The Treatment of Anxiety Disorders Clinician Guides and Patient Manuals
The Treatment of Anxiety Disorders Clinician Guides and Patient Manuals
The Treatment of Anxiety Disorders Clinician Guides and Patient Manuals
The Treatment of Anxiety Disorders brought together concise yet thorough theoretical reviews
with practical guides to treatment. In this completely revised second edition Gavin Andrews and
his co-authors review new developments in the research and treatment of anxiety disorders and
provide up-to-date treatment materials. Over half the material in the second edition is new, and
there is an entirely new section covering posttraumatic stress disorder. This is a unique and
authoritative overview of the recognition and treatment of anxiety disorders, giving Clinician
Guides and Patient Treatment Manuals for each. The Clinician Guides describe how to create
treatment programs, drawing upon materials and methods that the authors have used success-
fully in clinical practice for 15 years. The Patient Treatment Manuals provide session-by-session
resources for clinician and patient to work through, enabling each patient to better understand
and put into eVect the strategies of cognitive behavior therapy.
‘‘The Treatment of Anxiety Disorders is a well-referenced resource book and treatment guide.’’
ADAA Reporter
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The Treatment of
Anxiety Disorders
Clinician Guides and Patient Manuals
Second Edition
Gavin Andrews
Clinical Research Unit for Anxiety and Depression,
University of New South Wales at St. Vincent’s Hospital, Sydney
Mark Creamer
Australian Centre for Posttraumatic Mental Health (ACPMH), Melbourne
Rocco Crino
Anxiety Disorders Clinic, St. Vincent’s Hospital, Sydney
Caroline Hunt
School of Psychology, University of Sydney, Sydney
Lisa Lampe
Clinical Research Unit for Anxiety and Depression,
University of New South Wales at St. Vincent’s Hospital, Sydney
Andrew Page
School of Psychology, University of Western Australia, Perth
Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo
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isbn-13 978-0-511-06704-4 eBook (NetLibrary)
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isbn-10 0-511-06704-6 eBook (NetLibrary)
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isbn-13 978-0-521-78877-9 paperback
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isbn-10 0-521-78877-3 paperback
Every effort has been made in preparing this book to provide accurate and up-to-date
information which is in accord with accepted standards and practice at the time of
publication. Nevertheless, the authors, editors and publishers can make no warranties
that the information contained herein is totally free from error, not least because
clinical standards are constantly changing through research and regulation. The authors,
editors and publisher therefore disclaim all liability for direct or consequential
damages resulting from the use of material contained in this book. Readers are strongly
advised to pay careful attention to information provided by the manufacturer of any
drugs or equipment that they plan to use.
Although case histories are drawn from actual cases, every effort has been made to
disguise the identities of the individuals involved.
Contents
1 Read me 1
2 General issues in anxiety disorders 5
3 General issues in treatment: Clinician Guide 24
4 Panic disorder and agoraphobia: Syndrome 36
5 Panic disorder and agoraphobia: Treatment 54
6 Panic disorder and agoraphobia: Clinician Guide 65
7 Panic disorder and agoraphobia: Patient Treatment Manual 84
8 Social phobia: Syndrome 148
9 Social phobia: Treatment 164
10 Social phobia: Clinician Guide 177
11 Social phobia: Patient Treatment Manual 197
12 Specific phobias: Syndrome 261
13 Specific phobias: Treatment 271
14 Specific phobias: Clinician Guide 277
15 Specific phobias: Patient Treatment Manual 287
16 Obsessive–compulsive disorder: Syndrome 332
17 Obsessive–compulsive disorder: Treatment 346
v
vi Contents
References 555
Index 604
List of authors
Mark Creamer is Director of the Australian Centre for Posttraumatic Mental Health and a
Professor in the Department of Psychiatry at the University of Melbourne. He is a clinical
psychologist with many years of experience in the Weld of traumatic stress.
Rocco Crino is a clinical psychologist at St. Vincent’s Hospital. He is Director of the Anxiety
Disorders Clinic and Manager of Psychology at St. Vincent’s Hospital, Sydney.
Caroline Hunt is a clinical psychologist and Senior Lecturer in the School of Psychology,
University of Sydney. She is a clinician with many years of experience in the treatment of anxiety
disorders.
Lisa Lampe is a psychiatrist and Lecturer, School of Psychiatry, University of New South
Wales. She is a clinician with the Clinical Research Unit for Anxiety and Depression, Sydney,
and Director, Anxiety Disorders Program, Evesham Clinic, Cremorne, New South Wales.
Andrew Page is Associate Professor and Director of Clinical Psychology, School of Psychol-
ogy, University of Western Australia, Perth.
vii
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Preface to the second edition
The Wrst edition of this book was developed from the Patient Treatment Manuals
that had been used in the Clinical Research Unit for Anxiety and Depression for
the treatment of patients with anxiety disorders. Specialized treatment programs
for anxiety disorders were initiated in 1978 modeled on the treatment program for
adult stutterers with which Dr. Andrews had long been associated. John Franklin
designed and tested the Wrst program for patients with agoraphobia in 1979.
Since then programs for panic disorder and agoraphobia, social phobia, speciWc
phobias, generalized anxiety disorder, and obsessive–compulsive disorder have
been developed and tested. During these 20 years, many people have contributed
to the redevelopment and testing of the Manuals for the various programs.
SigniWcant contributions have been made by previous staV members of the unit, in
particular John Franklin, Paul Friend, Stephen MacMahon, Richard Mattick,
Carmen Moran, Conrad Newman, Susan Tanner, and Morison Tarrant. Robin
Harvey was the administrator of the Unit. Advice about the Wrst edition of this
book was forthcoming from Alex Blaszczynski, Anette Johansson, Colin MacLeod,
Richard Mattick, Hugh Morgan, Michael Nicholas, Cindy Page, Ron Rapee, Mark
Ryan, Derrick Silove, Michelle Singh, and Beth Spencer: their help is gratefully
acknowledged.
The second edition has been a much easier task. First, knowing that the Wrst
edition lacked a credible section on posttraumatic stress disorder, we invited Mark
Creamer, the Director of the Australian Centre for Posttraumatic Mental Health,
to contribute. Second, having taught from the book to graduate students and to
practicing clinicians for some 7 years we had clear ideas about the changes that
were necessary. Third, the explosive growth in the literature in the past 7 years
meant that revising the chapters was exciting, rather than boring. Fourth, the
natural development of the treatment programs in the clinic meant that the
treatment manuals are themselves quite altered and we are grateful for advice from
Stephanie Rosser and Merran Lindsay on this matter. Last, Dr. Page and Dr. Hunt
now work in clinics of other universities so their contributions contain knowledge
from those environments. Thus the book now comes from the clinics associated
ix
x Preface to the second edition
with four leading universities and is no longer the partisan view of CRUfAD.
Nevertheless we would recommend that readers supplement this book by recourse
to the CRUfAD website (www.crufad.org) for themselves and their patients.
The enthusiasm and guidance of Richard Barling and Pauline Graham of
Cambridge University Press is gratefully acknowledged.
Abbreviations
xi
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1
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situations. The book is written especially for psychiatrists and clinical psychol-
ogists to provide detailed knowledge about the process and pitfalls in conducting a
comprehensive cognitive behavioral program for the common anxiety disorders.
Clinical psychologists and psychiatrists learn about these techniques during their
training, but knowing about something is not equivalent to knowing how to do it.
The Patient Treatment Manuals are both the guidebook and the journey. They
allow clinicians to make the journey with the patient. In skilled hands these
programs comfort, commonly relieve, and quite frequently cure the disorder.
These programs can also ameliorate the underlying personality vulnerability to
anxiety.
This book contains six detailed Patient Treatment Manuals: for panic disorder
and agoraphobia, for social phobia, for speciWc phobias, for obsessive–compulsive
disorder, for generalized anxiety disorder and for posttraumatic stress disorder.
The publisher, Cambridge University Press, has agreed that these Manuals may be
photocopied by the purchaser of the book for the treatment of individual patients.
The Manuals are designed to be used as workbooks, and most patients annotate
and therefore personalize their copy with their own insights and with comments
from their clinician that are relevant to their particular circumstances. Apart from
copies of Manuals made by purchasers for their personal use in the treatment of
their patients, the Manuals – or indeed any other part of the book – may not be
copied, distributed, or sold. The standard provisions of copyright listed in the
front of the book apply.
Some patients with anxiety disorders can beneWt from simply being given the
Manual to read. However, most have already struggled to recover, and in these
persons signiWcant improvement and the prospect of cure come when a clinician
gives the appropriate Treatment Manual to a patient and then works through the
Manual with him or her, explaining, supervising, and supporting the process of
recovery. In this way the clinician’s expertise enables each patient to understand
and put into eVect the substance of the treatment. After treatment has concluded,
the Manuals, annotated with notes made during treatment, are commonly used by
patients to maintain their improvement and to inhibit relapse. In this sense they
do eventually become valid self-help manuals.
This book also contains separate Clinician Guides for the treatment of patients
with each of these disorders. These guides contain advice about the structures and
settings in which these programs have been shown to work, about patient charac-
teristics and behaviors that will require special skills if the progress of therapy is to
continue, and about critical issues in the therapeutic process. The guides are about
the art of therapy for patients with these disorders, and the Clinician Guides are
for clinicians’ eyes only. When the Wrst edition of this book was published the
Patient Treatment Manuals and the Clinician Guides were without precedent in
3 Read me
the therapy literature. They comprise three-quarters of the book. The remaining
quarter is much more conventional: an account of the scientiWc knowledge needed
for clinicians to understand the nature of the disorders aVecting their patients and
to evaluate the treatment options available.
When a clinician sees a patient with, say, agoraphobia and, after discussion of
the other possibilities, it is decided that a cognitive behavior therapy program is to
be the treatment of choice:
1. The clinician completes an assessment of symptoms and level of handicap,
incorporating appropriate rating scales and questionnaires, and then has the
patient identify and rate the extent to which their main problem interferes with
their life and activities.
2. The clinician explains the treatment to the patient using words like, ‘‘I am
going to teach you how to control your panics, enter feared situations, and
master your worrying thoughts. Here is a Manual that describes the program. I
want you to take the Manual home and look through it. Do remember to bring
it to your next session when we will begin to work through it together.’’
3. The patient is seen often, usually more than once per week, and at each session
a segment of the Manual is worked through, the clinician modifying the
information to make it appropriate to the patient’s disorder and level of
understanding. Homework exercises are then set and arrangements for the next
session are made.
4. Treatment proceeds quickly with most patients with agoraphobia improving
their panic control by session 3, being able to travel by session 6, and mastering
worrying thoughts by session 10. Treatment should conclude within 20
sessions with the clinician, the patient having spent an additional 40–60 hours
on homework during this time. The homework is focused on practicing the
anxiety management strategies, on graded exposure to feared situations, and
on identifying and combating dysfunctional cognitions.
5. When treatment concludes, the assessment measures made at the beginning are
repeated. Areas in which the patient needs to continue to make gains or to
consolidate are identiWed both from the therapy sessions and from the pattern
of scores on these measures. Patients are encouraged to continue their own
therapy by using both the Manual, now embellished with the additional
information, and techniques provided by the clinician during the therapy
sessions, and by periodic follow-up sessions with the clinician.
Clinicians of varying levels of expertise will use the book in diVerent ways.
Those new to the Weld, before treating a patient with, say, agoraphobia, should
read Chapters 2 and 3, the general overview and the general advice about treat-
ment, then proceed to Chapters 4 and 5 to review the scientiWc knowledge about
the nature and treatment of agoraphobia. Finally they should read Chapter 6, the
4 Treatment of Anxiety Disorders
Clinician Guide, about issues that may arise while treating patients with agora-
phobia, reading that in conjunction with Chapter 7, the Patient Treatment
Manual, for panic disorder and agoraphobia. Thus, when they begin to work with
the patient, they will be familiar with both the course of treatment outlined in the
Patient Treatment Manual and with the background information an experienced
clinician already has. Experienced and busy clinicians may initially skip the review
chapters but should still Wnd the general advice about treatment and the Clinician
Guide to agoraphobia essential, especially when diYculties arise during treatment.
In fact the Clinician Guide will be useful even when the Patient Treatment Manual
is not the principal treatment. That is to say, these treatment and clinician guide
chapters will also be valuable to many clinicians even when drug treatments are
being used, simply because many of the same diYculties will arise. In general,
clinicians using drugs as their main treatments will Wnd the chapters reviewing the
syndromes and those reviewing treatments to be informative, for patients invari-
ably ask about their disorder and expect their clinician to be conversant with the
literature.
This book is for practicing clinicians. It provides most of the information
needed for the successful treatment of patients with anxiety disorders.
2
NEUROTICISM
COPING
Figure 2.1 A model of the relationship among neuroticism, life events, appraisal, arousal, coping, and
symptoms of anxiety.
but adverse life events are neither necessary nor suYcient to explain the onset of
GAD. Many untoward life events that appear threatening at the time are found to
be benign. It is the appraisal of the event that conditionally identiWes an event as
potentially threatening.
Appraisal
When an untoward and potentially threatening event occurs one asks ‘‘Is this a
threat to me?’’, meaning is the threat unpredictable and uncontrollable. The event
is appraised in terms of one’s prior experience with similar events and in terms of
community knowledge about the level of threat associated with such events. Some
of this appraisal is deliberate whereas some, conducted at an automatic or
unconscious level, seems more driven by irrational thoughts of danger. When the
threat is ambiguous and accurate appraisal is diYcult, the automatic danger
schemas become more inXuential.
It is not the ‘‘things that go bump in the night’’ that produce anxiety but the
meaning given to them. For example, if one is awakened by a creaking door and
decides that the cat has caused the door to creak, then it is easy to go back to sleep.
If one decides that the noise could be caused by intruders, one instantly becomes
alert and anxious, with heart pounding and mouth dry as one rehearses what to
do. Once it has been established that the noise was caused by the cat, it is easy to go
back to sleep. Thus it is not the event but the thoughts about the event that cause
anxiety. Therefore the best way to reduce the anxiety is to evaluate the situation
carefully, decide what to do, then just do it. Most events that cause signiWcant
anxiety are complex and, as the full import of the event takes time to unfold,
appraisal and coping are iterative processes.
stopped for speeding, will get Wnes for noncompliance as well as for speeding, and
will remain aroused for a considerable time afterward. When confronted with the
truck, they will become so debilitated by anxiety that they will do exactly the
wrong thing and be killed.
Precisely because of the inXuence of trait anxiety or neuroticism on state
anxiety, the anxiety disorders used to be considered manifestations of personality
vulnerability. Neuroticism is probably the single most powerful risk factor and
determinant of symptoms. In our large twin sample (Andrews et al., 1990c), we
found neuroticism, measured by the Eysenck Personality Questionnaire Neuroti-
cism Scale (Eysenck and Eysenck, 1975), to be a stable characteristic, with test–
retest polychoric correlations of 0.9 at 4-, 8-, and 12-month intervals, even though
there is evidence of a gradual reduction over longer time periods. Krueger et al.
(2000) reported that the construct ‘‘stress reaction’’ was related (eVect size 0.7) to
current and future anxiety and depressive disorders. Neuroticism is clearly a
surface marker for some underlying trait related to the appearance of anxiety and
depressive symptoms.
There is a strong relationship between high neuroticism and anxiety disorders
(Brown et al., 1998). Patients with panic and agoraphobia, social phobia, OCD,
and GAD who do not have scores more than one standard deviation above the
mean are rare (Andrews et al., 1989), and should be investigated further. While
signiWcant, the association of neuroticism with PTSD is less absolute. Persons with
high neuroticism have been shown to experience an increased level of signiWcant
interpersonal life events regardless of whether questionnaire or interview methods
are used to determine the occurrence of signiWcant events (Poulton and Andrews,
1992). That both methods have conWrmed the relationship suggests that the
Wnding is not simply an artifact of a plaintive set. It is probably evidence of the
debilitating eVects of neuroticism and anxiety on interpersonal relationships.
High neuroticism scores are associated with the major anxiety disorders. A high
score is also associated with a more extensive lifetime history of neurotic illness
(Andrews et al., 1990c) and with a higher likelihood of relapse after treatment
(Andrews and Moran, 1988).
propensity to carry out this type of behavior. Locus of control scores behave as
though they were trait measures, being stable over time (test–retest polychoric
correlations at 4, 8, and 12 months being 0.7). Patients with anxiety disorders
characterize themselves as powerless on measures of locus of control, not only
unable to cope with adversity but unable to use external help to enable them to do
so (Sandler and Lakey, 1982). The higher the score (higher is used to mean more
external in orientation, more powerless), the greater is the history of past anxiety
disorder and the higher the probability of relapse after apparently successful
treatment (Andrews and Craig, 1988; Andrews and Moran, 1988).
Moderate anxiety can act as a positive force, potentiating eVective action.
However, anxiety that is too severe debilitates and reduces the individual’s ability
to perceive, reason, and act appropriately. Hence, integral to any notion of coping
with stress is the salience of some automatic defensive mechanism that functions
to maintain composure and limit the debilitating eVects of high anxiety. Vaillant
(1971) has shown the importance of such defense mechanisms in the long-term
adaptation of university graduates followed for 30 years. Mature defenses (antici-
pation, suppression, sublimation, humor) acknowledge the nature and extent of
the threat but directly limit the level of arousal and consequent anxiety. We have
used the Defense Style Questionnaire (Andrews et al., 1989; Andrews et al., 1993b)
to describe such mechanisms. The questionnaire functions as a trait measure
(test–retest correlation 0.75 over 1 to 18 months), shows a gradual maturation
with age, and discriminates people with anxiety disorders from normal controls.
This measure is abnormal in people with panic and agoraphobia, social phobia
and OCD, but, like neuroticism and locus of control, does not distinguish between
these disorders (Andrews et al., 1993b).
0.57 0.88
Hypothetical ILLNESS
state
0.87
Hypothetical VULNERABILITY
trait
0.83 0.54
Measures
Neuroticism Locus of control
Figure 2.2 The relation between the latent variable of vulnerability to illness as measured from Neuroti-
cism and Locus of Control measures and the latent variable of illness as measured from
lifetime prevalence of a neurotic diagnosis and symptoms of anxiety and depression over a
16-month period.
symptom measures taken on four occasions over the 16 months. Because the three
vulnerability measures (trait anxiety, locus of control, and defense style) are
correlated, there must be overlap in the domains of information tapped by each
questionnaire (Andrews et al., 1989). To elucidate this hypothesis we conducted a
multivariate genetic analysis of these three vulnerability factors. Results are dis-
played in Table 2.1 (for the full analysis, see Andrews, 1991). While each of the
three measures appears to be inXuenced by speciWc genetic and environmental
factors, there is a signiWcant loading on common genetic and environmental
factors that contributes to each measure. This Wnding is consistent with the
proposition that the three measures are interrelated – perhaps showing that
externalized locus of control and immature defense style are the consequence of
neuroticism, or perhaps showing that all three of these measures reXect some
common underlying pattern of neurological organization.
We have used canonical correlations in a group of adolescents to estimate the
relative importance of these three measures in determining anxiety and depressive
symptoms and report the following values: neuroticism 0.6, locus 0.2, defense style
0.3 (Andrews et al., 1993a). Their relative roles in determining chronicity once a
person is ill with the speciWc symptoms of an anxiety disorder may, of course, be
quite diVerent.
13 General issues in anxiety disorders
Table 2.1 Parameter estimates for the preferred multivariate model of the unique and
common individual environment (E) and additive genetic (H) components of the
vulnerability factors: neuroticism, locus of control and defense style
Vulnerability factor E H E H
Comorbidity
The occurrence of other disorders in association with speciWc anxiety disorders is
frequent (Kessler et al., 1994; Andrews, 1996a; Andrews et al., 2001a) and is of
therapeutic interest. If the association is because both disorders are due to the
same causative factor, then good treatment should target this vulnerability factor.
If the comorbid condition is secondary to the anxiety disorder, then treatment of
the anxiety disorder should also relieve this secondary illness. Finally, if the anxiety
disorder is secondary to the associated condition, then treatment of the primary
condition is essential.
2.0
CLINIC
Deviation from population means (SD units) 1.8
SAMPLE
1.6
1.4
1.2 TWIN
SAMPLE
1.0
0.8
0.6
0.4
0.2 Locus
Neuroticism
0.0
1 2 3 4 5
Number of diagnoses
Figure 2.3 The relation between vulnerability factors as measured by Locus of Control and Neuroticism
and number of neurotic diagnoses reported in lifetime to date for two samples – one drawn
from an anxiety disorders clinic and one from a quasi-population sample of adult twins
(redrawn from Andrews, 1991).
these scales measuring vulnerability to anxiety and depression, the more extensive
is the lifetime history of illness. The clinic attenders showed signiWcantly higher
vulnerability scores for a given illness history, which may indicate that illness in
the setting of a vulnerable personality determines the need to seek specialist
treatment, whereas illness alone is not so directly related to treatment-seeking.
Good treatment should therefore seek not only to remedy the individual symp-
toms but also to change the underlying vulnerability. If patients are to be cured,
i.e., after treatment have only the population risk of developing the same illness
anew, then such vulnerability must be lessened.
In an earlier study that involved a 15-year follow-up of patients initially
hospitalized with anxiety or depressive neuroses (Andrews et al., 1990a), we
searched for information available at the initial admission that might predict
long-term outcome. Personality was found to be the most important of the items
measured at intake. In a structural equation model, personality vulnerability, as
judged from measures of neuroticism at the initial admission, accounted for 20%
of the variance in outcome over 15 years. This eVect was not evident in patients
with aVective psychoses. We see this result as further support for the importance
of personality traits as determinants of the genesis and chronicity of anxiety and
depression, and another reason to recommend that attention to personality traits
be required if a treatment program seeks to do more than remedy the current
episode of illness.
The information from this method of examining the meaning behind the
comorbidity information is consistent with a two-factor theory of neurosis. The
Wrst factor is a general vulnerability to neurosis as evidenced by high trait anxiety
and poor coping. The second factor is a vulnerability to a speciWc disorder that is
presumably related (as most of the core disorders have Wrst symptoms in adoles-
cence or in early adult life) to familial, even nongenetic, inXuences that sensitize
one person to fears of bodily dysfunction, another to fears of social disapproval,
and a third to fears of harmful thoughts, and so on.
Substance abuse disorders are the other conditions that are reported to be more
frequent than expected in patients with anxiety disorders. There are three possible
mechanisms for such an association. First, a drug such as amphetamine or cocaine
could produce the symptoms of anxiety and, conceivably, those of an anxiety
disorder. There is a literature that the Wrst panic attack can occur while using drugs
(Moran, 1986) and that the Wrst panic can also follow drug or alcohol withdrawal.
The second association concerns the observation that many alcoholics and drug
users report that their dependence began as a mechanism to reduce their anxiety.
Reporting biases do aVect such rates, and Mulder et al. (1991) have discussed these
eVects. In which direction is the association? A review by Kushner et al. (1990)
concluded that in agoraphobia and social phobia the alcohol problems are more
likely to follow from attempts at self-medication of anxiety symptoms, whereas
the association in panic and GAD is more likely to follow pathological alcohol
consumption.
In our own clinic we examined the prevalence of substance use disorders among
patients being treated for panic, agoraphobia, or social phobia and compared
these rates with the risks in the general population. When the eVects of sex were
controlled, the overuse of alcohol and medication was raised in all diagnoses, with
the exception of males with panic disorder. Social phobics exhibited rates of
problem alcohol use three to Wve times greater than those in the control group. In
all diagnoses and sexes, rates of sedative or hypnotic abuse were six to 12 times
greater than the rates in the population. These high rates were deemed to be
secondary to the anxiety disorder.
discussed in the relevant chapters, but some of the general issues will be mentioned
here. A clinical diagnosis unsupported by other assessment tools may no longer be
good mental health practice. Unsupported diagnoses are no longer good practice
in any other branch of clinical medicine.
Forty-eight years ago, Meehl (1954) compared the accuracy of clinical versus
statistical prediction on the same data. He concluded that statistical predictions
were as least as accurate, and often more accurate, than the judgments of trained
clinicians. Clinicians were indignant at Meehl’s conclusions, for they considered
that their judgments were the ‘‘gold standard’’ against which the tests had been
developed and standardized. How could a statistical compilation of the tests be
better than their judgments about the tests? The answer lies in reliability. Clinical
judgment about the same data may vary from occasion to occasion and between
any two sets of clinicians. Statistical compilations do not vary in this manner.
Reliability is important because it is a prerequisite for validity. If a clinician cannot
reach the same diagnosis on two occasions when reviewing the same clinical data,
then the validity of at least one of the decisions is questionable. If two clinicians
given the same clinical data cannot agree, then both cannot be correct, and the
treatment prescribed by at least one of them will be wrong. Valid judgments
depend on reliable judgments.
Structured diagnostic instruments were developed to improve the reliability of
the clinical judgment as to how well a patient’s complaints satisWed the diagnostic
criteria. Such interviews have usually achieved their goal by modeling a clinical
interview, the gains in validity coming from standardizing the content of the
questions, as well as from the form of the interview and the scoring process. No
matter how perfect the structured diagnostic interview, validity will be limited to
the validity inherent in the diagnostic criteria on which that interview is based, and
by the exactness with which the interview elicits the behaviors, thoughts, and
feelings described by those diagnostic criteria. Interviews presently available were
reviewed by Page (1991b).
The Anxiety Disorders Interview Schedule for DSM-IV (ADIS-IV) (Brown et
al., 1994) is a semi-structured clinician administered diagnostic interview that
produces DSM-III-R diagnoses. This schedule is very thorough, covers all the
anxiety disorders, but can take two hours to administer. If the interviewer is
appropriately trained, the ADIS-IV can provide a detailed and reliable assessment.
The principal use is in small-scale clinical research requiring a very detailed
assessment.
The CIDI is a fully structured diagnostic interview that can be administered by a
trained interviewer. The computerized CIDI-Auto can be completed by an inter-
viewer or directly by the patient, the computer taking care of the logic of this
complex interview (Andrews and Peters, 1998). It was developed from the
20 Treatment of Anxiety Disorders
Diagnostic Interview Schedule under the auspices of the World Health Organiz-
ation and generates both ICD-10 and DSM-IV diagnoses. The CIDI is in modular
form and covers the major categories of mental disorders. The interviewer version
takes 30 minutes to cover the anxiety disorders, while the computerized version
takes virtually no clinician time. The CIDI is reliable and widely used, being
available in 14 languages. The principal uses are in epidemiological surveys,
clinical research, and in clinical practice. Validity studies suggest a need for greater
speciWcity, as the CIDI commonly identiWes more comorbid diagnoses than do
clinicians. However, diagnoses that are not critical can be quickly dismissed by the
clinician, while false negative diagnoses, which would be of greater concern, are
rare.
The Schedule for AVective Disorders and Schizophrenia (Endicott and Spitzer,
1978) is a semi-structured interview that has acceptable reliability and validity but,
being time consuming, is most appropriate for clinical research. The Schedule for
Clinical Assessment in Neuropsychiatry is a semi-structured diagnostic interview
for experienced clinicians that can generate DSM-IV and ICD-10 diagnoses,
although the scoring can be complex. This schedule aims to describe symptoms in
a fashion that is independent of the current classiWcations. Good clinical judgment
and considerable training is required before reliability is obtained. The Structured
Clinical Interview for DSM-IV (First et al., 1997) is a semi-structured interview.
The anxiety subsection is reliable and suitable for clinical research and practice.
However, training is required.
There are a large number of questionnaires and rating scales that have been
developed for the assessment of patients with anxiety disorders. Most clinicians
have areas of special interest and will already be using appropriate scales. Test
batteries suitable for clinical practice are described in subsequent chapters.
mental disorders was larger in those countries but because the burden of infectious
and perinatal diseases was less. Only three anxiety disorders, PTSD, OCD and
panic disorder, were included in the 1996 report, but it was of interest that the
burden of those three disorders was, in the established market economies, equival-
ent to the burden of schizophrenia, each accounting for one-tenth of the burden of
the mental disorders. The Wrst set of burden calculations to include all the anxiety
disorders was that published by Mathers et al. (1999). They reported that the
anxiety disorders accounted for 24% of the burden of mental disorders in Austra-
lia. AVective disorders accounted for a third of the burden and schizophrenia 5%
of the burden. Accompanying their estimates was a table of expenditure that
showed that the anxiety disorders accounted for only 8% of the mental health
system costs, despite accounting for 24% of the burden.
The anxiety disorders are common, probably the most common of all the
mental disorders. The reported lifetime risks for each disorder have varied con-
siderably according to the population being studied and the method being used.
The USA national comorbidity survey of adults aged 15 to 54 years reported that
17.2% of adults had met criteria for an anxiety disorder in the past 12 months.
These are the highest rates ever reported and this may be due to methodological
factors: Kessler et al. (1994) used commitment and stem probes to enhance
responses, adjusted for the higher morbidity among nonrespondents, used DSM-
III-R criteria that did not have the clinical signiWcance of DSM-IV criteria.
Furthermore they asked about simple phobias that are not often a focus of clinical
practice, utilized the wider DSM-III-R criteria for social phobia, and of unknown
importance, inferred 12-month risk by asking whether respondents, who had met
criteria in their lifetime, had had symptoms in the past 12 months, not whether
they had met criteria during that time. The matching 12-month data from the
Australian survey are presented in Table 2.2 (Andrews et al., 2001a). In this survey
it was ascertained that people had met criteria for an anxiety disorder during the
12-month period. In both surveys the anxiety disorders were the most common
class of mental disorder.
In the Australian survey of people aged 18 to 99 years (i.e., being representative
of the whole adult population), with exclusion criteria operationalized, DSM-IV
anxiety disorders had a 12-month prevalence of 5.6% and a one-month prevalence
of 3.8%. Those with current symptoms reported being unable to work, or having
to cut down on what they did, an average of 10 days out of the past 28 days, and
their SF-12 mental competency score was 35.9, signiWcantly below that of the
average for all people with a current mental disorder. Anxiety disorders are
disabling. Anxiety disorders were more common in females (odds ratio or
OR = 1.6), less common in people over 54 (OR 0.4), more common among those
separated, widowed or divorced (OR 1.9) or never married (OR 1.4), and less
22 Treatment of Anxiety Disorders
Table 2.2 Twelve month prevalences of anxiety disorders in Australia (DSM-IV) and the
USA (DSM-III-R), exclusion criteria not operationalized
% SE % SE
common among those with tertiary education or in the labor force (0.6). The
demographic correlates of depression were virtually identical.
These disorders commonly begin early. The median age of onset for speciWc
phobias is in childhood, for social phobias and OCD is in middle and late teenage,
respectively, and for panic, agoraphobia, and GAD it is between 20 and 30 years of
age. Many years pass between the onset of most disorders and patients obtaining
treatment. Overall females are more commonly aVected than males but in treat-
ment programs for social phobia, OCD, and GAD, the sex ratios are close to
parity. There is an important association between suicide attempts and anxiety
disorders in young people.
In the Australian survey (Andrews et al., 2001b), only 44% of current cases had
sought help ‘‘for a mental problem’’ in the previous 12 months. They were equally
distributed between people who saw a general practitioner only, who saw a
psychiatrist or psychologist as well, or who saw other health professionals. They
averaged nine consultations in the year and accounted for 39% of all consultations
for a mental problem. Half got a prescription, half got nonspeciWc counseling, and
only one-sixth got cognitive behavioral therapy, the treatment of choice. The
probability of seeking help was related to age, sex, disability, and marital status.
Only 20% of males aged less than 24 years or over 54 years consulted, whereas 75%
of females, aged 25 to 54 years and disabled and no longer married, consulted. The
perceived need for treatment among those who did not consult was for informa-
23 General issues in anxiety disorders
tion and psychological treatment, not for medication, the treatment most
commonly oVered. Perhaps that is why they did not consult.
In the past 20 years, there has been an explosive growth in knowledge about the
anxiety disorders. Diagnostic criteria are agreed upon, and diagnostic and other
assessment instruments have been shown to be reliable and valid. This book will
demonstrate that the treatments are eYcient and eVective. Information as to
causes, both speciWc and general, is emerging. It now behooves clinicians to treat
patients with anxiety disorders actively and well.
3
EVective treatments for the anxiety disorders are reviewed in this book. Some
treatments – the cognitive behavioral therapies (CBTs) for the major anxiety
disorders – are described in considerable detail. The background to the principal
cognitive behavioral techniques will be described in this chapter, together with the
clinical issues that are important if clinicians are to convert this group of tech-
niques into an eVective treatment.
once a strong proponent of exposure therapy, has argued that fear reduction is
possible by all of the above techniques.
Dearousal strategies
Hyperventilation control
Breathing more deeply than is normal is part of the normal physiological response
to threat. Hyperventilation to the point of developing symptoms (lightheaded-
ness, dizziness, shortness of breath, feelings of suVocation, tingling or numbness in
limbs, rapid heartbeat, chest pain or pressure, feelings of unreality) has long been
observed in patients with anxiety disorders (Lowry, 1967; de Ruiter et al., 1989a;
Holt and Andrews, 1989b). Kerr et al. (1937) used voluntary hyperventilation as
an educational technique for such patients, presumably to familiarize patients
with the cause of their symptoms. The emphasis in recent years has been on the
importance of the hyperventilation response as a complication to panic (Garssen
et al., 1983), and investigation of the treatment of overbreathing has been almost
totally conWned to this disorder. Rapee (1985b) presented a single case study in
which the importance of hyperventilation in panic attacks was demonstrated to
the patient by drawing attention to the similarity between the symptoms of panic
and the symptoms produced by voluntary hyperventilation. He then had the
patient repeatedly count her respiration rate at rest. Finally, the patient practiced
slowing her respiration to an 8-second cycle and was encouraged to use this
breathing rate whenever she noticed a panic attack beginning.
Clark et al. (1985) and Salkovskis (1986a) published two series of cases illustra-
ting the eVectiveness of voluntary hyperventilation for treating panic. After ex-
periencing the symptoms produced by a period of voluntary hyperventilation (a
form of interoceptive exposure), patients were able to control their panics better
because they could reattribute the cause of their panic symptoms. These patients
were then trained to breathe at a 5-second cycle and instructed to use this rate to
control panics whenever they occurred.
The traditional cure for the symptoms of hyperventilation is to breathe into a
paper bag to let the carbon dioxide level increase. There is no evidence that this
technique is eVective, presumably because it is never done as soon as the anxiety
begins, or continued for long enough to produce the desired eVect. The slow-
breathing technique appears to work because the patient can initiate the slow
breathing immediately anxiety or panic is anticipated and, because of the over-
learning produced by regular practice, the technique can be deployed even when
the patient is debilitated by the imminent anxiety or panic. Whether it works
because it corrects the hyperventilation, because it distracts from the situation, or
because it produces a relaxation response is unknown. There is sensible evidence
that total reliance on controlling panic attacks by hyperventilation control may be
26 Treatment of Anxiety Disorders
maladaptive as the person never learns that panic attacks are not dangerous
(Schmidt et al., 2000) but when coupled with interoceptive exposure to panic
symptoms it remains of value. Hyperventilation control is one control technique
that remains valuable when people are acutely anxious for whatever reason.
Meditation
Benson (1976) introduced a simpliWed yoga technique to the Western world in
which subjects were instructed to sit quietly in a comfortable position, close their
eyes, and concentrate on breathing and saying the word ‘‘one’’ each time they
breathed out. Continuing this for 10 to 20 minutes and concentrating on the task
whenever thoughts wandered, they would beneWt by a feeling of calmness and a
reversion of the Xight or Wght response. Benson produced data on the short-term
changes that would result. It has never been shown to be of beneWt in an anxiety
disorder but patients, especially those with high neuroticism scores, report beneWt.
Again this is a control of arousal technique but not one that can be used in any
acute situation.
Deep muscle relaxation was introduced to the Western world by Jacobson
(1962). This technique involves the alternate tensing and relaxing of all muscle
groups, often guided by a tape-recorded script. It, too, produces a lowering of
arousal but the results have never been shown to be superior to placebo in people
with anxiety disorders. Once people have learnt to use muscle contraction and
release to produce a relaxation response they can use the abbreviated form of
isometric deep muscle relaxation to produce a relaxation response in stressful
situations. The experience of being able to control arousal by using isometric
relaxation is beneWcial, and regular practice of progressive muscular relaxation is
beneWcial for the muscle tension that is seen in people with GAD.
Exposure
Graded exposure is perhaps the most powerful technique assisting patients to
overcome feared situations. The roots of these procedures are Wrmly based in
learning theory as habituation or graduated extinction. In short, the procedures
involve the gradual re-exposure of the individual to the fear- or anxiety-evoking
stimuli. On the basis of information supplied by the patient, the therapist devises a
series of exposure tasks arranged hierarchically, so that engagement in those
behaviors can be performed without overwhelming anxiety. Progress through the
hierarchy is systematic, commencing with behaviors that are minimally anxiety
provoking and progressing through mastery of those to tasks that are more anxiety
provoking.
Although similarities in form and mechanism may be noted with systematic
desensitization (which primarily involves exposure in imagination), the pro-
27 General issues in treatment: Clinician Guide
cedures involved in graded exposure diVer in two important ways. First, as much
as possible of the exposure is conducted in the real world rather than in imagin-
ation. Second, no competing response such as relaxation is taught, and no
response is designed to replace the anxiety response when the individual is
exposed to the fear-evoking stimuli. All persons have to learn for themselves that
their anxiety is groundless.
Exposure to fear-evoking cues as a method of alleviating anxiety is by no means
a new procedure. Johann Wolfgang von Goethe provided an excellent account of
self-directed exposure undertaken in the early 1770s to overcome a fear of heights,
noise, darkness, and blood injury. In describing his self-administered treatment,
he states, ‘‘Such troublesome and painful sensations I repeated until the impres-
sions became quite indiVerent to me’’ (cited by Eysenck, 1990).
Herzberg (1941) used graded exposure techniques to successfully treat a severe-
ly agoraphobic woman who was previously unable to leave her house. Grossberg
(1965) utilized graded exposure techniques in the treatment of a woman with a
circumscribed social phobia (fear of public speaking), allowing her to complete
the graduation requirements of the college. Since these early investigations,
controlled replication and extension of these applications have been undertaken,
with the result that exposure therapy has become an integral part of the behavioral
treatment of panic/agoraphobia, social phobia, speciWc phobias, OCD, and
PTSD.
Exposure to the feared stimulus, leading to the conclusion that the fear is
groundless, is the key. For many people the feared stimuli are the symptoms
themselves, e.g., rapid heart beat in panic, or intrusive thoughts in OCD. In-
teroceptive exposure refers to the graded exposure to such internal symptoms
until the suVerers lose their power to evoke anxiety. In panic disorder, interocep-
tive exposure is especially important in providing control.
Cognitive therapy
Although cognitive therapy is a relatively recent addition to behavioral pro-
cedures, the premise behind these techniques has a long history. The Wrst century
Greek philosopher Epictetus asserted that we are not aVected by events but by our
interpretation of those events. Changing the interpretation of events therefore
should exert an inXuence on the eVect those events have over the individual.
Cognitive methods such as those espoused by Ellis (1957, 1962) derive directly
from the belief that psychological disorders are the result of faulty or irrational
patterns of thinking. The therapeutic techniques utilized in Rational Emotive
Therapy aim to modify the irrational and faulty thinking and beliefs, replacing
them with more rational patterns, and therefore alleviating the disorder. The
essential feature is seen in the A-B-C-D-E paradigm.
28 Treatment of Anxiety Disorders
Clinical issues
Diagnosis
All persons likely to beneWt from treatments described in the manuals in this book
suVer from panic disorder, agoraphobia, social phobia, speciWc phobia, OCD,
GAD or PTSD. Failure to respond to previous treatment is not in itself a
contraindication. Severity and chronicity are, if anything, positive criteria on
which to select patients. Being severely handicapped and outraged at the interfer-
ence that the disorder has produced in their freedom to live normally provides
many patients with the impetus needed to work hard to recover. Recovery from an
anxiety disorder is hard work and requires considerable courage.
The clinician is responsible for the accurate diagnostic work-up required to
ensure that the symptoms meet the diagnostic criteria of ICD-10 or DSM-IV. A
behavioral analysis that makes clear the circumstances that aVect the occurrence of
the symptoms and the cognitions that co-occur is also required. Curiosity seems
to be the greatest attribute for a cautious clinician. ‘‘In case what occurred?’’ is the
key question that is commonly used to elucidate the Wnal fear. ‘‘In case I had a
heart attack’’, ‘‘In case others saw me anxious and thought me weak’’, ‘‘in case
harm to my family occurred’’, ‘‘In case everything went wrong’’, ‘‘In case the
memories came back’’ are the thoughts characteristic of the individual anxiety
disorders. Once the principal complaint is identiWed we recommend that the
patients rate the extent that the disorder interferes with their life and activities
(Figure 3.1). This scale serves two purposes: (1) it identiWes the patient’s principal
goal in coming for treatment right at the beginning; and (2), when used repeated-
ly, it provides a sensitive and personalized measure to assess the reduction in
handicap that follows good treatment.
Comorbidity
If two disorders coexist, and the anxiety disorder is judged to be primary and the
comorbid condition secondary, then obviously it is better to treat the anxiety
disorder. The single exception is substance abuse. Even persons who originally
took alcohol or benzodiazepines for their anxiety disorder must cease their drug
use before treatment for their anxiety disorder will be practical. Persons who have
taken benzodiazepines for a long time and have become very dependent on them
may not be able to be withdrawn and hence will not be able to fully beneWt from
the cognitive behavioral techniques. Some persons adjust to chronic benzo-
diazepine intake and it is a foolish clinician who seeks to get each and every such
patient to cease this medication. One must consider the gains and costs of such a
step. Withdrawal from benzodiazepines is diYcult. We recommend that persons
transfer to a long-acting benzodiazepine such as diazepam and then reduce their
31 General issues in treatment: Clinician Guide
After having discussed things with the doctor, you have said that your main
problem is:
At the present time, how much does this problem interfere with your life and
activities?
(please circle the number closest to your response on the rating scale below)
1 2 3 4 5 6 7
dose by 10% of the preceding dose every 3 days. Even so it may take 10 weeks to
withdraw and the last stages will be the most diYcult.
If the anxiety disorder appears in the setting of another disorder, and is
secondary to this disorder, then it will do little good to oVer treatment for anxiety
until the primary condition is resolved. If two conditions coexist but neither is
causative, then the clinician should treat either the disorder that is more disabling
or that which is easiest to remedy. The contraindication to treatment for anxiety
disorders is concurrent substance abuse, because people cannot learn to control
their anxiety while aVected by, or still craving, drugs or alcohol.
Florid and severe personality disorder is another contraindication, simply
because the anxiety is likely to be the least of the patient’s diYculties. Often
referrals of such patients to cognitive behavioral clinicians are acts of desperation
in the hope that, somewhere, something can be done. Patients with psychoses
certainly become anxious, and while the essential treatment should be aimed at the
psychosis, help with anxiety using cognitive behavioral techniques can be of value.
In our experience it is best if the therapist responsible for treating the psychosis
carries out the CBT, simply because this therapy has to blend with the other
treatments.
Patient motivation
The Wrst question to be asked is ‘‘Why did you come for treatment now?’’. If the
answer involves family, medical advisors, or other external factors then clinicians
should be cautious before accepting the patient for treatment and inquire further
32 Treatment of Anxiety Disorders
should determine the reasons for the hesitation and encourage the patient to
continue. Encouragement may take the form of pointing out the patient’s achieve-
ments to date, as well as the personal cost of continuing to be aVected by the
condition. Commonly, patients are more concerned with the tasks they must
complete as part of treatment. By focusing only on the task at hand, they tend to
lose sight of their achievements, as well as forgetting the distress and discomfort
their condition has caused them. Focusing the patient on these wider issues in
times of waning motivation often helps to stabilize the situation. Motivational
interviewing is discussed in Chapter 14.
In all anxiety disorders, patients have to face their fears if fears are to lose their
salience. Refusal by the patient may reXect poor program design or may be a
function of anticipatory anxiety. A re-examination of the program with the
patient may be required in order to determine whether the expected rate of
progress is too rapid or unrealistic. If it is, a more graded program of exposure can
be set. If anticipatory anxiety is the key, then reinforcing achievements as well as
analyzing the expected diYculties using cognitive restructuring may assist. Finally,
and of considerable importance, humor is an essential and invaluable tool for
assisting patients to deal with, and face, diYcult situations. Humor is, and always
has been, one of the best defenses against anxiety.
Therapist motivation
It is very easy for clinicians to become demoralized. By deWnition, all clinicians see
the diYcult-to-treat and slow-to-recover patients a large number of times. They
35 General issues in treatment: Clinician Guide
see the quick-to-recover patients much less frequently. Thus, whenever they look
at their appointment books they experience a sense of relative failure; the book is
full of the slow-to-improve patients. This is as it should be, for once the quick-to-
improve patients have recovered they do not return but continue with their lives
independently of continuing medical or psychological help. Colleagues reinforce
this whole process by saying they have just seen your patient who is once again
having diYculties. One forgets that, by deWnition, they will never see your other
patients who are doing well. We have done a number of follow-up studies and the
results have routinely been reassuring; the total cohort of patients does, on
average, twice as well as the patients who currently Wll the waiting room.
All this angst over therapist eVectiveness would be academic if demoralization
in the clinician did not lead to a sense of futility, a sense that carrying out speciWc
treatment programs may not be worthwhile, and the nihilistic idea that the ‘‘What
shall we do today?’’ type of therapy is permissible. It is not. The key message of this
book is that speciWc and eVective treatments exist. Therapists must therefore make
an accurate diagnosis and from this develop an appropriate therapy plan. Once
this plan is made, there is only one step to take. Just do the therapy to the best of
your, and your patient’s, abilities.
4
Individuals with panic disorder and agoraphobia present for treatment describing
‘‘panic attacks’’ and varying degrees of fear-driven situational avoidance. Corres-
pondingly, treatment aims to modify the symptoms that the person labels as
‘‘panic attacks’’ and to reduce any avoidance. Even though the causal link between
panic disorder and fearful avoidance is recognized, the major diagnostic systems
draw a qualitative distinction between the panic attacks and agoraphobic avoid-
ance.
Diagnosis
DSM-IV implies a temporal relationship between panic attacks and agoraphobic
avoidance. A panic attack is characterized by: fear; feeling dizzy or faint; choking,
shortness of breath, or smothering; and fears of dying, going crazy, or losing
control. Primacy is given to panic disorder, which describes recurrent unexpected
panic attacks or incapacitation caused by panic attacks (characterized by concern
about additional attacks or worry about the consequences of future attacks). A
diagnosis of panic disorder is typically given as occurring with or without agora-
phobia. Agoraphobia is deWned as ‘‘anxiety about being in places or situations in
which escape might be diYcult (or embarrassing) or in which help may not be
available in the event of having an unexpected or situationally predisposed panic
attack’’. Situations characteristically avoided include being outside the home
alone, traveling alone, being in tunnels, on bridges, and in open spaces. Agorapho-
bia without a history of panic attacks remains in the nosology, probably for
historical reasons. In epidemiological studies, the diagnosis appears not infre-
quently (e.g., Robins and Regier, 1991), but such cases are rarely seen in clinical
practice. When individual cases are examined, either they involve anxiety attacks
that do not meet the particular cut-oV scores for a DSM or ICD diagnosis of a
panic attack (Barlow, 1988), or they appear to be better described as a speciWc
phobia (i.e., claustrophobia; Friend and Andrews, 1990). In contrast to DSM-IV,
36
37 Panic disorder and agoraphobia: Syndrome
ICD-10 does not imply a primacy of panic attacks in its nosological structure.
Agoraphobia is listed under phobic anxiety disorders and is deWned behaviorally
by ‘‘an interrelated and often overlapping cluster of phobias embracing fears of
leaving home: fear of entering shops, crowds, and public places, or of traveling
alone in trains, buses, or planes . . . The lack of an immediately available exit is one
of the key features of many of these agoraphobic situations.’’ Although agorapho-
bia is acknowledged to occur with or without panic disorder, panic disorder (or
‘‘episodic paroxysmal anxiety’’) itself is placed within a category of ‘‘other anxiety
disorders’’.
Empirical studies favor the organization found in DSM-IV rather than in
ICD-10. In patients who seek treatment, panic disorder typically occurs before
agoraphobia (Aronson and Logue, 1987; Franklin, 1987; Garvey et al., 1987).
Agoraphobia is characterized less by a fear of certain situations and more by a fear
of having a panic in those situations (Franklin, 1987).
In terms of clinical practice, the separation between the two disorders primarily
serves a descriptive function indicating the extent to which a person is going to
require treatment that targets the agoraphobic avoidance in addition to merely the
panic. The greater the avoidance, the greater the amount and proportion of time
that will be spent modifying the avoidance. In our experience, it is very rare to see
an individual with long-standing panic attacks who has no situational avoidance
at all, just as it is very rare to see someone with agoraphobic avoidance who has no
attacks of anxiety.
In clinical settings, diagnoses are typically made following an interview with the
patient. When greater reliability and validity than the typical interview is desired,
structured diagnostic interviews provide an important and valuable clinical and
research resource. Selection of a structured diagnostic interview will ultimately
depend upon local needs, but arguably the most comprehensive, valid interview is
the revised Anxiety Disorders Interview Schedule (ADIS-R; Di Nardo and Barlow,
1988). It achieves in-depth coverage of the anxiety disorders, albeit at the expense
of covering a narrow range of disorders (Page, 1991b). If broader coverage is
required, the (computerized) Composite International Diagnostic Interview
(Peters and Andrews, 1995; Andrews et al., 1999b) is a particularly good candi-
date.
Clinical description
CASE ST UD Y
Ms. W., a 33-year-old female, presented to an anxiety clinic after reading a magazine article
describing hypochondriasis. For the past 10 years, she has received ‘‘far too many’’ medical
investigations because of her belief that she is having a heart attack.
38 Treatment of Anxiety Disorders
Investigations
A routine physical check-up, full blood count, and thyroid function test detected no pathol-
ogy. She reports drinking three cups of weak coffee per day and consumes one glass of wine
per day after reading that alcohol decreases the risk of heart attacks. She describes herself as
always being a ‘‘quiet, nervous type’’ with labile moods. Her responses to the Eysenck
Personality Questionnaire indicate high neuroticism and moderate introversion. Her scores
on the Agoraphobic Cognitions Questionnaire and the Anxiety Sensitivity Inventory were
both very high, while her score on the Beck Depression Inventory indicated very mild
depressive symptoms.
The above case study illustrates three common observations about panic dis-
order with agoraphobia. First, the disorder had a clear onset, which the suVerer
dated to her Wrst attack of panic (Uhde et al., 1985; Aronson and Logue, 1987;
Franklin, 1987; Garvey et al., 1987). Second, the avoidance of situations developed
subsequent to the panic attack, because she feared the consequences of having a
panic in certain situations (Goldstein and Chambless, 1978). Third, the panic
attack involved a dramatic increase in sympathetic arousal, the true origin of
which was unclear to the individual (Franklin, 1990b) and subsequently was
misinterpreted as a sign of serious physical pathology (Clark, 1986, 1988).
39 Panic disorder and agoraphobia: Syndrome
Differential diagnosis
A diagnosis of panic disorder must rule out physical and other psychological
pathology. Typically, individuals have Wrst presented to a medical practitioner
who will have conducted a full medical assessment. It is useful to ensure that
diseases that mimic panic attacks have been excluded at this time. Such patholo-
gies include hypoglycemia, hyperthyroidism, Cushing syndrome, pheochro-
mocytoma, vestibular disturbances, and mitral valve prolapse syndrome. It is also
necessary to evaluate the extent to which substance problems have caused or
exacerbated the presenting problem. Although the illicit drugs and alcohol quickly
come to mind, it is important to exclude excessive caVeine intake. DiVerential
diagnosis from other psychopathology can be more problematic. Disorders that
need to be actively excluded include many of the other anxiety disorders. In OCD,
the individual worries less that anxiety will cause a disease (e.g., a heart attack), but
that, by an act of omission or commission, some thought or behavior will cause
disease or injury. Although individuals with panic disorder exhibit PTSD-like
symptoms in response to their panic attacks (Barlow, 1988), the focus in PTSD is
the traumatic event that is the cause of the panicky symptoms. Although people
with agoraphobic avoidance may fear negative evaluation in social settings, their
fear is a consequence of what they believe the panic may cause them to do (e.g.,
lose bladder control). In contrast, in social phobia, the panic is a consequence of
the scrutiny of others (see Page, 1994c). When diVerential diagnosis between
social phobia and agoraphobia is diYcult, a potentially useful algorithm involves
coding +1 every time a patient endorses (1) feeling dizzy or lightheaded in a panic
attack, (2) avoiding traveling on public transportation alone, and a score of −1
every time a patient endorses (3) avoiding speaking to strangers, (4) fearing
blushing, shaking, or feeling foolish, and (5) fearing eating with others. Patients
with a score of zero or above are more likely to suVer from panic disorder and
agoraphobia, whereas patients who score −1 and lower are more likely to suVer
from social phobia (Page, 1994c). Separation anxiety disorder also needs to be
ruled out when making a diagnosis of agoraphobia. The principal diVerence will
be in terms of the age of onset, with separation anxiety disorder occurring in
children. In separation anxiety disorder, the child often (although not always)
worries about traumatic consequences happening to others (e.g., a parent) when
separated. In agoraphobia, individuals worry about possible traumatic events
befalling themselves when separated from supports and sources of help.
The most diYcult diVerential diagnosis is between claustrophobia and agora-
phobia. Agoraphobia has been deWned (in DSM-IV), in part, as anxiety about
being in places or situations from which escape might be diYcult or embarrassing.
Individuals with claustrophobia will report anxiety in the very same situations.
40 Treatment of Anxiety Disorders
Assessment
Having made a diagnosis, it is useful to assess formally the factors relevant to
treatment. While a behavioral analysis (Kirk, 1989; Schulte, 1997) will provide a
solid foundation for understanding the individual case and tailoring treatment
appropriately, standard assessments provide comparison data otherwise unavail-
able in a clinical interview.
Given that panic disorder and agoraphobia are argued to be manifestations of a
General Neurotic Syndrome (Andrews, 1990b), assessment should cover the
underlying neurotic vulnerability as well as the neurotic symptoms. The Neuroti-
cism subscale of the Eysenck Personality Questionnaire Revised (EPQ-R; Eysenck
and Eysenck, 1975) has proved itself in both research and clinical practice
(Andrews, 1996) as a good measure of the underlying vulnerability. The Depress-
ion Anxiety Stress Scale (DASS; Lovibond and Lovibond, 1995) is a particularly
useful measure of general neurotic symptoms. The DASS is a noncostly measure
that distinguishes between anxiety and depression better than do other measures
(Lovibond and Lovibond, 1995), it has excellent psychometric properties (Brown
et al., 1997) and the factor structure seems more stable than other measures.
In order to assess the more disorder-speciWc aspects of panic disorder and
agoraphobia, see Bouchard et al. (1997) and Page (1998a) for reviews. However,
by way of summary, Shear and Maser (1994) recommended that assessment cover
41 Panic disorder and agoraphobia: Syndrome
(1) panic frequency, severity, and duration, (2) panic-related phobias, (3) antici-
patory anxiety, (4) impairment and general quality of life, and (5) global problem
severity. In this context, the Panic and Agoraphobia Scale (P&A; Bandelow, 1995)
is a short clinician- or client-rated scale that is particularly good. A global severity
score can be obtained, but Wve subscales are also available (panic severity, fre-
quency, and duration; phobic avoidance anticipatory anxiety disability and
health-related worries). A similar measure is a clinician-scored diary called the
Panic-Associated Symptoms Scale (PASS; Scupi et al., 1992). The scale measures
situational panics, spontaneous panics, limited symptom attacks, anticipatory
anxiety, and phobic avoidance. A general severity score is obtainable by summing
the subscales. The P&A and PASS are similar, and clinician-rated versions corre-
late highly; however, they have diVerent strengths. The PASS does not rely on
retrospective reports, but the P&A is more time eYcient. Thus the P&A represents
a rapid, psychometrically sound (albeit retrospective) instrument to assess the
major aspects of panic disorder. If an additional assessment of agoraphobic
avoidance is required, the Mobility Inventory for Agoraphobia (Chambless et al.,
1985) is a 27-item scale designed to measure agoraphobic avoidance behavior both
alone and when accompanied. Further, it also provides an estimate of panic
frequency in the last week.
In addition to these general measures of the disorder, speciWc panic symptom
measures fall into two categories (Bouchard et al., 1997): assessments of panic-
related symptoms and panic-related cognitions. The panic-related symptom in-
strument with the most psychometric data is the Panic Attacks Symptom Ques-
tionnaire (PASQ; Clum et al., 1990). The PASQ has broad symptom coverage, it
focuses on the symptoms, and it measures symptom duration. In terms of
assessing panic-related cognitions the Agoraphobic Cognitions Questionnaire
(ACQ; Chambless et al., 1984) and the Body Sensations Questionnaire (BSQ)
stand out. The BSQ (Chambless, 1988) discriminates panic disorder patients from
normals and patients with other anxiety disorders. The ACQ further discriminates
panic disorder patients from those who also have agoraphobia (Chambless and
Gracely, 1989). Furthermore, the BSQ provides an index of fear intensity, whereas
the ACQ measures the frequency of catastrophic cognitions (Chambless, 1988).
Together the ACQ and BSQ provide a good assessment of cognitions associated
with panic disorder.
In summary, following diagnosis, a comprehensive assessment of panic dis-
order should include measures of common neurotic symptoms, the underlying
vulnerability, a treatment-sensitive assessment of panic and its consequences,
and indices of panic-related symptoms and cognitions. Each domain has a
number of potential candidate measures, of which a suggested list is included in
Table 4.1.
42 Treatment of Anxiety Disorders
Follow-
Domain Instrument Pre During Post up
Etiology
Vulnerability
Initially, it was hoped that there was a unique biological predisposition to panic
attacks. The four main pieces of evidence giving rise to this hope were diVerential
responses to particular pharmacological treatments, the speciWcity of responses to
biological challenge tests, the spontaneity of panic attacks, and a unique genetic
predisposition. However, when subjected to rigorous evaluation, the speciWcity
hypothesis has been usurped by a hypothesis of a general neurotic vulnerability.
First consider the speciWcity of treatment response: on the basis of pharmacologi-
cal dissection, Klein (1964) argued for a unique substrate to panic. Tricyclic
antidepressants reportedly blocked panic but not anticipatory anxiety, while
benzodiazepines reduced anticipatory anxiety but not panic. Although inferring
etiology solely on the basis of treatment response is questionable (Barlow and
Craske, 1988; Mattick et al., 1995), more recent studies have found that, in
contrast to Klein’s original position, tricyclics can alleviate generalized anxiety (see
Kahn et al., 1986; Hunt and Singh, 1991) and high dose/potency benzodiazepines
can reduce panic (Dunner et al., 1986). Second, it was hoped that certain challenge
tests would function as biological markers for panic attacks and panic disorder
(see Dager et al., 1987). Despite numerous attempts using a variety of substances
and procedures (e.g., sodium lactate, hyperventilation, carbon dioxide inhala-
tion), the diVerences between subjects with and without frequent panic attacks
have ultimately been attributable to baseline diVerences in arousal (e.g., Ehlers et
al., 1986a,b; Klein and Ross, 1986; Margraf et al., 1986; Ley, 1988; Holt and
43 Panic disorder and agoraphobia: Syndrome
Andrews, 1989a,b). That is to say, anxious subjects reach higher levels of arousal/
anxiety in response to the challenge than do controls, by virtue of their higher
baseline levels of arousal/ anxiety before the challenge test. Third, it was originally
argued that, because panic attacks were spontaneous, they must solely reXect the
operation or ‘‘Wring’’ of some endogenous dysfunction (Klein, 1981). The main
problem for this assertion is that the apparent spontaneity of panic cannot explain
the similarity in symptom proWles between situationally cued and ‘‘spontaneous’’
panic attacks (Margraf et al., 1987). Barlow (1988) has suggested that it is more
proWtable to describe panic attacks as being expected or unexpected and cued or
uncued. The term ‘‘uncued’’ is preferable to ‘‘spontaneous’’ because it describes
the phenomenon rather than carrying implicit assumptions about presumed
etiology. Furthermore, although the initial panic attack is a surprising and puz-
zling experience (Franklin, 1990a), the majority of panic disorder patients describe
their panic attacks as cued and expected (Goldstein and Chambless, 1978; Street,
Craske and Barlow cited by Barlow, 1988). The Wnal set of data expected to
support the unique etiology of panic attacks was the familial tendency observed in
panic disorder (see Crowe, 1985). As discussed in Chapter 2, the genetic studies
support the notion that there is a heritable component to panic disorder and
agoraphobia (e.g., Pauls et al., 1980; Crowe et al., 1983; Kendler et al., 1993).
However, the predisposition is not speciWc to panic or agoraphobia. Rather the
strongest statement the current data can support is that the predisposition is a
general trait of anxiety proneness (e.g., neuroticism; see Torgersen, 1983; Roth,
1984; Andrews et al., 1990b). The notion of a general predisposition to neurosis is
consistent with the Wnding that attacks of panic are found across the anxiety
disorders; the main distinctions between disorders can be made whether panics
are experienced as expected or unexpected, cued or uncued (Barlow, 1988), and
the meaning with which the symptoms are imbued. In addition to the general trait
of anxiety proneness, a number of risk factors have been associated with the onset
of panic disorder and agoraphobia. First, a variety of studies have found that
stressful life events precede the onset of the disorder (Faravelli, 1985; Faravelli and
Pallanti, 1989; Franklin and Andrews, 1989; Pollard et al., 1989). Interestingly, it
appears that it is not an increased frequency of life events per se that precedes the
onset of panic attacks, but a negative perception of the importance of the life
events by clinically anxious patients relative to normal controls. (Once again, there
were no diVerences between the various anxiety disordered groups, but all diVered
from normal controls.) The reason why life events are rated more negatively has
been attributed to a variety of factors, including personality factors (such as trait
anxiety or neuroticism, discussed in Chapter 2), social supports, physical health
(Roth and Holmes, 1985; Andrews, 1990a, 1991), and early loss (Faravelli et al.,
1985).
44 Treatment of Anxiety Disorders
By way of summary: panic disorder and agoraphobia share with the other
anxiety disorders a general tendency towards anxiety proneness. While the exact
nature of the phenotypic expression of the genotype is still debated (see Chapter
2), more recent theoretical accounts have speculated about the eVect of a non-
speciWc proneness to anxiety. Barlow (1988) has suggested that the increased
vulnerability implies that the Xight or Wght response (Cannon, 1927) is more easily
triggered. The emergency response may be triggered under potentially dangerous
circumstances (i.e., it is a ‘‘true alarm’’). Alternatively, it may be triggered in the
absence of potential danger but in response to the negative perception of life
stressors (i.e., it is a ‘‘false alarm’’). While various biological substrates have been
suggested (see Barlow, 1988; Gray, 1988; Gorman et al., 1989; Andrews et al.,
1990b), the key point is that the action tendencies of the Xight or Wght response are
triggered inappropriately. Consequently, the individual learns to expect that
certain situations will trigger the ‘‘alarm’’, so that one of the strongest predictors
of agoraphobic avoidance is the expectation that a panic attack (i.e., a false alarm)
will occur in a given situation (Telch et al., 1989). Although the anxiety response
may be more easily triggered in individuals with anxiety disorders, the failure to
clearly identify a unique biological substrate to panic attacks has meant that
attention has moved to searching for the etiological factors that channel an
individual with high trait anxiety to develop panic disorder and agoraphobia as
opposed to another anxiety disorder. One area of interest has been to examine the
cognitive processes of panickers; another has been to examine the role of hyper-
ventilation as a cause or exacerbater of panic attacks.
Hyperventilation
Hyperventilation describes increases in the rate or depth of breathing that pro-
duces a higher degree of ventilation than what is necessary to meet the body’s
demands. The end result is that alveolar and arterial carbon dioxide pressures
decrease (PCO2) and blood pH rises. Sustained hyperventilation produces a variety
of changes including arterial constriction, increased neural excitability, increased
lactic acid production, lowered arterial phosphate levels, and a decreased ability
for oxygen to pass from the blood to the body’s cells (Missri and Alexander, 1978;
Magarian, 1982; Ley, 1988). These physiological changes are believed to produce a
characteristic set of physical changes including dizziness, confusion, disorienta-
tion, light-headedness, and parasthesias. The particular pattern of symptoms has
been labeled the ‘‘hyperventilation syndrome’’. The similarity of the symptoms of
the hyperventilation syndrome to a panic attack (Garssen et al., 1992) has led to
two hypotheses. The Wrst hypothesis is that hyperventilation causes panic attacks;
the second is that hyperventilation is involved in the exacerbation of panic attacks.
The Wrst hypothesis is supported by a number of pieces of data including the
45 Panic disorder and agoraphobia: Syndrome
Wnding that patients with panic attacks recognize the symptoms produced by
voluntary hyperventilation as similar to the symptoms of panic. In addition,
during spontaneous panic attacks, PCO2 levels decrease (Salkovskis et al., 1986b;
Griez et al., 1988) suggesting that hyperventilation is occurring. However, there
are a number of Wndings not consistent with the hypothesis that panic attacks are
caused by hyperventilation alone (Gorman et al., 1984; Griez et al., 1988). These
data include Wndings that, while reported panic attacks produced by lactate
infusions were associated with hyperventilation (Gorman et al., 1984), voluntary
hyperventilation did not produce a clear panic attack (Gorman et al., 1984; Griez
et al., 1988), and although panics are associated with drops in PCO2, the decrease is
not of a suYcient magnitude to indicate acute hyperventilation (van Zijderveld et
al., 1999). Further, Hibbert and Pilsbury (1989) found no diVerence between the
symptoms of panic attacks with and without hyperventilation. Moreover only
around 50% of patients with panic disorder demonstrate reductions in arterial
PCO2 (Garssen et al., 1992). Finally, Roll (1987, cited by Garssen et al., 1992) has
demonstrated that a challenging mental task produced as frequent an endorse-
ment of symptoms associated with the hyperventilation syndrome (despite no
evidence of changes in end-tidal PCO2) as did the hyperventilation provocation test
(see also Hornsveld et al., 1990). Data from our group suggest that hyperventila-
tion may be one path leading to panic, but it is neither necessary nor suYcient.
Holt and Andrews (1989a) used hyperventilation (as well as other panic provoca-
tion procedures) and found that the chief diVerence between individuals with
panic disorder and other anxiety disorders was not in terms of the symptoms
generated but in the catastrophic interpretations placed on the symptoms. Fur-
thermore, hyperventilation was not found to be unique to panic disorder and
agoraphobia. Instead, hyperventilation appeared to occur during periods of high
anxiety (presumably thereby increasing the number of symptoms experienced in a
natural episode of high anxiety).
In summary, it appears that hyperventilation can produce symptoms that
overlap with those symptoms reported during a panic attack. In addition, a large
proportion of patients with panic disorder appear to hyperventilate during panic
attacks. However, it cannot be concluded that hyperventilation causes panic
attacks, because panic attacks can occur without evidence of hyperventilation,
hyperventilation does not always cause panic attacks, and the same symptoms can
be produced without hyperventilation. Rather, it appears that (some of ) the
symptoms of a panic attack can be produced by a variety of methods, one of which
is hyperventilation. The question then becomes, how do the symptoms produced
by hyperventilation (or any other means) relate to the experience of panic? One
answer to the question can be found among cognitive models of panic.
46 Treatment of Anxiety Disorders
Trigger
Perceived bodily sensations
Catastrophe-related thoughts
Situation previously associated with panic
Perception of imminent or
present threat
Apprehension
Figure 4.1 A cognitive model of panic attacks. (Modified from Salkovskis, PM (1988) Hyperventilation
and anxiety. Current Opinion in Psychiatry, 1, 78.)
Cognitions
Various models of the ways in which cognitive processes contribute to the
production of panic attacks (e.g., Clark, 1986, 1988; Beck, 1988, see Figure 4.1)
have been proposed. Although there are important diVerences between the ac-
counts, they share the common premise that patients with panic attacks process
information in the external environment, as well as internal somatic stimuli, as
though they were threatening. Before considering the models, it is worth examin-
ing the data regarding the ways in which individuals with panic attacks process
information diVerently from normal controls and individuals with other anxiety
disorders.
The Wrst area in which patients with panic disorder (with and without agora-
phobia) have been found to diVer from normal individuals is in their expectancies
of danger and in their perceptions of control. Individuals with panic attacks report
fearing loss of control. Consistent with this is the Wnding that when patients were
informed, during a carbon monoxide challenge test, that they could control the
intensity of their bodily sensations using a dial, only 20% reported a panic attack
(Sanderson et al., 1989). In contrast, 80% of patients who believed that they had
no control over the gas reported panic. Similarly, informing patients of the
47 Panic disorder and agoraphobia: Syndrome
certain bodily sensations that are once again interpreted in a threatening manner
and future attacks are anxiously anticipated.
These cognitive models have a rarely noted strength. None of the models is
inconsistent with any of the data discussed previously regarding biological predis-
positions to panic. For cognitive models, however, the sensations produced by any
putative pathophysiology are sensations that can be misinterpreted in the same
way as any other sensations. Another strength of the cognitive models is that they
can account for nocturnal panic attacks. While nocturnal panics have been
considered the sine qua non of a spontaneous panic (Roy-Byrne et al., 1988),
cognitive theorists respond that cognitive processing need not always be conscious
(see Mathews and MacLeod, 1986). Rather, since the person has spent their
waking hours selectively attuned to certain (‘‘threatening’’) somatic sensations,
when these occur during sleep the person responds to these with panic. That is to
say, in just the same way that people will respond to personally relevant material
while asleep (see Barlow, 1988), panickers will selectively encode and then respond
to panic symptoms.
Cognitive models of panic emphasize the catastrophic misinterpretations
placed upon internal bodily cues. Another approach to the same issue has been
discussed within the context of anxiety sensitivity. Anxiety sensitivity is a trait
construct, which describes individual diVerences in the tendency to interpret
anxiety symptoms in a catastrophic manner. It is acknowledged that somatic
symptoms and sensations may be produced by a variety of causes but not all
individuals will worry about them to the same extent (e.g., Clark and Hemsley,
1982; Griez and van den Hout, 1982; Starkman et al., 1985). Trait anxiety may
predispose individuals to ‘‘false alarms’’, but anxiety sensitivity may encourage an
individual to worry about the sensations. Consequently, anxiety sensitivity may be
related more strongly to panic disorder and agoraphobia than it will be to other
anxiety disorders. The construct of anxiety sensitivity diVers from other ap-
proaches to cognitive biases in anxiety problems in that it makes particular
assumptions about the construct, namely that anxiety sensitivity is a trait concep-
tually and empirically distinct from trait anxiety (see McNally, 1990).
In summary, cognitive models of anxiety suggest that the critical factor in the
development of a panic attack is not the experience of somatic sensations (what-
ever their origin), but the interpretation placed upon the sensations. In addition to
the empirical support for cognitive models of the maintenance of panic attacks, a
perhaps unexpected boon has been that cognitive models are becoming increas-
ingly powerful in predicting the degree of agoraphobic avoidance that develops in
a person with panic disorder.
49 Panic disorder and agoraphobia: Syndrome
Agoraphobic avoidance
The decision to separate individuals with panic disorder into those with and those
without agoraphobia is, at one level, a function of a classiWcatory system with a
penchant for categories rather than dimensions. However, people with panic
disorder present with varying degrees of agoraphobic avoidance and while border-
line cases are hard to dichotomize, there is no denying that individuals with
extensive avoidance present very diVerently from those without avoidance. Agora-
phobic avoidance has long been conceptualized in terms of conditioning, so that
pairing of situations with aversive events (e.g., panic attacks) leads the contextual
stimuli to acquire fear-provoking properties. The treatment consistent with this
theory involves exposing the individual to the feared situation until anxiety is
substantially reduced. The resulting exposure-based treatments have been repeat-
edly demonstrated to be eVective in reducing fear-driven avoidance (Emmelkamp,
1979).
Despite the evidence supporting a conditioning model of avoidance (Rachman,
1991), an examination of the predictors of avoidance behavior suggest that
cognitive processes are critical in the etiology of agoraphobia. In fact, the cognitive
variables appear to predict avoidance better than do those variables implicated by
a conditioning model (i.e., the frequency and severity of panics). Clum and
Knowles (1991; see also Andrews, 1993b) reviewed the literature pertaining to the
reasons for the development of avoidant behavior. They examined eight hypothe-
ses and concluded that, while panic attacks almost always precede the develop-
ment of agoraphobic avoidance (Uhde et al., 1985; Aronson and Logue, 1987;
Franklin, 1987; Garvey et al., 1987), the avoidance was not a function of the
severity or frequency of the panic attacks, or age at onset.
The research into the eVects of the duration of panic disorder and the location
of the Wrst panic attack was less consistent, but the Wndings could not be taken as
providing convincing support for the origin of agoraphobia in the characteristics
of the panic. In contrast, Clum and Knowles (1991) argued that the literature
supported the hypothesis that agoraphobic avoidance was predicted by three sets
of cognitions – situational negative outcome expectancies, catastrophic panic
outcomes, and an inability to cope with the panic symptoms. The Wrst cognitive
set associated with agoraphobic avoidance involved negative outcome expect-
ancies. Extensive avoidance was associated with expectations of situational fears,
rather than fears of the panic attack alone (Franklin, 1987; Noyes et al., 1987a;
Craske et al., 1988; Fleming and Falk, 1989). In addition, Telch et al. (1989) found
that the expectation of negative social (rather than physical) consequences distin-
guished avoidant from nonavoidant panickers. The second set of expectations
associated with avoidance involved the perception of a link between a given
50 Treatment of Anxiety Disorders
situation and a panic attack. For instance, Rapee and Murrell (1988) found that
individuals with panic disorder and marked avoidance were more likely to
perceive a link between situations and their panic attacks (see also Craske et al.,
1988; Adler et al., 1989; Telch et al., 1989). Finally, Clum and Knowles (1991)
suggested that coping strategies and associated self-eYcacy predicted the likeli-
hood of avoidance. A perception of being able to tolerate fear predicted less escape
and avoidance behavior (Craske et al., 1988). Avoidance behavior was associated
with a lack of conWdence regarding an ability to cope with future panic attacks
(Craske et al., 1988; Mavissakalian, 1988; Telch et al., 1989). Avoiders tended also
to use wishful thinking rather than social supports as coping strategies (Vitaliano
et al., 1987), and training suVerers in eVective coping strategies (e.g., breathing
retraining and relaxation) was associated with lower avoidance.
There are a series of important clinical implications that Xow from such data.
Agoraphobic avoidance is predicted by certain cognitions regarding panic attacks
in speciWc situations. First, people with greater degrees of avoidance tend to
perceive an association between certain situations and panic attacks. Therefore, it
might be argued that treatment needs to modify these beliefs. One way to achieve
this aim is to instruct patients regarding what are currently believed to be the true
causes of panic attacks (i.e., personality vulnerability, hyperventilation, cata-
strophic cognitions), thereby demonstrating that situations cannot in and of
themselves cause panic. Another strategy is to teach patients coping strategies so
that they are conWdent that they can stop panic occurring in ‘‘panicogenic’’
situations.
The second cognitive set found to be predictive of avoidance were catastrophic
expectations of aversive consequences of panic occurring in particular situations.
Treatment will need to modify this belief, especially since patients who cling to
these fears will be understandably reluctant to conduct graded exposure exercises
to these situations. Cognitive restructuring is one strategy to modify these beliefs,
as each catastrophic thought is evaluated and tested. For instance, fears of fainting
can be modiWed by instructing the patient in the origin of the feelings of faintness,
discussing why fainting is unlikely to occur (given its etiology), examining the
frequency of the feared outcome, and then recording the frequency of fainting in
subsequent graded exposure tasks. A perceived inability to cope with panic was
identiWed as the third cognitive set predictive of agoraphobic avoidance. Treat-
ment will need to modify this set of beliefs to fully overcome avoidance. Teaching
patients strategies that not only stop panic attacks but that serve to prevent future
panics are useful in modifying poor self-eYcacy. The perceived ability to cope
with panic attacks will be increased once the person has learned eVective anxiety-
management strategies and found them to be eVective while conducting graded
exposure exercises.
51 Panic disorder and agoraphobia: Syndrome
Course
The modal age for the development of the Wrst panic attack is between 15 and 19
years of age, and the age of onset of panic disorder tends to peak 10 years later in
the mid-20s and diminishes by the mid-40s. As with other anxiety disorders, some
studies have shown that stressful life events tend to precede the onset of the
disorder (e.g., Last et al., 1984; De Loof et al., 1989). However, as discussed earlier,
there are additional data suggesting that it is not so much the occurrence of
stressful life events that precedes panic, but a negative interpretation of these life
events (Rapee et al., 1990).
Epidemiology
Prior to DSM-III, panic disorder was not recognized as a separate diagnostic
category and the label agoraphobia did not describe the same disorder as it does
today. Therefore, some of the most useful estimates of the prevalence of the
disorders currently referred to as panic disorder and agoraphobia come from
Robins and Regier (1991). The lifetime frequency of panic disorder alone is just
under 2%, while the lifetime prevalence of agoraphobia (usually with panic
disorder) is just under 6%. Panic disorder and agoraphobia present diVerently in
terms of their sex distributions. Panic disorder has an annual incidence of 1.43 per
1000, with around a third of cases arising without agoraphobia (Eaton et al.,
1998). Panic typically (but not exclusively; Eaton et al., 1998) presents with an
equal sex ratio (Myers et al., 1984). This contrasts with agoraphobia, where
around three-quarters of suVerers are female (Yonkers et al., 1998). Interestingly,
the extent of avoidance appears to be associated with female gender, giving rise to
the Wnding that higher proportions of females with panic disorder also meet
criteria for a diagnosis of agoraphobia (see Clum and Knowles, 1991) and are also
more likely to experience a recurrence of panic symptoms than men (Yonkers et
al., 1998). While many mechanisms may be proposed to explain this, one possibil-
ity has been developed following the Wnding that the tendency to avoid agorapho-
bic situations is correlated with femininity scores on a sex-role scale (Chambless
and Mason, 1986; and see Reich et al., 1987). While being a female is associated
with higher femininity scores, males may score relatively highly in terms of
femininity and some females may score relatively lowly. Chambless and Mason
(1986) found that the more feminine that subjects of both genders rated them-
selves to be, the greater was the agoraphobic avoidance. Clum and Knowles (1991)
have extended this argument by placing this Wnding against the result that many
agoraphobics fear the humiliation that may follow a panic. They suggest that
femininity scores are associated with social sensitivity, and that the association
52 Treatment of Anxiety Disorders
between the disorder and gender comes about through the mediation of ‘‘feminin-
ity’’. Although one of the more appealing of recent explanations of sex diVerences,
the argument is weakened by the absence of similar diVerences in the sex ratio of
social phobia.
Notwithstanding, females with panic disorder and agoraphobia appear to be
more severe than males in terms of avoidance, catastrophic thoughts, number of
bodily sensations (Turgeon et al., 1998) and the course of panic disorder may be
more severe in women (Yonkers et al., 1998), with women being slightly less than
twice as likely to experience a re-emergence of symptoms than men (25% versus
15% at 6 months and 61% versus 41% and 3 years posttreatment). The reasons for
these sex diVerences are not clear, but at present it seems as likely that they reside
in psychological (e.g., greater harm avoidance in women, reducing compliance
with exposure instructions given in treatment) as in biological (e.g., cyclical
hormonal changes that modify the vulnerability to panic) diVerences (see Bekker,
1996).
Comorbidity
Individuals with panic disorder and agoraphobia tend to suVer additional psycho-
logical distress (Katon et al., 1987) and impaired quality of life (Markowitz et al.,
1989). Of particular concern is the occurrence of major depression, the preoccu-
pation with death (Overbeek et al., 1998), and elevated suicide rate among
individuals with panic disorder (Weissman et al., 1989). A diagnosis of panic
disorder is also associated with substance abuse, impaired social and marital
function, and Wnancial dependency (Markowitz et al., 1989). Further, if panic
disorder is comorbid with another diagnosis, the individual is more likely to seek
treatment for the comorbid disorder, than when there is no comorbid panic
(Boyd, 1986). In terms of etiology, one comorbidity is that which occurs with
speciWc phobias. Interestingly, Starcevic and Bogojevic (1997) found that death-
related phobia was the most proximal speciWc phobia that preceded the onset of
panic disorder and agoraphobia, suggesting that the arousal of these fears may
have some etiological signiWcance in the development of panic.
One complication that needs to be borne in mind is the co-occurrence of a
personality disorder. Individuals with panic disorder show an increased risk
(relative to the population) for personality disorders falling in the ‘‘anxious’’
cluster (i.e., DSM-IV’s cluster C, comprising dependent, avoidant, and obsessive–
compulsive personality disorders (Klass et al., 1989; Mauri et al., 1992)). As
Barlow (1988) noted, this pattern of comorbidity is not surprising, given the
postulation of a general neurotic syndrome. The strength of the association
appears to be a function of agoraphobic avoidance. That is to say, patients with
53 Panic disorder and agoraphobia: Syndrome
Summary
Individuals who present to clinics for treatment with agoraphobia almost always
have panic disorder. Panic disorder involves extreme attacks of anxiety that
perplex the individual, who in turn may misinterpret the anxiety response as a
signal of some mental or physical pathology. It appears that those who attribute
the causes of panic attacks to certain situations, who feel unable to manage panics
in certain situations, or who worry about the aversive consequences of panicking
in certain locations will develop agoraphobic avoidances.
5
In 1988, Barlow examined the evidence from around the world and concluded that
‘‘with speciWcally targeted psychological treatments, panic is eliminated in close to
100% of all cases, and these results are maintained at follow-ups of over 1 year. If
these results are conWrmed by additional research and replication, it will be one of
the most important and exciting developments in the history of psychotherapy’’
(Barlow, 1988; p. 447). The question facing researchers and clinicians alike is, with
the beneWt of more than a decade of subsequent research and replication, ‘‘Is it
possible to concur with Barlow’s statement?’’. The place to begin this evaluation is
by addressing the criteria of eVective treatment for panic disorder and agorapho-
bia.
Aims of treatment
Panic disorder and agoraphobia are currently conceptualized as two separate, but
frequently related, disorders. SpeciWcally, panic attacks are considered the ‘‘mo-
tor’’ that ‘‘drives’’ the agoraphobic avoidance (e.g., Clarke and Jackson, 1983).
Therefore, it would be expected that eVective long-term treatment for agorapho-
bia would require eVective long-term management of panic attacks. By extension,
the Wrst aim of an eVective treatment for agoraphobia (with panic disorder) would
be to stop panic attacks and their interference in an individual’s life. The second
aim would be to reduce any concurrent agoraphobic avoidance. Just as with the
speciWc phobias, avoidance will involve anticipatory anxiety and anxiety triggered
upon exposure and treatment will be more than simply ‘‘turning oV’’ avoidance.
However, an ideal treatment would do more than modify the existing symptoms;
it would reduce the vulnerability to the disorder. If the vulnerability to panic
disorder and agoraphobia (e.g., trait anxiety) could be modiWed, relapse would
presumably be decreased. In summary, eVective treatment of panic disorder and
agoraphobia will involve (1) the control of panic attacks, (2) the cessation of
fear-driven avoidance, and (3) reduction of the vulnerability.
54
55 Panic disorder and agoraphobia: Treatment
Nondrug treatments
Exposure
In vivo exposure has been one of the strongest and most consistently demon-
strated treatments for agoraphobic avoidance. In fact, it has often been demon-
strated to be superior to placebo interventions as well as other credible psychologi-
cal treatments (e.g., Mathews et al., 1981; Mavissakalian and Barlow, 1981;
Emmelkamp, 1982; Teusch and Boehme, 1999) – a none too easy achievement in
psychological research. Furthermore, when anti-exposure instructions are in-
cluded in comparison therapies, the strength of exposure becomes even more
evident (e.g., Greist et al., 1980; Telch et al., 1985). Barlow’s (1988) conclusion
that, following exposure alone, around 75% of agoraphobics (excluding dropouts)
will evidence some clinical beneWt is representative of most similar reviews (e.g.,
Mattick et al., 1990). Yet, despite the strength of in vivo exposure in the treatment
of agoraphobia, it is noteworthy that there remains little room for complacency.
Around one-quarter of patients do not experience any clinical improvement
during treatment, not all are completely symptom free at follow-up (e.g.,
McPherson et al., 1980), and not all those who beneWt from treatment maintain
their gains (Munby and Johnston, 1980). The research literature provides some
details about the ingredients of a successful exposure package.
First, it appears that the greater the exposure exercises resemble the real
situations avoided by individuals, the better is the outcome. For instance, in vivo
exposure is usually superior to imaginal exposure (e.g., Emmelkamp and Wessels,
1975). Second, the more frequently the person confronts their feared situation and
the greater the duration of exposure sessions, the higher is the proportion of
treatment completers who reach a high end-state functioning (e.g., Vermilyea et
al., 1984). Finally, it is probably the case that exposure that continues until anxiety
has subsided is preferable to shorter exposures (e.g., Stern and Marks, 1973; Foa et
al., 1980). For instance, Rayment and Richards (1998) found that allowing panic
symptoms to develop and pass predicted less avoidance of phobic situations.
However, while among speciWc phobics (see Marshall, 1985) continuing exposure
until anxiety decreased was superior to ‘‘escaping’’ when anxiety had risen, among
agoraphobics there are some data suggesting that both approaches are equally
eVective (de Silva and Rachman, 1984; Rachman et al., 1986; although cf. Rayment
and Richards, 1998).
One additional factor that may enhance exposure programs is an eVort to
assure that exposure brings about cognitive changes. Since certain cognitive
variables predict the degree of avoidance (Clum and Knowles, 1991), exposure
should also aim to modify the cognitions predictive of the avoidance. That is
to say, it is important to assure that exposure treatments include instruction
56 Treatment of Anxiety Disorders
regarding the true causes of panic attacks and be combined with training in
anxiety-management strategies. That said, it is apparent that the role that the
cognitive variables identiWed in cognitive theories play in treatment is not com-
pletely clear (Oei et al., 1999). For example Soechting et al. (1998) compared the
eYcacy of a cognitive and a behavioral rationale for exposure treatment among
people with panic disorder and agoraphobia, and there was no overall superior
eYcacy of the cognitive rationale. However, HoVart (1998) did Wnd that agora-
phobics given cognitive therapy showed superior outcomes to those who received
guided mastery and that a path analytic strategy implicated the variables identiWed
by cognitive models. In particular, it appears that changes in the situational fear of
agoraphobics is particularly mediated by changes in self-eYcacy, as opposed to
changes in catastrophic beliefs and perceived thought control (HoVart, 1995).
A further way in which the eYcacy of exposure-based programs has been
improved is with the involvement of spouses or partners in treatment. While a
complete discussion of all the Wndings regarding marital and family interventions
in agoraphobia is beyond the scope of the present book (see Daiuto et al., 1998), a
summary statement is in order. Barlow et al. (1984) found that among agorapho-
bics with apparently well-adjusted relationships, the inclusion of the partner in
treatment added little to improvement rates. In contrast, among individuals with
poorly adjusted relationships, the inclusion of a partner enhanced treatment
outcome, overriding any eVects of the poor interactions. Therefore it is useful
advice to include partners in exposure-based programs, particularly where there is
concern about the negative impact the relationship may have on treatment.
Behavioral therapy for couples may be a useful adjunct, but concurrent therapy
raises a number of other issues, including the diYculties of combining couple-
focused interventions and agoraphobic treatment (Daiuto et al., 1998). Thus our
practice is typically to sequence the treatment for agoraphobia and the couples
therapy, deciding on a case-by-case basis the order for particular clients.
Finally, one way that in vivo exposure programs have been improved is by the
addition of more and diVerent exposure. Fava et al. (1997) reported data that
suggested that additional exposure was beneWcial for patients who were not
initially responding to exposure. More novel treatments, e.g., ‘‘interoceptive
exposure’’ have been used to target panic attacks directly. People prone to panic
attacks are requested to engage in a series of exercises that produce sensations
similar to those that occur during a panic attack (Rapee and Barlow, 1990). For
instance, individuals who fear that tachycardia may signal a heart attack are
requested to run on the spot. The exercise produces a rapid heartbeat, which can
then be included in the person’s graded exposure hierarchy. We have demon-
strated that among agoraphobics the exercises tend to improve overall treatment
outcome (Page, 1994a; see also Ito et al., 1996) and Craske et al. (1997) found that
57 Panic disorder and agoraphobia: Treatment
Breathing retraining
Hyperventilation can produce symptoms similar to those experienced during a
panic attack and hyperventilation often occurs during a panic attack. Therefore, it
is reasonable to suppose that teaching individuals appropriate breathing strategies
aimed to control hyperventilation will alleviate panic symptoms and assist long-
term symptom management. An analysis of the treatment literature is compli-
cated by the variety of breathing techniques being taught (see Garssen et al., 1992).
For present purposes, attention will be limited to studies that compared breathing
retraining with exposure-based programs. Although breathing retraining alone
can reduce the frequency of panic attacks (Lum, 1983; Rapee, 1985b), given that
exposure-based programs have a demonstrated eYcacy, the clinically relevant
question is ‘‘Can breathing retraining enhance the eYcacy of standard exposure
treatments?’’. Three studies meet these criteria. One of the studies failed to
demonstrate a decrease in panic frequency following breathing retraining and
cognitive restructuring (de Ruiter et al., 1989b). This result is surprising, since
such a treatment should decrease the frequency of panic attacks (Clark et al., 1985;
Salkovskis et al., 1986a). Given the study’s failure to demonstrate a treatment
eVect, it is diYcult to interpret the comparisons with exposure treatments. The
remaining two studies failed to Wnd any posttreatment diVerences between expo-
sure-based programs with and without breathing retraining (Bonn et al., 1984;
Hibbert and Chan, 1989), leading to the conclusion that, while breathing retrain-
ing may reduce panic attacks, it does not improve exposure-based programs in the
short term. However, one study (Bonn et al., 1984) examined the patients at a
6-month follow-up point and found that the addition of breathing retraining to
58 Treatment of Anxiety Disorders
Relaxation
Another strategy that has been used in the treatment of panic disorder and
agoraphobia is relaxation. When the diVerent forms of relaxation are combined,
relaxation alone has been estimated to bring about a clinically signiWcant improve-
ment in around 47% of patients with panic disorder and agoraphobia (Michelson
and Marchione, 1991). However, in the context of panic disorder, applied relax-
ation has been found to be superior to progressive muscle relaxation (Ost, 1987b).
Applied relaxation is a rapid form of relaxation that enables individuals to elicit
the relaxation response quickly when needed. While eVective, Arntz and van den
Hout (1996) found that applied relaxation was less eVective than cognitive
therapy, particularly on measures of panic frequency. There have been some
suggestions that progressive muscle relaxation may detract from a cognitive
behavioral therapy (CBT) program for agoraphobia (Barlow et al., 1989). How-
ever, the design of the study involved the introduction of relaxation as one of the
Wrst components into a CBT program. If it is assumed that most individuals with a
chronic anxiety disorder will have been taught relaxation skills at some point, the
higher dropout rates observed in this condition could have occurred because the
patients became disillusioned with receiving a treatment they had already attemp-
ted. While further research is needed to address this question, it may be speculated
that it may be more helpful to include relaxation later, rather than earlier, in a
comprehensive CBT program.
al. (1992) similarly found that up to 90% of panic-disordered patients were panic
free following their combined panic control treatment. Furthermore, it is becom-
ing clear that the eVects of these treatment packages have a broader impact on the
clients, bringing about an overall improvement in quality of life (Telch et al.,
1995).
In addition, it is becoming increasingly clear that these treatment packages are
eVective not only in clinical research centers. The eVects transport well to self-help
delivery format (Gould et al., 1993; Gould and Clum, 1995) and can be main-
tained when face-to-face treatment is reduced in duration but compensated for by
a computer program that incorporates the basic principles of cognitive behavioral
treatment (Newman et al., 1997). The treatment packages can generalize favorably
to adolescent samples (Ollendick, 1995) and to settings that are representative of
community treatment, even when the patients are more severe than those typically
seen in research trials (e.g., Sanderson et al., 1998). When used in a community
mental health center, 87% of panic-disordered patients were panic free after 15
sessions of CBT (Wade et al., 1998); a Wgure that compares well with that obtained
in clinical research settings (e.g., Michelson and Marchione, 1991). The patients
also showed reductions in anticipatory anxiety, agoraphobic avoidance, generali-
zed anxiety, and depression; a pattern of data that once again would be expected
on the basis of research conducted in clinical research settings (Clum et al., 1993).
Manualized CBT-based treatment packages have also been criticized as being
inappropriate for clients with comorbid disorders (see Wilson, 1996). Marchand
et al. (1998) examined the rates of change in clients suVering from panic disorder
and agoraphobia with and without a comorbid personality disorder and found
that both groups responded to the treatment for the anxiety disorder; however,
clients with a personality disorder responded more slowly. In addition, HoVart
and Hedley (1997) noted that dependent personality traits appear particularly
detrimental to treatment progress, but that CBT for panic disorder and agorapho-
bia did reduce symptoms of personality disorder (especially avoidant and depend-
ent traits). Thus it seems more reasonable to conclude that clients with comorbid
personality disorders may require longer, rather than inherently diVerent, treat-
ment than those without personality disorders.
Drug treatments
Confronted with the increasingly favorable treatment outcomes associated with
cognitive behavioral packages, there are three possible reasons why pharmacologi-
cal interventions might be considered. First, it could be that pharmacological
interventions achieve the same outcomes as the CBT packages but at a cheaper
cost (Wnancially to the patient or in terms of therapist time), with fewer dropouts,
60 Treatment of Anxiety Disorders
lower relapse rates, and with fewer associated diYculties (such as side-eVects).
Second, it could be that pharmacological treatments may be useful adjuncts to the
CBT packages. Third, it could be that pharmacological interventions are useful
treatments to attempt with patients for whom a comprehensive and well-conduc-
ted CBT program has failed or to whom such a treatment is unacceptable. Before a
therapist can consider each possibility, it is necessary to evaluate the literature
regarding pharmacological interventions (Clum, 1989; Michelson and Marchione,
1991; Clum et al., 1993). There are Wve possible pharmacological interventions,
the tricyclic (antidepressants), the benzodiazepines (high and low potencies), the
beta blockers, the monoamine oxidase inhibitors, and the selective serotonin
re-uptake inhibitors (SSRIs). As with every medication there are pros, cons, and
guidelines for use, but at a general level of overall eYcacy it appears that the
low-dose benzodiazepines and the beta blockers (i.e., propranolol) have limited
eYcacy.
The tricyclics and the high-potency benzodiazepines have more acceptable
success rates. Holland et al. (1999) reported that the tricyclic clomipramine has a
slower therapeutic onset than the benzodiazepines alprazolam and adinazolam,
but that it reached the same rate of eYcacy as alprazolam (both being superior to
adinazolam) and had less frequent withdrawal problems. Den Boer (1998) noted
that a further advantage of the tricyclics over the benzodiazepines is that the
former have greater eVects on comorbid depression while being similarly eVective
in managing anxiety and agoraphobia.
Clum (1989) estimated (when dropouts are included) that behavior therapies in
general are successful with 54% of patients, tricyclics with 19%, and the high-
potency benzodiazepines with 42%. The unexpectedly low outcomes for the
tricyclics (Mattick et al., 1990) probably occur because studies have tended to use
people with panic disorder and agoraphobia (who are more diYcult to treat),
whereas studies with the high-potency benzodiazepines have tended to use sub-
jects with panic disorder alone (Clum, 1989). In a similar comparison, Michelson
and Marchione (1991) concluded that CBT packages are generally successful in
74% (including dropouts) of individuals with panic disorder and agoraphobia
(86% among panic disorder alone), the tricyclics in 45%, and the high-potency
benzodiazepines in 51%. Once again, the treatment outcomes for the low-potency
benzodiazepines and beta blockers are relatively low (13% and 8%, respectively).
Although the two reviews diVer in their Wnal estimates, the pattern of results is
similar, suggesting that – of the pharmacological treatments – high-potency
benzodiazepines and the tricyclics are the only interventions whose outcomes
approach the success obtained with a CBT package. If the choice of pharmacologi-
cal intervention were limited to these two classes of drug, it would be diYcult to
choose between them. On the one hand, the dropout rates for the tricyclics are
61 Panic disorder and agoraphobia: Treatment
higher than for the high-potency benzodiazepines (although this may reXect
diVerent sampling; Clum, 1989); but, on the other hand, the relapse rates for the
high-potency benzodiazepines are probably higher (Clum, 1989; Michelson and
Marchione, 1991). In terms of unwanted eVects, the tricyclics are unpopular
because of the anticholinergic side-eVects, but the high-potency benzodiazepines
are often avoided because of the possibility of dependence and also the negative
eVects upon memory (Kilic et al., 1999). Indeed, after demonstrating the eYcacy
of imipramine and (especially) alprazolam in treating panic disorder (Schweizer et
al., 1993), Rickels et al. (1993b) identiWed a ‘‘sobering fact [that] over the long
term (i.e., after taper), patients originally treated with imipramine or placebo did
as well at follow-up as patients treated with alprazolam, without the problems of
physical dependence and discontinuation that any long-term alprazolam therapy
entails’’ (ibid., p. 67).
Interestingly, Clum et al. (1993) subsequently identiWed some methodological
weaknesses in Clum’s (1989) early analysis. Using more stringent inclusion cri-
teria, the more recent meta-analysis continues to support some of the earlier
conclusions. In particular, the antidepressants continued to be identiWed as a
treatment of choice (although dropout rates were high) and psychological inter-
ventions were supported once more as a treatment of choice, with exposure or
Xooding being identiWed as a successful treatment. However, the support for the
high-potency benzodiazepines was much weaker than it had been in the earlier
analysis, perhaps because the earlier analysis had included some clinical trials, with
no control groups, that included only data from people who completed the trials.
In summary, it appears that the eYcacy of the CBT therapies is equaling, and
sometimes surpassing, that of the pharmacotherapies (Clum, 1989; Michelson and
Marchione, 1991). Furthermore, given the diYculties associated with medica-
tions, such as side-eVects and the possibility of dependence, psychological inter-
ventions should be the treatment of choice for panic disorder and agoraphobia.
Pharmacotherapies may be preferred because of their initial low cost; however, the
cost of continuing medication and the hidden cost of the higher rates of relapse
have yet to be factored into the equation. However, with the relatively recent
emergence of the SSRIs it is premature to draw strong conclusions about these
drugs. Nevertheless, the data to date are promising (e.g., Pollack et al., 1998; see
Boerner and Moeller, 1997). Finally, although rarely discussed in the literature,
just as there are some patients who Wnd the prospect of medication unacceptable,
there are some who will not participate in a CBT program. Given that the success
of a CBT program relies upon active participation, for these individuals pharma-
cotherapies may be preferred.
62 Treatment of Anxiety Disorders
conducted, it is apparent that there is presently strong support neither for nor
against combining benzodiazepines with CBT (see Spiegel and Bruce, 1997). Thus
a reasonable position would seem to be that combining benzodiazepines with
CBTs should await research support before being recommended as routine clinical
practice.
Summary
The treatment of panic disorder with agoraphobia is consistent with the etiology
models discussed. A comprehensive nondrug treatment package involves panic
control (e.g., education about anxiety, breathing retraining, panic provocation
exercises) as well as modiWcation of the agoraphobic avoidance and catastrophic
misinterpretations (in vivo exposure and cognitive restructuring). Drug treat-
ments, using high-potency benzodiazepines or the tricyclics, have been found to
yield similar rates of treatment success probably because they also decrease anxiety
(Barlow, 1988) and thereby facilitate exposure. However, while drug and nondrug
treatments are both eVective, there is one added bonus that is often not men-
tioned. There is evidence that CBT modiWes the vulnerability factors that give rise
to the disorder. For instance, Andrews and Moran (1988) found that an earlier
version of the Clinician Guide and Patient Manual substantially reduced neuroti-
cism scores and that the size of the decrease was predictive of subsequent relapse.
Given the long-term advantages of reducing vulnerability, a cognitive behavioral
intervention should probably be the treatment of choice (see also Nathan and
Gorman, 1998).
Yet, despite the success of CBTs for panic disorder and agoraphobia, there are
two words of caution. First, surveys of clients serve as a salutary reminder of state
of clinical practice. In a survey of 100 patients with panic disorder and agorapho-
bia, Bandelow et al. (1995) found that unproven treatments (e.g., herbal prepara-
tions) were overutilized and treatments with demonstrated eYcacy (e.g., CBT and
tricyclic antidepressants) were underutilized. Further, Wade et al. (1998) noted
that clinicians are often ambivalent about using a structured, short-term treat-
ment that requires adherence to a protocol, preferring to revert to more familiar
approaches of selecting treatments that they believe will be eVective for this
particular patient. Therefore, it is not only important that the outcomes of
research be disseminated, it is important that clinicians routinely use (and be
encouraged by their management structures to continue to use) established and
eYcacious treatments.
A closing word of caution can be taken from more recent work of Barlow
(1997). The present chapter opened with Barlow’s enthusiasm for this form of
treatment, and he quite reasonably persists with this enthusiasm, commenting
64 Treatment of Anxiety Disorders
that ‘‘cognitive-behavioral treatments yielded the highest mean eVect sizes [com-
paring] favorably with pharmacologic as well as combination drug and CBT
treatments’’ (Barlow, 1997: p. 34). However, his enthusiasm is now tempered by
data indicating that not insigniWcant numbers of patients continue to suVer from
panic continuously or continually following treatment. For instance, Barlow
described data from his group indicating that ‘‘while 74% of our patients re-
mained panic free at a 24-month follow-up when followed cross-sectionally and
57% had reached a state of ‘high end-state functioning’ that would represent a
state close to ‘cured,’ these numbers dropped notably when patients were followed
longitudinally . . . Thus, it seems that at least some of these patients do reasonably
well over the long term but continue to suVer from periods of exacerbation of their
Panic Disorder and Agoraphobia’’ (Barlow, 1997: p. 35). Therefore, attention
needs to continue to be allocated to those people who are less successful during
therapy and identify how treatment can be delivered or targeted more eVectively.
6
After formal diagnosis and assessment, two issues must be addressed before
treatment is planned. First, the clinician, by conducting a thorough behavioral
analysis, must identify the factors that trigger and maintain the panic attacks and
the avoidance behavior. Second, the clinician must consider the eVects of comor-
bid disorders on treatment.
Behavioral analysis
The general principles and practice of behavioral analysis have been outlined
elsewhere (Kirk, 1989; Schulte, 1997). However, in panic disorder and agorapho-
bia there are unique details to be considered. In terms of the antecedents of panic
attacks, it is necessary to evaluate the physical and psychological triggers. These
typically include situations previously associated with panic, certain physical
sensations, and particular worrying thoughts (e.g., ‘‘Oh no! What if I had a panic
attack right now?’’). In addition, panic attacks will be more likely to occur when
the person has been made more physically aroused as a result of being anxious,
stressed, hot, smoking, drinking alcohol, taking stimulant drugs (e.g., coVee), and
so on. In addition, panic attacks appear more likely when the individual is ‘‘run
down’’, perhaps because of illness (e.g., Xu), physical and psychological stress (e.g.,
childbirth), or sleep deprivation. Once a listing of antecedents has been made, the
consequences of panic attacks need to be identiWed. The consequences can be
divided into three categories. First, individuals may respond to panic attacks with
avoidance behavior. Commonly avoided agoraphobic situations have been de-
scribed earlier, but for present purposes it is worth noting that identifying the
cognitive link between panic attacks and avoidance will facilitate cognitive behav-
ioral treatment (e.g., ‘‘I avoid crowded trains because the air may run out when
everyone is breathing it’’). Second, the subtle avoidance strategies (e.g., the use of
safety signals) need to be identiWed. Finally, the social consequences of avoidance
need to be evaluated. For instance, individuals with dependent traits may welcome
the increased support given as a consequence of panic attacks and become more
65
66 Treatment of Anxiety Disorders
Format of treatment
Therapeutic outcome is a function of at least two sources of variance. One source
of variance is attributable to the treatment package. The second source of variance
in treatment outcome corresponds to the therapist’s ability to (1) enhance moti-
vation for treatment (discussed in more detail in Chapter 7), (2) enhance treat-
ment comprehension and compliance, and (3) successfully handle problems that
arise during treatment. The present chapter aims to make explicit the ways in
which a therapist can overcome some of these diYculties and maximize treatment
success. The Wrst issue is the structure of a treatment program. We will describe
our group program; but, for an individual patient, this would be modiWed by
assigning reading and exposure exercises for homework, reserving treatment
sessions for the discussion of progress, and for planning the next stages of the
intervention.
Day one
On the Wrst day most patients are highly anxious and it is most important to
establish rapport. After the usual introductions are completed, the therapist
should acknowledge the anxiety and make a list of everyone’s anxiety symptoms,
in part to conWrm the nature of panic and, in part, to allow group members to
68 Treatment of Anxiety Disorders
realize that others have the same symptoms. Other things to be done at this stage
include the following. Outline the program and distribute the manual.
Explain that the manual is the key to the program, and that patients should
personalize their copy by underlining especially relevant sections, and by
adding examples which are personally relevant.
Check that each patient has organized transport to and from the clinic.
Indicate that patients will be expected to use public transport or drive alone to and
from the clinic towards the end of the program.
If there are still individuals who are taking medication, check on the quantity and
type of medication that each person is taking.
To achieve the maximum beneWt from this program, encourage patients who are
taking benzodiazepines to cease these before beginning treatment. It is import-
ant that benzodiazepines are discontinued because they appear to block extinc-
tion learning (Bouton et al., 1990). In addition, as they provide a predictable
relief of symptoms 30 to 60 minutes after ingestion, patients do not learn that
their anxiety symptoms can be controlled by their new anxiety management
skills.
The therapist provides speciWc instructions for the directed exposure program but
does not accompany the patients on outings (apart from two brief group trips to
familiarize the patients with the local area). Although the itineraries for the group
trips and the individual assignments are predetermined, patients are encouraged
to modify these assignments, after consulting the therapist, so that they have more
relevance for them. As there is some evidence that patients do better if they
perceive control over their assignments, it is important to be Xexible and take into
account each patient’s needs. The group trips familiarize patients with the areas to
which they will be traveling subsequently on their own. It is important to explain
that the program is designed to ensure that they learn to cope with their own
anxiety, take responsibility for doing the assignments, and successfully enter
previously avoided situations. At all times the therapist aims to use language
readily understood by patients (e.g., Page, 1993). The therapist helps patients with
their assignments by rehearsing the steps necessary for each of the tasks before the
task is attempted. On the Wrst day therapists aim to cover the following material
and assignments:
∑ Material in Patient Treatment Manual: Section 1: The Nature of Anxiety, Panic
and Agoraphobia; and Section 2: Control of Hyperventilation.
∑ Accompanied group walk around the local area (duration 20 minutes).
∑ Individual assignment 1: Walk to closest bus stop and return to clinic. It is
important to emphasize that the assignments should be done in the order
shown, from least to most diYcult. When individual assignments are completed
they are ticked oV on a notice board, in part to reinforce the individual’s success
69 Panic disorder and agoraphobia: Clinician Guide
and in part to encourage recalcitrant group members. All group trips and
individual assignments are reviewed by the therapist. Any speciWc diYculties,
especially the panic-related cognitions, are identiWed and strategies to overcome
these diYculties outlined.
∑ Homework for day one: Monitor respiration rates and practice the slow-
breathing technique.
Day two
At the beginning of day two it is useful to ask about each patient’s attitude to the
program, to inquire about sleep the previous night, and to ask about each person’s
current level of anxiety. Patients are reminded that they will be expected to
attempt an individual assignment later in the day. Therapists should cover the
following material and assignments during day two:
∑ Review homework: respiratory monitoring, practice of the slow-breathing tech-
nique.
∑ Material in Patient Treatment Manual: Section 3: Relaxation Training; and
Section 4: Graded Exposure.
∑ Group practice of progressive muscle relaxation.
∑ Unaccompanied group walk around the block, walking further than the bus
stop in the previous day’s assignment. Individual assignment 2: same as group
walk but now completed alone.
∑ Homework for day two: respiratory rate monitoring, practice of slow-breathing
and relaxation techniques.
Day three
Therapists should cover the following material and assignments:
∑ Review homework: respiratory monitoring, practice of slow-breathing and
relaxation techniques.
∑ Group practice of progressive muscle relaxation.
∑ Unaccompanied group trip: travel by bus for two stops.
∑ Material in Patient Treatment Manual, Section 5: Thinking Straight.
∑ Homework for day three: respiratory monitoring, practice of slow-breathing
and relaxation techniques.
Day four
We remind patients about the group trip and the individual assignment scheduled
for later in the day. The section on Thinking Straight must be completed. All free
time is spent preparing and reviewing group and individual assignments, with an
emphasis on cognitive strategies. Therapists should cover the following assign-
ments:
70 Treatment of Anxiety Disorders
Day five
Therapists should cover the following material and assignments:
∑ Review homework: respiratory monitoring, slow-breathing and relaxation tech-
niques.
∑ Group practice of progressive muscle relaxation.
∑ Material in Patient Treatment Manual, Section 6: Producing the Panic Sensa-
tions.
∑ Unaccompanied group bus trip (15 stops) to major shopping center or mall,
remaining there for coVee. The purpose of this trip is to extend the patients’
range of travel away from the clinic and to expose them to a more crowded
shopping center with multilevel shops.
∑ Individual assignment 4: Repeat this day’s group assignment alone.
∑ DebrieWng after assignments: Review how the anxiety-management and cogni-
tive restructuring techniques were applied.
∑ Planning for week two: Before the end of the Wrst week all patients should have a
detailed plan for week two written in a diary format. Each patient should aim to
complete one Graded Exposure exercise and one Producing Panic Sensations
exercise every day. The therapist should help each patient to design their
individual assignments, using the goals and Graded Exposure hierarchies from
Section 3 and the Panic Sensations hierarchy from Section 5 of the Patient
Treatment Manual. The assignments should be relevant to the patient and
compatible with their usual activities. If any individual has not completed the
Wrst week’s individual assignments, they should complete those assignments
before continuing with the tasks for week two.
Day fifteen
Therapists should cover the following material and assignments:
∑ Review week two homework: respiratory monitoring, slow-breathing and relax-
71 Panic disorder and agoraphobia: Clinician Guide
Day sixteen
Therapists should cover the following material and assignments:
∑ Review: respiratory monitoring, practice of slow-breathing and relaxation tech-
niques.
∑ Group practice of progressive muscle relaxation.
∑ Unaccompanied group trip around the city. The purpose of this trip is to
demonstrate to the patients that they can cope with a 6-hour outing. A possible
trip can include lengthy bus trips, very short train trips, as well as the use of
elevators and escalators.
∑ DebrieWng after assignment: It is important to emphasize that this last exercise
has been long and tiring, and that tiredness should not be misidentiWed as
anxiety. Review how the anxiety-management and cognitive restructuring tech-
niques were applied.
∑ Homework for day sixteen: respiratory monitoring, practice of slow-breathing
and relaxation techniques.
Day seventeen
Therapists should cover the following material and assignments:
∑ Review: respiratory monitoring, practice of slow-breathing and relaxation tech-
niques.
72 Treatment of Anxiety Disorders
Day eighteen
Therapists should cover the following material and assignments:
∑ Review: respiratory monitoring, practice of slow-breathing and relaxation tech-
niques.
∑ Group practice of progressive muscle relaxation.
∑ Individual assignment 7: Travel by train for six stops, changing trains at one
station, using both surface and subway trains, if available.
∑ DebrieWng after assignments: Review how the anxiety-management and cogni-
tive restructuring techniques were applied.
∑ Homework for day eighteen: respiratory monitoring, practice of slow-breathing
and relaxation techniques.
Day nineteen
Therapists should cover the following material and assignments:
∑ Review: respiratory monitoring, practice of slow-breathing and relaxation tech-
niques.
∑ Group practice of progressive muscle relaxation.
∑ Material in Patient Treatment Manual, Section 9: Keeping Your Progress
Going.
∑ Individual assignment 8: Travel 30–40 stops by train, walking and catching
buses between stations and the clinic (this exercise should take 3–4 hours).
∑ Review of course: In this session the therapist reviews all the techniques that
have been taught during the course and restates how and when each technique
may be used. The essential instructions, printed on a card that may be carried in
a pocket or purse, are given to patients.
∑ Final instructions: Practice each day and do not make excuses for avoiding
anxiety-provoking situations or activities. Improvement will continue provided
you are prepared to keep entering anxiety-provoking situations and using the
anxiety-management techniques.
suVerers of agoraphobia were perplexed about the origin and real meaning of their
symptoms. The goal of the educational component of the Patient Treatment
Manual is to rectify this problem by providing a complete understanding of the
origin of every physical sensation and symptom. Doing so not only decreases
anxiety, but also lays the groundwork for cognitive restructuring. The Wrst two
sections in the Treatment Manual serve to bring the patient to the understanding
that panic attacks represent a misWring of the Xight or Wght response exacerbated
by hyperventilation and maladaptive cognitions. The Xight or Wght response has
misWred because its threshold for activation is too low. The increased sensitivity of
the Xight or Wght response has been caused by a nervous temperament, stress, and
a tendency to over breathe (see Chapter 4). The Wrst step in providing a new
conceptualization of panic is to agree upon a common domain of conversation.
The Manual achieves this by deWning agoraphobic avoidance and the symptoms of
a panic attack. When conducting group treatment, it is useful to construct a table
that all can see (on a blackboard or a sheet of paper) of each patient and their
symptoms. Doing so allows patients to see the similarities and diVerences between
themselves and other group members and deWnes the range of symptoms experi-
enced during panic attacks publicly. It is then possible to demonstrate that many
of the symptoms are similar to those found in the naturally occurring Xight or
Wght response. Worry about each symptom of panic can then be decreased by
drawing attention to the purpose of each physical change as a preparation for
danger. As a result, the person’s perception of panic changes from being just a
loose conglomeration of worrying symptoms to an ordered emergency response,
brilliantly designed to keep the individual safe. In a panic, it is not that the
symptoms are inherently dangerous it is just that the response is being triggered at
the wrong time and in the wrong place. Once a link has been made between the
Xight or Wght response and a panic attack, it is necessary to consolidate this
learning by explaining the origin of panic by discussing the putative etiology of a
decreased threshold of the Xight or Wght response. It identiWes stress, a nervous
temperament, and hyperventilation as three key causes of initial panic attacks. The
Patient Treatment Manual uses the metaphor of a car alarm to convey the message
that the Xight or Wght response can be triggered inappropriately if the Wring
mechanism is too sensitive. The metaphor helps patients to grasp the otherwise
abstract concept of a diVerential temperamental sensitivity to react to stressors
with anxiety. The Treatment Manual describes the mechanism of breathing and
the eVects of over breathing in detail. Consequently, it is necessary to take patients
slowly through the details to ensure understanding. Laying the groundwork at this
point makes it easier to respond to the complaint that slow breathing is simplistic
by referring the patient back to the explanation that panic attacks are the misWring
of the Xight or Wght response exacerbated by hyperventilation. It is not simplistic,
75 Panic disorder and agoraphobia: Clinician Guide
sign of anxiety to stop the spiral of anxiety into panic. Done at this time, the
person will be able to reverse quite quickly any changes caused by hyperventila-
tion. It will take longer to reverse the changes if they wait until hyperventilation
has aVected blood carbon dioxide levels. Even when slow breathing is used
successfully to control the beginning of a panic attack, it is useful to continue the
slow breathing for a couple more cycles. Otherwise, the person may continue with
their activity and notice the re-emergence of physical sensations that may initiate
the processes responsible for a panic. Another diYculty with the implementation
of the slow-breathing technique is when people take very large breaths. Conse-
quently, their breathing rate is reduced to a reasonable level, but the quantity of
carbon dioxide being expelled remains high. If this problem is suspected, the
typical signs that the therapist may observe include signiWcant rising and falling of
the shoulders and overextension of the chest area. A related diYculty is that the
person may breathe from the chest rather than from the diaphragm. Diaphrag-
matic breathing is usually recommended as the ‘‘correct’’ form of breathing at rest
and for patients with a tendency to overbreathe it is probably sensible, although
there is no empirical basis for this assertion (Weiss, 1989). Logically, it would be
expected that a person breathing from the chest would tend to take short shallow
breaths, which increase the amount of carbon dioxide expelled. Since expansion of
the chest is constrained by the rib cage it is also probable that a slow breathing rate
will be diYcult to sustain comfortably unless breathing is diaphragmatic. For these
reasons, we discourage chest breathing in patients prone to panic attacks (for a
discussion of teaching diaphragmatic breathing, see Weiss, 1989). A common
diYculty with slow breathing is neglecting to hold the breath at the start of each
slow-breathing cycle. This error, as well as decreasing the technique’s eVectiveness,
draws the attention of the therapist to a possible misunderstanding of the prin-
ciples underlying slow breathing. Holding the breath aims to increase blood levels
of carbon dioxide (by decreasing the rate with which the gas is expelled). Breathing
in and out on a 6-second cycle aims to ensure a respiration rate that is slow and
balanced (thereby preventing any new imbalance). Since the two components aim
to bring about diVerent eVects, it is equally important for patients not only to slow
their breathing frequency but also to regularly hold their breath to further increase
blood carbon dioxide levels. Therefore if the patient neglects one part of the
technique it is probable that the rationale has not been completely understood.
manner similar to Ost’s (1987b) applied relaxation. One frequently cited diYculty
with isometric relaxation as a panic control skill is the speed with which panic
attacks occur. Patients argue that almost before they know it, the panic is rising
rapidly, and they do not have the time to engage their relaxation techniques.
Because of the ubiquitousness of this diYculty we have taken to encouraging
patients to engage in progressive muscle relaxation before entering anxiety-
provoking situations, as a prophylactic measure. Isometric relaxation can be used
to manage tension during a panic, but in our program emphasis is placed upon the
need to Wrst bring hyperventilation under control. Patients are taught to hold their
breath at the Wrst sign of panic, to stop the spiral of anxiety into panic. Once the
slow breathing starts to work, the person is in a better position to tackle associated
problems such as muscle tension. They can then use cognitive restructuring
techniques to control worrying thoughts and they can use isometric relaxation to
reduce any tension. This choice of emphasis (i.e., stopping the escalation of
hyperventilation-induced symptoms versus stopping the escalation of physical
tension) is governed principally by reports from patients. They say that during a
panic their principal concern is the uncontrollable and rapid rise of the symptoms.
Therefore, we emphasize the need to use hyperventilation control to tackle this
part of the problem Wrst – only then moving on to modify other parts of the
vicious cycle of panic.
present section will consider only issues unique to agoraphobia. One common
diYculty in constructing a hierarchy is the patient who wants to dispense with
steps along the way, facing immediately the most feared situation. This desire
comes from two sources. First, the patient may be impatient and therefore
unwilling to ‘‘waste time’’ breaking the goal down (see Chapter 14). The second
reason why patients opt for Xooding is because panics are no longer frightening. If
they now consider that they have avoided situations for fear of panic and they can
now control panic attacks, all situations become equally safe. With such individ-
uals we have found it easiest to let them attempt to face the (previously) most
fear-provoking situation Wrst, simply because they invariably do it anyway. Never-
theless, it is useful to get the patients to agree to view the attempt as an experiment
and, if it fails, to commit themselves to trying a graded hierarchy (Miller and Page,
1991). Although patients may be timid about confronting their feared situations, a
related fear is therapist timidity. Timidity and maladaptive cognitions appear to
strike the novice therapist most commonly when conducting panic provocation
exercises, even though these exercises are intrinsically safe. The therapist must
communicate, in a calm manner, that to overcome fears those fears must be faced.
If the fear is of the internal bodily sensations, then these too must be confronted.
Only by facing the feared situation will anxiety be truly overcome. When the
rationale is clearly presented to patients who have had some success in controlling
panic attacks, we have found no diYculties with compliance. The panic provoca-
tion exercises function as a useful method for bringing about cognitive change as
well as rapidly decreasing the frequency of panic symptoms (Page, 1994). When
encouraging exposure to feared situations therapists must avoid a common trap.
Because individuals with panic disorder and agoraphobia are often afraid that
some catastrophe is imminent, they seek reassurance or safety in some person or
object (Rachman, 1984). Since these people and objects then become anxiety-
reducing mechanisms, they can attenuate the power of exposure-based programs.
Patients also have a tendency to attribute success to the presence of the safety
signal, thereby negating the hard-won gains of exposure therapy. There is a degree
of consistency across patients with panic and agoraphobia regarding the subtle
avoidance strategies used; the most common talismans that are carried in case they
may be needed to abort panic include anxiety medication, food, or drink (Barlow,
1988). Therapists should identify such safety signals and persuade patients to
relinquish them. Another common strategy used by patients to minimize anxiety
during exposure is distraction (see Clarke and Jackson, 1983). While distraction
may have helped suVerers of panic to cope with anxiety in the past, it does not
allow anxiety to extinguish or habituate. In addition, patients often spend so much
time distracting themselves that they fail to implement the new anxiety-manage-
ment techniques. While it is diYcult to encourage patients to give up one of the
79 Panic disorder and agoraphobia: Clinician Guide
few techniques that they have found useful, it is proWtable to do so. Once the
person can actively control panic attacks, the fear of panic decreases. Since panic
disorder is fundamentally a fear of future panics, it is only when the patient is
given a sense of true mastery over the panic that fear decreases (de Silva and
Rachman, 1984; Rachman et al., 1986). In addition to diYculties with grading
exposure tasks, there are some situations that are ungradable. Usually, diYculty in
grading a speciWed task can be overcome by imaginative and lateral thinking.
However, the feared outcome may be truly ungradable. For instance, one patient
with long-standing agoraphobia identiWed a primary fear to be ‘‘What if I panic,
and it lasts forever?’’. Every eVort to grade exposure tasks failed to modify this
fearful belief, because the patient was able to respond, ‘‘But I knew that the task
would be over in a set time and then the panic would end’’. It was only when
ungraded and essentially ‘‘open-ended’’ situations (e.g., long-distance train travel)
were attempted that anxiety began to decrease and the irrational cognition was
successfully challenged.
explicit the cognitive therapy that has, until now, been only modeled by the
therapist. This perception is fostered as patients are encouraged to increasingly
take responsibility for their own cognitive therapy. Patient independence in
cognitive therapy is developed by moving through three stages during treatment.
In the Wrst few days of therapy, the therapist models cognitive therapy by
reconceptualizing panic and agoraphobic avoidances as well as explicitly and
forcibly challenging any inaccurate and maladaptive beliefs. In the second stage,
Ellis’ model of cognitions is made explicit and panic attacks and agoraphobic
avoidance are conceptualized in cognitive terms. Patients are taught to challenge
and dispute irrational and maladaptive cognitions in the therapeutic context.
Therapist and patient work together, reWning the challenges so that they are
accurate, believable, and acceptable to the patient. Following this, the patient is
encouraged at every opportunity to identify and challenge any maladaptive cogni-
tions that occur, especially during panic attacks and graded exposure tasks. In the
Wnal stage, the therapist moves from a collaborative to provocative role. Once the
patient has begun to understand and successfully apply the cognitive skills, the
therapist begins to raise the stakes by deliberately Wnding weaknesses in the
person’s challenges. Patients do not Wnd this a novel situation, because whenever
they have previously tried to challenge maladaptive thoughts before, an internal
provocateur has attempted to pick holes in their new thoughts. However, for this
to be therapeutic, it is important to bring patients to a point where they begin to
Xounder, but then, using a careful Socratic approach, encourage development of
greater cognitive restructuring abilities. If the therapist provides a clear and simple
resolution when patients begin to Xounder, they will not acquire any greater skills
at challenging maladaptive cognitions. If the therapist leads them to develop a new
understanding, they acquire not only the adaptive cognition but also the means to
develop such thoughts in the future.
Problem solving
As the therapist works through the treatment program, challenges and questions
arise. Responding openly to any query encourages patients to express their doubts
and misgivings about the details of the program. Otherwise, the therapist runs the
risk of blithely progressing under the false impression that the patients have not
only understood but also accepted everything. In this context, it is useful to bear in
mind that, because anxiety-disordered patients are usually anxious, they may have
poor concentration. It is therefore important to speak slowly, using illustrations
where necessary. Complaints, diYculties, and questions commonly occur, despite
the best teaching. The following section provides some suggested answers and
resolutions. One problem often encountered among patients with severe agora-
phobic avoidance is ‘‘secondary gain’’. It appears that the person or a signiWcant
81 Panic disorder and agoraphobia: Clinician Guide
other serves to gain more from the continuation of the disorder than from its
amelioration. Although this behavior is by no means universal and almost certain-
ly does not cause agoraphobia, when present it makes therapeutic progress more
diYcult. Although such behavior can be construed as passive-aggressive, it is
perhaps more proWtable to conceptualize the actions as a problem requiring great
therapeutic skill to resolve. At the risk of trivializing the complexity of resolving
therapeutic resistance of this kind, it is useful to outline some principles. First, if
‘‘secondary gain’’ is considered a form of resistance, then motivational interview-
ing can be used to guide the therapist’s approach (see Chapter 14). The primary
aim will be to develop a discrepancy, so that the gains of recovery outweigh the
gains of remaining incapacitated. Second, it is probably helpful to view the
behavior as a sensible response to particular environmental contingencies (which
can be modiWed), rather than a defect in the person’s personality. Third, when the
partner (rather than the patient) is the primary hindrance, it is useful either to
discuss with the patient strategies whereby they may alter their partner’s behavior
or to involve the partner in treatment and perhaps oVer additional behavioral
relationship counseling (e.g., Barlow et al., 1984). One other problem encountered
during treatment is the eVect of intrusive or obsessional thoughts. It has been
documented that intrusive and obsessional thoughts are common in the general
population (Rachman, 1981). Similarly, individuals with panic disorder and
agoraphobia can worry about having unpleasant intrusive thoughts. Although the
problem may not warrant a diagnosis of OCD, patients will often reluctantly
confess, late in treatment, bizarre intrusive thoughts. They have secretly endured
these thoughts, convinced that they are true evidence of insanity. In group
treatment, when such ‘‘confessions’’ can be elicited, they are often greeted with
relief from other group members who too can ‘‘confess’’ to similar ideation. Once
brought into the open, the problem (if severe) can be tackled in the manner
described in Chapter 17.
Typical complaints
‘‘I have had this problem for years, I’ve had numerous treatments, I can’t get better
in three weeks!’’ Our group program for panic disorder with agoraphobia is run
intensively over 10 days spread over 3 weeks and concludes with patients making a
solo trip by bus, by train, and on foot that takes them many kilometers from the
clinic, a journey that takes the greater part of a day. For people who at the start of
treatment have great diYculty even coming to the clinic and who may have been
eVectively housebound for years, this rate of progress is hard to believe. This is
even more diYcult for patients who have had numerous failed treatment at-
tempts. Indeed, we too are constantly amazed at the degree and speed of recovery
82 Treatment of Anxiety Disorders
that occurs. We have found the best way to handle this comment, if it arises at the
initial treatment session, is to draw attention to the number of hours the person
will spend in the program. If the treatment program were spread over individual
1-hour weekly sessions, the person would be in treatment for 2 years. Patients can
conceive that they may be brought to this point within 2 years. The therapist can
then suggest that the group program compresses this treatment and allows
patients to rapidly build on their successes. If the comment arises later in therapy,
it is more useful to direct attention to the task at hand. That is to say, rather than
thinking (and usually worrying) about goals that are perceived to be unattainable,
the patient can be encouraged to successfully work to master the present task,
which is one step towards the seemingly impossible goal. ‘‘I can’t get to your clinic,
will you come to me?’’ Having made numerous failed attempts to take treatment
to housebound agoraphobics, we now insist that patients come to the clinic.
Although this may sound harsh, we have found that doing otherwise fosters
dependency. Patients do Wnd ways to attend the clinic – even individuals who have
been housebound. We have developed this practice from our experience and it is
for the same reason, the fostering of dependency, that we refuse to conduct an
inpatient program. If you elect to oVer a home-based program for those conWned
to their homes and Wnd it successful, please publish how you did it. A related issue
is accompanying patients upon their graded exposure assignments. We accom-
pany patients only on their very Wrst graded exposure assignment. After the Wrst
group walk, patients conduct the therapist-directed exposure tasks Wrst as a group
and then alone. Most patients are able to master fearful situations much more
easily when accompanied by the therapist. Although not accompanying patients
initially slows the rate of progress, in the long-term this strategy appears preferable
because the therapist does not become a safety signal (Rachman, 1984). In
addition, the patient learns from the beginning of therapy that self-control of
panics is possible and it is the way to overcome phobic disorders and ensure
independence. The one exception is the Wrst assignment after patients have
returned for the second half of their program. Many patients are demoralized at
this time, believing wrongly that they have made little progress. The therapist is
able to analyze what has been achieved, provide support and, more importantly,
observe each patient’s performance in vivo so that accurate feedback can be
provided. ‘‘Panics are unbearable, I can’t live like this any more!’’ Individuals with
panic disorder and agoraphobia have higher suicide rates than the general popula-
tion. Furthermore, given the comorbidity of the disorders with depression
(Andrews et al., 1990c) and alcohol problems (Page and Andrews, 1996), expres-
sions of hopelessness need to be taken seriously. Most often patients are using the
strongest language available to them, to communicate the incapacitation caused
by panics and the terror that haunts them. Therefore, the therapist must disen-
83 Panic disorder and agoraphobia: Clinician Guide
General summary
Conducting treatment for panic disorder and agoraphobia requires a thorough
understanding of the science behind the disorder and its treatment. However,
there is an art to presenting empirically validated techniques. This may explain
why clinicians unfamiliar with a cognitive behavioral formulation may have
slightly less impressive treatment outcomes when compared with those who are
more familiar with cognitive behavioral theories and interventions (e.g., compare
Welkowitz et al. (1991) and Gournay (1991) with Klosko et al. (1990)). The
present chapter has outlined the art of delivering an empirically validated treat-
ment technique, suggesting that maximum success attends those who can enhance
motivation for treatment, enhance treatment comprehension and compliance,
and successfully handle patients’ criticisms and diYculties.
7
This Manual is both a guide to treatment and a workbook for persons who suVer
from panic disorder and agoraphobia. During treatment, it is a workbook in
which individuals can record their own experience of their disorder, together with
the additional advice for their particular case given by their clinician. After
treatment has concluded, this Manual will serve as a self-help resource enabling
those who have recovered, but who encounter further stressors or diYculties, to
read the appropriate section and, by putting the content into action, stay well.
Contents
Section 1 86
1 The nature of anxiety, panic, and agoraphobia 86
1.1 How do panic disorder and agoraphobia develop? 88
1.1.1 Stress 88
1.1.2 Anxiety 88
1.1.3 Hyperventilation or overbreathing 89
1.1.4 Personality characteristics 89
1.2 The nature of panic 89
1.3 The development of situational fears 90
1.4 Subtle avoidances 92
1.5 Rationale of the program 93
1.6 Hindrances to recovery 94
1.7 The nature of anxiety: a true alarm 94
1.8 Anxiety: a false alarm 96
1.9 Why do I have false alarms? 97
1.10 The eVect of personality 97
1.11 Summary 98
1.12 Hyperventilation 98
1.13 Types of overbreathing 101
*Gavin Andrews, Mark Creamer, Rocco Crino, Caroline Hunt, Lisa Lampe and Andrew Page The Treatment
of Anxiety Disorders second edition © 2002 Cambridge University Press. All rights reserved.
85 Panic disorder and agoraphobia: Patient Treatment Manual
Section 2 104
2 Control of hyperventilation 104
2.1 Recognizing hyperventilation 104
2.2 Slow-breathing technique 105
2.2.1 Troubleshooting 106
2.3 Daily record of breathing rate 106
Section 3 107
3 Relaxation training 107
3.1 The importance of relaxation training 107
3.2 Recognizing tension 108
3.3 Relaxation training 110
3.3.1 Progressive muscle relaxation 110
3.3.2 Isometric relaxation 110
3.3.3 Further isometric exercises 112
3.3.4 DiYculties with relaxation 113
Sectn 4 114
4 Graded exposure 114
4.1 More about avoidance 114
4.2 Planning your program 115
4.3 Implementing your program 118
4.4 Practicing the steps 118
4.5 Facing fears in imagination 119
4.6 Achieving your own personal goals 119
Section 5 122
5 Thinking straight 122
5.1 Step 1: Identifying anxiety-provoking thoughts 124
5.1.1 Anxiety-provoking thoughts in panic disorder 124
5.1.2 Misinterpreting physical sensations 125
5.1.3 Situational fears and unhelpful thinking 125
5.1.4 Wishful thinking 127
5.1.5 More tips on detecting unhelpful thoughts 128
5.2 Step 2: Challenging anxiety-provoking thoughts 128
5.3 Step 3: Generating alternative thoughts 129
5.4 Troubleshooting 130
5.5 Summary 131
86 Treatment of Anxiety Disorders
Section 6 131
6 Producing the panic sensations 131
6.1 Panic sensations exercises 132
6.2 Constructing a stepladder of panic sensation exercises 134
6.3 Practicing the panic sensation exercises 134
6.4 Scheduling the panic sensation exercises during the program 134
6.5 Troubleshooting 135
6.6 Plan for break 136
Section 7 138
7 Producing panic sensations in your daily life 138
Section 8 141
8 More about thinking straight 141
8.1 Coping statements 143
8.2 Summary 144
Section 9 144
9 Keeping your progress going 144
9.1 Coping with setbacks or diYculties in making progress 144
9.1.1 Managing anxiety and hyperventilation 144
9.1.2 Planning of goals and steps 144
9.2 Emotional problems during setbacks 145
9.3 Expect lapse occasionally 145
9.4 Conclusion 146
Section 10 146
10 Recommended resources 146
10.1 Books 146
10.2 Video 147
10.3 Internet resources 147
SE C T I ON 1
1 The nature of anxiety, panic, and agoraphobia
Since the time of the ancient Greeks there have been consistent reports of a
disorder causing the most irrational fears in otherwise sane persons. It was not
until the latter part of the nineteenth century that this came to be known as
agoraphobia, which literally translated means ‘‘fear of the market place’’. More
recently, it has come to be known more generally as a fear of public places or open
spaces.
While fear of public places or open spaces does characterize the majority of
87 Panic disorder and agoraphobia: Patient Treatment Manual
suVerers of agoraphobia, recent evidence suggests that these situational fears are
not the primary fears in agoraphobia. It is the fear of panic or anxiety attacks,
regardless of where they occur, that is the primary fear in panic disorder and
agoraphobia.
Many people have attacks of panic. However, only a few people continue to
have frequent or distressing attacks of panic that begin to interfere with their
day-to-day functioning. When panic attacks are very frequent or when a person
spends a considerable amount of time fearfully anticipating the next attack of
panic, that individual may be said to suVer from panic disorder.
Some people with panic continue their daily lives despite the attacks of anxiety
that strike them out of the blue. For other people with panic, the attacks of anxiety
lead them to avoid situations for fear of panic. Typically, people who panic do so
for one of three reasons. First, they may avoid situations because they see a link
between the various situations and their panics. For example, panic attacks may
occur regularly in shopping centers, so the person comes to avoid these places.
Second, people with panic can avoid situations where a panic may occur because
of the physical or social eVects of panicking in that place. For instance, someone
who fears urinating during a panic may avoid places where people easily may
observe the consequences of such a loss of control. Finally, individuals may avoid
situations where they perceive that they do not have the resources to manage a
panic. For instance, a person may avoid driving if they fear that a panic may rob
them of the capacity to drive safely.
The avoidance of situations for fear of panic typically includes crowded areas,
open spaces, buses, trains, closed-in places, and being a long way from home or
help. Remember, these fearful avoidances are secondary to the basic fear: the fear
of panic. It is, therefore, more appropriate to describe agoraphobia as a fear of
panic attacks that may lead a person to avoid any situation or activities that they
think will provoke these attacks or prevent escape or hinder help arriving.
The distinction between primary and secondary fears is important. For individ-
uals with panic disorder it will be necessary to learn to control the primary fear, the
panic attacks. For individuals with panic disorder and agoraphobic avoidances,
the fact that the fear of situations is secondary to the fear of anxiety means that to
overcome the problems of agoraphobia it is necessary to learn to control the
anxiety and panic attacks. Once this primary fear is controlled, an individual with
agoraphobia can learn to overcome the situational fears. As individuals learn that
they can control their anxiety and their panics, they can confront those situations
that they have previously avoided, secured by the knowledge that they can prevent
panic attacks.
This primary fear in agoraphobia is often described as a fear of fainting or
collapsing, having a heart attack, going crazy, losing control of bowel or bladder,
88 Treatment of Anxiety Disorders
or in any other way losing personal control. The secondary or situational fears are
many and varied. These fears include any situation that an individual believes will
provoke or is associated with high anxiety. The important point here is that one
does not actually have to experience an anxiety attack in all of these situations, but
need only believe that the situation might provoke an attack. In this sense it is not
only the attacks of anxiety but the way in which an individual thinks about the
attacks that determines which situational fears develop. In our experience, almost
all people with a long-standing panic disorder come to avoid some situations for
fear of panic. The extent of your avoidance will determine the amount of time and
energy you will need to allocate to overcoming this problem.
Some disorders occasionally mistaken for agoraphobia include depression,
schizophrenia, social phobia, and obsessive–compulsive disorder. However, a
reasonable understanding of the nature of agoraphobia as previously described
generally allows for easy classiWcation of these disorders as not constituting
agoraphobia.
1.1.2 Anxiety
Both physical and psychological stress can produce an anxiety reaction. Becoming
anxious is not the inevitable consequence of stress, but it is a common result.
Often these stresses and the associated anxiety can be quite subtle, but it is in these
situations that a person is more vulnerable to a panic attack.
At some time or another everyone experiences stress and reacts by becoming
anxious. However, not everyone who experiences anxiety develops panic attacks.
The question arises why some people develop panics while others don’t. Unfortu-
nately, there is no single answer to this question as yet. There are, however, various
possible explanations. First, there is some evidence that people who develop panic
disorder and agoraphobia have been subjected to greater than normal amounts of
stress just prior to their Wrst attack, thus making them more vulnerable than
89 Panic disorder and agoraphobia: Patient Treatment Manual
others. Second, it may be the case that people who develop panic attacks are more
vulnerable than others to stress and to worry about panic attacks.
∑ ‘‘Jelly legs’’
∑ Blurred vision
∑ Muscle tension
∑ Feeling you can’t get your thoughts together or speak
∑ Fear you might die, lose control or act in a crazy way
When the panic becomes severe, most people try to get out of the particular
situation in the hope that the panic will stop, or else they get help so that should
they collapse, have a heart attack, or go crazy, there will be somebody with them
who will look after them. Occasionally, some people want to go somewhere alone
so that they do not embarrass themselves in some way.
The Wrst few times that someone experiences a panic attack are usually very
frightening because this is a new experience that is strange and abnormal. How-
ever, after many such experiences most people know deep down that they’re
unlikely to lose control, collapse, die, or go crazy. At least, they haven’t up till now.
However, many fear that the next time may be diVerent, that the next panic may
be the worst. Some people manage to resign themselves to the experience of panic,
even though they never like the experience.
Panics rarely come truly out of the blue. Even the Wrst attack usually occurs at a
time when the individual is under emotional pressure, or unwell (e.g., recovering
from the Xu), or when they are tired and exhausted and beginning to feel at the
end of their tether. A person’s Wrst panic attack is very uncommon when someone
is truly safe, genuinely relaxed, and free from stress.
which have in fact caused the attack, are not seen as the reasons by the suVerer.
This is because stress, anxiety, and overbreathing develop gradually, and the
individual is often unaware of their presence.
The individual with agoraphobia mistakenly explains the panic attack in terms
of the situation in which the panic was experienced. One way that this association
is made is by the process of conditioning. Because the experience of the panic and
the place in which it happened both occurred at the same time, the conditioning
process leads to an association between the two events being made in memory.
Your memory of the attack is associated with your memory of the situation in
which it occurred. It is this association that leads to the belief that the situation
caused the attack. This belief leads to the development of the situational fears and
the avoidance of certain situations.
As was mentioned previously, not all situations avoided by people with agora-
phobia have necessarily been the site of previous panic attacks. These individuals
need only think that a certain situation may provoke an attack to avoid it. This
explains the often widespread fears and avoidances held by people with agorapho-
bia. It also explains the speed with which these fears can develop. In fact, in 30% of
people with agoraphobia, widespread avoidance develops within one week of the
Wrst panic attack. The process by which these avoidance behaviors or fears spread
is known as generalization.
It is important that you understand the concepts of conditioning and generaliz-
ation because the successful treatment involves the breaking down of the associ-
ations between the panic attacks and the avoided situations that have been built up
by these two processes.
Another reason why people with panic attacks develop avoidance of feared
situations is because they see themselves as being unable to control a panic in that
situation. Because the panic is out of control, the person begins to worry about the
possible consequences of having a panic, the embarrassment or possible injury.
For example, you may worry that people will think less of you if you collapse in
public, or you may worry that if you were to lose control of your actions you may
injure yourself or loved ones. Whatever the reason, it appears sensible to avoid
situations in which the consequences of having a panic (such as driving a car) are
frightening.
Remember, the primary fear in agoraphobia is the fear of panic or anxiety
attacks, not the fear of certain places or situations. The situational fears are
secondary. Successful treatment involves, Wrst, learning to manage and control the
anxiety and panic attacks and then, second, with that knowledge, learning to
overcome the situational fears.
92 Treatment of Anxiety Disorders
anticipation of the worst and apprehension about what may be going to happen.
In addition, there are feelings that events could proceed uncontrollably or that one
may not have control over one’s own reactions. We will be looking at how such
thoughts can trigger, intensify, and prolong our anxiety reactions.
∑ Breathing speeds up and the nostrils and lungs open wider. This increases the
amount of oxygen available for the muscles.
∑ Heart rate and blood pressure increase so that the oxygen and nutrients
required by the muscles can be transported quickly to where they are needed.
∑ Blood is diverted to muscles, particularly the large muscles in the legs. Less
blood is allocated to areas that do not immediately require nutrition. Blood
moves away from the face and you may ‘‘pale with fear’’.
∑ Muscles tense, preparing you to respond quickly.
∑ Blood-clotting ability increases so that, were physical injury to occur, blood loss
would be minimized.
∑ Sweating increases to cool the body, stopping it from overheating when strenu-
ous physical activity begins. Blood vessels expand and move towards the skin to
cool the blood.
∑ The mind becomes focused. It becomes so preoccupied with the thought,
‘‘What is the danger and how can I get to safety?’’ that other things pass
unnoticed.
∑ Digestion is put on hold. The stomach stops digesting food. The mouth dries as
less saliva is produced. Food sits heavily in the stomach and nausea or ‘‘butter-
Xies’’ may occur. Instead, glucose is released to provide energy.
∑ The immune system slows down. In the short term, the body puts all of its
eVorts into escaping.
∑ Sphincter muscles around the bowel and bladder constrict so that no trail is left
by which a predator could track you down.
It is the automatic activation of this Xight or Wght response that allows you to
run and escape. The Xight or Wght response is an automatic reaction that will Wrst
lead you to Xee from danger. Only when escape is impossible will you turn and
Wght for your life. In contrast to this life-saving alarm, it is clear that not all anxiety
is of the same intensity. The prospect of examinations or a job interview may
increase anxiety but not usually to the same degree as if one were faced with a
vicious dog. However, whatever the degree of anxiety experienced, it is controlled
by the involuntary nervous system. Whether panic or vague worries, it is the Xight
or Wght response being triggered. The alarm is triggered, but to a lesser degree.
Also consider that anxiety helps you perform any skilled activity. If you are
totally relaxed when you take an exam, play a game, solve a quarrel between your
children or discuss a problem with your in-laws you will not do your best. To do
anything really well you need to be alert, anxious to do well, or ‘‘focused’’. Anxiety
in moderation can work well to make you more eYcient. People with anxiety
disorders often fear all anxiety, even anxiety that can help them to perform well.
They often worry that it may spiral out of control, and they may panic, and hence
try to avoid any anxiety.
96 Treatment of Anxiety Disorders
When people do get too anxious, the anxiety can interfere with performance, as
they are focused on the symptoms of anxiety and want to escape. High levels of
anxiety may lead to mistakes. The more diYcult the task, the more important it is
to manage anxiety carefully; ideally one should remain alert, tense and in control
for maximum eYciency. The relationship between anxiety and skill is shown in
the diagram. On this course we will teach a number of techniques for remaining
calm when the situation is appropriate, and alert, tense, and in control in diYcult
situations.
Very good
Performance
Average
Very poor
Anxiety level
If you have become anxious in situations in which other individuals would not
be so anxious, it suggests that your anxiety ‘‘alarm’’ (the Xight or Wght response) is
too sensitive. The alarm reaction, designed to protect you from dangerous buses,
charging bulls and other physical dangers, has been triggered at the wrong time.
The Xight or Wght response is useful in the short term, especially if the danger
can be avoided by physical exertion. But it is of no use in the long term and
certainly of little use in most stressful situations in the modern world. It doesn’t
help to run when the traYc cop pulls you over and it doesn’t help to Wght
physically when the boss threatens you. However, because the Xight or Wght
response was useful to our ancestors, it is still a part of our bodily make-up. It is no
wonder, then, that when we are threatened, we can’t get enough air, our hearts
pound, we feel nauseated, and the muscles in our arms and legs tingle and shake,
for all these responses would be useful if we could Xee or Wght.
The symptoms of a panic attack are, of course, very similar. This is because a
panic attack is the Xight or Wght response being triggered at the wrong time. But as
we know, there is no outside danger: the train is most probably not going to crash,
the supermarket will not catch Wre, we won’t suVocate waiting in the bank queue.
We know our anxiety is unreasonable. So people with panic attacks come to fear
themselves, fear that the panic will lead them to have a heart attack, lose control, or
die.
strategies that we will teach you will aid you to control this aspect of your
personality.
1.11 Summary
When people Wnd themselves in stressful or threatening situations, an automatic
physiological response is triggered. This response has been part of our physiologi-
cal make-up for perhaps thousands of years. It is a primitive response that
prepares people to protect themselves or escape from the source of stress. It
produces changes that prepare the body for vigorous physical action.
All of these changes are quickly reversed once vigorous physical activity has
been carried out. This explains why many people report the desire to run or in
some other way expend physical energy when placed in stressful situations. Today,
however, it is often the case that we are unable to immediately engage in such
physical activity and, therefore, are less able to reverse these changes.
This problem of reversing the Xight or Wght response is especially the case when
the response is activated by stressful or disturbing thoughts rather than physically
threatening situations. In this situation, the physical changes persist for longer
than they would in other situations. For people who are prone to worry excessive-
ly, these changes can be quite disturbing and a source of considerable anxiety.
This, of course, leads to further activation of the Xight or Wght response and the
whole cycle is continued. Treatment must therefore aim to break this vicious cycle.
One way is by controlling hyperventilation.
1.12 Hyperventilation
For the present, we shall turn our attention to one particular aspect of the Xight or
Wght response that is of most concern in panic disorder and agoraphobia, namely
the increase in rate of respiration, or overbreathing.
As we discussed in the context of the Wght or Xight response, the anxiety alarm
involves an increase in breathing. This overbreathing can make many of the
symptoms that occur in panic disorders and agoraphobia much worse than they
otherwise would be. These symptoms are important because people fear the
occurrence of the anxiety reaction even more than they fear danger in a feared
situation. Overbreathing has the power to make anxiety symptoms worse. Let us
see how this can happen. The diagram shows how the major components of
breathing link together.
Whenever we breathe in, oxygen goes into the lungs. The oxygen travels to the
blood where it is picked up by an ‘‘oxygen-sticky’’ chemical. This oxygen-sticky
chemical, called hemoglobin, carries the oxygen around the body. Oxygen is then
released by the hemoglobin for use by the body’s cells. The cells use the oxygen and
99 Panic disorder and agoraphobia: Patient Treatment Manual
LUNGS
BLOOD HEMOGLOBIN
BODY’S CELLS
generate a waste product – carbon dioxide. The carbon dioxide is released back to
the blood, taken to the lungs, and breathed out.
The puzzle is, if hemoglobin is ‘‘oxygen-sticky’’, then how did the oxygen
become unstuck? What is the key that unlocks the oxygen? The key is carbon
dioxide. Whenever the hemoglobin meets some carbon dioxide, the oxygen is
unlocked so that it can go into the body’s cells. Therefore, while it is important to
breathe in oxygen, it is just as important that there is carbon dioxide in the blood
to release the oxygen. Overbreathing makes anxiety worse not because you breathe
in too much oxygen but because you breathe out too much carbon dioxide.
Breathing ‘‘too much’’ has the eVect of decreasing the levels of carbon dioxide,
while breathing ‘‘too little’’ has the eVect of increasing levels of carbon dioxide.
The body works best when there is a balance between oxygen and carbon dioxide.
When you overbreathe, you end up with more oxygen than carbon dioxide in your
blood. When this imbalance happens a number of changes in the body occur.
One of the most important changes is a narrowing of certain blood vessels. In
particular, blood going to the brain is somewhat decreased. Coupled together with
this tightening of blood vessels is the fact that the hemoglobin increases its
‘‘stickiness’’ for oxygen. Thus less blood reaches certain areas of the body. Further-
more, the oxygen carried by this blood is less likely to be released to the cells.
Paradoxically, then, while overbreathing means we are taking in more oxygen, we
are actually getting less oxygen to certain areas of our brain and body. This results
in two broad categories of sensations.
Some sensations are produced by the slight reduction in oxygen to certain parts
of the brain. These symptoms include:
100 Treatment of Anxiety Disorders
∑ Breathlessness
∑ Light-headedness
∑ Dizziness
∑ Body feels diVerent or unreal
∑ Things around you seem unreal
∑ Confusion
∑ Increased heart rate
∑ Tingling, ‘‘pins and needles’’ or numbness in hands, feet or face
∑ Muscle stiVness
∑ Sweating hands
∑ Dry mouth or throat
It is important to remember that the reductions in oxygen are slight and totally
harmless.
One of the most distressing sensations caused by hyperventilation is a feeling
that you cannot get enough air. This can trick you into breathing even harder or
faster, which will just make the symptoms worse. If overbreathing continues,
further symptoms can appear such as:
∑ Vertigo
∑ Nausea
∑ A feeling of restricted breathing
∑ Chest pain, constriction or tenderness
∑ Muscle paralysis
∑ Increasing apprehension or fear
∑ Rising terror that something terrible is about to happen, for example, a heart
attack, brain hemorrhage, or even death
When individuals hyperventilate, they use more energy than they need to. This
may cause other symptoms:
∑ Feeling hot or Xushed
∑ Sweating
∑ Feeling tired
∑ Muscle fatigue, especially chest muscles
Looking at the lists of physical sensations produced by hyperventilation, there is
some overlap with symptoms commonly reported in panic attacks. It is also easy
to see how individuals might mistake the sensations produced by hyperventilation
as signs of some serious physical illness. When individuals do this, their anxiety
increases, they hyperventilate more, and thus worsen or prolong their symptoms.
It is important to remember that hyperventilation produces physical
sensations that are unpleasant (and, for some, frightening) but they are not
dangerous. The physical sensations produced may be experienced as physically
unpleasant, but will not harm you. When you stop hyperventilating (or
101 Panic disorder and agoraphobia: Patient Treatment Manual
when your body’s protective mechanisms step in), the sensations will go away.
Another requirement for survival is that the levels of oxygen and carbon dioxide
in the body are balanced. The body has a number of protective mechanisms that
prevent this relationship from becoming too unbalanced. When hyperventilation
occurs for a while, the body takes steps to correct it. There are many examples of
protective mechanisms in the body that maintain the body’s function. For
example, there is a protective mechanism that maintains blood pressure at a stable
level, thus preventing people from fainting every time they stand up. Other
protective mechanisms exist to regulate eating, sleep, and temperature. These
mechanisms are in-built, long lasting, and generally automatic.
Breathing has automatic and voluntary control. That is to say, when you are not
thinking about it, your body maintains your breathing rate. When you want to,
you can change your breathing rate, e.g., holding your breath under water. In
Section 1.13, you will learn that you can take advantage of this voluntary aspect of
breathing control to reduce the panic symptoms produced by hyperventilation.
Although people vary greatly in their response to overbreathing, the symptoms
listed are those most commonly reported. It is these symptoms of hyperventilation
that can make the symptoms of panic attacks much worse than they otherwise
would have been. Mild hyperventilation can also cause an individual to remain in
a state of perpetual apprehension.
At the risk of repetition, the most important point to be made about hyperven-
tilation is that it is not dangerous. Even though it can feel uncomfortable and
sometimes very unpleasant, severe anxiety alone does not harm you physically.
Increased breathing is part of the Xight or Wght response and so is part of a natural
biological response aimed at protecting the body from harm. Thus it is an
automatic reaction for the brain to immediately expect danger and for the
individual to feel the urge to escape.
Hyperventilation is often not obvious to the observer, or even to the persons,
themselves. It can be very subtle. This is especially true if the individual has been
slightly overbreathing over a long period of time. In this case, there can be a
marked drop in carbon dioxide but, because the body is able to compensate for
this drop, symptoms may not be produced. However, because carbon dioxide
levels are kept low, the body is less able to cope with further decreases and even a
slight change of breathing (e.g., a sigh, yawn, or gasp) can be enough to trigger
symptoms.
Trigger
Oh no...What if?
Breathe
faster
Fight or
Symptoms flight
Perceived
breathlessness
anxiety, such as when you are exposed to what you fear. The other is habitual: it
occurs most of the time and is essentially a bad breathing habit or style.
∑ Panting or rapid breathing: Such breathing tends to occur during periods of
acute anxiety or fear. This type of breathing will reduce carbon dioxide levels
very quickly and produce a rapid increase in anxiety.
∑ Sighing and yawning: Sighing and yawning tend to occur during periods of
disappointment or depression and both involve excessively deep breathing.
∑ Gasping: Gasping occurs when people think of frightening things such as doing
something that they have avoided for a long time.
∑ Chronic or habitual overbreathing: This type of breathing involves slight in-
creases in depth or speed of breathing sustained over a long period. Generally,
this happens during periods of worry. It is not enough to bring on a sense of
panic, but leaves the person feeling apprehensive, dizzy, and unable to think
clearly. If such people are placed in the presence of what they fear and increase
their breathing even by a little, this may trigger panic.
The relationship between phobic triggers and hyperventilation is summarized
in the above diagram.
panic attack can happen at any time. While panic symptoms can occur during
exercise and feel worse with exercise, they appear out of the blue and can even
occur during sleep. Lastly, if a doctor has checked your heart with an electrocar-
diogram (a device which measures electrical changes in the heart) and has given
you the all clear, then heart disease is unlikely to be causing the attacks. Heart
disease produces obvious changes in the electrical activity of the heart; panic
attacks just cause an increase in heart rate.
SE C T I ON 2
2 Control of hyperventilation
2.1 Recognizing hyperventilation
The Wrst step in preventing and controlling hyperventilation is to recognize how
and when you overbreathe.
Try monitoring your breathing rate now. Count one breath in and out as 1, the
next breath in and out as 2, and so on. It may be diYcult at Wrst, but don’t try to
change your breathing rate voluntarily. Write the answer here . As part of
treatment you will be required to monitor your breathing rate for 1 minute during
various times of the day. The form in Section 2.3 should be used for this purpose.
Now consider the following:
∑ Do you breathe too quickly? The average person only needs to take 10 to 12
normal breaths per minute at rest. If your rate of breathing is greater than this
then you must reduce it.
∑ Do you breathe too deeply? Does your chest sometimes feel overexpanded? You
should breathe from the abdomen and through the nose, consciously attempt-
ing to breathe in a smooth and light way. Breathing through the mouth is a bad
habit in most cases, and can be controlled by practice.
∑ Do you sigh or yawn more than others? Excessive sighing or yawning may be a
sign of hyperventilation.
∑ Do you gasp or take in a deep breath when for example, someone suggests an outing
or you hear the telephone ring? Taking one deep breath can trigger the hyperven-
tilation cycle in many people.
Apart from recognizing the way in which you overbreathe, it is also important
that you recognize the sorts of activities or events that may trigger overbreathing.
∑ Are you smoking too much or drinking too much tea or coVee? Tobacco, tea and
coVee are all stimulants that will accelerate the Wght or Xight response. Try to
reduce your smoking to a minimum and do not smoke just before anxiety-
provoking situations. Switch to decaVeinated coVee or tea during the program,
and later keep the number of cups you have to one or two per day. A signiWcant
105 Panic disorder and agoraphobia: Patient Treatment Manual
percentage of people have their panic attacks triggered by caVeine, and if you
Wnd you are one of these it will be better to avoid all caVeine.
∑ Are you drinking too much alcohol? Initially alcohol acts as a depressant; how-
ever, a few hours after drinking it acts as a stimulant. At this time and at times
when you experience ‘‘hangover’’ symptoms you are more susceptible to hyper-
ventilation attacks.
∑ Are you suVering from premenstrual tension or period pain? Some women experi-
ence an increase in bodily sensations in the week before their periods. For this
reason you may experience a worsening of panic-like sensations prior to
menstruation. Become aware of these changes and use the opportunity to deal
with a predictable period of increased bodily sensations and panic.
∑ Are you always rushing? Are you over conscientious – working too hard or too
fast? Slow down and give yourself adequate time to do things. Organize events
so that you are not always rushing from place to place. Physical activity will
increase your body’s need for oxygen, and, as a result, breathing rate and depth
of breathing will increase. You will achieve more by staying calm and working at
a reasonable pace.
2.2.1 Troubleshooting
You may Wnd the slow-breathing technique ‘‘unnatural’’ or uncomfortable.
Breathing at a rate of 10 breaths per minute is not unnatural, though for people
who have been overbreathing for a long time it may not be habitual. Regular
practice in a variety of settings will make the slow-breathing technique comfort-
able and habitual.
If you feel your symptoms are getting worse using this technique, ensure you are
keeping time with a watch. Simply counting to yourself may lead to accelerated
breathing.
Don’t expect too much too soon. Regular practice in ideal circumstances will
make it easier for you to use the technique in more tricky situations.
Focusing on breathing may seem ‘‘strange’’ for some people. Persevering with
the technique will reduce this feeling.
SE CT I O N 3
3 Relaxation training
3.1 The importance of relaxation training
Human beings have a built-in response to threat or stress known as the Xight or
Wght response. Part of this Xight or Wght response involves the activation of muscle
108 Treatment of Anxiety Disorders
tension, which helps us to perform many tasks in a more alert and eYcient
manner. In normal circumstances, the muscles do not remain at a high level of
tension all the time but become tensed and relaxed according to a person’s needs.
Thus a person may show Xuctuating patterns of tension and relaxation over a
single day according to the demands of the day, but this person would not be
considered to be suVering from tension.
If you remain tense after demanding or stressful periods have passed, you
remain more alert than is necessary and this sense of alertness ends up turning into
apprehension and anxiety. Constant tension makes people oversensitive and they
respond to smaller and smaller events as though they were threatening. By
learning to relax, you can gain control over these feelings of anxiety. In this
program, you will be taught how to recognize tension, how to achieve deep
relaxation, and how to relax in everyday situations. You will need to be an active
participant, committed to daily practice for 2 months or longer.
Since some tension may be good for you, it is important to discriminate when
tension is useful and when it is unnecessary. Actually, much everyday tension is
unnecessary. Only a few muscles are involved in maintaining normal posture, e.g.,
sitting, standing, or walking. Most people use more tension than is necessary to
perform these activities. Occasionally, an increase in tension is extremely beneW-
cial. For example, it is usually helpful to tense up when you are about to receive a
serve in a tennis game. Tension is unnecessary when (1) it performs no useful
alerting function, (2) when it is too high for the activity involved, or (3) when it
remains high after the activating situation has passed.
In order to be more in control of your anxiety, emotions, and general physical
well being, it is important to learn to relax. To do this you need to learn to
recognize tension; learn to relax your body in a general, total sense; and learn to let
tension go in speciWc muscles.
In each box of the Muscle tension rating form, place the number corresponding
to your level of tension:
0 1 2 3
Around eyes
Jaw
Side of neck
Top of scalp
Back of neck
Shoulders
Top of back
Lower back
Chest
Abdomen
Groin
Buttocks
Thighs
Knees
Calves
Feet
Upper arms
Lower arms
Hands
110 Treatment of Anxiety Disorders
∑ Pull the legs sideways in opposite directions while keeping them locked together
at the ankles.
Or
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow out of your muscles.
Choose other parts of the body to relax, e.g., the hands and arms:
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, tense hand and arm muscles by placing hands comfortably in
your lap, palm against palm, and pressing down with the top hand while trying
to lift the lower hand.
Or
∑ Place hands under the sides of chair and pull into the chair.
Or
∑ Grasp hands behind chair and try to pull them apart while simultaneously
pushing them in against the back of the chair.
Or
∑ Place hands behind the head, interlocking the Wngers, and while pushing the
head backward into hands try to pull hands apart.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow from your muscles.
If circumstances permit, continue with various muscle groups.
When standing in a public place:
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, straighten legs to tense all muscles, bending the knees back
almost as far as they will go.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow from your muscles.
Other exercises for hand and arm muscles:
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, cup hands together in front and try to pull them apart.
Or
112 Treatment of Anxiety Disorders
Instructions
Some example exercises are given below. Complete the remainder by starting with
those muscles that you rated as highly tense on the muscle tension rating form
earlier in this section. Write down some suggestions for putting tension in the
muscle area and then suggestions for relaxing that muscle. Give the suggestions a
try, but remember to tense gently and slowly.
Shoulders and neck Hunching shoulders up towards Letting shoulders drop and let
the head arms hang loose
work, go to a park. You may need to consider whether other factors are pre-
venting you from relaxing if you keep making the excuse that there’s no time.
5. ‘‘I’m not getting anything out of this.’’ Unfortunately, many people expect too
much too soon from relaxation training. People often exaggerate the speed of
recovery. You cannot expect to undo years of habitual tensing in a few
relaxation sessions. Impatience is one of the symptoms of anxiety and often
indicates a need to continue with relaxation training. Give the training time to
take eVect.
6. ‘‘I haven’t got the self-control.’’ You need to realize that quick, easy cures for
panic disorder calling for no eVort from you do not exist. The longest-lasting
treatment eVects occur when an individual takes responsibility for his or her
recovery. Responsibility means self-control, but self-control is diYcult if you
are not motivated.
SE C T I ON 4
4 Graded exposure
When a panic attack occurs for the Wrst time in a certain situation, most people
believe that, should they Wnd themselves in that same situation again, they would
be more than likely to panic. The occurrence of severe panics is very frightening
and so, as any sensible person would, suVerers soon learn to try to anticipate
situations likely to trigger their panics. For most people with panic disorder and
agoraphobia, these situations involve public transport, crowded, lonely, or closed-
in places – all situations from which it is impossible to escape easily or in which
help couldn’t easily arrive. The person usually feels that help is what is needed in a
severe panic. Occasionally, some people prefer to panic on their own, to save
themselves from possible embarrassment should they lose control.
Each time an individual with panic disorder and agoraphobia approaches some
feared situation worry and anxiety may begin to rise. If the person then avoids it,
in whole or in part, the fear increases because the drop in anxiety (which follows
the ‘‘escape’’) tells the person that the avoidance was a sensible strategy. Thus the
avoidance behavior is strengthened: after all if you can avoid panics by avoiding
situations, why not do so? Unfortunately, the panics really don’t stop; you just Wnd
more and more situations that could be ‘‘dangerous’’ and avoid them, too.
the same or similar situations in the past. But, due to the process of generalization,
a person need not actually have experienced a panic attack in a certain situation in
order to develop a fear of that situation.
Once situational fears are established, the individual with panic disorder and
agoraphobia develops an avoidance of the situation. The avoidance can be of
suYcient strength that the person never again enters the situation and therefore
never knows whether or not it would, in fact, trigger a panic attack. This is similar
to someone who, having once been frightened by a dog in a particular area,
thereafter avoids going down that street and thus never learns that the dog is no
longer there or is now tied up.
It is the goal of treatment to have you overcome avoidances and to break down
the association between panic attacks and speciWc situations, such as traveling by
bus or train, going far from home, or staying in small or closed-in places. The
process is gradual, as fears can often be made worse if the person suddenly forces
himself or herself without suYcient preparation and training in anxiety-manage-
ment skills to confront something he or she may have avoided for years. In this
situation, the anxiety produced by such a sudden exposure can actually strengthen
the association between the situation and the fear.
What then is the cure? If the fear is reinforced by leaving the situation, what
would happen if you stayed put? Actually, if you stayed in the situation for an hour
or so, the fear would eventually go, and the fear the next time you entered that
situation would be less. But few people with situational fears can actually stay in
the situation for the 1 or 2 hours required for a really big panic to wear oV. So they
keep avoiding those situations.
Instead, if the associations are to be weakened, exposure to the feared situations
must be gradual. First, you must learn to master situations associated with mild
anxiety and then progressively master situations associated with greater levels of
anxiety. It should be remembered that anxiety is diVerent from panic, and
moderate anxiety in new or previously feared situations is a perfectly normal and
reasonable response. Thus we do not expect you to wait until you are anxiety free
before you enter a situation. This program requires that you identify speciWc goals
that you wish to achieve and then break them down into small steps. Each step is
practiced and mastered before you move onto the next step. The skills you have
learned for the control of anxiety and hyperventilation are to be used when
practicing each step.
4. You should always be working on those activities that you can perform,
knowing you have a reasonably good chance of managing your anxiety. Some
people use the 75% rule: undertaking activities that you are 75% conWdent you
will be able to perform while managing your anxiety. If you use this rule you
can determine whether you are going from one step to another with too big a
jump, i.e., attempting a level that you are not ready for. If you feel less than 75%
certain of controlling your panic, modify that step so as to increase your
conWdence. Note: Do not use the 75% rule as a reason for avoiding activities –
you can always modify the activity in some way. All of your goals can be broken
down into smaller steps. Use this method to more easily achieve your goals.
We would now like you to practice making out a set of steps for each of the
following goals:
Steps:
Steps:
118 Treatment of Anxiety Disorders
I want to get out and about by myself I want to spend two hours a week shopping alone
in the nearest shops
I want to travel on buses I want to be able to travel from my home to the
city by bus alone
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Now select three (at the most) of the above goals that you would like to work on
Wrst, and write these below. Set out beneath each goal the steps you intend to take
in order to achieve it.
121 Panic disorder and agoraphobia: Patient Treatment Manual
1. Goal:
Steps:
2. Goal:
Steps:
3. Goal:
Steps:
122 Treatment of Anxiety Disorders
SE C T I ON 5
5 Thinking straight
This part of the program will help you to control the thoughts that accompany and
promote anxiety. This will be done by learning to label situations more appro-
priately and reduce the frequency, intensity and duration of upsetting emotional
reactions. The techniques in this chapter should be used along with other parts of
the treatment program.
All people have various thoughts, feelings, and behaviors in response to experi-
ences throughout their days. These thoughts, feelings, and behaviors inXuence
each other. Sometimes, however, people are unaware of these inXuences, especially
the inXuence of thoughts on feelings. It is easy to assume that events lead directly
to emotional responses (see the following diagram). This is very important,
because it may lead people to believe they have no inXuence over the way they
think, feel, or behave. The consequences are caused by the activating events.
However, in the same way that the roman alphabet does not run from A to C
without going through B, Activating events do not cause emotional Consequences
without going through our Beliefs. Let us consider for a moment what this means.
It means that the situations that appear to Activate the Consequence of a Panic
Attack, do so because of what we Believe about them.
Activating event:
SITUATION or EXPERIENCE
Consequence
EMOTIONAL RESPONSE AND BEHAVIOR
Activating event:
SITUATION or EXPERIENCE
Beliefs:
Consequences:
To make this more concrete, consider the following comparison between people
with and without panic disorder.
Beliefs: Beliefs:
What if I panic and can t get out? There are a lot of people here.
What if others can see I m anxious? I m glad I got a good seat in the middle.
Consequences: Consequences:
As you can see, the situation or Activating event is the same for both people.
What are diVerent are the Beliefs that they have. Therefore the emotional and
behavioral Consequences are quite diVerent too. Thus many individuals with
panic disorder and agoraphobia recognize that their emotional responses to
various situations (e.g., a cinema or a boat ride) diVer from those of others around
them. This occurs because the individual with panic labels such situations as
threatening or dangerous, and therefore feels anxious. It is important to realize it
is appropriate to feel anxious in response to objectively threatening or dangerous
situations. The problem in panic disorder is that the label is clearly unhelpful and
in many cases it is incorrect, because it is based on an exaggerated threat.
The individual with panic disorder and agoraphobia is responding appropriate-
ly to their thoughts; it’s just that the thoughts are not appropriate to the situation.
They have labeled the situation as being more threatening than they need to. By
changing the way you label or interpret events, you can gain more control over
your feelings, in a more helpful and adaptive way.
Some individuals with panic disorder and agoraphobia have been labeling or
interpreting places, events or interactions in unhelpful and fear-producing ways
for months to years. After many repetitions, such patterns of thinking may occur
124 Treatment of Anxiety Disorders
extremely quickly, and almost seem automatic. Some people even seem to become
experts at such unhelpful thinking patterns, and are able to make themselves
anxious in many diVerent situations, by applying unhelpful thinking patterns.
Avoiding situations only reinforces unhelpful and fear-producing thinking
habits, as it prevents individuals from getting new, helpful information. This
means they cannot prove their unhelpful beliefs to be wrong.
It is important to recognize that unhelpful thinking patterns are habits, and that
habits can be changed with eVort and practice. Identifying unhelpful thoughts
associated with anxiety is the Wrst step in changing your thinking.
Look through the list of physical sensations commonly associated with panic
attacks. Write down those physical sensations that occur during your panic attacks
and the beliefs you have about those sensations. When you have done this, we
will later Wnd alternative, less threatening, thoughts to challenge your original
beliefs.
This technique should be used with the technique of graded exposure, to help
you re-enter situations that you currently avoid because of anxiety.
The following examples come from individuals with panic disorder and agora-
phobia.
Example 1
Catching an express train, I’ll panic – being on a train I probably won’t lose control,
where I couldn’t get oV if I makes be lose control and panic I’ll just feel anxious
wanted to
I’ll go crazy if I can’t get out Even if I do feel anxious and
uncomfortable, that doesn’t
mean the situation is dangerous
What’ll people think of me? I’ve never done something out
of control on a train, and
probably won’t do something
this time either
If I can’t get out I’ll do I can use my techniques to
something stupid or out of manage my anxiety. People
control. Everyone is won’t notice me, and even if
watching me they do, they’ll just think I’m a
little tense
No one else feels this I know other people have panic
way attacks too
I must be loopy to feel this I’m not loopy, just anxious, and
way I’m doing something about that
Anxiety: 100% Anxiety: 40%
127 Panic disorder and agoraphobia: Patient Treatment Manual
Example 2
Walking into a train station, I’m going to have a heart attack I’m not having a heart attack. I’m
noticing a pounding heart, and die immediately experiencing an anxiety reaction
and getting suddenly anxious
There is something physically The unpleasant physical sensations
wrong with me are due to anxiety, which I have
learned to control
Breathing too hard will make the
symptoms worse, which proves it is
not a heart attack
I’ve never had a heart attack,
collapsed or died as a result of a
panic attack
I’d better sit down before I I don’t need to sit down, I can do my
collapse breathing exercise
Anxiety: 90% Anxiety: 35%
Unhelpful I didn’t get the job, which proves that I’m a failure. I’ll never get a job or have things go
right for me.
Helpful I’m disappointed I didn’t get the job, but I’ll get over it and cope in the meantime.
Unhelpful I feel really worthless now that I know what John’s been saying about me.
Helpful I’m sorry to hear John said that about me, but I’m not going to let myself get too upset by it.
128 Treatment of Anxiety Disorders
Unhelpful What if I can’t cope with this? I just know I’ll do something wrong.
Helpful I’m going to give this a try. I’ll do my best, and see how it goes.
Unhelpful thinking
∑ I must . . .
∑ I’ve got to . . .
∑ What if . . . [something happened] . . . that would be terrible.
∑ I couldn’t stand it if . . .
Wishful thinking
∑ It’ll work out.
∑ I don’t care . . .
∑ It wouldn’t have done any good anyway.
∑ I won’t be anxious at all.
Helpful thinking
∑ I’d like to . . .
∑ I’d prefer not to . . .
∑ It’s unlikely that . . . [something] . . . will actually happen.
∑ If things don’t go the way I want, I might be disappointed, but I’ll probably cope.
Now think of a recent situation where you felt anxious or had a panic attack.
Write down a description of the situation, and any anxiety-provoking thoughts
you may have had. Then write down some more helpful thoughts that could be
applied to that situation, in order to reduce your anxiety. There is also space for an
additional individual example.
5.4 Troubleshooting
1. ‘‘I don’t know what I’m thinking – I’m too scared.’’ Ask yourself, ‘‘What am I
scared of? What am I scared might happen?’’. It is diYcult to identify unhelpful
fears, especially to begin with. It may help to wait until the anxiety has dropped,
then think about the situation and associated fears. Re-entering a situation may
make the fears clearer.
2. ‘‘I can’t think of alternatives.’’ After many months to years of having anxiety-
provoking thoughts, it may be diYcult to think up less threatening alternatives.
Look at all available evidence, especially evidence that contradicts your
thoughts. Ask yourself why others around you do not fear the situation, and try
to consider what they might be thinking about the situation.
3. ‘‘I’m doing it and it’s not working.’’ Use all available techniques, including
relaxation and slow breathing, to reduce your anxiety. Do not expect to be
perfect at cognitive restructuring or expect the technique to work immediately.
131 Panic disorder and agoraphobia: Patient Treatment Manual
5.5 Summary
Let us take a moment to see where we are up to and to summarize what we have
learned by putting it into a series of steps.
Remember: The anxiety will always begin to fall within a few minutes and, if you act
promptly in controlling your breathing, you can prevent panic attacks.
SE CT I O N 6
6 Producing the panic sensations
One of the elements central to panic is the fearful reaction to bodily sensations,
such as a pounding heart, dizziness, etc. We deal with this subject towards the end
of the Wrst part of the program because the techniques involved are not easy for all
people to do and we want to be sure that you have some anxiety-management
132 Treatment of Anxiety Disorders
techniques. In this chapter we will deal with your reactivity to diVerent panic
sensations.
As we noted in the Wrst section of the Manual, diVerent sensations frighten
some people more than they frighten others. Just as you have been learning to
reduce your fear of particular sensations through regular graded exposure, you
can now begin to learn to reduce your fear of the frightening bodily sensations by
regular graded exposure. If you are not sure which symptoms are most relevant to
your fear we can use a series of exercises that bring on sensations similar to the
sensations experienced during anxiety and panic. In other words, you will expose
yourself to internal bodily feelings in the same way that you expose yourself to
feared situations through graded exposure. Fear reduction can be accomplished
only by repeatedly confronting the things that frighten you, in this case the bodily
feelings associated with panic.
Although you may not like the idea of deliberately bringing on the feelings that
are similar to those you experience when you panic, dealing with these fears is very
important. Many everyday experiences will cause you to feel sensations that are
similar to panic sensations. For example, any individual who engages in a hard
game of squash or goes for a jog may experience breathlessness, sweating and
light-headedness. These are normal reactions to the stress of exercise and should
not lead to fears of panic. In this part of the program we wish to dampen down, or
even extinguish, the anxiety produced by these harmless sensations.
In addition, performance of the exercises will provide you with a chance to
practice more purposefully the strategies you have acquired up to this point,
especially the rational thinking exercises. Their application during these repeated
practices will enhance their eVectiveness and their preparedness. The more you
rehearse a particular strategy, the more powerful and natural it becomes.
1. Hyperventilation
2. Shaking head
4. Step-ups
5. Holding breath
6. Body tension
7. Spinning
9. Chest breathing
If none of these exercises triggers some or other of your sensations, then you can
try to come up with some exercises of your own. For instance, if you are most
distressed by a dry mouth, you may wish to get some dental rolls and put them in
your mouth to soak up the saliva. Staring at a light for a few seconds and then
looking at a blank wall can create visual distortions that other people Wnd
distressing. Talk to your therapist about ways of creating the particular symptoms
that trouble you most.
134 Treatment of Anxiety Disorders
Do
∑ Bring on the sensations as strongly as you can during the exercises.
∑ Try to experience the sensations fully.
∑ Use the exercises as a chance to identify and challenge anxiety-provoking thoughts.
Don’t
∑ Use anxiety-management techniques before doing the exercises.
∑ Use distraction techniques during the exercises.
∑ Try to stop the sensations as soon as the time is up.
4. Once you have managed to bring anxiety associated with these exercises to a
minimal level (or even have no anxiety whilst doing them), you can extend
them by doing the following:
∑ Increasing the length of time by another 30 to 60 seconds.
∑ Standing up whilst doing the exercises.
∑ Doing the exercises in a park or other place away from help.
6.5 Troubleshooting
1. ‘‘I don’t need to do these exercises – I already know what my panic feels like.’’
These exercises allow controlled exposure to physical sensations associated
with panic attacks. Repeated exposure will reduce the amount of anxiety that
these normal, everyday physical sensations produce.
2. ‘‘These exercises don’t work, because I know that I’m safe.’’ Try doing these
exercises in a variety of settings: in the clinic, at home, or in a park. If you have
anxiety in any of these situations, try to examine the thoughts that are behind
this anxiety. For example, you may be more anxious at home than in the clinic,
because of a belief that you are somehow more at risk alone. Spend some time
challenging these unhelpful thoughts.
3. ‘‘I don’t feel anxious, because I’m in control of these physical sensations.’’ The
physical sensations produced are normal, everyday physical sensations. They
are the same as the physical sensations produced by daily activities, which may
trigger panic attacks in some people. Later in the program, we will be instruct-
ing people in how to incorporate these kinds of exercises in their day-to-day
lives.
4. ‘‘I can’t stand these sensations.’’ Try to identify the underlying thoughts that are
producing these fears, and challenge them. It is important to persevere with
these exercises, and gradually reduce your fear of them. This may take several
repetitions for some people. Some sensations may be unpleasant, but they need
not produce anxiety.
5. ‘‘I’m not having a good day today.’’ Most day-to-day illnesses can’t be predicted,
and sometimes it isn’t possible to avoid commitments because of them. It is
better to prepare for the colds and viral illnesses that aVect most people each
year, increasing your chances at better coping when they happen.
6. ‘‘These exercises will trigger a panic attack.’’ These exercises may increase
anxiety, because the physical sensations they cause generate anxiety-producing
thoughts. Try to identify these thoughts and challenge them with more adap-
tive and helpful thoughts. If necessary, use other techniques you have learned
to reduce your anxiety. Avoidance of physical sensations, like avoidance of
situations, does reduce anxiety in the long-term.
136 Treatment of Anxiety Disorders
DI ARY
Day:
Time
7–8
8–9 Breathing exercise
9–10
10–11
11–12
12–1 Breathing exercise
1–2
2–3
3–4
4–5
5–6
6–7 Breathing exercise
7–8
8–9
9–10 Breathing exercise
137 Panic disorder and agoraphobia: Patient Treatment Manual
SE C T I ON 7
7 Producing panic sensations in your daily life
Once panic attacks become regular, individuals with panic disorder and agora-
phobia can begin to misinterpret the physical sensations caused by everyday
activities as signals of panic. You may even have found that you avoid certain
activities because you are frightened by the sensations they produce. You might
avoid aerobic exercise because it makes your heart beat faster. You might not lift
heavy objects because it causes unpleasant physical sensations as a result of the
increased blood pressure. If the activities cause the sensations, you can then
misinterpret the sensations as signals of danger and a panic attack might occur.
The aim of this part of the program is to reduce any anxiety associated with
physical sensations produced by everyday activities.
As you begin these activities, it is important to note a diVerence between the
panic sensation exercises done previously and the activities outlined in this
chapter. When you did the exercises to produce the panic sensations, you would
have noticed that the sensations started and stopped roughly when the exercises
started and stopped. In contrast, when panic-like sensations are generated by daily
activities, their onset and oVset will be less clear. Do not worry about this. The
139 Panic disorder and agoraphobia: Patient Treatment Manual
more natural the activity is, the less likely it is that the sensations will start when
the activity begins and stop when the activity stops. Take, for example, going out
on a hot day. It takes some time to become hot and sweaty when you go outside
and it will take some time to cool down once you come inside again. This is just
what happens with natural everyday activities. However, if you worry about the
fact that the sensations are no longer as predictable as before and do not stop the
instant you stop the activity, you are just going to make the symptoms worse and
make it more likely that you will have a panic attack.
Following is a list of activities or places that may produce panic-like sensations.
Consider these activities and decide whether you avoid, or Wnd uncomfortable,
any of these activities for fear of having a panic attack. There may be other activities
of your own that you wish to add to the list.
∑ Heated vehicles or public transport
∑ Hot stuVy shops or shopping centers
∑ Watching medical programs
∑ Watching suspenseful TV programs or movies
∑ Watching sporting events on TV or in person
∑ Eating rich or heavy meals
∑ Arguments
∑ Amusement park rides
∑ Riding on boats or ferries
∑ Sexual activity
∑ Bushwalking
∑ Jogging or exercising of any kind
∑ Going to the gym or lifting weights
∑ Sports
∑ Dancing
∑ SurWng or swimming
∑ Getting up quickly from lying down
∑ Running up hills or stairs
∑ Walking in hot or humid conditions
∑ Heavily air-conditioned places
∑ Having showers with doors and windows closed
∑ Hot or steamy rooms
If you avoid any of these activities or places for fear of panic you should apply
your anxiety-management techniques, speciWcally graded exposure and straight
thinking. Begin with exposure to the least anxiety-provoking activity. The goal is
to repeat the activity a number of times until only mild anxiety is experienced.
Then move on to the next most anxiety-provoking activity. Below list up to Wve
activities you are aware of avoiding for fear of panic:
140 Treatment of Anxiety Disorders
Goals:
Now choose one goal you would like to start working on in the near future.
Write down the goal in the space provided, then break it down into steps. Also,
write down any anxiety-provoking thoughts you may have about doing this
activity, and then challenge and replace those thoughts.
Goal:
Steps:
Anxiety-provoking thoughts
Helpful thoughts
141 Panic disorder and agoraphobia: Patient Treatment Manual
As with the graded exposure tasks you have been carrying out the important points to
remember are:
SE CT I O N 8
8 More about thinking straight
Having discussed previously how unhelpful thoughts can be identiWed, chal-
lenged, and disputed we shall consider another method. Rather than engaging in a
mental exercise of weighing up the evidence a person can actively go out and seek
evidence for and against the belief.
Examples of unhelpful thoughts include:
If you had these thoughts you could argue with yourself about their truth.
However, a better test would be to try to go out without the tablets, to see whether
the anxiety decreased if you went near what you feared and stayed there, or to see
whether the air ran out and you suVocated in a tiny room. Obviously to achieve
this result the graded exposure exercises you planned are very relevant. Not only
will they help to elicit the thoughts (what better time to identify thoughts than
when you’re afraid) but you will be able to test them at the same time.
We now know that unhelpful thoughts (e.g., ‘‘I will panic and collapse’’) can
make your fears much worse than they otherwise would have been. Sometimes it is
possible to think yourself into a fearful state without even being near what you
fear. Disputing the unhelpful thought will decrease the power they have over your
feelings. As you begin to replace the unhelpful thoughts with helpful ones, your
feelings will become more appropriate to the situation you face.
You have all been identifying, challenging and disputing your unhelpful
thoughts, but it is not always that easy. To give you some extra help there are four
142 Treatment of Anxiety Disorders
types of question you can ask yourself that may make the unhelpful aspects of the
thoughts more clear.
1. ‘‘What is the evidence for what I thought?’’ Ask yourself whether other people
would accept the thought as correct. From your or other people’s experience,
what is the evidence that what you believe is true? Ask yourself whether you are
jumping to conclusions by basing what you think on poor evidence. How do
you know what you think is right?
e.g., If I panic I will deWnitely lose control.
2. ‘‘What alternatives are there to what I thought?’’ Is the thought the only one you
could have? Perhaps there are alternative explanations of an event or ways of
thinking about something. Determine whether any of these have better evi-
dence for them or would be more helpful in overcoming your feelings.
e.g., My heart is beating fast – I must be having a heart attack.
3. ‘‘What is the eVect of thinking the way I do?’’ Establish in your own mind what
your goals are and then ask whether the way you are thinking is helping you to
achieve those goals or is it taking you further away.
e.g., I failed in my exposure task, I’ll never improve, I might as well give up.
4. ‘‘What thinking errors am I making?’’ Some examples of common thinking
errors include:
(i) Thinking in all-or-nothing terms. This is black-and-white thinking in which
things are seen as all good or all bad, safe or dangerous – there is no middle
ground.
e.g., I know panic attacks are very dangerous.
(ii) Using ultimatums. Beware of words like always, never, everyone, no-one,
everything, or nothing. Ask yourself whether the situation really is as
clear-cut as you are thinking.
e.g., No-one else has a fear like mine, everyone else in the group is
improving so much faster than me.
(iii) Condemning yourself on the basis of a single event. Because there is one thing
that you cannot or have not done you then label yourself a failure or
worthless.
e.g., I avoided doing my exposure task today, I am a complete failure.
(iv) Concentrating on weaknesses and forgetting strengths. Try to think of other
times you have attempted or even been successful at something and think
about the resources that you really do have.
e.g., I haven’t made any progress and that’s just typical of me.
(v) Overestimating the chances of disaster. Things will certainly go wrong and
there is danger in the world, but are you overestimating these? How likely is
it that what you expect will really happen?
e.g., I could never hyperventilate alone because I might go crazy or die.
143 Panic disorder and agoraphobia: Patient Treatment Manual
(vi) Exaggerating the importance of events. Often we think that some event will be
much more important than it turns out to be. Ask yourself, ‘‘What diVer-
ence will it make in a week or 10 years? Will I still feel this way?’’
e.g., My breathing rate is not decreasing as fast as everyone else in the
group.
(vii) Fretting about the way things ought to be. Telling yourself that things should
be diVerent or that you must act in a certain way indicates that you may be
worrying about how things ‘‘ought’’ to be rather than dealing with them as
they are. Challenge the ‘‘should’s’’ and ‘‘must’s’’. Why should it be that way?
Why must you act that way?
e.g., I ought to be better by now.
(viii) Pessimism about a lack of ability to change a situation leads to feelings of
depression and lowered self-esteem. There may be no solution but you will
not know until you try. Ask yourself whether you are really trying to Wnd
answers and solutions.
e.g., I’ll never completely get over my panics.
(ix) Predicting the future. Just because you acted a certain way in the past does
not mean that you have to act that way forever more. Predicting what you
will do on the basis of past behavior means that you will cut yourself oV from
the possibility of change.
e.g., I’m a nervous person, I’ll always be afraid.
most important source of praise is from inside you, because you know yourself
best and what your actions mean to you.
8.2 Summary
SE C T I ON 9
9 Keeping your progress going
9.1 Coping with setbacks or difficulties in making progress
Setbacks or diYculties in making progress are generally the consequence of either
poor management or poor planning of goals and steps. If you should experience
such diYculties, you must carefully analyze the way in which you carry out these
two exercises.
lie between the last step you completed successfully and the step with which you
are now having diYculty?
∑ Do you need to practice new steps more frequently and for longer periods
before moving on to more diYcult ones?
∑ Is your level of certainty of success too high or too low?
∑ If your objectives are too easy or too diYcult you will not make progress. Are
you sure that you are not expecting too much of yourself?
∑ Make sure that you give yourself suYcient praise for your achievements.
Remember that the key to success is gradual but regular progress.
cope with that and I’m not going to turn it into an excuse for giving up altogether.
Now I’ll get out my Manual and start again.’’ Of course, some people do stop
things like relaxation training or slow breathing when they have been feeling okay
for some time.
This is Wne, so long as you keep aware of any stress or anxiety that may be
creeping back into your life, and restart the training as soon as you become aware
of any increase. Also, it will be important to reinstate such techniques if you have
recently experienced any stressful life event.
9.4 Conclusion
You now have three skills that you have been taught and now need to practice. You
need to use the various exposure tasks, working up the graded ‘‘stepladders’’ of
anxiety, to reduce your fear of your panic. Relaxation exercises will help to reduce
your general level of tension before the exposure task and the isometric exercises
will regulate tension during exposure. Slow breathing will help to keep control of
any anxiety you may experience. By thinking straight you will be able to stop
anxiety from spiraling into panic.
SE C T I ON 1 0
10 Recommended resources
The following books are available from most good bookstores, some news-stands,
and over the internet. If in doubt, ask whether the book can be ordered. We also
suggest that you use your local library to gain access to many of these books. When
you read these or any similar books on the management of anxiety or depression,
remember that they are best regarded as guidelines only. Be critical in both a
positive and negative sense when reading these books, so that you get what is best
for you out of them. Most of these books are inexpensive.
10.1 Books
Barlow D and Rapee R. (1997) Mastering Stress: A Lifestyle Approach. Killara, NSW: Lifestyle
Press.
Burns DD. (1999) The Feeling Good Handbook, revised edition. New York: Penguin.
Copeland ME. (1992) The Depression Workbook: A Guide for Living with Depression and Manic
Depression. New York: New Harbinger.
Davis M, Eshelman ER and McKay M. (1995) The Relaxation and Stress Reduction Workbook,
fourth edition. Oakland, CA: New Harbinger.
Ellis A and Harper R. (1979) A New Guide to Rational Living. Hollywood, CA: Wilshire Book
147 Panic disorder and agoraphobia: Patient Treatment Manual
Company.
Emery G. (2000) Overcoming Depression: A Cognitive-Behavior Protocol for the Treatment of
Depression. Oakland, CA: New Harbinger.
Greenberger D and Padesky C. (1995) Mind Over Mood. New York: Guilford.
Marks IM. (2001) Living with Fear. New York: McGraw-Hill.
McKay M and Fanning P. (1987) Self-Esteem: A Proven Program of Cognitive Techniques for
Assessing, Improving and Maintaining Your Self-Esteem. Oakland, CA: New Harbinger.
McKay M, Davis M, and Fanning P. (1995) Messages: The Communication Skills Book. Oakland,
CA: New Harbinger.
McKay M, Davis M, and Fanning P. (1997) Thoughts and Feelings: Taking Control of Your Moods
and Your Life. Oakland, CA: New Harbinger.
Meichenbaum D. (1983) Coping With Stress. London: Century Publishing.
Page A. (1993) Don’t Panic! Overcoming Anxiety, Phobias and Tension. Sydney: Gore Osment.
Walker CE. (1975) Learn to Relax: 13 Ways to Reduce Tension. Englewood CliVs, NJ: Prentice
Hall.
Weekes C. (1966) Self-Help For Your Nerves. Sydney: Angus and Robertson.
Weekes C. (1972) Peace From Nervous SuVering. Sydney: Angus and Robertson.
10.2 Video
Rapee R, Lampe L. (1998). Fight or Xight? Overcoming Panic and Agoraphobia. Available from
Monkey See Productions. P.O. Box 167, Waverley, NSW 2024 Australia.
Social phobia
Syndrome
Clinical description
Social phobia is characterized by phobic anxiety and avoidance of social or
performance situations. There is fear of scrutiny, of doing or saying something
that would be embarrassing, and of being seen to be anxious. Central to the
disorder is an underlying fear of negative evaluation (Beck et al., 1985; Liebowitz et
al., 1985; Lucock and Salkovskis, 1988; Mattick and Peters, 1988; Mattick et al.,
1989). Both the probability and anticipated detrimental consequences (cost) of
negative evaluation are exaggerated. Social phobia for many patients is a chronic
and disabling condition, with a signiWcant morbidity in terms of personal distress,
failure to achieve full social, occupational and personal potential, and signiWcant
psychiatric comorbidity. Cognitive, behavioral, and physiological aspects of the
disorder have been recognized.
Individuals with social phobia experience many of the same anxiety symptoms
as people with other anxiety disorders. However, the symptoms that are most
troubling are those which are most visible to others: 77% reported blushing,
sweating or trembling as an accompanying symptom in one study (Mersch et al.,
1995). Individuals with social phobia worry that these symptoms indicate to
others that they are anxious. They worry that if they are viewed as being inappro-
priately anxious they will be evaluated negatively.
Avoidance is the most prominent behavioral symptom of social phobia. Many
patients will avoid the feared situations when possible, but will endure with
intense anxiety when the negative consequences of avoidance are perceived to
outweigh the negative consequences of attending. Social situations that cause
anxiety may have primarily an interactional focus (e.g., initiating and maintaining
conversations, meeting or ‘‘getting to know’’ others) or a performance focus (e.g.,
public speaking, presentations in meetings and tutorials, writing or signing one’s
name in front of others). Situations that involve actual or possible scrutiny may
also trigger anxiety (e.g., standing in line, using public transport, using public
toilets, using the telephone when others are around, eating or drinking in public,
148
149 Social phobia: Syndrome
crowded situations including shops and cinemas). Most patients with social
phobia fear more than one situation (Turner and Beidel, 1989; Manuzza et al.,
1995).
less disabling, associated with less comorbidity and better prognosis (Manuzza et
al., 1995; Kessler et al., 1999b). Comorbid depression and alcohol abuse become
increasingly more common along the spectrum from discrete to generalized social
phobia to social phobia comorbid with APD (Turner et al., 1986; Holt et al., 1992;
Lepine and Pelissolo, 1998; Stein and Chavira, 1998). Greater autonomic arousal is
evident in social phobia limited to a fear of public speaking (Stein, 1998).
Currently there is most support for the view that social phobia and APD
represent diVerent points on a spectrum whereby the comorbid condition is
associated with greater severity and pervasiveness of anxiety and distress, more
comorbidity, and greater functional impairment (Holt et al., 1992; Turner et al.,
1992b; Rapee, 1995; Boone et al., 1999). Estimated rates of comorbid APD in
social phobia vary from 18% to 84% (Alnaes and Torgersen, 1988b; Schneier et al.,
1991; Turner et al., 1991; Holt et al., 1992; Mersch et al., 1995; Baillie and Lampe,
1998; Turk et al., 1998). In studies utilizing DSM-III-R criteria there is little to
distinguish between those with generalized social phobia alone and those in whom
the condition is comorbid with APD on feared situations, general cognitive focus,
subjective situational anxiety and perceived impairment of performance (Holt et
al., 1992; Turner et al., 1992b) but the latter exhibit greater avoidance and overall
distress (Turner et al., 1986). First-degree relatives of probands with generalized
social phobia show markedly elevated rates of APD as compared with relatives of
controls without social phobia (Stein et al., 1998). DSM-IV made signiWcant
revisions to the criteria for APD, for which there is some empirical support (Baillie
and Lampe, 1998). The greater emphasis on fears of rejection and humiliation,
and the sense of personal inadequacy and inferiority required to make the
diagnosis may enable the identiWcation of a group of individuals who diVer in
signiWcant ways from the currently recognized subtypes of social phobia and who
may have needs currently unmet by existing treatment programs.
Case 1
Patient identification
Mrs. B is a 45-year-old woman who is married with two children. She works part-time with
her husband in their own business.
worries about blushing and fears her hands may shake as she is serving guests or eating, and
others will think her odd or weak. Her anxiety is worst when she feels she is the center of
attention. Recently Mrs. B felt so anxious before the event she convinced her husband to
make an excuse and take their guests to a restaurant without her. When asked about other
difficult situations Mrs. B says that she is comfortable with friends she knows well, but that
she does become very anxious about meeting new people socially and would prefer to avoid
it. She is uncomfortable signing anything with someone watching and will avoid doing so
whenever possible. She is highly anxious about public speaking and her husband takes
responsibility for any meetings or presentations that are necessary to advance the business.
She also never joined parent or community groups, despite having some interest in doing so.
Family history
Mrs. B described her father as a quiet, gentle man who socialized little outside the family, but
her mother was sociable and outgoing. She has one brother who is much like her in
personality.
Premorbid personality
She describes herself as always having been ‘‘shy’’, meaning that she has always felt anxious
meeting new people, feeling self-conscious and fearful of saying something foolish or
appearing socially inadequate. She was always a little anxious at the start of each school year,
but quickly settled in, enjoyed school, and always had a small group of close friends. She is
confident with people she knows well, in knowing her job and in her intimate relationships.
Diagnosis
Social phobia, generalized subtype.
Mrs. B is typical of patients at the milder end of the social phobia spectrum, who are able to
enjoy some satisfying social relationships and who are minimally impaired. This case illus-
trates the problems of making the generalized versus discrete distinction: Mrs. B’s fears
involve only two types of situation, meeting new people and public speaking. However, she
encounters, or avoids because of her anxiety, many situations of these types. She also admits
to a fear of scrutiny, and it may emerge during treatment that she has problems with a wider
range of situations than she currently realizes, because she has adapted her activities around
her fears over the years.
Case 2
Patient identification
Mr. P is a 35-year-old single clerk.
department since he left school, and in the same position for the past 10 years. However, his
employer is ‘‘restructuring’’ and he has learned that he is to be moved to a different position
where he will be expected to learn new skills and be part of a team. This has made Mr. P
extremely anxious and he does not think he will be able to cope. Getting to know new people
terrifies him: ‘‘I never know what to say. I make people uncomfortable and they don’t want
me around.’’ However, he can cope better if he knows he will only have to see someone once
or twice – when he has to establish any type of relationship with another person he becomes
convinced that they will soon learn that he is inadequate, even worthless, and will reject him.
He is fearful of meeting the new demands that will be placed on him: ‘‘If I can’t do it they’ll be
angry [and reject me].’’ Mr. P also worries about others seeing his anxiety, especially the fact
that he tends to sweat profusely when anxious, but says that this does not tend to be much of
a problem in practice because for years he has avoided any situation that will trigger his
anxiety. Mr. P lives with his parents, and they take care of all outside chores such as shopping
and even buying his clothes. Mr. P’s only outings are to work. He utilizes his employer’s
flexible hours arrangement to avoid traveling on the bus at peak hours, because he is acutely
uncomfortable in crowds. In his current work situation he shares a large office with two
others who are often out on field work. He has one friend from school who visits him
occasionally, and on very rare occasions he has gone out with this friend to a bar, where the
alcohol has enabled him to tolerate the situation. He has never had an intimate relationship
and never accepts social invitations.
Previous history
Mr. P was treated for depression in his early 20s. There have been other periods of his life
where he has felt depressed but has not sought treatment. Mr. P has used alcohol to excess
intermittently but has never missed work because of his drinking.
Family history
Mr. P is an only child. His parents are both quiet and have never socialized outside the home.
Mrs. P had postnatal depression after Mr. P’s birth. He describes her as ‘‘nervy’’.
almost all eye contact, although this improved somewhat as the interview progressed. His
history was halting and his speech was quiet and colorless. His affect was anxious and
dysphoric. There was no evidence of thought disorder, delusions, or hallucinations.
Diagnosis
Social phobia, generalized subtype.
Avoidant personality disorder.
This example illustrates the typically earlier onset of symptoms when social phobia is
comorbid with APD, the typically very negative self-beliefs and the generalized anxiety and
avoidance that is driven primarily by fear of rejection. Mr. P expects rejection because he
believes himself inferior and unable to meet the social expectations of others. The avoidance
in APD is so extensive that anxiety may not be a prominent presenting complaint, in contrast
to social phobia. An earlier age at onset of symptoms has been associated with greater
disability in social phobia. This may explain at least some of the greater disability and
impairment seen in APD. Although duration of illness is not linked to outcome, age at onset
was found to be a powerful predictor of recovery in a Canadian epidemiological study (DeWit
et al., 1999). Those aged 7 years or less at onset of the disorder were least likely to recover.
Epidemiology
Epidemiological and clinical surveys in the past decade have put the lifetime
prevalence of social phobia at between 9.5% and 16% in Western nations,
154 Treatment of Anxiety Disorders
general population: 37% with nongeneralized social phobia and 64% with general-
ized social phobia in a clinical sample had never married (Manuzza et al., 1995). A
small study of media respondents found that those meeting criteria for social
phobia were signiWcantly more likely than a group meeting criteria for panic
disorder to be single, living alone and unemployed, despite a higher level of
education (Norton et al., 1996). The degree of impairment, disability and co-
morbidity increases along the spectrum from discrete to generalized social phobia
to social phobia comorbid with APD.
Differential diagnosis
Axis I disorders
Social phobia may be confused with agoraphobia, since many of the same types of
situation will be avoided. However, the underlying fearful cognitions, the reasons
for avoiding, will diVer. The person with social phobia may dislike shopping
centers, crowded trains, and queues because of the risk of scrutiny and the
diYculty of escaping in case they embarrass themselves. The person with agora-
phobia may dislike these same situations because of the diYculty of escaping in
case of physical harm. Embarrassment will not be the main focus of the fear. A
useful distinguishing exercise can be to ask a patient whether they would be
anxious if they could be completely alone in the feared situations: the person with
agoraphobia will Wnd this a frightening proposition, whereas an individual with
social phobia will report that if there were no one else around they would not have
the problem. Social phobia may also be confused with simple phobia when there
appears to be only one feared situation. If the fear is of scrutiny or embarrassment,
a diagnosis of social phobia takes precedence, but may be subtyped as non-
generalized. In clinical practice, a careful history will usually reveal that more than
one situation is avoided. A loss of conWdence and social withdrawal are common
features of major depression. There may even be associated social anxiety. How-
ever, the history of premorbidly normal social functioning excludes social phobia.
Social anxiety and avoidance is frequently reported in body dysmorphic disorder
and to exclude this condition it can be helpful to ask patients whether there is
some particular aspect of their appearance or behavior that they fear will attract a
negative reaction from others. Whilst individuals with social phobia may have a
range of concerns regarding their presentation to others, individuals with body
dysmorphic disorder typically manifest a marked preoccupation with a quite
speciWc perceived defect while appearing normal in reality. Social phobia may be
comorbid with body dysmorphic disorder in 11% to 12% of cases (Wilhelm et al.,
1997).
157 Social phobia: Syndrome
Assessment
There are now a large number of measures speciWcally designed for use in social
phobia. The choice of assessment instrument will be aVected by whether the
clinician wishes to measure symptoms, discriminate between individuals with
social phobia and nonanxious individuals or those meeting criteria for other
anxiety disorders, measure treatment outcome, or conduct research. The Fear of
Negative Evaluation Scale (FNE; Watson and Friend, 1969) is a 30-item true–false
self-report questionnaire that provides a measure of apprehension about others’
evaluations, distress over negative evaluations, and the expectation of negative
evaluation. Means of around 24 have been described in social phobic populations
(Heimberg et al., 1988). The FNE is useful in conWrming the presence, and
perhaps extent, of social evaluative anxiety. However, available evidence suggests
that it does not reliably discriminate social phobia from other anxiety disorders
(apart from speciWc phobias), and it is not recommended for use as a diagnostic
tool (Turner et al., 1987; Oei et al., 1991). Several newer measures have been
developed, including the Social Phobia Scale (SPS; Mattick and Clarke, 1998), the
Social Interaction Anxiety Scale (SIAS; Mattick and Clarke, 1998), the Social
Phobia and Anxiety Inventory (SPAI; Turner et al., 1989, 1996), and the Liebowitz
Social Anxiety Scale (LSAS; Liebowitz, 1987). The psychometric properties of
these scales are gradually being established. The SPS has been shown to be most
closely associated with scrutiny fears, and the SIAS with fears of social interaction
(Cox et al., 1998; Ries et al., 1998). The SPAI asks individuals about somatic
symptoms of social anxiety. The SPAI and LSAS also aim to measure avoidance
behaviors in social phobia, although the fear/anxiety and avoidance subscales of
the LSAS have been shown to be highly correlated (Cox et al., 1998; Safren et al.,
158 Treatment of Anxiety Disorders
1999). Overall, there has been consistent failure to demonstrate any reliable
association between verbal report measures and observable behavior. The SPAI
and SIAS may be particularly sensitive measures in their ability to distinguish
between speciWc and generalized subtypes of social phobia (Ries et al., 1998), and
the SPAI also has a high degree of speciWcity in distinguishing social phobia from
other anxiety disorders (Cox et al., 1998; Peters, 2000). All the newer measures
appear sensitive to treatment change (Ries et al., 1998).
Etiology
Etiological theories of social phobia have been proposed, encompassing genetic/
biological, environmental and cognitive behavioral domains. Research to date has
suggested heritable factors that include a general vulnerability to anxiety disorders
(Andrews et al., 1990a; Kendler et al., 1992a; Manuzza et al., 1995; Beidel, 1998).
The general vulnerability probably corresponds to an elevated trait anxiety,
common to all anxiety disorders and also found in some depressive disorders
(Andrews et al., 1990a; Parker et al., 1999).
Several family studies have now shown an increased incidence of social phobia
in Wrst-degree relatives of probands with social phobia. A recent study using twin
data across two measurement occasions (allowing better control over sources of
measurement error, including diagnostic unreliability) has found substantial
increases in the heritability estimates for all phobias. It is now estimated that
genetic factors account for approximately 50% of the variance in liability to
develop social phobia (Kendler et al., 1999). Generalized social phobia appears to
show the strongest association with genetic/biological factors. More relatives of
probands with social phobia than control probands met criteria for social phobia
in the study of Manuzza et al. (1995), although there did not appear to be a greater
rate of generalized than nongeneralized social phobia in these relatives. In a later
study utilizing a similar design, Stein et al. (1998a) found a greatly increased
incidence of generalized social phobia (26.4%) but not the nongeneralized form in
the relatives of clinic attenders with generalized social phobia as compared with
relatives of controls (2.7%).
In their seminal work, Kagan et al. (1988) identiWed a temperamental construct,
which they referred to as behavioral inhibition to the unfamiliar (BI), and
suggested that it represents a putative biological basis for shy behavior. They
found in a longitudinal study that extreme shyness (deWned as inhibition in social
situations) at age 2 years was predictive of inhibition at age 7 years. Similarly,
extreme disinhibition remained relatively stable over time. Further research has
sought to establish the relationship of BI to the later emergence of anxiety
disorders and the utility of early intervention strategies. Behavioral inhibition has
159 Social phobia: Syndrome
since been linked both to panic disorder/agoraphobia and to social phobia, but
not to speciWc phobia, OCD, GAD or aVective disorder (Beidel, 1998; Mick and
Telch, 1998; Cooper and Eke, 1999). The children in the longitudinal cohort
described by Kagan had signiWcantly higher rates of phobic disorder of childhood
than the uninhibited children. Inhibited children also seem more likely to have
parents with social phobia, especially if the child has BI in association with
multiple anxiety disorders (Knowles et al., 1995). DeWnitions of the BI construct
encompassed both social and nonsocial novelty. Preliminary evidence suggests
that BI in response to social novelty may be more linked to later social phobia, but
the same study failed to Wnd a close relationship between panic/agoraphobia and
nonsocial novelty (Van Ameringen et al., 1998). A stronger association with
generalized than with nongeneralized social phobia has been reported (Wittchen
et al., 1999). It remains unclear at present whether BI is a general vulnerability
factor related to the development of social phobia and agoraphobia but not that of
speciWc phobias or whether there is a particular relationship with social anxiety.
The neurobiology of social phobia remains poorly understood. Biological
correlates of social dominance, social aYliation and attachment have been identi-
Wed in animals (e.g., Stein, 1998) that have potential for the development and
study of human models. There is preliminary evidence for both serotonergic and,
alone of the anxiety disorders, dopaminergic dysfunction in social phobia (Nutt et
al., 1998; Stein, 1998).
Several psychological models of social phobia have been proposed (for a review,
see Mattick et al., 1995). Many studies have sought to assess the association of
social phobia with childhood environmental factors but rely on recall of distant
events, and hence are subject to unreliable accuracy of both recall and causal
attribution. Aversive conditioning models have been proposed but the data suVer
from the limitations of retrospective studies. There may be some role for aversive
social events, perhaps making some contribution to the initiation or maintenance
of social phobia: typically 60% of subjects report such events (Mattick et al., 1995).
Preparedness conditioning theories of social phobia suggest that certain types of
social interaction may have a particular salience such that individuals may more
readily learn particular associations. Öhman’s (1986) work strongly suggests that
humans readily learn to fear critical, angry or rejecting faces but does not explain
fear of scrutiny (Mattick et al., 1995). The social learning model (e.g., Bandura,
1977) may have some relevance to the acquisition of phobias (there is some
experimental evidence for this in primates), but has not yet been studied with
respect to social phobia. However, Kendler et al. (1992a, 1999) concluded that
familial environmental inXuences on social phobia are small or insigniWcant.
Individual-speciWc environmental inXuences may account for 40% to 60% of the
etiology of social phobia. A model of social skills deWcits as a causal inXuence in
160 Treatment of Anxiety Disorders
social phobia has also been suggested. It is now realized that an apparent lack of
skill may represent either a true skills deWcit or an inhibition of skill expression.
There is an association between severity of social phobia and poor social skills, but
a causal relationship has not been established.
Cognitive theories of the initiation and maintenance of emotional disorder have
been applied to social phobia, and now represent the strongest area of research
interest among psychological theories (e.g., Clark and Wells, 1995; Rapee and
Heimberg, 1997). In social phobia, the underlying cognitive set, or ‘‘schema’’, is
seen to include beliefs that negative evaluation is a catastrophic outcome with a
high probability of occurring as a result of any one of several contingencies speciWc
to the individual (e.g., Clark and Wells, 1995; Leary and Kowalski, 1995: Rapee
and Heimberg, 1997). Evidence is available, from our laboratory and others
(Lucock and Salkovskis, 1988; Rapee and Lim, 1992), that individuals with social
phobia underestimate their social performance, overestimate the probability of
negative social outcome, and overestimate how bad it would be if the feared
outcome occurred. Individuals with social phobia have more negative thoughts in
social situations than other anxious and nonanxious controls and show a prepon-
derance of negative thoughts prior to treatment (Bruch et al., 1991). Data are
available that support a cognitive vulnerability factor of discrepancy between
individuals’ views of themselves as they are and their view of how others see them
(Mattick et al., 1995). These patients also tend to attribute more responsibility for
negative outcomes to themselves rather than to external factors, in a pattern
opposite to those who are not particularly socially anxious (Hope et al., 1989).
Recently, there has been considerable research interest from an information-
processing perspective, seeking to understand how individuals with social phobia
process information about themselves and their environment in social situations.
Several cognitive ‘‘biases’’ have been identiWed that result in hypervigilance for
social cues and inXuence the individual to interpret the cues in a manner consist-
ent with the underlying cognitive schemas of social phobia, even though the
interpretations may not be particularly realistic or helpful to that individual. An
interpretive bias ensures that scrutiny, criticism, and negative evaluation are
detected even when realistically not apparent, and an attentional bias towards
threat cues (physiological symptoms of anxiety, presence of others who may
potentially scrutinize) maintains overestimates of probability and cost of negative
social outcomes (Hope et al., 1989; Mattick et al., 1995). Interpretation bias may
also lead an individual to misinterpret interoceptive information as disastrous and
to interpret an ambiguous social situation as negative. Individuals with social
phobia consistently tended towards a negative interpretation of self-relevant
situations, even when presented with positive alternatives in one study (Amir et
al., 1998a). It is suggested that this may be a relative negative bias as compared
161 Social phobia: Syndrome
with the generally more positive interpretations that nonsocially anxious individ-
uals make (Constans et al., 1999). Individuals with prominent social-evaluative
concerns have been shown to focus their attention on themselves in social
situations, attempting to create an image of how they would appear to others,
often referred to as ‘‘the observer perspective’’ (Wells and Papageorgiou, 1999).
This contrasts with the cognitive experience of individuals with normal levels of
social anxiety whose attention is focused mostly on aspects of the social interac-
tion or situation. Self-focused attention is postulated to prevent the individual
from gaining more accurate information about the situation and others’ responses
that might disconWrm negative expectations. The beneWts of exposure were en-
hanced in a single small case series when individuals with social phobia were
encouraged to focus attention on actual social cues rather than becoming pre-
occupied with their own thoughts and feelings (Wells and Papageorgiou, 1998)
and reduced self-focused attention was linked to better outcome in a study of
group cognitive behavioral therapy (Woody et al., 1997).
Memory and judgment biases have also been reported in socially anxious
individuals, although there have also been negative Wndings for memory bias
(Hope et al., 1989; Mattick et al., 1995; Amir et al., 1998b; Constans et al., 1999).
Comorbidity
ECA (Schneier et al., 1992), National Comorbidity Survey (NCS; Magee et al.,
1996) and National Survey of Mental Health and Wellbeing in Australia
(NSMHWB, Lampe et al., unpublished data) data indicate a high rate of comor-
bidity between social phobia and other Axis I conditions, particularly other
anxiety disorders and major depression (Table 8.1). In the NCS, 81% of persons
with social phobia reported at least one other lifetime DSM-III-R disorder. In
contrast to other anxiety disorders (excluding speciWc phobia) and to depression,
social phobia most often preceded the comorbid disorder (typically in about 70%
to 80% of cases in both the ECA and NCS studies; Schneier et al., 1992; Kessler et
al., 1999b).
Depression, suicidal ideation and suicide attempts occur in social phobia at
greater than population rates. However, an elevated frequency of suicide attempts
in social phobia appears to be mostly, though not completely, related to the
presence of comorbid conditions. According to ECA data, the rate was approxi-
mately 14 times the population frequency. In the NSMHWB survey, the presence
of a comorbid Axis I disorder resulted in a tripling of the rate of suicidal ideation,
but without a corresponding increase in suicide attempts. When social phobia was
comorbid with anxious personality disorder (closely related to APD) both suicidal
ideation and attempts were reported at signiWcantly higher rates – suicide
162 Treatment of Anxiety Disorders
Table 8.1. Comorbidity in social phobia compared across three epidemiological surveys
attempts were reported at almost four times the frequency of that in uncom-
plicated social phobia. An early study (Amies et al., 1983) found that parasuicidal
acts were more common in a socially phobic sample than in a comparison group
meeting criteria for agoraphobia, but more recent epidemiological and clinical
studies have failed to conWrm this Wnding (Cox et al., 1994; Norton et al., 1996;
Montgomery, 1998). The risk of depression does not appear to increase with
duration of social phobia, but may be reduced if social phobia remits (Kessler et
al., 1999a). Clinical samples have also shown elevated rates of depression, suicidal
ideation and suicide attempts in social phobia comorbid with other Axis I or with
Axis II conditions (Amies et al., 1983; Turner et al., 1991; Weiller et al., 1996). The
presence of depression is likely to obscure the diagnosis of social phobia in
primary care (Weiller et al., 1996). Alcohol abuse is another important area of
comorbidity. Excessive use of alcohol has been reported in 16% to 36% in clinical
samples with social phobia (Amies et al., 1983; Liebowitz et al., 1985; Schneier et
al., 1989). SigniWcantly, in the Schneier et al. (1989) study, the rate of alcoholism
as deWned by research diagnostic criteria was twice the population rate for men,
but three to four times the population rate for women, suggesting that women
with social phobia may be particularly at risk of developing alcohol abuse.
Epidemiological studies generally Wnd the rate of alcohol abuse or dependence in
social phobia to be one to two times the population prevalence but have not
163 Social phobia: Syndrome
Summary
Social phobia is a fear of negative evaluation that results in signiWcant avoidance of
social situations. AVected individuals overestimate the probability and adverse
consequences of negative evaluation and process social information in ways that
maintain such estimates. The disorder aVects men and women almost equally,
begins most commonly in the second decade of life, and has a chronic course. It is
associated with signiWcant personal distress and secondary morbidity, and
commonly results in failure to achieve full social and occupational potential.
9
Social phobia
Treatment
Aims of treatment
The aims of treatment are symptom reduction and improved function. Elimin-
ation of all anxiety is unlikely (and unnecessary), and the therapist has a role in
helping the patient to set realistic goals for therapy. Psychological and pharmacol-
ogical treatments are available for social phobia. The treatments for which there is
most evidence of eYcacy are cognitive and exposure-based treatments, social skills
training packages, antidepressant medication and benzodiazepine anxiolytics. In
general, outcome is related to severity of symptoms at pretreatment.
social skills of patients with social phobia, comparing those with and without
avoidant personality disorder. They found that patients with social phobia alone
felt anxious, and perceived that others found them anxious and inadequate, but in
fact had appropriate social skills. Those with APD were found to be markedly
lacking in social skills. However, the authors were unable to exclude profound
inhibition in social situations as the underlying cause giving rise to the appearance
of skills deWcits: in APD, severe anxiety related to a core schema that social error
will lead to rejection can result in profound social inhibition and avoidance.
Whatever the relation of social skills to social phobia may be, social skills
training packages demonstrate an eVectiveness equal to exposure therapy. This
appears to be the case where participants’ existing social skills have not been
assessed (Van Dam-Baggen and Kraaimaat, 2000) and is not improved by at-
tempting to direct those with skills deWcits towards social skills training (Wlazlo et
al., 1990). Maintenance of therapeutic eVects to 2 years has been demonstrated.
For patients who are ‘‘socially dysfunctional’’ and who have social phobia, social
skills training has been reported to be superior to bibliotherapy, group discussion,
and psychoanalytical group psychotherapy. For these patients, who would prob-
ably meet criteria for APD, it does not seem that the eVect of social skills training is
enhanced by the addition of propranolol, anxiety-management techniques such as
relaxation, or by cognitive strategies. On the other hand, those with APD improve
to an equivalent degree when they are treated with cognitive behavioral therapy
(CBT). Emmelkamp et al. (1985a), comparing exposure and cognitive therapy,
noted that improvement in social anxiety can occur in the presence of persisting
poor social skills and that, conversely, treatment failure is not predicted by poor
social skills. Social skills training is a complex package with components of
exposure and desensitization, behavioral rehearsal, and modeling of appropriate
behavior (Emmelkamp et al., 1985a; Marks, 1985) – it remains unclear which
aspect(s) of the package may be eVective. The most active ingredient appears to be
the exposure component, since patients do equally well whether they have formal
social skills training or are given homework requiring social interaction
(Stravynski and Greenberg, 1989; Stravynski et al., 2000). In patients with APD,
social skills training may have the beneWt of improving social performance and
increasing prosocial behaviors.
Behavioral treatments
Recognition of the success of exposure and desensitization techniques in treating
other phobic disorders led to trials of these techniques in the management of
social phobia. Studies using imaginal desensitization techniques were largely
completed prior to the publication of DSM-III, and used subjects variously
diagnosed as socially phobic, socially dysfunctional, and socially anxious. In a
166 Treatment of Anxiety Disorders
review of these techniques, Marks (1985) found that in general they were not very
eVective in treating the problems under study, although there are some reports of
eVectiveness equal to social skills training (Shaw, 1979; Stravynski and Greenberg,
1989). Graded exposure to feared social situations, within a group treatment
setting and in vivo, is the most common behavioral technique currently in use. It
has been shown to reduce the physiological symptoms of anxiety in feared
situations, and reduce avoidance of targeted situations (Emmelkamp et al., 1985b;
Wlazlo et al., 1990). Exposure alone results in signiWcant improvement in social
phobia. However, given the evidence for the importance of cognitive factors in
social phobia, it is of signiWcant interest to compare the results of exposure therapy
to cognitive therapy and of exposure alone to the combination of cognitive and
exposure therapies.
100
90
Mean % of BAT completed COMB
80
70 CR
60 EXP
50
40
30 WLC
20
10
0
Pre Post F/U
Assessment occasion
Figure 9.1 Behavioral approach test (BAT) mean scores (percentage) before (Pre) and after (Post)
treatment, and at 3-month follow-up (F/U). CR, cognitive restructuring without exposure;
EXP, guided exposure; COMB, guided exposure with cognitive restructuring; WLC, wait-list
control. (Redrawn with permission from Peters (1985), unpublished honors thesis, Univer-
sity of New South Wales.)
suggest that the addition of cognitive therapy may provide no advantage over
exposure alone (Biran et al., 1981; Stravynski et al., 1983; Van Velzen et al., 1997).
Taylor (1996), in a recent meta-analysis, located 25 studies using DSM criteria and
comparing two active treatments or using a placebo or wait-list control. Most
studies included a majority of participants with generalized social phobia. In this
analysis, exposure therapy, cognitive therapy, social skills training and combined
cognitive therapy and exposure were all eVective relative to wait-list control, but
only combined cognitive therapy and exposure yielded a signiWcantly greater eVect
size than a placebo. There was a trend for the combined treatment to show larger
eVect sizes. In this analysis the eVect sizes for both pill- and attention-control
placebo were similar at 0.4 to 0.5, while eVect sizes of the active treatments ranged
from 0.6 (for social skills training and for cognitive therapy alone) to 1.0 (for
combined cognitive and exposure therapy). All active treatment conditions
showed increased eVect sizes at 3 months posttreatment, at which time there was
little diVerence between them due largely to the signiWcant gains that occurred in
the cognitive therapy and social skills training groups. At 3 months all eVect sizes
were close to 1.0.
A similar Wnding has been reported by Mattick et al. (1989; see Figure 9.1) and
Salaberria and Echeburua (1998). In these studies, the exposure-only group
actually showed some deterioration at follow-up. Gould et al. (1997a) required a
no-treatment or wait-list control or psychological placebo for studies selected for
168 Treatment of Anxiety Disorders
meta-analysis. Sixteen studies were identiWed, of which six were also included in
the Taylor (1996) meta-analysis. Most of the diVerences are explained by the
inclusion of more early studies (including pre-DSM-III) and exclusion of studies
comparing only active treatments in the Gould et al. (1997) meta-analysis. Despite
these, and other minor methodological diVerences, the Wndings were similar, with
average eVect sizes of 0.8 for combined exposure plus cognitive restructuring, and
0.6 for cognitive therapy alone and for social skills training. However, a slight
advantage was reported for exposure alone, with an average eVect size of 0.89.
Most studies did not report follow-up data for the control condition (understand-
ably, since most such research is conducted in clinical settings where patients who
meet criteria for social phobia are seeking treatment and those randomized to
wait-list or placebo already suVer considerable delay). Therefore, eVect sizes were
calculated comparing posttreatment and 3-month follow-up data for the active
treatment conditions only. Mean eVect sizes for diVerent treatments, based on
seven studies were: exposure alone (four studies; two negative eVect sizes) 0.16;
cognitive therapy alone (one study) 0.62; social skills training (one study) 0;
combined exposure plus cognitive therapy (six studies; one negative eVect size)
0.23.
On reviewing individual studies that compare exposure with cognitive inter-
ventions and anxiety management strategies, it seems that slightly diVerent symp-
toms (behavioral, cognitive, and physiological) may be targeted by each treat-
ment, but that these diVerences largely disappear at follow-up (Butler et al., 1984;
Heimberg et al., 1985; Jerremalm et al., 1986; Mattick et al., 1989; Hope et al.,
1995). It has also been suggested by some authors that certain symptom proWles
may respond best to particular aspects of a cognitive behavioral package and that
not all components may be necessary for all patients. The limited evidence from
studies of circumscribed social phobia would support this view. Ost et al. (1981)
found some evidence for this view in an early study, but were unable to replicate
their Wndings later (Jerremalm et al., 1986). Negative Wndings were also reported
by Wlazlo et al. (1990).
In summary, we recommend a combined cognitive behavioral treatment pack-
age for social phobia because it is not yet possible to match symptom proWles with
speciWc treatment strategies, and because there is some evidence to suggest that
gains from exposure-only treatments may not be as well maintained in the long
term as the gains that result from combined cognitive behavioral treatments.
2000). A dropout rate of 34% was reported by Van Velzen et al. (1997) from their
exposure-based individual treatment, which they argued may have been more
frightening for participants without the assistance of cognitive strategies or the
support of a group (although clinical observation would suggest that the prospect
of group treatment can be frightening: perhaps once enrolled in group treatment,
the support provided may enhance continuation). Dropout rates for social skills
training show more variation, having been estimated as ranging between 4% and
25% (Taylor, 1996; Gould et al., 1997a; Stravynski and Greenberg, 1998).
Long-term outcome
All the studies reviewed demonstrated maintenance of gains at follow-up periods
of 3 to 6 months. It is important to determine whether results can be maintained
in the longer term. There is now preliminary evidence of sustained improvement
over 5 years (Heimberg et al., 1993). Patients who had earlier received treatment in
either cognitive behavioral group therapy or a control condition comprising
education and supportive psychotherapy (reported by Heimberg et al., 1990a)
were re-evaluated after a period of 4.5 to 6.25 years after treatment. Those who had
received the CBT remained more improved on a variety of behavioral and
self-report measures than those treated in the alternative condition. More import-
antly, global measures suggested that they continued to function well. It was noted
that patients who participated in the long-term follow-up were less impaired pre-
and posttreatment than those who were not re-evaluated at the long-term follow-
up (Heimberg et al., 1993). However, there were no diVerences in pretreatment
severity between long-term follow-up participants who received education sup-
port or CBT.
Predictors of outcome
Symptom severity at baseline is the strongest and most consistent predictor of
outcome, for both drug and psychological treatments (Otto et al., 2000). Symp-
tom severity in turn is related to the subtype of social phobia (generalized versus
nongeneralized) and the presence of comorbid conditions, the most studied being
depression and APD. Consistent Wndings are that the rate of improvement, or
degree of change, in social phobia is very similar no matter what the comorbidity
or pretreatment symptom burden, but severity of symptoms and degree of
impairment posttreatment are most closely related to pretreatment levels. In other
words, CBT is likely to be of beneWt no matter how severe symptoms are, but
functional outcome will be poorer for the more severely impaired individual.
Predictive factors that have been identiWed generally account for only a small part
of the variance, and seem to become of even less predictive value as follow-up
periods lengthen.
170 Treatment of Anxiety Disorders
Depression
Individuals with generalized social phobia and avoidant personality disorder but
no depression improve to the same degree as those with generalized social phobia
alone, but show more impairment before and after treatment (Heimberg et al.,
1990b; Hope et al., 1995; Feske et al., 1996; Turner et al., 1996). At least some of the
diVerence in symptom severity has been attributed to the presence of comorbid
depression, depression and APD showing some independence of eVects in one
study (Feske et al., 1996). In this study, the presence of comorbid APD was related
to a poorer functional outcome, while comorbid depression reduced the degree of
improvement/rate of change. The presence of depressive symptoms accounted for
5% of the variance in outcome at 6-month follow-up, as did treatment expect-
ancy, in the study of Chambless et al. (1997). At follow-up, depression was a more
important predictor of outcome than APD. Scholing and Emmelkamp (1999)
found that depression was a weak predictor of outcome at posttreatment but not
at 18-month follow-up.
Treatment format
Most reported studies conducted group cognitive behavioral treatment of social
phobia. Wlazlo et al. (1990) compared individual with group social skills training
and found an advantage for the group condition. There are few trials comparing
group with individual cognitive behavioral treatment, but neither Scholing and
Emmelkamp (1993) nor a recent meta-analysis (Gould et al., 1997a) found
signiWcant diVerences between reported outcomes of group and individual treat-
ment programs. Butler (1989a), in an excellent review, has commented on the
diYculties of creating adequate exposure conditions for social phobia as a func-
tion of the often brief and unexpected nature of many types of social interaction.
For this reason, group treatment might be expected to have an advantage because
of the prolonged exposure intrinsic to this treatment format. A prolonged group
exposure situation provides the opportunity to habituate to the anxiety provoked
by exposure to strangers. As the group becomes acquainted, there is also the
opportunity for exposure to fears of interacting with a group of people who are
better known, and whose opinions may therefore matter more to the individual.
Research limitations
Existing CBT treatment literature suVers from several methodological limitations.
Early studies using DSM-III may have excluded more severe cases of social phobia,
since hierarchical rules prevented those diagnosed with APD from also being given
a diagnosis of social phobia. Studies that employ clinical samples often also have a
signiWcant proportion of participants on psychotropic medication, including
benzodiazepines and antidepressants, who are free to seek additional treatment
between posttreatment and follow-up: such factors cannot always be controlled
for given small sample sizes. The speciWc requirements of an adequate and
appropriate control condition for trials of psychological treatments were recog-
nized years ago (Heimberg et al., 1990a; Kendall and Lipman, 1991), yet there are
still relatively few reported trials employing the type of placebo condition that
provides a more robust test of psychological treatments. However, the number of
trials using at least a wait-list control is large enough to establish the eYcacy of the
psychological treatments reviewed above in relieving at least some of the burden of
social phobia. Comparison between studies and treatments is rendered diYcult
by the wide range of outcome measures used across studies, and the adoption
of a small number of well-validated measures of symptom burden and social
172 Treatment of Anxiety Disorders
functioning (e.g., see Bobes, 1998; Cox et al., 1998; Lampe, 2000) would assist the
interpretation of results.
Pharmacological treatments
Several classes of drug have been the subject of research. These are beta blockers,
anxiolytics of the benzodiazepine class, and antidepressants.
Beta blockers
Beta blockers – such as propranolol or atenolol – may be of value in reducing
peripheral symptoms resulting from hyperactivity of the beta-adrenergic nervous
system, such as tremor, sweating, blushing, dry mouth, and palpitations
(Marshall, 1992; Roy-Byrne and Wingerson, 1992). In this context, beta blockers
are frequently used in the management of performance anxiety. Twenty-seven
percent of performing artists reported using them in one study (Marshall, 1992).
Individuals with performance anxiety will in many cases meet criteria for social
phobia, DSM-III-R circumscribed type (Clark and Agras, 1991). There is some
rationale for the use of beta blockers in that physiological symptoms of anxiety are
often interpreted catastrophically, a factor that has been proposed as important in
the maintenance of social phobia (Clark and Wells, 1995; Wells and Papageorgiou,
2000). Therefore, minimizing or eliminating these symptoms may result in fewer
anxiety-provoking irrational cognitions and less anxiety. However, evidence for
the eYcacy of beta blockers in generalized social phobia is lacking. Atenolol was no
better than placebo in the studies by Liebowitz et al. (1988) and Turner et al.
(1994). Side-eVects may include depression, sleep disturbance, and broncho-
constriction in susceptible patients, especially with noncardioselective beta
blockers. Beta blockers may also cause bradycardia and hypotension and possibly
dose-related cognitive and psychomotor impairment. In those whose social
anxiety is not limited to public speaking or other discrete performance situations,
a beta blocker is likely to be of little value.
Benzodiazepines
Uncontrolled trials have suggested that benzodiazepines can be of value in the
treatment of social phobia (Ontiveros and Fontaine, 1990). Munjack et al. (1990)
compared clonazepam to no treatment for patients meeting DSM-III-R criteria
for social phobia, generalized subtype. Patients receiving the drug (average dose
2.75 mg per day) improved on cognitive measures of social phobia, but at post-
treatment were not engaging in any more exposure than the nontreatment group,
and there was no real diVerence between the groups in level of disability secondary
to social phobia. No follow-up was reported. Clonazepam (up to 4 mg per day)
173 Social phobia: Treatment
rated variable using the last observation carried forward method (Otto et al.,
2000). Dropout rates of 25% for CBGT and 40% for clonazepam were reported as
not signiWcantly diVerent. Both conditions showed improvement with eVect sizes
of 0.92 for CBGT and 0.99 for clonazepam (calculated from data provided in Otto
et al., 2000, Table 1, p. 352). CBGT and phenelzine were superior to placebo and
an Education + Support control condition, with the phenelzine group showing an
earlier improvement and superiority to CBGT on some measures (Heimberg et al.,
1998). EVect sizes for phenelzine over placebo were of the order of 0.6 to 0.7 and
for CBGT were more variable, ranging from 0.1 to 0.44.
Limited evidence suggests that individuals treated with both medication and
CBT do no better than those treated with a single therapeutic modality, or may
even do somewhat worse (e.g., Clark and Agras, 1991).
Long-term outcome
To date, studies of discontinuation of pharmacotherapy have resulted in high
relapse rates, even, in one case, after active treatment had been administered for up
to 2 years (Versiani et al., 1996). The depression literature has shown that CBT
results in a reduction in the frequency and severity of relapse. Future research in
social phobia must be directed towards establishing whether treatment gains are
maintained and whether maintenance of gains requires continued administration
of the drug or could be improved with the addition of CBT.
Summary
The core elements of social phobia are now well deWned. Successful treatments
have been identiWed and include CBT, MAOIs and SSRIs. Functional outcome of
CBT is related to pretreatment symptom severity. There is reasonable evidence
that gains from CBT can be maintained in the medium term, with a need for more
long-term studies. There is as yet no evidence that gains from drug treatment can
be maintained once medication is withdrawn. The speciWc active ingredients of
CBT programs remain largely unknown, and there remains a need for more
dismantling studies. In view of the long-term outcome, CBT is the treatment of
choice for social phobia. When social phobia is complicated by conditions for
which there are established and indicated drug treatments, these drugs should be
used as appropriate. There is good evidence for reduction of reported levels of
social anxiety and self-reported avoidance of nominated social situations after
treatment with either antidepressant therapy or CBT. It has not been demon-
strated that a reduction in measures of social anxiety equates with more functional
social interaction in the real world. The challenge for social phobia outcome
research in the twenty-Wrst century is to Wnd and implement measures of
176 Treatment of Anxiety Disorders
functional outcome: how well do our treatments assist individuals to achieve their
goals of social function in work, family and community social domains? There is
also a need for more studies to assess the long-term outcome of treatment, and to
maximize therapeutic eVectiveness for the individual.
10
Social phobia
Clinician Guide
Assessment
Diagnosis
This aspect has been covered in detail in Chapter 9. Correct diagnosis is essential.
The core cognitions of social phobia diVer from those of the other anxiety
disorders: the cognitive component of treatment must be directed at the core
cognitive distortions of social phobia to be maximally eVective.
The presence or absence of comorbid conditions will inXuence treatment
priorities, choice of treatment format and response to treatment.
frequently reported. Conversely, social anxiety and concerns about negative evalu-
ation occur in other anxiety disorders (Rapee et al., 1988). When more than one
anxiety disorder is present, the underlying concerns that maintain the anxiety may
cover several diVerent cognitive themes. In individual treatment, a comprehensive
approach may be planned to cover all areas of concern. Group cognitive behavior
therapy (CBT) may be available oVering either general anxiety-management
strategies or targeting a speciWc anxiety disorder. In the Wrst case it is important
that participants realize that the techniques being taught may be successfully
applied to any phobic disorder and may also be useful in a wide range of emotional
problems. Ideally, some guidance should be given as to how to apply these
techniques. In general, if group treatment with a speciWc anxiety disorder focus is
the available format, the patient should be directed to the group treatment
program aimed towards the principal or most disabling concern. The patient can
later be assisted to apply learned strategies to other problem areas.
Symptomatic assessment
A detailed history should be taken of the patient’s physiological, behavioral, and
cognitive symptoms of anxiety. How symptoms are related across these domains is
also important. In the behavioral assessment, patients should be asked about
situations that are avoided and in which anxiety is experienced. Note that patients
may say that they have no trouble with a particular situation because they are
avoiding it completely. Individuals may also be using safety behaviors, designed to
reduce the likelihood of the feared symptom, or to reduce the likelihood of others
noticing or thinking negatively of it should it occur (e.g., wearing a high collar to
hide any Xushing of the neck). Many patients structure their lives around their
social phobia, incorporating avoidance into every aspect of their daily routines.
Hence, it is important to ask patients what they would like to be able to do. This will
help to formulate the goals of treatment. Physiological symptoms of anxiety are
prominent (Amies et al., 1983) and distressing. It is important to determine which
symptoms are experienced as particularly troubling, the frequency with which
they occur, and the personal meaning of such symptoms. Some symptoms will be
feared but rarely happen; others will in reality occur frequently – diVerent
treatment approaches are required. Knowing why such symptoms are feared will
assist with eVective cognitive challenging and graded exposure. It is important to
ask about ‘‘embarrassing’’ types of symptom that patients will not volunteer
because they fear your negative evaluation: fear of vomiting, urination, defecation,
incontinence, burping, Xatus.
Assessment instruments
A number of diagnostic instruments of established reliability and validity are
available for use with DSM-IV and ICD-10 (including the Structured Clinical
Interview for DSM-IV Axis I Disorders (SCID), Anxiety Disorders Interview
Schedule for DSM-IV (ADIS-IV), and the Composite International Diagnostic
Interview (CIDI)), although not usually available outside of research settings.
Symptom measures have been discussed in Chapter 9. Many patients are interest-
ed to know their scores on such measures and those which are sensitive to change,
such as the Social Phobia Scale (SPS), Social Interaction Anxiety Scale (SIAS),
Social Phobia and Anxiety Inventory (SPAI) and the Liebowitz Social Anxiety
Scale (LSAS), are useful aids in assessing treatment eVectiveness. The Personality
Disorder Examination (Loranger, 1988), the International Personality Disorder
Examination (Loranger et al., 1997) and the Structured Clinical Interview for
180 Treatment of Anxiety Disorders
Treatment format
Social phobia may be treated individually or in a group setting in massed sessions
or in sessions distributed over time. Feske et al. (1996) found no diVerence in
outcome between 32 hours of massed group treatment and 42 hours of more
spaced group treatment. In many treatment settings, group programs may not be
available. Where such programs are available, the following considerations may
also assist in deciding on the treatment format to recommend.
1. Individual therapy
∑ Will take 10 to 20 hours of therapist time, with social phobia uncomplicated
by signiWcant other Axis I disorders or personality disorder.
∑ Useful where feared events or situations are unusual or particularly embar-
rassing to discuss.
∑ Preferable when comorbid conditions make a group format unsuitable for
the patient, or where the patient is likely to behave in a way that will impair
the access of other group members to eVective treatment.
∑ May represent more eYcient use of patient time in circumscribed social
phobias: but note that a minority of those who present for treatment of social
phobia have truly circumscribed fears (Mattick et al., 1989; Holt et al., 1992;
Schneier et al., 1992; Eng et al., 2000).
∑ Can provide more Xexibility in terms of scheduling and content.
2. Group therapy
∑ Generally involves around 24 to 50 hours of treatment over a number of
sessions, typically held at weekly intervals.
∑ EYcient use of therapist time.
∑ BeneWt of peer support and modeling.
∑ Opportunity not present in the individual therapy setting for exposure
experiences such as public speaking, social interaction, scrutiny and per-
formance under observation within a therapeutic setting.
It is our belief that some exposure to group treatment confers a clinical
advantage to the majority of suVerers with generalized social phobia. It provides
lengthy periods of exposure to others, which permits habituation to anxiety. Given
the brief nature of many social interactions, and the often great degree of avoid-
ance, this may be a Wrst opportunity to learn that, with persistence in the
anxiety-provoking situation, the level of anxiety will eventually diminish. It may
also be the Wrst opportunity that many participants have to meet others with the
disorder and to Wnd that they are not alone. Furthermore, in the group setting
181 Social phobia: Clinician Guide
there is the important advantage of positive peer inXuence. The reports of peers
that practice the recommended techniques resulting in improvement tend to carry
more weight than didactic statements by the therapist. The group permits some
types of exposure exercise that are not possible in individual therapy, in a
supportive setting.
It is entirely understandable that, given the nature of the disorder, many
individuals react with anxiety to the suggestion of participating in a group
treatment program. In most cases, the individual readily appreciates the potential
value of such a program once the rationale for group treatment is described.
However, a minority, particularly those who also meet criteria for avoidant
personality disorder, may require some individual therapy before they can con-
sider the prospect of group treatment without extreme anxiety.
Treatment schedule
The program is run as a closed group, and patients are expected to attend all
sessions. Most cognitive behavioral group programs are scheduled as weekly
sessions of 2 to 212 hours over 10 to 12 weeks. We have also used formats of 3 full
days followed by a number of shorter weekly sessions, and a series of 3–5 full days
separated by intervals of 1 or 2 weeks. All formats have shown equivalent eVective-
ness, and hence it appears that groups may be scheduled in a manner that suits the
participants and the institution.
182 Treatment of Anxiety Disorders
We believe that the breaks between treatment sessions are an important part of
the therapy; however, since they allow time for participants to practice their new
skills, and achieve some success, but also encounter problems and diYculties that
can provide the opportunity for discussion in the group and hence further
learning and skills enhancement. Recent work on relapse prevention has high-
lighted the need for patients to learn to cope with failure and diYculties adaptively
(Whisman, 1990; Wilson, 1992).
∑ Early assistance with some strategies to manage this anxiety. For example,
participants may Wnd it helpful to remind themselves of their motivation for
attending, and to remember that they survived the Wrst day, perhaps even with a
gradual reduction in the level of anxiety experienced.
Problem solving
It is not uncommon to have a person fail to turn up at the Wrst session despite
conWrming their intention to attend perhaps only a short time before the group
starts. For some patients, the anxiety on the day seems too great and they deal with
it by avoiding the situation. Such individuals will usually be followed up to
determine the reasons for nonattendance and the best course of action, but it is
not recommended that they attend the current group unless able to come in and
start immediately, i.e., in the current session. If the patient returns much later,
they will have missed important educational aspects of the program and will not
have been part of the developing rapport between group members. These factors
may impede the individual’s progress and reinforce their anxiety, further dimin-
ishing their chances of persisting with the program.
Occasionally, patients will fail to return for the second treatment session. A
follow-up phone call as soon as practicable is valuable: it reinforces the supportive
aspect of the therapeutic alliance and allows an opportunity to reassess the most
appropriate format of treatment. In general, when the individual has unrealistic
anxieties about the group that are amenable to cognitive challenge, and when his
or her anxiety responds to the empathy and support of the therapist, a successful
return to the same group is often possible – preferably that same day, or at the very
next session. Otherwise, the same considerations as noted above will apply.
At times during the group, participants may experience extreme distress or
anxiety, and may cry or leave the room upset. Common reasons for leaving are
severe anxiety, usually related to some particular cognition, especially regarding
perceived negative evaluation from other group members. Serious decompensa-
tion (e.g., frank paranoia) is occasionally seen and warrants psychiatric assess-
ment. It is appropriate to acknowledge distress but in a way that does not demean
or embarrass the patient, or detract from the development of mastery and
responsibility. Empathic inquiry into the individual’s emotional state, if necessary
gentle reminders to use anxiety-management strategies, and permission to do
what they feel is necessary to cope, is often suYcient. At a convenient break, the
therapist should talk to the patient privately to ascertain what the problem may
have been, and devise a management plan if the issue has not resolved. The calm
and accepting way in which the disturbance is handled demonstrates that expres-
sion of strong emotions does not necessarily attract negative evaluation, that
184 Treatment of Anxiety Disorders
anxiety and distress within the group is not unusual, and that the therapist has
faith in the patient’s ability to cope. These episodes can be valuable learning
experiences for both the patient and the group.
The person with social phobia is likely to be highly anxious and acutely sensitive
to criticism. The degree of anxiety, coupled with an underlying cognitive bias to
interpret situations negatively, may impair attention and realistic appraisal of the
situation. When social phobia is complicated by avoidant personality disorder
there are in addition distorted ideas about rejection (e.g., that if someone disagrees
with the individual this equals rejection as a person). The person with social
phobia also fears negative evaluation from the therapist. In a group situation, the
therapist may need to disagree somewhat with a participant’s opinion (e.g., that
social phobia is caused by one’s parents) but must be sensitive about the ways in
which such disagreement is expressed. Rather than assert that an expressed
opinion is incorrect, it may be more helpful to suggest alternative interpretations.
Similarly, when giving feedback about a participant’s performance or manner of
relating. In general, the fear of negative evaluation also means that individuals
with social phobia are very compliant with requests, tasks, and homework.
However, they are reluctant to express disagreement or ask questions, so that the
therapist should initiate discussion at certain points and be alert for signs of
incomprehension or dissension.
Time management
In general the program is worked through in the order in which chapters are set
out in the Manual. The Wrst priorities of treatment are to educate about anxiety
and panic, and teach methods of anxiety management. Initially participants are
taught a technique of hyperventilation control, since most individuals Wnd this a
useful anxiety management strategy, which can be quickly mastered. The prin-
ciples of CBT are outlined, and patients are introduced to a model of social
phobia. Some discussion of the individual’s experience of social phobia in relation
to this model is often useful at this point. This may also be a convenient time to
introduce discussion of ‘‘embarrassing’’ symptoms or else fear of negative evalu-
ation may mean that these are never disclosed. Next, work begins to identify and
challenge the speciWc underlying cognitions that drive the individual’s social
phobia. This work will continue throughout the course of treatment, the eventual
goal being the identiWcation and challenge of underlying schemas. Exposure
exercises should begin early. At this stage the behavioral analysis may be com-
pleted in more detail than may have been possible initially, since many patients
have avoidance strategies of which they are unaware prior to treatment. Once this
core material has been covered, sessions can usefully be divided into sections
comprising review of homework tasks, discussion of any here-and-now issues or
185 Social phobia: Clinician Guide
problems, the topic for that session (in the early stages), and planning of between-
session goals and exercises, including cognitive and exposure-based tasks. Home-
work may include reading material (e.g., the appropriate section of the Patient
Treatment Manual), exposure tasks, behavioral experiments, and cognitive chal-
lenging exercises.
In the group setting, some exposure exercises are usually carried out during the
session. These may include various types of interaction or performance, including
public-speaking or role-play exercises tailored to individual areas of diYculty.
The sections of the Patient Treatment Manual will be discussed in more detail
below.
Education: what is social phobia (Sections 1.1–1.5) and the nature of anxiety (Section 2)
Treatment begins with education about the nature of anxiety and social phobia. At
this point, many patients often raise their own theories about why they have social
phobia. In some cases, they unequivocally blame some other person, often a
parent. This is a good time to discuss the multiple inXuences (biological, psycho-
logical, and environmental) on the development of social phobia, and to stress
that, whatever the cause or causes, something can be done to improve the
situation. The individual’s experience of anxiety should be discussed. In the group
situation, the similarities and diVerences in participants’ experience of anxiety can
be explored. The exercise, ‘‘Make a List of Situations in Which You Would Feel
Very Anxious’’ can be another useful group exercise. Once patients have com-
pleted their own list, a group list can be generated for the whiteboard. This may be
saved so that the therapist and group members can check that exposure tasks over
the coming sessions target these situations. Once again, patients will see how much
they have in common. In individual treatment, the list of diYcult situations will
form the basis of the graded exposure hierarchy. At this stage, patients are often
unable to appreciate how so many seemingly diVerent situational fears can have
anything in common and may ask about this. They may also point out that
‘‘sometimes this is a problem, and sometimes it isn’t. It’s totally unpredictable’’. In
fact, the list will be logically understandable in terms of the individual’s speciWc
underlying fears. Until they have learned about the inXuence of cognitions on the
experience of anxiety it may be diYcult to be persuaded of this. It is probably best
to say that this issue will be discussed at a later stage, and that it will probably turn
out that their fears are more predictable than it currently seems.
It is helpful to discuss the Yerkes–Dodson curve (Yerkes and Dodson, 1908) in
detail. We often begin by asking patients to predict what they think might be the
relationship between anxiety and performance. The actual shape of the curve
usually comes as a surprise. Many patients who attend for treatment believe that
any anxiety is abnormal and hope that treatment will eliminate all anxiety. This
186 Treatment of Anxiety Disorders
concept should be discussed with reference to the implications from the Yerkes–
Dodson curve (and reinforced by real life experience) that not only is it not
necessary to eliminate all anxiety, but some anxiety can even be helpful. Suggest
that the aim should be to keep to the left side of the curve, entering situations with
as low an initial anxiety level as is reasonable and possible, but remembering that
some anxiety can improve performance (Section 2.3).
pay the individual any particular attention. Hence, the hypothesis in the Patient
Treatment Manual (i.e., that no-one is really very interested in the individual with
social phobia) is given some support. The technique of guided discovery may be
used to help individuals to reach this conclusion and realize that their initial
predictions overestimated the probability of a negative outcome. The Patient
Treatment Manual details the most common types of cognitive distortions or
‘‘errors’’ in social phobia. This may assist mastery of the skill of cognitive
challenging. Individuals usually take a signiWcant amount of time to master the
technique and to begin to see results. Once the basic skills have been introduced, a
signiWcant proportion of session time is spent in reviewing and Wne-tuning an
individual’s application of the techniques in every day life. In general, patients will
need to identify and challenge underlying unhelpful cognitions repeatedly with
therapist guidance. As their skill level increases, patients can be gradually encour-
aged to take more responsibility for identifying and challenging their own beliefs.
The ‘‘downward arrow’’ or ‘‘Xow of thought’’ techniques are introduced early to
help to uncover core schemas. In time, most patients will be able to identify a
number of underlying core schemas operating in most social situations. SpeciWc
behavioral experiments may be devised to help to challenge these. Cognitive
restructuring is most eVective in social phobia when it is linked to exposure to
feared situations. It is introduced before graded exposure, as we have found that
patients Wnd it easier to engage in exposure tasks if they can reduce their level of
anxiety beforehand using cognitive challenging.
Graded exposure
This concept is one of the more diYcult aspects of the program for individuals in
therapy to grasp. To be most eVective, exposure should be targeted at speciWc
underlying concerns. For example, consider the goal of having a meal at a
restaurant with friends. The graded exposure program will be diVerent for the
person whose main fear is that their hands will shake as compared with the person
whose main fear is that they will not be able to make conversation. The former
needs practice with eating, drinking, and writing under scrutiny, but the latter
needs practice making social conversation. Patients Wnd it hard to generate steps
of variable diYculty. When the goal cannot be easily divided into steps, individ-
uals Wnd it particularly hard to generate steps involving situations that are
diVerent from the goal, yet similar enough to provoke the same underlying fear
and therefore engage anxiety related to the goal. Versions of a performance target
will result in desensitization, generalizing to the principal target when the inter-
mediate step engages the speciWc underlying fear and is successfully achieved.
Considerable practice is usually required. There are several practice examples in
the Patient Treatment Manual that are usefully worked through. In a group
treatment program, each patient can be asked to volunteer their suggestions in
turn. Participants will learn from their peers, and the therapist will have the
opportunity to illustrate that there is no single ‘‘right’’ answer, but that there are
several useful approaches, and that the speciWc program will vary according to the
speciWc underlying fears. The ‘‘who, what, when, where, how long’’ format is an
attempt to make the process a little easier by using a ‘‘formula’’. Each category can
be altered for most tasks. Within these categories much can be modiWed to alter
the degree of diYculty. The following list provides a format for modifying such
tasks to form a graded hierarchy.
189 Social phobia: Clinician Guide
Who: Vary who will be present and what their relationship is to the patient, e.g.,
authority Wgure, family, close friend, acquaintance, colleague, stranger. Vary
how many people will be present.
What: Vary exactly what is to be done: should focus on behavior rather than style,
e.g., to give a 5-minute talk, but not ‘‘to be free from anxiety’’ or ‘‘to give an
outstanding oration’’.
When: Vary the time of day, for this may inXuence the individual’s energy level
and motivation and how many other people may be around. The degree of
advance warning inXuences anticipatory anxiety.
Where: Vary the setting. Consider such factors of potential importance as relative
ease of escape, how much the setting results in a feeling of being under scrutiny
(e.g., open-plan restaurant versus booths), who else is likely to be there.
Locations include work, home, public places, friends’ homes, family homes.
How long: Vary how long the activity will last. Could the patient leave earlier; how
long will the patient expect to perform that activity in that situation; should
they remain after the activity has been completed?
their behavior, since this represents a greater perceived risk for negative evalu-
ation. Posttask discussion may center around how much attention was really paid
by others, how unusual various behaviors really are, and how much negative
evaluation assertive or unusual behavior really attracts. Participants may be asked
to predict the outcome before they set out and compare the actual outcome on
their return. Other tasks are negotiated with reference to the hierarchy of feared
situations already established for the individual. Throughout the practice of
graded exposure it is stressed that the goal is to develop eVective anxiety-manag-
ment strategies and reduce fear, rather than achieve a ‘‘perfect’’ performance in
the practice situation.
In a group program, graded exposure is undertaken within the group, outside
the group during therapy time, and by the individual between meetings. Some
tasks are set by the therapist to be carried out either as a group, in pairs, or
individually: these are usually the tasks that serve as behavioral experiments that
will challenge common underlying beliefs in social phobia. Role-play exposure to
challenging situations may also be undertaken in the group setting. Types of
situation that are challenging for the majority of participants are chosen. Typically
these include meeting new people (especially potential dates) and making conver-
sation, and various types of situation requiring the exercise of assertiveness skills
such as resolving conXicts, making requests, and handling criticism. We have
found a public-speaking exercise to be particularly valuable in a group setting.
This task is chosen because it will provoke anxiety in the majority of participants.
It can be structured to provide a demonstration of the application and eVective-
ness of graded exposure and of cognitive challenging in reducing the anxiety
provoked by exposure situations. Individuals give talks of gradually increasing
duration to their fellow participants. We alternate between prepared and im-
promptu talks to provide exposure to both anticipatory anxiety as well as give
practice at coping with the unexpected. It also provides the opportunity for an
extremely useful exercise, which challenges beliefs about how anxious an individ-
ual believes they look. In this exercise, participants are videotaped giving their talk
in front of the group. Before watching the videos each participant is asked to give a
Subjective Units of Distress (SUDs) rating to how anxious they felt while giving
their talk. This is recorded against the appropriate individual’s name on a white-
board. Next, each video is watched in turn. After each video, the individual on the
tape is asked to rate how anxious they feel they looked on the video. Finally, the
group is asked to provide an honest appraisal of how anxious they feel the person
looked ((S)UDs scores are roughly averaged to give a group measure). This
process is repeated after each video is viewed. Typically, each individual rates
himself or herself as highly anxious, then is surprised to see that he or she deWnitely
does not look as anxious as they felt, although he or she still tends to give
294 Treatment of Anxiety Disorders
explains the lack of memory. However, it is also possible that some people’s fears
have always been with them. Whichever one (or combination) of these causes
started the phobia in the Wrst place, what is now important is to identify what
keeps the phobia going in the present.
We will discuss the factors that keep a phobia going as the program continues.
However, by way of summary, it is clear that people with phobias worry more
about the objects and situations that are the focus of their fear than others do and
they worry more than is necessary. We will consider these worries and how to
challenge them in Section 5. Another factor that maintains avoidance – Xeeing
from or never even facing what you fear. The problem is that avoidance helps in
the short term, but in the long term it causes the phobia to grow. We will discuss
avoidance and how to stop it causing phobias to grow in Section 4. Finally, phobic
anxiety is excessive and unreasonable. Thus, by deWnition, the anxiety and fear is
more intense than it should be. Two factors that we know can elevate anxiety and
fear are muscle tension and overbreathing. We will consider muscle tension and
how to combat it in Section 3, but for the time being we will turn our attention to
overbreathing.
LUNGS
BLOOD HEMOGLOBIN
BODY’S CELLS
unlocked so that it can go into the body’s cells. Therefore, while it is important to
breathe in oxygen, it is just as important that there is carbon dioxide in the blood
to release the oxygen. Overbreathing makes anxiety worse, not because you
breathe in too much oxygen but because you breathe out too much carbon
dioxide.
Breathing ‘‘too much’’ has the eVect of decreasing the levels of carbon dioxide,
while breathing ‘‘too little’’ has the eVect of increasing levels of carbon dioxide.
The body works best when there is a balance between oxygen and carbon dioxide.
When you overbreathe, you end up with more oxygen than carbon dioxide in your
blood. When this imbalance happens, a number of changes occur in the body.
One of the most important changes is a narrowing of certain blood vessels. In
particular, blood going to the brain is somewhat decreased. Coupled together with
this tightening of blood vessels is the fact that the hemoglobin increases its
‘‘stickiness’’ for oxygen. Thus less blood reaches certain areas of the body. Further-
more, the oxygen carried by this blood is less likely to be released to the cells.
Paradoxically, then, while overbreathing means we are taking in more oxygen, we
are actually getting less oxygen to certain areas of our brain and body. This results
in two broad categories of sensations:
1. Some sensations are produced by the slight reduction in oxygen to certain parts
of the brain. These symptoms include:
∑ Dizziness
∑ Light-headedness
∑ Confusion
296 Treatment of Anxiety Disorders
∑ Blurred vision
∑ Feelings of unreality
2. Some symptoms are produced by the slight reduction in oxygen to certain parts
of the body. These symptoms include:
∑ Increase in heartbeat to pump more blood around
∑ Breathlessness
∑ Numbness and tingling in the extremities
∑ Cold, clammy hands
∑ StiVness in the muscles
It is important to remember that the reductions in oxygen are slight and totally
harmless.
Hyperventilation is also responsible for a number of overall eVects. The act of
overbreathing is hard, physical work. Hence, the individual may often feel hot,
Xushed, and sweaty. Because it is hard work to overbreathe, doing it for a long
time can result in tiredness and exhaustion.
People who overbreathe often tend to breathe from their chest rather than their
diaphragm. As the chest muscles are not made for breathing, they tend to become
tired and tense. Thus these people can experience symptoms of chest tightness or
even chest pains.
If overbreathing continues, a second stage of hyperventilation is reached. This
produces symptoms such as:
∑ Severe vertigo
∑ Dizziness and nausea
∑ An inability to breathe freely
∑ A crushing sensation or sharp pains in the chest
∑ Temporary paralysis of muscles in diVerent parts of the body
∑ Actual momentary loss of consciousness (‘‘blackouts’’)
∑ Rising terror that something terrible is about to happen, for example, a heart
attack, brain hemorrhage, or even death
The symptoms in the second stage of hyperventilation are produced by the
body’s automatic defence reaction to decreasing levels of carbon dioxide. This
defence reaction forcibly restricts the person’s breathing, allowing carbon dioxide
levels to return to normal.
At the risk of repetition, the most important point to be made about hyperven-
tilation is that it is not dangerous. Increased breathing is part of the Xight or Wght
response and so is part of a natural biological response aimed at protecting the
body from harm. Thus it is an automatic reaction for the brain to immediately
expect danger and for the individual to feel the urge to escape.
Hyperventilation is often not obvious to the observer, or even to the persons
experiencing it. It can be very subtle. This is especially true if the individual has
297 Specific phobias: Patient Treatment Manual
been slightly overbreathing over a long period of time. In this case, there can be a
marked drop in carbon dioxide but, because the body is able to compensate for
this drop, symptoms may not be produced. However, because carbon dioxide
levels are kept low, the body is less able to cope with further decreases and even a
slight change of breathing (e.g., a sigh, yawn, or gasp) can be enough to trigger
symptoms.
Trigger
Oh no...What if?
Breathe
faster
Fight or
Symptoms flight
Perceived
breathlessness
that when you do not use the anxiety response to Xee or Wght, you may feel
confused, unreal, and distracted. Nevertheless, you are still able to think and
function normally. You are still able to decide what action to take in response to
panic; that is, whether to stay or leave.
SE CT I O N 2
2 Control of hyperventilation
2.1 Recognizing hyperventilation
The Wrst step in preventing and controlling hyperventilation is to recognize how
and when you overbreathe.
Try monitoring your breathing rate now. Count one breath in and out as 1, the
next breath in and out as 2, and so on. It may be diYcult at Wrst, but don’t try to
change your breathing rate voluntarily. Write the answer here . As part of
treatment you will be required to monitor your breathing rate for 1 minute during
various times of the day. The form in Section 2.3 should be used for this purpose.
Now consider the following:
∑ Do you breathe too quickly? The average person only needs to take 10 to 12
300 Treatment of Anxiety Disorders
breaths per minute at rest. If your rate of breathing is greater than this, then you
must reduce it.
∑ Do you breathe too deeply? Does your chest sometimes feel overexpanded? You
should breathe from the abdomen and through the nose, consciously attempt-
ing to breathe in a smooth and light way.
∑ Do you breathe from your chest? Sit with your arms folded lightly across your
tummy and while breathing naturally observe your arms, chest, and shoulders.
While all three will move, the main movement should be in your tummy if you
are breathing correctly from your diaphragm.
∑ Do you sigh or yawn more than others? Become aware of when you sigh or yawn
and avoid taking deep breaths at these times.
∑ Do you gasp or take in a deep breath when, for example, someone mentions
what you fear? Taking one deep breath can trigger the hyperventilation cycle in
many people.
∑ Do you breathe through your mouth? You are more likely to hyperventilate if
you breathe through your mouth. Whenever you notice this, you should
consciously revert to breathing through your nose.
SE C T I ON 3
3 Relaxation training
3.1 The importance of relaxation training
Human beings have a built-in response to threat or stress known as the Xight or
Wght response. Part of this Xight or Wght response involves the activation of muscle
tension, which helps us to perform many tasks in a more alert and eYcient
manner. In normal circumstances, the muscles do not remain at a high level of
tension all the time but become tensed and relaxed according to a person’s needs.
Thus a person may show Xuctuating patterns of tension and relaxation over a
single day according to the demands of the day, but this person would not be
considered to be suVering from tension.
If you remain tense after demanding or stressful periods have passed, you
remain more alert than is necessary and this sense of alertness ends up turning into
apprehension and anxiety. Constant tension makes people oversensitive and they
respond to smaller and smaller events as though they were threatening. By
learning to relax, you can gain control over these feelings of anxiety. In this
program, you will be taught how to recognize tension, how to achieve deep
relaxation, and how to relax in everyday situations. You will need to be an active
participant, committed to daily practice for 2 months or longer.
Since some tension may be good for you, it is important to discriminate when
tension is useful and when it is unnecessary. Actually, much everyday tension is
unnecessary. Only a few muscles are involved in maintaining normal posture, e.g.,
sitting, standing, walking. Most people use more tension than is necessary to
perform these activities. Occasionally, an increase in tension is extremely beneW-
cial. For example, it is usually helpful to tense up when you are about to receive a
serve in a tennis game. Tension is unnecessary when (1) it performs no useful
alerting function, (2) it is too high for the activity involved, or (3) it remains high
after the activating situation has passed.
In order to be more in control of your anxiety, emotions, and general physical
well-being, it is important to learn to relax. To do this you need to learn to
recognize tension; learn to relax your body in a general, total sense; and learn to let
tension go in speciWc muscles.
Where do you feel tension? For the next 12 days we want you to monitor the
tension in your body. Use the following form to indicate the location of your
tension and the degree of tension. Always choose approximately the same time
each day to monitor your tension. Before your evening meal is usually a good time
for this.
In each box place the number corresponding to your level of tension
0 1 2 3
Jaw
Top of scalp
Back of neck
Shoulders
Top of back
Lower back
Chest
Abdomen
Groin
Buttocks
Thighs
Knees
Calves
Feet
Top of arms
Lower arms
Hands
304 Treatment of Anxiety Disorders
∑ Pull the legs sideways in opposite directions while keeping them locked together
at the ankles.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow out of your muscles.
∑ Choose other parts of the body to relax, e.g., the hands and arms.
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, tense hand and arm muscles by placing hands comfortably in
your lap, palm against palm, and pressing down with the top hand while trying
to lift the lower hand.
Or
∑ Place hands under the sides of chair and pull into the chair.
Or
∑ Grasp hands behind chair and try to pull them apart while simultaneously
pushing them in against the back of the chair.
Or
∑ Place hands behind the head, interlocking the Wngers, and while pushing the
head backward into hands try to pull hands apart.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow from your muscles.
If circumstances permit, continue with various muscle groups.
When standing in a public place:
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, straighten legs to tense all muscles, bending the knees back
almost as far as they will go.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow from your muscles.
Other exercises for hand and arm muscles:
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, cup hands together in front and try to pull them apart.
Or
∑ Cup hands together behind and try to pull them apart.
306 Treatment of Anxiety Disorders
Or
∑ Tightly grip an immovable rail or bar and let the tension Xow up the arms.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow from your muscles.
Shoulders and neck Hunching shoulders up towards Letting shoulders drop and let
the head arms hang loose
work, go to a park. You may need to consider whether other factors are
preventing you from relaxing if you keep making the excuse that there’s no
time.
5. ‘‘I’m not getting anything out of this.’’ Unfortunately, many people expect too
much too soon from relaxation training. People often exaggerate the speed of
recovery. You cannot expect to undo years of habitual tensing in a few
relaxation sessions. Impatience is one of the symptoms of anxiety and often
indicates a need to continue with relaxation training. Give the training time to
take eVect.
6. ‘‘I haven’t got the self control.’’ You need to realize that quick, easy cures for
phobias calling for no eVort from you do not exist. The longest-lasting treat-
ment eVects occur when an individual takes responsibility for his or her
recovery. Responsibility means self-control, but self-control is diYcult if you
are not motivated.
SE C T I ON 4
4 Graded exposure
One of the hallmarks of a phobia is that the feared object or situation is avoided or
endured with considerable distress. Remember that the sorts of avoidance that we
are talking about are not only the obvious ones (e.g., running away from or not
going near what you fear) but also the more subtle ones (e.g., thinking about
something else). However, avoiding the feared object or situation is good in the
short term but its longer-term implications are not good. Whether you avoid in a
subtle or obvious way, the result is the same. Each time a person with a phobia
approaches some situation and then avoids it, in whole or in part, the fear
subsequently increases because the drop in anxiety (which follows the ‘‘escape’’) is
rewarding. Thus the avoidance is rewarded: after all, if you can avoid the fear by
avoiding, why not do so? Unfortunately, the fear really doesn’t stop, you just Wnd
more and more situations that could be ‘‘dangerous’’ and avoid them also.
What, then, is the way out? If leaving the situation strengthens the fear, what
would happen if you stayed put? Actually, if you stayed in the situation for an hour
or so, the fear would eventually go and the fear the next time you entered that
situation would be less. But few people with situational fears can actually stay in
the situation for the time required for intense fear to wear oV. So they keep
avoiding those situations.
The best remedy is to control the level of the fear using hyperventilation control,
relaxation, and straight thinking (which will be discussed in Section 5), and then
309 Specific phobias: Patient Treatment Manual
stay in a situation until you are calmer. Obviously, intense fear will take substan-
tially longer to decrease than would lower levels of anxiety. For this reason, it is
recommended that you begin with situations associated with small amounts of
anxiety and work up to situations associated with higher levels of anxiety. In this
way, you will experience anxiety, but only levels that you will be able to manage
relatively quickly. As a result, you will have more successes in managing your fear.
But how do you organize such experiences? First, you make a list of all the
situations in which you are likely to ever have your phobic fears. Next, you rank
those situations in terms of the fear associated with them. Put them into a fear
‘‘stepladder’’, beginning with the least fear provoking and moving through to the
most feared situations. Then, you work your way up the ‘‘stepladder’’, staying
again and again in a situation at each level until the situation loses its power to
evoke excessive anxiety. This procedure is discussed in more detail in the following
sections.
associated with what you fear. By way of illustration, consider a person who has a
phobia about being trapped in elevators. Exposure to the elevator will reduce the
anxiety associated with elevators but it is possible, though not very probable on
any day, that the person could get trapped in an elevator. In such a situation, the
person is faced with two diYculties. The Wrst is coping with any anxiety and fear,
which would involve breathing control, relaxation, and thinking straight. The
second problem is how to get out of the elevator. Being prepared to cope with this
eventuality will help to minimize worry about what may happen and also would
make responding more eYcient.
Think about what you fear and how you may choose to cope with any possible
diYculties. Remember, this is an exercise in planning helpful and eVective coping
strategies for possible eventualities, not a chance to worry about everything that
you fear.
Only imagine one scene at a time. You do not have to imagine all scenes in a single
session.
Practice examples
We would now like you to practice making out a similar set of steps for each of the
following goals:
1. Goal: Traveling up the tallest available building in an elevator.
Steps:
In the space below, we would like you to work out up to 10 goals of your own
choosing. These goals should vary in diYculty from those things that you hope to
achieve in the next few weeks to those that may take longer to attain.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Now select three (at the most) of the above goals that you would like to work on
Wrst, and write these below. Set out beneath each goal the steps you intend to take
in order to achieve it.
1. Goal:
Steps:
315 Specific phobias: Patient Treatment Manual
2. Goal:
Steps:
3. Goal:
Steps:
SE CT I O N 5
5 Thinking straight
This part of the program is designed to help you to control the kinds of thoughts
that occur when you are in the presence of something you fear. These thoughts not
only accompany your anxiety reactions but can also promote them. You will
achieve this control by learning procedures that reduce the frequency, intensity,
and duration of upsetting emotional reactions by labeling the situation more
appropriately and accurately. Simply put, the procedures you will practice involve
learning how to ‘‘think straight.’’
Why did Peter become anxious and climb the stairs? The most accurate answer
is ‘‘Peter made Peter anxious’’. To make this clear, consider another version of the
same story:
Peter is on an errand from work and enters an office building. He approaches the elevator
and thinks to himself, ‘‘The office is on the 15th floor. What if the elevator broke down?
Chances are that it will not, and even if it did, I would be able to use the telephone in the
elevator to call for assistance. There is no need to worry unnecessarily.’’ He becomes less
anxious and enters the elevator.
As you can see, the situation is exactly the same in the two stories except for two
important features. First of all, Peter’s thoughts have changed. Second, Peter’s
emotional reaction has changed: in the Wrst scene he became anxious; in the
second he remained in a pleasant mood. Peter’s emotional reaction is no accident:
the elevator hadn’t made him afraid. Rather, it was the catastrophic thoughts that
Peter had that caused him to feel afraid.
Putting this all together, there was an activating event, i.e., the elevator. This was
presumed to lead to the consequence of Peter feeling afraid and later angry with
his boss. However, in the expanded story, it was apparent that Peter’s explanation
was incomplete because there were a number of intervening beliefs or thoughts
that he had. Thus, the way in which emotions are produced can be written as As,
Bs, and Cs. A is the Activating event, B is the Beliefs or thoughts that a person has
about the activating event and its meaning, while C is the emotional and behav-
ioral Consequence of having those beliefs and thoughts about the event. In other
words, the activating event does not cause the consequence on its own, but, rather,
it is the way we think about the activating event that causes the emotional
consequence.
Beliefs Beliefs
‘‘What if it is poisonous?’’ ‘‘I’ve been told it is harmless’’
‘‘Any movement means that the spider is ‘‘I’ve never been so close to one of these
about to kill me ’’ spiders before’’
Consequences Consequences
Anxious and refuse to touch it Relaxed
On edge and desiring to escape Settles down to study the spider
At its heart, the unhelpful thinking that makes the fears of people with phobias
much more intense than they need to be involves overly pessimistic ratings of the
probability and cost of danger. The greater the chance of something bad happening
(i.e., the probability) and the worse that the event will be (i.e., the cost), then the
more a person is going to worry about it. For example, a person with height
phobia may start to climb a steep ladder and think that the probability that they
will fall from the Wfth step is about 80% (i.e., the probability is high) and that they
will almost certainly die from the injuries (i.e., the cost is high). Quite reasonably,
the person will be afraid of climbing the ladder.
Sometimes a person with a phobia will be afraid because their estimates of
probability and cost are both high. Other times, the worry may arise because one
or other is excessively high. For instance, a person who is afraid of Xying may agree
that the airplane they may Xy in is less likely to crash than the car they drove to the
airport in, but they may think that the cost of a crash is greater in an airplane
because most car accidents are not fatal.
However, this isn’t the whole story. Estimates of probability and cost change as
a person gets closer to what it is that they fear. Interestingly, estimates of the
probability and cost of danger are higher when people consider confronting what
they fear than when they are actually in its presence. You may have noticed this
yourself, that you can be more worried when thinking about facing your fears than
when you actually face them.
These worries that are based upon overly high ratings of the probability and cost
of danger can encourage a person to avoid fear-provoking situations. Avoiding
situations only strengthens unhelpful and fear-producing thinking habits, as it
318 Treatment of Anxiety Disorders
prevents individuals from getting new, helpful information that the probability
and cost are not as high as you may be thinking.
Given the thoughts a person with a phobia is having, the fear is reasonable. The
problem is that the thoughts are not appropriate to the situation. They have
labeled the situation as more threatening than they need to or they have worried
that danger is more likely than it is. By changing the way a person labels or
interprets events, a person can gain more control over their feelings in a more
helpful and adaptive way.
It is important to recognize that unhelpful thinking patterns are habits, and that
habits can be changed with eVort and practice. Identifying unhelpful thoughts
associated with anxiety is the Wrst step in changing your thinking.
features: other people, limited opportunities to leave, and limited control over
their direction.
Catching an express train, I’ll panic – being on a train I probably won’t lose control;
where I couldn’t get oV if I makes be lose control and panic I’ll just feel anxious
wanted to I’ll go crazy if I can’t get out Even if I do feel anxious and
What’ll people think of me? uncomfortable that doesn’t
If I can’t get out I’ll do mean the situation is dangerous
something stupid or out of I’ve never done something out
control of control on a train, and
I won’t cope probably won’t do something
No-one else feels this way this time either
I can use my techniques to
manage my anxiety
People won’t notice me, and,
even if they do, they’ll just think
I’m a little tense
I must be loopy to feel this way I’m not loopy, just anxious, and
I’m doing something about that
320 Treatment of Anxiety Disorders
Now think of a recent situation where you felt anxious because of your phobia.
Write down a description of the situation and any anxiety-provoking thoughts
that you may have had. Then write down some more helpful thoughts that could
be applied to that situation, in order to reduce your anxiety. There is also space for
an additional individual example.
This technique should be used with the technique of graded exposure, to help
you re-enter situations that you currently avoid because of anxiety.
Helpful thinking is not simply positive thinking; it does not reject all negative
thoughts. It is looking at things in a way that is most helpful given the facts. It is
therefore important to distinguish helpful thinking from unhelpful positive, or
wishful, thinking.
Some examples of the diVerence between unhelpful, helpful, and wishful thinking are:
Unhelpful What if I can’t cope with this? I just know I’ll do something wrong.
Helpful I’m going to give this a try. I’ll do my best, and see how it goes.
able. If so, face your disappointment, but don’t make a catastrophe of it either! It is
sometimes diYcult to tell the diVerence between unhelpful, wishful, and helpful
thinking. Here are some clues to help clarify these:
Unhelpful thinking
I must . . .
I’ve got to . . .
What if . . . [something happened] . . . that would be terrible.
I couldn’t stand it if . . .
Wishful thinking
It’ll work out.
I don’t care . . .
It wouldn’t have done any good anyway.
I won’t be anxious at all.
Helpful thinking
I’d like to . . .
I’d prefer not to . . .
It’s unlikely that . . . [something] . . . will actually happen.
If things don’t go the way I want, I might be disappointed, but I’ll use my anxiety
management skills to help me cope.
Troubleshooting
1. ‘‘I don’t know what I’m thinking – I’m too scared.’’ Ask yourself ‘‘What am I
scared of? What am I scared might happen?’’. It is diYcult to identify unhelpful
fears, especially to begin with. It may help to wait until the anxiety has dropped,
then think about the situation and associated fears. Re-entering a situation may
make the fears clearer.
2. ‘‘I can’t think of alternatives.’’ After many months to years of having anxiety-
provoking thoughts, it may be diYcult to think up less threatening alternatives.
Look at all available evidence, especially evidence that contradicts your
thoughts. Ask yourself why others around you do not fear the situation, and try
to consider what they might be thinking about the situation.
3. ‘‘I’m doing it and it’s not working.’’ Use all available techniques, including
relaxation and slow breathing, to reduce your anxiety. Do not expect to be
perfect at controlling your thoughts or expect the technique to work immedi-
ately. Changing well-established patterns takes time and eVort.
4. ‘‘I still feel anxious.’’ Straight thinking is designed to provide more helpful and
appropriate responses to given situations, events or interactions. If the reality is
that a particular situation is associated with some anxiety for most people, do
not expect to use the technique to reduce all anxiety.
322 Treatment of Anxiety Disorders
5. ‘‘I don’t believe my new thoughts.’’ This may occur if you have not addressed all
of your anxiety-provoking thoughts. Go back and look at the original thought,
and try to think whether there are any related thoughts that still cause anxiety.
Also, you don’t have to believe your new thoughts immediately, as part of the
exercise is to disprove your old, unhelpful thoughts. Try to act as if your new
thoughts are true, and see what happens.
Coping statements
There are times when you may need some shortcuts to coping with feelings. Here
are a few:
1. Have a cue that makes you turn a potentially bad feeling into a coping one. For
example, if you feel butterXies in the stomach, instead of saying ‘‘Oh no, I’m
really getting anxious and upset’’ say ‘‘I know what these feelings mean. They
mean I’m getting anxious. That means: slow down, regulate my breathing and
do some isometric exercises.’’
2. Develop some personal self-statements, such as ‘‘Take this step by step’’,
‘‘Don’t jump to conclusions’’ or ‘‘This fear can’t hurt me – I can tolerate it’’.
Make these statements up yourself so that they are relevant to your life.
3. Don’t always put yourself down. Don’t say, ‘‘A baby should be able to do this’’,
‘‘I’m hopeless’’ or ‘‘I’ll never get the hang of this’’. As long as you say these sorts
of things to yourself you make them come true (but only for as long as you say
them, fortunately).
4. Praise yourself. Say things like ‘‘That was good’’ or ‘‘I felt I was having a bad day
this morning, but I still managed to get on the crowded train.’’ Remember the
most important source of praise is from inside you, because you know yourself
best and what your actions mean to you.
will be able to wait in the feared situation until the anxiety levels have decreased
signiWcantly to levels that are mild to moderate.
Over the next few weeks you will need to keep a record of your daily activities.
This will help you to remember what you did, the steps forward, and the
diYculties. To help in planning, below is a schedule that you can complete. On the
Wrst page, you can plan what you are going to do. Remember that your aim should
be to attempt a graded exposure exercise and a relaxation session every day.
Following the plan is room for you to write any comments that you may have
about the activities. On the pages after the plan are tables for you to write in the
unhelpful thoughts and level of fear that occurs during your graded exposure
exercises. You can then write down helpful thoughts so that you will be better able
to manage your fear.
DI A R Y
Day:
Time
7–8
8–9 Breathing exercise
9–10
10–11
11–12
12–1 Breathing exercise
1–2
2–3
3–4
4–5
5–6
6–7 Breathing exercise
7–8
8–9
9–10 Breathing exercise
324 Treatment of Anxiety Disorders
Exercise 2
SE CT I O N 6
6 Blood and injury phobia
6.1 Fear and fainting
Blood and injury phobias are relatively common, being found in about 4% of
people. People with blood and injury phobias can be divided into two overlapping
groups. On the one hand, there are those who experience fear when faced with
blood or injury. On the other hand, there are those who faint when faced with
blood or injury. Therefore, some people experience only fear, some only fainting,
and others both.
The skills that have been covered in the Patient Treatment Manual so far have
addressed fear and how to cope with it. These same skills are just as applicable for
dealing with blood and injury fears as for any other phobia: you must continue to
expose yourself to the distressing situations and wait for the discomfort to
decrease. What has not been covered is how to control fainting when in the
presence of blood or injury. This requires additional skills, but, before describing
these, we shall consider why the fainting occurs.
Among individuals with blood and injury phobias, fainting is extremely
common and is associated with a characteristic pattern of physiological respon-
ding. The particular pattern of responding has been called ‘‘vasovagal syncope’’.
The vasovagal syncope involves a two-stage process. In the Wrst stage, an increase
in heart rate and blood pressure occurs. This happens because there is an increase
in arousal caused by the sympathetic part of the involuntary nervous system. It is
the sympathetic branch of the involuntary nervous system that is responsible for
the Xight or Wght response and activation of it will trigger the fear reactions
described in Section 1 of the Manual. However, the involuntary nervous system
has another branch that opposes the sympathetic branch. This so-called parasym-
pathetic branch of the involuntary nervous system serves to regulate the body and
does the opposite to the sympathetic part of the nervous system. In people with a
blood and injury phobia, this compensation is very rapid and tends to be an
overcompensation. The heart slows too much and the blood pressure falls too low.
Therefore the blood (obeying gravity) will run away from the brain, causing a
deWciency in oxygen for the brain cells. If you do not lie down at this stage, the
brain will shut down and you fall unconscious. This reaction, when you think
about it, is really quite sensible because you are forced to lie down and the blood
can return to your brain cells.
As you can see from this description, the fainting is beyond your control. The
changes in heart rate and blood pressure are controlled by the autonomic part of
the nervous system, which is not under direct conscious control. The reason why
326 Treatment of Anxiety Disorders
your brain responds this way is not entirely clear but some parts of the puzzle are
available. It is now known that just under half the number of people with blood
and injury phobias have other members of their family who faint. Interestingly, it
was also found that while people who fainted were more likely to report a parent
who also did, people who reported fear of blood and injury did not report that
their parent did. This suggests that the fainting may be inherited but the fear is not.
It has also been found that people who faint tend to be more empathic; that is, they
are more able to see things from another person’s point of view. It is possibly the
ability to be able to ‘‘get inside another person’s shoes’’ that leads to people
fainting when they witness, think, or hear about injuries.
Hearing these facts about fainting may lead you to feel frustrated. ‘‘If I have
inherited it from my family and it is controlled by the nonconscious part of my
brain, what can I do?’’ The answer is that just because the fainting may be inherited
and controlled unconsciously does not mean that you cannot control it. Think for
a moment: can you increase your heart rate and blood pressure at will? If you run
quickly up a steep Xight of stairs, your heart rate and blood pressure will increase.
If you sit down and do relaxation exercises, they will decrease. Thus you can
engage in certain activities that can change these processes. Section 6.3 will
therefore go on to describe what techniques you can do to avoid fainting. These
activities are a little more practical and unobtrusive than running up stairs.
Slow breathing
People with blood and injury fears may increase their breathing rates when a
needle is placed on their arm. As you will remember, overbreathing has a number
of results one of which is feeling faint. You should monitor your breathing rate
and check to see whether it is elevated before you start your ‘‘fear stepladder’’. Also
check to see whether it is subtly increasing during exposure. In order to counter
these experiences, you will need to use your hyperventilation control exercise.
The most important point to remember is that slow breathing will be of most
use early in the physical reaction.
As the heart rate increases and the body prepares itself for danger, slow
breathing will help to restore the normal level of arousal to the body. However,
once you are aroused you need to stop the rapid decrease in heart rate and blood
pressure. For this, a diVerent skill is needed.
327 Specific phobias: Patient Treatment Manual
Applied tension
The second technique you will need to learn and master is ‘‘applied tension’’. The
aim of applied tension is to counteract the drop in blood pressure so that you have
control over your reactions. Essentially it aims to increase physical arousal, much
the same as running up a set of stairs would do, in a manner that is appropriate to
most medical settings. The steps involved require you to:
∑ Tense muscles in the arms, chest, and legs simultaneously.
∑ Continue to apply the tension until there is a feeling of warmth in the face
(usually about 10 to 20 seconds).
∑ Release the tension and relax to starting level (without becoming too relaxed
remember the technique is applied tension).
∑ Wait 20 seconds.
∑ Repeat the whole cycle a minimum of Wve times and always until the feeling of
faintness has signiWcantly decreased to manageable levels.
∑ You will need to be able to identify your particular signals of fainting, which
may include light-headedness or dizzy feelings.
This technique will need to be incorporated into your exposure tasks and
combined with relaxation and slow breathing. As you develop your skill with
breathing control and applied tension, you will become able to discriminate when
the best time is to apply the slow breathing and the applied tension. The rule of
thumb is that you begin with slow breathing to keep you relaxed as you move into
the situation but then switch (still keeping an eye on your breathing rate) as you
approach the blood or injury stimulus or when you notice the very Wrst signs of
faintness. The Wrst signs are diVerent for diVerent people, but some commonly
reported ones include dizziness, a cold sweat (across the forehead), a queasy
feeling in the stomach, or nausea.
A commonly reported problem with applied tension is headaches. This indi-
cates that you are applying too much tension. This problem is solved by increasing
the length of time between muscle tensions from 20 seconds to a time when the
headaches do not occur. Also you can try to avoid tensing muscles in the face (e.g.,
the jaw and eyebrows) that constrict and cause pressure to be applied to the head.
Another problem is diYculty in identifying the muscles to tense and how to make
them taut. Looking back at the isometric exercises for some ideas may be helpful.
Many people Wnd it useful to imagine they are a bodybuilder and think about how
a bodybuilder would tense those muscles. One other problem is that tensing
muscles can make receiving injections more painful. You will need to be able to
relax the muscle group in which the injection will be given (typically the non-
dominant arm) while maintaining tension in your other arm, torso, and legs.
328 Treatment of Anxiety Disorders
SE C T I ON 7
7 Keeping your progress going
7.1 Coping with setbacks or difficulties in making progress
Setbacks or diYculties in making progress are generally the consequence of either
poor management or poor planning of goals and steps. If you should experience
such diYculties, you must carefully analyze the way in which you carry out these
two exercises.
to factors such as outside stressors, the Xu, or school holidays. In such cases, the
setback is often viewed as devastating because it has a lot of emotional meaning for
the person, who has put considerable eVort into recovering. This eVort is not
wasted, and after the stressors pass you will Wnd it easier to get yourself out and
about again. This pattern has been demonstrated again and again. Therefore, if
you have a setback, don’t add to the problem with all the old catastrophic,
emotional, and self-destructive ideas. Keep practicing all the techniques you have
been taught and you will be able to make progress. If you feel that you have
genuinely lost the skills necessary to control anxiety and panic, then you may want
to consider retreatment. Most people do not lose the skills but need some
Wne-tuning of their skills. ‘‘Booster’’ sessions or follow-up meetings are the best
way to receive this form of assistance.
7.4 Conclusion
You now have three skills that you have been taught and now need to practice. You
need to use the various exposure tasks, working up the fear stepladder, to reduce
your fear. Relaxation will help to reduce your general levels of tension before the
exposure task, and the isometric exercises will regulate tension during exposure.
Slow breathing will help to keep control of any anxiety that you may experience
and by thinking straight you will be able to stop anxiety from spiraling out of
control.
330 Treatment of Anxiety Disorders
SE C T I ON 8
8 Recommended resources
The following books are available from most large bookstores, many smaller ones,
and some news-stands. If in doubt, ask whether the book can be ordered. We also
suggest that you use your local library to gain access to many of these books. When
you read these or any similar books on the management of anxiety, remember that
they are best regarded as guidelines only. Be critical in both a positive and negative
sense when reading these books, so that you get what is best for you out of them.
Most of these books are inexpensive.
8.1 Books
Barlow D and Rapee R. (1997) Mastering Stress: A Lifestyle Approach. Killara, NSW: Lifestyle
Press.
Burns DD. (1999) The Feeling Good Handbook, revised edition. New York: Penguin.
Copeland ME. (1992) The Depression Workbook: A Guide for Living with Depression and Manic
Depression. New York: New Harbinger.
Davis M, Eshelman ER and McKay M. (1995) The Relaxation and Stress Reduction Workbook,
fourth edition. Oakland, CA: New Harbinger.
Ellis A and Harper R. (1979) A New Guide to Rational Living. Hollywood, CA: Wilshire Book
Company.
Emery G. (2000) Overcoming Depression: A Cognitive-Behavior Protocol for the Treatment of
Depression. Oakland, CA: New Harbinger.
Greenberger D and Padesky C. (1995) Mind Over Mood. New York: Guilford.
Marks IM. (2001) Living with Fear. New York: McGraw-Hill.
McKay M and Fanning P. (1987) Self-Esteem: A Proven Program of Cognitive Techniques for
Assessing, Improving and Maintaining Your Self-Esteem. Oakland, CA: New Harbinger.
McKay M, Davis M and Fanning P. (1995) Messages: The Communication Skills Book. Oakland,
CA: New Harbinger.
McKay M, Davis D and Fanning P. (1997) Thoughts and Feelings: Taking Control of Your Moods
and Your Life. Oakland, CA: New Harbinger.
Meichenbaum D. (1983) Coping With Stress. London: Century Publishing.
Page A. (1993) Don’t Panic! Overcoming Anxiety, Phobias and Tension. Sydney: Gore Osment.
Walker CE. (1975) Learn to Relax: 13 Ways to Reduce Tension. Englewood CliVs, NJ: Prentice
Hall.
Weekes C. (1966) Self-Help For Your Nerves. Sydney: Angus and Robertson.
Weekes C. (1972) Peace From Nervous SuVering. Sydney: Angus and Robertson.
8.2 Video
Rapee R, Lampe L. (1998). Fight or Flight? Overcoming Panic and Agoraphobia. Monkey See
Productions. P.O. Box 167, Waverley, NSW 2024 Australia.
331 Specific phobias: Patient Treatment Manual
Obsessive–compulsive disorder
Syndrome
Diagnostic criteria
Obsessions are deWned as ideas, thoughts, images and impulses that enter the
subject’s mind repeatedly. They are recognized as a product of the subject’s own
mind, are perceived as intrusive and senseless, and eVorts are made to resist,
ignore or suppress such thoughts. Compulsions are repetitive or stereotyped
behaviors that are performed in response to an obsession in order to prevent the
occurrence of an unlikely event or to prevent discomfort. Resistance is often
evident, but may be minimal in longstanding cases. The diagnosis of OCD is to be
made if the individual experiences both obsessions and compulsions, obsessions
alone or compulsions alone, given that such symptoms are time consuming or
332
333 Obsessive–compulsive disorder: Syndrome
CASE VIGN ET TE
Patient identification
Mr. P is a 30 year old father of two children who presents with a 9-year history of compulsive
behavior. At the time of presentation, he was engaging in extensive checking behavior that
significantly interfered with his life.
Presenting problem
Because of thoughts that something terrible may happen and he may inadvertently be
responsible for harm befalling loved ones, neighbors, or other people, Mr. P states that he
must check ‘‘dangerous’’ items repeatedly before being able to leave his home. He performs
his checking in a ritualized manner, ensuring that electrical items are switched off and at
times has to count to 4 as he stares at each item. If he is interrupted while completing these
behaviors or feels under pressure, he must recommence his checking rituals. Similarly, if the
thought that something may have been left on reoccurs while checking, the time spent
ritualizing is considerably extended by his need to check repetitively. In addition to ensuring
that possibly harmful events are unlikely to occur, Mr. P feels that he must check that all taps
are turned off and has difficulty in writing and posting cheques and letters. He reports that he
is consistently late in getting out of the house and was in fact asked to resign from his last two
positions of employment as a result of his constant tardiness.
sessions as he felt his mood had improved and there was little further to be gained by
continuing to attend. He remained handicapped by his obsessional behavior. There were no
other psychiatric interventions until his current referral to a specialist unit.
Differential diagnosis
The diagnosis of OCD should not be made if the thoughts or behavior are
ego-syntonic or pleasurable, and resistance to such thoughts is primarily a func-
tion of deleterious consequences. Where the obsessional thought has developed
into an overvalued idea, the diagnosis of OCD is still possible if the suVerer is able
to eventually acknowledge that the belief is unfounded. The co-occurrence of
depression in OCD is frequently noted in the literature. Where major depressive
symptoms precede the onset of OCD symptoms or where both depressive and
obsessional symptoms equally predominate, a diagnosis of depression may be
indicated and the primary depressive disorder should be addressed. In making the
diVerential diagnosis, a qualitative diVerence is often noted between obsessional
and depressive thoughts, particularly with regard to the perceived senselessness
and resistance to the thought. The absence of compulsive rituals in those suVering
from depression also assists in making the diVerential diagnosis. Similar qualitat-
ive diVerences are evident in relation to stereotyped behavior in schizophrenia,
where the behavior is often engaged in as a result of Wxed beliefs or delusional ideas
or in response to other psychotic symptoms.
The symptoms of generalized anxiety disorder (GAD) may be distinguished
from OCD on a number of dimensions. In terms of content, the anxious cogni-
tions of GAD are usually concerned with problems of everyday living (health,
family, Wnances, work, etc.) as opposed to the frequently encountered themes of
dirt/contamination, violence, sex, aggression and blasphemy in OCD suVerers.
The absence of rituals – either overt or covert – in response to the worrying
thoughts in GAD is another often noted diVerence and may well be a reXection of
the degree of resistance to the thoughts. DiVerentiation may also be made in terms
335 Obsessive–compulsive disorder: Syndrome
Spectrum disorders
A growing trend in the literature has been concerned with the classiWcation of a
variety of impulse control and other disorders as ‘‘obsessional’’. The notion that
patients experience a subjective urge to complete behaviors – as well as anxiety
relief upon their completion – has led some authors to speculate that a number of
disparate disorders, such as trichotillomania, sexual compulsions, kleptomania,
borderline personality disorder, or Tourette’s Syndrome, may be related to OCD
along an impulsive–compulsive continuum. Although individuals with a spec-
trum disorder may respond to thoughts, urges, or preoccupations with particular
maladaptive behaviors, the relationship of their disorder to OCD is questionable
at a number of levels. OCD is characterized by intrusive, unwanted thoughts while
many of the spectrum disorders are characterized by thoughts or preoccupations
that are perceived as appropriate and rational. As the content or cognitive
component of their symptoms is markedly diVerent from OCD, the reasons for
engaging in the particular behavior are diVerent. While behaviors associated with
spectrum disorders may appear to have a sense of compulsion, important dif-
ferences are noteworthy in that the behaviors themselves are gratifying or pleasur-
able (e.g., impulse control disorders), are in response to an urge rather than an
intrusive thought (Tourette’s syndrome, trichotillomania), or to a physical symp-
tom or sensation (hypochondriasis), or are selectively purposeful (eating dis-
orders) or in response to a delusional belief (body dysmorphic disorder). In
contrast, rituals or behaviors in OCD are engaged in to reduce distress or anxiety
associated with the perceived threat resulting from the intrusive thought. Cogni-
tive factors involved in the mediation of OCD have been reported in a number of
investigations and these further diVerentiate OCD from spectrum disorders.
InXated responsibility has been proposed by investigators as an essential element
in the development of OCD (Salkovskis, 1989; Salkovskis and Kirk, 1997).
Thought–action fusion interacting with inXated responsibility is also considered
to be cognitive bias directly involved in the development and maintenance of
OCD (Rachman, 1997). Danger expectancies rather than responsibility have been
336 Treatment of Anxiety Disorders
Sex ratio
Black (1974) summarized 11 studies of OCD and reported that of 1336 cases, 651
were male and 685 female, suggesting an almost equal sex ratio. Similarly,
Yaryura-Tobias and Neziroglu (1983) reported an equal sex ratio in their review of
six OCD studies, while another study reporting on a clinical cohort (Noshirvani et
al., 1991) found a slightly higher proportion of women. Rasmussen and Eisen
(1992) also reported a slightly higher proportion of women (53.8%) in a large
cohort of 560 OCD patients. The opposite has generally been the case with child
and adolescent studies, which have tended to indicate a predominance of males
(Swedo et al., 1989, Rapoport, 1990). However, this may in part be due to an
earlier onset in males than in females.
Age of onset
In reviewing a number of studies, Black (1974) found that the majority of cases
had an onset of OCD between ages 10 and 40 years. The distribution, however, was
337 Obsessive–compulsive disorder: Syndrome
skewed, with 21% beginning between ages 10 and 15 years. Mean age of onset was
10–15 years, with 10% having syndrome onset prior to age 10 and 9% after age 40
years. Noshirvani et al. (1991), reporting on a large clinical cohort (N=307), found
a signiWcantly earlier onset in males (5–15 years). The mean age of onset was 22
years, with the vast majority (92%) commencing between ages 10 and 40 years.
Earlier onset for males was also reported in childhood onset OCD (Rapoport,
1990). Similarly, in another large clinical cohort of 560 individuals, Rasmussen
and Eisen (1992) report, the mean onset age as 20.9±9.8 years. Males were
reported to have a signiWcantly earlier onset (19.5±9.6 years), as compared
with females (22.0±9.8 years). Sixty-Wve percent of suVerers were found to have
illness onset prior to age 25 years, and fewer than 15% reported onset after age 35
years.
Course of illness
Prior to the development of eVective treatments of OCD, Ingram (1961) reported
a constant worsening in 39% of 89 inpatients, a constant and static unremitting
course in 15%, a Xuctuating course with periods of worsening and relative
improvement in 33% and a phasic course with periods of remission in 13%. An
early follow-up study of OCD suVerers by Kringlen (1965) found that 5% had a
constant worsening, 30% were constant and static, 20% Xuctuating and 5%
phasic. More recently, Rasmussen and Eisen (1992) reported that 85% had a
continuous and Xuctuating course, 10% had a deteriorative course and 2% were
classiWed as episodic. More recently, Skoog and Skoog (1999), in a 40 to 50 year
follow-up of OCD patients found that 83% of patients had improved over the
follow-up period, and 48% showed clinical recovery. However, 37% still had
diagnosable OCD after 50 years, and only 20% of the sample showed complete
recovery. Overall, clinical and subclinical symptoms were still evident in two-
thirds of the sample at follow-up, and 10% of the sample showed a deteriorating
course.
the same purpose as overt behavioral rituals. The presence of covert compulsions
has been recognized for some time. Foa and Tillmans (1980) have suggested that
the deWnition of compulsions be broadened to include both overt and covert
behaviors. Further support for this notion is found in the work conducted by
Salkovskis and Westbrook (1989), who diVerentiated between obsessional ideas
and cognitive rituals. They deWned obsessional ideas as the original anxiety-
arousing intrusions. In contrast, cognitive rituals are deWned as thoughts that the
patients voluntarily initiate to attempt to reduce the anxiety or discomfort
aroused by obsessional ideas. Within this approach, cognitive rituals are also often
referred to as ‘‘neutralizing’’ thoughts. DSM-IV criteria now acknowledge the
presence of covert compulsions and revision of the diagnostic criteria include
neutralizing thoughts within the compulsion deWnition. Although obsessional
ruminators are conceptualized as being similar to individuals with obsessions and
overt compulsions, a number of diVerences have been noted by Arts et al. (1993),
who, in comparing 26 ruminators to 48 patients with both obsessions and
compulsions, reported that the former group were more depressed, were more
often married, had achieved a lower level of education, were older at symptom
onset and were more often on medication.
The types of obsessional thoughts and compulsive behaviors have been reported
to be consistent across cultures (Tseng; 1973, Mahgoub and Abdel-HaWez, 1991;
Okasha et al., 1994) and time, with similar phenomenological reports and clinical
descriptions appearing in medical writings of the last century (Berrios, 1985).
Obsessional thoughts are often concerned with worries of contamination, harm-
ing others, or going against social mores such as swearing or making inappropriate
sexual advances in public (Marks, 1987). Rasmussen and Eisen (1992) reported
that 50% of 560 OCD patients had obsessions regarding contamination, 42%
pathological doubt, 33% somatic obsessions, 32% need for symmetry, 31%
aggressive, and 24% sexual. Compulsive behavior has generally been categorized
as washing, checking, repeating and ordering, with both adult and child suVerers
exhibiting similar phenomenology (Last and Strauss, 1989; Swedo et al., 1989).
Washing or cleaning, which generally aVects more women than men, is character-
ized by a fear of contamination and associated washing, decontaminating or
cleaning rituals, with extensive avoidance of the contaminant. Washing/cleaning
compulsions were evident in 50% of 560 OCD patients investigated by Rasmussen
and Eisen (1992). Checking behaviors were evident in 61% of the their sample,
with patients engaging in repeated checking in order to prevent a dreaded event or
disaster from occurring. Counting was evident in 36%, a need to ask or confess in
34%, a need for symmetry or precision in 28%, and hoarding in 18% of the
sample. In another large clinical cohort, Noshirvani et al. (1991) reported signiW-
cantly more compulsive washing in females and signiWcantly more checking in
339 Obsessive–compulsive disorder: Syndrome
males. Compared with late onset cases, early onset cases exhibited signiWcantly
more checking and fewer washing rituals. Obsessional slowness without visible
rituals has also been reported, though to a much lesser extent than other presenta-
tions, and is most likely a function of mental checking or the need to follow
a meticulous preset order (Rachman, 1974; Marks, 1987; Ratnasuriya et al.,
1991).
The utility of classifying subjects according to phenomenology is questionable,
given that suVerers often have more than one obsession and more than one form
of ritual. In a large cohort of 560 OCD patients (Rasmussen and Eisen, 1992), 72%
experienced multiple obsessions and 58% experienced multiple compulsions.
Other research suggests that phenomenology may change over time (Marks, 1987;
Hodgson and Rachman, 1977). A more promising classiWcation with implications
for behavioral treatment was proposed by Foa et al. (1985), and is based on the
presence or absence of external cues, disastrous consequences and either overt or
covert anxiety-reducing responses. ClassiWcation according to these criteria hold
implications for the cognitive behavioral treatment of the disorder and would
therefore be of greater clinical utility to the practicing clinician. A comprehensive
behavioral program should include exposure to all cues, both internal and exter-
nal, as well as response prevention that focuses on overt and covert rituals in
addition to avoidance.
Assessment instruments
A thorough assessment of OC symptomatology for the purposes of designing a
behavioral program relies heavily on clinical interview. No instrument will pro-
vide the clinician with the detailed and often idiosyncratic information regarding
the cues that create anxiety or discomfort, the responses (rituals) to those cues,
and the avoidance that the patient often engages in to minimize their discomfort.
Despite these limitations, it is good clinical practice to utilize assessment instru-
ments that may provide an independent validation of treatment eVectiveness. An
often-used therapist-administered instrument utilized in both clinical practice
and research settings that focuses on target obsessions and compulsions is the
Yale–Brown Obsessive Compulsive Scale (Goodman et al., 1989). The Maudsley
Obsessive Compulsive Inventory (Hodgson and Rachman, 1977) is a 30 item
‘‘true–false’’ self-report inventory that is also often used in the treatment of OCD.
The major shortcoming of this instrument is that it asks the patient to rate the
presence or absence of symptoms and therefore does not lend itself to changes in
interference, severity or frequency as a result of treatment. A more comprehensive
instrument, the Padua Inventory (Sanavio, 1988) consists of 60 items reXecting
OC symptoms that the patient rates in terms of degree of disturbance. In its
340 Treatment of Anxiety Disorders
original version, the Padua Inventory was found to be signiWcantly correlated with
measures of neuroticism and trait anxiety. A revision of the Padua was undertaken
by Burns et al. (1996) in order to delete items that overlapped with worry. This
resulted in a 39 item questionnaire (WSUR revision) consisting of Wve subscales:
obsessional thoughts about harm to self or others, obsessional impulses to harm
self or others, contamination obsessions and washing compulsions, checking
compulsions, and dressing or grooming compulsions.
Genetics
At the time of writing, there is growing evidence for a contribution from genetic
factors in some OCD presentations. The evidence for possible genetic predisposi-
tion in OCD derives from two sources: twin studies and investigations of the
Wrst-degree relatives of OCD suVerers. Early twin studies reporting concordance
may be criticized on the basis of failing to establish Wrm diagnoses of either
342 Treatment of Anxiety Disorders
zygosity or OCD (Hoaken and Schnurr, 1980). However, even in those studies
where zygosity was established and diagnosis conWrmed (WoodruV and Pitts,
1964; Marks et al., 1969; McGuYn and Mawson, 1980), the eVects of social
learning cannot be ruled out.
As with the twin studies, early investigations of Wrst-degree relatives of OCD
suVerers can be criticized on a number of grounds. The use of loose diagnostic
criteria, confounding of obsessional symptoms and traits, absence of control data,
as well as reliance on information provided by the proband rather than direct
interview of the relatives renders the Wndings of early investigations, as well as
some later studies (Insel, Hoover and Murphy, 1983; Rasmussen and Tsuang,
1986) diYcult to interpret. However, more recent studies, have attempted to
overcome such methodological Xaws through the use of structured diagnostic
interviews and direct relative interview. A study by Black et al. (1992) used the
Diagnostic Interview Schedule to assess the prevalence of OCD in the relatives of
OCD suVerers and normal controls. The authors found that, while Wrst-degree
relatives of probands with OCD were signiWcantly more likely to develop anxiety
disorders than relatives of the control group, the prevalence of OCD in both the
index and control relatives did not exceed the estimated occurrence in the general
population. Pauls et al. (1995), however, reported that the morbid risk for OCD
was signiWcantly higher in OCD proband relatives (10.3%) as compared with
relatives of controls (1.3%). The addition of subthreshold OCD raised the morbid
risk to 18.2%.
In contrast, studies that have utilized structured interviews to assess Wrst-degree
relatives of children and adolescent suVerers report a considerably higher inci-
dence of diagnosable OCD. Riddle et al. (1990) directly interviewed parents of
children with OCD using a standard clinical assessment. Results showed that 71%
of 21 children or adolescents with OCD had a parent with OCD (N=4) or
obsessional symptoms (N=11), indicating that 37.5% of parents had diagnosable
or subthreshold OCD. Lenane et al. (1990) reported similar results, with diagnos-
able OCD being found in 25% of fathers and 9% of mothers of 46 children with
OCD. With the inclusion of subclinical OCD, age-corrected morbidity risk was
estimated at 35%, not unlike the Wndings of Riddle et al. (1990).
The discrepancy between the child and adult studies may be a function of
diVerences between childhood/adolescent onset OCD and later or adult onset
OCD. In one early study, Bellodi et al. (1992) reported a morbid risk of 3.4% in the
Wrst-degree relatives of 92 OCD patients. Separation of the probands according to
age of onset, however, resulted in a morbid risk of 8.8% of relatives of probands
with onset prior to age 14 years and 3.4% for relatives of probands with a later
onset. More recently, Nestadt et al. (2000) reported that the lifetime prevalence in
relatives of 80 OCD patients was signiWcantly higher than controls (11.7% versus
2.7%). When the sample was divided into early onset (5–17 years) and late onset
343 Obsessive–compulsive disorder: Syndrome
(over 18 years) groups, the prevalence of OCD in relatives was 13.8% and 0%,
respectively.
To some extent, OCD is familial, particularly in early onset OCD. However,
while the above studies indicate that familial factors may play a role in some forms
of OCD, there are a signiWcantly large proportion of probands in all of the cited
studies that have no family history of OCD. Thus genetics, while important, do
not provide a total answer.
Comorbidity
Depression
The occurrence of obsessional symptoms in depressive illness suVerers has been
noted by a number of authors (Gittleson, 1966; Kendell and Discipio, 1970), as has
the high incidence of depressed mood in OCD suVerers (Rosenberg, 1968;
Goodwin, 1969; Rasmussen and Tsuang, 1986). However, the obsessional symp-
toms seen in patients with depressive illness are generally not of the intensity seen
in patients with OCD, and recovery from depression has been shown to result in a
reduction of obsessional symptoms. Other studies also indicate that obsessional
features in depression appear to parallel the course of the primary illness and that,
if present beforehand, will revert to their original intensity after resolution of the
depression (Videbech, 1975; Marks, 1987).
The presence of depressed mood or depressive symptoms has consistently been
shown to be a frequent complication of OCD (Rosenberg, 1968; Goodwin et al.,
1969; Black and Noyes, 1990), and some authors have suggested a psychobiologi-
cal link between depression and OCD (Hudson and Pope, 1990). Studies of child,
adolescent, and adult OCD suVerers report high rates of depressed mood, with
between 20% and 35% of OCD clinic attenders meeting criteria for major
depression (Rasmussen and Tsuang, 1986; Swedo et al., 1989; Sanderson et al.,
1990). Lifetime prevalence has been reported as aVecting up to 67% of OCD
patients (Rasmussen and Eisen, 1992). However, such clinical data need to be
interpreted cautiously, as many OCD suVerers tend to seek help only when
depressed (Marks, 1987). It is, moreover, important to carefully assess the severity
of depression in OCD patients presenting for treatment – particularly as the
presence of severe depression hinders the eVectiveness of behavioral interventions
in OCD (Foa et al., 1983a,b). Aside from improving less than suVerers with mild
or moderate depression, OCD suVerers with severe depression also tend to have a
higher relapse rate. Where such patients present for treatment, the possibility of
combining behavioral treatment with antidepressant medication, preferably with
antidepressant medication which has 5HT reuptake inhibiting properties, needs to
be carefully considered.
344 Treatment of Anxiety Disorders
Anxiety disorders
The co-occurrence of anxiety disorders in OCD suVerers is considerable. Similar
results are reported in both epidemiological and clinic samples for adults, adoles-
cents, and children (Rasmussen and Tsuang, 1986; Flament et al., 1988; Karno et
al., 1988; Swedo et al., 1989; Brown and Barlow, 1992; Crino and Andrew, 1996a).
Severity of co-occurring anxiety disorders should be assessed by the clinician, as
these conditions may require intervention after, or even before, the obsessional
problems have been addressed. Alternatively, these ‘‘conditions’’ may be second-
ary to the obsessional complaints, so that what appears to be agoraphobic avoid-
ance or social phobic concerns may be the direct result of the obsessional fears or
attempts by the suVerer to keep their rituals hidden from others. For example, a
patient with contamination concerns may experience diYculty in using public
transport, eating or drinking away from home, or other situations that may expose
the individual to contamination and therefore be wrongly identiWed as suVering
from a phobia. If there is a clear co-occurring anxiety disorder, it should be the
patient’s decision as to which disorder should be dealt with Wrst, and such a
decision should be made on the basis of level of interference with their life.
Personality disorder
The relationship between OCD and axis II diagnoses have generated considerable
interest among researchers. Findings suggest that anywhere from 48% (Jenike et
al., 1986) to 87.5% (Black et al., 1993) of OCD patients have one or more
personality disorders, as diagnosed by a variety of instruments. The results of
many of these studies are questionable on a number of grounds. First, the validity
of the instruments is uncertain, particularly as there is no ‘‘gold standard’’ against
which to compare the various questionnaires. Second, the confounding of state
and trait is certainly an issue worthy of consideration when eVective treatment of
the obsessional symptoms in OCD subjects results in a marked lowering of
personality disorder diagnoses (cf. JoVe and Regan, 1988; Mavissakalian et al.,
1990). One would expect the enduring maladaptive traits that constitute personal-
ity disorder should persist after the Axis I condition is treated. EVective treatment
of OCD and other anxiety disorder patients, however, results in the majority of
patients leading essentially normal lives, uncomplicated by any obvious Axis II
pathology. Results from our clinic (Crino and Andrews, 1996b) suggest that the
rate of personality disorders in OCD and other anxiety disorders is relatively low,
and that minor but important diVerences between the anxiety disorders exist
when one takes a dimensional rather than categorical view of personality disorder.
345 Obsessive–compulsive disorder: Syndrome
Conclusion
Many facts regarding OCD and its possible causes remain unknown despite the
extraordinary burgeoning of research in this area in recent years. While there is
general agreement of the diagnostic criteria across the two major classiWcation
systems as well as acknowledgment of the frequently encountered complication of
depression in OCD, much still remains to be learned of the etiology, comorbidity,
and other complications of what remains a puzzling and, if left untreated,
crippling disorder. One important question that continues to re-occur in the
recent literature is the possibility that OCD is a heterogeneous disorder. Taking
such a view would go part of the way to explain some of the disparate Wndings
noted above (e.g. genetics, relationship to TS, diVering cognitive styles, etc.)
Nevertheless, eVective treatments for OCD are available and, either alone or in
combination, will result in the majority of patients gaining control over their
disorder.
17
Obsessive–compulsive disorder
Treatment
Although OCD has been recognized for centuries, eVective treatment for this
condition has been available only for the past four decades. The treatments of
choice for OCD are behavior therapy, consisting of exposure and response
prevention, and selective serotonin reuptake-inhibiting medications. Recent stu-
dies have also included speciWc cognitive techniques targeting the appraisals of
intrusive thoughts, responsibility for harm and threat estimates. Whether the
addition of such techniques results in superior eYcacy is yet to be demonstrated in
further trials. Nevertheless, the use of cognitive techniques to challenge the
dysfunctional appraisal of intrusive thoughts is warranted in individuals with
cognitive styles that interfere with treatment. Cure of OCD is not commonplace.
The primary goal of treatment in the majority of cases is to have the individual
control the disorder rather than the obsessional disorder control the individual.
Achievement of this goal allows the patient to minimize the impact and eVects of
the disorder on their daily life and enhances their ability to reach their full
potential.
Behavioral therapy
The basic principles of exposure and response prevention include the deliberate
exposure to obsessional cues and prevention of the behaviors that the suVerer
typically engages in to lessen the anxiety, discomfort, or distress associated with
the feared stimuli. Repeatedly employing prolonged exposure (45 minutes to 2
hours) to the obsessional cues, with strict response prevention, allows habituation
to take place. Exposure tasks are arranged hierarchically, with treatment com-
mencing with the least anxiety-provoking situation and progressing rapidly
through the hierarchy.
In reviewing the results of more than 200 OCD patients treated with behavior
therapy in several countries, Foa et al. (1985) reported that 51% of suVerers
achieved at least a 70% reduction in symptoms. Thirty-nine percent of patients
346
347 Obsessive–compulsive disorder: Treatment
achieved reductions ranging from 31% to 69%, and 10% were considered failures,
failure being deWned as patients with an improvement of 30% or less. At follow-up
(mean duration 1 year), the number of failures increased from 10% to 24%.
However, 76% of patients remained improved to a degree rated as moderately
improved or better.
Further evidence for the eYcacy of exposure and response prevention is reXec-
ted in a long-term follow-up of nine cohorts from Wve countries conducted by
O’Sullivan et al. (1991). Both self- and assessor ratings were used, and two cohorts
had received exposure plus either clomipramine or placebo. The overall dropout
rate was reported at 9% and – of a total of 223 patients – 87% were followed up for
a mean of 3 years (range 1 to 6 years). All studies reported a signiWcant improve-
ment at posttreatment, which remained evident at follow-up, with 78% of individ-
uals remaining improved. On average, there was a 60% improvement in target
rituals as compared with pretreatment. These Wndings need to be tempered with
the fact that approximately 25% of patients refuse behavior therapy when oVered,
because of the time commitment, or because of fears of overwhelming anxiety
when confronting their triggers, or because they fear that the dreaded outcome
from not performing their ritual will eventuate (Greist, 1998). In our experience,
motivational interventions may assist in those who do not wish to make the time
commitment, cognitive techniques may assist those who fear the dreaded out-
come, while a more graded approach to exposure may assist those who fear
overwhelming anxiety or panic.
Although the utilization of exposure and response prevention techniques have
had a signiWcant impact upon the treatment of individuals with compulsive
rituals, the eYcacy of behavioral techniques in the treatment of obsessional
thoughts has, until recently, been considered problematic. However, Salkovskis
and Westbrook (1989), employing revised habituation procedures in which the
subjects were exposed to obsessional thoughts via loop tapes and avoided cogni-
tive neutralizing, reported a favorable outcome in four subjects. More recently,
Freeston et al. (1997) randomly assigned 29 OCD patients without overt rituals to
a wait-list control condition or a comprehensive cognitive behavioral program
that involved a cognitive model of obsessions, cognitive restructuring of the
dysfunctional assumptions, loop tape and in vivo exposure and response preven-
tion, and relapse prevention. SigniWcant improvement was reported in Yale–
Brown Obsessive Compulsive Scale (YBOCS) scores, self-report of OCD symp-
toms and self-reported anxiety, with 77% of treatment completers (N = 22)
showing clinically signiWcant changes.
348 Treatment of Anxiety Disorders
Cognitive therapy
The eYcacy of cognitive interventions in the treatment of OCD has been inves-
tigated by a number of researchers. The contribution of self-instructional training
(SIT) to exposure and response prevention was examined by Emmelkamp et al.
(1980). Fifteen patients received either self-controlled exposure or exposure com-
bined with SIT. No group diVerences were found at posttreatment or 1- or
6-month follow-up. Emmelkamp et al. (1988) compared self-controlled exposure
and response prevention to rational emotive therapy (RET) in 18 OCD suVerers
and reported that cognitive therapy was as eVective as exposure and response
prevention. In a replication, Emmelkamp and Beens (1991) compared six sessions
of RET to six sessions of exposure followed by a 4-week waiting period and six
further sessions of exposure for both groups. Although no diVerence was found
between the RET condition and exposure condition, there was no indication that
RET enhanced outcome when combined with exposure and response prevention.
In a larger study, Van Oppen et al. (1995) randomly allocated 71 patients to either
self-controlled exposure or a cognitive therapy condition on the basis of work of
Beck (1976) and Salkovskis (1989). Both conditions led to signiWcant improve-
ment and there were some indications that cognitive therapy may have been
superior; however, the diVerences were not signiWcant when initial diVerences
between conditions were taken into account. EVect sizes tended to be larger in the
cognitive therapy condition and there were signiWcantly more patients rated as
recovered in the cognitive condition. Although the authors discuss the results in
terms of the eYcacy of cognitive techniques, the addition of behavioral experi-
ments to test the empirical basis of dysfunctional assumptions (exposure) after six
sessions of cognitive therapy would tend to confound the observed outcome. No
study directly comparing cognitive techniques alone, cognitive techniques com-
bined with exposure, and exposure alone has yet been conducted.
fered signiWcantly from treated patients in Wve areas: they were less obsessive
compulsive, they had more discongruent treatment expectations, they were more
critical of the therapist, they experienced less anxiety in homework exposure, and
they were less often pressured by signiWcant others to continue treatment. Foa et
al. (1983a,b), attempting to determine predictors of outcome, found that signiW-
cant depression may aVect outcome when exposure and response prevention is
used by inXuencing reactivity and habituation between sessions. Similarly, the
presence of overvalued ideation has been noted to aVect outcome negatively (Foa,
1979). In contrast, Lelliot et al. (1988) found that patients with bizarre and Wxed
beliefs responded well to treatment. While there was a signiWcant correlation
between clinical improvement on a number of measures and the reduction of
Wxity of obsessional beliefs, the Wxity of such beliefs did predict severity of target
rituals at 1-year follow-up (Basoglu et al., 1988). More recently, Ito et al. (1995)
reported that reduction in Wxity of OCD beliefs parallelled improvements in other
measures of OCD symptoms.
Other factors that may aVect the success of treatment include excessive behav-
ioral or cognitive avoidance and excessive arousal in the presence of feared stimuli
(Foa et al., 1983a). In the Wrst case, attention-focusing techniques while using in
vivo exposure may assist in promoting habituation. Excessive arousal may be a
function of the program design, and require a reanalysis of the fear-evoking
potential of the stimuli so that arousal is kept at moderate levels, thereby promo-
ting emotional processing and habituation. Clinical factors not found to inXuence
treatment include age at symptom onset. In fact, Foa et al. (1983a) reported that
the younger the individual was when symptoms began, the better maintained was
the improvement at follow-up. Similarly, neither duration of symptoms nor
symptom severity was associated with poor outcome. The types of ritual (washing
versus checking) were also not predictive of outcome with exposure and response
prevention. In contrast, Basoglu et al. (1988) reported that severe rituals and social
disability predicted poorer outcome in patients treated with clomipramine and
exposure. Similarly, Cottraux et al. (1993), in examining predictors of treatment
outcome in 60 patients treated with behavior therapy, Xuvoxamine or a combina-
tion, found that high avoidance was the best single predictor of poor outcome.
While depression was not a signiWcant predictor of outcome in a number of other
studies (Basoglu et al., 1988; Hoogduin and Duivenvoorden, 1988; O’Sullivan et
al., 1991; Riggs et al., 1992), depression predicted failure in Cottraux et al.’s (1993)
study. Severe depression was also associated with poorer outcome in a follow up of
72 OCD patients treated with behavior therapy (Foa et al., 1981).
More recently, Castle et al. (1994) examined outcome predictors for 178
outpatients with OCD. Forty-one patients who dropped out of treatment did not
diVer signiWcantly in terms of demographic or illness variables or initial rating
350 Treatment of Anxiety Disorders
scale scores. As with data from Foa et al. (1983a), age, age of onset, and illness
duration were not signiWcantly associated with outcome, nor were meticulous or
anxious personality traits. Patients living alone were signiWcantly less likely to be
classiWed as ‘‘much improved’’. The ‘‘much improved’’ group had signiWcantly
lower initial scores on global phobia as well as ratings of work and home
impairment, and were more likely to have had a co-therapist. While gender was
not a predictor of outcome, predictors of outcome diVered between the sexes.
Factors associated with a good outcome for women were being in paid employ-
ment, having a co-therapist (relative, friend or appropriate other), and low initial
severity ratings of global phobia, impairment of work and home activity, and
compulsion checklist. For men, however, the only factor to approach statistical
signiWcance was living alone, which was associated with less improvement.
Keijsers et al. (1994) also reported greater initial severity of obsessional com-
plaints to be associated with poorer outcome but also reported that poorer
motivation, dissatisfaction with the therapeutic relationship and longer duration
of complaints predicted poorer immediate (posttreatment) outcome for ‘‘obses-
sive fear’’, while higher pretreatment levels of depression predicted poorer out-
come of compulsive behavior.
In summary, the most consistent outcome predictor appears to be symptom
severity, with the more severely symptomatic patients tending to have a poorer
outcome. The role of depression as a predictor of outcome remains unresolved,
with some studies reporting less improvement in depressed patients (e.g., Foa et
al., 1983b; Cottraux et al., 1993) while others report no association (e.g., Basoglu
et al., 1988; Hoogduin and Diuvenvoorden, 1988; Castle et al., 1994). Overvalued
ideation and Wxity of beliefs have also been delineated as possible predictors of
outcome.
Pharmacotherapy
Although a wide variety of medications have been utilized in the treatment of
OCD, there is little doubt as to the consistent eYcacy of serotonin reuptake
inhibitors (SSRIs), of which clomipramine is the most widely researched. Placebo
controlled trials have in general attested to its eYcacy and comparison to other
antidepressants have also demonstrated its superiority in decreasing obsessional
symptoms ( Greist, 1990a; Jenike, 1990a). Average symptom reduction, however,
is only moderate (Zak et al., 1988; De Veaugh-Geiss et al., 1989; Greist, 1990a).
Although not as extensively researched as clomipramine, other more potent
SSRI appear to be of equal beneWt in the treatment of OCD, and in general have
the added beneWt of a lower side-eVect proWle. The eYcacy of Xuoxetine at three
Wxed doses (20, 40, and 60 mg) was examined in a multicenter trial by Tollefson et
351 Obsessive–compulsive disorder: Treatment
al. (1994), who reported symptom reduction of 32.1%, 32.4%, and 35.1%, re-
spectively, as compared with 8.5% for placebo after a 13 week trial. Pigott et al.
(1990) in a randomized double-blind crossover design compared clomipramine
to Xuoxetine and reported similar therapeutic eVects. Fluvoxamine has also been
shown to be superior to placebo in the treatment of OCD in a number of
double-blind studies (e.g., Goodman et al., 1990; Perse et al., 1987; Jenike et al.,
1990b) and in a multicenter trial (Goodman et al., 1992). Fluvoxamine was also
compared with desipramine in a study by Goodman et al. (1990) and was found to
be superior in reducing the severity of OC symptoms. A direct comparison of
Xuvoxamine with clomipramine by Lorin et al. (1996) reported similar levels of
symptom reduction in a similar proportion of patients in both groups. Sertraline,
another SSRI, has also had mixed results initially, with one placebo controlled
study Wnding no eVect in a small number of patients (Jenike et al., 1990a). Other
studies have attested to the eYcacy of sertraline in OCD. Chouinard et al. (1990)
reported that sertraline resulted in signiWcant decreases in OCD symptoms on
three of the four measures used. Greist et al. (1995) reporting on a large multicen-
ter placebo controlled trial of Wxed-dose sertraline (50, 100, 200 mg) found that
doses of 50 mg and 200 mg were signiWcantly more eVective than placebo in
reducing obsessional symptoms. More recently, Kronig et al. (1999) found sertra-
line at varying doses from 50 to 200 mg per day to be signiWcantly more eVective
than placebo on all measures used. Paroxetine has also been reported to be more
eVective than placebo in a multicenter trial but only at doses of 40 mg and 60 mg
per day, with 20 mg being no diVerent from placebo (Hollander et al., 2000).
There also is growing evidence concerning the eVectiveness of citalopram in the
treatment of OCD (Kopenon et al., 1997). Mundo et al. (1997) reported equal
eVectiveness of Xuvoxamine, paroxetine and citalopram in a single-blind com-
parative trial of 30 patients with OCD.
The issue of treatment-refractory OCD patients has been addressed by a
number of authors, and several pharmacological agents (e.g., lithium, buspirone,
haloperidol, olanzapine) have been suggested as possible augmenting strategies.
Few controlled trials of such substances have been reported. However, in a recent
placebo controlled trial, McDougle et al. (2000) found augmentation of SSRIs
with risperidone to be of assistance in patients who did not respond to SSRI
monotherapy. The issue of how to deWne a treatment-refractory patient was
addressed by Rasmussen and Eisen (1997), who suggested that the emerging
consensus is ‘‘someone who has failed both adequate trials of an SSRI and
exposure with response prevention’’ (ibid., p. 11), rather than monotherapy with
either exposure or SSRIs.
Perhaps the major diYculty with the use of SSRIs in the treatment of OCD is the
high relapse rate with medication discontinuation. For example, Pato et al. (1988)
352 Treatment of Anxiety Disorders
Conclusions
The eVective cognitive behavioral treatment of OCD requires intensive interven-
tion on the part of the therapist and strong motivation on the part of the patient.
The decision as to whether to combine pharmacological and behavioral treatment
should be made in consultation with the patient. In the presence of a severe major
depressive illness, the decision is clear: a combined approach may be the most
eVective. If the patient is drug naı̈ve, hesitant about taking medication, or cannot
tolerate the side-eVects, then behavior therapy alone may well be the treatment of
choice. Given the high relapse rate associated with medication discontinuation,
pharmacotherapy in the absence of behavioral therapy does not constitute an
adequate or appropriate treatment of OCD.
18
Obsessive–compulsive disorder
Clinician Guide
Common questions
Patients referred for treatment will often ask a number of questions about their
condition and the proposed treatment. As much as possible, individuals are
encouraged to ask questions, and answers are given on the basis of available
knowledge regarding OCD. Common questions include those relating to the cause
of their condition. Apart from discussing the research Wndings to date, it is
pointed out that there is no one cause of OCD: it is not as simple as a ‘‘biochemical
imbalance’’, nor genes, nor individual psychological factors, nor environment but
a complex condition due to a combination of a variety of complex factors.
Educating the patient about OCD, its many causal factors and its treatment is an
important step in bringing about a cognitive shift from the helpless attitude of
many suVerers to having a good understanding of the condition, its maintaining
factors, and what patients can do to assist in their own treatment.
354
355 Obsessive–compulsive disorder: Clinician Guide
Assessment
Perhaps the most important aspect of the cognitive behavioral treatment of OCD
is the detailed assessment of the problem behaviors. Because of inadequate
assessment, many diYculties commonly arise in the treatment of the condition.
While standardized assessment forms may yield information and clues as to
symptoms that may have been missed on initial interview, the assessment process
is interactive. The therapist tests hypotheses with the patient not only on the basis
of information obtained in the initial stages of treatment but more importantly on
information gained throughout the treatment process. In other words, assessment
is an ongoing activity. It is rarely the case that suVerers will be able to elucidate all
of the necessary information in the Wrst one or two sessions. In addition, a
proportion of patients will be reticent in giving full details of their symptoms
because of embarrassment. In the Wrst instance, it is a matter of modifying the
program as more information is made available. Where embarrassment plays a
role, it is important to reassure the patient that, as an experienced therapist, you
have seen similar symptoms in OCD suVerers. It may be worthwhile oVering
examples of obsessional symptoms in order to allay any anxieties that the patient
may have about being negatively evaluated by the therapist or others because of
their symptoms.
Assessment should focus on the presence or absence of internal cues (e.g.,
images, thoughts, urges), and external cues (contaminants, situations, etc.) that
elicit the urge to ritualize. Rituals, particularly covert rituals or cognitive neutraliz-
ing, need to be carefully assessed. Reasons for ritualizing should also be noted, as
they may have implications for the exposure program and provide clues in
relation to avoidance and therefore to further exposure tasks. Avoidance of
situations by OCD suVerers is often considerable, relating to situations, objects,
and so forth, that the suVerer knows will provoke discomfort and the urge to
ritualize. In addition to discussing avoided situations with the suVerer, it is often
worthwhile discussing the patient’s obsessional symptoms with a signiWcant other,
who can provide further information relating to triggers, rituals, and avoidance.
Assessment of individuals presenting with obsessional thoughts and no overt
rituals requires close attention. It is essential that the intrusive thought be identi-
Wed correctly in order for exposure to be eVective. Similarly, it is necessary to
identify cognitive neutralizing of the obsessional thought. While suVerers are
often able to verbalize the intrusive cognition, it is sometimes diYcult to identify
the covert neutralization of the thought, as it may be a repetition of the thought
itself – or perhaps even an image of the actions involved in the thought – both of
which may be anxiety-provoking and therefore diYcult to distinguish from the
original anxiety-arousing intrusion. For example, one suVerer presented with
356 Treatment of Anxiety Disorders
intrusive thoughts and images of harming a loved one while asleep. The intrusions
appeared to take the form of verbal thoughts – ‘‘I will kill him’’ – as well as images
of the actions being carried out. Detailed questioning of the suVerer indicated that
the ‘‘intrusive’’ image, while anxiety provoking, was in response to the thought
and was voluntarily produced because it served to reassure the suVerer that she
could never perform such a terrible act. It may be helpful to deWne the neutralizing
behavior for the suVerer in terms of any cognitive behavior in which they
voluntarily engage as a response to their intrusive thought. Recording of the
thought on a loop cassette tape and playing the same back to the patient may also
yield important information as to neutralizing cognitions.
Cognitive assessment is equally important when dealing with individuals who
present with obsessional thoughts and no overt rituals or those who present with
thoughts of harm to others through some act of their own or through their own
negligence. Such assessment is focused on the appraisals and beliefs the individuals
have of their thought (‘‘I may act on the thought’’), as well as the occurrence of the
thought (‘‘having this thought means that I want it to happen’’, or ‘‘having the
thought means I’m an evil person’’, etc.). Freeston et al. (1996b) proposed Wve
groupings of beliefs and appraisals commonly present among OCD patients: (1)
overestimating the importance of the thought through thought–action fusion,
magical thinking and distorted Cartesian thinking; (2) exaggerating responsibility
for events that are beyond the person’s control and the consequences of being
responsible for harm; (3) a need to seek absolute certainty or completeness or
complete control over thoughts and actions; (4) overestimating the probability
and consequences of negative events; and (5) beliefs that the anxiety caused by the
thoughts is dangerous or unacceptable (Freeston et al., 1996b). As patients may
have one or a series of beliefs regarding the intrusions as well as diVering
dysfunctional assumptions of the same thought, the individual examples of
cognitive styles are by no means mutually exclusive. The authors give excellent
descriptions of speciWc interventions that may be utilized to challenge the beliefs
and assumptions associated with the thoughts and the reader is encouraged to
obtain the journal article.
Treatment process
It is essential that the patient has a good grasp of the treatment rationale. Taking
time to explain graded exposure, response prevention, and habituation – using
examples from daily life – will help to ensure that the suVerer has a good
understanding of the procedures without engendering further anxiety and pre-
cipitating a Xight from the clinician’s oYce. A typical example one might give to
patients is that of learning to drive a motor vehicle. The majority of people upon
357 Obsessive–compulsive disorder: Clinician Guide
entering a car for their Wrst driving lesson will feel quite anxious and uncomfort-
able, trying to remember all of the basic things to look out for as well as control the
motor vehicle. However, with repeated exposure, the anxiety gradually subsides to
the point that, after performing the driving behavior innumerable times, the
driver feels no anxiety and doesn’t even have to think about their routine behavior.
Clinical examples of exposure and habituation from previously treated cases will
also serve to reinforce the principles for the patient.
When discussing the treatment rationale with the patient, a graded approach
should be emphasized. Often, patients envisage being asked to do the impossible:
not ritualizing at all when exposed to the most ‘‘noxious’’ stimulus. Unless
clariWed and explained to the patient, such a misconception will place the clinician
in the same position as many ‘‘helpful’’ friends and relatives who have suggested to
the suVerer that, if he or she does not like being the way they are, they should just
put a stop to their behavior. By explaining the fact that exposure will be graded,
with the patient and therapist working through a graded hierarchy of stimuli and
the patient being asked to refrain from engaging in rituals to a gradually increasing
number of stimuli, the task does not seem as insurmountable as being told that
total exposure will take place and absolutely no rituals are allowed. As part of the
rationale, it is imperative that the suVerer is made aware that they will be taking a
very active part in their own treatment and should in fact take on the role of
co-therapist in the treatment program.
stimulus object) or they may attempt to cope by delaying their rituals (e.g., ‘‘I will
wash my hands later today and touch as little as I can in the meantime’’). While
such techniques may lead to a reduction in distress during the session, habituation
or decreases in discomfort between sessions will not occur. Again, in such
circumstances, it is important to remind the suVerer of the treatment rationale
and reinforce the notion that there is little to gain by utilizing such methods. If,
however, such methods are being utilized by the patient because the distress
associated with the stimulus is greater than expected, then it is likely that a more
detailed behavioral assessment is required and a more gentle rate of progress
implemented.
Where the suVerer experiences obsessional thoughts without overt rituals,
program design and implementation follow lines similar to the treatment of
suVerers with behavioral rituals. Intrusive thoughts are identiWed, as are the covert
neutralizing responses to such thoughts. Obsessions are rated hierarchically and
the patient is requested to refrain from engaging in covert neutralization. Expo-
sure consists of having the patient record their least anxiety-engendering or
distressing thought on a loop cassette tape. On replay, anxiety or discomfort
ratings are noted. Replaying of the taped thoughts in the early stages of treatment
may also assist in the identiWcation of any covert neutralizing responses. Patients
are requested to refrain from any neutralizing behaviors and are required to listen
to the tape and allow the recorded thoughts to guide their thinking. For example, a
suVerer with intrusive blasphemous thoughts who prays in response to those
thoughts is asked to listen to the taped blasphemous thoughts and not engage in
prayers. As with compulsive ritualizers, it is often useful to allow the suVerer to
experience anxiety or discomfort reduction within the initial treatment sessions
and set similar tasks as homework assignments. As habituation to each thought
takes place, variations in procedures such as listening to the tape in previously
avoided situations or varying the tone or loudness of the recorded thoughts
should be implemented. In the case of the individual described above, for
example, this may involve having the patient listen to the recorded blasphemous
thoughts while sitting near or in a church, and so forth.
An alternative method to loop tape exposure, which has led to equal success at
our unit, follows the same principles without the taped exposure and relies on
spontaneous thought occurrence and voluntary cessation of cognitive neutraliz-
ing. Avoidance of situations that may trigger the intrusive thought is often
considerable. For example, intrusive sexual thoughts will often result in the person
avoiding to look at, or be near, triggering stimuli such as same-sex individuals,
children or animals; intrusive blasphemous thoughts will often result in avoidance
of anything of a religious nature; and intrusive thoughts about harm will often
result in avoidance of objects with which to cause harm, especially in the presence
359 Obsessive–compulsive disorder: Clinician Guide
of the loved ones or persons involved in such thoughts. Individuals are given a
thorough rationale for the maintenance of the intrusion and the associated worry.
This is followed by identiWcation of all intrusive thoughts as well as the associated
neutralizing or avoidance. Dysfunctional beliefs are challenged, and the patient is
encouraged to passively accept the thought whenever it occurs, live with the
anxiety until it fades, while exposure to previously avoided situations is conducted
in a hierarchical fashion. To some, such exposure may be viewed as behavioral
experiments aimed at testing the patient’s beliefs and assumptions rather than
exposure per se, but what’s in a name?
Whether the clinician decides on a loop tape or relies on spontaneous exposure,
the challenging of dysfunctional assumptions in obsessional ruminators and those
who fear causing harm to others by their thoughts is an essential step in ensuring
the success of exposure treatment. For example, a 23-year-old female was referred
to our unit after having failed in treatment at another clinic. The primary concerns
were intrusive thoughts of molesting children. There was considerable avoidance
of children and places where children could be encountered (e.g., friends’ homes,
shopping centers, schools, parks, etc.). SpeciWc neutralizing strategies included
trying to push the thoughts out of her head, arguing with the thoughts in order to
reassure herself that her sexual preference was for adult heterosexual relationships,
telling herself that she would never act on the thoughts and that she would commit
suicide if there was ever any chance of acting on the thoughts. Although she had
undergone a well-designed treatment program that included exposure to the
thought as well as previously avoided situations and prevention of the neutralizing
responses, few gains were made. On assessment, it became apparent that treatment
gains were minimized by the fact that her beliefs about the intrusive thoughts had
not been addressed. Her underlying assumptions regarding the thoughts included
the notion that only very disturbed individuals would have such thoughts, that she
did not have OCD, and that perhaps she was a sexual deviate after all. Challenging
these assumptions at a number of levels included education about the fact that
intrusive thoughts are common human phenomena and that what diVerentiates
OCD from normal intrusive thoughts is the meaning and importance individuals
attach to intrusive thoughts. The notion that having an inappropriate thought
directly reXects on the individual’s nature was challenged by having her examine
other inappropriate thoughts to which no meaning was attached, as well as having
her discuss with signiWcant others (family who were aware of her concerns) the
nature of inappropriate thoughts that they had experienced. Such techniques,
aimed at changing her appraisal of the intrusive thoughts, led to signiWcant
improvement with exposure-based treatment.
Unlike overt rituals, cognitive neutralizing is considerably more diYcult to
identify and control. Consequently, the clinician is much more reliant on the
360 Treatment of Anxiety Disorders
Homework assignments
Homework assignments in which the patient is required to perform the exposure
tasks conducted during the treatment session are an integral part of treatment.
Little is to be gained if the patient engages only in exposure and response
prevention in the clinic setting. In order to ensure habituation to the anxiety-
evoking stimulus, exposure and self-directed response prevention need to be
conducted repeatedly and such tasks should be included as part of the homework
assignments. Diary notes of each assignment should be kept by the suVerer and
ratings of discomfort and urge to ritualize (overtly or covertly) included in the
diary. Involvement of signiWcant others, such as partners or family members, as
co-therapists will assist in ensuring that the required tasks are carried out as
instructed. However, at all times it is emphasized that the suVerer himself or
herself is responsible for the implementation of the program.
Follow-up
It is essential that OCD patients be seen on a regular basis for at least 12 months
following intensive treatment. Invariably, suVerers will experience short-term
diYculties in maintaining their gains, particularly as novel situations or thoughts
provoke the urge to ritualize. The clinician needs to encourage the adoption of the
principles of exposure and response prevention for each of the novel as well as the
familiar stimuli. Although total cures are relatively rare, the goal of controlling the
361 Obsessive–compulsive disorder: Clinician Guide
disorder rather than the disorder controlling the suVerer is both realistic and
achievable in the majority of cases.
Problem solving
When using any cognitive behavioral procedure, it is important for the suVerer to
be aware that they will be taught skills with which to deal with their own disorder.
That is to say, they will not be ‘‘treated’’ in the traditional sense of the word and be
passive recipients of the techniques that will alleviate their distress. This is much
more the case in the treatment of obsessional disorders, particularly as ritual
prevention must be self-directed and voluntary. As part of the treatment rationale,
the patient should be made aware of the expectation that they will take an active
part in their own treatment, being primarily responsible for the proper implemen-
tation of the techniques and therefore directly responsible for their own treatment
gains. The role of the therapist is described as that of an instructor or teacher
whose principal task includes encouraging the suVerer to face the various anxiety-
provoking situations in a planned and systematic fashion. At all stages, the patient
is encouraged to assist in their program design and he or she should be encouraged
to take on the role of co-therapist in the assessment phase, for without total
cooperation in the assessment of obsessional symptoms, program outcome will be
less than satisfactory.
Reassurance
Invariably, OCD suVerers will request reassurance from their treating clinician.
While this reassurance is conWned to possible outcome of treatment or the
rationale for exposure, the clinician is on safe ground in reassuring the patient
about the techniques being used. However, reassurance relating to the possibilities
of danger or harm must be diligently avoided by the therapist. If one considers that
in the majority of cases, the OCD suVerer engages in repetitive ritualized overt or
covert behaviors in order to minimize the risk of harm to themselves or others,
reassurance of the lack of danger by the therapist will serve only to replace one
anxiety-reducing behavior (washing, checking, praying, etc.) with another, i.e.,
checking with or gaining reassurance from the therapist. Once given, the patient
will constantly seek the clinician’s reassurance that the behavior engaged in poses
no threat to the suVerer or signiWcant others. Needless to say, the exposure
program will then be confronted with major diYculties, as it becomes the
clinician’s permission that allows the behavior to be performed rather than the
patient taking the risk in performing the behavior. Another pitfall in treating some
patients is that the clinician inadvertently reassures the patient by setting the
exposure task. Responsibility for any disastrous consequence is transferred from
362 Treatment of Anxiety Disorders
the patient to the clinician, as the task was conducted only at the clinician’s
request. In such cases, it is always helpful to have the patient select the exposure
task without input from the clinician. Similarly, some individuals with intrusive
unpleasant thoughts or images will, in each treatment session, insist on giving the
clinician a detailed account of each occurrence of the intrusive thought and image,
the content of the thoughts/images and every situation in which they occurred.
This need to ‘‘confess all’’ is a more subtle way of gaining reassurance, for as the
clinician sits impassively listening, the patient knows there is nothing to be
concerned about because the clinician has not reacted in shock or horror by falling
out of the chair. In such cases, it is better for the session to focus on more general
issues such as frequency of the thoughts, intensity of anxiety, duration, neutraliz-
ing, etc. rather than speciWc individual instances of intrusive thought occurrences.
In general, reassurance-seeking behavior should be dealt with by explaining to the
patient that assurances regarding the lack of possible harm from any action is an
impossibility, and that, in order to eVectively overcome OCD, the patient must
learn to live with the doubt.
19
Obsessive–compulsive disorder
Patient Treatment Manual*
This Manual is both a guide to treatment and a workbook for persons who suVer
from obsessive–compulsive disorder. During treatment, it is a workbook in which
individuals can record their own experience of their disorder, together with the
additional advice for their particular case given by their clinician. After treatment
has concluded, this Manual will serve as a self-help resource enabling those who
have recovered, but who encounter further stressors or diYculties, to read the
appropriate section and, by putting the content into action, stay well.
Contents
Section 1 364
1 The nature of obsessive–compulsive disorder 364
1.1 Symptoms of obsessive–compulsive disorder 365
Section 2 366
2 The causes and treatment of obsessive–compulsive disorder 366
2.1 The biochemical theory 367
2.2 The genetic theory 367
2.3 Learning theory 367
2.4 Cognitive theory 368
2.5 Psychoanalytical theory 368
2.6 The treatment of obsessive–compulsive disorder 368
2.6.1 Medication 369
2.6.2 Behavior Therapy 369
Section 3 371
3 Exposure and response prevention 371
3.1 Obsessional thoughts 372
3.2 Basic rules for success 373
*Gavin Andrews, Mark Creamer, Rocco Crino, Caroline Hunt, Lisa Lampe and Andrew Page The Treatment
of Anxiety Disorders second edition © 2002 Cambridge University Press. All rights reserved.
364 Treatment of Anxiety Disorders
Section 4 375
4 The treatment program 375
4.1 Program design 376
4.1.1 Avoidance 379
4.2 Exposure tasks 380
Section 5 382
5 Recommended reading 382
5.1 Recommended paperbacks 382
SE C T I ON 1
1 The nature of obsessive–compulsive disorder
Obsessive–compulsive disorder (OCD) is an anxiety disorder that, until quite
recently, was regarded as a rare condition. Recent studies have shown that OCD is
considerably more common than was previously thought and as many as 2 in
every 100 people may suVer from the condition.
OCD is characterized by persistent, intrusive, unwanted thoughts that the
suVerer is unable to control. Such thoughts are often very distressing and result in
discomfort. Many OCD suVerers also engage in rituals or compulsions that are
persistent needs or urges to perform certain behaviors in order to reduce their
anxiety or discomfort or to prevent some dreaded event from occurring. More
often than not, the rituals are associated with an obsessional thought. For example,
washing in order to avoid contamination follows thoughts about possible con-
tamination. For some, there is no apparent connection between the intrusive
thought and the behavior, e.g., not stepping on cracks in the sidewalk in order to
avoid harm befalling one’s family. Others have no compulsive behaviors and suVer
from obsessional thoughts alone, while still others do not experience obsessions
but have compulsive rituals alone.
The one common element to the various symptoms in OCD is anxiety or
discomfort. For those suVering both obsessional thoughts and compulsive rituals,
it is the anxiety or discomfort associated with the thought that drives the ritual. In
other words, the ritual is performed to reduce the anxiety produced by the
thought. For those suVering from obsessional thoughts alone, anxiety is often
associated with the thought, and mental rituals, distraction, or avoidance may be
used to lessen the discomfort and ensure that the fearful event does not occur. It’s
much the same for those with compulsive rituals alone in that the behavior is
performed in order to lessen the urge to ritualize. The role of anxiety is important
in OCD and will be discussed in much greater detail in subsequent sections.
365 Obsessive–compulsive disorder: Patient Treatment Manual
Most OCD suVerers can see the uselessness and absurdity of their actions but
still feel compelled to perform their various rituals. They know that their hands are
not dirty or contaminated and they know that their house will not burn down if
they leave the electric kettle switched on at the wall. Because they are aware of how
irrational their behavior is, many suVerers are ashamed of their actions and go to
great lengths to hide their symptoms from family, friends, and, unfortunately,
even their doctors. It is extremely important that your therapist is aware of all of
your symptoms no matter how embarrassing or shameful they may be, as this is
the only way that a suitable treatment program can be designed for you. Rest
assured that a therapist experienced in the treatment of OCD will have heard of
symptoms worse than yours many times over.
type of symptom so that individuals may engage in more than one type of ritual or
have more than one type of obsessional thought. Another point to note is that
symptoms change over time and someone who is predominately a washer may,
over time, develop checking rituals that eventually supersede the original com-
plaint. In addition to changes in symptoms, the course of the disorder may also
Xuctuate over time, with periods of worsening and periods of improvement. Other
suVerers may Wnd that their symptoms remain static, while yet others may Wnd a
gradual worsening of symptoms since the onset of the disorder.
For many suVerers of OCD, these symptoms take up a great deal of time, often
resulting in their being late for appointments and work and causing considerable
disruption and interference with their lives. Apart from disrupting their own lives,
it also frequently interferes with the lives of family members, as the typical suVerer
often asks the other members to do things a certain way or not to engage in certain
behaviors, as this may prompt the suVerer to engage in rituals. Thus the symptoms
are controlling, frustrating, and irritating not only to the patients, but also to their
families, friends, and workmates.
Avoidance of certain situations or objects that may trigger discomfort and
rituals is also quite common among OCD suVerers. It seems logical to avoid
contact with contaminants if you are a person who washes compulsively, or to
avoid going out of the house if you must check all the electrical equipment, the
doors, and windows. While this seems like a reasonable way of coping, it actually
adds to the problem, as the typical suVerer avoids more and more situations and
gradually the problem comes to rule their life. Moreover, avoidance does little to
deal with the problem as it serves only to reinforce the idea that such situations are
dangerous. Because the situation or object is constantly avoided, there is no
opportunity for the individual to learn that there is no danger.
SE C T I ON 2
2 The causes and treatment of obsessive–compulsive disorder
At the time of writing, no one is certain of the causes of OCD. Though there are a
number of theories that attempt to explain the development of the condition, in
general there is little evidence to support any one of them exclusively. In fact, it
may be best to consider OCD as a complex problem with complex causative
factors. It is most likely that a combination of psychological, biological, environ-
mental and other factors result in the development of the disorder. We do know
that for some the onset is during childhood, while for others the onset may be
during adolescence or early adulthood. We also know that in some cases the onset
367 Obsessive–compulsive disorder: Patient Treatment Manual
is sudden, while others have a slow, insidious onset. Some of the theories that have
been proposed to explain the development of OCD follow and are for information
purposes only.
and, as a result, this issue will be dealt with in much greater detail in subsequent
sections.
ior therapy too diYcult initially may beneWt from a course of medication so that
eVective behavior therapy can be undertaken.
2.6.1 Medication
The medications that have been found to be particularly helpful in the treatment
of OCD come from the antidepressant family of drugs and include clomipramine,
Xuoxetine, Xuvoxamine, and sertraline. They have speciWc eVects on serotonin
levels in the brain. Serotonin is the biochemical substance that some researchers
believe is involved in OCD. In general, these medications have been shown to be
eVective for some OCD suVerers and assist them in bringing their symptoms
under control. If one of these medications is prescribed for you, you should be
made aware of possible side-eVects and report their occurrence to your therapist.
It is important to remember that these medications are not a cure for OCD. In
addition, research indicates that ceasing the medication in the short term generally
results in a return of symptoms. It could be that suVerers need to remain on the
medication for long periods of time or that behavior therapy should be used in
conjunction with the drug.
Engaging in the ritual brings about an immediate and dramatic decrease in both
these measures.
Urge/ 4
discomfort
Though the decrease may be short lived, the individual very quickly learns that
the discomfort may be reduced again by performing the ritual. The more anxious
the individual feels, the more ritualizing they engage in. This is further worsened
by their inability to concentrate on what they are doing to the extent that they are
unsure that the ritual was conducted properly. This adds to their anxiety, which
they try to bring under control by ritualizing further. For example, an individual
who checks electrical equipment, doors, and windows prior to leaving home learns
very quickly that checking alleviates the discomfort associated with the thought
that the house may burn down or be broken into. The individual may have to
perform the checking rituals a number of times in order to gain some relief. If he
or she is under pressure from other sources and is preoccupied or distracted by
these other worries, then they will have to engage in the rituals many more times
because they may not have been done ‘‘correctly’’ the Wrst few times. Having seen
how compulsive rituals are maintained, the important question is what can be
done to break the vicious cycle between the discomfort-producing thought and
the anxiety-reducing rituals. Again, research into the condition provides the
answer.
371 Obsessive–compulsive disorder: Patient Treatment Manual
SE CT I O N 3
3 Exposure and response prevention
Investigators looking at the phenomenology of OCD examined what happened
when suVerers were exposed to stimuli that triggered rituals and were asked not to
engage in their rituals. Initially, there was a signiWcant rise in anxiety, discomfort,
and urge to ritualize. Rather than continue to get worse, however, this rise
remained quite steady and then gradually decreased so that by the end of the
session, the level of discomfort had almost returned to normal. When this process
was repeated again and again, the surprising Wnding was that the initial discomfort
and anxiety was less with each exposure and the time taken to return to normal
was shortened so that eventually exposure to the stimulus would result in a
‘‘hiccup’’ in anxiety that would then quickly settle. The initial Wndings of this
research are demonstrated in the following diagram.
Urge/
discomfort
confronted with triggers for the rituals, but the most important change is that the
individual is now in a position to control the problem rather than be controlled by
it.
When suVerers are made aware of this form of treatment, the initial reaction is
either one of disbelief that such simple methods may work or, alternatively, that it
appears extremely diYcult. First, this form of treatment is not as simple as it
seems. The approach must be structured, planned, and systematic in order to have
maximum beneWt. The individual needs to be motivated and consistent in his or
her eVorts to overcome the problem and faithfully follow all homework and clinic
assignments. Approaching the problem in a haphazard manner will invariably
result in a less than optimal outcome, with suVerers feeling disappointed, frus-
trated, and hopeless. A consistent and planned approach ensures that the problem
is dealt with in a systematic manner. Any diYculties encountered can be quickly
dealt with by the patient with the assistance of the therapist. Second, for those who
see this approach as too diYcult, the fact that the treatment program is planned by
you in conjunction with the therapist ensures that the pace is at a level you are
capable of mastering and the various steps can be graded to maximize your
chances of success.
problems have been with you for a considerable period of time and are probably
well ingrained in your daily routine. Overcoming these diYculties will most
certainly take time and you should allow yourself as much time as it takes to get
yourself better. You don’t need to add to your diYculties by being impatient.
Second, progress is not in a straight line but tends to be Xuctuating so that having
occasional bad days is the rule rather than the exception. The two graphs below are
to demonstrate the diVerence between what people expect to happen and what
actually happens.
EXPECTATION ACTUAL
IMPROVEMENT
IMPROVEMENT
Time Time
Most people expect the response to treatment to be linear, i.e. they start
treatment and expect to get better and better. What actually happens, however, is
that there are Xuctuations from day to day, with some days being worse or better
than others. When the Xuctuations in the right-hand graph above are evened out
(dotted line), it becomes obvious that the individual is improving, even though at
times it may not feel as though they are getting better. They may even feel as
though they are slipping back. It is important to reassure yourself that having a
bad day does not mean that the situation is hopeless or that you are back to square
one. In fact, the only individuals sure to return to square one are those who lose
their motivation and no longer persist with the program.
Another basic requirement for a positive outcome is, for want of a better word,
honesty. You need to be honest with yourself and your therapist in terms of your
fears, avoidance, rituals, and thoughts. At times, individuals who know they have
to be exposed to situations that they have avoided for long periods of time will
avoid telling the therapist about similar situations or will not complete homework
assignments. This does nothing to help the suVerer overcome the problem in any
way. Telling yourself that the problem will be dealt with later is just another form
375 Obsessive–compulsive disorder: Patient Treatment Manual
As you progress through the program, you will gradually gain conWdence in dealing with the OCD
problems. In order to gain this sense of mastery over the problem, it is essential that you do not use
anxiety-reducing drugs, illegal drugs, or alcohol while participating in the program, as use of such
substances results in your attributing positive changes to the drugs rather than to yourself.
SE CT I O N 4
4 The treatment program
In previous sections an outline of the rationale and principles of treatment have
been discussed. This section will review some of the important points and discuss
the design of your treatment program. As mentioned above, treatment consists of
repeatedly exposing the individual for prolonged periods (45 minutes to 2 hours)
to circumstances that produce discomfort. In the initial sessions, such exposure
will be under the supervision of your therapist, who will be with you throughout
the task. Sessions may be conducted at the clinic, at your home, or in other settings
where the rituals are a problem. The exposure is graded so that moderately
disturbing situations are eVectively dealt with before you proceed to more diYcult
376 Treatment of Anxiety Disorders
ones. By breaking down the problems into steps and mastering each step before
moving on to the next, you will Wnd that what may seem like insurmountable
problems become manageable. The sessions are held daily, with daily homework
tasks being set during each session.
The importance of homework tasks cannot be overestimated, as it is with
performance of these tasks that most of the treatment gains will occur. It is of little
use to engage in the exposure and response prevention only while at the clinic. By
completing your homework tasks faithfully, you are ensuring that what is being
achieved at the clinic will transfer to the outside environment as well as reinforcing
what has been learned during each session. Throughout the exposure, individuals
are requested to refrain from ritualizing, regardless of the urges to do so. You
should be prepared to experience some discomfort but you can rest assured that it
will be considerably less than what you will anticipate. In fact, this is one of the
major diYculties when describing this type of treatment to patients. Most suf-
ferers fear that when exposed to a stimulus that evokes discomfort their anxiety
will continue to rise for as long as they do not perform the ritual, until it eventually
becomes unbearable. This is not the case. As described in previous sections, the
discomfort will peak and then gradually decay, and each subsequent exposure will
be less distressing and the decay will occur more rapidly.
Cue or trigger: Touching a cup or plate that someone else has used at my home
Ritual: Washing my hands with disinfectant repeatedly until they feel clean SUDs
377 Obsessive–compulsive disorder: Patient Treatment Manual
Example 2
Ritual: Telling myself I love my child and would never harm it and making SUDs
sure my partner is around when I’m near the child
Example 3
Ritual: Listen for the click of the lock and return six times to make sure the
door is Wrmly locked SUDs
Cue or trigger:
Ritual: SUDs
Cue or trigger:
Ritual: SUDs
378 Treatment of Anxiety Disorders
Cue or trigger:
Ritual: SUDs
Cue or trigger:
Ritual: SUDs
Cue or trigger:
Ritual: SUDs
Cue or trigger:
Ritual: SUDs
379 Obsessive–compulsive disorder: Patient Treatment Manual
4.1.1 Avoidance
Individuals with OCD will often avoid situations that will provoke the thoughts or
urge to ritualize. For example, someone with intrusive blasphemous thoughts may
avoid church or anything of a religious nature. Someone with a fear of being
contaminated may avoid hospitals, doctors’ surgeries, people who are ill, etc. In
this section, please list all situations, objects, etc. that you avoid because they will
cause you discomfort.
Avoidance SUD
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
380 Treatment of Anxiety Disorders
1.
2.
3.
4.
5.
381 Obsessive–compulsive disorder: Patient Treatment Manual
Exposure session
Session number: Date:
Exposure task 1:
DiYculties:
Exposure Task 2:
DiYculties:
Comments:
382 Treatment of Anxiety Disorders
SE C T I ON 5
Recommended reading
5.1 Recommended paperbacks
The following books are available from most large bookstores, many smaller ones,
and some newsstands. If in doubt, ask if the book can be ordered. We also suggest
that you use your local library to gain access to these books. When you read these
or any similar books on the management of anxiety, remember that they are best
regarded as guidelines only. Be critical in both a positive and negative sense when
reading these books, so that you get what is best for you out of them. These books
are inexpensive.
Foa E, Wilson R. (1991) Stop Obsessing! How to Overcome Your Obsessions and Compulsions.
Bantam Books.
Steketee G, White K. (1990) When Once Is Not Enough: Help for Obsessive Compulsives. Oakland,
CA: New Harbinger.
20
Clinical description
GAD is characterized by generalized and persistent symptoms of anxiety, which
are driven by worry. The worry is out of proportion to the feared event, pervasive,
and diYcult for the individual to control. The content of these worries usually
covers several domains, primarily concerns for one’s family, Wnances, work and
personal health. Individuals with this disorder usually describe themselves as
sensitive or nervous by nature, and their tendency to worry is usually longstand-
ing, or at least of several months duration. The symptoms of anxiety usually
involve motor tension (such as restlessness, trembling, or muscle tension) and
overarousal (feeling keyed up or ‘‘on edge’’, irritable, or experiencing diYculty
concentrating). Longstanding worry and anxiety may contribute to excessive
tiredness, tension headaches, epigastric disturbances, and insomnia.
CASE VIGN ET TE
Patient identification
Ms. G is a woman in her mid 30s. She is married with two children now aged 4 and 7 years.
Presenting problem
Ms. G had been troubled by worry for many years. She described herself as ‘‘a born worrier’’.
Recently she had particularly worried about her family’s health – fears that had been
exacerbated by her husband suffering a serious illness several years previously. She stated
‘‘since then every time he mentions something, however minor, feeling tired, not eating as
much as I think he should, I worry that he’s getting sick again. And I won’t stop worrying until
he’s been to see the GP and I’m convinced that it is nothing serious. And the kids too, I know
it’s ridiculous, but I’m constantly thinking about what might happen to them, even to the
point of thinking how I would cope, and having to visit them in hospital, and worse . . .’’. She
had tried to deal with these worries by seeking reassurance from family, friends and her
general practitioner. Other worries included what other people thought of her, whether she
might have said something to upset them. If her husband was late home – or even if he
wasn’t late – she worried that he had been in an accident. Some time ago she became
concerned about global warming and the possibility that she might lose her house to
flooding.
In regard to associated symptoms of anxiety, Ms. G reported feeling jumpy and nervous for
much of the time. She said ‘‘I’ve never really been able to sit still, I always have to be on the
386 Treatment of Anxiety Disorders
go’’. She also described significant muscle tension that sometimes resulted in aching and
stiffness in her neck and shoulders. During periods of increased worry she reported difficulty
getting to sleep and a loss of appetite.
Diagnosis
Prior to DSM-III-R, GAD had the status of a residual diagnostic category. Partly as
a result of this residual position, the validity of the disorder has been brought
under question. However DSM-III-R and DSM-IV no longer describe GAD as a
residual category, consistent with evidence that it can exist independently of
anxiety that is related only to the anticipation of panic or exposure to phobic or
obsessive concerns (often simply referred to as anticipatory anxiety) (Barlow et al.,
1986a). Thus a diagnosis of GAD can be made in a person with panic disorder
provided that the worry is unrelated to having a panic attack. Likewise, GAD and
social phobia can coexist if anxiety is not only related to a fear of negative
evaluation but also results from the presence of pervasive worries about day-to-
day concerns.
An additional change to DSM-IV has been the exclusion of autonomic symp-
toms from the list of required somatic symptoms. The low rate of endorsement of
autonomic symptoms by GAD patients (Marten et al., 1993), together with the
Wnding that symptoms within the motor tension and scanning and vigilance
clusters are more closely associated with independent measures of GAD than
symptoms from the autonomic activity cluster (Brown et al., 1995) support this
change. Data from a nonclinical population using the Depression, Anxiety and
Stress Scale (Lovibond and Lovibond, 1995) also supports the notion that worry is
more closely associated with tension or stress symptoms than with the autonomic
cluster of symptoms (Lovibond, 1998). Similar Wndings in a nonclinical sample,
387 Generalized anxiety disorder: Syndrome
and clinical interest, as there is considerable overlap between these two disorders.
Breslau and Davis (1985) argued that – given the scant evidence of temporal
separation of episodes in patients who meet criteria for both GAD and depression
– either the designation of residual status to GAD is justiWed or GAD may
constitute a subtype of major depressive disorder. The lack of speciWcity of
response to pharmacotherapy across GAD and major depression has also led to
speculation that GAD may be a prodromal or residual entity of a mood disorder
(Casacalenda and Boulenger, 1998). On the other hand, there are studies that
suggest that GAD and major depressive disorder can be discriminated signiWcantly
in terms of scores on the Hamilton Depression and Anxiety Rating Scales (Riskind
et al., 1987; Copp et al., 1990) or the Depression Anxiety Stress Scales (Lovibond
and Lovibond, 1995; Brown et al., 1997). A large study of female twins assessing
the role of genetic factors in the etiology of GAD has found that these genetic
factors were completely shared with those for major depressive disorder (Kendler
et al., 1992b). The Wndings suggest that, in women, the genetic vulnerability to
GAD and major depression is likely to be the same, but whether one or the other
disorder develops is likely to be a result of environmental experiences.
A more diYcult diVerential diagnosis may occur in the case of GAD and
dysthymia. In a review of the relationship between these two disorders, Riskind et
al. (1991) pointed out that both disorders are characteristically low grade, cross-
situational, and chronic. They concluded, on the basis of a systematic search of the
literature and unpublished data sets, that support for the diVerentiation between
GAD and dysthymia is equivocal.
OCD is commonly comorbid with GAD (Sanderson and Wetzler, 1991) and
hence may pose another diVerential diagnosis dilemma. While the worry shown
by GAD patients may often appear to be obsessive and ruminative in nature, it is
possible to clinically diVerentiate between the worry observed in GAD and the
obsessive thoughts observed in OCD. Turner et al. (1992a) Wrst reviewed these two
types of thinking process, and noted that while there are shared features, the two
can be diVerentiated. GAD worries are typically self-initiated (as opposed to the
unwanted and intrusive nature of obsessions), are ego-syntonic (as opposed to
ego-dystonic), and are related to an undeWned set of ongoing concerns in an
individual’s life (as opposed to being conWned to a speciWc set of concerns, such as
contamination, violence, or blasphemy). Likewise Abramowitz and Foa (1998)
argued that worry in GAD and obsession in OCD are distinct phenomena. They
found that the presence of comorbid GAD in patients with OCD was not
associated with severity of obsessions or compulsions, but rather with greater
levels of indecision, an excessive sense of responsibility, and excessive worry about
everyday concerns. Langlois et al. (2000a,b) found a number of diVerences, but
also some overlap, between worry and obsessions in a nonclinical population and
389 Generalized anxiety disorder: Syndrome
Comorbidity
Since GAD has been able to be diagnosed independently from other disorders, the
problem of high comorbidity with other anxiety and depressive disorders has
become apparent. Studies of both clinical and community samples have shown
that ‘‘pure’’ cases of GAD are rare (Sanderson and Wetzler, 1991; Brown and
Barlow, 1992; Brawman-Mintzer et al., 1993; Wittchen et al., 1994; Yonkers et al.,
1996). Using NCS data, Wittchen et al. (1994) reported comorbidity with another
mental disorder in 90.4% of the sample with a lifetime history of GAD. The most
frequent comorbid disorders were major depression, panic disorder, and (for
current comorbidity only) agoraphobia. The odds ratios reported were not
strongly aVected by the use of diagnostic hierarchy rules. Judd et al. (1988)
reported that 84% of the NSC GAD sample had a comorbid lifetime mood
disorder.
Even when other diagnoses are not met, a large proportion of GAD patients
report experiencing at least one panic attack (73%; Sanderson and Barlow, 1990)
390 Treatment of Anxiety Disorders
and experience social phobic concerns (75%; Rapee et al., 1988). Moreover, Rapee
et al. (1988) found that 79% of patients with a primary diagnosis of GAD reported
at least one moderate fear, and 61% of patients report sometimes avoiding at least
one social situation.
Maser (1998) has argued that the high rates of clinical or subclinical GAD
comorbid with other anxiety or depressive disorders may be responsible for the
broad occurrence of worry across these other disorders, and a resulting lack of
speciWcity of this feature. Using ECA data, Bienvenu et al. (1998) compared the
demographic and comorbidity proWles across Wve samples comprising patients
with a DSM-III-R diagnosis and four subthreshold groups. They found groups
were comparable in respect to the demographic and comorbidity variables
whether or not the worry criterion was met or whether the anxiety and associated
symptoms were of 1 month or 6 months duration. The only group that diVered
from the GAD diagnosis group was that which had less than the required six
associated symptoms. These authors argue against the construct validity of the
DSM-III-R diagnostic criteria for GAD.
The associated somatic symptoms also suVer from a lack of diagnostic speciWc-
ity. Brown et al. (1995) reported that, while most of a sample of patients with GAD
endorsed the three of six symptoms required in DSM-IV, a large proportion of
patients with other anxiety or mood disorders also fulWlled this criterion. How-
ever, not all patients with a principal diagnosis of another anxiety disorder meet
diagnostic criteria for GAD (Sanderson and Wetzler, 1991), suggesting that, while
symptoms of generalized anxiety are common to other anxiety disorders, these
symptoms are not synonymous with the syndrome of GAD.
But there is also evidence supporting the validity of GAD as an independent
diagnostic construct. An assessment of the genetic and environmental contribu-
tions speciWc and common to GAD and panic disorder in a cohort of male–male
twin pairs has shown a genetic liability that is speciWc to panic disorder, suggesting
that the two disorders are at least partially etiologically distinct (Scherrer et al.,
2000). Breitholtz et al. (1999) found signiWcant diVerences in the content of
thinking between GAD and panic disorder patients, hence supporting the cogni-
tive speciWcity of the two disorders. Likewise, Abramowitz and Foa (1998) have
argued that worry in GAD and obsessions in OCD are distinct phenomena. They
found that the presence of comorbid GAD in patients with OCD was not
associated with severity of obsessions or compulsions but rather with greater levels
of indecision, an excessive sense of responsibility, and excessive worry about
everyday concerns. Brown et al. (1993) found that, while many of a sample of
OCD patients endorsed worry symptoms, OCD and GAD patient groups could be
reliably distinguished diagnostically by clinical interview. Lastly, an examination
of the construct validity of diagnoses across the anxiety and depressive disorders
showed that patients with a diagnosis of GAD had a unique score proWle across a
number of self-report measures, and that proWle signiWcantly diVerentiated pa-
tients with GAD from other diagnostic groups (Zinbard and Barlow, 1996).
392 Treatment of Anxiety Disorders
worry as an attempt to avoid negative events or prepare for the worst; because the
worst rarely eventuates, the function of worry is negatively reinforced. Lastly,
worry about relatively unimportant day-to-day concerns may function as a dis-
traction from more emotionally laden topics.
Davey and Levy (1998) have investigated the process of catastrophic worry,
typically associated with a ‘‘What if . . .’’ questioning style, where worriers adopt
progressively worse and worse outcomes related to a speciWc topic. Of prime
interest was the question of what caused worriers to continue to generate cata-
strophic steps despite increases in subjective discomfort. During a ‘‘catastrophiz-
ing interview’’, chronic worriers displayed a general perseverative iterative style in
that they were more willing than nonworriers to catastrophize across a range of
topics, including those that were novel or pleasant. They also found that chronic
worriers tended to couch their catastrophizing in terms of personal inadequacies,
perhaps stemming from dysfunctional beliefs. Davey and Levy hypothesized that
core beliefs of self-doubt might make it diYcult for individuals to obtain closure
on their problems, leading to more catastrophizing steps, and hence greater
opportunity to perceive the negative consequences that might result from personal
inadequacies.
matters than the panic disorder patients. Conversely, the panic disorder patients
had more thoughts of physical catastrophe. Across worry topics, patients with
GAD worry more about remote and future events than do anxious control
patients (Dugas et al., 1998).
The level of perceived control over worries can discriminate GAD patients from
nonanxious controls: GAD patients perceive less control over their worries and
report a greater proportion of unprecipitated worries (Craske et al., 1989). Butler
and Booth (1991) have pointed out additional features that tend to characterize
the cognitions of patients with GAD. Accordingly, the worries of these patients
tend to reXect a perceived vulnerability and threat (e.g., ‘‘Something will go
wrong’’) and a perceived lack of personal coping skills (e.g., ‘I won’t be able to
manage’’).
nonanxious control group. Even when the number of events were controlled, the
GAD patients perceived minor events to be signiWcantly more stressful. This
Wnding is in keeping with Barlow’s model that predicts that an increasing vulner-
ability to anxiety guarantees that the relatively minor events or disruptions to
one’s life become the focus of worry.
Drawing from evidence of the nature of worry in GAD and data from informa-
tion-processing paradigms in anxious individuals, Rapee (1991b) has developed a
model of the maintenance of GAD from an information-processing perspective.
In summary, individuals with high levels of generalized anxiety have been shown
to allocate extensive attentional resources to the detection of threatening informa-
tion and hence have a ‘‘lower threshold’’ for threatening information (e.g.,
MacLeod et al., 1986; Dibartolo et al., 1997). There is evidence that threat-related
information may be more accessible in memory to these individuals, resulting
from selective encoding of further such information (e.g., Butler and Mathews,
1983; MacLeod and McLaughlin, 1995). Drawing on models of semantic net-
works, Rapee (1991b) proposed that once threat-related information has been
accessed, there is activation of the anxiety node, which in turn will further lower
the threshold for threat-related material. Activation of the anxiety node will also
elicit information about potential responses to the threat, and the likelihood that
these responses will successfully deal with the threat. It is argued that, if the
information is consistent with successful control of the threat, then the activation
of the anxiety node will be inhibited. Patients with generalized anxiety report that
they lack control over threat and hence are less likely to experience this inhibition.
Rapee has further argued that worry is a conscious and attention-demanding
process that, through its hypothesized activity in working memory, may have an
inhibitory eVect on anxious aVect. The resulting reduction of anxiety may thereby
reinforce the role of worry.
Dugas et al. (1998) have developed a cognitive behavioral model of GAD in
which a primary role is given to the concept of ‘‘intolerance of uncertainty’’,
contributing to the typical ‘‘What if . . .’’ questioning style of these patients. Some
preliminary support has been given to the role of this construct in worry. An
experimental study that aimed to manipulate the level of intolerance of uncertain-
ty in a nonclinical sample indicated that greater levels of intolerance of uncertainty
led to reports of increased worry (Ladouceur et al., 2000b). Second, beliefs about
worry such as ‘‘worry helps to avoid disappointment’’ or ‘‘worry protects loved
ones’’, like Borkovec et al.’s ‘‘worry to avoid negative events’’, may be negatively
reinforced by the nonoccurrence of the feared event central to the worry. Third,
GAD patients lack conWdence in their own ability to solve problems rather than
lack problem-solving skills per se (Ladouceur et al., 1998). Lastly the model
incorporates the role of cognitive avoidance, which, in keeping with Borkovec et
396 Treatment of Anxiety Disorders
Conclusions
The concept of worry and the associated somatic symptoms of motor tension and
vigilance are central features of GAD. Little is known about speciWc etiology, but
GAD is likely to share a common vulnerability with other anxiety and depressive
disorders. A number of theoretical models have been developed and the research
294 Treatment of Anxiety Disorders
explains the lack of memory. However, it is also possible that some people’s fears
have always been with them. Whichever one (or combination) of these causes
started the phobia in the Wrst place, what is now important is to identify what
keeps the phobia going in the present.
We will discuss the factors that keep a phobia going as the program continues.
However, by way of summary, it is clear that people with phobias worry more
about the objects and situations that are the focus of their fear than others do and
they worry more than is necessary. We will consider these worries and how to
challenge them in Section 5. Another factor that maintains avoidance – Xeeing
from or never even facing what you fear. The problem is that avoidance helps in
the short term, but in the long term it causes the phobia to grow. We will discuss
avoidance and how to stop it causing phobias to grow in Section 4. Finally, phobic
anxiety is excessive and unreasonable. Thus, by deWnition, the anxiety and fear is
more intense than it should be. Two factors that we know can elevate anxiety and
fear are muscle tension and overbreathing. We will consider muscle tension and
how to combat it in Section 3, but for the time being we will turn our attention to
overbreathing.
LUNGS
BLOOD HEMOGLOBIN
BODY’S CELLS
unlocked so that it can go into the body’s cells. Therefore, while it is important to
breathe in oxygen, it is just as important that there is carbon dioxide in the blood
to release the oxygen. Overbreathing makes anxiety worse, not because you
breathe in too much oxygen but because you breathe out too much carbon
dioxide.
Breathing ‘‘too much’’ has the eVect of decreasing the levels of carbon dioxide,
while breathing ‘‘too little’’ has the eVect of increasing levels of carbon dioxide.
The body works best when there is a balance between oxygen and carbon dioxide.
When you overbreathe, you end up with more oxygen than carbon dioxide in your
blood. When this imbalance happens, a number of changes occur in the body.
One of the most important changes is a narrowing of certain blood vessels. In
particular, blood going to the brain is somewhat decreased. Coupled together with
this tightening of blood vessels is the fact that the hemoglobin increases its
‘‘stickiness’’ for oxygen. Thus less blood reaches certain areas of the body. Further-
more, the oxygen carried by this blood is less likely to be released to the cells.
Paradoxically, then, while overbreathing means we are taking in more oxygen, we
are actually getting less oxygen to certain areas of our brain and body. This results
in two broad categories of sensations:
1. Some sensations are produced by the slight reduction in oxygen to certain parts
of the brain. These symptoms include:
∑ Dizziness
∑ Light-headedness
∑ Confusion
296 Treatment of Anxiety Disorders
∑ Blurred vision
∑ Feelings of unreality
2. Some symptoms are produced by the slight reduction in oxygen to certain parts
of the body. These symptoms include:
∑ Increase in heartbeat to pump more blood around
∑ Breathlessness
∑ Numbness and tingling in the extremities
∑ Cold, clammy hands
∑ StiVness in the muscles
It is important to remember that the reductions in oxygen are slight and totally
harmless.
Hyperventilation is also responsible for a number of overall eVects. The act of
overbreathing is hard, physical work. Hence, the individual may often feel hot,
Xushed, and sweaty. Because it is hard work to overbreathe, doing it for a long
time can result in tiredness and exhaustion.
People who overbreathe often tend to breathe from their chest rather than their
diaphragm. As the chest muscles are not made for breathing, they tend to become
tired and tense. Thus these people can experience symptoms of chest tightness or
even chest pains.
If overbreathing continues, a second stage of hyperventilation is reached. This
produces symptoms such as:
∑ Severe vertigo
∑ Dizziness and nausea
∑ An inability to breathe freely
∑ A crushing sensation or sharp pains in the chest
∑ Temporary paralysis of muscles in diVerent parts of the body
∑ Actual momentary loss of consciousness (‘‘blackouts’’)
∑ Rising terror that something terrible is about to happen, for example, a heart
attack, brain hemorrhage, or even death
The symptoms in the second stage of hyperventilation are produced by the
body’s automatic defence reaction to decreasing levels of carbon dioxide. This
defence reaction forcibly restricts the person’s breathing, allowing carbon dioxide
levels to return to normal.
At the risk of repetition, the most important point to be made about hyperven-
tilation is that it is not dangerous. Increased breathing is part of the Xight or Wght
response and so is part of a natural biological response aimed at protecting the
body from harm. Thus it is an automatic reaction for the brain to immediately
expect danger and for the individual to feel the urge to escape.
Hyperventilation is often not obvious to the observer, or even to the persons
experiencing it. It can be very subtle. This is especially true if the individual has
297 Specific phobias: Patient Treatment Manual
been slightly overbreathing over a long period of time. In this case, there can be a
marked drop in carbon dioxide but, because the body is able to compensate for
this drop, symptoms may not be produced. However, because carbon dioxide
levels are kept low, the body is less able to cope with further decreases and even a
slight change of breathing (e.g., a sigh, yawn, or gasp) can be enough to trigger
symptoms.
Trigger
Oh no...What if?
Breathe
faster
Fight or
Symptoms flight
Perceived
breathlessness
that when you do not use the anxiety response to Xee or Wght, you may feel
confused, unreal, and distracted. Nevertheless, you are still able to think and
function normally. You are still able to decide what action to take in response to
panic; that is, whether to stay or leave.
SE CT I O N 2
2 Control of hyperventilation
2.1 Recognizing hyperventilation
The Wrst step in preventing and controlling hyperventilation is to recognize how
and when you overbreathe.
Try monitoring your breathing rate now. Count one breath in and out as 1, the
next breath in and out as 2, and so on. It may be diYcult at Wrst, but don’t try to
change your breathing rate voluntarily. Write the answer here . As part of
treatment you will be required to monitor your breathing rate for 1 minute during
various times of the day. The form in Section 2.3 should be used for this purpose.
Now consider the following:
∑ Do you breathe too quickly? The average person only needs to take 10 to 12
300 Treatment of Anxiety Disorders
breaths per minute at rest. If your rate of breathing is greater than this, then you
must reduce it.
∑ Do you breathe too deeply? Does your chest sometimes feel overexpanded? You
should breathe from the abdomen and through the nose, consciously attempt-
ing to breathe in a smooth and light way.
∑ Do you breathe from your chest? Sit with your arms folded lightly across your
tummy and while breathing naturally observe your arms, chest, and shoulders.
While all three will move, the main movement should be in your tummy if you
are breathing correctly from your diaphragm.
∑ Do you sigh or yawn more than others? Become aware of when you sigh or yawn
and avoid taking deep breaths at these times.
∑ Do you gasp or take in a deep breath when, for example, someone mentions
what you fear? Taking one deep breath can trigger the hyperventilation cycle in
many people.
∑ Do you breathe through your mouth? You are more likely to hyperventilate if
you breathe through your mouth. Whenever you notice this, you should
consciously revert to breathing through your nose.
SE C T I ON 3
3 Relaxation training
3.1 The importance of relaxation training
Human beings have a built-in response to threat or stress known as the Xight or
Wght response. Part of this Xight or Wght response involves the activation of muscle
tension, which helps us to perform many tasks in a more alert and eYcient
manner. In normal circumstances, the muscles do not remain at a high level of
tension all the time but become tensed and relaxed according to a person’s needs.
Thus a person may show Xuctuating patterns of tension and relaxation over a
single day according to the demands of the day, but this person would not be
considered to be suVering from tension.
If you remain tense after demanding or stressful periods have passed, you
remain more alert than is necessary and this sense of alertness ends up turning into
apprehension and anxiety. Constant tension makes people oversensitive and they
respond to smaller and smaller events as though they were threatening. By
learning to relax, you can gain control over these feelings of anxiety. In this
program, you will be taught how to recognize tension, how to achieve deep
relaxation, and how to relax in everyday situations. You will need to be an active
participant, committed to daily practice for 2 months or longer.
Since some tension may be good for you, it is important to discriminate when
tension is useful and when it is unnecessary. Actually, much everyday tension is
unnecessary. Only a few muscles are involved in maintaining normal posture, e.g.,
sitting, standing, walking. Most people use more tension than is necessary to
perform these activities. Occasionally, an increase in tension is extremely beneW-
cial. For example, it is usually helpful to tense up when you are about to receive a
serve in a tennis game. Tension is unnecessary when (1) it performs no useful
alerting function, (2) it is too high for the activity involved, or (3) it remains high
after the activating situation has passed.
In order to be more in control of your anxiety, emotions, and general physical
well-being, it is important to learn to relax. To do this you need to learn to
recognize tension; learn to relax your body in a general, total sense; and learn to let
tension go in speciWc muscles.
Where do you feel tension? For the next 12 days we want you to monitor the
tension in your body. Use the following form to indicate the location of your
tension and the degree of tension. Always choose approximately the same time
each day to monitor your tension. Before your evening meal is usually a good time
for this.
In each box place the number corresponding to your level of tension
0 1 2 3
Jaw
Top of scalp
Back of neck
Shoulders
Top of back
Lower back
Chest
Abdomen
Groin
Buttocks
Thighs
Knees
Calves
Feet
Top of arms
Lower arms
Hands
304 Treatment of Anxiety Disorders
∑ Pull the legs sideways in opposite directions while keeping them locked together
at the ankles.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow out of your muscles.
∑ Choose other parts of the body to relax, e.g., the hands and arms.
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, tense hand and arm muscles by placing hands comfortably in
your lap, palm against palm, and pressing down with the top hand while trying
to lift the lower hand.
Or
∑ Place hands under the sides of chair and pull into the chair.
Or
∑ Grasp hands behind chair and try to pull them apart while simultaneously
pushing them in against the back of the chair.
Or
∑ Place hands behind the head, interlocking the Wngers, and while pushing the
head backward into hands try to pull hands apart.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow from your muscles.
If circumstances permit, continue with various muscle groups.
When standing in a public place:
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, straighten legs to tense all muscles, bending the knees back
almost as far as they will go.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow from your muscles.
Other exercises for hand and arm muscles:
∑ Take a small breath and hold it for up to 7 seconds.
∑ At the same time, cup hands together in front and try to pull them apart.
Or
∑ Cup hands together behind and try to pull them apart.
306 Treatment of Anxiety Disorders
Or
∑ Tightly grip an immovable rail or bar and let the tension Xow up the arms.
∑ After 7 seconds, breathe out and slowly say the word ‘‘relax’’ to yourself.
∑ Let all the tension go from your muscles.
∑ Close your eyes.
∑ For the next minute, each time you breathe out, say the word ‘‘relax’’ to yourself
and let all the tension Xow from your muscles.
Shoulders and neck Hunching shoulders up towards Letting shoulders drop and let
the head arms hang loose
work, go to a park. You may need to consider whether other factors are
preventing you from relaxing if you keep making the excuse that there’s no
time.
5. ‘‘I’m not getting anything out of this.’’ Unfortunately, many people expect too
much too soon from relaxation training. People often exaggerate the speed of
recovery. You cannot expect to undo years of habitual tensing in a few
relaxation sessions. Impatience is one of the symptoms of anxiety and often
indicates a need to continue with relaxation training. Give the training time to
take eVect.
6. ‘‘I haven’t got the self control.’’ You need to realize that quick, easy cures for
phobias calling for no eVort from you do not exist. The longest-lasting treat-
ment eVects occur when an individual takes responsibility for his or her
recovery. Responsibility means self-control, but self-control is diYcult if you
are not motivated.
SE C T I ON 4
4 Graded exposure
One of the hallmarks of a phobia is that the feared object or situation is avoided or
endured with considerable distress. Remember that the sorts of avoidance that we
are talking about are not only the obvious ones (e.g., running away from or not
going near what you fear) but also the more subtle ones (e.g., thinking about
something else). However, avoiding the feared object or situation is good in the
short term but its longer-term implications are not good. Whether you avoid in a
subtle or obvious way, the result is the same. Each time a person with a phobia
approaches some situation and then avoids it, in whole or in part, the fear
subsequently increases because the drop in anxiety (which follows the ‘‘escape’’) is
rewarding. Thus the avoidance is rewarded: after all, if you can avoid the fear by
avoiding, why not do so? Unfortunately, the fear really doesn’t stop, you just Wnd
more and more situations that could be ‘‘dangerous’’ and avoid them also.
What, then, is the way out? If leaving the situation strengthens the fear, what
would happen if you stayed put? Actually, if you stayed in the situation for an hour
or so, the fear would eventually go and the fear the next time you entered that
situation would be less. But few people with situational fears can actually stay in
the situation for the time required for intense fear to wear oV. So they keep
avoiding those situations.
The best remedy is to control the level of the fear using hyperventilation control,
relaxation, and straight thinking (which will be discussed in Section 5), and then
309 Specific phobias: Patient Treatment Manual
stay in a situation until you are calmer. Obviously, intense fear will take substan-
tially longer to decrease than would lower levels of anxiety. For this reason, it is
recommended that you begin with situations associated with small amounts of
anxiety and work up to situations associated with higher levels of anxiety. In this
way, you will experience anxiety, but only levels that you will be able to manage
relatively quickly. As a result, you will have more successes in managing your fear.
But how do you organize such experiences? First, you make a list of all the
situations in which you are likely to ever have your phobic fears. Next, you rank
those situations in terms of the fear associated with them. Put them into a fear
‘‘stepladder’’, beginning with the least fear provoking and moving through to the
most feared situations. Then, you work your way up the ‘‘stepladder’’, staying
again and again in a situation at each level until the situation loses its power to
evoke excessive anxiety. This procedure is discussed in more detail in the following
sections.
associated with what you fear. By way of illustration, consider a person who has a
phobia about being trapped in elevators. Exposure to the elevator will reduce the
anxiety associated with elevators but it is possible, though not very probable on
any day, that the person could get trapped in an elevator. In such a situation, the
person is faced with two diYculties. The Wrst is coping with any anxiety and fear,
which would involve breathing control, relaxation, and thinking straight. The
second problem is how to get out of the elevator. Being prepared to cope with this
eventuality will help to minimize worry about what may happen and also would
make responding more eYcient.
Think about what you fear and how you may choose to cope with any possible
diYculties. Remember, this is an exercise in planning helpful and eVective coping
strategies for possible eventualities, not a chance to worry about everything that
you fear.
Only imagine one scene at a time. You do not have to imagine all scenes in a single
session.
Practice examples
We would now like you to practice making out a similar set of steps for each of the
following goals:
1. Goal: Traveling up the tallest available building in an elevator.
Steps:
In the space below, we would like you to work out up to 10 goals of your own
choosing. These goals should vary in diYculty from those things that you hope to
achieve in the next few weeks to those that may take longer to attain.
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Now select three (at the most) of the above goals that you would like to work on
Wrst, and write these below. Set out beneath each goal the steps you intend to take
in order to achieve it.
1. Goal:
Steps:
315 Specific phobias: Patient Treatment Manual
2. Goal:
Steps:
3. Goal:
Steps:
SE CT I O N 5
5 Thinking straight
This part of the program is designed to help you to control the kinds of thoughts
that occur when you are in the presence of something you fear. These thoughts not
only accompany your anxiety reactions but can also promote them. You will
achieve this control by learning procedures that reduce the frequency, intensity,
and duration of upsetting emotional reactions by labeling the situation more
appropriately and accurately. Simply put, the procedures you will practice involve
learning how to ‘‘think straight.’’
Why did Peter become anxious and climb the stairs? The most accurate answer
is ‘‘Peter made Peter anxious’’. To make this clear, consider another version of the
same story:
Peter is on an errand from work and enters an office building. He approaches the elevator
and thinks to himself, ‘‘The office is on the 15th floor. What if the elevator broke down?
Chances are that it will not, and even if it did, I would be able to use the telephone in the
elevator to call for assistance. There is no need to worry unnecessarily.’’ He becomes less
anxious and enters the elevator.
As you can see, the situation is exactly the same in the two stories except for two
important features. First of all, Peter’s thoughts have changed. Second, Peter’s
emotional reaction has changed: in the Wrst scene he became anxious; in the
second he remained in a pleasant mood. Peter’s emotional reaction is no accident:
the elevator hadn’t made him afraid. Rather, it was the catastrophic thoughts that
Peter had that caused him to feel afraid.
Putting this all together, there was an activating event, i.e., the elevator. This was
presumed to lead to the consequence of Peter feeling afraid and later angry with
his boss. However, in the expanded story, it was apparent that Peter’s explanation
was incomplete because there were a number of intervening beliefs or thoughts
that he had. Thus, the way in which emotions are produced can be written as As,
Bs, and Cs. A is the Activating event, B is the Beliefs or thoughts that a person has
about the activating event and its meaning, while C is the emotional and behav-
ioral Consequence of having those beliefs and thoughts about the event. In other
words, the activating event does not cause the consequence on its own, but, rather,
it is the way we think about the activating event that causes the emotional
consequence.
Beliefs Beliefs
‘‘What if it is poisonous?’’ ‘‘I’ve been told it is harmless’’
‘‘Any movement means that the spider is ‘‘I’ve never been so close to one of these
about to kill me ’’ spiders before’’
Consequences Consequences
Anxious and refuse to touch it Relaxed
On edge and desiring to escape Settles down to study the spider
At its heart, the unhelpful thinking that makes the fears of people with phobias
much more intense than they need to be involves overly pessimistic ratings of the
probability and cost of danger. The greater the chance of something bad happening
(i.e., the probability) and the worse that the event will be (i.e., the cost), then the
more a person is going to worry about it. For example, a person with height
phobia may start to climb a steep ladder and think that the probability that they
will fall from the Wfth step is about 80% (i.e., the probability is high) and that they
will almost certainly die from the injuries (i.e., the cost is high). Quite reasonably,
the person will be afraid of climbing the ladder.
Sometimes a person with a phobia will be afraid because their estimates of
probability and cost are both high. Other times, the worry may arise because one
or other is excessively high. For instance, a person who is afraid of Xying may agree
that the airplane they may Xy in is less likely to crash than the car they drove to the
airport in, but they may think that the cost of a crash is greater in an airplane
because most car accidents are not fatal.
However, this isn’t the whole story. Estimates of probability and cost change as
a person gets closer to what it is that they fear. Interestingly, estimates of the
probability and cost of danger are higher when people consider confronting what
they fear than when they are actually in its presence. You may have noticed this
yourself, that you can be more worried when thinking about facing your fears than
when you actually face them.
These worries that are based upon overly high ratings of the probability and cost
of danger can encourage a person to avoid fear-provoking situations. Avoiding
situations only strengthens unhelpful and fear-producing thinking habits, as it
318 Treatment of Anxiety Disorders
prevents individuals from getting new, helpful information that the probability
and cost are not as high as you may be thinking.
Given the thoughts a person with a phobia is having, the fear is reasonable. The
problem is that the thoughts are not appropriate to the situation. They have
labeled the situation as more threatening than they need to or they have worried
that danger is more likely than it is. By changing the way a person labels or
interprets events, a person can gain more control over their feelings in a more
helpful and adaptive way.
It is important to recognize that unhelpful thinking patterns are habits, and that
habits can be changed with eVort and practice. Identifying unhelpful thoughts
associated with anxiety is the Wrst step in changing your thinking.
features: other people, limited opportunities to leave, and limited control over
their direction.
Catching an express train, I’ll panic – being on a train I probably won’t lose control;
where I couldn’t get oV if I makes be lose control and panic I’ll just feel anxious
wanted to I’ll go crazy if I can’t get out Even if I do feel anxious and
What’ll people think of me? uncomfortable that doesn’t
If I can’t get out I’ll do mean the situation is dangerous
something stupid or out of I’ve never done something out
control of control on a train, and
I won’t cope probably won’t do something
No-one else feels this way this time either
I can use my techniques to
manage my anxiety
People won’t notice me, and,
even if they do, they’ll just think
I’m a little tense
I must be loopy to feel this way I’m not loopy, just anxious, and
I’m doing something about that
320 Treatment of Anxiety Disorders
Now think of a recent situation where you felt anxious because of your phobia.
Write down a description of the situation and any anxiety-provoking thoughts
that you may have had. Then write down some more helpful thoughts that could
be applied to that situation, in order to reduce your anxiety. There is also space for
an additional individual example.
This technique should be used with the technique of graded exposure, to help
you re-enter situations that you currently avoid because of anxiety.
Helpful thinking is not simply positive thinking; it does not reject all negative
thoughts. It is looking at things in a way that is most helpful given the facts. It is
therefore important to distinguish helpful thinking from unhelpful positive, or
wishful, thinking.
Some examples of the diVerence between unhelpful, helpful, and wishful thinking are:
Unhelpful What if I can’t cope with this? I just know I’ll do something wrong.
Helpful I’m going to give this a try. I’ll do my best, and see how it goes.
able. If so, face your disappointment, but don’t make a catastrophe of it either! It is
sometimes diYcult to tell the diVerence between unhelpful, wishful, and helpful
thinking. Here are some clues to help clarify these:
Unhelpful thinking
I must . . .
I’ve got to . . .
What if . . . [something happened] . . . that would be terrible.
I couldn’t stand it if . . .
Wishful thinking
It’ll work out.
I don’t care . . .
It wouldn’t have done any good anyway.
I won’t be anxious at all.
Helpful thinking
I’d like to . . .
I’d prefer not to . . .
It’s unlikely that . . . [something] . . . will actually happen.
If things don’t go the way I want, I might be disappointed, but I’ll use my anxiety
management skills to help me cope.
Troubleshooting
1. ‘‘I don’t know what I’m thinking – I’m too scared.’’ Ask yourself ‘‘What am I
scared of? What am I scared might happen?’’. It is diYcult to identify unhelpful
fears, especially to begin with. It may help to wait until the anxiety has dropped,
then think about the situation and associated fears. Re-entering a situation may
make the fears clearer.
2. ‘‘I can’t think of alternatives.’’ After many months to years of having anxiety-
provoking thoughts, it may be diYcult to think up less threatening alternatives.
Look at all available evidence, especially evidence that contradicts your
thoughts. Ask yourself why others around you do not fear the situation, and try
to consider what they might be thinking about the situation.
3. ‘‘I’m doing it and it’s not working.’’ Use all available techniques, including
relaxation and slow breathing, to reduce your anxiety. Do not expect to be
perfect at controlling your thoughts or expect the technique to work immedi-
ately. Changing well-established patterns takes time and eVort.
4. ‘‘I still feel anxious.’’ Straight thinking is designed to provide more helpful and
appropriate responses to given situations, events or interactions. If the reality is
that a particular situation is associated with some anxiety for most people, do
not expect to use the technique to reduce all anxiety.
322 Treatment of Anxiety Disorders
5. ‘‘I don’t believe my new thoughts.’’ This may occur if you have not addressed all
of your anxiety-provoking thoughts. Go back and look at the original thought,
and try to think whether there are any related thoughts that still cause anxiety.
Also, you don’t have to believe your new thoughts immediately, as part of the
exercise is to disprove your old, unhelpful thoughts. Try to act as if your new
thoughts are true, and see what happens.
Coping statements
There are times when you may need some shortcuts to coping with feelings. Here
are a few:
1. Have a cue that makes you turn a potentially bad feeling into a coping one. For
example, if you feel butterXies in the stomach, instead of saying ‘‘Oh no, I’m
really getting anxious and upset’’ say ‘‘I know what these feelings mean. They
mean I’m getting anxious. That means: slow down, regulate my breathing and
do some isometric exercises.’’
2. Develop some personal self-statements, such as ‘‘Take this step by step’’,
‘‘Don’t jump to conclusions’’ or ‘‘This fear can’t hurt me – I can tolerate it’’.
Make these statements up yourself so that they are relevant to your life.
3. Don’t always put yourself down. Don’t say, ‘‘A baby should be able to do this’’,
‘‘I’m hopeless’’ or ‘‘I’ll never get the hang of this’’. As long as you say these sorts
of things to yourself you make them come true (but only for as long as you say
them, fortunately).
4. Praise yourself. Say things like ‘‘That was good’’ or ‘‘I felt I was having a bad day
this morning, but I still managed to get on the crowded train.’’ Remember the
most important source of praise is from inside you, because you know yourself
best and what your actions mean to you.
will be able to wait in the feared situation until the anxiety levels have decreased
signiWcantly to levels that are mild to moderate.
Over the next few weeks you will need to keep a record of your daily activities.
This will help you to remember what you did, the steps forward, and the
diYculties. To help in planning, below is a schedule that you can complete. On the
Wrst page, you can plan what you are going to do. Remember that your aim should
be to attempt a graded exposure exercise and a relaxation session every day.
Following the plan is room for you to write any comments that you may have
about the activities. On the pages after the plan are tables for you to write in the
unhelpful thoughts and level of fear that occurs during your graded exposure
exercises. You can then write down helpful thoughts so that you will be better able
to manage your fear.
DI A R Y
Day:
Time
7–8
8–9 Breathing exercise
9–10
10–11
11–12
12–1 Breathing exercise
1–2
2–3
3–4
4–5
5–6
6–7 Breathing exercise
7–8
8–9
9–10 Breathing exercise
324 Treatment of Anxiety Disorders
Exercise 2
SE CT I O N 6
6 Blood and injury phobia
6.1 Fear and fainting
Blood and injury phobias are relatively common, being found in about 4% of
people. People with blood and injury phobias can be divided into two overlapping
groups. On the one hand, there are those who experience fear when faced with
blood or injury. On the other hand, there are those who faint when faced with
blood or injury. Therefore, some people experience only fear, some only fainting,
and others both.
The skills that have been covered in the Patient Treatment Manual so far have
addressed fear and how to cope with it. These same skills are just as applicable for
dealing with blood and injury fears as for any other phobia: you must continue to
expose yourself to the distressing situations and wait for the discomfort to
decrease. What has not been covered is how to control fainting when in the
presence of blood or injury. This requires additional skills, but, before describing
these, we shall consider why the fainting occurs.
Among individuals with blood and injury phobias, fainting is extremely
common and is associated with a characteristic pattern of physiological respon-
ding. The particular pattern of responding has been called ‘‘vasovagal syncope’’.
The vasovagal syncope involves a two-stage process. In the Wrst stage, an increase
in heart rate and blood pressure occurs. This happens because there is an increase
in arousal caused by the sympathetic part of the involuntary nervous system. It is
the sympathetic branch of the involuntary nervous system that is responsible for
the Xight or Wght response and activation of it will trigger the fear reactions
described in Section 1 of the Manual. However, the involuntary nervous system
has another branch that opposes the sympathetic branch. This so-called parasym-
pathetic branch of the involuntary nervous system serves to regulate the body and
does the opposite to the sympathetic part of the nervous system. In people with a
blood and injury phobia, this compensation is very rapid and tends to be an
overcompensation. The heart slows too much and the blood pressure falls too low.
Therefore the blood (obeying gravity) will run away from the brain, causing a
deWciency in oxygen for the brain cells. If you do not lie down at this stage, the
brain will shut down and you fall unconscious. This reaction, when you think
about it, is really quite sensible because you are forced to lie down and the blood
can return to your brain cells.
As you can see from this description, the fainting is beyond your control. The
changes in heart rate and blood pressure are controlled by the autonomic part of
the nervous system, which is not under direct conscious control. The reason why
326 Treatment of Anxiety Disorders
your brain responds this way is not entirely clear but some parts of the puzzle are
available. It is now known that just under half the number of people with blood
and injury phobias have other members of their family who faint. Interestingly, it
was also found that while people who fainted were more likely to report a parent
who also did, people who reported fear of blood and injury did not report that
their parent did. This suggests that the fainting may be inherited but the fear is not.
It has also been found that people who faint tend to be more empathic; that is, they
are more able to see things from another person’s point of view. It is possibly the
ability to be able to ‘‘get inside another person’s shoes’’ that leads to people
fainting when they witness, think, or hear about injuries.
Hearing these facts about fainting may lead you to feel frustrated. ‘‘If I have
inherited it from my family and it is controlled by the nonconscious part of my
brain, what can I do?’’ The answer is that just because the fainting may be inherited
and controlled unconsciously does not mean that you cannot control it. Think for
a moment: can you increase your heart rate and blood pressure at will? If you run
quickly up a steep Xight of stairs, your heart rate and blood pressure will increase.
If you sit down and do relaxation exercises, they will decrease. Thus you can
engage in certain activities that can change these processes. Section 6.3 will
therefore go on to describe what techniques you can do to avoid fainting. These
activities are a little more practical and unobtrusive than running up stairs.
Slow breathing
People with blood and injury fears may increase their breathing rates when a
needle is placed on their arm. As you will remember, overbreathing has a number
of results one of which is feeling faint. You should monitor your breathing rate
and check to see whether it is elevated before you start your ‘‘fear stepladder’’. Also
check to see whether it is subtly increasing during exposure. In order to counter
these experiences, you will need to use your hyperventilation control exercise.
The most important point to remember is that slow breathing will be of most
use early in the physical reaction.
As the heart rate increases and the body prepares itself for danger, slow
breathing will help to restore the normal level of arousal to the body. However,
once you are aroused you need to stop the rapid decrease in heart rate and blood
pressure. For this, a diVerent skill is needed.
327 Specific phobias: Patient Treatment Manual
Applied tension
The second technique you will need to learn and master is ‘‘applied tension’’. The
aim of applied tension is to counteract the drop in blood pressure so that you have
control over your reactions. Essentially it aims to increase physical arousal, much
the same as running up a set of stairs would do, in a manner that is appropriate to
most medical settings. The steps involved require you to:
∑ Tense muscles in the arms, chest, and legs simultaneously.
∑ Continue to apply the tension until there is a feeling of warmth in the face
(usually about 10 to 20 seconds).
∑ Release the tension and relax to starting level (without becoming too relaxed
remember the technique is applied tension).
∑ Wait 20 seconds.
∑ Repeat the whole cycle a minimum of Wve times and always until the feeling of
faintness has signiWcantly decreased to manageable levels.
∑ You will need to be able to identify your particular signals of fainting, which
may include light-headedness or dizzy feelings.
This technique will need to be incorporated into your exposure tasks and
combined with relaxation and slow breathing. As you develop your skill with
breathing control and applied tension, you will become able to discriminate when
the best time is to apply the slow breathing and the applied tension. The rule of
thumb is that you begin with slow breathing to keep you relaxed as you move into
the situation but then switch (still keeping an eye on your breathing rate) as you
approach the blood or injury stimulus or when you notice the very Wrst signs of
faintness. The Wrst signs are diVerent for diVerent people, but some commonly
reported ones include dizziness, a cold sweat (across the forehead), a queasy
feeling in the stomach, or nausea.
A commonly reported problem with applied tension is headaches. This indi-
cates that you are applying too much tension. This problem is solved by increasing
the length of time between muscle tensions from 20 seconds to a time when the
headaches do not occur. Also you can try to avoid tensing muscles in the face (e.g.,
the jaw and eyebrows) that constrict and cause pressure to be applied to the head.
Another problem is diYculty in identifying the muscles to tense and how to make
them taut. Looking back at the isometric exercises for some ideas may be helpful.
Many people Wnd it useful to imagine they are a bodybuilder and think about how
a bodybuilder would tense those muscles. One other problem is that tensing
muscles can make receiving injections more painful. You will need to be able to
relax the muscle group in which the injection will be given (typically the non-
dominant arm) while maintaining tension in your other arm, torso, and legs.
328 Treatment of Anxiety Disorders
SE C T I ON 7
7 Keeping your progress going
7.1 Coping with setbacks or difficulties in making progress
Setbacks or diYculties in making progress are generally the consequence of either
poor management or poor planning of goals and steps. If you should experience
such diYculties, you must carefully analyze the way in which you carry out these
two exercises.
to factors such as outside stressors, the Xu, or school holidays. In such cases, the
setback is often viewed as devastating because it has a lot of emotional meaning for
the person, who has put considerable eVort into recovering. This eVort is not
wasted, and after the stressors pass you will Wnd it easier to get yourself out and
about again. This pattern has been demonstrated again and again. Therefore, if
you have a setback, don’t add to the problem with all the old catastrophic,
emotional, and self-destructive ideas. Keep practicing all the techniques you have
been taught and you will be able to make progress. If you feel that you have
genuinely lost the skills necessary to control anxiety and panic, then you may want
to consider retreatment. Most people do not lose the skills but need some
Wne-tuning of their skills. ‘‘Booster’’ sessions or follow-up meetings are the best
way to receive this form of assistance.
7.4 Conclusion
You now have three skills that you have been taught and now need to practice. You
need to use the various exposure tasks, working up the fear stepladder, to reduce
your fear. Relaxation will help to reduce your general levels of tension before the
exposure task, and the isometric exercises will regulate tension during exposure.
Slow breathing will help to keep control of any anxiety that you may experience
and by thinking straight you will be able to stop anxiety from spiraling out of
control.
330 Treatment of Anxiety Disorders
SE C T I ON 8
8 Recommended resources
The following books are available from most large bookstores, many smaller ones,
and some news-stands. If in doubt, ask whether the book can be ordered. We also
suggest that you use your local library to gain access to many of these books. When
you read these or any similar books on the management of anxiety, remember that
they are best regarded as guidelines only. Be critical in both a positive and negative
sense when reading these books, so that you get what is best for you out of them.
Most of these books are inexpensive.
8.1 Books
Barlow D and Rapee R. (1997) Mastering Stress: A Lifestyle Approach. Killara, NSW: Lifestyle
Press.
Burns DD. (1999) The Feeling Good Handbook, revised edition. New York: Penguin.
Copeland ME. (1992) The Depression Workbook: A Guide for Living with Depression and Manic
Depression. New York: New Harbinger.
Davis M, Eshelman ER and McKay M. (1995) The Relaxation and Stress Reduction Workbook,
fourth edition. Oakland, CA: New Harbinger.
Ellis A and Harper R. (1979) A New Guide to Rational Living. Hollywood, CA: Wilshire Book
Company.
Emery G. (2000) Overcoming Depression: A Cognitive-Behavior Protocol for the Treatment of
Depression. Oakland, CA: New Harbinger.
Greenberger D and Padesky C. (1995) Mind Over Mood. New York: Guilford.
Marks IM. (2001) Living with Fear. New York: McGraw-Hill.
McKay M and Fanning P. (1987) Self-Esteem: A Proven Program of Cognitive Techniques for
Assessing, Improving and Maintaining Your Self-Esteem. Oakland, CA: New Harbinger.
McKay M, Davis M and Fanning P. (1995) Messages: The Communication Skills Book. Oakland,
CA: New Harbinger.
McKay M, Davis D and Fanning P. (1997) Thoughts and Feelings: Taking Control of Your Moods
and Your Life. Oakland, CA: New Harbinger.
Meichenbaum D. (1983) Coping With Stress. London: Century Publishing.
Page A. (1993) Don’t Panic! Overcoming Anxiety, Phobias and Tension. Sydney: Gore Osment.
Walker CE. (1975) Learn to Relax: 13 Ways to Reduce Tension. Englewood CliVs, NJ: Prentice
Hall.
Weekes C. (1966) Self-Help For Your Nerves. Sydney: Angus and Robertson.
Weekes C. (1972) Peace From Nervous SuVering. Sydney: Angus and Robertson.
8.2 Video
Rapee R, Lampe L. (1998). Fight or Flight? Overcoming Panic and Agoraphobia. Monkey See
Productions. P.O. Box 167, Waverley, NSW 2024 Australia.
331 Specific phobias: Patient Treatment Manual
Obsessive–compulsive disorder
Syndrome
Diagnostic criteria
Obsessions are deWned as ideas, thoughts, images and impulses that enter the
subject’s mind repeatedly. They are recognized as a product of the subject’s own
mind, are perceived as intrusive and senseless, and eVorts are made to resist,
ignore or suppress such thoughts. Compulsions are repetitive or stereotyped
behaviors that are performed in response to an obsession in order to prevent the
occurrence of an unlikely event or to prevent discomfort. Resistance is often
evident, but may be minimal in longstanding cases. The diagnosis of OCD is to be
made if the individual experiences both obsessions and compulsions, obsessions
alone or compulsions alone, given that such symptoms are time consuming or
332
333 Obsessive–compulsive disorder: Syndrome
CASE VIGN ET TE
Patient identification
Mr. P is a 30 year old father of two children who presents with a 9-year history of compulsive
behavior. At the time of presentation, he was engaging in extensive checking behavior that
significantly interfered with his life.
Presenting problem
Because of thoughts that something terrible may happen and he may inadvertently be
responsible for harm befalling loved ones, neighbors, or other people, Mr. P states that he
must check ‘‘dangerous’’ items repeatedly before being able to leave his home. He performs
his checking in a ritualized manner, ensuring that electrical items are switched off and at
times has to count to 4 as he stares at each item. If he is interrupted while completing these
behaviors or feels under pressure, he must recommence his checking rituals. Similarly, if the
thought that something may have been left on reoccurs while checking, the time spent
ritualizing is considerably extended by his need to check repetitively. In addition to ensuring
that possibly harmful events are unlikely to occur, Mr. P feels that he must check that all taps
are turned off and has difficulty in writing and posting cheques and letters. He reports that he
is consistently late in getting out of the house and was in fact asked to resign from his last two
positions of employment as a result of his constant tardiness.
sessions as he felt his mood had improved and there was little further to be gained by
continuing to attend. He remained handicapped by his obsessional behavior. There were no
other psychiatric interventions until his current referral to a specialist unit.
Differential diagnosis
The diagnosis of OCD should not be made if the thoughts or behavior are
ego-syntonic or pleasurable, and resistance to such thoughts is primarily a func-
tion of deleterious consequences. Where the obsessional thought has developed
into an overvalued idea, the diagnosis of OCD is still possible if the suVerer is able
to eventually acknowledge that the belief is unfounded. The co-occurrence of
depression in OCD is frequently noted in the literature. Where major depressive
symptoms precede the onset of OCD symptoms or where both depressive and
obsessional symptoms equally predominate, a diagnosis of depression may be
indicated and the primary depressive disorder should be addressed. In making the
diVerential diagnosis, a qualitative diVerence is often noted between obsessional
and depressive thoughts, particularly with regard to the perceived senselessness
and resistance to the thought. The absence of compulsive rituals in those suVering
from depression also assists in making the diVerential diagnosis. Similar qualitat-
ive diVerences are evident in relation to stereotyped behavior in schizophrenia,
where the behavior is often engaged in as a result of Wxed beliefs or delusional ideas
or in response to other psychotic symptoms.
The symptoms of generalized anxiety disorder (GAD) may be distinguished
from OCD on a number of dimensions. In terms of content, the anxious cogni-
tions of GAD are usually concerned with problems of everyday living (health,
family, Wnances, work, etc.) as opposed to the frequently encountered themes of
dirt/contamination, violence, sex, aggression and blasphemy in OCD suVerers.
The absence of rituals – either overt or covert – in response to the worrying
thoughts in GAD is another often noted diVerence and may well be a reXection of
the degree of resistance to the thoughts. DiVerentiation may also be made in terms
335 Obsessive–compulsive disorder: Syndrome
Spectrum disorders
A growing trend in the literature has been concerned with the classiWcation of a
variety of impulse control and other disorders as ‘‘obsessional’’. The notion that
patients experience a subjective urge to complete behaviors – as well as anxiety
relief upon their completion – has led some authors to speculate that a number of
disparate disorders, such as trichotillomania, sexual compulsions, kleptomania,
borderline personality disorder, or Tourette’s Syndrome, may be related to OCD
along an impulsive–compulsive continuum. Although individuals with a spec-
trum disorder may respond to thoughts, urges, or preoccupations with particular
maladaptive behaviors, the relationship of their disorder to OCD is questionable
at a number of levels. OCD is characterized by intrusive, unwanted thoughts while
many of the spectrum disorders are characterized by thoughts or preoccupations
that are perceived as appropriate and rational. As the content or cognitive
component of their symptoms is markedly diVerent from OCD, the reasons for
engaging in the particular behavior are diVerent. While behaviors associated with
spectrum disorders may appear to have a sense of compulsion, important dif-
ferences are noteworthy in that the behaviors themselves are gratifying or pleasur-
able (e.g., impulse control disorders), are in response to an urge rather than an
intrusive thought (Tourette’s syndrome, trichotillomania), or to a physical symp-
tom or sensation (hypochondriasis), or are selectively purposeful (eating dis-
orders) or in response to a delusional belief (body dysmorphic disorder). In
contrast, rituals or behaviors in OCD are engaged in to reduce distress or anxiety
associated with the perceived threat resulting from the intrusive thought. Cogni-
tive factors involved in the mediation of OCD have been reported in a number of
investigations and these further diVerentiate OCD from spectrum disorders.
InXated responsibility has been proposed by investigators as an essential element
in the development of OCD (Salkovskis, 1989; Salkovskis and Kirk, 1997).
Thought–action fusion interacting with inXated responsibility is also considered
to be cognitive bias directly involved in the development and maintenance of
OCD (Rachman, 1997). Danger expectancies rather than responsibility have been
336 Treatment of Anxiety Disorders
Sex ratio
Black (1974) summarized 11 studies of OCD and reported that of 1336 cases, 651
were male and 685 female, suggesting an almost equal sex ratio. Similarly,
Yaryura-Tobias and Neziroglu (1983) reported an equal sex ratio in their review of
six OCD studies, while another study reporting on a clinical cohort (Noshirvani et
al., 1991) found a slightly higher proportion of women. Rasmussen and Eisen
(1992) also reported a slightly higher proportion of women (53.8%) in a large
cohort of 560 OCD patients. The opposite has generally been the case with child
and adolescent studies, which have tended to indicate a predominance of males
(Swedo et al., 1989, Rapoport, 1990). However, this may in part be due to an
earlier onset in males than in females.
Age of onset
In reviewing a number of studies, Black (1974) found that the majority of cases
had an onset of OCD between ages 10 and 40 years. The distribution, however, was
337 Obsessive–compulsive disorder: Syndrome
skewed, with 21% beginning between ages 10 and 15 years. Mean age of onset was
10–15 years, with 10% having syndrome onset prior to age 10 and 9% after age 40
years. Noshirvani et al. (1991), reporting on a large clinical cohort (N=307), found
a signiWcantly earlier onset in males (5–15 years). The mean age of onset was 22
years, with the vast majority (92%) commencing between ages 10 and 40 years.
Earlier onset for males was also reported in childhood onset OCD (Rapoport,
1990). Similarly, in another large clinical cohort of 560 individuals, Rasmussen
and Eisen (1992) report, the mean onset age as 20.9±9.8 years. Males were
reported to have a signiWcantly earlier onset (19.5±9.6 years), as compared
with females (22.0±9.8 years). Sixty-Wve percent of suVerers were found to have
illness onset prior to age 25 years, and fewer than 15% reported onset after age 35
years.
Course of illness
Prior to the development of eVective treatments of OCD, Ingram (1961) reported
a constant worsening in 39% of 89 inpatients, a constant and static unremitting
course in 15%, a Xuctuating course with periods of worsening and relative
improvement in 33% and a phasic course with periods of remission in 13%. An
early follow-up study of OCD suVerers by Kringlen (1965) found that 5% had a
constant worsening, 30% were constant and static, 20% Xuctuating and 5%
phasic. More recently, Rasmussen and Eisen (1992) reported that 85% had a
continuous and Xuctuating course, 10% had a deteriorative course and 2% were
classiWed as episodic. More recently, Skoog and Skoog (1999), in a 40 to 50 year
follow-up of OCD patients found that 83% of patients had improved over the
follow-up period, and 48% showed clinical recovery. However, 37% still had
diagnosable OCD after 50 years, and only 20% of the sample showed complete
recovery. Overall, clinical and subclinical symptoms were still evident in two-
thirds of the sample at follow-up, and 10% of the sample showed a deteriorating
course.
the same purpose as overt behavioral rituals. The presence of covert compulsions
has been recognized for some time. Foa and Tillmans (1980) have suggested that
the deWnition of compulsions be broadened to include both overt and covert
behaviors. Further support for this notion is found in the work conducted by
Salkovskis and Westbrook (1989), who diVerentiated between obsessional ideas
and cognitive rituals. They deWned obsessional ideas as the original anxiety-
arousing intrusions. In contrast, cognitive rituals are deWned as thoughts that the
patients voluntarily initiate to attempt to reduce the anxiety or discomfort
aroused by obsessional ideas. Within this approach, cognitive rituals are also often
referred to as ‘‘neutralizing’’ thoughts. DSM-IV criteria now acknowledge the
presence of covert compulsions and revision of the diagnostic criteria include
neutralizing thoughts within the compulsion deWnition. Although obsessional
ruminators are conceptualized as being similar to individuals with obsessions and
overt compulsions, a number of diVerences have been noted by Arts et al. (1993),
who, in comparing 26 ruminators to 48 patients with both obsessions and
compulsions, reported that the former group were more depressed, were more
often married, had achieved a lower level of education, were older at symptom
onset and were more often on medication.
The types of obsessional thoughts and compulsive behaviors have been reported
to be consistent across cultures (Tseng; 1973, Mahgoub and Abdel-HaWez, 1991;
Okasha et al., 1994) and time, with similar phenomenological reports and clinical
descriptions appearing in medical writings of the last century (Berrios, 1985).
Obsessional thoughts are often concerned with worries of contamination, harm-
ing others, or going against social mores such as swearing or making inappropriate
sexual advances in public (Marks, 1987). Rasmussen and Eisen (1992) reported
that 50% of 560 OCD patients had obsessions regarding contamination, 42%
pathological doubt, 33% somatic obsessions, 32% need for symmetry, 31%
aggressive, and 24% sexual. Compulsive behavior has generally been categorized
as washing, checking, repeating and ordering, with both adult and child suVerers
exhibiting similar phenomenology (Last and Strauss, 1989; Swedo et al., 1989).
Washing or cleaning, which generally aVects more women than men, is character-
ized by a fear of contamination and associated washing, decontaminating or
cleaning rituals, with extensive avoidance of the contaminant. Washing/cleaning
compulsions were evident in 50% of 560 OCD patients investigated by Rasmussen
and Eisen (1992). Checking behaviors were evident in 61% of the their sample,
with patients engaging in repeated checking in order to prevent a dreaded event or
disaster from occurring. Counting was evident in 36%, a need to ask or confess in
34%, a need for symmetry or precision in 28%, and hoarding in 18% of the
sample. In another large clinical cohort, Noshirvani et al. (1991) reported signiW-
cantly more compulsive washing in females and signiWcantly more checking in
339 Obsessive–compulsive disorder: Syndrome
males. Compared with late onset cases, early onset cases exhibited signiWcantly
more checking and fewer washing rituals. Obsessional slowness without visible
rituals has also been reported, though to a much lesser extent than other presenta-
tions, and is most likely a function of mental checking or the need to follow
a meticulous preset order (Rachman, 1974; Marks, 1987; Ratnasuriya et al.,
1991).
The utility of classifying subjects according to phenomenology is questionable,
given that suVerers often have more than one obsession and more than one form
of ritual. In a large cohort of 560 OCD patients (Rasmussen and Eisen, 1992), 72%
experienced multiple obsessions and 58% experienced multiple compulsions.
Other research suggests that phenomenology may change over time (Marks, 1987;
Hodgson and Rachman, 1977). A more promising classiWcation with implications
for behavioral treatment was proposed by Foa et al. (1985), and is based on the
presence or absence of external cues, disastrous consequences and either overt or
covert anxiety-reducing responses. ClassiWcation according to these criteria hold
implications for the cognitive behavioral treatment of the disorder and would
therefore be of greater clinical utility to the practicing clinician. A comprehensive
behavioral program should include exposure to all cues, both internal and exter-
nal, as well as response prevention that focuses on overt and covert rituals in
addition to avoidance.
Assessment instruments
A thorough assessment of OC symptomatology for the purposes of designing a
behavioral program relies heavily on clinical interview. No instrument will pro-
vide the clinician with the detailed and often idiosyncratic information regarding
the cues that create anxiety or discomfort, the responses (rituals) to those cues,
and the avoidance that the patient often engages in to minimize their discomfort.
Despite these limitations, it is good clinical practice to utilize assessment instru-
ments that may provide an independent validation of treatment eVectiveness. An
often-used therapist-administered instrument utilized in both clinical practice
and research settings that focuses on target obsessions and compulsions is the
Yale–Brown Obsessive Compulsive Scale (Goodman et al., 1989). The Maudsley
Obsessive Compulsive Inventory (Hodgson and Rachman, 1977) is a 30 item
‘‘true–false’’ self-report inventory that is also often used in the treatment of OCD.
The major shortcoming of this instrument is that it asks the patient to rate the
presence or absence of symptoms and therefore does not lend itself to changes in
interference, severity or frequency as a result of treatment. A more comprehensive
instrument, the Padua Inventory (Sanavio, 1988) consists of 60 items reXecting
OC symptoms that the patient rates in terms of degree of disturbance. In its
340 Treatment of Anxiety Disorders
original version, the Padua Inventory was found to be signiWcantly correlated with
measures of neuroticism and trait anxiety. A revision of the Padua was undertaken
by Burns et al. (1996) in order to delete items that overlapped with worry. This
resulted in a 39 item questionnaire (WSUR revision) consisting of Wve subscales:
obsessional thoughts about harm to self or others, obsessional impulses to harm
self or others, contamination obsessions and washing compulsions, checking
compulsions, and dressing or grooming compulsions.
Genetics
At the time of writing, there is growing evidence for a contribution from genetic
factors in some OCD presentations. The evidence for possible genetic predisposi-
tion in OCD derives from two sources: twin studies and investigations of the
Wrst-degree relatives of OCD suVerers. Early twin studies reporting concordance
may be criticized on the basis of failing to establish Wrm diagnoses of either
342 Treatment of Anxiety Disorders
zygosity or OCD (Hoaken and Schnurr, 1980). However, even in those studies
where zygosity was established and diagnosis conWrmed (WoodruV and Pitts,
1964; Marks et al., 1969; McGuYn and Mawson, 1980), the eVects of social
learning cannot be ruled out.
As with the twin studies, early investigations of Wrst-degree relatives of OCD
suVerers can be criticized on a number of grounds. The use of loose diagnostic
criteria, confounding of obsessional symptoms and traits, absence of control data,
as well as reliance on information provided by the proband rather than direct
interview of the relatives renders the Wndings of early investigations, as well as
some later studies (Insel, Hoover and Murphy, 1983; Rasmussen and Tsuang,
1986) diYcult to interpret. However, more recent studies, have attempted to
overcome such methodological Xaws through the use of structured diagnostic
interviews and direct relative interview. A study by Black et al. (1992) used the
Diagnostic Interview Schedule to assess the prevalence of OCD in the relatives of
OCD suVerers and normal controls. The authors found that, while Wrst-degree
relatives of probands with OCD were signiWcantly more likely to develop anxiety
disorders than relatives of the control group, the prevalence of OCD in both the
index and control relatives did not exceed the estimated occurrence in the general
population. Pauls et al. (1995), however, reported that the morbid risk for OCD
was signiWcantly higher in OCD proband relatives (10.3%) as compared with
relatives of controls (1.3%). The addition of subthreshold OCD raised the morbid
risk to 18.2%.
In contrast, studies that have utilized structured interviews to assess Wrst-degree
relatives of children and adolescent suVerers report a considerably higher inci-
dence of diagnosable OCD. Riddle et al. (1990) directly interviewed parents of
children with OCD using a standard clinical assessment. Results showed that 71%
of 21 children or adolescents with OCD had a parent with OCD (N=4) or
obsessional symptoms (N=11), indicating that 37.5% of parents had diagnosable
or subthreshold OCD. Lenane et al. (1990) reported similar results, with diagnos-
able OCD being found in 25% of fathers and 9% of mothers of 46 children with
OCD. With the inclusion of subclinical OCD, age-corrected morbidity risk was
estimated at 35%, not unlike the Wndings of Riddle et al. (1990).
The discrepancy between the child and adult studies may be a function of
diVerences between childhood/adolescent onset OCD and later or adult onset
OCD. In one early study, Bellodi et al. (1992) reported a morbid risk of 3.4% in the
Wrst-degree relatives of 92 OCD patients. Separation of the probands according to
age of onset, however, resulted in a morbid risk of 8.8% of relatives of probands
with onset prior to age 14 years and 3.4% for relatives of probands with a later
onset. More recently, Nestadt et al. (2000) reported that the lifetime prevalence in
relatives of 80 OCD patients was signiWcantly higher than controls (11.7% versus
2.7%). When the sample was divided into early onset (5–17 years) and late onset
343 Obsessive–compulsive disorder: Syndrome
(over 18 years) groups, the prevalence of OCD in relatives was 13.8% and 0%,
respectively.
To some extent, OCD is familial, particularly in early onset OCD. However,
while the above studies indicate that familial factors may play a role in some forms
of OCD, there are a signiWcantly large proportion of probands in all of the cited
studies that have no family history of OCD. Thus genetics, while important, do
not provide a total answer.
Comorbidity
Depression
The occurrence of obsessional symptoms in depressive illness suVerers has been
noted by a number of authors (Gittleson, 1966; Kendell and Discipio, 1970), as has
the high incidence of depressed mood in OCD suVerers (Rosenberg, 1968;
Goodwin, 1969; Rasmussen and Tsuang, 1986). However, the obsessional symp-
toms seen in patients with depressive illness are generally not of the intensity seen
in patients with OCD, and recovery from depression has been shown to result in a
reduction of obsessional symptoms. Other studies also indicate that obsessional
features in depression appear to parallel the course of the primary illness and that,
if present beforehand, will revert to their original intensity after resolution of the
depression (Videbech, 1975; Marks, 1987).
The presence of depressed mood or depressive symptoms has consistently been
shown to be a frequent complication of OCD (Rosenberg, 1968; Goodwin et al.,
1969; Black and Noyes, 1990), and some authors have suggested a psychobiologi-
cal link between depression and OCD (Hudson and Pope, 1990). Studies of child,
adolescent, and adult OCD suVerers report high rates of depressed mood, with
between 20% and 35% of OCD clinic attenders meeting criteria for major
depression (Rasmussen and Tsuang, 1986; Swedo et al., 1989; Sanderson et al.,
1990). Lifetime prevalence has been reported as aVecting up to 67% of OCD
patients (Rasmussen and Eisen, 1992). However, such clinical data need to be
interpreted cautiously, as many OCD suVerers tend to seek help only when
depressed (Marks, 1987). It is, moreover, important to carefully assess the severity
of depression in OCD patients presenting for treatment – particularly as the
presence of severe depression hinders the eVectiveness of behavioral interventions
in OCD (Foa et al., 1983a,b). Aside from improving less than suVerers with mild
or moderate depression, OCD suVerers with severe depression also tend to have a
higher relapse rate. Where such patients present for treatment, the possibility of
combining behavioral treatment with antidepressant medication, preferably with
antidepressant medication which has 5HT reuptake inhibiting properties, needs to
be carefully considered.
344 Treatment of Anxiety Disorders
Anxiety disorders
The co-occurrence of anxiety disorders in OCD suVerers is considerable. Similar
results are reported in both epidemiological and clinic samples for adults, adoles-
cents, and children (Rasmussen and Tsuang, 1986; Flament et al., 1988; Karno et
al., 1988; Swedo et al., 1989; Brown and Barlow, 1992; Crino and Andrew, 1996a).
Severity of co-occurring anxiety disorders should be assessed by the clinician, as
these conditions may require intervention after, or even before, the obsessional
problems have been addressed. Alternatively, these ‘‘conditions’’ may be second-
ary to the obsessional complaints, so that what appears to be agoraphobic avoid-
ance or social phobic concerns may be the direct result of the obsessional fears or
attempts by the suVerer to keep their rituals hidden from others. For example, a
patient with contamination concerns may experience diYculty in using public
transport, eating or drinking away from home, or other situations that may expose
the individual to contamination and therefore be wrongly identiWed as suVering
from a phobia. If there is a clear co-occurring anxiety disorder, it should be the
patient’s decision as to which disorder should be dealt with Wrst, and such a
decision should be made on the basis of level of interference with their life.
Personality disorder
The relationship between OCD and axis II diagnoses have generated considerable
interest among researchers. Findings suggest that anywhere from 48% (Jenike et
al., 1986) to 87.5% (Black et al., 1993) of OCD patients have one or more
personality disorders, as diagnosed by a variety of instruments. The results of
many of these studies are questionable on a number of grounds. First, the validity
of the instruments is uncertain, particularly as there is no ‘‘gold standard’’ against
which to compare the various questionnaires. Second, the confounding of state
and trait is certainly an issue worthy of consideration when eVective treatment of
the obsessional symptoms in OCD subjects results in a marked lowering of
personality disorder diagnoses (cf. JoVe and Regan, 1988; Mavissakalian et al.,
1990). One would expect the enduring maladaptive traits that constitute personal-
ity disorder should persist after the Axis I condition is treated. EVective treatment
of OCD and other anxiety disorder patients, however, results in the majority of
patients leading essentially normal lives, uncomplicated by any obvious Axis II
pathology. Results from our clinic (Crino and Andrews, 1996b) suggest that the
rate of personality disorders in OCD and other anxiety disorders is relatively low,
and that minor but important diVerences between the anxiety disorders exist
when one takes a dimensional rather than categorical view of personality disorder.
345 Obsessive–compulsive disorder: Syndrome
Conclusion
Many facts regarding OCD and its possible causes remain unknown despite the
extraordinary burgeoning of research in this area in recent years. While there is
general agreement of the diagnostic criteria across the two major classiWcation
systems as well as acknowledgment of the frequently encountered complication of
depression in OCD, much still remains to be learned of the etiology, comorbidity,
and other complications of what remains a puzzling and, if left untreated,
crippling disorder. One important question that continues to re-occur in the
recent literature is the possibility that OCD is a heterogeneous disorder. Taking
such a view would go part of the way to explain some of the disparate Wndings
noted above (e.g. genetics, relationship to TS, diVering cognitive styles, etc.)
Nevertheless, eVective treatments for OCD are available and, either alone or in
combination, will result in the majority of patients gaining control over their
disorder.
17
Obsessive–compulsive disorder
Treatment
Although OCD has been recognized for centuries, eVective treatment for this
condition has been available only for the past four decades. The treatments of
choice for OCD are behavior therapy, consisting of exposure and response
prevention, and selective serotonin reuptake-inhibiting medications. Recent stu-
dies have also included speciWc cognitive techniques targeting the appraisals of
intrusive thoughts, responsibility for harm and threat estimates. Whether the
addition of such techniques results in superior eYcacy is yet to be demonstrated in
further trials. Nevertheless, the use of cognitive techniques to challenge the
dysfunctional appraisal of intrusive thoughts is warranted in individuals with
cognitive styles that interfere with treatment. Cure of OCD is not commonplace.
The primary goal of treatment in the majority of cases is to have the individual
control the disorder rather than the obsessional disorder control the individual.
Achievement of this goal allows the patient to minimize the impact and eVects of
the disorder on their daily life and enhances their ability to reach their full
potential.
Behavioral therapy
The basic principles of exposure and response prevention include the deliberate
exposure to obsessional cues and prevention of the behaviors that the suVerer
typically engages in to lessen the anxiety, discomfort, or distress associated with
the feared stimuli. Repeatedly employing prolonged exposure (45 minutes to 2
hours) to the obsessional cues, with strict response prevention, allows habituation
to take place. Exposure tasks are arranged hierarchically, with treatment com-
mencing with the least anxiety-provoking situation and progressing rapidly
through the hierarchy.
In reviewing the results of more than 200 OCD patients treated with behavior
therapy in several countries, Foa et al. (1985) reported that 51% of suVerers
achieved at least a 70% reduction in symptoms. Thirty-nine percent of patients
346
347 Obsessive–compulsive disorder: Treatment
achieved reductions ranging from 31% to 69%, and 10% were considered failures,
failure being deWned as patients with an improvement of 30% or less. At follow-up
(mean duration 1 year), the number of failures increased from 10% to 24%.
However, 76% of patients remained improved to a degree rated as moderately
improved or better.
Further evidence for the eYcacy of exposure and response prevention is reXec-
ted in a long-term follow-up of nine cohorts from Wve countries conducted by
O’Sullivan et al. (1991). Both self- and assessor ratings were used, and two cohorts
had received exposure plus either clomipramine or placebo. The overall dropout
rate was reported at 9% and – of a total of 223 patients – 87% were followed up for
a mean of 3 years (range 1 to 6 years). All studies reported a signiWcant improve-
ment at posttreatment, which remained evident at follow-up, with 78% of individ-
uals remaining improved. On average, there was a 60% improvement in target
rituals as compared with pretreatment. These Wndings need to be tempered with
the fact that approximately 25% of patients refuse behavior therapy when oVered,
because of the time commitment, or because of fears of overwhelming anxiety
when confronting their triggers, or because they fear that the dreaded outcome
from not performing their ritual will eventuate (Greist, 1998). In our experience,
motivational interventions may assist in those who do not wish to make the time
commitment, cognitive techniques may assist those who fear the dreaded out-
come, while a more graded approach to exposure may assist those who fear
overwhelming anxiety or panic.
Although the utilization of exposure and response prevention techniques have
had a signiWcant impact upon the treatment of individuals with compulsive
rituals, the eYcacy of behavioral techniques in the treatment of obsessional
thoughts has, until recently, been considered problematic. However, Salkovskis
and Westbrook (1989), employing revised habituation procedures in which the
subjects were exposed to obsessional thoughts via loop tapes and avoided cogni-
tive neutralizing, reported a favorable outcome in four subjects. More recently,
Freeston et al. (1997) randomly assigned 29 OCD patients without overt rituals to
a wait-list control condition or a comprehensive cognitive behavioral program
that involved a cognitive model of obsessions, cognitive restructuring of the
dysfunctional assumptions, loop tape and in vivo exposure and response preven-
tion, and relapse prevention. SigniWcant improvement was reported in Yale–
Brown Obsessive Compulsive Scale (YBOCS) scores, self-report of OCD symp-
toms and self-reported anxiety, with 77% of treatment completers (N = 22)
showing clinically signiWcant changes.
348 Treatment of Anxiety Disorders
Cognitive therapy
The eYcacy of cognitive interventions in the treatment of OCD has been inves-
tigated by a number of researchers. The contribution of self-instructional training
(SIT) to exposure and response prevention was examined by Emmelkamp et al.
(1980). Fifteen patients received either self-controlled exposure or exposure com-
bined with SIT. No group diVerences were found at posttreatment or 1- or
6-month follow-up. Emmelkamp et al. (1988) compared self-controlled exposure
and response prevention to rational emotive therapy (RET) in 18 OCD suVerers
and reported that cognitive therapy was as eVective as exposure and response
prevention. In a replication, Emmelkamp and Beens (1991) compared six sessions
of RET to six sessions of exposure followed by a 4-week waiting period and six
further sessions of exposure for both groups. Although no diVerence was found
between the RET condition and exposure condition, there was no indication that
RET enhanced outcome when combined with exposure and response prevention.
In a larger study, Van Oppen et al. (1995) randomly allocated 71 patients to either
self-controlled exposure or a cognitive therapy condition on the basis of work of
Beck (1976) and Salkovskis (1989). Both conditions led to signiWcant improve-
ment and there were some indications that cognitive therapy may have been
superior; however, the diVerences were not signiWcant when initial diVerences
between conditions were taken into account. EVect sizes tended to be larger in the
cognitive therapy condition and there were signiWcantly more patients rated as
recovered in the cognitive condition. Although the authors discuss the results in
terms of the eYcacy of cognitive techniques, the addition of behavioral experi-
ments to test the empirical basis of dysfunctional assumptions (exposure) after six
sessions of cognitive therapy would tend to confound the observed outcome. No
study directly comparing cognitive techniques alone, cognitive techniques com-
bined with exposure, and exposure alone has yet been conducted.
fered signiWcantly from treated patients in Wve areas: they were less obsessive
compulsive, they had more discongruent treatment expectations, they were more
critical of the therapist, they experienced less anxiety in homework exposure, and
they were less often pressured by signiWcant others to continue treatment. Foa et
al. (1983a,b), attempting to determine predictors of outcome, found that signiW-
cant depression may aVect outcome when exposure and response prevention is
used by inXuencing reactivity and habituation between sessions. Similarly, the
presence of overvalued ideation has been noted to aVect outcome negatively (Foa,
1979). In contrast, Lelliot et al. (1988) found that patients with bizarre and Wxed
beliefs responded well to treatment. While there was a signiWcant correlation
between clinical improvement on a number of measures and the reduction of
Wxity of obsessional beliefs, the Wxity of such beliefs did predict severity of target
rituals at 1-year follow-up (Basoglu et al., 1988). More recently, Ito et al. (1995)
reported that reduction in Wxity of OCD beliefs parallelled improvements in other
measures of OCD symptoms.
Other factors that may aVect the success of treatment include excessive behav-
ioral or cognitive avoidance and excessive arousal in the presence of feared stimuli
(Foa et al., 1983a). In the Wrst case, attention-focusing techniques while using in
vivo exposure may assist in promoting habituation. Excessive arousal may be a
function of the program design, and require a reanalysis of the fear-evoking
potential of the stimuli so that arousal is kept at moderate levels, thereby promo-
ting emotional processing and habituation. Clinical factors not found to inXuence
treatment include age at symptom onset. In fact, Foa et al. (1983a) reported that
the younger the individual was when symptoms began, the better maintained was
the improvement at follow-up. Similarly, neither duration of symptoms nor
symptom severity was associated with poor outcome. The types of ritual (washing
versus checking) were also not predictive of outcome with exposure and response
prevention. In contrast, Basoglu et al. (1988) reported that severe rituals and social
disability predicted poorer outcome in patients treated with clomipramine and
exposure. Similarly, Cottraux et al. (1993), in examining predictors of treatment
outcome in 60 patients treated with behavior therapy, Xuvoxamine or a combina-
tion, found that high avoidance was the best single predictor of poor outcome.
While depression was not a signiWcant predictor of outcome in a number of other
studies (Basoglu et al., 1988; Hoogduin and Duivenvoorden, 1988; O’Sullivan et
al., 1991; Riggs et al., 1992), depression predicted failure in Cottraux et al.’s (1993)
study. Severe depression was also associated with poorer outcome in a follow up of
72 OCD patients treated with behavior therapy (Foa et al., 1981).
More recently, Castle et al. (1994) examined outcome predictors for 178
outpatients with OCD. Forty-one patients who dropped out of treatment did not
diVer signiWcantly in terms of demographic or illness variables or initial rating
350 Treatment of Anxiety Disorders
scale scores. As with data from Foa et al. (1983a), age, age of onset, and illness
duration were not signiWcantly associated with outcome, nor were meticulous or
anxious personality traits. Patients living alone were signiWcantly less likely to be
classiWed as ‘‘much improved’’. The ‘‘much improved’’ group had signiWcantly
lower initial scores on global phobia as well as ratings of work and home
impairment, and were more likely to have had a co-therapist. While gender was
not a predictor of outcome, predictors of outcome diVered between the sexes.
Factors associated with a good outcome for women were being in paid employ-
ment, having a co-therapist (relative, friend or appropriate other), and low initial
severity ratings of global phobia, impairment of work and home activity, and
compulsion checklist. For men, however, the only factor to approach statistical
signiWcance was living alone, which was associated with less improvement.
Keijsers et al. (1994) also reported greater initial severity of obsessional com-
plaints to be associated with poorer outcome but also reported that poorer
motivation, dissatisfaction with the therapeutic relationship and longer duration
of complaints predicted poorer immediate (posttreatment) outcome for ‘‘obses-
sive fear’’, while higher pretreatment levels of depression predicted poorer out-
come of compulsive behavior.
In summary, the most consistent outcome predictor appears to be symptom
severity, with the more severely symptomatic patients tending to have a poorer
outcome. The role of depression as a predictor of outcome remains unresolved,
with some studies reporting less improvement in depressed patients (e.g., Foa et
al., 1983b; Cottraux et al., 1993) while others report no association (e.g., Basoglu
et al., 1988; Hoogduin and Diuvenvoorden, 1988; Castle et al., 1994). Overvalued
ideation and Wxity of beliefs have also been delineated as possible predictors of
outcome.
Pharmacotherapy
Although a wide variety of medications have been utilized in the treatment of
OCD, there is little doubt as to the consistent eYcacy of serotonin reuptake
inhibitors (SSRIs), of which clomipramine is the most widely researched. Placebo
controlled trials have in general attested to its eYcacy and comparison to other
antidepressants have also demonstrated its superiority in decreasing obsessional
symptoms ( Greist, 1990a; Jenike, 1990a). Average symptom reduction, however,
is only moderate (Zak et al., 1988; De Veaugh-Geiss et al., 1989; Greist, 1990a).
Although not as extensively researched as clomipramine, other more potent
SSRI appear to be of equal beneWt in the treatment of OCD, and in general have
the added beneWt of a lower side-eVect proWle. The eYcacy of Xuoxetine at three
Wxed doses (20, 40, and 60 mg) was examined in a multicenter trial by Tollefson et
351 Obsessive–compulsive disorder: Treatment
al. (1994), who reported symptom reduction of 32.1%, 32.4%, and 35.1%, re-
spectively, as compared with 8.5% for placebo after a 13 week trial. Pigott et al.
(1990) in a randomized double-blind crossover design compared clomipramine
to Xuoxetine and reported similar therapeutic eVects. Fluvoxamine has also been
shown to be superior to placebo in the treatment of OCD in a number of
double-blind studies (e.g., Goodman et al., 1990; Perse et al., 1987; Jenike et al.,
1990b) and in a multicenter trial (Goodman et al., 1992). Fluvoxamine was also
compared with desipramine in a study by Goodman et al. (1990) and was found to
be superior in reducing the severity of OC symptoms. A direct comparison of
Xuvoxamine with clomipramine by Lorin et al. (1996) reported similar levels of
symptom reduction in a similar proportion of patients in both groups. Sertraline,
another SSRI, has also had mixed results initially, with one placebo controlled
study Wnding no eVect in a small number of patients (Jenike et al., 1990a). Other
studies have attested to the eYcacy of sertraline in OCD. Chouinard et al. (1990)
reported that sertraline resulted in signiWcant decreases in OCD symptoms on
three of the four measures used. Greist et al. (1995) reporting on a large multicen-
ter placebo controlled trial of Wxed-dose sertraline (50, 100, 200 mg) found that
doses of 50 mg and 200 mg were signiWcantly more eVective than placebo in
reducing obsessional symptoms. More recently, Kronig et al. (1999) found sertra-
line at varying doses from 50 to 200 mg per day to be signiWcantly more eVective
than placebo on all measures used. Paroxetine has also been reported to be more
eVective than placebo in a multicenter trial but only at doses of 40 mg and 60 mg
per day, with 20 mg being no diVerent from placebo (Hollander et al., 2000).
There also is growing evidence concerning the eVectiveness of citalopram in the
treatment of OCD (Kopenon et al., 1997). Mundo et al. (1997) reported equal
eVectiveness of Xuvoxamine, paroxetine and citalopram in a single-blind com-
parative trial of 30 patients with OCD.
The issue of treatment-refractory OCD patients has been addressed by a
number of authors, and several pharmacological agents (e.g., lithium, buspirone,
haloperidol, olanzapine) have been suggested as possible augmenting strategies.
Few controlled trials of such substances have been reported. However, in a recent
placebo controlled trial, McDougle et al. (2000) found augmentation of SSRIs
with risperidone to be of assistance in patients who did not respond to SSRI
monotherapy. The issue of how to deWne a treatment-refractory patient was
addressed by Rasmussen and Eisen (1997), who suggested that the emerging
consensus is ‘‘someone who has failed both adequate trials of an SSRI and
exposure with response prevention’’ (ibid., p. 11), rather than monotherapy with
either exposure or SSRIs.
Perhaps the major diYculty with the use of SSRIs in the treatment of OCD is the
high relapse rate with medication discontinuation. For example, Pato et al. (1988)
352 Treatment of Anxiety Disorders
Conclusions
The eVective cognitive behavioral treatment of OCD requires intensive interven-
tion on the part of the therapist and strong motivation on the part of the patient.
The decision as to whether to combine pharmacological and behavioral treatment
should be made in consultation with the patient. In the presence of a severe major
depressive illness, the decision is clear: a combined approach may be the most
eVective. If the patient is drug naı̈ve, hesitant about taking medication, or cannot
tolerate the side-eVects, then behavior therapy alone may well be the treatment of
choice. Given the high relapse rate associated with medication discontinuation,
pharmacotherapy in the absence of behavioral therapy does not constitute an
adequate or appropriate treatment of OCD.
18
Obsessive–compulsive disorder
Clinician Guide
Common questions
Patients referred for treatment will often ask a number of questions about their
condition and the proposed treatment. As much as possible, individuals are
encouraged to ask questions, and answers are given on the basis of available
knowledge regarding OCD. Common questions include those relating to the cause
of their condition. Apart from discussing the research Wndings to date, it is
pointed out that there is no one cause of OCD: it is not as simple as a ‘‘biochemical
imbalance’’, nor genes, nor individual psychological factors, nor environment but
a complex condition due to a combination of a variety of complex factors.
Educating the patient about OCD, its many causal factors and its treatment is an
important step in bringing about a cognitive shift from the helpless attitude of
many suVerers to having a good understanding of the condition, its maintaining
factors, and what patients can do to assist in their own treatment.
354
355 Obsessive–compulsive disorder: Clinician Guide
Assessment
Perhaps the most important aspect of the cognitive behavioral treatment of OCD
is the detailed assessment of the problem behaviors. Because of inadequate
assessment, many diYculties commonly arise in the treatment of the condition.
While standardized assessment forms may yield information and clues as to
symptoms that may have been missed on initial interview, the assessment process
is interactive. The therapist tests hypotheses with the patient not only on the basis
of information obtained in the initial stages of treatment but more importantly on
information gained throughout the treatment process. In other words, assessment
is an ongoing activity. It is rarely the case that suVerers will be able to elucidate all
of the necessary information in the Wrst one or two sessions. In addition, a
proportion of patients will be reticent in giving full details of their symptoms
because of embarrassment. In the Wrst instance, it is a matter of modifying the
program as more information is made available. Where embarrassment plays a
role, it is important to reassure the patient that, as an experienced therapist, you
have seen similar symptoms in OCD suVerers. It may be worthwhile oVering
examples of obsessional symptoms in order to allay any anxieties that the patient
may have about being negatively evaluated by the therapist or others because of
their symptoms.
Assessment should focus on the presence or absence of internal cues (e.g.,
images, thoughts, urges), and external cues (contaminants, situations, etc.) that
elicit the urge to ritualize. Rituals, particularly covert rituals or cognitive neutraliz-
ing, need to be carefully assessed. Reasons for ritualizing should also be noted, as
they may have implications for the exposure program and provide clues in
relation to avoidance and therefore to further exposure tasks. Avoidance of
situations by OCD suVerers is often considerable, relating to situations, objects,
and so forth, that the suVerer knows will provoke discomfort and the urge to
ritualize. In addition to discussing avoided situations with the suVerer, it is often
worthwhile discussing the patient’s obsessional symptoms with a signiWcant other,
who can provide further information relating to triggers, rituals, and avoidance.
Assessment of individuals presenting with obsessional thoughts and no overt
rituals requires close attention. It is essential that the intrusive thought be identi-
Wed correctly in order for exposure to be eVective. Similarly, it is necessary to
identify cognitive neutralizing of the obsessional thought. While suVerers are
often able to verbalize the intrusive cognition, it is sometimes diYcult to identify
the covert neutralization of the thought, as it may be a repetition of the thought
itself – or perhaps even an image of the actions involved in the thought – both of
which may be anxiety-provoking and therefore diYcult to distinguish from the
original anxiety-arousing intrusion. For example, one suVerer presented with
356 Treatment of Anxiety Disorders
intrusive thoughts and images of harming a loved one while asleep. The intrusions
appeared to take the form of verbal thoughts – ‘‘I will kill him’’ – as well as images
of the actions being carried out. Detailed questioning of the suVerer indicated that
the ‘‘intrusive’’ image, while anxiety provoking, was in response to the thought
and was voluntarily produced because it served to reassure the suVerer that she
could never perform such a terrible act. It may be helpful to deWne the neutralizing
behavior for the suVerer in terms of any cognitive behavior in which they
voluntarily engage as a response to their intrusive thought. Recording of the
thought on a loop cassette tape and playing the same back to the patient may also
yield important information as to neutralizing cognitions.
Cognitive assessment is equally important when dealing with individuals who
present with obsessional thoughts and no overt rituals or those who present with
thoughts of harm to others through some act of their own or through their own
negligence. Such assessment is focused on the appraisals and beliefs the individuals
have of their thought (‘‘I may act on the thought’’), as well as the occurrence of the
thought (‘‘having this thought means that I want it to happen’’, or ‘‘having the
thought means I’m an evil person’’, etc.). Freeston et al. (1996b) proposed Wve
groupings of beliefs and appraisals commonly present among OCD patients: (1)
overestimating the importance of the thought through thought–action fusion,
magical thinking and distorted Cartesian thinking; (2) exaggerating responsibility
for events that are beyond the person’s control and the consequences of being
responsible for harm; (3) a need to seek absolute certainty or completeness or
complete control over thoughts and actions; (4) overestimating the probability
and consequences of negative events; and (5) beliefs that the anxiety caused by the
thoughts is dangerous or unacceptable (Freeston et al., 1996b). As patients may
have one or a series of beliefs regarding the intrusions as well as diVering
dysfunctional assumptions of the same thought, the individual examples of
cognitive styles are by no means mutually exclusive. The authors give excellent
descriptions of speciWc interventions that may be utilized to challenge the beliefs
and assumptions associated with the thoughts and the reader is encouraged to
obtain the journal article.
Treatment process
It is essential that the patient has a good grasp of the treatment rationale. Taking
time to explain graded exposure, response prevention, and habituation – using
examples from daily life – will help to ensure that the suVerer has a good
understanding of the procedures without engendering further anxiety and pre-
cipitating a Xight from the clinician’s oYce. A typical example one might give to
patients is that of learning to drive a motor vehicle. The majority of people upon
357 Obsessive–compulsive disorder: Clinician Guide
entering a car for their Wrst driving lesson will feel quite anxious and uncomfort-
able, trying to remember all of the basic things to look out for as well as control the
motor vehicle. However, with repeated exposure, the anxiety gradually subsides to
the point that, after performing the driving behavior innumerable times, the
driver feels no anxiety and doesn’t even have to think about their routine behavior.
Clinical examples of exposure and habituation from previously treated cases will
also serve to reinforce the principles for the patient.
When discussing the treatment rationale with the patient, a graded approach
should be emphasized. Often, patients envisage being asked to do the impossible:
not ritualizing at all when exposed to the most ‘‘noxious’’ stimulus. Unless
clariWed and explained to the patient, such a misconception will place the clinician
in the same position as many ‘‘helpful’’ friends and relatives who have suggested to
the suVerer that, if he or she does not like being the way they are, they should just
put a stop to their behavior. By explaining the fact that exposure will be graded,
with the patient and therapist working through a graded hierarchy of stimuli and
the patient being asked to refrain from engaging in rituals to a gradually increasing
number of stimuli, the task does not seem as insurmountable as being told that
total exposure will take place and absolutely no rituals are allowed. As part of the
rationale, it is imperative that the suVerer is made aware that they will be taking a
very active part in their own treatment and should in fact take on the role of
co-therapist in the treatment program.
stimulus object) or they may attempt to cope by delaying their rituals (e.g., ‘‘I will
wash my hands later today and touch as little as I can in the meantime’’). While
such techniques may lead to a reduction in distress during the session, habituation
or decreases in discomfort between sessions will not occur. Again, in such
circumstances, it is important to remind the suVerer of the treatment rationale
and reinforce the notion that there is little to gain by utilizing such methods. If,
however, such methods are being utilized by the patient because the distress
associated with the stimulus is greater than expected, then it is likely that a more
detailed behavioral assessment is required and a more gentle rate of progress
implemented.
Where the suVerer experiences obsessional thoughts without overt rituals,
program design and implementation follow lines similar to the treatment of
suVerers with behavioral rituals. Intrusive thoughts are identiWed, as are the covert
neutralizing responses to such thoughts. Obsessions are rated hierarchically and
the patient is requested to refrain from engaging in covert neutralization. Expo-
sure consists of having the patient record their least anxiety-engendering or
distressing thought on a loop cassette tape. On replay, anxiety or discomfort
ratings are noted. Replaying of the taped thoughts in the early stages of treatment
may also assist in the identiWcation of any covert neutralizing responses. Patients
are requested to refrain from any neutralizing behaviors and are required to listen
to the tape and allow the recorded thoughts to guide their thinking. For example, a
suVerer with intrusive blasphemous thoughts who prays in response to those
thoughts is asked to listen to the taped blasphemous thoughts and not engage in
prayers. As with compulsive ritualizers, it is often useful to allow the suVerer to
experience anxiety or discomfort reduction within the initial treatment sessions
and set similar tasks as homework assignments. As habituation to each thought
takes place, variations in procedures such as listening to the tape in previously
avoided situations or varying the tone or loudness of the recorded thoughts
should be implemented. In the case of the individual described above, for
example, this may involve having the patient listen to the recorded blasphemous
thoughts while sitting near or in a church, and so forth.
An alternative method to loop tape exposure, which has led to equal success at
our unit, follows the same principles without the taped exposure and relies on
spontaneous thought occurrence and voluntary cessation of cognitive neutraliz-
ing. Avoidance of situations that may trigger the intrusive thought is often
considerable. For example, intrusive sexual thoughts will often result in the person
avoiding to look at, or be near, triggering stimuli such as same-sex individuals,
children or animals; intrusive blasphemous thoughts will often result in avoidance
of anything of a religious nature; and intrusive thoughts about harm will often
result in avoidance of objects with which to cause harm, especially in the presence
359 Obsessive–compulsive disorder: Clinician Guide
of the loved ones or persons involved in such thoughts. Individuals are given a
thorough rationale for the maintenance of the intrusion and the associated worry.
This is followed by identiWcation of all intrusive thoughts as well as the associated
neutralizing or avoidance. Dysfunctional beliefs are challenged, and the patient is
encouraged to passively accept the thought whenever it occurs, live with the
anxiety until it fades, while exposure to previously avoided situations is conducted
in a hierarchical fashion. To some, such exposure may be viewed as behavioral
experiments aimed at testing the patient’s beliefs and assumptions rather than
exposure per se, but what’s in a name?
Whether the clinician decides on a loop tape or relies on spontaneous exposure,
the challenging of dysfunctional assumptions in obsessional ruminators and those
who fear causing harm to others by their thoughts is an essential step in ensuring
the success of exposure treatment. For example, a 23-year-old female was referred
to our unit after having failed in treatment at another clinic. The primary concerns
were intrusive thoughts of molesting children. There was considerable avoidance
of children and places where children could be encountered (e.g., friends’ homes,
shopping centers, schools, parks, etc.). SpeciWc neutralizing strategies included
trying to push the thoughts out of her head, arguing with the thoughts in order to
reassure herself that her sexual preference was for adult heterosexual relationships,
telling herself that she would never act on the thoughts and that she would commit
suicide if there was ever any chance of acting on the thoughts. Although she had
undergone a well-designed treatment program that included exposure to the
thought as well as previously avoided situations and prevention of the neutralizing
responses, few gains were made. On assessment, it became apparent that treatment
gains were minimized by the fact that her beliefs about the intrusive thoughts had
not been addressed. Her underlying assumptions regarding the thoughts included
the notion that only very disturbed individuals would have such thoughts, that she
did not have OCD, and that perhaps she was a sexual deviate after all. Challenging
these assumptions at a number of levels included education about the fact that
intrusive thoughts are common human phenomena and that what diVerentiates
OCD from normal intrusive thoughts is the meaning and importance individuals
attach to intrusive thoughts. The notion that having an inappropriate thought
directly reXects on the individual’s nature was challenged by having her examine
other inappropriate thoughts to which no meaning was attached, as well as having
her discuss with signiWcant others (family who were aware of her concerns) the
nature of inappropriate thoughts that they had experienced. Such techniques,
aimed at changing her appraisal of the intrusive thoughts, led to signiWcant
improvement with exposure-based treatment.
Unlike overt rituals, cognitive neutralizing is considerably more diYcult to
identify and control. Consequently, the clinician is much more reliant on the
360 Treatment of Anxiety Disorders
Homework assignments
Homework assignments in which the patient is required to perform the exposure
tasks conducted during the treatment session are an integral part of treatment.
Little is to be gained if the patient engages only in exposure and response
prevention in the clinic setting. In order to ensure habituation to the anxiety-
evoking stimulus, exposure and self-directed response prevention need to be
conducted repeatedly and such tasks should be included as part of the homework
assignments. Diary notes of each assignment should be kept by the suVerer and
ratings of discomfort and urge to ritualize (overtly or covertly) included in the
diary. Involvement of signiWcant others, such as partners or family members, as
co-therapists will assist in ensuring that the required tasks are carried out as
instructed. However, at all times it is emphasized that the suVerer himself or
herself is responsible for the implementation of the program.
Follow-up
It is essential that OCD patients be seen on a regular basis for at least 12 months
following intensive treatment. Invariably, suVerers will experience short-term
diYculties in maintaining their gains, particularly as novel situations or thoughts
provoke the urge to ritualize. The clinician needs to encourage the adoption of the
principles of exposure and response prevention for each of the novel as well as the
familiar stimuli. Although total cures are relatively rare, the goal of controlling the
361 Obsessive–compulsive disorder: Clinician Guide
disorder rather than the disorder controlling the suVerer is both realistic and
achievable in the majority of cases.
Problem solving
When using any cognitive behavioral procedure, it is important for the suVerer to
be aware that they will be taught skills with which to deal with their own disorder.
That is to say, they will not be ‘‘treated’’ in the traditional sense of the word and be
passive recipients of the techniques that will alleviate their distress. This is much
more the case in the treatment of obsessional disorders, particularly as ritual
prevention must be self-directed and voluntary. As part of the treatment rationale,
the patient should be made aware of the expectation that they will take an active
part in their own treatment, being primarily responsible for the proper implemen-
tation of the techniques and therefore directly responsible for their own treatment
gains. The role of the therapist is described as that of an instructor or teacher
whose principal task includes encouraging the suVerer to face the various anxiety-
provoking situations in a planned and systematic fashion. At all stages, the patient
is encouraged to assist in their program design and he or she should be encouraged
to take on the role of co-therapist in the assessment phase, for without total
cooperation in the assessment of obsessional symptoms, program outcome will be
less than satisfactory.
Reassurance
Invariably, OCD suVerers will request reassurance from their treating clinician.
While this reassurance is conWned to possible outcome of treatment or the
rationale for exposure, the clinician is on safe ground in reassuring the patient
about the techniques being used. However, reassurance relating to the possibilities
of danger or harm must be diligently avoided by the therapist. If one considers that
in the majority of cases, the OCD suVerer engages in repetitive ritualized overt or
covert behaviors in order to minimize the risk of harm to themselves or others,
reassurance of the lack of danger by the therapist will serve only to replace one
anxiety-reducing behavior (washing, checking, praying, etc.) with another, i.e.,
checking with or gaining reassurance from the therapist. Once given, the patient
will constantly seek the clinician’s reassurance that the behavior engaged in poses
no threat to the suVerer or signiWcant others. Needless to say, the exposure
program will then be confronted with major diYculties, as it becomes the
clinician’s permission that allows the behavior to be performed rather than the
patient taking the risk in performing the behavior. Another pitfall in treating some
patients is that the clinician inadvertently reassures the patient by setting the
exposure task. Responsibility for any disastrous consequence is transferred from
362 Treatment of Anxiety Disorders
the patient to the clinician, as the task was conducted only at the clinician’s
request. In such cases, it is always helpful to have the patient select the exposure
task without input from the clinician. Similarly, some individuals with intrusive
unpleasant thoughts or images will, in each treatment session, insist on giving the
clinician a detailed account of each occurrence of the intrusive thought and image,
the content of the thoughts/images and every situation in which they occurred.
This need to ‘‘confess all’’ is a more subtle way of gaining reassurance, for as the
clinician sits impassively listening, the patient knows there is nothing to be
concerned about because the clinician has not reacted in shock or horror by falling
out of the chair. In such cases, it is better for the session to focus on more general
issues such as frequency of the thoughts, intensity of anxiety, duration, neutraliz-
ing, etc. rather than speciWc individual instances of intrusive thought occurrences.
In general, reassurance-seeking behavior should be dealt with by explaining to the
patient that assurances regarding the lack of possible harm from any action is an
impossibility, and that, in order to eVectively overcome OCD, the patient must
learn to live with the doubt.
19
Obsessive–compulsive disorder
Patient Treatment Manual*
This Manual is both a guide to treatment and a workbook for persons who suVer
from obsessive–compulsive disorder. During treatment, it is a workbook in which
individuals can record their own experience of their disorder, together with the
additional advice for their particular case given by their clinician. After treatment
has concluded, this Manual will serve as a self-help resource enabling those who
have recovered, but who encounter further stressors or diYculties, to read the
appropriate section and, by putting the content into action, stay well.
Contents
Section 1 364
1 The nature of obsessive–compulsive disorder 364
1.1 Symptoms of obsessive–compulsive disorder 365
Section 2 366
2 The causes and treatment of obsessive–compulsive disorder 366
2.1 The biochemical theory 367
2.2 The genetic theory 367
2.3 Learning theory 367
2.4 Cognitive theory 368
2.5 Psychoanalytical theory 368
2.6 The treatment of obsessive–compulsive disorder 368
2.6.1 Medication 369
2.6.2 Behavior Therapy 369
Section 3 371
3 Exposure and response prevention 371
3.1 Obsessional thoughts 372
3.2 Basic rules for success 373
*Gavin Andrews, Mark Creamer, Rocco Crino, Caroline Hunt, Lisa Lampe and Andrew Page The Treatment
of Anxiety Disorders second edition © 2002 Cambridge University Press. All rights reserved.
364 Treatment of Anxiety Disorders
Section 4 375
4 The treatment program 375
4.1 Program design 376
4.1.1 Avoidance 379
4.2 Exposure tasks 380
Section 5 382
5 Recommended reading 382
5.1 Recommended paperbacks 382
SE C T I ON 1
1 The nature of obsessive–compulsive disorder
Obsessive–compulsive disorder (OCD) is an anxiety disorder that, until quite
recently, was regarded as a rare condition. Recent studies have shown that OCD is
considerably more common than was previously thought and as many as 2 in
every 100 people may suVer from the condition.
OCD is characterized by persistent, intrusive, unwanted thoughts that the
suVerer is unable to control. Such thoughts are often very distressing and result in
discomfort. Many OCD suVerers also engage in rituals or compulsions that are
persistent needs or urges to perform certain behaviors in order to reduce their
anxiety or discomfort or to prevent some dreaded event from occurring. More
often than not, the rituals are associated with an obsessional thought. For example,
washing in order to avoid contamination follows thoughts about possible con-
tamination. For some, there is no apparent connection between the intrusive
thought and the behavior, e.g., not stepping on cracks in the sidewalk in order to
avoid harm befalling one’s family. Others have no compulsive behaviors and suVer
from obsessional thoughts alone, while still others do not experience obsessions
but have compulsive rituals alone.
The one common element to the various symptoms in OCD is anxiety or
discomfort. For those suVering both obsessional thoughts and compulsive rituals,
it is the anxiety or discomfort associated with the thought that drives the ritual. In
other words, the ritual is performed to reduce the anxiety produced by the
thought. For those suVering from obsessional thoughts alone, anxiety is often
associated with the thought, and mental rituals, distraction, or avoidance may be
used to lessen the discomfort and ensure that the fearful event does not occur. It’s
much the same for those with compulsive rituals alone in that the behavior is
performed in order to lessen the urge to ritualize. The role of anxiety is important
in OCD and will be discussed in much greater detail in subsequent sections.
365 Obsessive–compulsive disorder: Patient Treatment Manual
Most OCD suVerers can see the uselessness and absurdity of their actions but
still feel compelled to perform their various rituals. They know that their hands are
not dirty or contaminated and they know that their house will not burn down if
they leave the electric kettle switched on at the wall. Because they are aware of how
irrational their behavior is, many suVerers are ashamed of their actions and go to
great lengths to hide their symptoms from family, friends, and, unfortunately,
even their doctors. It is extremely important that your therapist is aware of all of
your symptoms no matter how embarrassing or shameful they may be, as this is
the only way that a suitable treatment program can be designed for you. Rest
assured that a therapist experienced in the treatment of OCD will have heard of
symptoms worse than yours many times over.
type of symptom so that individuals may engage in more than one type of ritual or
have more than one type of obsessional thought. Another point to note is that
symptoms change over time and someone who is predominately a washer may,
over time, develop checking rituals that eventually supersede the original com-
plaint. In addition to changes in symptoms, the course of the disorder may also
Xuctuate over time, with periods of worsening and periods of improvement. Other
suVerers may Wnd that their symptoms remain static, while yet others may Wnd a
gradual worsening of symptoms since the onset of the disorder.
For many suVerers of OCD, these symptoms take up a great deal of time, often
resulting in their being late for appointments and work and causing considerable
disruption and interference with their lives. Apart from disrupting their own lives,
it also frequently interferes with the lives of family members, as the typical suVerer
often asks the other members to do things a certain way or not to engage in certain
behaviors, as this may prompt the suVerer to engage in rituals. Thus the symptoms
are controlling, frustrating, and irritating not only to the patients, but also to their
families, friends, and workmates.
Avoidance of certain situations or objects that may trigger discomfort and
rituals is also quite common among OCD suVerers. It seems logical to avoid
contact with contaminants if you are a person who washes compulsively, or to
avoid going out of the house if you must check all the electrical equipment, the
doors, and windows. While this seems like a reasonable way of coping, it actually
adds to the problem, as the typical suVerer avoids more and more situations and
gradually the problem comes to rule their life. Moreover, avoidance does little to
deal with the problem as it serves only to reinforce the idea that such situations are
dangerous. Because the situation or object is constantly avoided, there is no
opportunity for the individual to learn that there is no danger.
SE C T I ON 2
2 The causes and treatment of obsessive–compulsive disorder
At the time of writing, no one is certain of the causes of OCD. Though there are a
number of theories that attempt to explain the development of the condition, in
general there is little evidence to support any one of them exclusively. In fact, it
may be best to consider OCD as a complex problem with complex causative
factors. It is most likely that a combination of psychological, biological, environ-
mental and other factors result in the development of the disorder. We do know
that for some the onset is during childhood, while for others the onset may be
during adolescence or early adulthood. We also know that in some cases the onset
367 Obsessive–compulsive disorder: Patient Treatment Manual
is sudden, while others have a slow, insidious onset. Some of the theories that have
been proposed to explain the development of OCD follow and are for information
purposes only.
and, as a result, this issue will be dealt with in much greater detail in subsequent
sections.
ior therapy too diYcult initially may beneWt from a course of medication so that
eVective behavior therapy can be undertaken.
2.6.1 Medication
The medications that have been found to be particularly helpful in the treatment
of OCD come from the antidepressant family of drugs and include clomipramine,
Xuoxetine, Xuvoxamine, and sertraline. They have speciWc eVects on serotonin
levels in the brain. Serotonin is the biochemical substance that some researchers
believe is involved in OCD. In general, these medications have been shown to be
eVective for some OCD suVerers and assist them in bringing their symptoms
under control. If one of these medications is prescribed for you, you should be
made aware of possible side-eVects and report their occurrence to your therapist.
It is important to remember that these medications are not a cure for OCD. In
addition, research indicates that ceasing the medication in the short term generally
results in a return of symptoms. It could be that suVerers need to remain on the
medication for long periods of time or that behavior therapy should be used in
conjunction with the drug.
Engaging in the ritual brings about an immediate and dramatic decrease in both
these measures.
Urge/ 4
discomfort
Though the decrease may be short lived, the individual very quickly learns that
the discomfort may be reduced again by performing the ritual. The more anxious
the individual feels, the more ritualizing they engage in. This is further worsened
by their inability to concentrate on what they are doing to the extent that they are
unsure that the ritual was conducted properly. This adds to their anxiety, which
they try to bring under control by ritualizing further. For example, an individual
who checks electrical equipment, doors, and windows prior to leaving home learns
very quickly that checking alleviates the discomfort associated with the thought
that the house may burn down or be broken into. The individual may have to
perform the checking rituals a number of times in order to gain some relief. If he
or she is under pressure from other sources and is preoccupied or distracted by
these other worries, then they will have to engage in the rituals many more times
because they may not have been done ‘‘correctly’’ the Wrst few times. Having seen
how compulsive rituals are maintained, the important question is what can be
done to break the vicious cycle between the discomfort-producing thought and
the anxiety-reducing rituals. Again, research into the condition provides the
answer.
371 Obsessive–compulsive disorder: Patient Treatment Manual
SE CT I O N 3
3 Exposure and response prevention
Investigators looking at the phenomenology of OCD examined what happened
when suVerers were exposed to stimuli that triggered rituals and were asked not to
engage in their rituals. Initially, there was a signiWcant rise in anxiety, discomfort,
and urge to ritualize. Rather than continue to get worse, however, this rise
remained quite steady and then gradually decreased so that by the end of the
session, the level of discomfort had almost returned to normal. When this process
was repeated again and again, the surprising Wnding was that the initial discomfort
and anxiety was less with each exposure and the time taken to return to normal
was shortened so that eventually exposure to the stimulus would result in a
‘‘hiccup’’ in anxiety that would then quickly settle. The initial Wndings of this
research are demonstrated in the following diagram.
Urge/
discomfort
confronted with triggers for the rituals, but the most important change is that the
individual is now in a position to control the problem rather than be controlled by
it.
When suVerers are made aware of this form of treatment, the initial reaction is
either one of disbelief that such simple methods may work or, alternatively, that it
appears extremely diYcult. First, this form of treatment is not as simple as it
seems. The approach must be structured, planned, and systematic in order to have
maximum beneWt. The individual needs to be motivated and consistent in his or
her eVorts to overcome the problem and faithfully follow all homework and clinic
assignments. Approaching the problem in a haphazard manner will invariably
result in a less than optimal outcome, with suVerers feeling disappointed, frus-
trated, and hopeless. A consistent and planned approach ensures that the problem
is dealt with in a systematic manner. Any diYculties encountered can be quickly
dealt with by the patient with the assistance of the therapist. Second, for those who
see this approach as too diYcult, the fact that the treatment program is planned by
you in conjunction with the therapist ensures that the pace is at a level you are
capable of mastering and the various steps can be graded to maximize your
chances of success.
problems have been with you for a considerable period of time and are probably
well ingrained in your daily routine. Overcoming these diYculties will most
certainly take time and you should allow yourself as much time as it takes to get
yourself better. You don’t need to add to your diYculties by being impatient.
Second, progress is not in a straight line but tends to be Xuctuating so that having
occasional bad days is the rule rather than the exception. The two graphs below are
to demonstrate the diVerence between what people expect to happen and what
actually happens.
EXPECTATION ACTUAL
IMPROVEMENT
IMPROVEMENT
Time Time
Most people expect the response to treatment to be linear, i.e. they start
treatment and expect to get better and better. What actually happens, however, is
that there are Xuctuations from day to day, with some days being worse or better
than others. When the Xuctuations in the right-hand graph above are evened out
(dotted line), it becomes obvious that the individual is improving, even though at
times it may not feel as though they are getting better. They may even feel as
though they are slipping back. It is important to reassure yourself that having a
bad day does not mean that the situation is hopeless or that you are back to square
one. In fact, the only individuals sure to return to square one are those who lose
their motivation and no longer persist with the program.
Another basic requirement for a positive outcome is, for want of a better word,
honesty. You need to be honest with yourself and your therapist in terms of your
fears, avoidance, rituals, and thoughts. At times, individuals who know they have
to be exposed to situations that they have avoided for long periods of time will
avoid telling the therapist about similar situations or will not complete homework
assignments. This does nothing to help the suVerer overcome the problem in any
way. Telling yourself that the problem will be dealt with later is just another form
375 Obsessive–compulsive disorder: Patient Treatment Manual
As you progress through the program, you will gradually gain conWdence in dealing with the OCD
problems. In order to gain this sense of mastery over the problem, it is essential that you do not use
anxiety-reducing drugs, illegal drugs, or alcohol while participating in the program, as use of such
substances results in your attributing positive changes to the drugs rather than to yourself.
SE CT I O N 4
4 The treatment program
In previous sections an outline of the rationale and principles of treatment have
been discussed. This section will review some of the important points and discuss
the design of your treatment program. As mentioned above, treatment consists of
repeatedly exposing the individual for prolonged periods (45 minutes to 2 hours)
to circumstances that produce discomfort. In the initial sessions, such exposure
will be under the supervision of your therapist, who will be with you throughout
the task. Sessions may be conducted at the clinic, at your home, or in other settings
where the rituals are a problem. The exposure is graded so that moderately
disturbing situations are eVectively dealt with before you proceed to more diYcult
376 Treatment of Anxiety Disorders
ones. By breaking down the problems into steps and mastering each step before
moving on to the next, you will Wnd that what may seem like insurmountable
problems become manageable. The sessions are held daily, with daily homework
tasks being set during each session.
The importance of homework tasks cannot be overestimated, as it is with
performance of these tasks that most of the treatment gains will occur. It is of little
use to engage in the exposure and response prevention only while at the clinic. By
completing your homework tasks faithfully, you are ensuring that what is being
achieved at the clinic will transfer to the outside environment as well as reinforcing
what has been learned during each session. Throughout the exposure, individuals
are requested to refrain from ritualizing, regardless of the urges to do so. You
should be prepared to experience some discomfort but you can rest assured that it
will be considerably less than what you will anticipate. In fact, this is one of the
major diYculties when describing this type of treatment to patients. Most suf-
ferers fear that when exposed to a stimulus that evokes discomfort their anxiety
will continue to rise for as long as they do not perform the ritual, until it eventually
becomes unbearable. This is not the case. As described in previous sections, the
discomfort will peak and then gradually decay, and each subsequent exposure will
be less distressing and the decay will occur more rapidly.
Cue or trigger: Touching a cup or plate that someone else has used at my home
Ritual: Washing my hands with disinfectant repeatedly until they feel clean SUDs
377 Obsessive–compulsive disorder: Patient Treatment Manual
Example 2
Ritual: Telling myself I love my child and would never harm it and making SUDs
sure my partner is around when I’m near the child
Example 3
Ritual: Listen for the click of the lock and return six times to make sure the
door is Wrmly locked SUDs
Cue or trigger:
Ritual: SUDs
Cue or trigger:
Ritual: SUDs
378 Treatment of Anxiety Disorders
Cue or trigger:
Ritual: SUDs
Cue or trigger:
Ritual: SUDs
Cue or trigger:
Ritual: SUDs
Cue or trigger:
Ritual: SUDs
379 Obsessive–compulsive disorder: Patient Treatment Manual
4.1.1 Avoidance
Individuals with OCD will often avoid situations that will provoke the thoughts or
urge to ritualize. For example, someone with intrusive blasphemous thoughts may
avoid church or anything of a religious nature. Someone with a fear of being
contaminated may avoid hospitals, doctors’ surgeries, people who are ill, etc. In
this section, please list all situations, objects, etc. that you avoid because they will
cause you discomfort.
Avoidance SUD
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
380 Treatment of Anxiety Disorders
1.
2.
3.
4.
5.
381 Obsessive–compulsive disorder: Patient Treatment Manual
Exposure session
Session number: Date:
Exposure task 1:
DiYculties:
Exposure Task 2:
DiYculties:
Comments:
382 Treatment of Anxiety Disorders
SE C T I ON 5
Recommended reading
5.1 Recommended paperbacks
The following books are available from most large bookstores, many smaller ones,
and some newsstands. If in doubt, ask if the book can be ordered. We also suggest
that you use your local library to gain access to these books. When you read these
or any similar books on the management of anxiety, remember that they are best
regarded as guidelines only. Be critical in both a positive and negative sense when
reading these books, so that you get what is best for you out of them. These books
are inexpensive.
Foa E, Wilson R. (1991) Stop Obsessing! How to Overcome Your Obsessions and Compulsions.
Bantam Books.
Steketee G, White K. (1990) When Once Is Not Enough: Help for Obsessive Compulsives. Oakland,
CA: New Harbinger.
20
Clinical description
GAD is characterized by generalized and persistent symptoms of anxiety, which
are driven by worry. The worry is out of proportion to the feared event, pervasive,
and diYcult for the individual to control. The content of these worries usually
covers several domains, primarily concerns for one’s family, Wnances, work and
personal health. Individuals with this disorder usually describe themselves as
sensitive or nervous by nature, and their tendency to worry is usually longstand-
ing, or at least of several months duration. The symptoms of anxiety usually
involve motor tension (such as restlessness, trembling, or muscle tension) and
overarousal (feeling keyed up or ‘‘on edge’’, irritable, or experiencing diYculty
concentrating). Longstanding worry and anxiety may contribute to excessive
tiredness, tension headaches, epigastric disturbances, and insomnia.
CASE VIGN ET TE
Patient identification
Ms. G is a woman in her mid 30s. She is married with two children now aged 4 and 7 years.
Presenting problem
Ms. G had been troubled by worry for many years. She described herself as ‘‘a born worrier’’.
Recently she had particularly worried about her family’s health – fears that had been
exacerbated by her husband suffering a serious illness several years previously. She stated
‘‘since then every time he mentions something, however minor, feeling tired, not eating as
much as I think he should, I worry that he’s getting sick again. And I won’t stop worrying until
he’s been to see the GP and I’m convinced that it is nothing serious. And the kids too, I know
it’s ridiculous, but I’m constantly thinking about what might happen to them, even to the
point of thinking how I would cope, and having to visit them in hospital, and worse . . .’’. She
had tried to deal with these worries by seeking reassurance from family, friends and her
general practitioner. Other worries included what other people thought of her, whether she
might have said something to upset them. If her husband was late home – or even if he
wasn’t late – she worried that he had been in an accident. Some time ago she became
concerned about global warming and the possibility that she might lose her house to
flooding.
In regard to associated symptoms of anxiety, Ms. G reported feeling jumpy and nervous for
much of the time. She said ‘‘I’ve never really been able to sit still, I always have to be on the
386 Treatment of Anxiety Disorders
go’’. She also described significant muscle tension that sometimes resulted in aching and
stiffness in her neck and shoulders. During periods of increased worry she reported difficulty
getting to sleep and a loss of appetite.
Diagnosis
Prior to DSM-III-R, GAD had the status of a residual diagnostic category. Partly as
a result of this residual position, the validity of the disorder has been brought
under question. However DSM-III-R and DSM-IV no longer describe GAD as a
residual category, consistent with evidence that it can exist independently of
anxiety that is related only to the anticipation of panic or exposure to phobic or
obsessive concerns (often simply referred to as anticipatory anxiety) (Barlow et al.,
1986a). Thus a diagnosis of GAD can be made in a person with panic disorder
provided that the worry is unrelated to having a panic attack. Likewise, GAD and
social phobia can coexist if anxiety is not only related to a fear of negative
evaluation but also results from the presence of pervasive worries about day-to-
day concerns.
An additional change to DSM-IV has been the exclusion of autonomic symp-
toms from the list of required somatic symptoms. The low rate of endorsement of
autonomic symptoms by GAD patients (Marten et al., 1993), together with the
Wnding that symptoms within the motor tension and scanning and vigilance
clusters are more closely associated with independent measures of GAD than
symptoms from the autonomic activity cluster (Brown et al., 1995) support this
change. Data from a nonclinical population using the Depression, Anxiety and
Stress Scale (Lovibond and Lovibond, 1995) also supports the notion that worry is
more closely associated with tension or stress symptoms than with the autonomic
cluster of symptoms (Lovibond, 1998). Similar Wndings in a nonclinical sample,
387 Generalized anxiety disorder: Syndrome
and clinical interest, as there is considerable overlap between these two disorders.
Breslau and Davis (1985) argued that – given the scant evidence of temporal
separation of episodes in patients who meet criteria for both GAD and depression
– either the designation of residual status to GAD is justiWed or GAD may
constitute a subtype of major depressive disorder. The lack of speciWcity of
response to pharmacotherapy across GAD and major depression has also led to
speculation that GAD may be a prodromal or residual entity of a mood disorder
(Casacalenda and Boulenger, 1998). On the other hand, there are studies that
suggest that GAD and major depressive disorder can be discriminated signiWcantly
in terms of scores on the Hamilton Depression and Anxiety Rating Scales (Riskind
et al., 1987; Copp et al., 1990) or the Depression Anxiety Stress Scales (Lovibond
and Lovibond, 1995; Brown et al., 1997). A large study of female twins assessing
the role of genetic factors in the etiology of GAD has found that these genetic
factors were completely shared with those for major depressive disorder (Kendler
et al., 1992b). The Wndings suggest that, in women, the genetic vulnerability to
GAD and major depression is likely to be the same, but whether one or the other
disorder develops is likely to be a result of environmental experiences.
A more diYcult diVerential diagnosis may occur in the case of GAD and
dysthymia. In a review of the relationship between these two disorders, Riskind et
al. (1991) pointed out that both disorders are characteristically low grade, cross-
situational, and chronic. They concluded, on the basis of a systematic search of the
literature and unpublished data sets, that support for the diVerentiation between
GAD and dysthymia is equivocal.
OCD is commonly comorbid with GAD (Sanderson and Wetzler, 1991) and
hence may pose another diVerential diagnosis dilemma. While the worry shown
by GAD patients may often appear to be obsessive and ruminative in nature, it is
possible to clinically diVerentiate between the worry observed in GAD and the
obsessive thoughts observed in OCD. Turner et al. (1992a) Wrst reviewed these two
types of thinking process, and noted that while there are shared features, the two
can be diVerentiated. GAD worries are typically self-initiated (as opposed to the
unwanted and intrusive nature of obsessions), are ego-syntonic (as opposed to
ego-dystonic), and are related to an undeWned set of ongoing concerns in an
individual’s life (as opposed to being conWned to a speciWc set of concerns, such as
contamination, violence, or blasphemy). Likewise Abramowitz and Foa (1998)
argued that worry in GAD and obsession in OCD are distinct phenomena. They
found that the presence of comorbid GAD in patients with OCD was not
associated with severity of obsessions or compulsions, but rather with greater
levels of indecision, an excessive sense of responsibility, and excessive worry about
everyday concerns. Langlois et al. (2000a,b) found a number of diVerences, but
also some overlap, between worry and obsessions in a nonclinical population and
389 Generalized anxiety disorder: Syndrome
Comorbidity
Since GAD has been able to be diagnosed independently from other disorders, the
problem of high comorbidity with other anxiety and depressive disorders has
become apparent. Studies of both clinical and community samples have shown
that ‘‘pure’’ cases of GAD are rare (Sanderson and Wetzler, 1991; Brown and
Barlow, 1992; Brawman-Mintzer et al., 1993; Wittchen et al., 1994; Yonkers et al.,
1996). Using NCS data, Wittchen et al. (1994) reported comorbidity with another
mental disorder in 90.4% of the sample with a lifetime history of GAD. The most
frequent comorbid disorders were major depression, panic disorder, and (for
current comorbidity only) agoraphobia. The odds ratios reported were not
strongly aVected by the use of diagnostic hierarchy rules. Judd et al. (1988)
reported that 84% of the NSC GAD sample had a comorbid lifetime mood
disorder.
Even when other diagnoses are not met, a large proportion of GAD patients
report experiencing at least one panic attack (73%; Sanderson and Barlow, 1990)
390 Treatment of Anxiety Disorders
and experience social phobic concerns (75%; Rapee et al., 1988). Moreover, Rapee
et al. (1988) found that 79% of patients with a primary diagnosis of GAD reported
at least one moderate fear, and 61% of patients report sometimes avoiding at least
one social situation.
Maser (1998) has argued that the high rates of clinical or subclinical GAD
comorbid with other anxiety or depressive disorders may be responsible for the
broad occurrence of worry across these other disorders, and a resulting lack of
speciWcity of this feature. Using ECA data, Bienvenu et al. (1998) compared the
demographic and comorbidity proWles across Wve samples comprising patients
with a DSM-III-R diagnosis and four subthreshold groups. They found groups
were comparable in respect to the demographic and comorbidity variables
whether or not the worry criterion was met or whether the anxiety and associated
symptoms were of 1 month or 6 months duration. The only group that diVered
from the GAD diagnosis group was that which had less than the required six
associated symptoms. These authors argue against the construct validity of the
DSM-III-R diagnostic criteria for GAD.
The associated somatic symptoms also suVer from a lack of diagnostic speciWc-
ity. Brown et al. (1995) reported that, while most of a sample of patients with GAD
endorsed the three of six symptoms required in DSM-IV, a large proportion of
patients with other anxiety or mood disorders also fulWlled this criterion. How-
ever, not all patients with a principal diagnosis of another anxiety disorder meet
diagnostic criteria for GAD (Sanderson and Wetzler, 1991), suggesting that, while
symptoms of generalized anxiety are common to other anxiety disorders, these
symptoms are not synonymous with the syndrome of GAD.
But there is also evidence supporting the validity of GAD as an independent
diagnostic construct. An assessment of the genetic and environmental contribu-
tions speciWc and common to GAD and panic disorder in a cohort of male–male
twin pairs has shown a genetic liability that is speciWc to panic disorder, suggesting
that the two disorders are at least partially etiologically distinct (Scherrer et al.,
2000). Breitholtz et al. (1999) found signiWcant diVerences in the content of
thinking between GAD and panic disorder patients, hence supporting the cogni-
tive speciWcity of the two disorders. Likewise, Abramowitz and Foa (1998) have
argued that worry in GAD and obsessions in OCD are distinct phenomena. They
found that the presence of comorbid GAD in patients with OCD was not
associated with severity of obsessions or compulsions but rather with greater levels
of indecision, an excessive sense of responsibility, and excessive worry about
everyday concerns. Brown et al. (1993) found that, while many of a sample of
OCD patients endorsed worry symptoms, OCD and GAD patient groups could be
reliably distinguished diagnostically by clinical interview. Lastly, an examination
of the construct validity of diagnoses across the anxiety and depressive disorders
showed that patients with a diagnosis of GAD had a unique score proWle across a
number of self-report measures, and that proWle signiWcantly diVerentiated pa-
tients with GAD from other diagnostic groups (Zinbard and Barlow, 1996).
392 Treatment of Anxiety Disorders
worry as an attempt to avoid negative events or prepare for the worst; because the
worst rarely eventuates, the function of worry is negatively reinforced. Lastly,
worry about relatively unimportant day-to-day concerns may function as a dis-
traction from more emotionally laden topics.
Davey and Levy (1998) have investigated the process of catastrophic worry,
typically associated with a ‘‘What if . . .’’ questioning style, where worriers adopt
progressively worse and worse outcomes related to a speciWc topic. Of prime
interest was the question of what caused worriers to continue to generate cata-
strophic steps despite increases in subjective discomfort. During a ‘‘catastrophiz-
ing interview’’, chronic worriers displayed a general perseverative iterative style in
that they were more willing than nonworriers to catastrophize across a range of
topics, including those that were novel or pleasant. They also found that chronic
worriers tended to couch their catastrophizing in terms of personal inadequacies,
perhaps stemming from dysfunctional beliefs. Davey and Levy hypothesized that
core beliefs of self-doubt might make it diYcult for individuals to obtain closure
on their problems, leading to more catastrophizing steps, and hence greater
opportunity to perceive the negative consequences that might result from personal
inadequacies.
matters than the panic disorder patients. Conversely, the panic disorder patients
had more thoughts of physical catastrophe. Across worry topics, patients with
GAD worry more about remote and future events than do anxious control
patients (Dugas et al., 1998).
The level of perceived control over worries can discriminate GAD patients from
nonanxious controls: GAD patients perceive less control over their worries and
report a greater proportion of unprecipitated worries (Craske et al., 1989). Butler
and Booth (1991) have pointed out additional features that tend to characterize
the cognitions of patients with GAD. Accordingly, the worries of these patients
tend to reXect a perceived vulnerability and threat (e.g., ‘‘Something will go
wrong’’) and a perceived lack of personal coping skills (e.g., ‘I won’t be able to
manage’’).
nonanxious control group. Even when the number of events were controlled, the
GAD patients perceived minor events to be signiWcantly more stressful. This
Wnding is in keeping with Barlow’s model that predicts that an increasing vulner-
ability to anxiety guarantees that the relatively minor events or disruptions to
one’s life become the focus of worry.
Drawing from evidence of the nature of worry in GAD and data from informa-
tion-processing paradigms in anxious individuals, Rapee (1991b) has developed a
model of the maintenance of GAD from an information-processing perspective.
In summary, individuals with high levels of generalized anxiety have been shown
to allocate extensive attentional resources to the detection of threatening informa-
tion and hence have a ‘‘lower threshold’’ for threatening information (e.g.,
MacLeod et al., 1986; Dibartolo et al., 1997). There is evidence that threat-related
information may be more accessible in memory to these individuals, resulting
from selective encoding of further such information (e.g., Butler and Mathews,
1983; MacLeod and McLaughlin, 1995). Drawing on models of semantic net-
works, Rapee (1991b) proposed that once threat-related information has been
accessed, there is activation of the anxiety node, which in turn will further lower
the threshold for threat-related material. Activation of the anxiety node will also
elicit information about potential responses to the threat, and the likelihood that
these responses will successfully deal with the threat. It is argued that, if the
information is consistent with successful control of the threat, then the activation
of the anxiety node will be inhibited. Patients with generalized anxiety report that
they lack control over threat and hence are less likely to experience this inhibition.
Rapee has further argued that worry is a conscious and attention-demanding
process that, through its hypothesized activity in working memory, may have an
inhibitory eVect on anxious aVect. The resulting reduction of anxiety may thereby
reinforce the role of worry.
Dugas et al. (1998) have developed a cognitive behavioral model of GAD in
which a primary role is given to the concept of ‘‘intolerance of uncertainty’’,
contributing to the typical ‘‘What if . . .’’ questioning style of these patients. Some
preliminary support has been given to the role of this construct in worry. An
experimental study that aimed to manipulate the level of intolerance of uncertain-
ty in a nonclinical sample indicated that greater levels of intolerance of uncertainty
led to reports of increased worry (Ladouceur et al., 2000b). Second, beliefs about
worry such as ‘‘worry helps to avoid disappointment’’ or ‘‘worry protects loved
ones’’, like Borkovec et al.’s ‘‘worry to avoid negative events’’, may be negatively
reinforced by the nonoccurrence of the feared event central to the worry. Third,
GAD patients lack conWdence in their own ability to solve problems rather than
lack problem-solving skills per se (Ladouceur et al., 1998). Lastly the model
incorporates the role of cognitive avoidance, which, in keeping with Borkovec et
396 Treatment of Anxiety Disorders
Conclusions
The concept of worry and the associated somatic symptoms of motor tension and
vigilance are central features of GAD. Little is known about speciWc etiology, but
GAD is likely to share a common vulnerability with other anxiety and depressive
disorders. A number of theoretical models have been developed and the research
397 Generalized anxiety disorder: Syndrome
they continue to generate will add greatly to our understanding of this disorder.
The weak evidence of diagnostic reliability, the high rates of comorbidity and the
need for greater speciWcity of certain features of GAD are some of the issues that
require further investigation. Even if GAD comes to hold a unique position within
the anxiety disorders – as the ‘‘basic’’ anxiety disorder – it is unlikely that it will
disappear from the diagnostic classiWcation systems. Epidemiological surveys have
shown that GAD is prevalent, chronic, and largely unremitting. Despite the
disability associated with the disorder, the majority of suVerers do not receive
treatment. However, Chapter 21 will demonstrate that treatments are available
that produce clinically signiWcant and long-lasting improvement.
21
The goal of the treatment of GAD is the reduction of impairment that results from
both cognitive and somatic symptoms of anxiety: the worry or anxious expecta-
tion, and the accompanying symptoms of tension and overarousal. This chapter
aims to summarize the evidence for the eVectiveness of psychological and pharma-
cological treatments for GAD.
Psychological treatments
Since the Wrst edition of this book was published, Wve reviews of the psychological
treatment of GAD have been published (Barlow et al., 1998; Borkovec and
Whisman, 1996; Fisher and Durham, 1999; Gale and Oakely-Browne, 2000; Gould
et al., 1997). All agree that a cognitive behavioral approach is eVective for this
disorder, a Wnding that is consistent with previous quantitative and qualitative
reviews (e.g., Marks, 1989; Butler and Booth, 1991; Hunt and Singh, 1991;
Durham and Allan, 1993). Hence, there is general agreement that cognitive
behavioral therapy yields statistically and clinically signiWcant improvement for
the majority of patients, and that this change is maintained for up to a year
following the end of treatment.
However there is less agreement on the extent to which diVerent therapies
produce diVerential eVects. For example, Barlow et al. (1998: 311) stated ‘‘Until
recently, most studies have not demonstrated diVerential rates of eYcacy for
active treatment techniques, although most studies have shown that active treat-
ments are superior to non-directive approaches and uniformly superior to no
treatment’’. Fisher and Durham (1999) applied Jacobson’s criteria for clinical
signiWcance to six randomised controlled trials using the State–Trait Anxiety
Inventory, Trait Version (STAI-T) as an outcome measure and showed that both
cognitive behavioral therapy and applied relaxation produced recovery rates at
6-month follow-up of 50% to 60%. On the other hand, their results indicated
that some individual therapies (behavior therapy and analytical therapy) were
ineVective, with recovery rates of 11% and 4%, respectively. Of further interest
398
399 Generalized anxiety disorder: Treatment
was the Wnding that individual therapy produced higher recovery rates than the
same treatment delivered in a group format. Fisher and Durham (1999) con-
cluded that while cognitive behavioral therapy may not be the only treatment to
deliver reasonable treatment outcome eVects, it is unlikely that the eVects ob-
served were solely due to spontaneous remission, regression to the mean, or
placebo factors.
Gould et al. (1997b) reported the results of a meta-analysis of 22 controlled
trials of broadly deWned ‘‘cognitive behavioral therapies’’. They concluded that
there were no signiWcant diVerences between the eight trials of cognitive and
behavioral techniques (mean anxiety eVect size of 0.91) and the three trials of
relaxation training (mean anxiety eVect size of 0.64). Of note was the Wnding that
the mean eVect size for measures of depression was also substantial across the
‘‘cognitive behavior therapies’’ (mean depression eVect size of 0.77). In the trials
where follow-up data were available, the analysis conWrmed that the beneWcial
eVects of therapy were maintained over time. Analyses were conducted to statisti-
cally assess the inXuence of a range of variables – including sex, duration of
disorder, use of concurrent medication, group versus individual format, or treat-
ment duration – but no variable was found to be signiWcantly associated with
outcome.
Combining information from a range of available evidence, Gale and Oakely-
Browne’s (2000) contribution to the British Medical Journal Clinical Evidence
series concluded that the only intervention likely to be eVective with a high degree
of reliability is cognitive behavioral therapy. The approach used in this review
grades intervention studies in their ability to predict treatment eVectiveness (with
systematic reviews with meta-analysis of randomized controlled trials seen to
provide the most reliable evidence and expert opinion as the least reliable).
Cognitive behavioral therapy was deemed to be eVective on the basis of two
systematic reviews of randomized controlled trials that found it to be more
eVective than remaining on a wait-list, anxiety-management training alone, or
nondirective therapy. However, applied relaxation was deemed to be of unknown
eVectiveness as one systematic review had not established or excluded a clinically
important diVerence between applied relaxation and cognitive therapy.
In conclusion, the reviews are largely in agreement despite the use of diVerent
methods to summarize the treatment outcome results. Cognitive behavioral
therapy is certainly superior to no treatment and appears to be superior to
nondirective treatments. Of interest, however, is a recent trial in adults over 55
years of age that found no diVerences between group-based cognitive behavior
therapy or supportive psychotherapy at posttreatment and at the 6-month follow-
up across all measures of anxiety, worry, and depression (Stanley et al., 1996). As
Stanley et al. pointed out, it remains to be seen whether potential diVerences in the
400 Treatment of Anxiety Disorders
may be possible that the conduct of the therapy in such large-sized groups may
have diluted the treatment eVects.
Two studies have demonstrated that cognitive or cognitive behavioral therapy
produced signiWcantly greater improvement than the other active treatments
tested. Butler et al. (1991) compared cognitive behavioral therapy to behavior
therapy and found at the 6-month follow-up that cognitive behavioral therapy
produced signiWcantly greater improvements than behavior therapy on measures
of anxiety, depression and cognition. Furthermore, there were fewer dropouts
from therapy in the cognitive behavioral condition. Durham and colleagues
compared cognitive therapy, analytical therapy (delivered by experienced thera-
pists across two levels of intensity) and anxiety-management training (delivered
by inexperienced therapists) (Durham et al., 1994, 1999). At the 1-year follow-up
cognitive therapy was signiWcantly more eVective than analytical therapy or the
anxiety-management training. The results suggested that cognitive therapy de-
livered weekly showed greater improvement over the follow-up on some measures
than when delivered fortnightly. The authors suggest that a higher intensity
treatment may be important in a disorder that is often characterized by high rates
of comorbidity and disablement, which in themselves appear to inXuence progno-
sis following treatment (Durham et al., 1997).
As worry has been given a central role in GAD, it seems important that speciWc
therapeutic strategies be directed towards the cognitive aspects of this disorder. In
Chapter 20, we saw that individuals who suVer from GAD describe their worries as
diYcult to control, excessive and hence out of proportion to the actual reality of
the feared outcome. The characteristics of these cognitive aspects are amenable to
cognitive therapy that aims to address unrealistic and erroneous beliefs, attitudes,
and expectations. The eYcacy of cognitive behavioral treatment packages for this
disorder tend to support the case for such an approach to the amelioration of
worrying thoughts, particularly in studies in which the measurement of worry has
been included (e.g., Lindsay et al., 1987; Butler et al., 1991). In further support is
the Wnding from one study that higher levels of apprehensive expectation or worry
prior to cognitive behavioral treatment was signiWcantly predictive of greater
anxiety symptoms following treatment, irrespective of the level of anxiety symp-
toms prior to treatment (Butler, 1993).
More recently there has been an emergence of treatment packages speciWcally
designed to address worry, with the rationale that a decrease in worry will produce
concomitant changes in related subsystems (such as a decrease in somatic symp-
toms of anxiety) without these subsystems being speciWcally targeted (such as by
relaxation training). Such treatments have been derived directly from research
into the psychopathology of worry and conceptual models of GAD. Ladouceur
et al. (2000a) conducted a wait-list controlled trial of a cognitive behavioral
402 Treatment of Anxiety Disorders
common in primary care and whose suVerers tend not to reach specialist treat-
ment programs.
Pharmacological treatments
For many years, benzodiazepines were the preferred pharmacotherapy for GAD
and considered the treatment of choice (e.g., Rickels, 1987; Dubovsky, 1990;
Gorman and Papp, 1990). There is ample evidence to conclude that the benzo-
diazepines are safe and provide eVective symptomatic relief for the majority of
patients. Furthermore, numerous trials have shown that all benzodiazepine
groups appear to be equally eVective (Gould et al., 1997b; Roy-Byrne and Cowley,
1998). In their meta-analytical study, Gould et al. (1997b) reported a mean anxiety
eVect size of 0.70 across 23 controlled trials of benzodiazepine therapy, equivalent
to that calculated across all the ‘‘cognitive behavioral’’ therapies included in that
study. While benzodiazepines undoubtedly produce good short-term treatment
eVects, side-eVects include impaired cognitive performance, drowsiness and leth-
argy with high doses, and physical and psychological dependence following
prolonged use. Discontinuation of benzodiazepine treatment can result in re-
bound anxiety or an intensiWcation of previous symptoms in 25% to 75% of
individuals, in a withdrawal syndrome in 40% to 100%, and a relapse of original
symptoms in 63% to 81% of individuals (Dubovsky, 1990). Few pharmacotherapy
studies address long-term outcome, but in one study using DSM-III-diagnosed
patients, discontinuation of diazepam (when provided as the sole treatment)
resulted in a reversal of treatment eVects (Power et al., 1990). Although there is
little research on long-term pharmacotherapy, some patients will have taken
benzodiazepines for many years without tolerance to their anxiolytic eVects (da
Roza Davis and Gelder, 1991). However, medical, ethical, and legal concerns
surrounding the long-term use of these drugs, particularly in regard to the
potential for dependence, have led to recommendations of intermittent usage,
using the lowest eVective dose for the shortest possible time (Rickels, 1987;
Gorman and Papp, 1990). Gale and Oakley-Browne (2000) have concluded in
their evidence-based review that, although benzodiazepines are, compared with
placebo, an eVective and rapid treatment for GAD, they are not a beneWcial
treatment because of the trade-oV between beneWts and harms. In particular, they
state that benzodiazepines have been found to increase the risk of dependence,
sedation, industrial accidents and road traYc accidents. Furthermore, ben-
zodiazepines have been associated with neonatal and infant mortality when used
in late pregnancy or while breastfeeding (Gale and Oakely-Browne, 2000).
Benzodiazepines should be used particularly cautiously in older adults because of
the greater sensitivity to adverse eVects (Sheikh and Cassidy, 2000).
404 Treatment of Anxiety Disorders
cantly greater than placebo-treated groups and equivalent to the other active
medications studied.
The treatment literature conWrms that benzodiazepine treatment is eVective in
the short-term treatment of generalized anxiety. However the high risk of depend-
ence and the common return of symptoms following discontinuation preclude the
usefulness of these drugs in a chronic disorder. Buspirone, with equal eVectiveness
and an absence of dependence, may well provide a better treatment option, but
tends not to be widely prescribed. This may be due to the lag in eVect, so that
neither patients nor their doctors may be prepared to tolerate the several weeks
that may occur before a decrease in anxiety is experienced. In many of the earlier
pharmacological studies reviewed, it is unknown how many patients would have
fulWlled DSM-IV diagnostic criteria. Furthermore, there is a paucity of long-term
data for any pharmacotherapy, despite epidemiological evidence that for most
individuals GAD is a chronic disorder. Given the increased importance of the
concept of worry in the disorder, particular attention should be paid to the
measurement of the cognitive components of anxiety. It is of interest that most
studies that compared anxiolytic and antidepressant medications concluded that
while overall the outcomes were equivalent, the antidepressant medication pro-
duce greater improvements in measures of psychic symptoms of anxiety.
showed higher rates of subsequent treatment (54% of the group) and lower rates
of ‘‘clinically signiWcant change’’ (30% to 70%) at 6 months following treatment.
While the Wndings of Power et al. (1990) require replication, they do suggest
that the judicious use of long-acting benzodiazepines may not signiWcantly
interfere with cognitive behavioral therapy in individuals who have sought treat-
ment for GAD. However, the cognitive behavioral treatments achieved similar
clinical change in the absence of active pharmacological treatment. Therefore,
while the use of benzodiazepines may not interfere with cognitive behavioral
therapy, they do not appear to add to the treatment eVect and the potential for
adverse eVects must be taken into consideration. In contrast, a review of psycho-
logical treatments in GAD (Durham and Allan, 1993) found that, across a number
of studies, outcomes indicating above-average improvement in symptom
measures and clinically signiWcant changes were associated with patient samples
that were free from anxiolytic medication. No data appear to be available concern-
ing the combined use of psychological treatment and antidepressant medication.
Clearly, the role of pharmacotherapy as an adjunct to psychological treatment in
GAD has yet to be established.
Conclusions
The cognitive behavioral therapies appear to be at least as eVective in the short
term as pharmacotherapy, cause no adverse eVects in terms of side-eVects and
withdrawal syndromes, and aim to increase coping skills, and hence increase the
sense of control and mastery in patients. In other anxiety disorders, the same
strategies have been shown to bring about long-term changes in measures thought
to represent vulnerability to neurosis (Hunt and Andrews, 1998). Our present
knowledge suggests that treatment should include, at the very least, education
about the nature of the disorder and should address the beliefs, attitudes, and
expectations relevant to an individual’s worries and fears.
Despite the existence of eYcacious treatments, there is still much to be done.
For example, it will be important to replicate many of the reported treatment
eVects in DSM-IV samples and in the delivery of treatment in routine care.
Furthermore, the development of treatments appropriate to the primary care
setting will be important for the majority of GAD suVerers who will never reach
specialist treatment settings. It will also be important for future outcome studies
to target the prominent feature of worry in terms of assessment and treatment.
22
The present chapter aims to guide clinicians in the principles of treatment and the
use of the treatment Manual, as well as highlight some of the more common
problems encountered in therapy. While further studies are needed to identify the
active components of eVective treatment for generalized anxiety disorder, it
appears that two core elements are:
∑ An underlying rationale, based on the ‘‘coping skills’’ model of cognitive
behavioral therapy, where patients are taught skills to manage their anxiety and
to take responsibility for change and control over their thoughts, feelings, and
behavior.
∑ Cognitive therapy with the goal of bringing the process of worry under the
patients control.
Relaxation training, usually a form of progressive muscle relaxation, is a useful
adjunct to treatment, particularly where the eVects of chronic and high levels of
muscle tension trouble an individual.
Assessment
It is assumed that before the commencement of treatment, a clinical assessment
will have ruled out comorbid diagnoses in need of immediate speciWc treatment,
such as a major depressive episode. Where depression is present, it becomes the
treatment priority and the need for further treatment of anxiety symptoms
reviewed when the depression is resolved. Given the phenomenological similari-
ties between the two disorders, it is often necessary to establish from historical
information whether GAD existed before the onset of a major depressive episode,
or to assess whether a GAD continues to exist following eVective treatment of the
depressive disorder.
While patients with a primary diagnosis of GAD will not always meet criteria for
another diagnosis, they will often have concerns and behaviors that are character-
istic of other anxiety disorders. Panic attacks, social anxiety, phobic avoidance,
obsessions, and illness anxiety are common. The treating clinician will therefore
407
408 Treatment of Anxiety Disorders
need to be able to recognize these diVerent features and address these in the course
of treatment. For example, some time can be spent focusing speciWcally on fears of
scrutiny and negative evaluation or fears that a physical sensation is really a sign of
a serious, life-threatening illness within the framework of the cognitive behavioral
approach. The use of a slow-breathing exercise (possibly due to its meditation-like
features) can provide temporary control over acute episodes of high anxiety for
many individuals. Hence patients can be relatively quickly provided with an
increased sense of control that allows them to recognize the triggers of their
anxiety and implement cognitive strategies. The diVerentiation between obsessive
thoughts and worries or ruminations has been outlined in Chapter 20, and careful
assessment may be required to diVerentiate these types of thinking. It will also be
important that the individuals themselves are taught to recognize the diVerence
between obsessions and worries/ruminations and then implement the appropriate
management strategy (see treatment of obsessive thoughts in Chapter 17).
The relationship between diVerent thoughts, feelings, or behaviors may require
a certain amount of detective work between the patient and the therapist. Like-
wise, the formulation of strategies to deal with such diYculties may not be entirely
straightforward. A collaborative approach with the patient is vital, with interven-
tion often framed in the following way: ‘‘I wonder whether these factors could be
causing this problem? What strategies do you think would be useful, given our
understanding of anxiety and the strategies we have learned about so far? How
about we put them into practice and see whether they make a diVerence?’’
Therapists should help patients to use any problems or setbacks that occur during
the course of treatment to provide them with more evidence to reWne problem
formulations and treatment strategies. For example, a thorough behavioral for-
mulation will help to identify situations, events, thoughts, feelings, or behaviors
that continue to trigger or maintain anxiety and hence provide a guide for
improving intervention strategies.
Format
It is likely that most clinicians using this Manual will be seeing patients on an
individual basis. Although the group versus individual format has not been
studied directly, it appears that there is some advantage in an individual approach.
While the structure of treatment can be Xexible, treatment should begin with a
discussion of the goals of treatment for each individual. Between-session monitor-
ing of situations that trigger anxiety, avoidance, and worries can begin from the
Wrst sessions and will help the individual to develop a greater awareness of the
incidence and impact of their worry. The presentation of information and skills as
laid out in the Patient Treatment Manual is a good guide for the order in which
409 Generalized anxiety disorder: Clinician Guide
topics can be covered, beginning with the presentation of information about the
nature of the disorder and the rationale for treatment. Butler and Booth (1991)
suggested that a treatment formulation should be developed at approximately the
fourth treatment session. Further sessions can then be spaced on a weekly (or
2-weekly) basis, over which time skills are consolidated and applied in the
patient’s ongoing life and problems in progress pinpointed and solved. At the
Anxiety Disorders Unit, Sydney, individuals are seen on average for 1 hour weekly
for 8 weeks, then again at a 1-month follow-up session. Later sessions focus on
review and practice of the skills, tailored to each individual’s needs. Appropriate
sections can be used from the Patient Treatment Manuals provided in this book
for the other anxiety disorders if necessary (e.g., dealing with social anxieties from
the Social Phobia Patient Treatment Manual).
The pace of change in individuals in treatment is variable. An expectation of
complete absence of anxiety and worry by the end of treatment is unrealistic for
the majority of individuals. However, it will be important that patients exhibit
evidence that they can successfully apply the skills that are being taught and that
they have consolidated their skills and are able to continue to apply these without
regular therapist contact. Evidence should be sought for such progress, including
the spontaneous and successful use of cognitive strategies outside of the sessions
or the completion of graded exposure tasks.
to come. It may be important to point out that years of habitual thinking and
behaving will not change overnight. It will be critical to ensure that clinicians’ and
patients’ goals and expectations of therapy are matched. For example, if the
patient’s goal is to ‘‘get rid of the anxiety’’, the clinician should present a realistic
alternative such as ‘‘to better manage anxiety (which is an inevitable part of
human existence) so that it ceases to interfere with functioning and cause undue
distress’’. An adequate discussion of such issues, outlining the goals of therapy,
and the provision of information about the nature of anxiety will account for at
least the Wrst session of treatment.
General issues
An emphasis on regular homework is as important in the treatment of this
disorder as in all other anxiety disorders. Patients will soon learn that the strategies
must be well practiced if they are to be successful, particularly in the face of high
levels of anxiety. The importance of regular between-session practice of techniques
when anxiety is relatively low may need to be addressed throughout treatment.
Butler and Booth (1991) outlined the shared characteristics of successful treat-
ments, which include:
∑ A treatment goal of increased self-control and independence on the part of the
patient.
∑ The use of Patient Treatment Manuals, the provision of information about the
nature of anxiety, and a rationale for treatment, record keeping, and homework.
∑ A collaborative relationship between the patient and therapist.
∑ A structure to treatment so that eYcient use is made of time and the important
points of therapy are salient.
Butler and Booth (1991) also suggested that therapists make use of ‘‘formula-
tions’’ and ‘‘blueprints’’ in their treatment programs. Formulations of patients’
problems provide a framework to clarify understanding of symptoms and the
factors maintaining those symptoms in the context of a cognitive behavioral
model of anxiety. These formulations aid in the generation of hypotheses from
which treatment strategies are planned. Blueprints, or detailed plans of work to be
done, that explicitly outline aspects of treatment that have been useful during
treatment can be generated and kept for future reference so that future anxiety
problems can be dealt with eYciently should they arise. The core speciWc treat-
ment strategies are covered in detail in the Patient Treatment Manual. The
material covered is relatively straightforward for a clinician with a good grounding
in cognitive behavioral theory and techniques.
Relaxation therapy
It is unclear that progressive muscle relaxation per se is critical to the amelioration
of GAD symptoms, particularly given the apparent eYcacy of treatments that do
411 Generalized anxiety disorder: Clinician Guide
not contain this component (e.g., Durham et al., 1997; Ladouceur et al., 2000a).
Furthermore, it is possible that the eYcacious eVects of applied relaxation as a
treatment package may be due to the consequence of providing an alternative
strategy to engagement in worry in the face of triggers of worry. However, because
many patients complain of high levels of tension and its eVects, it is a useful skill
that will help individuals to bring their somatic symptoms under control. Regular
practice of relaxation exercises is always encouraged, but it is not recommended
that a large proportion of treatment contact time be spent on this component.
Used alone, relaxation appears to be no more eVective than a placebo (see e.g.,
Hunt and Singh, 1991).
Cognitive therapy
One of the core features of GAD is the pervasive nature of the worry or concern,
unlike the concerns of patients with other anxiety disorders that tend to be fairly
discrete or limited to one general domain. The wide range of worries, beliefs, and
expectations found in patients with GAD will require Xexibility on the part of the
therapist, who may need to address unhelpful thinking over a number of domains.
Worry in generalized anxiety disorder is certainly characterized by catastrophic
interpretations, often couched in terms of personal inadequacies (Butler and
Booth, 1991; Breitholtz et al., 1999; Davey and Levy, 1998; Molina et al., 1998).
These catastrophic interpretations are particularly amenable to standard cognitive
interventions that aim to address unrealistic and erroneous beliefs, attitudes, and
expectations. More often than not, the thinking of individuals with GAD will be
colored by a general perception of threat and they will react with alarm to a
multitude of cues in their day-to-day lives. Such threats can include the telephone
ringing (bringing news of some disaster), meetings with work colleagues (who will
Wnally discover the individual’s incompetence), or symptoms of the Xu (a deadly
virus that the doctors will again ignore).
Often, individuals will feel overwhelmed when they become more aware of the
pervasiveness of their unhelpful thinking. It is then useful to look for general
patterns or themes that can then be targeted. For example, a belief that one is
incompetent can drive a multitude of smaller crises whenever performance is
required or decisions are to be made. Addressing the broad fear (e.g., ‘‘I’m
incompetent, it’s just that nobody has noticed yet’’) and getting individuals to
consider the objective evidence (e.g., ‘‘I’m still employed; nobody has ever com-
plained about my work; my friends all seem to like me; I always manage to get
done what needs to be done’’) may circumvent a number of day-to-day anxieties.
This approach will also serve to make vague and abstract worries more concrete
(see below). However, the individual will need to regularly challenge and dispute
their unhelpful thinking whenever in the presence of cues that may trigger it.
Completing cognitive exercises in writing early in treatment is vital for the success
412 Treatment of Anxiety Disorders
are more concrete or speciWc may also aid the identiWcation of solutions to
potential problems or help to invalidate those worries that are abstract in nature
(e.g., ‘‘I won’t cope’’ or ‘‘I’m incompetent’’).
A key component of the cognitive behavioral model of GAD proposed by Dugas
et al. (1998) is an intolerance of uncertainty. It follows that an important aim of
treatment will be to teach patients to become more tolerant of uncertainty in the
face of ambiguity, both by directly challenging beliefs that certainty is either
achievable or necessary, and indirectly through the use of behavioral experiments.
For example, individuals can be encouraged to undertake activities or make
decisions without the need for excessive amounts of information or reassurance
from others and thus test whether the potential negative outcomes do in fact
occur. Unhelpful beliefs about worry that may serve to maintain worry (Dugas et
al., 1998; Wells and Carter, 1999) can also be challenged directly (e.g., ‘‘What
evidence is there that worry is helping you solve your problems?’’) or more
indirectly (e.g., ‘‘Can we stop the worry and see if the feared event actually
eventuates?’’).
Lastly, because an important goal of treatment is for patients to function
independently of the therapist, the use of reassurance that may in fact discourage
patients from evaluating and challenging their own unhelpful thoughts should be
avoided. While the therapist should provide accurate information about the
disorder, its treatment, and prognosis, one should be wary of providing answers
for patients who continually ask questions such as ‘‘Is this pain really just
anxiety?’’ or ‘‘Will I ever get over this?’’ Such reassurance seeking is best redirected
back to the patient to be dealt with using cognitive techniques. For example, ‘‘I
can’t answer that question. What do you think, given the evidence and our
discussions about anxiety?’’.
Graded exposure
Many individuals with GAD have avoidance of certain situations that will need to
be addressed during the course of therapy, using the principles of graded expo-
sure. However, it is widely acknowledged that much of the avoidance behavior of
these individuals can be quite subtle, and can include things such as avoiding any
stimuli that might be a reminder of their fears (e.g., reading newspapers, talking to
certain people, thinking about certain issues), avoiding interactions that might
cause conXict with others, avoiding solving certain problems, or even forms of
‘‘internal avoidance’’ to prevent full engagement in certain activities (e.g., using
distraction methods, such as counting or singing to oneself). Distraction will not
be a useful anxiety-management technique if it prevents individuals from disput-
ing core beliefs, solving problems, or exposing themselves to what they fear. Most
subtle avoidance can be addressed using the basic principles of graded exposure:
414 Treatment of Anxiety Disorders
setting speciWc behavioral goals that can be broken down into smaller steps if
necessary.
Many patients engage in a range of other unhelpful behaviors in an attempt to
relieve anxiety and distress in the short term (e.g., reassurance seeking, checking)
and these may need to be addressed using the principles of exposure and response
prevention. For example, individuals who worry constantly about the safety of a
loved one may contact them frequently when separated, just to reassure them-
selves that the loved one has come to no harm. Dealing with this worry will
necessarily involve exposure to the cues that may trigger the worry (e.g., separ-
ation from the loved one) and prevention of the reassuring behavior.
and who therefore may take some time to change the traits that make them
vulnerable to anxiety. The reasonable goal that anxiety is to be controlled rather
than ‘‘cured’’ can be reinforced when providing information about anxiety,
making it clear that it is a normal physiological response that may in fact be useful
in a number of situations in an individual’s everyday life.
Conclusions
In conclusion, to return to the advice of Butler and Booth (1991), two of the most
important skills that a clinician can have in dealing with GAD patients are clarity
and creativity. Following latest developments in regard to the psychopathology of
the disorder (in particular worry) will help clinicians to develop more speciWc, and
we hope eVective, treatment strategies for their patients. It is likely that a cognitive
behavioral framework provides clarity and direction to the treatment process,
while the scientist-practitioner approach allows Xexibility and creativity in dealing
with individuals with GAD.
23
This Manual is both a guide to treatment and a workbook for people who suVer
from generalized anxiety disorder. During treatment, it is a workbook in which
individuals can record their own experience of generalized anxiety disorder,
together with the additional advice for their particular case given by their clinician.
After treatment has concluded, this Manual can serve as a self-help resource when
challenges or diYculties are faced.
Contents
Section 1 419
1 What is generalized anxiety disorder? 419
1.1 Generalized anxiety disorder and everyday worry 420
1.2 Medication 420
1.2.1 Antidepressant medication 420
1.2.2 Sedatives, tranquilizers, and sleeping pills 421
Section 2 421
2 The nature of anxiety and worry 421
2.1 The nature of anxiety 421
2.1.1 The anxiety cycle 423
2.1.2 Anxiety and performance 423
2.1.3 Chronic anxiety 424
2.1.4 Why do the symptoms of tension and anxiety begin? 425
2.2 The nature of worry 426
2.2.1 Worry about worry 427
2.2.2 Behaviors that can maintain worry and anxiety 427
2.2.3 Keeping a record of your anxiety or worry 429
*Gavin Andrews, Mark Creamer, Rocco Crino, Caroline Hunt, Lisa Lampe and Andrew Page The Treatment
of Anxiety Disorders second edition © 2002 Cambridge University Press. All rights reserved.
418 Treatment of Anxiety Disorders
Section 3 432
3 Relaxation strategies 432
3.1 What is relaxation training? 432
3.2 Importance of relaxation training 432
3.3 Components of relaxation training 433
3.3.1 Recognizing tension 433
3.3.2 Relax your body in a general, total sense: achieving the relaxation
response 434
3.3.3 Let tension go in speciWc muscles: isometric relaxation 435
3.4 Important points about learning to relax quickly 436
3.5 DiYculties with relaxation 437
Section 4 438
4 Thinking strategies 438
4.1 Identifying anxiety-provoking thoughts 440
4.2 Challenging anxiety-provoking thinking 441
4.2.1 What is the evidence for what I thought? 441
4.2.2 What alternatives are there to what I thought? 442
4.2.3 What is the eVect of thinking the way I do? 442
4.2.4 What thinking errors am I making? 443
4.3 Generating alternative thinking 445
4.4 Assumptions and core beliefs 446
Section 5 448
5 Managing worry 448
5.1 Problem solving 449
5.2 Indecision 449
5.3 Worry about worry 450
5.4 Letting go of worries 451
Section 6 451
6 Structured problem solving 451
6.1 Setting up a problem-solving session 452
6.2 Identifying problems 452
6.3 Step 1: DeWning problems and goals 453
6.4 Step 2: Generating solutions through brainstorming 454
6.5 Step 3: Evaluating the solutions 454
6.6 Step 4: Choosing the optimal solution 454
6.7 Step 5: Planning 455
6.8 Step 6: Review 456
6.9 When things don’t go as planned 456
6.10 Problem-solving practice 456
419 Generalized anxiety disorder: Patient Treatment Manual
Section 7 457
7 Dealing with behaviors that maintain anxiety or worry 457
Section 8 462
8 Keeping your practice going 462
8.1 Dealing with setbacks 462
8.2 Expect to lapse occasionally 462
8.3 Long-lasting change 463
Section 9 464
9 Further reading 464
SE CT I O N 1
This program will aim to teach you to manage your worry and anxiety by learning
to change the way you think and the way you react to your thinking and other
events. In essence you will be learning new methods of control.
It is important to realize that achieving control of worry and anxiety is a skill
that has to be learnt. To be eVective, the skill must be practiced regularly and you
will need to take responsibility for change. The more you put into the program,
the more you will get out of it. It is not the severity of your anxiety, or how long
you have been anxious, or how old you are that predicts the success of this
program, but rather it is your motivation to change your reactions.
1.2 Medication
You may be taking medication to help you cope with anxiety. If you are taking
medication, you may need to talk about the issues discussed below with your
therapist.
SE CT I O N 2
2 The nature of anxiety and worry
2.1 The nature of anxiety
Anxiety is a normal and healthy reaction. It describes a series of changes in the
body, and in the way we think and behave, that enable us to deal with threat or
danger; changes that can be very useful if you have to respond very quickly.
Consider the following: You are crossing a wide and busy road at a pedestrian
crossing. You suddenly notice a truck that has failed to slow down and will
probably not stop, and it is heading in your direction. You start running
for the safety of the sidewalk some meters away. The brain becomes aware of
danger. Automatically, hormones are released and the involuntary nervous system
sends signals to various parts of the body to produce the changes listed
below.
422 Treatment of Anxiety Disorders
And so you are able to run very quickly to the side of the road and escape being
knocked down by the truck.
As you can see, this series of reactions, known as the ‘‘Wght or Xight’’ response,
account for the many and varied feelings you can experience when you are
anxious. In your mind you feel fear and apprehension; you are ‘‘on edge’’, ‘‘keyed
up’’, and worried.
In your body, you may experience one or a number of the following sensations:
∑ Trembling or shaking
∑ Restlessness
∑ Muscle tension
∑ Sweating
∑ Shortness of breath
∑ Pounding or racing heart
∑ Cold and clammy hands
∑ Fast breathing
∑ Dry mouth
∑ Hot Xushes or chills
∑ Feeling sick or nauseated
∑ ‘‘ButterXies’’ in the stomach
This Wght or Xight response is useful in the short term, especially if the danger
can be dealt with by physical exertion. But it is of no use in the long term and
certainly of little use in most stressful situations today – it does not help to run
when the traYc cop pulls you over and it doesn’t help to Wght physically when you
are threatened by the boss. However, because the Wght or Xight response was
useful when, in the distant past we regularly had to deal with physical danger, it
remains part of our physical make-up. It is no wonder that when we are
423 Generalized anxiety disorder: Patient Treatment Manual
threatened, we can’t get enough air, our hearts pound, we feel nauseated, and our
arms and legs tremble and shake, as all these responses would be useful if we could
Xee or Wght.
Anxiety triggers:
Fear-provoking thoughts
Feelings, images, or situations
Perception of threat
“Fight or flight”
response
Worry about
This reaction is understandable, for if you don’t know how to control anxiety, it is
probably better to have too little than too much. When people do get too anxious,
their skill at problem solving, managing children, or meeting deadlines at work
declines rapidly. Extreme anxiety interferes with the ability to think clearly and act
sensibly. This, as everyone knows, is the sort of anxiety that robs us of our capacity
to do things as well as we are able. In fact, the more diYcult the task, the more
important it is to manage anxiety carefully; ideally, one should be mildly anxious,
alert, tense, and in control, for maximum eYciency.
The relationship between anxiety and skill is shown in the diagram. It is,
therefore, important to learn strategies for remaining calm when appropriate, and
alert, tense, and in control in diYcult situations.
Very good
Performance
Average
Very poor
When you experience these problems, the anxiety has begun to interfere with
your everyday life. Because anxiety is a normal, in-built, and at times useful
response, you will never banish it completely from your life, but the good news is
that you can learn to manage and control it.
several smaller problems, that may exceed your normal powers of adaptation.
When high levels of stress occur, anxiety can result if they produce in you a sense
of threat and lack of control.
It is clear that individuals with generalized anxiety disorder worry largely about
events that are remote (as opposed to in the immediate future) and which are
unlikely to happen. This sort of worry is rarely helpful as it is unlikely to promote
eVective problem solving. For example, worrying that a relative might develop a
life-threatening illness in the absence of any risk factors (a remote and unlikely
event) will not aVect the likelihood of it happening. However, adaptive worry
might take place prior to an important exam if the worry led to a good problem-
solving behavior – a time-table of study.
bodily sensation that might mean you are ill. Continually seeking reassurance
from others might relieve the anxiety in the short term, but the relief is usually
only temporary. Because you are never really allowed to deal with the initial
worry yourself, you can come to depend on this reassurance, and unfortunately
come to need it more and more to relieve anxiety.
∑ Other forms of checking include obsessively reviewing the report for work or
study to make sure that it is perfect, or not being able to take a break until all the
tasks for the day are complete (and we all know how likely that goal is to be
achieved!!). While there is not a lot of evidence that this type of checking
ensures that work is perfect, or that everything gets done, the individual never
learns that their work can be acceptable without the checking or that they can
take breaks and still get things done. Instead, goals are set too high, and the
individual becomes upset, anxious, and demoralized when he or she doesn’t
achieve what has been planned.
∑ Avoidance of situations or events that are thought to produce anxiety. For
example, avoiding listening to the news because stories of disasters or illness will
trigger worry about personal disaster or illness. Or avoiding people because of
what they might say to you. Or avoiding any situation in which the chances of
danger have been overestimated. Avoidance can seriously limit your life and the
possibility of enjoying a range of activities that are so much a part of everybody’s
life. When avoidance is based on an overestimation of danger, it is unnecessary
and the belief of danger is never disconWrmed.
∑ Procrastination, a special form of avoidance, which involves not beginning a task
because of the anxiety associated with a possible negative outcome. Many times
tasks are started only when the negative consequences of not starting outweigh
the negative consequences associated with completing the task – some tasks
never get started at all! For example, consider a dressmaker who can never start
on special orders because of her fear that her client would not like the Wnished
product and therefore think less of her both professionally and personally. In
most cases, the feared consequences are overly negative, usually catastrophic,
and not based on reality.
∑ Another form of avoidance is trying to suppress or control worry. Unfortunately,
the worry might well be made stronger by attempts to suppress it, possibly just
because you are purposefully focusing your attention on it. Some research has
suggested that the process of deliberately suppressing thoughts can cause them
to intrude into your mind more forcefully when the thoughts are no longer
being actively suppressed. This process has been called a rebound eVect.
Alternative strategies for dealing with worry that do not maintain the anxiety
and worry are covered in later sections of the Manual.
429 Generalized anxiety disorder: Patient Treatment Manual
Date:
SE C T I ON 3
3 Relaxation strategies
3.1 What is relaxation training?
Relaxation is the voluntary letting go of tension. This tension can be physical
tension in the muscles or it can be mental, or psychological, tension. When we
physically relax, the impulses arising in the various nerves in the muscles change
the nature of the signals that are sent to the brain. This change brings about a
general feeling of calm, both physically and mentally. Muscle relaxation has a
widespread eVect on the nervous system and therefore should be seen as a physical
treatment, as well as a psychological one. Section 3 will discuss how to recognize
tension, how to achieve deep relaxation, and how to relax in everyday situations.
You will need to be an active participant in relaxation, committed to daily practice
for 2 months or longer.
extremely beneWcial. For example, it is usually helpful to tense up when you are
about to receive a serve in a tennis game. Likewise, it is probably helpful to tense
up a bit before a job interview. This tension keeps you keen and alert. Do not
become frightened of this type of tension.
The tension is unnecessary when:
∑ It performs no useful alerting function.
∑ It is too high for the activity involved.
∑ It remains high after the activating situation has passed.
Note that these responses are opposite to the ‘‘Wght or Xight’’ response.
3.3.2 Relax your body in a general, total sense: achieving the relaxation response
Progressive muscle relaxation means that the muscles are relaxed in a progressive
manner, usually starting with the hands and arms and ending with the leg muscles.
Relaxation exercises should be done at least once a day to begin with, preferably
before any activity that might prove diYcult. Initially, do the exercises in a quiet
room, free from interruption, so that you can give your entire concentration to
relaxation. Explaining the exercises to those you live with will generally lessen any
embarrassment and aid in cooperation in minimizing interruptions. Select a
comfortable chair with good support for your head and shoulders.
If a chair does not provide good support, use cushions placed against a wall.
Some people prefer to do the exercises lying down, but do not use this position if
you are likely to fall asleep. These relaxation exercises are not meant to put you to
sleep, since you cannot learn to relax while asleep. Sleep is not the same as
relaxation – consider those times when you have awakened tense. If you do want
some method to put you to sleep, go over the relaxation exercises in your mind or
keep a relaxation tape speciWcally for that purpose. As you master the relaxation
exercises, try inducing deep relaxation in various postures and situations.
It is usually not a good idea to practice progressive muscle relaxation while
performing activities that require a high degree of alertness, e.g., driving a car or
operating a machine. Instead, use one of the speciWc muscle exercises described
further on.
When possible, it is advisable that you use the relaxation exercises as a prepara-
tion for some activity over which you anticipate diYculty. Decide which form of
relaxation you will use, arrange your seating appropriately, Wnish all you need to
do, and then start the exercises. It is important that you have nothing external to
think about while you are relaxing. Therefore, if you are expecting a phone call,
leave the phone oV the hook; likewise, don’t start cooking just before relaxing if
435 Generalized anxiety disorder: Patient Treatment Manual
something might boil over. When you are relaxing, you can be comfortably aware
that any distractions that occur are not important and don’t require your atten-
tion.
During the relaxation avoid tensing the muscles too tightly or they may become
overly tense and then diYcult to relax, or you may even cause cramping. About
60% to 70% of your maximum tension is usually recommended.
After you have Wnished the relaxation, don’t jump up right away. First, you
might feel momentarily dizzy and misinterpret this normal reaction as a sign of
some other problem. Second, you might get straight back into the old habit of
tensing. Get up slowly and try to preserve the state of relaxation for as long as
possible. Set about your activities in a slow and peaceful manner.
Remember, relaxation is a skill and, as such, improves with practice. Do not
despair if you do not reach deep levels of relaxation during your early sessions. The
more frequently you practice relaxation, the deeper the relaxation will be, and the
longer lasting the eVect.
You will need to commit yourself to at least 8 weeks of daily practice in order to
achieve really long-lasting eVects. Naturally, longer is even better. Some people
continue daily relaxation many years after leaving treatment. If you can do this, we
recommend it. However, not all people continue relaxation in this way. It is our
experience that people who beneWt most from relaxation either practice regularly
or practice immediately when they notice any increase in tension or anxiety.
too much tension. These are meant to be gentle and slow exercises. The aim of the
exercise is to relax you, not to get you even more tense. If circumstances do not
allow you to hold the tension for 7 seconds, you can still beneWt from putting in
the tension slowly over some period of time and releasing it in the same manner.
SE C T I ON 4
4 Thinking strategies
Humans are thinking, feeling, and behaving beings. These three aspects of our
make-up interact with each other. However, thoughts can often go unrecognized
and we fail to realize the important role they play in the way we feel and behave.
People often presume that events lead directly to feelings.
This presumption is important because it may lead people to believe that they
have no inXuence over the way they think, feel or behave. But thoughts intervene
between A and C, so the true association is:
THOUGHTS OR BELIEFS
“I must be really stupid. The boss will be really annoyed. I’ll lose my job.”
Another important point is that diVerent people will often have very diVerent
thoughts, and therefore very diVerent reactions, in response to the same event.
Consider the following example. Three people are waiting at a bus stop. They see
the bus approach, hail the bus – and it just drives past without stopping.
∑ The Wrst person gets angry and clenches their Wsts.
∑ The second person gets anxious and their heart starts to pound.
∑ The third person shrugs their shoulders and gets on with reading the newspaper.
The same event produced three diVerent responses, because it is not the event
that directly produced the feelings and behavior, but rather the thoughts the three
people had about the event.
∑ The Wrst person might have thought, ‘‘That driver should have stopped! Now
I’m going to be late for an important meeting!’’.
∑ The second person might have thought ‘‘I’m going to be late, I’ll never get
everything done in time, and the rest of the day will be a disaster!’’.
∑ The third might have thought ‘‘I might be late, but there’s not much I can do
about it right now’’.
So people can respond diVerently to the same situation. Their emotional
response and behavior (C) is related to the way they think about or interpret (B)
any given situation or event (A).
If you are like the Wrst or second person in the example above you might tend to
see things as worse than they need be, and you may be causing yourself unneces-
sary anxiety. All people who have suVered anxiety for many years develop habitual
and unhelpful ways of thinking about situations. They often tend to expect the
worst; often so much so that they bring the ‘‘worst’’ on. The way an individual
reacts to events and to people is largely tied into the expectations and assumptions
that that individual holds about particular situations and their self. Some of these
expectations and assumptions may not be particularly helpful.
Expectations such as:
∑ ‘‘I know that something dreadful is going to happen.’’
∑ ‘‘I can’t concentrate and it’s aVecting my whole life.’’
∑ ‘‘I’ll always be anxious.’’
∑ ‘‘My worry will drive me crazy.’’
∑ ‘‘Everyone will see that I’m not coping.’’
. . . are likely to increase anxiety.
Typically, these expectations and assumptions have been built up over a
number of years, so much so that they at times seem automatic. They do, however,
have signiWcant implications for how upset you feel and how you actually behave.
It is important to recognize that unhelpful thinking patterns are habits, and that
habits can be changed with eVort and practice. Identifying unhelpful thoughts
associated with anxiety is the Wrst step in changing your thinking.
440 Treatment of Anxiety Disorders
1. If people still spoke to you after you were anxious when you went out with
them.
2. If the feared event happened if you stopped worrying about it.
3. Whether or not you still got things done if you did slow down.
In weighing up the evidence, ask yourself:
Advantages of having to get it right Disadvantages of having to get it right all the
all the time time
think through the arguments for and against. If it is not your fault, stop
blaming yourself (even if you cannot think of anyone or anything else to
blame).
‘‘I’m too weak to deal with my worry.’’
Taking things personally: Are you ‘‘personalizing’’ everything so that it has
relevance to you or caused by you when in fact it has nothing to do with you?
‘‘That woman in the magazine with cancer is the same age as me, I could get
cancer.’’
Expecting perfection: People invariably make mistakes. Accepting imperfection
does not mean accepting low standards but it means acknowledging mistakes
and learning from them rather than being paralyzed by failure.
‘‘It’s got to be exactly right, or it is not even worth starting.’’
Using double standards: Many people expect of themselves what they would not
expect of others. Ask yourself, ‘‘How would I react if it was someone else in my
situation? Would I be so hard on them?’’
‘‘I can’t possibly say that I disagree with them; they’d be annoyed and dislike
me.’’
Overestimating the chances of disaster: Things will certainly go wrong and there is
danger in the world, but are you overestimating these? How likely is it that what
you expect will really happen?
‘‘I might lose my way; my car will break down; I’ll be stranded, or bashed or
raped.’’
Exaggerating the importance of events: Often we think that some event will be
much more important than it turns out to be. Ask yourself, ‘‘What diVerence
will it make in a week or 10 years? Will I still feel this way?’’
‘‘That Wght we had yesterday has ruined everything.’’
Fretting about the way things ought to be: Telling yourself that things should be
diVerent or that you must act in a certain way indicates that you may be
worrying about how things ‘‘ought’’ to be rather than dealing with them as they
are.
‘‘I must get rid of this worry. It’s not normal.’’
I can do nothing to change the situation: Pessimism about a lack of ability to
change a situation leads to feelings of depression and lowered self-esteem.
There may be no solution, but you will not know until you try. Ask yourself
whether you are really trying to Wnd answers and solutions.
‘‘I can’t help the way I think. I can’t change or control my feelings.’’
Predicting the future: Just because you acted a certain way in the past does not
mean that you have to act that way forevermore. Predicting what you will do on
the basis of past behavior means that you will cut yourself oV from the
possibility of change.
‘‘I usually get anxious at parties, so I know I won’t enjoy the next one.’’
445 Generalized anxiety disorder: Patient Treatment Manual
Blaming the past: Just because certain things happened in the past doesn’t mean
that signiWcant changes cannot be made by you for the future.
‘‘My past is the cause of all my problems. It will continue to aVect me and I will
never change.’’
What if everything goes wrong? Its unlikely that everything will go wrong.
Worrying about something that may go wrong
won’t stop it from happening. I will only plan
for things that are likely to happen
I’m not good enough to do this well I like to do things well most of the time but
like everyone, I will occasionally make a
mistake. I may feel bad, but I can handle that. I
will try my best
Surely these feelings really mean that I have a I am feeling symptoms of anxiety, which I
serious illness know cannot harm me. I am unlikely to have
anything seriously wrong with me that all the
doctors have missed
I keep thinking that something dreadful will There is no evidence that anything bad is
happen to the people close to me about to happen. I won’t dwell on future
events that are unlikely to happen
446 Treatment of Anxiety Disorders
Helpful thinking does not reject all negative thoughts; it is not simply wishful
thinking. It involves looking at things in a way that is most realistic, given the facts.
For example:
Unhelpful thinking
‘‘I didn’t get the job, which proves that I am a failure. I’ll never get a job or have things go
right for me.’’
Helpful thinking
‘‘I am disappointed I didn’t get that job, but I can cope.’’
Wishful thinking
‘‘Who cares! I didn’t want the job anyway.’’
Unhelpful thinking
‘‘What if I can’t cope with this? It will be absolutely disastrous.’’
Helpful thinking
‘‘I’m going to give this a try. I’ll give it my best shot and see how it goes.’’
Wishful thinking
‘‘It’ll be easy!’’
Date:
Describe the situation Identify and list automatic thoughts Objective reappraisal
How strong was that feeling % How strong was that feeling %
SE C T I ON 5
5 Managing worry
Individuals with generalized anxiety worry a lot. These worries tend to center on
everyday things; we all worry to some extent about problems that might arise at
home or at work, about illness or injury aZicting ourselves or our family, about
diYculties in our relationships with others, or even Wnancial pressures. Individ-
uals with generalized anxiety will recognize that they worry excessively about these
things, that the worries are often unrealistic, and that the worry takes up a large
part of their typical day. Unfortunately, it is this type of worry that can interfere
with daily functioning, and can increase anxiety and tension levels.
Excessive worry or ruminating about events that are unlikely to happen can
make you feel worse than you need to and may even increase feelings that you
449 Generalized anxiety disorder: Patient Treatment Manual
cannot cope. It may feel as though by worrying about things you might be able to
anticipate and avoid future catastrophes, but in reality the worry does not lead to
productive or constructive action. Instead, problems remain unsolved, fears are
not confronted, and the unhelpful beliefs about events or situations continue
unchallenged. In the following sections more practical steps for helping to deal
with worry are described.
5.2 Indecision
Determine whether the worry is driven by indecision. Many individuals with
generalized anxiety disorder are anxious that they might do something wrong or
make the wrong decision. They may be overly perfectionistic. The anxiety may
cause these individuals to procrastinate or continually put oV making a decision,
or they may deliberately continue to ‘‘worry through’’ the decision in an attempt
to ensure that they don’t make a mistake. For example, people may Wnd them-
selves going through a lengthy series of questions and answers about major life
decisions such as ‘‘Am I in the right job?’’, ‘‘Am I in the right relationship?’’. Or
there may be a series of day-to-day decisions that cause worry, such as ‘‘Should I
go to that party?’’ ‘‘What present should I buy my partner?’’ or ‘‘Which task
should I start Wrst?’’
Unfortunately this ‘‘worrying it through’’ process does not usually help to Wnd
the ‘‘right’’ decision (as there may not be such a thing as the ‘‘right’’ or ‘‘wrong’’
answer) but instead increases and extends feelings of anxiety and uncertainty,
thereby feeding the indecision. Furthermore, this process may cause you to come
up with a wider range of catastrophic consequences that you would otherwise have
come up with. In other words, the more you worry, the more and more negative
you may become.
Sometimes people will not want to make a decision until they believe they have
all the information relevant to that decision. For example, every travel agent will
need to be contacted to check out every deal before the holiday can be booked, or
450 Treatment of Anxiety Disorders
every consequence has to be thought out before a plan embarked upon. Unfortu-
nately it is rarely necessary to have this level of certainty before making a decision,
and impossible to be free from any doubt.
If your worry is driven by indecision:
∑ Determine whether there is any unhelpful thinking that lies behind your worry.
For example, ‘‘Is there really a ‘right’ answer to your decision?’’ ‘‘Realistically,
what would really happen if you made a decision one way or the other?’’
‘‘What’s the worst that could happen?’’ ‘‘What evidence is there that you are
unable to make a decision?’’
∑ If there is a decision to be made, set a reasonable amount of time to reach a
decision, and then act on it! The problem-solving strategy described in Section 6
can be helpful here.
∑ Then make sure that you don’t engage in any further worry about the decision
(see Section 5.4).
Ask yourself:
∑ ‘‘What is the eVect of thinking this way?’’
∑ ‘‘What is the evidence to support these beliefs?’’
∑ ‘‘What alternative explanations might there be?’’
∑ ‘‘What is more likely based on past experience?’’
For example, if you worry that you will be unable to control your worry, ask
yourself what typically happens when you do worry. Are you really never able to
stop it? What eventually stops the worry? So next time, how likely is it that the
worry will go on and on forever? What do you think would happen if you tried to
postpone the worry by telling yourself that you will give yourself time to think
about it later in the day? Why don’t you try this and see what happens? What
would happen if you deliberately tried to lose control through worry?
Positive beliefs about worry can be challenged using similar strategies. For
example, ask yourself when worrying about the worst possible outcome has
actually helped you to cope with the outcome? It is likely that the answer to this
question would be that the worst possible outcome has never come about! Would
451 Generalized anxiety disorder: Patient Treatment Manual
you really be increasing the chances that a bad thing would happen by not
worrying about it? Why don’t you stop worrying about it and see if it really
happens?
SE CT I O N 6
6 Structured problem solving
Our lives are full of problems to be solved, ranging from major life crises to the
more mundane hassles of our day-to-day lives. However, no matter how small or
452 Treatment of Anxiety Disorders
trivial the matter, if problems remain unsolved, or if the way they are resolved is
unsatisfactory, they can lead to feelings of uncontrollability or the perception of
threat, which are major contributors to anxiety.
Structured problem solving is a useful strategy for anyone with problems,
whether those problems are related to anxiety, or other personal matters, such as
dealing with a diYcult colleague at work. The approach can also be used by groups
of people, such as families, friends, and workmates. For example, your family may
be facing Wnancial diYculties and may need to cut expenses, or they may have a
problem in that nobody is prepared to do the dishes in the evening. Problem
solving can also be applied to achieving goals, such as getting a job, planning a
social activity, or improving one’s Wtness.
There are no perfect or ideal solutions to problems, but the structured problem-
solving approach aims to lead you to the most eVective plan for action.
∑ Consider the content of your worries. Is there a problem that requires solving
behind these worries?
Write down some of your problems and goals in the spaces below
454 Treatment of Anxiety Disorders
1.
2.
3.
4.
5.
6.
diYcult to implement, even though it may not be the ideal solution. At least, you
can get started right away. The problem may not be solved immediately, but you
might have made a diVerence, and what you learn by trying might be useful the
second time around. This is preferable to choosing a solution that is doomed to
failure because you have been overly ambitious.
Outline the solution (or combination of solutions) you have agreed upon in the space
below.
1.
2.
3.
4.
The following checklist applies to any problem and is helpful to see whether you
have planned properly.
∑ Do you have the necessary resources available (time, skills, equipment, money)
or are you able to arrange the necessary resources or help?
∑ Do you have the agreement or cooperation of other people that might be
involved in the plan?
∑ Have all the steps been examined for possible diYculties?
∑ Have any strategies been planned to cope with likely diYculties? Setting speci-
Wed times or deadlines will minimize the risk of procrastination.
∑ Have any strategies been planned to cope with any negative (or positive)
consequences?
∑ Have diYcult parts of the plan been rehearsed, e.g., a telephone call, conversa-
tion, interview, or speech?
∑ Has a time been set for a review of the overall progress of the plan?
456 Treatment of Anxiety Disorders
Step 2: List all possible solutions: Put down all ideas, even bad ones. List the solutions without
evaluation at this stage.
1.
2.
457 Generalized anxiety disorder: Patient Treatment Manual
3.
4.
5.
6.
Step 3: Assess each possible solution: Quickly go down the list of possible solutions and assess the main
advantages and disadvantages of each one.
Step 4: Choose the ‘‘best’’ or most practical solution: Choose the solution that can be carried out most
easily to solve (or to begin to solve) the problem.
Step 5: Plan how to carry out the best solution: List the resources needed and the major pitfalls to
overcome. Practice diYcult steps, make notes of information needed.
Step 6: Review progress and be pleased with any progress: Focus on achievement Wrst. Identify what has
been achieved, then what still needs to be achieved. Go through steps 1 to 6 again in the light of
what has been achieved or learned.
SE CT I O N 7
7 Dealing with behaviors that maintain anxiety or worry
When anxiety occurs for the Wrst time with a certain situation, most people believe
that, should they confront that same situation again, they would be more than
likely to become anxious. Likewise, certain activities or problems may also have
become associated over time with discomfort or anxiety. The occurrence of
anxiety is unpleasant and so, as any sensible person would, suVerers soon learn to
try to anticipate the situations or events likely to trigger their anxiety.
Of course, it is quite helpful to behave in a way to minimize objective danger,
such as getting your doctor to check an unusual mole on your arm or avoiding
deserted parts of the city late at night. On these occasions the anxiety that causes us
to act in these ways will serve a useful purpose. The problem is that when they are
anxious, individuals with generalized anxiety will often avoid situations that are
458 Treatment of Anxiety Disorders
The problem with these behaviors is that the relief is only temporary.
In practice, the things we avoid become harder and harder to do, and gradually we avoid
more and more things.
The need to seek reassurance becomes greater, and more and more reassurance is required
to relieve the anxiety.
When anxiety is relieved by something we do, the fear can be made even worse,
because the feeling of relief and drop in anxiety following the behavior tell us that
the behavior was sensible. Thus, the behavior is reinforced or strengthened; after
all, if you can avoid anxiety by acting in a particular way, why not do so?
Unfortunately, you just identify more and more situations as diYcult and avoid
them also.
Then what is the cure? If avoiding the things you fear makes them harder and
harder to face, what would happen if you started to confront your fears? If the fear
is reinforced by seeking reassurance, what would happen if you prevented yourself
from checking? Actually, if you confronted your fears or doubts for long enough,
it would eventually go, and the fear the next time you encountered that situation
would be less. However, most people don’t like to put this to the test, so they keep
avoiding those situations or seeking reassurance.
One good way to break behaviors is to start with easy situations and slowly build
up enough conWdence to face the harder things. The other important strategy is to
control the level of the anxiety using the breathing exercise and controlling
worrying thoughts, and then stay with the situation until you have become more
calm.
But how do you organize such experiences? First, you need to identify all
behaviors that might be maintaining anxiety.
You have already made a list of:
∑ Situations or circumstance that trigger worry or anxiety.
∑ The situations that you avoid because of anxiety or worry.
∑ Behaviors you engage in response to your worry.
Make sure that you include things that might not be obvious at Wrst, such as
certain topics of conversation or news items, missed opportunities, uncertainty,
thoughts of illness or accidents, not accepting invitations, putting things oV, or
cutting activities short.
459 Generalized anxiety disorder: Patient Treatment Manual
Then you plan ways of changing the behavior so that it no longer prevents you
from facing what you fear. Some examples are listed below:
Next, rank those situations or circumstances in terms of the anxiety that they
cause, or would potentially cause. If the anxiety is too high to allow you to directly
change that behavior then:
1. You can break down the behavior into smaller, more manageable steps.
2. You might need to address unrealistic worries about the outcome of this
change in behavior.
Read newspaper story about cancer - how common it is and its consequences 70%
Leave all new letters unopened and e-mail unchecked for one day 100%
Carefully monitor and record your progress on the sheets provided. This will
help you to both structure your progress and give you feedback as to how you are
doing. Make sure a task is attempted every day until you feel comfortable with the
situation.
460 Treatment of Anxiety Disorders
SE C T I ON 8
8 Keeping your practice going
Some people have diYculty keeping up practice of their anxiety-management
skills. This diYculty may be because they don’t think that they are making any
progress, even though other people may see a change. Progress is often slow, and
sometimes diYcult to notice over a number of days. Take care not to underrate
your achievements. Learn to praise yourself for your eVorts in attempting new
ways to deal with diYcult situations, as well as your successes. Remember that
praising yourself is an important factor in maintaining motivation, particularly in
the early stages following treatment.
‘‘I’m really hopeless. I’m right back where I started from. I’ll never be able to change.’’
‘‘I’m disappointed that I have let things slip, but I can deal with that and I’m not going to turn it into an
excuse for giving up altogether. Now, I’ll get out my Manual and start my practice again.’’
Therefore, if you have a setback don’t add to the problem with all the old
catastrophic and unhelpful ideas. Keep practicing all the techniques you have been
taught and you will still be making progress.
Of course, many people do stop things like relaxation when they have been
feeling okay for some time. This is Wne, so long as you keep aware of any stress or
anxiety that may be creeping back into your life, and restart the exercises as soon as
you become aware of any increase. It will also be important to reinstate such
techniques if you have recently experienced any stress or life event.
It may also be helpful to revisit some of the thinking strategies you found useful
over treatment. For example, rather than trying to deal with unhelpful worries in
your mind, write them down! You will remember that this helps you to distance
yourself from your fears and to be more realistic in your thinking.
SE C T I ON 9
9 Further reading
There is no evidence-based self-help book speciWcally for GAD available right
now. However, this may be useful as a general reference:
Barlow DH, Rapee RM. (1991) Mastering Stress: A Lifestyle Approach. Dallas, TX: American
Health Publishing Co.
24
Historical context
Recent years have seen an extraordinary growth in awareness of traumatic stress,
not only among health workers but also among the general public. This increased
awareness might suggest that mental health professionals have only just dis-
covered the fact that human beings experience a psychological reaction following
exposure to trauma or, worse, that the disorder has just been ‘‘invented’’. It is
important, therefore, to understand the historical context of PTSD.
The notion that an individual may experience psychological problems following
a traumatic experience is not new, with references dating back nearly three
thousand years to Homer’s Iliad. Shakespeare provided several descriptions of
traumatic stress reactions, as have other writers throughout history. It was not
until early this century, however, that the condition became the focus of interest
from a scientiWc perspective. Several leading Wgures in the burgeoning Weld of
psychiatry at that time, such as Freud, Kraepelin, and Janet, commented on the
existence and nature of traumatic stress reactions following accidents, Wres, and
other traumatic events. Wartime experiences, notably in the American Civil War
and the First World War, prompted physicians to speculate on the cause of
posttrauma reactions. The condition was thought initially to be a result of organic
damage to the brain caused by explosions on the battleWeld and thus the term
‘‘shell shock’’ was coined during the First World War. It was not until later that the
psychological basis of the disorder was widely accepted and clinicians began to
recognize that terms such as ‘‘shell shock’’, ‘‘war neurosis’’, and ‘‘combat fatigue’’
all referred to the same phenomenon. Gradually, it was acknowledged also that
these disorders were essentially no diVerent from traumatic stress reactions seen in
civilians following nonmilitary traumas such as transport accidents, Wres, natural
disasters, and violent assault.
Despite interest in the area over many decades, the disorder was not formally
recognized until 1980, with the publication of DSM-III. The term ‘‘posttraumatic
stress disorder’’ was proposed and the diagnostic criteria were delineated. With
465
466 Treatment of Anxiety Disorders
that formal recognition, the area became accepted as a legitimate focus of empiri-
cal research and theoretical debate. In 1987, the diagnostic criteria were modiWed
signiWcantly in DSM-III-R and further minor changes were made in the latest
edition, DSM-IV. The most recent version of the International ClassiWcation of
Diseases, ICD-10, has included the category of PTSD for the Wrst time.
not unusual in more chronic forms of the disorder, the problem in more acute
forms is often the opposite. That is to say, trauma survivors tend to report
overwhelming emotions, with highly labile aVect (although loving feelings may
still elude them). The Wnal symptom in this cluster refers to a sense of fore-
shortened future (C7); the person’s sense of mortality has been brought home to
them to such an extent that it is impossible for them to imagine a long and happy
life in the future.
While the DSM-IV includes active avoidance and numbing of responsiveness
within the same symptom cluster, there is increasing evidence that the two may
represent separate constructs (Foa et al., 1995b). Those authors speculate also that
the numbing symptoms are central to the diagnosis of PTSD, diVerentiating it
from more common, but less pathological, psychological responses to trauma.
Certainly, clinical experience suggests that, if a trauma survivor does not meet
criteria for a formal diagnosis of PTSD, it is often because the person does not have
suYcient numbing symptoms.
The Wnal cluster of symptoms are those of persistently increased arousal. Sleep
disturbance (criterion D1) appears to be almost universal in the early days
posttrauma. Some trauma survivors report that they are frightened to go to sleep
because of the intrusive images and nightmares while, for others, fears for their
safety are enough to keep them awake. These disturbed patterns often develop into
chronic problems with the establishment of habitual poor sleep hygiene. Anger
and irritability (D2) are also common. These symptoms can be very destructive to
support networks, with the survivor alienating the very people who are trying to
help (such as family, friends, and helping professionals). In more chronic PTSD,
especially among veteran populations, explosive and consuming anger is often a
central component of the initial presentation. Concentration is likely to be
disturbed (D3), often as a result of the frequent intrusions. Individuals with PTSD
tend to be hypervigilant (D4) – always on the look-out for signs of potential
danger – a feature that is often quite noticeable in the clinical interview. The Wnal
arousal symptom is that of exaggerated startle response (D5). This is characterized
not only by an excessive physiological arousal when startled but also by a failure to
habituate to repeated presentations of the startle stimulus. Two of these hy-
perarousal symptoms are required for a diagnosis of PTSD.
DSM-IV requires that symptoms in B, C and D have been present for at least 1
month (criterion E). In line with other DSM-IV diagnoses is the requirement that
the disturbance must cause signiWcant distress or functional impairment (cri-
terion F). The disorder is speciWed as acute if duration of symptoms is less than 3
months and chronic if 3 months or more. It could be argued that 3 months is a
little premature to be referring to the disorder as ‘‘chronic’’. Nevertheless, the
distinction is an important one and may prompt appropriate research into
469 Posttraumatic stress disorder: Syndrome
hours per night before the incident to 4–5 hours. He reported problems with concentration,
being unable to read books or focus on television programs, and complained of problems
with memory and decision making. He talked of being hypervigilant when away from home,
particularly when out at night (which he tried to avoid if at all possible). The course of
symptoms over the previous 18 months had been relatively stable, with a slight reduction in
intrusive symptoms accompanied by an increase in avoidance and emotional numbing.
A brief interview with Mr. D.’s wife confirmed the above story. In particular, she empha-
sized the social withdrawal and emotional numbing aspects of his current presentation,
saying that he had become ‘‘a different man to the one I’ve known for the last 18 years’’.
History
There was no significant prior psychiatric or medical history. The oldest of three children, his
childhood was relatively stable, although he reported that he was shy at school and a ‘‘bit of a
loner’’ as a child. He described his mother as a nervous woman who tended to shun social
contact. His father drank fairly heavily, although Mr. D. did not remember any episodes of
associated violence. He described his family as being ‘‘no nonsense – when things went
wrong you didn’t complain or talk about it, just got on with life’’. He completed school and
went on to teacher training. Although he worked for 10 years as a teacher, he never enjoyed it
and was pleased to be offered voluntary early retirement. Over the past 7 years he has had
several jobs and has been with the security firm for the last 2 years. He married his wife, also a
teacher, when they were both at college and has two children aged 7 and 10 years. The
relationship is strong, although it has been put under considerable pressure since the
trauma. He has many acquaintances, but few (if any) close friends.
Permorbid personality
Mr. D. described himself as being a happy and outgoing person prior to the trauma, although
on closer questioning his social contact seemed to revolve almost entirely around sport. Not
particularly psychologically minded, his habitual style of coping with stress appeared to be
one of avoidance and denial.
Mental state
Mr. D. presented as a casually dressed man of above-average intelligence who appeared
haggard and tired. Although initially quite defensive and tense (he insisted on taking a chair
facing the door), he loosened up and eventually spoke freely and openly about his history
and current problems. His affect varied from flat to dysthymic, often on the edge of tears. He
showed little insight and was unable to understand why he had not recovered from the
event, seeing it as a sign of weakness. He was pessimistic about the future and reported
feeling guilty about his behavior towards his family. There was no evidence of thought
disorder, hallucinations, or delusions. Having made the decision to seek treatment, he
seemed highly motivated to work on his problems.
Formulation
Mr. D. clearly meets criteria for a diagnosis of chronic PTSD, with evidence of a traumatic
experience, several re-experiencing symptoms, widespread avoidance and numbing, and
471 Posttraumatic stress disorder: Syndrome
persistent hyperarousal. Although there is evidence also of depression, this seems secondary
to the PTSD and would not warrant a separate diagnosis. Despite an absence of prior trauma
history or psychiatric problems, there is some evidence of vulnerability in terms of a prior
tendency towards anxiety (in both him and his parents) and a pattern of coping with stress
characterized by avoidance and denial. Although these strategies have worked well in the
past, they have prevented him from integrating his experience and moving on. The traumatic
memories remain unchanged and continue to invade consciousness causing frequent dis-
tress. His attempts to deal with the memories by increased avoidance, denial, and emotional
numbing, while not always successful, have resulted in social and occupational problems.
Comorbidity
It is important to recognize that comorbidity is the norm, rather than the
exception, in chronic PTSD. For example, Kulka and his colleagues (1990)
reported that 98% of Vietnam veterans with PTSD had, at some stage, qualiWed for
another DSM-III-R diagnosis. The National Comorbidity Survey (Kessler et al.,
1995) reported that 88% of men and 79% of women with chronic PTSD meet
criteria for at least one other psychiatric diagnosis.
Although not a formal diagnosis, feelings of guilt are reported frequently by
survivors of trauma. This symptom was included in DSM-III but was dropped
from the revised version in 1987. These feelings of guilt may be about behavior
required for survival, about the fact that the individual survived while others did
not, or about reactions and behavior since the event. Symptoms of depression are
common also following trauma. Indeed, it is clear from the PTSD criteria outlined
above that many symptoms overlap between the two diagnostic categories, some-
times presenting a problem for diVerential diagnosis. Indeed, an additional formal
diagnosis is often warranted: major depression is the most common comorbid
condition occurring with chronic PTSD (in around 46% of cases; Kessler et al.,
1995). Other anxiety disorders, particularly in the form of panic disorder and
social phobia, may occur in 20% to 30% of individuals with chronic PTSD.
Substance abuse and dependence is a frequent complication, occurring in around
52% of men and 28% of women with chronic PTSD. This use of both licit and
illicit drugs is often conceptualized as part of the avoidance and numbing compo-
nent of PTSD, as the suVerer attempts to block out the painful memories and
feelings. Somatic symptoms, including gastrointestinal problems, aches and pains,
cardiovascular symptoms, and psychosexual diYculties may be present, particu-
larly in more chronic forms, as well as poor health behavior (such as smoking,
poor diet, lack of exercise).
Although this discussion has focused on the comorbid conditions that may
occur along with PTSD, it is important to remember also that many of these
disorders may develop as sequelae of trauma in the absence of PTSD. It is
important to resist the temptation to diagnose PTSD simply because the person
has experienced a signiWcant trauma when an alternative diagnosis may be more
appropriate.
473 Posttraumatic stress disorder: Syndrome
approach at the expense of a more rigorous assessment may not be in the client’s
best interest over the longer term.
A comprehensive assessment should include not only mental state, current
functioning, and life circumstances, but also details of the traumatic experience,
prior history of trauma, and pretrauma functioning. The clinician needs to cover
the presence and course of core PTSD symptoms, as well as likely comorbid
conditions such as depression, anxiety, and substance abuse. In order to under-
stand the client’s reaction to the experience, information must be collected also
regarding the broader social context.
In most clinical settings, an unstructured interview will comprise the primary, if
not the only, assessment strategy. In suspected cases of PTSD, however, there is
often a need for more objective assessment that will stand up to the rigorous
scrutiny expected in a psycho-legal context. With our current state of knowledge,
there is no ‘‘gold standard’’ for diagnosing PTSD. Rather, a multifaceted approach
incorporating information from a variety of sources is recommended. In clinical
settings, the combination of a structured clinical interview and self-report inven-
tories comprise the optimum strategy. In research settings, the addition of a third
category of data in the form of psychophysiological measures provides an extra
degree of objectivity, although this approach is rarely practical in clinical contexts.
Self-report measures
A multitude of inventories exist for the assessment of PTSD symptoms and several
excellent reviews exist (e.g., Solomon et al., 1996; Norris and Riad, 1997). The best
self-report measures are psychometrically robust, relatively nonintrusive, and
often (although not always) reasonably inexpensive. They have the advantage of
assessing how the clients view their symptoms without being inXuenced by the
presence of an interviewer. Equally, they are easy to fake and may be susceptible to
symptom exaggeration or minimization. As such, self-report measures should
never be used as the only, or even the primary, diagnostic tool. On the other hand,
they can function as excellent screening instruments: those clients who score
highly can be targeted for more intensive interview procedures. Finally, they are
useful for repeated assessments in assessing change as a function of treatment. The
following provides a brief overview of some of the more commonly used self-
report instruments that may be useful in the psychological assessment of trau-
matic stress.
Many of the more comprehensive self-report measures of psychopathology
have been used in the assessment of traumatic stress reactions and PTSD. For
example, Keane and his colleagues have developed a 49-item PTSD scale from the
MMPI (PK subscale; Keane et al., 1984). Similarly, several attempts have been
made to derive a PTSD scale from the Symptom Checklist 90-R (SCL-90-R;
Derogatis, 1977). The best known of these is the Crime-Related PTSD Scale
(CR-PTSD; Saunders et al., 1990). While these global measures of psychopathol-
ogy have useful research applications, scales developed speciWcally for traumatic
stress are more appropriate in most clinical settings.
The Mississippi Scale (Keane et al., 1988), available in both combat and civilian
versions, functions as a good indicator of PTSD severity and has excellent
psychometric properties. The recommended cutoV for a probable PTSD diagnosis
varies, although 107 was suggested by the original authors. The Penn Inventory
(Hammarberg, 1992) is a 26-item scale designed to apply to all types of traumatic
event. It requires respondents to select the most appropriate of four possible
statements for each question. A cutoV score of 35 provided reasonable sensitivity
and speciWcity in PTSD diagnosis across a range of populations (Hammarberg,
478 Treatment of Anxiety Disorders
1992). The oldest and most widely used self-report measure for the assessment of
traumatic stress is the Impact of Event Scale (Horowitz et al., 1979). This 15-item
scale takes about 5 minutes to complete and comparative data are available for a
wide range of traumatized populations. Developed prior to the recognition of
PTSD in 1980, the scale is limited by its exclusive emphasis on intrusion and
avoidance symptoms. In order to address this deWciency, the IES-R has recently
been published (Weiss and Marmar, 1997). This revised scale includes additional
items that reXect the arousal symptom cluster in PTSD. At this stage, insuYcient
data are available to comment on the reliability and validity of this new scale.
None of the above scales are tied speciWcally to the DSM symptoms of PTSD.
Rather, they provide a more general evaluation of the severity of traumatic stress
reactions. A few currently available scales, on the other hand, are designed to
reXect the DSM content exactly. The Posttraumatic Stress Disorder Checklist
(PCL; Weathers et al., 1993) covers the 17 PTSD symptoms, with each rated on a
Wve-point scale from ‘‘not at all’’ to ‘‘extremely’’. The scale is brief, taking only 5
minutes to complete, and possesses excellent psychometric qualities (Blanchard et
al., 1996a). A score of 50 is recommended as the diagnostic cutoV. Another
DSM-speciWc scale is the self-report version of the PSS-I structured interview
discussed above. The PSS-S (Foa et al., 1993) consists of the 17 items rated on a
four-point scale from ‘‘not at all’’ to ‘‘very much’’. Finally, the Davidson Trauma
Scale (DTS; Zlotnick et al., 1996) is a similar self-report measure allowing for both
frequency and intensity ratings. Although the authors report good psychometric
properties, additional research is required to provide further validation of this
measure.
have actually experienced them Wrst-hand. Resnick (1993) suggested that a history
of unstable employment or previous incapacitating illnesses, emphasis on re-
experiencing (rather than avoidance and numbing) symptoms, and lack of sexual
dysfunction or nightmares are all potential indicators of malingering in PTSD.
Contradictions in the clinical presentation (such as being unable to work but
retaining an active social life, or complaining of emotional detachment and high
irritability in the absence of any marital discord) should be a cause for concern.
Similarly, several features of PTSD may be directly observable to the clinician
during the interview (e.g., hypervigilance, Xattened aVect) and those observations
can be compared with the patient’s report. Informant interviews, particularly with
a spouse or partner, can shed a great deal of light on the validity of the patient’s
report. If good diagnostic practices are adopted, it is not an easy task to deceive an
experienced clinician with a thorough knowledge of the disorder. Equally, unless
we are to adopt an attitude of constant disbelief, assuming that everyone with
PTSD is malingering until proved otherwise, occasionally even the best clinicians
will be deceived.
Summary
PTSD is a severe psychiatric disorder that develops in a minority of trauma
survivors. It is important to distinguish this more severe reaction from normal,
albeit highly distressing, reactions that will occur in most people following a
traumatic event. The disorder is characterized by intrusive memories of the
trauma, attempts to block those memories out, and persistent hyperarousal. The
likelihood of developing PTSD is dependent upon a complex interaction of
pretrauma vulnerability, severity of the trauma, and the posttrauma recovery
environment.
25
Aims of treatment
It is reasonable to assume that virtually all human beings will experience a
psychological reaction to very frightening or upsetting events. This raises ques-
tions about what constitutes an adaptive psychological response to trauma and, as
a corollary, what are reasonable treatment goals. Severe traumatic events
profoundly aVect survivors’ views of themselves and the world. In most cases, it is
reasonable to suggest that the survivor will never be the same person again.
Equally, those changes need not all be bad. Recovery from trauma can result in
personal growth, with the development of improved coping strategies and more
adaptive models of the self and the world.
Ideally, treatment would serve to eliminate all the symptoms of PTSD and
return the survivor to pretrauma levels of functioning. In reality, that will not
always be possible. As with other disorders, factors such as the severity of the
condition, chronicity, and comorbidity (particularly in the form of axis II dis-
orders) are likely to aVect treatment eYcacy. In acute cases of PTSD with few
complications, it is reasonable to expect a high degree of success with relatively few
sessions (6 to 10). In such cases, elimination of PTSD symptoms, a return to prior
functioning, and low risk of relapse would be achievable goals. (Importantly, this
is not to imply that the person will never again experience distressing memories of
the event but, rather, that such intrusive phenomena will be infrequent and
manageable). On the other hand, treatment goals for a Vietnam veteran with, for
480
481 Posttraumatic stress disorder: Treatment
example, a 30-year history of PTSD, high levels of comorbid alcohol abuse, and
poor social and occupational functioning, would be more conservative. It may be
a question of helping that person to manage the symptoms more eVectively,
reducing their impact on quality of life, relationships, and general functioning.
Anxiety management
PTSD is an anxiety disorder characterized by persistent arousal, with high levels of
fear relating to trauma-related memories and external cues. This, in combination
with a poor understanding of their own psychological reactions, leaves many
survivors feeling vulnerable and out of control. Thus a vital step in the early part of
treatment is that of teaching a repertoire of simple strategies to manage the arousal
and distress. These interventions do not address the underlying causes and are not
usually seen as a treatment for PTSD per se. Rather, they provide ways to manage
anxiety and distress when it occurs. As such, they are an important precursor to
the painful process of exposure.
Anxiety management may be conceptualized under the three broad headings of
physical, cognitive, and behavioral components, with interventions delivered in all
three domains. The more physically oriented strategies, which directly address the
hyperarousal aspects of traumatic stress reactions, are an excellent starting point.
Clinical experience suggests that they often produce rapid eVects that not only
assist the survivor in feeling better but, perhaps more importantly, improve
482 Treatment of Anxiety Disorders
Exposure treatments
It is reasonable to assume that all successful treatments of PTSD involve some kind
of opportunity to confront the traumatic memories. Exposure-based treatments,
widely used in the management of anxiety disorders for many years, constitute a
central component of treatments for PTSD. Initially, these approaches were based
on the assumption that fear is acquired and maintained by the processes of
classical and operant conditioning of stimuli related to the traumatic incident. The
concept of extinction, or habituation, has been used to explain fear reduction
following prolonged exposure to the traumatic stimuli. More recently, Foa and
Kozak (1986) have proposed the notion of emotional processing to explain
anxiety reduction during exposure. They suggested that the processing of correct-
ive information results in changes to the traumatic memory network, modifying
both the stimulus–response connections and the meaning attached to the experi-
483 Posttraumatic stress disorder: Treatment
Cognitive restructuring
Cognitive restructuring, based on the work of Beck and his colleagues (1979), is
sometimes included under the heading of anxiety management. However, the
techniques of cognitive therapy have been used to directly treat the core symptoms
of PTSD. Cognitive processing therapy (CPT; Resick and Schnicke, 1992) com-
prises cognitive restructuring with speciWc reference to Wve primary themes:
safety, trust, power, self-esteem, and intimacy. Clients in CPT are taught to
identify maladaptive cognitions (or ‘‘stuck points’’) and to vigorously challenge
them using a list of dispute questions. A detailed description of the procedure has
been provided by Resick and Schnicke (1993). Various adaptations of cognitive
therapy and CPT have now been trialled in the treatment of PTSD.
Anxiety management
Regrettably, few of the anxiety-management strategies described above have been
empirically evaluated in isolation for the treatment of traumatic stress reactions. It
is diYcult, therefore, to comment on the eYcacy of any individual component.
484 Treatment of Anxiety Disorders
Exposure treatments
A large body of empirical support now exists for the eYcacy of exposure treatment
in PTSD, with the Wrst controlled trials published in 1989. In a study of 24 combat
veterans, Keane and his colleagues (1989) found signiWcant improvements in
anxiety (40% reduction in symptoms) and depression (39% reduction), as well as
in the re-experiencing symptoms of PTSD (35% reduction), using imaginal
exposure compared with a wait-list control. Similar results have been achieved in
other studies of combat veterans with PTSD (e.g., Cooper and Clum, 1989;
Boudewyns and Hyer, 1990). While all of those studies suVered some method-
ological Xaws, they provided important preliminary evidence for the beneWts of
exposure in PTSD, particularly with regard to the re-experiencing symptoms.
As noted above, Foa et al. (1991b) found PE to be marginally superior to SIT,
and considerably superior to both supportive counseling and a wait-list control, in
485 Posttraumatic stress disorder: Treatment
45 female assault survivors with PTSD. As noted above, SIT was superior at
posttreatment, but subjects in this group tended to show some relapse at follow-
up. Those in the PE group, on the other hand, showed a slower but continued
improvement. This Wnding is interesting, perhaps suggesting that the SIT was
eVective for symptom management but did little to modify the traumatic memo-
ries in the longer term. Thus, while PE is a more diYcult and painful process, it
does seem to produce more meaningful and lasting curative eVects. Also noted
above is the second study by the same group (Foa et al., 1999), which conWrmed
the superiority of PE over both SIT and a combination of the two. The fact that the
combination treatment was less eVective than PE alone is intriguing. The most
likely explanation is that session lengths in all groups were identical. Thus the
combination group received less time on exposure and anxiety management than
the single modality equivalents. It may be that an extended treatment protocol,
allowing adequate time for both components, would prove superior.
Two other studies are worthy of note, since they investigated PTSD patients
with a variety of traumatic stressors rather than focusing solely on veterans or
female assault victims. Thompson et al. (1995) conducted an open trial with 23
PTSD patients, providing eight weekly exposure sessions. While the results must
be interpreted cautiously given the absence of a control condition, signiWcant
improvements in PTSD symptoms were obtained across several objective
measures. In an interesting variation, Richards et al. (1994) compared imaginal
with in vivo exposure in the treatment of PTSD, using a cross-over design. They
found surprisingly high symptom reduction of 65% to 80% following treatment,
with no patients continuing to meet criteria for PTSD at posttreatment or 1 year
follow-up. The only diVerence between exposure types was found on phobic
avoidance, with in vivo being superior regardless of the order of presentation.
In summary, controlled treatment outcome research has consistently provided
support for the use of exposure techniques in the treatment of PTSD.
Cognitive restructuring
Resick and Schnicke (1992) evaluated a group version of CPT with 19 rape victims
and compared it with a wait-list control group. They reported a 40% reduction in
PTSD symptoms in the CPT group, as compared with 1.5% for the wait-list
controls. These results are encouraging, although interpretation is hampered by
the absence of a credible control treatment. Two recent studies with mixed PTSD
samples have addressed this issue by investigating both cognitive therapy and
exposure. Marks et al. (1998) compared four treatment approaches: (1) imaginal
and in vivo exposure, (2) cognitive restructuring, (3) a combination of exposure
and cognitive restructuring, and (4) relaxation. Exposure, cognitive restructuring,
and the combination group all produced global improvements, but no signiWcant
486 Treatment of Anxiety Disorders
Drug treatments
Since several useful reviews of pharmacological interventions in PTSD exist (e.g.,
Friedman, 1997; Yehuda et al., 1998), this section will attempt to provide only a
broad overview of the area. Drug treatments may serve several functions in the
treatment of PTSD. First, since confronting the trauma as part of treatment is
inevitably distressing, medication may serve as an adjunct to psychological inter-
ventions. Drugs may serve to moderate the arousal and distress, allowing the
patient to tolerate the diYcult process of modifying, and coming to terms with,
the traumatic memories. Second, drugs may be used to treat comorbid conditions,
such as depression, that may interfere with treatment of the core PTSD symptoms.
Finally, pharmacotherapy may be viewed as directly relieving the primary PTSD
symptoms, a position that has strengthened with the increasing recognition of
biological alterations in PTSD. This, however, remains a goal for the future. To
date, no drug has been developed speciWcally for PTSD and, instead, drugs
developed for depression and anxiety have been tested with varying degrees of
success.
The new generation of antidepressants, selective serotonin reuptake inhibitors
(SSRIs), have emerged recently as the Wrst choice of drug treatments for PTSD.
This is despite the fact that few randomized clinical trials have been published to
date (van der Kolk et al., 1994; Connor et al., 1999). Those studies reported
improvement in civilian samples, but van der Kolk et al. (1994) found that
Xuoxetine was no better than placebo in treating veterans with combat-related
488 Treatment of Anxiety Disorders
PTSD. Several open trials have suggested that SSRIs produce marked reductions in
overall PTSD symptomatology. In particular, the apparent capacity of SSRIs to
reduce the emotionally numbing symptoms of PTSD has provoked much interest,
since other drugs have failed to moderate this aspect of the disorder. The SSRIs
remain promising medications in the treatment of PTSD, partly because of their
purported ability to target the whole syndrome and partly because of the relatively
low side-eVects proWle. Drugs such as trazadone and nefazadone, which are
serotonergic antidepressants with both SSRI and 5-hydroxytryptamine type 2
receptor blockade properties, also have potential. Although these are yet to be
tested in adequately controlled trials, multisite trials of nefazadone are currently in
progress.
Of the older antidepressants, the monoamine oxidase inhibitors (MAOIs) have
produced improvements in two out of three randomized trials, particularly with
reference to the re-experiencing symptoms. In practice, however, clinicians are
reluctant to prescribe these agents because of concerns about the dietary restric-
tions. The newer breed of MAOIs such as moclobemide, known as reversible
inhibitors of monoamine oxidase type A (RIMAs), do not have these problems but
have yet to be tested in PTSD. Three randomized trials have investigated tricyclic
antidepressants in PTSD, along with numerous open trials and case reports. The
results have been mixed and generally moderate in magnitude. With the advent of
SSRIs, the tricyclics are no longer a Wrst-line drug in PTSD treatment.
Anxiolytic drugs, particularly the benzodiazepines, have been prescribed widely
for PTSD in some clinical settings. While they may produce modest reductions in
generalized anxiety, evidence from both randomized and open trials suggests that
they are no better than placebo in reducing core PTSD symptoms. Indeed, there is
some evidence that they may impede recovery when used in the Wrst few weeks
following the trauma (Gelpin et al., 1996). On the other hand, antiadrenergic
agents such as clonidine and propranolol may be helpful. Although no ran-
domized trials exist as yet, several open trials suggest improvement in hy-
perarousal and intrusion symptoms (Yehuda et al., 1998). Further, clonidine has
been proposed as a useful intervention in the very acute stages of traumatic stress
such as combat stress reaction (Friedman et al., 1993).
Several other classes of medication have been used in the treatment of PTSD,
although none has been adequately evaluated at this stage. Open trials of anticon-
vulsant agents, such as carbamazepine and valproate, have suggested some role for
this class of medication in PTSD, particularly with reference to the arousal
symptom cluster. Although antipsychotic drugs were used in the past, the advent
of more appropriate medications has rendered this class of medication less useful
in PTSD, except in cases presenting with frank psychotic symptoms. While
suggestions that the endogenous opioid system is dysregulated in PTSD have led
489 Posttraumatic stress disorder: Treatment
Primary prevention
Primary prevention aims to reduce the incidence of new cases through interven-
tion before the disorder occurs. These interventions are provided to the whole of
the aVected population, with no attempt to identify high-risk survivors (although
that may be an important outcome of the process). Much debate has revolved
around the area of psychological debrieWng as described by Mitchell and Bray
(1990). As noted by several authors (Kenardy et al., 1996; Rose and Bisson, 1998),
there is a paucity of adequate empirical evidence to support the use of brief early
interventions, such as debrieWng, following trauma. That is not to say that
debrieWng is not helpful – the methodological problems inherent in the available
research simply do not permit Wrm conclusions to be drawn either way. There is
an urgent need for rigorous evaluation of debrieWng strategies to answer not only
the obvious questions regarding the eYcacy of debrieWng, but also a range of other
very basic questions about which, at present, there is little consensus. What exactly
is debrieWng? What are the goals? To whom is it suited – which populations and
following which types of incident? When should it be provided? Who should
provide it? And, perhaps most importantly, can debrieWng be harmful? A compre-
hensive discussion of this debate is beyond the scope of this chapter. SuYce to say
490 Treatment of Anxiety Disorders
criteria for PTSD versus 70% of the latter group. Five and a half months postas-
sault, victims in the active condition were signiWcantly less depressed, and had
signiWcantly less severe re-experiencing symptoms, than victims in the control
condition. Interestingly, the rate of PTSD in the wait-list condition had dropped
to 20% by follow-up, providing further evidence of the trend towards recovery
over the Wrst 6 months posttrauma, even in the absence of formal treatment.
The advent of ASD as a diagnostic category has provided the opportunity to
determine whether speciWc interventions may prevent the progression from ASD
to PTSD. Although only one controlled trial is available at this time, many more
are likely to appear in the literature over the coming months. Bryant and col-
leagues (1998) investigated survivors of civilian trauma with a diagnosis of ASD,
comparing a cognitive behavioral therapy (CBT) intervention (similar to that of
Foa et al.’s study) with supportive counseling (SC). Only 8% of patients in the
CBT group met criteria for PTSD at posttreatment, as compared with 83% in the
SC condition. At 6-month follow-up, the Wgures were 17% and 67%, respectively,
with the CBT group showing signiWcantly greater reductions in intrusive, avoid-
ance, and depressive symptomatology. In a subsequent extension of that study,
Bryant and colleagues (1999) found that prolonged exposure, as well as a combi-
nation of prolonged exposure and anxiety management, were both superior to
supportive counseling. Interestingly, the combination treatment was not superior,
suggesting that exposure may be the most critical component.
In summary, there is now suYcient evidence to suggest that it is worth targeting
symptomatic survivors in the immediate aftermath of trauma with the provision
of speciWc interventions. Such treatment can be expected to signiWcantly reduce
the subsequent prevalence of more serious and chronic pathology such as PTSD.
Conclusions
The controlled outcome studies quoted above, at Wrst sight, provide impressive
support for various approaches to the treatment of chronic PTSD. However, it is
important to be cautious in our optimism. The treatment of chronic PTSD (i.e., of
more than 3 months duration) has yet to achieve the levels of eYcacy obtainable in
the treatment of most other anxiety disorders. As a rule of thumb, around
one-third of patients with chronic PTSD do very well following treatment.
Another third do reasonably well – although they will probably not meet criteria
for a formal diagnosis of PTSD at posttreatment, many problems remain and
impairment of psychosocial functioning continues. The Wnal one-third of patients
fail to respond in any signiWcant way to treatment. The elucidation of those factors
that will predict response to treatment, as well as which treatment modality is
suited to which patients, is a major challenge for the Weld.
26
Assessment issues
A detailed discussion of assessment strategies for PTSD was provided in Chapter
24. The purpose of this section is to elucidate some additional factors to be
considered when assessing for treatment purposes. A thorough assessment of the
patient’s history, current psychosocial functioning, and diagnosis is required
before an adequate formulation of the case can be made and a management plan
developed. A detailed discussion of psychiatric interviewing is beyond the scope of
this chapter and only those issues particularly relevant to survivors of trauma will
be discussed in this section. Key issues to look for in the history include previous
episodes of psychiatric disorder (or simply ‘‘bad nerves’’), as well as prior treat-
ment experience and pretrauma coping strategies. IdentiWcation of these factors
492
493 Posttraumatic stress disorder: Clinician Guide
will assist in the formulation of realistic treatment goals and selection of interven-
tion strategies with an improved chance of success. It is important also to take a
history of prior traumatic experiences. Clearly, this latter area may be highly
sensitive and relevant information may not necessarily emerge in the Wrst session.
While the utmost care must be taken not to assume the existence of prior trauma
on the basis of symptom proWle or treatment response, the clinician is nevertheless
advised to keep the possibility in mind. Clinical experience suggests that it is not
unusual for current presentations to be exacerbated by activation of prior trau-
matic memory networks, even if the patient does not necessarily make the
connection.
The patient’s current social context – their ‘‘recovery environment’’ – may
impact upon the eYcacy of treatment. Thus assessment should include evaluation
of support networks and close interpersonal relationships, and should attempt to
gauge the attitude of signiWcant others to the person’s traumatic experience and
psychological response. Social support and validation of the experience by signiW-
cant others appear to facilitate eVective recovery. Active involvement of spouses
and partners (with the patient’s approval) in both assessment and treatment
phases is strongly encouraged. Where social support is obviously lacking, it may be
worth attempting to address this issue by means of a skills-development, problem-
solving approach in the initial stages of treatment. Evaluation of occupational
functioning is important also. Clinical experience suggests that the structure
provided by daily routines is important in restoring a sense of control. Equally, an
overcommitment to work is often used by PTSD suVerers as an avoidance strategy
– keeping busy every minute of the day helps to prevent the memories from
returning. Although this, like many avoidance behaviors, may be an eVective
strategy for some people some of the time, it precludes the possibility of confront-
ing and modifying the traumatic memories and will interfere with longer-term
recovery.
Since PTSD is routinely associated with comorbidity, a thorough assessment of
other conditions, particularly substance abuse, depression, and other anxiety
disorders, is essential in planning an eVective intervention strategy. The next
section discusses the implications of chronicity and comorbidity for treatment.
and treating a Vietnam veteran with a 30-year history of the disorder, several failed
marriages, an unstable employment history, substance abuse, anger problems, and
a pension claim currently pending. It is beyond the scope of this chapter to discuss
all the issues associated with the latter example. SuYce to say that issues of good
clinical management become of paramount importance. Change will be slow and
eVective case management is essential. Psychosocial issues other than core PTSD
symptoms will need to be addressed, including relationships, occupational func-
tioning, and social reintegration.
The appropriate management of comorbid conditions is, more often than not,
an important factor in the treatment of PTSD. The two most common Axis I
conditions associated with chronic PTSD are substance abuse and depression.
Each of these will be dealt with brieXy, although it must be stated at the outset that
empirical data on the treatment of comorbid conditions in PTSD are lacking and
decisions often need to be based on informed clinical judgment.
Substance abuse
Substance abuse, particularly in the form of alcohol, is a common complication in
survivors of trauma. Regular alcohol use, notwithstanding its obvious drawbacks,
can be an eVective way for PTSD patients to manage the intrusion and arousal
symptoms. As such, it is best conceptualized as part of the avoidance and
emotional numbing component of the disorder. Care must be taken when asking
people to give up this crutch without providing alternative coping strategies. This
raises one of the more diYcult clinical decisions in the treatment of PTSD: should
the substance abuse be treated Wrst, aiming for a period of sobriety prior to
addressing the PTSD, or should the two disorders be treated concurrently? There
is no easy answer. One argument proposes that the primary reason the person is
abusing alcohol is to manage the PTSD symptoms and, thus, amelioration of those
symptoms must occur before (or concomitant with) attempting to reduce the
substance abuse. The alternative argument proposes that eVective processing and
modiWcation of the traumatic memories is not possible while the person continues
to abuse alcohol or other drugs. Some clinicians believe that the decision can be
made on the basis of history: if the person was abusing substances prior to the
trauma (even if the abuse has signiWcantly worsened since), then the behavior is
not fundamentally trauma related and should be treated separately and prior to
the PTSD. If the abuse only commenced following the trauma, it should be treated
in conjunction with the traumatic stress.
In the Wnal analysis, it will be a clinical decision based on a range of factors.
There is no doubt that sobriety is preferable and that, at the very least, the
substance abuse must be under control prior to PTSD treatment. The severity of
the abuse is an important consideration and the person must be able to attend
495 Posttraumatic stress disorder: Clinician Guide
treatment without being under the inXuence of drugs. As a guide, we suggest that
the early stages of treatment (as discussed below) can, and should, proceed in
conjunction with treatment for the substance abuse, since they are likely to
facilitate change in that area. It is doubtful that the more intensive stages of
exposure and cognitive restructuring will be eVective in the context of ongoing
substance abuse.
Depression
The second common comorbid condition in PTSD is depression, again raising the
diYcult question of which disorder to treat Wrst. As with substance abuse, an
evaluation of whether the depression is secondary to the PTSD or a primary
disorder in itself may facilitate decision making, although, of course, this is not a
clear dichotomy. The severity of the depression will be an important factor also.
Milder forms of the disorder are more likely to resolve with improvements in
other areas and are less likely to interfere with PTSD treatment. As in the
treatment of other anxiety disorders, however, more severe depression is likely to
impact negatively on the treatment process and outcome.
Thus, when moderate to severe depression is diagnosed, it is recommended that
attention be paid to that disorder prior to addressing the PTSD symptoms.
Psychological or pharmacological interventions may be useful. Both of these may
have additional advantages in providing some amelioration of core PTSD symp-
toms, which may, in turn, facilitate subsequent psychological interventions
directed at the traumatic memories.
Impediments in treatment
There are many potential impediments to the treatment of PTSD, several of which
(such as comorbid conditions and poor rapport or client motivation) are
common to any psychological intervention. A few, however, are particularly
relevant to PTSD and are worthy of consideration if treatment does not seem to be
progressing as expected.
The issue of secondary gain, particularly in the form of monetary compensa-
tion, can be a complicating factor in recovery from trauma. There is no clear or
automatic relationship – many people who fail to show a good recovery are not
seeking compensation, and many who are awaiting the outcome of a claim are still
able to beneWt considerably from treatment. Nevertheless, in an ideal world, it
would be wise to ensure that all compensation claims are resolved prior to
commencing treatment. In the real world that is not possible and often the best
that can be done is to raise the issue openly and to discuss the implications with
the patient. Through this process of open discussion, the clinician may be able to
496 Treatment of Anxiety Disorders
gauge the extent to which the patient feels a need to retain a symptom proWle for
the purposes of compensation. This, in turn, may inXuence the goals and type of
treatment provided. It may be possible also to convince the patient that a good
psychological recovery will, in the long term, contribute more to their happiness
and well-being than any compensation payout. Finally, it is advisable for the
treating clinician not to provide assessment reports for compensation or other
psycho-legal purposes. This is obviously a diYcult issue, with the clinician in this
situation often arguing that he or she knows the patient best and is therefore in the
optimum position to provide such a report. However, the conXict in roles is
unavoidable and the blurring of boundaries has the potential to impact negatively
on both the treatment and assessment roles. It may be better to explain the
situation openly to the patient at the outset, oVering instead to refer on to a
trusted colleague for the assessment reports.
Reference has already been made to the issue of prior trauma. It is important to
reiterate that assumptions by clinicians about the existence of prior trauma, and
subsequent attempts to ‘‘unearth’’ previously inaccessible memories, are both
unethical and dangerous. Guidelines regarding such procedures are available from
most professional organisations. Equally, to ignore the possibility of prior trauma
as an inXuence on current functioning is almost negligent. Thus the clinician must
walk a Wne line between, on the one hand, encouraging the client to (perhaps
unconsciously) generate false memories and, on the other, providing a safe
environment in which genuine traumatic experiences can be revealed. Nondirec-
tive questions, such as ‘‘have you had other experiences in your past that were very
frightening or distressing?’’ or ‘‘Have there been times in your life when you’ve felt
like this before?’’ can be useful in accessing important information. If therapy
targeted at the most recent trauma is progressing well, this is unlikely to be an
issue. However, if the patient is not progressing as expected, one hypothesis may
be the existence of prior traumatic experiences. Revelations of prior trauma
provide the clinician with an opportunity to make links between those experiences
and the more recent events, with the possibility of treating the earlier traumatic
memories more directly if appropriate. It is not unusual, particularly in patients
who habitually deal with stress by avoidance and denial (e.g., not uncommon in
emergency workers) for the opportunity to make those links to be a turning point
in treatment.
Although the issue of guilt will be discussed further below, it warrants separate
attention at this stage, since clinical experience suggests that it often interferes with
treatment. By deWnition, those things about which survivors feel most guilty are
those that they are most reluctant to acknowledge and admit to another person.
This is particularly a problem with veteran populations, since many acts commit-
ted in the context of war are unacceptable when viewed later from a civilian
497 Posttraumatic stress disorder: Clinician Guide
perspective. As with prior trauma, issues of guilt will often emerge quite naturally
during treatment and can be dealt with by normal therapeutic processes. In some
cases, however, guilt feelings may be particularly strong and may not be acknow-
ledged even in response to direct questioning. A failure to progress in treatment
may prompt the clinician to hypothesize about the existence of unresolved guilt
and to gently probe the patient with appropriate questions. Again, clinical experi-
ence suggests that an opportunity to acknowledge the guilt, often for the Wrst time,
and to re-evaluate those self-appraisals in the context of therapy may be a turning
point in treatment.
Treatment process
The major stages of treatment are shown in Table 26.1. As a general guideline, the
interventions are presented in the order in which they appear in the table,
although we recommend that attempts be made to integrate the exposure and
cognitive restructuring components. It is recommended that all treatment sessions
be taped so that clients have an opportunity to review and consolidate the
information. As noted below, exposure components will be taped separately and
therefore we recommend the use of two tapes for each client, one being reserved
exclusively for the exposure.
Psychoeducation
Psychoeducation in traumatic stress is an important Wrst step in treatment. It can
do much to reduce the secondary distress (about the symptoms) and to enhance
the credibility of the therapist and the collaborative nature of the relationship. The
sudden onset of symptoms following trauma can be extremely frightening, es-
pecially for someone with no prior psychiatric history. The person may believe
that they are going crazy and will never recover. A poor understanding of personal
reactions may prompt denial, avoidance, and withdrawal, often with associated
substance abuse, which may serve to impede recovery. On the other hand, a good
understanding of traumatic stress reactions is the Wrst step in cementing the
therapeutic relationship, managing symptoms eVectively, and working on the
recovery process.
The content of this phase would normally include common responses to
trauma, much as outlined in the accompanying Patient Treatment Manual. Care
should be taken not to minimize these reactions and the commonly used phrase
‘‘normal reactions in a normal person to an abnormal event’’ is not always
appropriate. If patients have developed PTSD, their reaction is not (statistically)
normal. Even if they do not have the full disorder, their reaction is far from normal
in terms of their own experience and the phrase may sound dismissive of the level
499 Posttraumatic stress disorder: Clinician Guide
Symptom management
Most clients presenting with PTSD or other traumatic stress disorders are feeling
frightened, vulnerable, and out of control. While the psychoeducation will have
helped them to understand what is happening to them, they now need strategies to
manage the symptoms in order to regain a feeling of control. A detailed descrip-
tion of the range of possible strategies is beyond the scope of this section and
clinicians are referred to other chapters in this book (e.g., Chapters 7, 15 and 23)
for excellent descriptions of some key anxiety management interventions. Never-
theless, the following provides a summary under the broad headings of physiologi-
cal, cognitive, and behavioral strategies as they apply to the treatment of traumatic
stress.
It is important not to overwhelm the patient with too many strategies, but
rather to think about which will work best for each particular case. Then, if it is
worth teaching, it is worth teaching properly. Provide a rationale for, and a
description of, the strategy, before modeling and practicing it in the session.
Discuss any problems or misunderstandings as they arise and adjust as necessary.
It is then vital to emphasize the importance of practicing the skill (often several
times a day) in nonstressful environments before attempting to use it to control
anxiety in a diYcult (particularly trauma-related) situation. It is better to teach
and consolidate a few skills well than to provide a plethora of strategies that are
poorly understood and unlikely to be eVective.
A Wrst step is often to introduce the concept of SUDs – subjective units of
distress. (A copy of this scale appears in the Patient Treatment Manual.) This is a
‘‘fear thermometer’’ that clients use to rate their current level of anxiety or distress
on a scale of 0 (‘‘perfectly relaxed and calm’’) to 100 (‘‘the worst imaginable
anxiety or distress’’). This is important in helping the person to self-monitor the
eVects of the anxiety-management interventions, providing a more objective
measure of their eYcacy. It will also be a vital component of the subsequent
exposure treatment. Introducing it at this stage has the added beneWt of providing
the patient with plenty of opportunities to practice rating his or her own anxiety
before being asked to do so in the more diYcult phase of exposure.
500 Treatment of Anxiety Disorders
Physiological arousal is a key feature of traumatic stress and any strategy that
assists in reducing arousal is likely to be beneWcial. This may be particularly
important in the acute stages posttrauma – clinical experience suggests that
eVective arousal management in the Wrst few hours or days may facilitate subse-
quent recovery. Physically orientated strategies are appealing not only for their
eYcacy in producing rapid results, but also because they are easy, nonthreatening
(and nonpsychological) interventions to use while the patient is still feeling very
vulnerable. A Wrst option adopted by many therapists is that of breathing control,
an area well covered in several other chapters in this book, as well as in the Patient
Treatment Manual (Chapter 27). Progressive muscle and isometric relaxation
strategies, also covered well elsewhere in this book, are often useful. Other
suggestions involve dietary advice, including the reduction of stimulants such as
caVeine and nicotine, as well as aerobic exercise.
Cognitive strategies are usually designed to give the patient some control over
the intrusive cognitions, but care must be taken not to give contradictory mess-
ages. It should be emphasized that thinking about the trauma is not a bad thing to
do – on the contrary, it will be a central component of treatment further down the
track. However, it is important to do this in a controlled manner for limited times
during the day. If the thoughts are intruding constantly, they simply result in high
distress and the person may feel unable to focus on anything else. Thus these
strategies will help to limit the time spent thinking about the trauma in order to
reduce distress and facilitate a return to more normal functioning. Distraction
techniques are commonly used – anything from counting backwards from 100 in
7s to asking patients to describe their current surroundings in great detail. Again,
see the Patient Treatment Manual for more information on such strategies. Many
people with PTSD are good at imaging. However, if imaginal techniques are to be
used for arousal reduction in PTSD, it is essential that the patient, not the
therapist, describes the scene, since there is too much danger of unwittingly
introducing potentially traumatic elements into the scenario. Some people Wnd
imagining a safe place, and describing it in great detail, to be a useful technique
that provides not only a distraction from the painful memories but also a sense of
security.
Behaviorally orientated techniques usually revolve around scheduling activities
and providing structure to the person’s day. It is often a good idea to encourage
people to resume a normal routine as quickly as reasonably possible following a
trauma, although they should be reminded to take it easy and not throw them-
selves into work as a way of avoiding the unpleasant memories. Scheduling
pleasant activities is often important, since the core symptoms of PTSD are likely
to produce anhedonia and loss of interest. It is particularly important to recom-
mend that the person makes an eVort to undertake activities with other family
501 Posttraumatic stress disorder: Clinician Guide
members. This helps to reduce the social withdrawal and isolation that can place
an enormous strain on relationships.
Although the bulk of this section has referred to anxiety management, since that
is a fundamental part of treatment for all traumatic stress reactions, more chronic
presentations may require symptom management for other problems. Anger is
often a primary presenting problem in chronic PTSD (especially in veterans). The
consuming and explosive nature of anger, and its impact on social networks, often
necessitates direct intervention prior to addressing core PTSD symptoms. Similar-
ly, depression that does not ameliorate over the Wrst few sessions will impact
negatively on subsequent treatment and should be addressed. Empirically
validated behavioral strategies may be used to address other areas of diYculty such
as sleep disturbance, substance abuse, and assertion (see e.g., the Social phobia:
Patient Treatment Manual, Chapter 11).
The purpose of the symptom-management component of treatment for PTSD
is to help the person to develop some control over the distressing symptoms in the
early stages of treatment. The strategies are generally simple and relatively quick to
teach and to learn. It is recommended, therefore, that one or two interventions
from each of the physical, cognitive, and behavioral domains be provided to the
patient over the Wrst few weeks. It is important that some progress is made in
symptom management before moving on to the most important aspect of treat-
ment, exposure to the traumatic memories.
least, however, a signiWcant reduction must take place before the session is
terminated, even if this means prolonging the session longer than usual.
Fourth, each item on the hierarchy needs to be repeated as often as is necessary
for it to evoke only minimal anxiety. This repetition may occur within a single
session, within multiple sessions, or between sessions as discussed below. Finally,
exposure needs to be functional, which means that the aVective components of the
memory must be accessed along with the stimulus material. Individuals with
PTSD become adept at telling their story in a detached, unemotional manner,
accessing only part of the traumatic memory network. This process is not likely to
be therapeutic. However, a few probing questions are usually suYcient to access
the accompanying aVect, allowing habituation to occur.
trauma is likely to cause high anxiety and the patient may require considerable
reassurance prior to commencing the imaginal exposure. Then the patient is asked
to describe the experience in detail and to continue the description until the event
is over and a point of safety is reached. Although Foa and Rothbaum (1998)
suggested that the client be told to recount the trauma in the present tense with
eyes closed on the Wrst presentation, in routine clinical practice the therapist may
decide to titrate the distress by allowing a past-tense narrative with eyes open. This
provides an opportunity for an initial sense of mastery and gives the therapist
important information about likely diYcult points on subsequent exposures.
Assuming the SUDs are manageable, however, a move to present tense with eyes
closed is recommended as soon as possible. Similarly, the client may be allowed to
skip over the worst aspects on earlier sessions. On later presentations, however, the
therapist should use prompts with stimulus cues (e.g., ‘‘What does he smell like?’’
or ‘‘Describe her face’’) and response cues (e.g., ‘‘What are you feeling now?’’ or
‘‘What are you thinking now?’’) as appropriate. It is also useful to provide
supportive comments throughout the process (e.g., ‘‘You’re doing really well’’ or
‘‘I know it’s diYcult, but stay with that image for a while’’). As the SUDs gradually
reduce over repeated sessions, more attention is paid to the speciWc elements of the
memory that are most distressing. Later sessions may focus primarily on repeated
exposure to those most upsetting parts. It is important in these later sessions to
maximize the cues in all sensory modalities (sights, sounds, smells, tastes, sensa-
tions). Elements of cognitive restructuring are also routinely incorporated into the
imaginal exposure, as discussed below.
The client should be asked for a SUDs rating every 5 minutes throughout the
exposure, which is recorded by the therapist and discussed at the end of the
session. The therapist should not rely exclusively on SUDs reports but, rather,
should observe the client closely for signs of distress or avoidance. If the anxiety
has reduced appreciably, that should be reinforced. If not, it is important to
reassure the client that it will reduce with persistent confrontation of the memory.
Adequate time should be allocated at the end of the session to discuss the
experience and to unwind. Some therapists provide a separate room for patients to
recover in their own time before going home and may use a relaxation procedure
at this point.
Repeated exposure to the traumatic memory is best achieved by taping the
session and instructing the client to listen to the tape daily at home. Obviously,
this component requires some clinical judgment and there may be occasions when
the therapist decides that this may not be the best course of action. At the very
least, it is important to provide clear structure and guidelines for this homework
and to ensure that support is available should the experience prove too distressing.
An example of appropriate guidelines for taped exposure homework is provided
in the Patient Treatment Manual.
505 Posttraumatic stress disorder: Clinician Guide
A Wnal point to consider during the exposure process concerns the client’s
knowledge about the experience. Indeed, it has been suggested that a key to
eVective recovery from trauma is the ability to answer fundamental questions
about what happened and why it happened (Figley, 1985). Therapists often
assume that the survivor is clear about all the details – after all, they were there,
surely they know what happened? In reality, many survivors of trauma have very
confused and fragmented memories of the experience, with a poor understanding
of exactly what happened, how it happened, and why it happened. Misunder-
standings, and gaps in the memory, may make successful exposure treatment
more diYcult. Obviously, some of these questions will remain unanswerable and
others will resolve as part of the exposure process. However, therapists should be
constantly aware of opportunities to Wll in gaps in the trauma memory in order to
assist the client to ‘‘put the pieces of the jigsaw together’’ and make sense of the
experience. Are there other people they can talk to, such as emergency services
personnel or others present at the scene? Is there written information from media
reports that they can read about the incident, or video footage to view, that would
help make sense of what happened? Occasionally, the therapist is able to support
and empower the client in accessing such information. The opportunity to Wnd
out more about what happened (and possibly why) can do a great deal to assist
survivors in understanding, and coming to terms with, their experiences.
minimize avoidance. Foa and Rothbaum (1998) suggested that asking clients to
recount the most diYcult aspects using a ‘‘slow motion’’ strategy, with thoughts,
feelings, and physical sensations slowed down, may help to maintain full engage-
ment and minimize avoidance. An alternative form of dissociation is often
mentioned in the context of exposure. This is opposite to the detached, disengaged
form described above, characterized instead by an overinvolvement in the mem-
ory and a vivid Xashback experience as if the event were recurring again. It is not
possible to modify the traumatic memory network eVectively, incorporating new
information, while experiencing a Xashback. The therapist should therefore make
every eVort to bring the client back into the ‘‘here and now’’ before proceeding
with the exposure. Instructions to open their eyes, look around, feel the chair,
describe the room, check date, time and place, and so on, are all useful in dealing
with such dissociative episodes during exposure. Having said that, if the exposure
is conducted carefully according to the guidelines described above, such dissocia-
tive Xashback experiences should be a rare occurrence.
Contraindications for exposure are basically common sense. Timing is import-
ant: does the client feel suYciently in control (having mastered some key symp-
tom management strategies) and is rapport adequate? Acute life crises, current
substance abuse, severe psychiatric comorbidity, and a history of noncompliance
with treatment should all suggest caution in the use of exposure. While the
possibility of iatrogenic eVects with exposure, as with any other potent interven-
tion, should not be ignored, the likelihood of adverse reactions can be minimized
by sensible clinical practice.
Cognitive restructuring
Cognitive restructuring in PTSD is designed to assist the client in identifying
dysfunctional thoughts and beliefs about the world, other people, or themselves
that have developed from, or been strengthened by, the traumatic experience.
There are many ways to go about the process of cognitive restructuring and good
descriptions of its application in PTSD are provided elsewhere (Resick and
Schnicke, 1993; Foa & Rothbaum, 1998).
Foa and Rothbaum (1998) identiWed Wve common themes of dysfunctional
belief (and associated negative thoughts) that frequently occur following trauma.
The Wrst two of these relate to pretrauma beliefs about the self and the world, with
extreme views in either direction rendering the person vulnerable to poor pos-
ttrauma adjustment. On the one hand, a prior negative view of the self may be
reinforced by the traumatic experience (e.g., ‘‘this proves that I’m really no
good’’). On the other hand, prior unrealistic beliefs of invulnerability and personal
competence may be shattered by the experience, leaving the person confused and
insecure. Similarly, pretrauma beliefs about the safety of the world may be aVected
507 Posttraumatic stress disorder: Clinician Guide
in the same way. Prior perceptions of the world, and other people, as being
dangerous will be reinforced by the trauma, while unrealistic views of the world as
always safe will be shattered by the trauma. More Xexible and realistic prior views
of the self and the world are likely to be associated with improved posttrauma
adjustment. The third category relates to beliefs about reactions during the
trauma, leading to negative self-perceptions (e.g., ‘‘I should have fought back’’, or
‘‘I can’t trust myself’’). The fourth relates to beliefs about the PTSD symptoms
themselves (such as ‘‘I’m going crazy’’ or ‘‘I’ll never recover’’), while the Wnal
theme relates to beliefs about the reactions of others (such as ‘‘Everyone thinks it
was my fault’’ or ‘‘They think I’m overreacting’’).
The client is helped to identify the negative automatic thoughts and dysfunc-
tional beliefs present following the trauma, and to treat them as hypotheses rather
than facts. Therapist and client can then work together in a collaborative fashion
to challenge and dispute the negative cognitions, eventually replacing them with
more balanced and rational alternatives. While there are several ways to go about
this process, it is common to work through a series of questions, as shown in the
Patient Treatment Manual. The important point common to all eVective cognitive
therapy is that the process of challenging and disputing the automatic thoughts
and dysfunctional beliefs is an active and rigorous intellectual task. It is not
suYcient to simply replace the maladaptive cognitions with an adaptive alterna-
tive; the individual must make an eVort to really understand why the thought is
based upon faulty logic.
Many survivors of trauma seek unrealistic assurances, wishing to replace the
distress-producing thoughts with beliefs that are patently untrue. A common
example of this is to seek an assurance that they will never experience such an
event again. (‘‘If you could promise me that this will never happen again, I’d be
alright’’). Clearly, it is not possible to provide such an assurance. Rather, the
therapist needs to work with the client to realistically evaluate the risks and the
potential eVects. A common theme in all anxiety disorders is the tendency to
overestimate the probability of a bad event occurring, as well as to overestimate
the negative consequences should it occur. The latter, of course, are diYcult
cognitions to challenge in PTSD. However, therapists need to assist clients in
focusing on what few positives there are: the fact that they did survive, that they
are recovering, and that they have learnt skills that will help them in the extremely
unlikely event that it should happen again.
The timing of cognitive restructuring in PTSD is important if its eYcacy is to be
optimized. Although exposure work is routinely commenced prior to the cogni-
tive interventions, in practice the two are inextricably entwined. Exposure often
helps to integrate the fragmented traumatic memory, bringing to light informa-
tion that casts a new perspective on the event. These new perspectives are often
508 Treatment of Anxiety Disorders
best dealt with by cognitive restructuring. Indeed, it may be postulated that the
real therapeutic ingredient of any exposure treatment is actually the processing of
new information. Appraisals, interpretations, and beliefs are central to our under-
standing of traumatic stress, which is characterized by shattered assumptions
about fundamental issues such as safety, trust, and personal worth. While some of
these may be resolved by a pure exposure paradigm alone, in most cases cognitive
restructuring needs to be woven into the later stages of exposure. This is particu-
larly relevant from the perspective of cognitive processing models of PTSD which
postulate that the traumatic memory network must be activated before it can be
modiWed. The interpretations and beliefs associated with the experience need to be
restructured in the context of the entire memory network. Therapists should
therefore be prepared to do at least some of the cognitive challenging work during
the later exposure sessions when target thoughts and beliefs are activated.
dangerous part of town, on my own, in the early hours of the morning. I won’t do
that again’’). Characterological self-blame, however, is potentially much more
problematic (‘‘It was my fault it happened because I’m such a worthless person’’).
In such cases, the therapist needs to highlight the logical errors inherent in global
self-rating, drawing the distinction between a bad, or unwise, behavior and a bad
person. This is particularly important when working with someone who did,
undeniably, ‘‘do something bad’’ during the traumatic event: e.g., by mistake or
design, the person did something that resulted in the death or suVering of
innocent others. It is counter-therapeutic to pretend that it did not happen or that
it was an acceptable way to behave. Rather, the client needs to be assisted in
understanding that it is illogical and unhelpful to generalize from a single mistake
or negative act to rate their whole selves. The Weld of rational emotive therapy
(RET) is notably strong on this issue and interested readers are referred to
standard RET texts (e.g., Walen et al., 1992) for a more detailed elucidation of this
concept.
can cope with it. It will pass. Now, what strategies can I use to take control and
help myself to feel better?’’).
∑ Session 4
∑ Check homework and coping (15 minutes)
∑ Exposure (45 minutes)
∑ Continue cognitive restructuring (30 minutes)
∑ Session 5
∑ Check homework (15 minutes)
∑ Cognitive restructuring (15 minutes)
∑ Relapse prevention (45 minutes)
∑ Closure & termination (15 minutes)
Conclusions
While the treatment of PTSD (and ASD) has come a long way in the past 10 years,
there is still much to learn about these complex disorders. Expectations of
treatment outcome must remain modest. As a rule of thumb, it can be expected
that around one-third of patients will respond very well to treatment, making
close to a full recovery. Another one-third will show clear beneWts, probably not
meeting criteria for a formal diagnosis at posttreatment but continuing to experi-
ence milder adjustment problems and interference in social and occupational
functioning. Research data are not yet available regarding continued recovery in
this subpopulation, although anecdotal evidence would suggest that signiWcant
changes from pretrauma functioning may remain in the long term. Often these
changes are described by partners in terms of their loved ones being somewhat
more withdrawn and less spontaneous than they used to be, with perhaps a slight
Xattening of aVect. The Wnal one-third of patients with PTSD seem to gain little
from existing treatment approaches. A major challenge for the Weld is that of
identifying potential nonresponders prior to treatment and designing alternative
strategies (perhaps with a more symptom-management, social problem-solving
focus) for that group.
27
This Manual is both a guide to treatment and a workbook for persons who suVer
from posttraumatic stress disorder. During treatment, it is a workbook in which
individuals can record their own experience of their disorder, together with the
additional advice for their particular case given by their clinician. After treatment
has concluded, this Manual will serve as a self-help resource enabling those who
have recovered, but who encounter further stressors or diYculties, to read the
appropriate section and, by putting the content into action, stay well.
Contents
Section 1 514
1 The nature of traumatic stress and posttraumatic stress disorder 514
1.1 What is a traumatic event? 515
1.2 What is posttraumatic stress disorder? 515
1.3 Common symptoms of posttraumatic stress disorder 515
1.3.1 Intrusive symptoms 516
1.3.2 Avoidance symptoms 516
1.3.3 Arousal symptoms 517
1.4 Associated problems 518
1.5 Why do traumatic stress reactions develop? 519
1.6 The process of treatment and recovery 520
Section 2 521
2 Stabilization of a crisis and engagement in treatment 521
Section 3 522
3 Education and information 522
*Parts of this Manual were adapted from What Is PTSD: Information for Veterans and Their Families, written
by Mark Creamer, David Forbes, and Grant Devilly, and produced by the Australian Centre for Posttrau-
matic Mental Health, Melbourne, Australia.
Gavin Andrews, Mark Creamer, Rocco Crino, Caroline Hunt, Lisa Lampe and Andrew Page The Treatment
of Anxiety Disorders second edition © 2002 Cambridge University Press. All rights reserved.
513 Posttraumatic stress disorder: Patient Treatment Manual
Section 4 523
4 Managing anxiety and distress 523
4.1 Hints for coping 524
4.2 Overview of anxiety management 526
4.3 Subjective units of distress (SUDs) 527
4.4 Managing the physical symptoms 527
4.5 Managing problems with thoughts 530
4.5.1 Distraction 530
4.5.2 Thought stopping 531
4.5.3 Self-statements 532
4.6 Changing behaviors 533
4.7 Arousal and anger 534
Section 5 535
5 Exposure therapy: confronting feared situations 535
5.1 Planning your program 537
5.2 Implementing your program 537
5.3 Practicing the steps 538
Section 6 538
6 Exposure therapy: confronting the memories 538
6.1 What is imaginal exposure? 539
6.2 Therapist-assisted imaginal exposure 540
6.3 Self-directed imaginal exposure 541
6.4 Exposure: can I cope with it? 543
Section 7 543
7 Cognitive restructuring 543
7.1 The process of cognitive restructuring 544
Section 8 546
8 Relapse prevention 546
Section 9 548
9 Concluding comments 548
Section 10 548
10 Recommended resources 548
10.1 Books 548
10.2 Internet resources 548
514 Treatment of Anxiety Disorders
SE C T I ON 1
Experience of a traumatic event can shatter a person’s life, leaving him or her
feeling vulnerable and frightened. It is very important to remember that recovery
is possible and that you can lead a normal, happy life again. This does not mean
that you will forget what happened to you or that you will never again be
distressed by memories and reminders of the event. A certain amount of distress
when you think about what happened is part of being a normal, caring human
being and we certainly do not want you to have no feelings. However, the distress
will become less frequent and more manageable – it will no longer control your life
as it may do now. Recovery also does not mean that you will be exactly the same
person that you were before the trauma. Such powerful experiences may change
people in many ways, not all of them negative. As people recover from trauma,
they may Wnd themselves stronger than before, perhaps more caring and with a
more balanced and sensible view about what is important in their lives.
By seeking some help, you have taken the Wrst steps to recovery. The purpose of
this Manual is to help you through the treatment process in a step-by-step fashion.
There is a great deal of information here – take it slowly and read each section as
often as necessary until you understand it before moving on. You will be asked to
write things down from time to time, so we suggest that you Wnd an exercise book
to use for those tasks that you will keep adding to throughout your recovery. Try
not to worry if it all seems too diYcult at the moment – recovery from trauma is
often a long process and you need to take things one day at a time, recognizing
small improvements as they occur. It can be a long journey, but it will be worth it.
complex mix of what the person was like before the trauma, his or her experience
of other frightening events in the past, the severity of the current trauma, and what
else is happening as he or she tries to recover. Regardless of the causes, eVective
treatment does a great deal to improve the chances of recovery.
Anxiety
Anxiety is a state of apprehension and worry that something unpleasant is about to
happen. It is often accompanied by a range of physical symptoms (such as
sweating, racing heart, and breathing diYculties) that are, in themselves, very
frightening. Sometimes people experiencing these symptoms believe that they are
going to die from a heart attack or go crazy. Anxiety can be speciWc to certain
situations (such as social events, crowded places, or public transport), or it can be
a general state of worry about many things in our lives. If you are having
signiWcant problems in these areas, be sure to tell your therapist. Treatment (as
outlined in other chapters in this book) can be very eVective.
Depression
Depression is a general state of low mood and a loss of interest or pleasure in
activities that were once enjoyed. Life becomes Xat and gray, and nothing seems
fun, exciting, or enjoyable anymore. These depressed states can be very intense,
leading to a total withdrawal from others and a state of numbness, or they can be
lower in intensity – just feeling ‘‘down in the dumps’’. They may last for as little as
a few hours or as long as months or even years. In more severe cases, the person
may believe that life is no longer worth living. Many people who suVer from PTSD
over a long period develop signiWcant problems with depression. Again, it is
important to tell your therapist if these problems apply to you. It can be treated
eVectively with psychological treatments and/or prescription drugs.
519 Posttraumatic stress disorder: Patient Treatment Manual
Guilt
People with PTSD often report strong feelings of guilt, shame, and remorse. This
may be about the fact that they survived while others did not; it may be about what
they had to do to survive; it may be related to how they have coped or acted since
the trauma. Guilt is often the most diYcult thing to talk about, especially if you
feel that you did something wrong or acted in a bad way. However, it is very
important that you work on those feelings as part of your PTSD treatment, so be
sure to tell your therapist about those feelings.
experience that is, by its very nature, overwhelming. It contains lots of new
information that is hard to accept or understand. It does not Wt with our view of
the world or ourselves – the way we think things are or should be. Human beings
have a natural tendency to try to make sense of things that happen around them.
When people experience a trauma, the event keeps coming back into their mind in
an attempt to make sense of what happened. This is the body’s natural way of
trying to deal with, or come to terms with, diYcult experiences and seems to work
well for many stressful life events. However, due to the high level of distress
associated with memories of more severe trauma, the thoughts and feelings tend
to be pushed away to protect the person from this distress. The result is that, whilst
the memory may go away for a while, the need for it to be dealt with has not been
addressed and it keeps coming back. The movement backward and forward from
intrusive thoughts and feelings about the trauma to avoidance and numbing can
then continue almost indeWnitely unless the cycle is addressed in some way.
Throughout this alternating between short bursts of painful memories and
periods of avoidance and numbing, the sense of feeling keyed-up persists. The
traumatized person has been through an event that threatened their life, or the life
of someone else, so the mind and body stay on alert to make sure that no future
potential dangers will be missed. It is safer to get it wrong by overestimating
potential threat than to risk the possibility of missing any future threat. The
persistent activation of this threat detection system, however, leaves the
traumatized person feeling keyed-up or on edge much of the time. In addition, the
threat detection system is so sensitive that it is constantly going oV when there is
no danger in such a way that interferes with the person’s capacity to live a normal
and happy life.
Traumatic stress reactions, therefore, are sensible and adaptive both as part of
survival during the trauma and in attempts to come to terms with the trauma
afterward. Once we recognize where these symptoms come from, it is easier to
understand the typical traumatic stress reactions. The diYcult part is letting go of
these reactions now that they have ceased to provide beneWt and are interfering
with the traumatized person’s quality of life.
SE CT I O N 2
2 Stabilization of a crisis and engagement in treatment
People who have been through a trauma often have other diYcult situations to
deal with in the aftermath. These may be legal issues, family disruptions, Wnancial
problems, or a multitude of other crises. It is important that any current life crises
are resolved, or at least put ‘‘on hold’’, before the real treatment of PTSD can
begin. It is not possible to devote the necessary concentration, time, and energy to
your recovery if you are constantly worried about your job, your relationship,
your children, or other important life areas. That is not to say that you have to be
able to solve all those problems before you can work on your PTSD, but you will
need to be able to put them to one side for a while to concentrate on your
treatment. Therapy is hard work – there is no easy way to do it – and you will need
to devote all your personal resources to the task. If other life issues are worrying
you, it is important that you discuss these with your therapist as they arise so that
they do not interfere too much with your treatment.
The Wrst part of treatment will often be devoted to developing a relationship
with the therapist (or the treatment team if you are taking part in a group
program). You will need to spend some time getting to know each other, and
building trust, if you are to work on the diYcult issues. We call this process
‘‘engagement’’. For many people with PTSD, this is a very diYcult process –
experience of a traumatic event often makes it very hard to trust another person,
particularly someone whom you have never met before. In many cases, you will
522 Treatment of Anxiety Disorders
need to tell your therapist about experiences and feelings that you have never
discussed with anyone. We need to recognize that this is a diYcult process that will
take a lot of courage, but it will be worth it and it is the only way to recovery.
SE C T I ON 3
3 Education and information
PTSD can sometimes feel like an incomprehensible cloud that hangs over all areas
of the person’s life. The Wrst step in treatment is to understand exactly what
trauma is, why we have the symptoms we do and, therefore, why it is treated the
way it is. In this regard, you have come a long way already by reading the sections
above. You need to know what the common signs and symptoms are, and you
need to recognize that you are not alone – many people who have experienced
traumatic events have responded in exactly the same way you have. You need to
understand why the symptoms have appeared – the fact that they were very useful
for survival while the traumatic events were happening but that they are no longer
useful. They have become ‘‘maladaptive’’ and now serve only to create problems
and distress for you. You need to understand what treatment will involve and how
it may aVect you. It is very important that you feel able to ask your therapist
questions about the nature of your problems and the process of treatment. He or
she will not have all the answers, but together you will reach a better understand-
ing of what has happened and how you will recover.
Sometimes people who have been through a traumatic event have trouble
understanding what happened and why it happened. You may Wnd yourself
constantly asking questions such as ‘‘How did this happen’’ or ‘‘Why me?’’. This is
partly because, when we are under threat, our attention is very focused on the
source of the danger and we do not take in all the other things that are happening
around us. We may end up with a distorted and confused memory of the
experience, so that it becomes diYcult to understand and make sense of the event.
This confusion often stops us from being able to put the experience behind us. For
this reason, your therapist may help you to Wnd out more about what happened
during the event. This process is important in being able to ‘‘put the pieces of the
jigsaw puzzle together’’ and make sense of your experience. A good understanding
of exactly what happened, and why it happened, often facilitates recovery.
Although we have put this under the heading ‘‘Education and information’’, it
is actually something that may happen at several stages throughout treatment and
you need to make sure that you are ready before you pursue these options. When
you are feeling reasonably conWdent, however, ask yourself what other informa-
tion you need to help you to understand what happened and why it happened.
523 Posttraumatic stress disorder: Patient Treatment Manual
Quick strategies to
manage escalations
Anxiety
High anxiety
and panic
Routine strategies to
lower overall levels
Time
∑ Is there anyone else you can talk to who may be able to clarify things for you and
help you to reach a better understanding of your experience (such as others who
were there, police oYcers, or ambulance oYcers)?
∑ Is there anything you can read that will help to Wll in the missing pieces (such as
media reports, police statements, or reports from a trial or coroner’s inquest)?
Sometimes, reading accounts written by other survivors of trauma can be useful
in understanding your reactions.
∑ Occasionally there may even be video footage available from news reports or
other sources: is there anything you can watch that will help you to Wll in the
gaps?
Unfortunately, of course, it is not always possible to Wll in all the gaps in your
understanding of the event. Sometimes we may never Wnd out exactly what
happened (or, more commonly, why it happened) and treatment needs to focus
on helping us learn to live with that uncertainty.
SE CT I O N 4
4 Managing anxiety and distress
The next step is to help you to feel more in control of your reactions. We will do
this in several parts. First, there are many simple things you can do in your
day-to-day life that will make you feel more in control and less distressed. There is
524 Treatment of Anxiety Disorders
nothing magical about these ‘‘Hints for coping’’ – most are simply common sense
– but they can make a real diVerence. The second part involves more speciWc
strategies that your therapist will teach you to control your anxiety and distress.
Some of these are useful in lowering your overall level of tension and stress – the
more relaxed you are in general, the better you will cope when the memories
return or you are confronted with other unexpected diYculties. Everyone experi-
ences increases in anxiety and distress at those times. If your overall level of stress
is high, these escalations will take you up into the level of high anxiety and panic
(the top graph in the Wgure above). If your overall level is lower, the shape will be
the same – you will still react to negative events, but your anxiety and distress will
not reach the same heights (the lower graph in the Wgure). We will call these
‘‘routine strategies’’, since we want them to become part of your everyday routine.
Examples would be regular exercise, rest, sensible diet, and relaxation (see below).
Other strategies are designed to help you to deal more speciWcally with diYcult
situations when you can feel your anxiety escalating and you are beginning to feel
overwhelmed. These require a lot of practice, but are very useful to use when the
feelings of distress and anxiety are particularly strong.
time, plan your activities for the day). Routine is very important in helping us to
feel in control and to function eVectively. If you feel able, return to work, study,
or other routines as soon as possible but take it easy – don’t expect too much of
yourself and don’t use work as a way of avoiding painful feelings.
∑ Ask for support and help from your family, friends, church, or other commu-
nity resources when you need it. This is not a sign of weakness. In general, other
people are very keen to help as long as you let them know what you want. If they
do not oVer, it may simply be because they are unsure of what to do.
∑ Spend time with other people, but don’t feel that you have to talk about the
trauma. Talk about football, books, or the weather; go to a movie or a concert;
try to do some enjoyable things with others. This is part of resuming a normal
life.
∑ Focus on your strengths and coping skills. It may not feel like it at times, but you
have many strengths and strategies to deal with diYcult times. Remember that
you are not alone. Many other survivors over the centuries have experienced
these kinds of problems and the vast majority have recovered well.
appreciated. OVer praise. Make a point of saying something nice to each other
every day. Good relationships are characterized by lots of positive interactions,
but they require hard work.
unpleasant signs and symptoms that may follow, causes people to feel scared and
vulnerable. In an attempt to cope, they may try to withdraw from other people and
the outside world, shutting down as a means of self-protection. If we are to
eVectively manage the anxiety and distress that follows a traumatic experience, we
will need to address all three aspects: the physical components, the thoughts, and
the behavior.
It is important to remember that the goal is not to make the unpleasant feelings
go away altogether – that is neither possible nor desirable. Rather, the goal is to
keep them manageable – to keep them under control and to stop them escalating
into extreme anxiety and panic. Practice is essential to master most of the
following techniques. Try to set aside some time each day (preferably twice a day)
to practice. If you wait until you are tense and frightened before you try the
technique, it will not work. Once you have practiced them regularly, however, they
will become more automatic and eVective. They will become important tools in
helping you to manage anxiety and distress. Keep a diary of your practice sessions,
noting down the SUDs level (see below) before and after. This will give both you
and your therapist a good idea of how you are progressing.
The following sections discuss strategies in each of the three domains. Other
chapters in this book contain very good descriptions of several anxiety-manage-
ment strategies. You may wish to talk to your therapist about getting copies of
some of the relevant sections.
0 Totally relaxed
40
60
eat properly, get enough rest, and try to cut down on stimulants (such as coVee,
tea, cola, chocolate, and cigarettes), you will go a long way towards reducing the
chronic arousal that is part of PTSD. In this section, we will look at two speciWc
strategies to reduce arousal. The Wrst is a simple breathing control strategy
designed to reduce your rate and depth of breathing and help you to feel more
relaxed and in control.
Often when people are frightened or upset, they start to breathe faster. An
increase in breathing is part of the Wght or Xight response – we need more oxygen
if we are to Wght or run away. However, breathing too deeply and too fast when we
529 Posttraumatic stress disorder: Patient Treatment Manual
are not using up a lot of energy tends to make us more anxious and often causes
unpleasant physical symptoms such as dizziness, tightness in the chest, and a
feeling of being short of breath. When we are upset, we may be told to ‘‘take a few
deep breaths’’. However, this is not quite right. When we are feeling anxious or
frightened, we don’t need to take a deep breath; we need to take a normal breath in
and exhale slowly. Breathing out is associated with relaxation, not breathing in.
While concentrating on a long, slow exhalation, it’s a good idea to say a word like
‘‘relax’’ or ‘‘calm’’ to yourself. Any word that is associated with feeling peaceful
and at ease will do Wne. Try to drag out the word to match the long, slow
exhalation, as in ‘‘r-e-e-e-l-a-a-a-x’’ or ‘‘c-a-a-a-a-a-l-m’’.
The next thing to remember is to slow your breathing down. Remember that
taking in too much air causes an increase in anxiety and unpleasant physical
symptoms. So, what we need to do is to slow our breathing down and take in less
air. We do this by taking smaller breaths and by pausing between breaths to space
them out. It is also important to try to breathe in through your nose, not through
your mouth. When you have taken a normal breath in through your nose, hold
your breath for a count of 4 before exhaling slowly.
Practice this type of breathing at least twice a day. That way, when you become
frightened or anxious, you will be ready to use the technique to help you to calm
down.
The second physical intervention we will discuss is relaxation training, or
progressive muscle relaxation (PMR). The breathing control described above,
once you have mastered it, is an excellent strategy for dealing with rapid increases
in anxiety that may occur when you experience memories of the trauma or Wnd
yourself in a frightening situation. PMR is designed to deal with the more
pervasive, chronic tension and stress associated with PTSD. If you can lower your
general level of arousal or ‘‘uptightness’’, you will be much less likely to overreact
in response to minor perceived threats. This is just like a coiled spring – the more
wound up it is, the more likely it is to explode under pressure. The world will seem
like a safer place.
PMR is usually done by listening to a tape, which will take you through a series
of exercises in which you will be asked to tense up and relax various muscle
530 Treatment of Anxiety Disorders
groups. By gradually working through your whole body, from head to toe, you will
achieve a state of physical relaxation that, with practice, you will be able to
maintain through much of the day. Your therapist will make a tape for you to use
at home. Alternatively, many libraries or community health centers will be able to
provide one for you. Excellent descriptions of relaxation training appear in other
Patient Treatment Manuals contained in this book and will not be repeated here.
If you decide to try this approach (and we strongly recommend that you do), ask
your therapist to copy one of the relevant sections for you. Making relaxation a
regular part of your daily routine will go a long way to help you in managing the
physical symptoms of PTSD.
4.5.1 Distraction
One simple way that, with practice, can be very eVective is distraction. An obvious
example would be getting on with an activity that is absorbing (and we hope
enjoyable) to occupy your mind. Can you think of something that you could do to
distract yourself? Passive activities (like reading, or watching TV) do not usually
work, as your concentration may not be good enough. Rather, you will need to do
something more active that involves both physical and mental aspects. Games,
crafts, and other creative activities are often good.
It is also good to practice a purely mental distraction technique that you can use
anywhere, anytime. There are many things that you could try and the following list
provides some examples. They are particularly good because no-one else can see
you doing them. Do not try to do them all – pick one or two that feel as though
they may work for you and practice regularly. Even with practice, you must expect
the thoughts to intrude again from time to time. That’s OK – just go back to the
distracting thoughts as often as necessary.
531 Posttraumatic stress disorder: Patient Treatment Manual
4.5.3 Self-statements
One Wnal area we would like to discuss under the heading of managing thought
problems is that of ‘‘self-statements’’. At present, it is likely that many of your
thoughts are negative: worrying about the safety of yourself or others, concerned
that you will never recover, and so on. These negative thoughts feed into your
anxiety and distress, making it much worse. We will address this issue again later.
For the time being, we are going to suggest that you simply work out some simple
things that you can say to yourself to help you calm down and relax when you are
in a diYcult situation or when you are feeling overwhelmed by painful memories.
A famous psychologist, Donald Meichenbaum, has suggested that we should break
up each event into several stages.
First, what can we say to ourselves when we are preparing for something diYcult?
This helps you to re-evaluate the actual probability of the feared negative event
533 Posttraumatic stress disorder: Patient Treatment Manual
It’s natural to be nervous about going into the city given my traumatic
experiences, but the likelihood of anything bad happening is very remote. Just
relax and slow down my breathing. I may not feel great, but I can cope. Now,
what is it that I need to do?
Like everything else, the more you practice using these self-statements, the more
eVective they will be in helping you to manage your anxiety at diYcult times. This
will become especially important as we move on to the next stage of treatment.
SE CT I O N 5
5 Exposure therapy: confronting feared situations
The next part of treatment is the most diYcult and painful – confronting the
feared situations and traumatic memories. It is also the most important. Your
therapist will not start this process until you are ready and will take you through at
a pace that you can manage. Most people Wnd that it is not nearly as diYcult as
they expect it to be and there is often a tremendous sense of relief and achievement
as the feared situations and painful memories are confronted and dealt with.
Not surprisingly, anxiety frequently causes people to stay away from frightening
situations. It is quite normal for people to want to escape or avoid situations,
thoughts, memories, or feelings that are painful or distressing. However, this is
one of the major impediments to recovery. Avoidance and escape provide tempor-
ary relief – the anxiety reduces – but the next time the person encounters that
situation again, he or she is likely to become anxious long before it is planned to
occur. We call this ‘‘anticipatory anxiety’’. The more the situation is avoided, the
more the person continues to believe that it is dangerous. Further, even if the
person does not avoid, the anxiety may continue to build once they are in the
situation. Very often people believe that if they do not leave the situation they will
‘‘lose control’’, ‘‘go crazy’’, ‘‘have a heart attack’’, or have some other dire
consequences. At the very least, they are likely to believe that the unpleasant
feelings will be intolerable. Exposure therapy aims to show that this is not the case
by helping the person to confront the feared situation. The important thing to
remember when you are confronting something that you are frightened of
(whether it is a situation or a memory) is that the anxiety will come down if you
stay there long enough. There is no answer to the question of how long is enough.
In some cases, the anxiety may drop considerably in 15 to 20 minutes. In other
cases, it may take as long as an hour or more but it will reduce eventually. It is vital
that you try to stay in the feared situation long enough for the anxiety to reduce. It
is important to note also that anxiety often increases before it starts to drop. This
temporary increase is often enough to make people avoid or escape – it is vital that
you stay with the feared situation through this phase until the anxiety reduces.
This pattern is shown in the Wgure overleaf. You will notice that the drop in
anxiety is not smooth – you may notice occasional small increases – but the
general trend is downwards. Exposure is done in a controlled and gradual fashion
so that discomfort is kept manageable. By building upon repeated successes in
facing these feared situations, you will eventually be able to confront them without
anxiety and no longer avoid them.
In many ways, this approach is common sense. Let’s take an example of a little
boy who is standing on the beach when a big wave knocks him over. He becomes
536 Treatment of Anxiety Disorders
very frightened of the sea and refuses to go to the beach the next day. How would
his mother or father help? In order to overcome the fear, his parents may take him
for a walk along the beach, staying away from the sea, holding his hand and
reassuring him. Gradually, they walk closer and closer to the water’s edge.
Eventually, the boy is able to go into the sea again unaided. This is a simple
example, but exactly the same process applies to treating more severe and complex
fears in adults.
This section discusses confronting activities, places, people, or objects that you
have become frightened of since the trauma. We call this type of exposure ‘‘in
vivo’’. In vivo simply means ‘‘in real life’’. When we are confronting memories, we
have to do it in imagination, so we call it imaginal exposure – which is discussed in
the next section. In conducting exposure treatment, your therapist will work with
you in constructing a hierarchy – a list of feared situations in order of diYculty.
Treatment involves tackling each item, one at a time, and moving on to the next
only when you are conWdent to do so. More diYcult items may be broken up into
several steps. Exposure treatment can be diYcult and painful, but it is the most
eVective way of treating many anxieties.
537 Posttraumatic stress disorder: Patient Treatment Manual
used for making any comments about the exercise. This will help both you and
your therapist keep track of your exposure progress.
SE C T I ON 6
6 Exposure therapy: confronting the memories
A form of exposure therapy is also used to treat distressing memories of the
trauma. We call it ‘‘imaginal exposure’’. In Section 5, we talked about confronting
feared situations such as places, people, and activities. In cases of PTSD, however,
the most ‘‘feared situation’’ is actually the painful memories of your experience.
These memories are so frightening, and cause so much distress, that the person
tries to avoid or escape from them by blocking them out. Imaginal exposure
treatments are used to assist in confronting the memories. Exposure is only one
539 Posttraumatic stress disorder: Patient Treatment Manual
term used to describe this process. Some people talk about ‘‘trauma focus work’’,
‘‘working through the trauma’’, ‘‘coming to terms with the experience’’ or simply
‘‘confronting the memories’’.
After a trauma, we often try to Wle away our memory of what happened, putting it to the back of
our mind. It’s as if we are trying to pack the event away into a box. We then use a little strength
to keep the lid tightly closed and try to leave it undisturbed. However, over time, two things
happen. Firstly, our strength begins to wane and it becomes more of an eVort to keep it sealed
(that is, to stop the memories from coming back). Secondly, due to the pressure, the box begins
to lose its shape and small cracks begin to appear. What we experience as symptoms (such as
memories of the trauma, and having nightmares and disturbed sleep) is like the content of the
box spilling out through these cracks. This is usually very frightening, so we try to avoid
anything that reminds us of the trauma. We try to stop thinking and talking about what
happened and how we felt. In this way, the content of the box becomes a ‘‘ghost’’ which we have
learned to fear and which we are terriWed of confronting. As part of therapy, we are going to
open the box and inspect the content for what it really is. We will talk through what happened
and how you felt. We will be inspecting the ‘‘ghosts’’ that have been created and throwing away
any maladaptive and distressing beliefs you may have about the event. We Wnd that once the
trauma has been dealt with in this manner the symptoms become much less severe and less
frequent.
When dentists work on a decayed tooth, they don’t just slap the Wlling on top of the decay. If
they did, it might be Wne for a few weeks or months, but the problems would keep coming back
as the tooth continued to deteriorate. Instead, they spend some time drilling and scraping,
cleaning out all the decay before putting the tooth back together. This is a very unpleasant and
painful process, but we know it is worth going through this short-term pain for the long-term
gain. Traumatic memories are a bit like tooth decay. We need to make sure that we have
confronted all aspects of the trauma before we try to put the event behind us. We need to give
ourselves time to face up to even the worst parts of the experience so that there are no skeletons
in the closet to come and haunt us in the future. Like the dentist’s drilling, it is a painful process
but an important part of recovery.
A Wnal analogy comes from the work of Edna Foa, one of the leading experts in
the treatment of PTSD:
Suppose you have eaten a very large and heavy meal that you are unable to digest. This is an
uncomfortable feeling. But when you have digested the food, you feel a great sense of relief.
540 Treatment of Anxiety Disorders
Flashbacks, nightmares, and troublesome thoughts continue to occur because the traumatic
event has not been adequately digested. Treatment will help you to start digesting your heavy
memories so that they will stop interfering with your daily life. (E. B. Foa and B. O. Rothbaum
(1998) Treating the Trauma of Rape, p. 160)
Exposure-based treatments are not for everybody. In some cases, if the trauma
occurred many years ago and the memories are not causing too much of a
problem, it may be best not to drag everything up again. Talk to your therapist
about whether this approach would be beneWcial for you.
∑ Step 1: Preparation.
∑ Plan an activity to do immediately afterwards (e.g., go for a walk, visit or ring
a friend; do an enjoyable absorbing activity, not an addictive activity like
watching TV or drinking, or an emotional shutdown like hiding away on
your own).
∑ Choose a private place with no interruptions (take the phone oV the hook, let
others know you are not to be disturbed).
∑ Identify two people you can contact immediately if you need help: keep their
phone numbers handy.
∑ BrieXy relax yourself and try to clear your mind of other thoughts and
worries: note down your SUDs level on a piece of paper.
∑ Step 2: Confront the memory safely.
∑ Listen to the tape and try to focus on what is being said: try not to imagine
other, more frightening parts – just concentrate on the tape.
∑ Equally, try to imagine it happening as if you were experiencing it again.
What can you see, hear, smell, touch, taste? What are you feeling and
thinking?
∑ When reminded to do so on the tape, note your SUDs level. If it is above 90,
take a moment to remind yourself where you are; you are safe here and now;
you can feel as upset as you need to in the memory.
∑ Don’t stop the tape in the middle: stick with the memory through to the end.
∑ Step 3: At the end of the tape, pause and open your eyes.
∑ Look around, feel the chair, remind yourself where you are and that you are
safe.
∑ Note your SUDs level and use an arousal management strategy if necessary
(such as breathing control or relaxation).
∑ Step 4: Process the memory by writing down some or all of:
∑ What new (or old) pieces of the memory did you discover or became clearer?
∑ Are you now thinking diVerently about any aspects?
∑ What feelings or thoughts are going through your mind right now?
∑ What parts of the memory are still too upsetting to remember or accept?
∑ What do you still want to change about the event or its aftermath? How can
you achieve that?
∑ What did you do that you should be able to feel good about?
∑ Step 5: Relax and do your planned activity.
SE CT I O N 7
7 Cognitive restructuring
One eVect that exposure may have is to bring to the surface unhelpful thoughts
and beliefs that have arisen as a result of your experiences. In order to recover
eVectively from the trauma, it may be necessary to challenge those thoughts and
beliefs (we call them ‘‘cognitions’’), and try to replace them with something more
rational and realistic. In PTSD, this process is best carried out in conjunction with
the process of exposure, modifying the unhelpful cognitions as they arise.
Following a traumatic experience, people may be left with a range of negative
thoughts about what happened, as well as about themselves and the world. For
example, many people are left feeling vulnerable and insecure. They may think
that the world has become a dangerous place and that other people are nasty,
cruel, and out to take advantage. Similarly, many people experience feelings of
guilt and shame following trauma. They may think that they are bad or evil for
acting in the way they did during or after the incident; they may think that what
happened was their fault; they may see themselves as weak or inadequate for not
coping better. Sometimes, there may be elements of truth in these thoughts.
Usually, however, they are completely untrue or, at least, grossly exaggerated. This
kind of thinking leads to all sorts of unpleasant emotions such as depression and
guilt, anxiety and fear, and anger. An important part of recovery involves identi-
fying those maladaptive thoughts, challenging them, and replacing them with a
more realistic view of yourself and the world.
544 Treatment of Anxiety Disorders
The next stage is to pick one of the key themes that is leading you to feel an
unpleasant emotion. Which one makes you feel angry? Or frightened? Or guilty?
Or sad? Try to express it as a single statement of opinion, such as ‘‘all men are bad’’
or ‘‘it was all my fault’’. In particular, look for statements beginning with ‘‘I’’, such
as ‘‘I’m weak and hopeless’’ or ‘‘I’m not safe anywhere’’. Write this thought or
belief at the top of a clean sheet in your exercise book. Then go through and try to
answer the following questions. Some of them may not apply to every thought, but
most will – they will help you to re-evaluate whether your thoughts and beliefs are
really true.
What is the evidence? Here we want you to become a scientist and really think
about the objective evidence for and against the thought. Is it really true? Are
you 100% sure? Do the facts of the situation back up what you think or
contradict it? Write out all the evidence you can think of for and against the
thought. In most cases, you will Wnd that it is not completely true. (Indeed, it
may turn out to be completely false.)
What alternative views are there? How do other people think about this? Would
other people agree with you? Is there another way of looking at it? Are there
other explanations? Try to generate as many alternative explanations as you can
and review the evidence for and against them. When you look at it objectively,
which explanation is most likely to be correct?
Am I thinking in all-or-nothing, black-and-white terms? Am I using terms like all,
always, never? Nothing is all bad or all good, no person is either perfect or
worthless. Try to look for a more balanced view, with a more realistic assess-
ment of the situation.
Am I overestimating my responsibility? Things happen for all sorts of complex
reasons, many of which we may never understand. Be very careful not to take
too much responsibility for things over which you do not have control.
Are my judgments based on how I feel, rather than what is actually happening? If
you feel guilty, you are likely to assume things must have been your fault. If you
feel frightened, you may assume that you are not safe. If you feel depressed, you
may assume that things will never get better. Feelings are not a good basis on
which to make rational judgments. Put the feelings to one side for a moment
and look for objective evidence.
Am I over-focusing on one aspect and forgetting other aspects? Am I looking only
at the negative side and ignoring the neutral or positive things? If we focus only
on small parts of the whole picture, we will end up with a very distorted view of
reality.
How likely is it? Am I confusing a low probability with a high probability? How
likely is it that what you fear will actually happen? Understandably, many
trauma survivors fear a recurrence of the event but, realistically, how likely is it?
546 Treatment of Anxiety Disorders
SE C T I ON 8
8 Relapse prevention
The Wnal stage of treatment will look at relapse prevention. Recovery is not just
about getting better; it is about staying better. Some simple strategies will help you
to get through diYcult times in the future. There are a few simple points to
remember in relapse prevention:
∑ Lapses are to be expected from time to time: When you are reminded of your
traumatic experience (such as hearing of a similar event, or experiencing
something else frightening) it is natural for you to become a little distressed.
This is part of a normal human reaction and, as long as it is not too severe or
lasts too long, you should not consider it to be a problem. You can cope with
being upset for a while. It becomes a problem if you are not expecting it and you
547 Posttraumatic stress disorder: Patient Treatment Manual
tell yourself that you have ‘‘fallen in a heap’’ or that you are ‘‘back to square
one’’. Simply use it as a reminder to practice your coping strategies a bit more
for a few days.
∑ Be aware of the early warning signs: Keep an eye on yourself and try to notice
when you are not coping so well. The earlier that you can recognize that things
are not right, the easier it will be to do something about it. The longer you leave
it, the worse it will get, and the more diYcult it will become to pull yourself out
again. It will be easier to recognize the early warning signs if you are aware of the
kinds of things that may precipitate a lapse.
∑ Identify high risk situations: Spend some time thinking about what kinds of
things may cause you to become upset – the more prepared you are, the better
you will cope. The kinds of things that upset most trauma survivors are
powerful reminders or news of similar incidents, an experience similar to the
original trauma, and other life stresses such as Wnancial or family problems.
What kinds of things may cause you to become upset and think about the
trauma again?
∑ Generate a plan to cope: Write down on a card what you will do if and when you
are upset again about the trauma. The kinds of things to include are:
∑ Who will you call? Write down the names and phone numbers.
∑ Physical coping strategies: Which arousal management strategies worked best
for you? Write down one or two (such as breathing control, go for a walk,
listen to the relaxation tape) as a reminder to do them.
∑ Cognitive coping strategies: Write out a coping self-statement that you can use
such as ‘‘I expect to feel upset when I’m reminded of what happened, but
that’s okay – I may not like it but I can cope with it. I don’t have to make it
worse by exaggerating it. Now, what can I do to make myself feel better?’’ You
may wish also to jot down any other strategies that worked well for you such
as your favorite distraction technique or thought stopping.
∑ Behavioral coping strategies: Write down one or two things you can do to get
you back on track – visit a friend, go to a movie, get involved in an engrossing
hobby or task.
∑ Be positive: Remind yourself that you expected this from time to time and that
you will get over it quickly. Try to view it as an opportunity to practice your
skills and become a stronger person.
∑ Get professional help if necessary: No matter how well you have recovered from
the original trauma, sometimes a relapse may be just too much for you to cope
with alone. Don’t hesitate to get some professional help if necessary. It does not
mean that you are weak or that you are back to square one, simply that you need
some extra support to get over a diYcult time. It may require only one or two
sessions.
548 Treatment of Anxiety Disorders
SE C T I ON 9
9 Concluding comments
If you have worked your way through this Manual, with or without a therapist,
you will have come a long way to recovering from an experience that changed your
life. As we noted at the beginning, you will never be quite the same person again.
But over the course of your recovery you have learnt many new skills that will
stand you in good stead in the future. Importantly, you have faced one of the worst
things that life can throw at you and you have come through it. You have survived.
Give yourself a pat on the back and remember that, if you can deal with this, you
can deal with almost anything.
SE C T I ON 1 0
10 Recommended resources
The following books are available from most large bookstores, many smaller ones,
and some news-stands. If in doubt, ask whether the book can be ordered. We also
suggest that you use your local library to gain access to some of these books. When
you read these or any similar books on the management of anxiety, remember that
they are best regarded as guidelines only. Be critical in both a positive and negative
sense when reading these books, so that you get what is best for you out of them.
Most of these books are inexpensive.
10.1 Books
Allen JG. (1999) Coping With Trauma: A Guide To Self Understanding. Washington, DC:
American Psychiatric Press.
Herbert C and Wetmore A. (1999) Overcoming Traumatic Stress: A Self Help Guide Using
Cognitive Behavioral Techniques. London: Robinson Publishing Ltd.
Matsakis A. (1996) I Can’t Get Over It: A Handbook For Trauma Survivors, 2nd Edition. Oakland
CA: New Harbinger Publications.
Matsakis A. (1998) Trust After Trauma: A Guide To Relationships For Survivors And Those Who
Love Them. Oakland CA: New Harbinger Publications.
Rosenbloom D, Williams MB and Watkins B. (1999) Life After Trauma: A Workbook For
Healing. New York: Guilford.
Schiraldi GR. (2000) The Posttraumatic Stress Disorder Sourcebook. Lincolnwood, IL: Lowell
House Publications.
Conclusions
Part of this book has been quite conventional. The reviews of the syndromes and
treatments in relation to panic and agoraphobia, social phobia, speciWc phobias,
obsessive–compulsive disorder, generalized anxiety disorder and posttraumatic
stress disorder are brief, succinct overviews designed for busy clinicians. The
discussion of general issues in the etiology and treatment of the anxiety disorders
is also essential information for the practicing clinician. The Clinician Guides and
the Patient Treatment Manuals are, however, quite unusual. These Guides and
Manuals need to be placed in context.
There is an art and a science to good medical practice. Because the science tends
to predominate, the art of treatment is seldom discussed, either at a general or a
speciWc level. Elsewhere, we have called attention to the need for the elements of
good clinical care to be made explicit. Good clinical care needs to be taught to
trainee psychiatrists and clinical psychologists for use with patients for whom
there is no speciWc remedy immediately applicable to their disorder (Andrews,
1993a). This book is diVerent. It is about treating persons with chronic anxiety
disorders who, if expertly treated with speciWc remedies, can be expected to
recover. This recovery has been made possible by the scientiWc advances that have
occurred in our understanding of the treatment of the anxiety disorders. Much of
this book is focused on the cognitive behavioral treatments simply because the
instructions for prescribing medications are relatively simple and, courtesy of
advertising by the pharmaceutical industry, do not need repeating in a book on the
treatment of anxiety disorders. The cognitive behavioral treatments are less well
known and, being both nonproprietary and not for proWt, are neither as widely
promoted nor as readily available as are the drug therapies.
There is a greater problem. The amount of evidence for the eYcacy of psycho-
therapy is less plentiful than the evidence that is routinely provided by the
pharmaceutical industry to the national regulatory authorities in each country.
This evidence is provided as part of the process of having products cleared for
marketing and, in many countries, for subsidy. In the Wrst edition of this book,
much of the evidence about the eYcacy of cognitive behavioral therapy came from
550
551 Conclusions
trials in which the progress of treated groups were compared to their own
pretreated status, or else were compared to the progress of wait-list or no
treatment control groups.
While aggregating evidence of eVectiveness from such trials can be satisfactory,
in the Wnal analysis evidence from randomized placebo controlled trials is neces-
sary. This type of trial is necessary to control for the three factors that can produce
improvement even when the treatment being studied has no speciWc value. The
Wrst of these factors is spontaneous remission of the disorder over the duration of
treatment and assessment. Spontaneous remission is likely to be more important
when this duration extends over months or years. The next factor is regression to
the mean. Persons with chronic and Xuctuating disorders seek treatment when
their symptoms are most disabling and, with the passage of time and even in the
absence of treatment, these symptoms will improve to their average level, thus
imitating treatment-related beneWt. The last of these confounds is the placebo
eVect, which identiWes the improvement that occurs due to the morale-raising
eVect of seeing an interested clinician and expecting to beneWt from a notionally
eVective treatment. In a randomized controlled design, a placebo control group
controls for all these factors whereas wait-list or no-treatment control groups
satisfy only the Wrst two.
Randomized placebo controlled trials are the standard method by which the
eYcacy of a new treatment is assessed. The most informative design is a placebo
controlled comparison trial in which the new treatment is compared with a
placebo and with a proven and accepted treatment. Even so, the results of a single
trial should be taken cautiously, because – even given the control – chance factors
might have contributed to the improvement observed in the treated group. Once
replicated by independent scientists, acceptance of the Wnding depends on two
other factors. The Wrst factor is the power of the treatment as measured by the
superiority over the placebo treatment, for this power indicates the likely robust-
ness of the Wnding. The second factor is the number of subjects in the trials, for this
will indicate the probability that the results will be applicable to other subjects.
These issues are not completely independent and stronger treatments are usually
accepted on evidence from fewer subjects, given that the proviso of independent
replication is met.
The number of replication studies in the literature varies with the length of time
a treatment has been available, the funds for such research, and the ease of
mounting a placebo controlled trial. For example, when alprazolam was intro-
duced for panic disorder, the manufacturer funded a series of multicenter and
multinational placebo and comparison trials of the drug. The placebo, an inert
replica tablet, was simple to manufacture, measurement was standardized, and the
results at the end of treatment were clear. In contrast, there are relatively few
552 Treatment of Anxiety Disorders
patients in the active treatment groups was 73, double the number required to
meet the threshold requirements at this level of eVectiveness.
Generalized anxiety disorder: We located four randomized controlled trials in
generalized anxiety disorder that compared CBT with an appropriate placebo
condition (Borkovec et al., 1987; Lindsay et al., 1987; Power et al., 1989, 1990).
The treatments were well deWned and the cognitive therapies were based on the
procedures described by Beck and Emery (1979) but also included relaxation
training and graded exposure where appropriate. The average eVect size from
the 57 subjects in the four trials was 2.07, considerably above the threshold
required.
Obsessive–compulsive disorder: Four randomized placebo-controlled trials were
identiWed (Roper et al., 1975; Marks et al., 1980, 1988, Lindsay et al., 1997) in
which graded exposure, coupled with response prevention, was utilized as the
speciWc treatment. The mean eVect size was 1.81, and the number of patients in
the treatment groups was 33, very few indeed but above the threshold required.
There is supporting evidence that, unlike the drug remedies, the beneWts of
these treatments are stable and continue for months or years after treatment has
concluded. The number of studies and the number of subjects in the studies is
small compared with the amount of evidence for eVectiveness of drugs in these
disorders. While this diVerence in the number of studies is the result of both the
money available and the ease of doing the drug trials, it remains important that the
proponents of the nondrug therapies see that more studies are done. It will be clear
from the chapters of this second edition that more research has been done and that
now there is suYcient evidence for the eYcacy of CBT in social phobia and
posttraumatic stress disorder as well as in panic, generalized anxiety disorder and
obsessive–compulsive disorder.
That CBT works is established (Nathan and Gorman, 1998). The larger question
is whether it is more cost eVective than the alternative therapies. Hofmann and
Barlow (1999) considered such data to be lacking but oVered a model that
compared CBT in anxiety disorders to the costs of three diVerent drug therapies.
In the initial months the costs of CBT were greater but, as no further treatment
was required, the costs of the repeated visits to the doctor and the costs of
continuing the medications meant that within the year the costs of drug treat-
ments exceeded the costs of CBT. When a treatment is both more eVective and
cheaper it is said to dominate the alternative treatments. Our modeling for the
clinical practice guidelines for the Royal Australian and New Zealand College of
Psychiatrists is showing, exactly as we showed in depression (Andrews et al.,
2000), that CBT for panic disorder/agoraphobia dominates the drug therapies in
that it is both cheaper and more eVective.
There is both an art and a science to good clinical practice. The scientiWc
554 Treatment of Anxiety Disorders
information from the randomized placebo controlled trials has been summarized
in the chapters on treatment and operationalized in the Patient Treatment Man-
uals. Although the content of these Manuals is based on research, the form of the
Manuals – how the techniques are sequenced, how each technique is presented
and reinforced with patient exercises – is the result of our clinical experience over
20 years of treating patients with these disorders. Thus the manuals contain both
art and science.
The Clinician Guides are again diVerent. As new staV members joined the
Clinical Research Unit for Anxiety Disorders and took responsibility for con-
ducting these treatment programs, we discovered an increase in their eVectiveness
as therapists that reached an asymptote after they had treated their third or fourth
group. Discussing these Wndings, we concluded that it was not their technical
competence at guiding patients through the Manuals that had changed but rather
their ability to recognize and manage diYculties that individual patients experi-
enced with aspects of the program. For this reason we began to write a series of
Clinician Guides.
Like the Patient Treatment Manuals, these Clinician Guides were initially
written to a set design. However, we soon realized that, while all diYculties were at
times evident with patients regardless of diagnosis, there were domains of diY-
culty particularly associated with certain disorders. Furthermore, it became evi-
dent that the way of presenting the solutions diVered depending on the patient’s
principal diagnosis. The Clinician Guides in this book are therefore both speciWc
and general; each is written from the viewpoint of a clinician treating only patients
with that particular diagnosis but each contains information of general import-
ance in the treatment of patients with any of the anxiety disorders. Thus the
Clinician Guides are our view of the art of clinical practice.
References
Abramowitz JS, Foa EB. (1998) Worries and obsessions in individuals with obsessive–compul-
sive disorder with and without comorbid generalized anxiety disorder. Behaviour Research
and Therapy, 36, 695–700.
Adler CM, Craske MG, Kirschenbaum S, Barlow DH. (1989) ‘‘Fear of panic’’: an investigation of
its role in panic occurrence, phobic avoidance, and treatment outcome. Behaviour Research
and Therapy, 27, 391–6.
Agras SW, Sylvester D, Oliveau D. (1969) The epidemiology of common fears and phobias.
Comprehensive Psychiatry, 10, 439–47.
Akiskal HS. (1998) Toward a deWnition of generalized anxiety disorder as an anxious tempera-
ment type. Acta Psychiatrica Scandinavica, 98 (Suppl. 393), 66–73.
Alnaes R, Torgersen S. (1988a) DSM-III symptom disorders (axis I) and personality disorders
(axis II) in an outpatient population. Acta Psychiatrica Scandinavica, 78, 348–55.
Alnaes R, Torgersen S. (1988b) The relationship between DSMIII symptom disorders (axis I)
and personality disorders (axis II) in an outpatient population. Acta Psychiatrica Scandina-
vica, 78, 485–92.
Amies PL, Gelder MG, Shaw PM. (1983) Social phobia: a comparative clinical study. British
Journal of Psychiatry, 142, 174–9.
Amir N, Foa EB, Coles ME. (1998) Automatic activation and strategic avoidance of threat-
relevant information in social phobia. Journal of Abnormal Psychology, 107, 285–90.
Anderson DJ, Noyes R, Crowe RR. (1984) A comparison of panic disorder and generalized
anxiety disorder. American Journal of Psychiatry, 141, 572–5.
Andrews G. (1981) A prospective study of life events and psychological symptoms. Psychological
Medicine, 77, 795–801.
Andrews G. (1988) Stressful life events and anxiety. In Burrows G, Noyes R, Roth M (Eds),
Handbook of Anxiety, Vol. 2: ClassiWcation, Etiological Factors and Associated Disorders.
Amsterdam: Elsevier.
Andrews G. (1990a) Neurosis, personality and cognitive behaviour therapy. In McNaughton N,
Andrews G (Eds), Anxiety. Dunedin: Otago University Press.
Andrews G. (1990b) ClassiWcation of neurotic disorders. Journal of the Royal Society of Medicine,
83, 606–7.
Andrews G. (1990c) England: an innovative community psychiatric service. Lancet, 335,
1087–8.
555
556 References
Andrews G. (1991) Anxiety, personality and anxiety disorders. International Review of Psychia-
try, 3, 293–302.
Andrews G. (1993a) The essential psychotherapies. British Journal of Psychiatry, 162, 447–51.
Andrews G. (1993b) Panic and generalized anxiety disorders. Current Opinion in Psychiatry, 6,
191–4.
Andrews G. (1996a) Comorbidity and the general neurotic syndrome. British Journal of
Psychiatry, 168 (Suppl. 30), 76–84.
Andrews G. (1996b) Talk that works: the rise of cognitive behaviour therapy. British Medical
Journal, 313, 1501–2.
Andrews G. (2000) The anxiety disorder inclusion and exclusion criteria in DSM-IV and
ICD-10. Current Opinion in Psychiatry, 13, 139–41.
Andrews G, Craig A. (1988) Prediction of outcome after treatment for stuttering. British Journal
of Psychiatry, 153, 236–40.
Andrews G, Moran C. (1988) Exposure treatment of agoraphobia with panic attacks: are drugs
essential? In Hand I, Wittchen H-U (Eds), Panic and Phobias II. Treatments and Variables
AVecting Course and Outcome. Heidelberg: Springer-Verlag.
Andrews G, Peters L. (1998) Psychometric properties of the CIDI. Social Psychiatry and
Psychiatric Epidemiology, 33, 80–8.
Andrews G, Tennant CC, Hewson D, Vaillant G. (1978) Life event stress, social support, coping
style and risk of psychological impairment. Journal of Nervous and Mental Disease, 16,
307–16.
Andrews G, Pollock C, Stewart G. (1989) The determination of defense style by questionnaire.
Archives of General Psychiatry, 46, 455–60.
Andrews G, Neilson MD, Hunt C, Stewart GW, Kiloh LG. (1990a) Diagnosis, personality and
the long-term outcome of depression. British Journal of Psychiatry, 157, 13–18.
Andrews G, Stewart G, Allen R, Henderson, AS. (1990b) The genetics of six neurotic disorders: a
twin study. Journal of AVective Disorders, 19, 23–9.
Andrews G, Stewart G, Morris-Yates A, Holt P, Henderson S. (1990c) Evidence for a general
neurotic syndrome. British Journal of Psychiatry, 157, 6–12.
Andrews G, Crino RD, Hunt C, Lampe L, Page A. (1992) A List of Essential Psychotherapies.
Proceedings of the Annual Conference of the Royal Australian and New Zealand College of
Psychiatrists. Canberra: Royal Australian and New Zealand College of Psychiatrists.
Andrews G, Page AC, Neilson MD. (1993a) Sending your teenagers away: controlled stress
decreases neurotic vulnerability. Archives of General Psychiatry, 50, 585–9.
Andrews G, Singh M, Bond, M. (1993b) The Defense Style Questionnaire. Journal of Nervous
and Mental Disease, 181, 246–56.
Andrews G, Hall W, Teesson M, Henderson S. (1999a) The Mental Health of Australians.
Canberra: Commonwealth Department of Health and Aged Care.
Andrews G, Slade T, Peters L. (1999b) ClassiWcation in psychiatry: ICD-10 versus DSM-IV.
British Journal of Psychiatry, 174, 3–5.
Andrews G, Henderson S, Hall W. (2001a) Prevalence, comorbidity, disability and service
utilisation: an overview of the Australian national mental health survey. British Journal of
Psychiatry, 178, 145–53.
557 References
Andrews G, Issakidis C, Carter G. (2001b) The shortfall in mental health service utilization.
British Journal of Psychiatry, 179, 417–25.
Andrews G, Sanderson K, Corry J, Lapsley HM. (2000) Using epidemiological data to model
eYciency in reducing the burden of depression. Journal of Mental Health Policy and Econ-
omics.
APA (American Psychiatric Association). (1980) Diagnostic and Statistical Manual of Mental
Disorders, 3rd Edition (DSM-III). Washington, DC: American Psychiatric Association.
APA (American Psychiatric Association). (1987) Diagnostic and Statistical Manual of Mental
Disorders, 3rd Edition, Revised (DSM-III-R). Washington, DC: American Psychiatric Associ-
ation.
APA (American Psychiatric Association). (1994) Diagnostic and Statistical Manual of Mental
Disorders, 4th Edition (DSM-IV). Washington, DC: American Psychiatric Association.
Arntz A, van den Hout M. (1996) Psychological treatments of panic disorder without agorapho-
bia: cognitive therapy versus applied relaxation. Behaviour Research and Therapy, 34, 113–21.
Aronson TA, Logue CM. (1987) On the longitudinal course of panic disorder: development
history and predictors of phobic complications. Comprehensive Psychiatry, 28, 344–55.
Arts W, Hoogduin K, Schaap C, De Haan E. (1993) Do patients suVering from obsessions alone
diVer from other obsessive compulsives? Behaviour Research and Therapy, 31, 119–32.
Baillie AJ, Lampe LA. (1998) Avoidant personality disorder: empirical support for DSM-IV
revisions. Journal of Personality Disorders, 12, 23–30.
Bakker A, van Balkom AJLM, Spinhoven P, Blaauw BMJW, van Dyck R. (1998) Follow-up on
the treatment of panic disorder with or without agoraphobia: a quantitative review. Journal of
Nervous and Mental Disease, 186, 414–19.
Baldwin D, Bobes J, Stein DJ, Scharwachter I, Faure M. (1999) Paroxetine in social phobia/social
anxiety disorder. British Journal of Psychiatry, 175, 120–6.
Ballenger JC, Davidson JRT, Lecrubier Y, Nutt DJ, Bobes J, Beidel DC, Ono Y, Westenberg
HGM. (1998) Consensus statement on social anxiety disorder from the International Con-
sensus Group on Anxiety and Depression. Journal of Clinical Psychiatry, 59 (Suppl. 17),
54–60.
Bandelow B. (1995) Assessing the eYcacy of treatments for panic disorder and agoraphobia: II.
The Panic and Agoraphobia Scale. International Clinical Psychopharmacology, 10, 73–81.
Bandelow B, Sievert K, Roethemeyer M, Hajak G, Ruther E. (1995). What treatments do
patients with panic disorder and agoraphobia get? European Archives of Psychiatry & Clinical
Neuroscience, 245, 165–71.
Bandura A. (1977) Self-eYcacy: toward a unifying theory of behavioural change. Psychological
Review, 84, 191–215.
Barlow DH. (1988) Anxiety and Its Disorders: The Nature and Treatment of Anxiety and Panic.
New York: Guilford.
Barlow DH. (1997). Cognitive-behavioral therapy for panic disorder: current status. Journal of
Clinical Psychiatry, 58 (Suppl. 2), 32–7.
Barlow DH. (2000) Unraveling the mysteries of anxiety and its disorders from the perspective of
emotion theory. American Psychologist, 51, 1247–63.
Barlow DH, Craske MG. (1988) The phenomenology of panic. In Rachman S, Maser JD (Eds),
558 References
Boerner RJ, Moeller H-J. (1997) The value of selective serotonin re-uptake inhibitors (SSRIs) in
the treatment of panic disorder with and without agoraphobia. International Journal of
Psychiatry in Clinical Practice, 1, 59–67.
Bonn JA, Readhead CPA, Timmons BH. (1984) Enhanced behavioral response in agoraphobic
patients pretreated with breathing retraining. Lancet, ii, 665–9.
Boone ML, McNeil DW, Masia CL, Turk CL, Carter LE, Ries BJ, Lewin MR. (1999) Multimodal
comparisons of social phobia subtypes and avoidant personality disorder. Journal of Anxiety
Disorders, 13, 271–92.
Borkovec TD, Costello E (1993) EYcacy of applied relaxation and cognitive-behavioral therapy
and the treatment of generalized anxiety disorder. Journal of Consulting and Clinical Psychol-
ogy, 61, 611–19.
Borkovec TD, Whisman MA. (1996) Psychosocial treatment for generalized anxiety disorder. In
Mavissakalian MR, Prien RF (Eds), Long-term Treatments of Anxiety Disorders. Washington,
DC: American Psychiatric Press, pp. 171–99.
Borkovec TD, Robinson E, Pruzinsky T, Depree JA. (1983) Preliminary exploration of worry:
some characteristics and processes. Behaviour Research and Therapy, 21, 9–16.
Borkovec TD, Mathews AM, Chambers A, Ebrahimi S, Lytle R, Nelson R. (1987) The eVects of
relaxation training with cognitive or nondirective therapy and the role of relaxation-induced
anxiety in the treatment of generalized anxiety. Journal of Consulting and Clinical Psychology,
55, 883–8.
Borkovec TD, Ray WJ, Stoeber J. (1998) Worry: a cognitive phenomenon intimately linked to
aVective, physiological, and interpersonal behavioral processes. Cognitive Therapy and Re-
search, 22, 561–76.
Bouchard S, Pelletier MH, Gauthier JG, Côté Laberge B. (1997) The assessment of panic using
self-report: a comprehensive survey of validated instruments. Journal of Anxiety Disorders, 11,
89–111.
Boudewyns PA, Hyer L. (1990) Physiological response to combat memories and preliminary
outcome in Vietnam veteran PTSD patients treated with direct therapeutic exposure. Behav-
ior Therapy, 21, 63–87.
Bourdon KH, Boyd JH, Rae DS, Burns BJ, Thompson JW, Locke BZ. (1988) Gender diVerences
in phobias: results of the ECA community survey. Journal of Anxiety Disorders, 2, 227–41.
Bourque P, Ladouceur R. (1980) An investigation of various performance-based treatments
with agoraphobics. Behaviour Research and Therapy, 18, 161–70.
Bouton ME, Kenney FA, Rosengard C. (1990) State-dependent fear extinction with two
benzodiazepine tranquilizers. Behavioral Neuroscience, 104, 44–55.
Bouwer C, Stein DJ. (1998) Use of the selective serotonin reuptake inhibitor citalopram in the
treatment of generalized social phobia. Journal of AVective Disorders, 49, 79–82.
Bowman D, Scogin F, Floyd M, Patton E, Gist L. (1997). EYcacy of self-examination therapy in
the treatment of generalized anxiety disorder. Journal of Counseling Psychology, 44, 267–73.
Boyd J. (1986) Use of mental health services for the treatment of panic disorder. American
Journal of Psychiatry, 143, 1569–74.
Brantley PJ, Mehan DJ, Ames SC, Jones GN. (1999) Minor stressors and generalized anxiety
disorder among low-income patients attending primary care clinics. Journal of Nervous and
561 References
Century-Crofts.
Carlson EB. (1996) Trauma Research Methodology. Lutherville, MD: Sidran Press.
Casacalenda N, Boulenger J-P. (1998) Pharmacologic treatments eVective in both generalized
anxiety disorder and major depressive disorder: clinical and theoretical implications. Cana-
dian Journal of Psychiatry, 43, 722–30.
Castle DJ, Deale A, Marks IM, Cutts F, Chadhoury Y, Stewart A. (1994) Obsessive–compulsive
disorder: prediction of outcome from behavioural psychotherapy. Acta Psychiatrica Scandi-
navica, 89, 393–8.
Cath DC, van der Wetering BJM, van Woerkom TCAM, Hoogduin CAL, Roos, RAC, Rooij-
mans HGM. (1992) Mental play in Gilles de la Tourette’s syndrome and obsessive compulsive
disorder. British Journal of Psychiatry, 161, 542–5.
Chaleby KS, Raslan A. (1990) Delineation of social phobia in Saudi Arabians. Social Psychiatry
and Psychiatric Epidemiology, 25, 324–7.
Chambless DL. (1988) Body sensations questionnaire. In Hersen M, Bellack A (Eds), Dictionary
of Behavioral Assessment Techniques. New York: Pergamon.
Chambless DL. (1990) Spacing of exposure sessions in treatment of agoraphobia and simple
phobia. Behavior Therapy, 18, 225–32.
Chambless DL, Gracely EJ. (1989) Fear of fear and the anxiety disorders. Cognitive Therapy and
Research, 13, 9–20.
Chambless DL, Mason J. (1986) Sex, sex-role stereotyping and agoraphobia. Behaviour Research
and Therapy, 24, 231–5.
Chambless DL, Foa EB, Groves GA, Goldstein AJ. (1982) Exposure and communications
training in the treatment of agoraphobia. Behaviour Research and Therapy, 20, 219–31.
Chambless DL, Caputo GC, Bright P, Gallagher R. (1984) Assessment of fear in agoraphobics:
the Body Sensations Questionnaire and the Agoraphobic Cognitions Questionnaire. Journal
of Consulting and Clinical Psychology, 52, 1090–7.
Chambless DL, Caputo GC, Jasin SE, Gracely EJ, Williams C. (1985) The Mobility Inventory for
Agoraphobia. Behaviour Research and Therapy, 23, 35–44.
Chambless DL, Goldstein AA, Gallagher R, Bright P. (1986) Integrating behavior therapy and
psychotherapy in the treatment of agoraphobia. Psychotherapy: Theory, Research, and Practice,
23, 150–9.
Chambless DL, Tran GQ, Glass CR. (1997) Predictors of response to cognitive-behavioral group
therapy for social phobia. Journal of Anxiety Disorders, 11, 221–40.
Chorpita BF, Tracey SA, Brown TA, Collica TJ, Barlow DH. (1997) Assessment of worry in
children and adolescents: an adaptation of the Penn State Worry Questionnaire. Behaviour
Research and Therapy, 35, 569–81.
Chouinard G, Goodman W, Greist J, Jenike M, Rasmusson S, White K, Hackett E, GaVney M,
Bick P. (1990) Results of a double blind placebo controlled trial of a new serotonin uptake
inhibitor, sertraline, in the treatment of obsessive compulsive disorder. Psychopharmacology,
26, 279–84.
Clark DB, Agras WS. (1991) The assessment and treatment of performance anxiety in musi-
cians. American Journal of Psychiatry, 148, 598–605.
Clark DM. (1986) A cognitive approach to panic. Behaviour Research and Therapy, 24, 461–70.
564 References
Clark DM. (1988) A cognitive model of panic attacks. In Rachman S, Maser JD (Eds), Panic:
Psychological Perspectives. Hillsdale, NJ: Lawrence Erlbaum.
Clark DM, Hemsley DR. (1982) The eVects of hyperventilation: individual variability and its
relation to personality. Journal of Behavior Therapy and Experimental Psychiatry, 13, 41–7.
Clark DM, Wells A. (1995) A cognitive model of social phobia. In Heimberg RG, Liebowitz MR,
Hope DA, Schneier FR (Eds), Social Phobia: Diagnosis, Assessment and Treatment. New York:
Guilford Press, pp. 69–93.
Clark DM, Salkovskis PM, Chalkley AJ. (1985) Respiratory control as a treatment for panic
attacks. Journal of Behavior Therapy and Experimental Psychiatry, 16, 23–30.
Clark LA, Watson D. (1991) Tripartite model of anxiety and depression: psychometric evidence
and taxonomic implications. Journal of Abnormal Psychology, 100, 316–36.
Clarke JC, Jackson JA. (1983) Hypnosis and Behavior Therapy. New York: Springer-Verlag.
Clum GA. (1989) Psychological interventions vs. drugs in the treatment of panic. Behavior
Therapy, 20, 429–57.
Clum GA, Knowles SL. (1991) Why do some people with panic disorder become avoidant? A
review. Clinical Psychology Review, 11, 295–313.
Clum GA, Broyles S, Borden J, Watkins PL. (1990) Validity and reliability of the panic attack
symptoms and cognitions questionnaires. Special Issue: DSM-IV and the psychology litera-
ture. Journal of Psychopathology and Behavioral Assessment, 12, 233–45.
Clum GA, Clum GA, Searles R. (1993) A meta-analysis of treatments for panic disorder. Journal
of Consulting and Clinical Psychology, 61, 317–26.
Cohen J. (1992) A power primer. Psychological Bulletin, 112, 155–9.
Coles ME, Heimberg RG. (2000) Patterns of anxious arousal during exposure to feared
situations in individuals with social phobia. Behaviour Research and Therapy, 38, 405–24.
Connolly J, Hallam RS, Marks IM. (1976) Selective association of fainting with blood–injury–
illness fear. Behaviour Research and Therapy, 7, 8–13.
Connor KM, Davidson JRT. (1998) Generalized anxiety disorder: neurobiological and phar-
macotherapeutic perspectives. Biological Psychiatry, 44, 1286–94.
Connor KM, Sutherland SM, Tupler LA, Malik ML, Davidson JRT. (1999) Fluoxetine in
post-traumatic stress disorder – randomised, double-blind study. British Journal of Psychia-
try, 175, 17–22.
Constans JI, Penn DL, Ihen GH, Hope DA. (1999) Interpretive biases for ambiguous stimuli in
social anxiety. Behaviour Research and Therapy, 37, 643–51.
Cooper NA, Clum GA. (1989) Imaginal Xooding as a supplementary treatment for PTSD in
combat veterans: a controlled study. Behavior Therapy, 20, 381–91.
Cooper PJ, Eke M. (1999) Childhood shyness and maternal social phobia: a community study.
British Journal of Psychiatry, 174, 439–43.
Copp JE, Schwiderski UE, Robinson DS. (1990) Symptom comorbidity in anxiety and depress-
ive disorders. Journal of Clinical Psychopharmacology, 10 (3, Suppl.), 52S–60S.
Costa P, Herbst JH, McCrae RR, Siegler IC. (2000) Personality at midlife: stability, intrinsic
maturation, and response to life events. Assessment, 7, 365–78.
Costa PT, McCrae RR. (1992) Normal personality assessment in clinical practice: the NEO
personality inventory. Psychological Assessment, 4, 5–13.
565 References
iterative style as features of the catastrophizing process. Journal of Abnormal Psychology, 107,
576–86.
Davidson J, Smith R, Kudler H. (1989) Validity and reliability of the DSM-III criteria for
posttraumatic stress disorder. Experience with a structured interview. Journal of Nervous and
Mental Disease, 177, 336–41.
Davidson JRT, Potts NLS, Richichi EA, Krishnan R, Ford SM, Smith R, Wilson WH. (1993)
Treatment of social phobia with clonazepam and placebo. Journal of Clinical Psychophar-
macology, 13, 423–8.
Davidson JRT, Hughes DC, George LK, Blazer DG. (1994) The boundary of social phobia:
exploring the threshold. Archives of General Psychiatry, 51, 975–83.
de Haan E, Hoogduin K, Buitelaar J, Keijsers G. (1998) Behaviour therapy versus clomipramine
for the treatment of obsessive compulsive disorder in children and adolescents. Journal of the
American Academy of Child and Adolescent Psychiatry, 37, 1022–9.
De Loof C, Zandbergen H, Lousberg T, Pols H, Griez E. (1989) The role of life events in the
onset of panic disorder. Behaviour Research and Therapy, 27, 461–3.
De Ruiter C, Garssen B, Rijken H, Kraaimaat F. (1989a) The hyperventilation syndrome in
panic disorder, agoraphobia, and generalized anxiety disorder. Behaviour Research and
Therapy, 27, 447–52.
De Ruiter C, Rijken H, Garssen B, Kraaimaat F. (1989b) Breathing retraining, exposure, and a
combination of both, in the treatment of panic disorder with agoraphobia. Behaviour
Research and Therapy, 27, 647–55.
De Silva P, Rachman SJ. (1984) Does escape behaviour strengthen agoraphobic avoidance? A
preliminary study. Behaviour Research and Therapy, 22, 87–91.
De Veaugh-Geiss J, Katz RJ, Landau P. (1989) Preliminary results from a multicentre trial of
clomipramine in obsessive compulsive disorder. Psychopharmacology Bulletin, 25, 36–40.
DeFries JC, Gervais MC, Thomas EA. (1978) Response for 30 generations of selection for open
Weld activity in laboratory mice. Behavior Genetics, 8, 3–13.
den Boer JA. (1998) Pharmacotherapy of panic disorder: DiVerential eYcacy from a clinical
viewpoint. Journal of Clinical Psychiatry, 59, 30–6.
Denney DR, Sullivan DJ, Thiry MR. (1977) Participant modelling and self-verbalization train-
ing in the reduction of spider fears. Journal of Behavior Therapy and Experimental Psychiatry,
8, 247–53.
Derogatis LR. (1977) SCL-90 Revised Version Manual-1. Baltimore, MD: Johns Hopkins School
of Medicine.
Devilly G, Spence S. (1999) The relative eYcacy and treatment distress of EMDR and a
cognitive-behavior trauma treatment protocol in the amelioration of posttraumatic stress
disorder. Journal of Anxiety Disorders, 13, 131–57.
Devilly G, Spence S, Rapee R. (1998) Statistical and reliable change with eye movement
desensitization and reprocessing: treating trauma within a veteran population. Behavior
Therapy, 29, 435–55.
DeWit DJ, Ogborne A, OVord DR, MacDonald K. (1999) Antecedents of the risk of recovery
from DSM-III-R social phobia. Psychological Medicine, 29, 569–82.
Di Nardo PA, Barlow DH. (1988) Instructions for the Anxiety Disorders Interview Schedule –
567 References
(Eds), Psychiatric Disorders in America: The Epidemiological Catchment Area Study. New York:
Free Press.
Eaton WW, Anthony JC, Romanoski A, Tien A, Gallo J, Cai G, Neufeld K, Schlaepfer T,
Laugharne J, Chen LS. (1998) Onset and recovery from panic disorder in the Baltimore
Epidemiologic Catchment Area follow-up. British Journal of Psychiatry, 173, 501–7.
Ehlers A, Margraf J, Davies S, Roth WT. (1988) Selective processing of threat cues in subjects
with panic attacks. Cognition and Emotion, 2, 201–20.
Ehlers A, Margraf J, Roth WT. (1986a) The authors’ reply. Psychiatry Research, 19, 165–7.
Ehlers A, Margraf J, Roth WT, Taylor CB, Maddock RJ, Sheikh J, Kopell ML, McClenahan KL,
Gossard D, Blowers GH, Agras WS, Kopell BS. (1986b) Lactate infusions and panic attacks:
do patient and controls respond diVerently? Psychiatry Research, 17, 295–308.
Eley TC, Plomin R. (1997) Genetic analyses of emotionality. Current Opinion in Neurobiology, 7,
279–84.
Elkin I, Shea T, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR,
Docherty JP, Fiester SJ, ParloV MB. (1989) National Institute of Mental Health treatment of
depression collaborative research program. Archives of General Psychiatry, 46, 971–82.
Ellis A. (1957) Outcome of employing three techniques of psychotherapy. Journal of Clinical
Psychology, 13, 344–50.
Ellis A. (1962) Reason and Emotion in Psychotherapy. New York: Lyle Stuart.
Ellis A, Harper RA. (1975) A New Guide to Rational Living. North Hollywood, CA: Wilshire.
Emmelkamp PMG. (1979) The behavioral study of clinical phobias. In Hersen M, Eisler RM,
Miller PM (Eds), Progress in Behavior ModiWcation, Vol. 8. New York: Academic Press.
Emmelkamp PMG. (1982) Phobic and Obsessive–Compulsive Disorders: Theory, Research, and
Practice. New York: Plenum Press.
Emmelkamp PMG, Beens H. (1991) Cognitive therapy with obsessive–compulsive disorder: a
comparative evaluation. Behaviour Research and Therapy, 29, 293–300.
Emmelkamp PMG, Felten M. (1985) Cognitive and physiological changes during prolonged
exposure in vivo: a comparison with agoraphobics as subjects. Behaviour Research and
Therapy, 23, 219–23.
Emmelkamp PMG, Wessels H. (1975) Flooding in imagination vs. Xooding in vivo: a compari-
son with agoraphobics. Behaviour Research and Therapy, 13, 7–15.
Emmelkamp PMG, van der Helm M, van Zantin BL, Plochg I. (1980) Treatment of obsessive
compulsive patients: the contribution of self-instructional training to the eVectiveness of
exposure. Behaviour Research and Therapy, 18, 61–6.
Emmelkamp PMG, Mersch P-P, Vissia E. (1985a) The external validity of analogue outcome
research: evaluation of cognitive and behavioural interventions. Behavior Research and
Therapy, 23, 83–6.
Emmelkamp PMG, Mersch P-P, Vissia E, van der Helm M. (1985b) Social phobia: a compara-
tive evaluation of cognitive and behavioral interventions. Behavior Research and Therapy, 23,
365–9.
Emmelkamp PMG, Visser S, Hoekstra RJ. (1988) Cognitive therapy versus exposure in vivo in
the treatment of obsessive–compulsives. Cognitive Therapy and Research, 12, 103–14.
Endicott J, Spitzer RL. (1978) A diagnostic interview: the schedule for aVective disorders and
569 References
Foa EB, Tillmans A. (1980) The treatment of obsessive compulsive neurosis. In Goldstein A, Foa
EB (Eds), Handbook of Behavioural Interventions: A Clinical Guide. New York: Wiley.
Foa EB, Jameson JS, Turner RM, Payne LL. (1980) Massed vs. spaced exposure sessions in the
treatment of agoraphobia. Behaviour Research and Therapy, 18, 333–8.
Foa EB, Steketee GS, Grayson JB. (1981) Success and failure in treating obsessive–compulsives.
Biological Psychiatry, 5, 1099–1102.
Foa EB, Grayson JB, Steketee G, Doppelt HG, Turner RM, Latimer PR. (1983a) Success and
failure in behavioral treatment of obsessive compulsives. Journal of Consulting and Clinical
Psychology, 51, 287–97.
Foa EB, Steketee GS, Grayson JB, Doppelt HG. (1983b) Treatment of obsessive–compulsives:
when do we fail? In Foa EB, Emmelkamp PMG (Eds), Failures in Behavior Therapy. New
York: Wiley.
Foa EB, Steketee GS, Ozarow BJ. (1985) Behaviour therapy with obsessive compulsives: from
therapy to treatment. In Mavissakalian M, Turner SM, Michelsen L (Eds), Obsessive Compul-
sive Disorder: Psychological and Pharmacological Treatments. New York: Plenum Press.
Foa EB, Feske U, Murdock TB, Kozak MJ, McCarthy PR. (1991a) Processing of threat-related
information in rape victims. Journal of Abnormal Psychology, 100, 156–62.
Foa EB, Rothbaum BO, Riggs DS, Murdock TB. (1991b) Treatment of posttraumatic stress
disorder in rape victims: a comparison between cognitive-behavioral procedures and coun-
seling. Journal of Consulting and Clinical Psychology, 59, 715–23.
Foa EB, Riggs DS, Dancu CV, Rothbaum BO. (1993) Reliability and validity of a brief
instrument for assessing post-traumatic stress disorder. Journal of Traumatic Stress, 6,
459–73.
Foa EB, Hearst-Ikeda ID, Perry KJ. (1995a) Evaluation of a brief cognitive-behavioral program
for the prevention of chronic PTSD in recent assault victims. Journal of Consulting and
Clinical Psychology, 63, 948–55.
Foa EB, Riggs DS, Gershuny BS. (1995b) Arousal, numbing, and intrusion: symptom structure
of PTSD following assault. American Journal of Psychiatry, 152, 116–20.
Foa EB, Dancu CV, Hembree EA, Jaycox LH, Meadows EA, Street GP. (1999) A comparison of
exposure therapy, stress inoculation training, and their combination for reducing posttrau-
matic stress disorder in female assault victims. Journal of Consulting and Clinical Psychology,
67, 194–200.
Foa EB, Keane TM, Friedman MJ. (2000) EVective Treatments for PTSD. New York: Guilford
Press.
Fones CSL, Manfro GG, Pollack MH. (1998) Social phobia: an update. Harvard Review of
Psychiatry, 5, 247–59.
Forsyth JP, Chorpita BF. (1997) Unearthing the non-associative origins of fears and phobias: a
rejoinder. Journal of Behavior Therapy and Experimental Psychiatry, 28, 297–305.
Foulds J, Wiedmann K, Patterson J, Brooks N. (1990) The eVects of muscle tension on cerebral
circulation in blood-phobic and non-phobic subjects. Behaviour Research and Therapy, 28,
481–6.
Franklin JA. (1987) The changing nature of agoraphobic fears. British Journal of Clinical
Psychology, 26, 127–33.
571 References
Franklin JA. (1990a) Behavioural therapy for panic disorder. In McNaughton N, Andrews G
(Eds), Anxiety. Dunedin: Otago University Press.
Franklin JA. (1990b) Agoraphobia: its nature, development and treatment. Unpublished doc-
toral dissertation. Sydney: University of New South Wales.
Franklin JA. (1991) Agoraphobia. International Review of Psychiatry, 3, 151–62.
Franklin JA, Andrews G. (1989) Stress and the onset of agoraphobia. Australian Psychologist, 24,
203–19.
Freeston MH, Rheaume J, Letarte H, Dugas MJ, Ladouceur R. (1994) Why do people worry?
Personality and Individual DiVerences, 17, 791–802.
Freeston MH, Dugas MJ, Ladouceur R. (1996a) Thoughts, images, worry and anxiety. Cognitive
Therapy and Research, 20, 265–73.
Freeston MH, Rheaume J, Ladouceur R. (1996b) Correcting faulty appraisals of obsessional
thoughts. Behavior Research and Therapy, 34, 433–46.
Freeston M, Ladoucer R, Gagnon F, Thibodeau N, Rheaume J, Letarte H, Bujold A. (1997)
Cognitive-behavioral treatment of obsessive thoughts: a controlled study. Journal of Consult-
ing and Clinical Psychology, 65, 405–13.
Friedman MJ. (1997) Drug treatment for PTSD: answers and questions. Annals of the New York
Academy of Science, 821, 359–71.
Friedman, MJ, Charney, DS, Southwick SM. (1993) Pharmacotherapy for recently evacuated
military casualties. Military Medicine, 158, 493–7.
Friend P, Andrews G. (1990) Agoraphobia without panic attacks. In McNaughton N, Andrews
G (Eds), Anxiety. Dunedin: Otago University Press.
Frueh BC, Gold PB, de Arellano MA. (1997) Symptom overreporting in combat veterans
evaluated for PTSD: diVerentiation on the basis of compensation seeking status. Journal of
Personality Assessment, 68, 369–84.
Furmark T, Tillfors M, Everz P-O, Marteinsdottir I, Gefvert O, Fredrickson M. (1999) Social
phobia in the general population: prevalence and sociodemographic proWle. Social Psychiatry
and Psychiatric Epidemiology, 34, 416–24.
Furmark T, Tillfors M, Stattin H, Ekselius L, Fredrikson M. (2000) Social phobia subtypes in the
general population revealed by cluster analysis. Psychological Medicine, 30, 1335–44.
Fyer AJ. (1987) Simple phobia. Modern Problems in Pharmacopsychiatry, 22, 174–92.
Fyer AJ, Mannuzza S, Gallops MS, Martin LY, Aaronson C, Gorman JM, Liebowitz MR, Klein
DF. (1990) Familial transmission of simple phobias and fears: a preliminary report. Archives
of General Psychiatry, 47, 252–6.
Gale C, Oakley-Browne M. (2000) Extracts from ‘‘Clinical Evidence’’: anxiety disorder. British
Medical Journal, 321, 1204–7.
Garssen B, van Veenendaal W, Bloemink R. (1983) Agoraphobia and the hyperventilation
syndrome. Behaviour Research and Therapy, 21, 643–9.
Garssen B, de Ruiter C, van Dyck R. (1992) Breathing retraining: a rational placebo? Clinical
Psychology Review, 12, 141–53.
Garvey MJ, Noyes R, Cook B. (1987) Does situational panic disorder represent a speciWc panic
disorder subtype? Comprehensive Psychiatry, 28, 329–33.
Garvey MJ, Cook B, Noyes R. (1988) The occurrence of a prodrome of generalized anxiety in
572 References
Gould RA, Clum GA. (1995) Self-help plus minimal therapist contact in the treatment of panic
disorder: a replication and extension. Behavior Therapy, 26, 533–46.
Gould RA, Clum GA, Shapiro D. (1993) The use of bibliotherapy in the treatment of panic: a
preliminary investigation. Behavior Therapy, 24, 241–52.
Gould RA, Buckminster S, Pollack MH, Otto MW, Yap L. (1997a) Cognitive-behavioral and
pharmacological treatment for social phobia: a meta-analysis. Clinical Psychology: Science and
Practice, 4, 291–306.
Gould RA, Otto MW, Pollack MH, Yap L. (1997b) Cognitive behavioural and pharmacological
treatment of generalized anxiety disorder: a preliminary meta-analysis. Behavior Therapy, 28,
285–305.
Gournay KJM. (1991) The failure of exposure treatment in agoraphobia: implications for the
practice of nurse therapists and community psychiatric nurses. Journal of Advanced Nursing,
16, 1099–109.
Gray JA. (1988) A neuropsychological basis of anxiety. In Last CA, Hersen M (Eds), Handbook of
Anxiety Disorders. Elmsford, NY: Pergamon Press.
Gray JA, McNaughton N. (2000) The Neuropsychology of Anxiety, 2nd Edition. New York:
Oxford University Press.
Green BL. (1996) Traumatic stress and disaster: mental health eVects and factors inXuencing
adaptation. In Mak FL, Nadelson CC (Eds), International Review of Psychiatry, Vol. 2.
Washington, DC: American Psychiatric Press.
Greist J, Chouinard G, DuBoV E, Halaris A, Kim SW, Koran L, Liebowitz M, Lydiard RB,
Rasmussen S, White K, Sikes C. (1995) Double blind parallel comparison of three doses of
sertraline and placebo in outpatients with obsessive compulsive disorder. Archives of General
Psychiatry, 52, 289–95.
Greist JH. (1990a) Medication management of obsessive compulsive disorder. Today’s Thera-
peutic Trends, 7, 13–27.
Greist JH. (1990b) Treatment of obsessive–compulsive disorder: psychotherapies, drugs and
other somatic treatments. Journal of Clinical Psychiatry, 51 (8, Suppl.), 44–50.
Greist JH. (1998) The comparative eVectiveness of treatments for obsessive–compulsive dis-
order. Bulletin of the Meninger Clinic, 62 (Suppl. A), A65–A81.
Greist JH, Marks IM, Berlin F, Gourney K, Noshirvani, H. (1980) Avoidance versus confronta-
tion of fear. Behavior Therapy, 11, 1–14.
Griez E, van den Hout MA. (1982) EVects of carbon dioxide–oxygen inhalations on subjective
anxiety and some neurovegetative parameters. Journal of Behavior Therapy and Experimental
Psychiatry, 13, 27–32.
Griez E, Zandbergen J, Lousberg H, van den Hout M. (1988) EVects of low pulmonary CO2 on
panic anxiety. Comprehensive Psychiatry, 29, 49–58.
Grossberg JM. (1965) Successful behavior therapy in a case of speech phobia (‘‘stage fright’’).
Journal of Speech and Hearing Disorders, 30, 285–8.
Hafner RJ, Marks IM. (1976) Exposure in vivo of agoraphobics: contributions of diazepam,
group exposure, and anxiety evocation. Psychological Medicine, 6, 71–88.
Hamilton M. (1959) The assessment of anxiety states by rating. British Journal of Medical
Psychology, 2, 50–9.
574 References
Hoehn-Saric R. (1998) Psychic and somatic anxiety: worries, somatic symptoms and physio-
logical changes. Acta Psychiatrica Scandinavica, 98 (Suppl. 393), 32–8.
Hoehn-Saric R, McLeod DR, Zimmerli WD. (1988) DiVerential eVects of alprazolam and
imipramine in generalized anxiety disorder: somatic versus psychic symptoms. Journal of
Clinical Psychiatry, 49, 293–301.
HoVart A. (1995) Cognitive mediators of situation fear in agoraphobia. Journal of Behavior
Therapy and Experimental Psychiatry, 26, 313–20.
HoVart A. (1998) Cognitive and guided mastery therapy of agoraphobia: long-term outcome
and mechanisms of change. Cognitive Therapy and Research, 22, 195–207.
HoVart A, Hedley LM. (1997) Personality traits among panic disorder with agoraphobia
patients before and after symptom-focused treatment. Journal of Anxiety Disorders, 11, 77–87.
Hofmann SG. (2000) Self-focused attention before and after treatment of social phobia.
Behaviour Research and Therapy, 38, 717–25.
Hofmann SG, Barlow DH. (1999) The costs of anxiety disorders: implications for psychosocial
interventions. In Miller NE, Magruder KM (Eds), Cost EVectiveness of Psychotherapy. New
York: Oxford University Press.
Hofmann SG, Lehman CL, Barlow DH. (1997) How speciWc are speciWc phobias? Journal of
Behavior Therapy and Experimental Psychiatry, 28, 233–40.
Hohagen F, Winkelmann G, Rasche-Raeuchle H, Hand I, Koenig, A, Muenchau N, Hiss H,
Geiger-Kabisch C, Kaeppler C, Schramm P, Rey E, AldenhoV J, Berger M. (1998) Combina-
tion of behaviour therapy with Xuvoxamine in comparison with behaviour therapy and
placebo: results of a multicentre study. British Journal of Psychiatry, 173 (Suppl. 35), 71–78.
Holland RL, Musch BC, Hindmarch I. (1999) SpeciWc eVects of benzodiazepines and tricyclic
antidepressants in panic disorder: comparisons of clomipramine with alprazolam SR and
adinazolam SR. Human Psychopharmacology, 14, 119–24.
Hollander E, Kaplan A, Allen A, Cartwright C. (2000) Pharmacotherapy for obsessive–compul-
sive disorder. Psychiatric Clinics of North America, 23, 643–56.
Holt CS, Heimberg RG, Hope DA. (1992) Avoidant personality disorder and the generalized
subtype of social phobia. Journal of Abnormal Psychology, 101, 318–25.
Holt PE, Andrews G. (1989a) Provocation of panic: three elements of the panic reaction in four
anxiety disorders. Behaviour Research and Therapy, 27, 253–61.
Holt PE, Andrews G. (1989b) Hyperventilation and anxiety in panic disorder, social phobia,
GAD, and normal controls. Behaviour Research and Therapy, 27, 453–60.
Holzer JC, Goodman WK, McDougle, CJ, Baer L, Boyarsky BK, Leckman JF, Price LH. (1994)
Obsessive–compulsive disorder with and without a chronic tic disorder: a comparison of
symptoms in 70 patients. British Journal of Psychiatry, 164, 469–73.
Hoogduin CAL, Diuvenvoorden HJ. (1988) A decision model in the treatment of obsessive–
compulsive neurosis. British Journal of Psychiatry, 152, 516–21.
Hope DA, Gansler DA, Heimberg RG. (1989) Attentional focus and causal attributions in social
phobia: implications from social psychology. Clinical Psychology Review, 9, 49–60.
Hope DA, Rapee RM, Heimberg RG, Dombeck MJ. (1990) Representations of self in social
phobia: vulnerability to social threat. Cognitive Therapy and Research, 14, 177–89.
Hope DA, Heimberg RG, Bruch MA. (1995) Dismantling cognitive-behavioral group therapy
576 References
Oei TPS, Llamas M, Devilly GJ. (1999) The eYcacy and cognitive processes of cognitive
behaviour therapy in the treatment of panic disorder with agoraphobia. Behavioural and
Cognitive Psychotherapy, 27, 63–88.
OVord DR, Boyle MH, Campbell D, Goering P, Lin E, Wong M, Racine A. (1996) One-year
prevalence of psychiatric disorder in Ontarians 15 to 64 years of age. Canadian Journal of
Psychiatry, 41, 559–63.
Öhman A. (1986) Face the beast and fear the face: animal and social fears as prototypes for
evolutionary analyses of emotion. Psychophysiology, 23, 123–45.
Öhman A, Eriksson A, Olofsson C. (1975a) One-trial learning and superior resistance to
extinction of autonomic responses conditioned to potentially phobic stimuli. Journal of
Comparative and Physiological Psychology, 8, 619–27.
Öhman A, Erixon G, Lofberg I. (1975b) Phobias and preparedness: phobic versus neutral
pictures as conditioned stimuli for human autonomic responses. Journal of Abnormal Psy-
chology, 4, 41–5.
Öhman A, Freidrikson M, Hugdahl K, Rimmo P. (1976) The premise of equipotentiality in
human classical conditioning: conditioned electrodermal responses to potentially phobic
stimuli. Journal of Experimental Psychology: General, 105, 331–7.
Okasha A, Saad A, Khalil AH, Seif El Dawla A, Yehia N. (1994) Phenomenology of obsessive
compulsive disorder; a transcultural study. Comprehensive Psychiatry, 35, 191–7.
Oliver N, Page AC. (2002). Fear reduction during in-vivo exposure to blood–injection stimuli:
distraction vs attentional focus. British Journal of Clinical Psychology, in press.
Ollendick TH. (1995) Cognitive behavioral treatment of panic disorder with agoraphobia in
adolescents: a multiple baseline design analysis. Behavior Therapy, 26, 517–31.
Ontiveros A, Fontaine R. (1990) Social phobia and clonazepam. Canadian Journal of Psychiatry,
35, 439–41.
Öst L-G. (1978) Behavioral treatment of thunder and lightning phobics. Behaviour Research and
Therapy, 16, 197–207.
Öst L-G. (1987a) Age at onset in diVerent phobia. Journal of Abnormal Psychology, 6, 223–9.
Öst L-G. (1987b) Applied relaxation: description of a coping technique and review of controlled
studies. Behaviour Research and Therapy, 25, 397–409.
Öst L-G. (1989) One session treatment for speciWc phobias. Behaviour Research and Therapy, 27,
1–7.
Öst L-G, Breitholtz E. (2000). Applied relaxation vs. cognitive therapy in the treatment of
generalized anxiety disorder. Behaviour Research and Therapy, 38, 777–90.
Öst L-G, Jerremalm A, Johansson J. (1981) Individual response patterns and the eVects of
diVerent behavioral methods in the treatment of social phobia. Behavior Research and
Therapy, 19, 1–16.
Öst L-G, Lindahl I-L, Sterner U, Jerremalm A. (1984a) Exposure in vivo vs applied relaxation in
the treatment of blood phobia. Behaviour Research and Therapy, 22, 205–16.
Öst L-G, Sterner U, Lindahl, I-L. (1984b) Physiological responses in blood phobics. Behaviour
Research and Therapy, 22, 109–17.
Öst L-G, Sterner U. (1987) Applied tension: a speciWc method for treatment of blood phobia.
Behaviour Research and Therapy, 25, 25–9.
589 References
Öst L-G, Sterner U, Fellenius J. (1989) Applied tension, applied relaxation, and the combination
in the treatment of blood phobia. Behaviour Research and Therapy, 27, 109–21.
O’Sullivan G, Noshirvani H, Marks I, Montiero W, Lelliot P. (1991) Six year follow-up after
exposure and clomipramine therapy for obsessive compulsive disorder. Journal of Clinical
Psychiatry, 52, 150–5.
Otto MW, Pollack MH, Gould RA, Worthington JJ, McArdle ET, Rosenbaum JF. (2000) A
comparison of the eYcacy of clonazepam and cognitive-behavioral group therapy for the
treatment of social phobia. Journal of Anxiety Disorders, 14, 345–58.
Overbeek T, Rikken J, Schruers K, Griez E. (1998) Suicidal ideation in panic disorder patients.
Journal of Nervous and Mental Disease, 186, 577–80.
Page AC. (1991a) Simple phobias. International Review of Psychiatry, 3, 175–84.
Page AC. (1991b) An assessment of structured diagnostic interviews for adult anxiety disorders.
International Review of Psychiatry, 3, 265–78.
Page AC. (1993) Don’t Panic! Overcoming Anxiety, Phobias and Tension. Sydney: Gore Osment.
Page AC. (1994a) Panic provocation in the treatment of agoraphobia: a preliminary investiga-
tion. Australian and New Zealand Journal of Psychiatry, 28, 82–6.
Page AC. (1994b) Blood–injury phobia. Clinical Psychology Review, 14, 443–61.
Page AC. (1994c) Distinguishing panic disorder and agoraphobia from social phobia. Journal of
Nervous and Mental Disease, 182, 611–17.
Page AC. (1996) Blood–injury–injection fears in medical practice. Medical Journal of Australia,
164, 189.
Page AC. (1998a) Assessment of panic disorder. Current Opinion in Psychiatry, 11, 137–41.
Page AC. (1998b) Blood–injury–injection fears: nature, assessment, and management. Behav-
iour Change, 15, 160–4.
Page AC, Andrews G. (1996) Do speciWc anxiety disorders show speciWc drug problems?
Australian and New Zealand Journal of Psychiatry, 30, 410–14.
Page AC, Bennett K, Carter O, Smith J, Woodmore K. (1997) The Blood-Injection Symptom
Scale (BISS): assessing a structure of phobic symptoms elicited by blood and injections.
Behaviour Research and Therapy, 35, 457–64.
Parker G, Wilhelm K, Mitchell P, Austin M-P, Roussos J, Gladstone G. (1999). The inXuence of
anxiety as a risk to early onset major depression. Journal of AVective Disorders, 52, 11–17.
Pato MT, Zohar-Kadouch R, Zohar J, Murphy DL. (1988) Return of symptoms after discon-
tinuation of clomipramine in patients with obsessive compulsive disorder. American Journal
of Psychiatry, 145, 1521–5.
Pauls DL, Bucher KD, Crowe RR, Noyes R. (1980) A genetic study of panic disorder pedigrees.
American Journal of Human Genetics, 32, 639–44.
Pauls DL, Alsobrook JP, Goodman W, Rasmussen S, Leckman JF. (1995) A family study of
obsessive–compulsive disorder. American Journal of Psychiatry, 152, 76–84.
Pavlov IP. (1927) Conditioned ReXexes. London: Oxford.
Pelcovitz D, van der Kolk B, Roth S, Mandel F, Kaplan S, Resick P. (1997) Development of a
criteria set and a Structured Interview for Disorders of Extreme Stress (SIDES). Journal of
Traumatic Stress, 10, 3–16.
Penfold K, Page AC. (1999). Distraction enhances within-session fear reduction during in vivo
590 References
Rachman SJ. (1974) Primary obsessional slowness. Behaviour Research and Therapy, 12, 9–18.
Rachman SJ. (1981) Part 1. Unwanted intrusive cognitions. Advances in Behavior Research and
Therapy, 3, 89–99.
Rachman SJ. (1984) Agoraphobia: a safety-signal perspective. Behaviour Research and Therapy,
22, 59–70.
Rachman SJ. (1990) The determinants and treatment of simple phobias. Advances in Behaviour
Research and Therapy, 12, 1–30.
Rachman SJ. (1991) Neo-conditioning and classical theory of fear acquisition. Clinical Psychol-
ogy Review, 11, 155–73.
Rachman SJ. (1993) Obsessions, responsibility and guilt. Behaviour Research and Therapy, 31,
149–54.
Rachman SJ. (1997) A cognitive theory of obsessions. Behavior Research and Therapy, 35,
379–91.
Rachman S, Bichard S. (1988) The overprediction of fear. Clinical Psychology Review, 8, 303–12.
Rachman SJ, Craske M, Tallman K, Solyom C. (1986) Does escape behavior strengthen
agoraphobic avoidance? A replication. Behavior Therapy, 17, 366–84.
Raguram R, Bhide AY. (1985) Patterns of phobic neurosis: a retrospective study. British Journal
of Psychiatry, 147, 557–60.
Rapee RM. (1985a) Distinctions between panic disorder and generalized anxiety disorder:
clinical presentation. Australian and New Zealand Journal of Psychiatry, 19, 227–32.
Rapee RM. (1985b) A case of panic disorder treated with breathing retraining. Journal of
Behavior Therapy and Experimental Psychiatry, 16, 63–5.
Rapee RM. (1991a) The conceptual overlap between cognition and conditioning in clinical
psychology. Clinical Psychology Review, 11, 193–204.
Rapee RM. (1991b) Generalized anxiety disorder: a review of clinical features and theoretical
concepts. Clinical Psychology Review, 11, 419–40.
Rapee RM. (1995) Descriptive psychopathology of social phobia. In Heimberg RG, Leibowitz
MR, Hope DA, Schneier FR (Eds), Social Phobia: Diagnosis, Assessment, and Treatment. New
York: Guilford Press.
Rapee RM, Barlow DH. (1990) The assessment of panic disorder. In McReynolds P, Rosen JC,
Chelune G (Eds), Advances in Psychological Assessment, Vol. 7. New York: Plenum Press.
Rapee RM, Heimberg RG. (1997) A cognitive-behavioural model of anxiety in social phobia.
Behaviour Research and Therapy, 35, 741–56.
Rapee RM, Lim L. (1992) Discrepancy between self and observer ratings of performance in
social phobics. Journal of Abnormal Psychology, 101, 728–31.
Rapee RM, Murrell E. (1988) Predictors of agoraphobic avoidance. Journal of Anxiety Disorders,
2, 203–18.
Rapee RM, Mattick RP, Murrell E. (1986) Cognitive mediation in the aVective component of
spontaneous panic attacks. Journal of Behavior Therapy and Experimental Psychiatry, 17,
245–53.
Rapee RM, Sanderson WC, Barlow DH. (1988) Social phobia features across the DSM-III-R
anxiety disorders. Journal of Psychopathology and Behavioural Assessment, 10, 287–99.
Rapee RM, Litwin EM, Barlow DH. (1990) Impact of life events on subjects with panic disorder
592 References
Riddle MA, Scahil L, King R, Hardin MT, Towbin KE, Ort SI, Leckman JF, Cohen DJ. (1990)
Obsessive–compulsive disorder in children and adolescents: phenomenology and family
history. Journal of the American Academy of Child and Adolescent Psychiatry, 29, 766–72.
Rickels K, Downing R, Schweizer E, Hassan, H. (1993a). Antidepressants for the treatment of
generalised anxiety disorder: a placebo-controlled comparison of imipramine, trazodone and
diazepam. Archives of General Psychiatry, 50, 884–95.
Rickels K, Schweizer E, Weiss S, Zavodnick S. (1993b) Maintenance drug treatment of panic
disorder, II: short- and long-term outcome after drug taper. Archives of General Psychiatry,
50, 61–8.
Rickels K, Schweizer E, DeMartinis N, Mandos L, Mercer C. (1997). Gepirone and diazepam in
generalized anxiety disorder: a placebo-controlled trial. Journal of Clinical Psychopharmacol-
ogy, 17, 272–277.
Ries BJ, McNeil DW, Boone ML, Turk CL, Carter LE, Heimberg RG. (1998) Assessment of
contemporary social phobia verbal report instruments. Behaviour Research and Therapy, 36,
983–94.
Riggs DS, Hiss H, Foa EB. (1992) Marital distress and the treatment of obsessive–compulsive
disorder. Behavior Therapy, 23, 585–97.
Riggs DS, Rothbaum BO, Foa EB. (1995) A prospective examination of symptoms of posttrau-
matic stress disorder in victims of nonsexual assault. Journal of Interpersonal Violence, 10,
201–14.
Riskind JH, Beck AT, Brown G, Steer RA. (1987) Taking the measure of anxiety and depression:
validity of the reconstructed Hamilton scales. Journal of Nervous and Mental Disease, 22,
474–8.
Riskind JH, Moore R, Harman B, Hohmann AA, Beck AT, Stewart B. (1991) The relation of
generalized anxiety disorder to depression in general and dysthymic disorder in particular. In
Rapee RM, Barlow DH (Eds), Chronic Anxiety. Generalized Anxiety Disorder and Mixed
Anxiety–Depression. New York: Guilford.
Robins LN, Regier DA. (1991) Psychiatric Disorders in America. New York: Macmillan.
Rocca P, Fonzo V, Scotta M, Zanalda E, Ravizza L. (1997). Paroxetine eYcacy in the treatment
of generalized anxiety disorder. Acta Psychiatrica Scandinavica, 95, 444–50.
Roemer L, Borkovec M, Posa S, Borkovec TD. (1995) A self-report diagnostic measure of
generalized anxiety disorder. Journal of Behaviour Therapy and Experimental Psychiatry, 26,
345–50.
Roper G, Rachman S, Marks I. (1975) Passive and participant modelling in exposure treatment
of obsessive-compulsive neurotics. Behaviour Research and Therapy, 13, 271–9.
Rose RJ, Ditto WB. (1983) A developmental-genetic analysis of common fears from early
adolescence to early adulthood. Child Development, 54, 361–8.
Rose S, Bisson J. (1998) Brief early interventions following trauma: a systematic review of the
literature. Journal of Traumatic Stress, 11, 697–710.
Rosenberg CM. (1968) Complications of obsessional neurosis. British Journal of Psychiatry, 114,
477–8.
Roth DL, Holmes DS. (1985) InXuence of physical Wtness in determining the impact of stressful
life events on physical and psychological health. Psychosomatic Medicine, 47, 164–73.
594 References
Roth M. (1984) Agoraphobia, panic disorder and generalized anxiety disorder: some implica-
tions of recent advances. Psychiatric Developments, 2, 31–52.
Roth M, Argyle N. (1988) Anxiety, panic and phobic disorders: an overview. Journal of
Psychiatric Research, 22 (1, Suppl.), 33–54.
Rothbaum BO, Foa EB, Riggs DS, Murdock T, Walsh W. (1992) A prospective examination of
post-traumatic stress disorder in rape victims. Journal of Traumatic Stress, 5, 455–75.
Roy-Byrne PP, Cowley DS (1998) Pharmacological treatment of panic, generalized anxiety, and
phobic disorders. In Nathan PE, Gorman JM (Eds), A Guide to Treatments That Work. New
York: Oxford University Press.
Roy-Byrne P, Mellman TA, Uhde TW. (1988) Biological Wndings in panic disorder: neuroen-
docrine and sleep-related abnormalities. Journal of Anxiety Disorders, 2, 17–29.
Roy-Byrne PP, Wingerson D. (1992) Pharmacotherapy of anxiety disorders. In Tasman A, Riba
MB (Eds), Review of Psychiatry, Vol. 11. Washington DC: American Psychiatric Press.
Ruch LO, Leon JJ. (1983) Sexual assault trauma and trauma change. Women and Health, 8,
5–21.
Safren SA, Heimberg RG, Horner KJ, Juster HR, Schneier FR, Liebowitz MR. (1999) Factor
structure of social fears: the Liebowitz Social Anxiety Scale. Journal of Anxiety Disorders, 13,
253–70.
Salaberria K, Echeburua E. (1998) Long-term outcome of cognitive therapy’s contribution to
self-exposure in vivo to the treatment of generalized social phobia. Behavior ModiWcation, 22,
262–84.
Salkovskis PM. (1989) Obsessions and compulsions. In Scott J, Williams JMG, Beck A (Eds),
Cognitive Therapy in Clinical Practice. London: Routledge.
Salkovskis PM, Kirk J. (1997) Obsessive–compulsive disorder. In Clark DM, Fairburn CG (Eds),
Cognitive Behaviour Therapy: Science and Practice. New York: Oxford University Press.
Salkovskis PM, Westbrook D. (1989) Behaviour therapy and obsessional ruminations: can
failure be turned into success? Behaviour Research and Therapy, 27, 149–60.
Salkovskis PM, Jones DRO, Clark DM. (1986a) Respiratory control in the treatment of panic
attacks: replication and extension with concurrent measurement of behaviour and PCO.
British Journal of Psychiatry, 148, 526–32.
Salkovskis PM, Warwick HMC, Clark DM, Wessels DJ. (1986b) A demonstration of acute
hyperventilation during naturally occurring panic attacks. Behaviour Research and Therapy,
24, 91–4.
Salkovskis PM, Atha C, Storer D. (1990) Cognitive-behavioural problem solving in the treat-
ment of patients who repeatedly attempt suicide. British Journal of Psychiatry, 157, 871–6.
Salkovskis PM, Clark DM, Hackman A. (1991) Treatment of panic attacks using cognitive
therapy without exposure or breathing retraining. Behaviour Research and Therapy, 29,
161–6.
Sanavio E. (1988) Obsessions and compulsions: the Padua Inventory. Behaviour Research and
Therapy, 26, 169–77.
Sanderson WC, Barlow DH. (1990) A description of patients diagnosed with DSM-III-R GAD.
Journal of Nervous and Mental Disease, 178, 588–91.
Sanderson WC, Wetzler S. (1991) Chronic anxiety and generalized anxiety disorder: issues in
595 References
comorbidity. In Rapee RM, Barlow DH (Eds), Chronic Anxiety. Generalized Anxiety Disorder
and Mixed Anxiety–Depression. New York: Guilford, pp. 119–35.
Sanderson WC, Rapee RM, Barlow DH. (1989) The inXuence of an illusion of control on panic
attacks induced via inhalation of 5.5% carbon dioxide-enriched air. Archives of General
Psychiatry, 46, 157–62.
Sanderson WC, Di Nardo PA, Rapee RM, Barlow DH. (1990). Syndrome co-morbidity in
patients diagnosed with DSM IIIR anxiety disorder. Journal of Abnormal Psychology, 99,
308–12.
Sanderson WC, Raue PJ, Wetzler S. (1998) The generalizability of cognitive behavior therapy for
panic disorder. Journal of Cognitive Psychotherapy, 12, 323–30.
Sandler IN, Lakey B. (1982) Locus of control as a stress moderator: the role of control
perceptions and social support. American Journal of Community Psychology, 10, 65–72.
Sartorius N, de Girolamo G, Andrews G, German GA, Eisenberg L. (1993) Treatment of Mental
Disorders. Washington, DC: American Psychiatric Press.
Saunders BE, Arata CM, Kilpatrick DG. (1990) Development of a crime-related posttraumatic
stress disorder scale for women within the Symptom Checklist 90 Revised. Journal of
Traumatic Stress, 3, 439–48.
Saxena S, Rauch SL. (2000) Functional neuroimaging and the neuroanatomy of obsessive
compulsive disorder. Psychiatric Clinics of North America, 23, 563–86.
Saxena S, Brody AL, Schwartz JM, Baxter LR. (1998) Neuroimaging and frontal-subcortical
circuitry in obsessive–compulsive disorder. British Journal of Psychiatry, 173 (Suppl. 35),
26–37.
Scherrer JF, True WR, Xian H, Lyons MJ, Eisen SA, Goldberg J, Lin N, Tsuang MT. (2000).
Evidence for genetic inXuences common and speciWc to symptoms of generalized anxiety and
panic. Journal of AVective Disorders, 57, 25–35.
Schmidt NB. (1999) Panic disorder: cognitive behavioral and pharmacological treatment
strategies. Journal of Clinical Psychology in Medical Settings, 6, 89–111.
Schmidt NB, Woolaway-Bickel K, Trakowski J, Santiago H, Storey J, Koselka M, Cook J. (2000)
Dismantling cognitive behavioral treatment for panic disorder: questioning the utility of
breathing retraining. Journal of Consulting and Clinical Psychology, 68, 417–24.
Schneier FR, Martin LY, Liebowitz MR, Gorman MD, Fyer AJ. (1989) Alcohol abuse in social
phobia. Journal of Anxiety Disorders, 3, 15–23.
Schneier FR, Spitzer RL, Gibbon M, Fyer AJ, Liebowitz, MR. (1991) The relationship of social
phobia subtypes and avoidant personality disorder. Comprehensive Psychiatry, 32, 496–502.
Schneier FR, Johnson J, Hornig CD, Liebowitz MR, Weissman MM. (1992) Social phobia:
comorbidity and morbidity in an epidemiological sample. Archives of General Psychiatry, 49,
282–8.
Schneier FR, Goetz D, Campeas R, Fallon B, Marshall R, Liebowitz MR. (1998) Placebo-
controlled trial of moclobemide in social phobia. British Journal of Psychiatry, 172, 70–7.
Schulte D. (1997) Behavioural analysis: does it matter? Behavioural and Cognitive Psychotherapy,
25, 231–49.
Schwartz (1998) Neuroanatomical aspects of cognitive behavioural therapy response in obsess-
ive–compulsive disorders. An evolving perspective on brain and behaviour. British Journal of
596 References
Patient Version (SCID-P, Version 2.0). Washington, DC: American Psychiatric Press.
Stanley MA, Novy DM. (2000) Cognitive-behavior therapy for generalized anxiety in late life: an
evaluative overview. Journal of Anxiety Disorders, 14, 191–207.
Stanley MA, Beck JG, Glassco JD. (1996). Treatment of generalized anxiety in older adults: A
preliminary comparison of cognitive-behavioural and supportive approaches. Behavior Ther-
apy, 27, 565–81.
Starcevic V, Bogojevic G. (1997) Comorbidity of panic disorder with agoraphobia and speciWc
phobia: relationship with the subtypes of speciWc phobia. Comprehensive Psychiatry, 38,
315–20.
Starcevic V, Bogojevic G. (1999) The concept of generalized anxiety disorder: between the too
narrow and too wide diagnostic criteria. Psychopathology, 32, 5–11.
Starkman MN, Zelnik TC, Nesse RM, Cameron OG. (1985) Anxiety in patients with pheoch-
romocytomas. Archives of Internal Medicine, 145, 248–52.
Stein M, Forde D, Anderson G, Walker J. (1997) Obsessive–compulsive disorder in the
community: an epidemiologic survey with clinical reappraisal. American Journal of Psychiatry,
154, 1120–6.
Stein MB. (1998) Neurobiological perspectives on social phobia: from aYliation to zoology.
Biological Psychiatry, 44, 1277–85.
Stein MB, Chavira, DA. (1998) Subtypes of social phobia and comorbidity with depression and
other anxiety disorders. Journal of AVective Disorders, 50 (Suppl.), S11–S16.
Stein MB, Chartier MJ, Hazen Al, Kozak MV, Tancer ME, Lander S, Furer P, Chubaty D, Walker
JR. (1998a) A direct-interview family study of generalized social phobia. American Journal of
Psychiatry, 155, 90–7.
Stein MB, Liebowitz MR, Lydiard RB, Pitts CD, Bushnell W, Gergel I. (1998b) Paroxetine
treatment of generalized social phobia (social anxiety disorder): a randomized controlled
trial. Journal of the American Medical Association, 220, 708–13.
Stein MB, Fyer AJ, Davidson JRT, Pollack MH, Wiita B. (1999) Fluvoxamine treatment of social
phobia (social anxiety disorder): a double-blind, placebo-controlled study. American Journal
of Psychiatry, 156, 756–60.
Steptoe A, Wardle J. (1988) Emotional fainting and the psychophysiologic response to blood
and injury: autonomic mechanisms and coping strategies. Psychosomatic Medicine, 50,
402–17.
Stern R. (1978) Behavioural Techniques: A Therapist’s Manual. New York: Academic Press.
Stern RS, Marks IM. (1973) Brief and prolonged Xooding: a comparison of agoraphobic
patients. Archives of General Psychiatry, 28, 270–6.
Stöber J. (1998) Worry, problem elaboration and suppression of imagery: the role of concrete-
ness. Behaviour Research and Therapy, 36, 751–6.
Stöber J, Borkovec TD. (In press) Reduced concreteness of worry in generalized anxiety
disorder: Wndings from a therapy study. Cognitive Therapy and Research.
Stravynski A. (1983) Behavioral treatment of psychogenic vomiting in the context of social
phobia. Journal of Nervous and Mental Disease, 171, 448–51.
Stravynski A, Greenberg D. (1989) Behavioural psychotherapy for social phobia and dysfunc-
tion. International Review of Psychiatry, 1, 207–18.
598 References
Stravynski A, Greenberg D. (1998) The treatment of social phobia: a critical assessment. Acta
Pyschiatrica Scandinavica, 98, 171–81.
Stravynski A, Marks I, Yule W. (1982) Social skills problems in neurotic outpatients. Archives of
General Psychiatry, 39, 1378–85.
Stravynski A, Lamontagne Y, Lavellee Y-J. (1986) Clinical phobias and avoidant personality
disorder among alcoholics admitted to an alcoholism rehabilitation setting. Canadian Journal
of Psychiatry, 31, 714–19.
Stravynski A, Arbel N, Bounader J, Gaudette G, Lachance L, Borgeat F, Fabian J, Lamontagne Y,
Sidoun P, Todorov C. (2000) Social phobia treated as a problem in social functioning: a
controlled comparison of two behavioural group approaches. Acta Psychiatrica Scandinavica,
102, 188–98.
Sturgis ET, Scott R. (1984) Simple phobia. In Turner SH (Ed), Behavioural Theories and
Treatment of Anxiety. New York: Plenum Press.
Swedo SE, Rapoport JL, Leonard H, Lenane M, Cheslow D. (1989) Obsessive–compulsive
disorder in children and adolescents: clinical phenomenology of 70 consecutive cases.
Archives of General Psychiatry, 46, 335–41.
Tallis F, Eysenck M, Mathews A. (1992) A questionnaire for the measurement of nonpathologi-
cal worry. Personality and Individual DiVerences, 13, 161–8.
Tarrier N, Pilgrim H, SommerWeld C, Faragher B, Reynolds M, Graham E, Barrowclough C.
(1999) A randomized trial of cognitive therapy and imaginal exposure in the treatment of
chronic posttraumatic stress disorder. Journal of Consulting and Clinical Psychology, 67,
13–18.
Taylor FK. (1966) Psychopathology: Its Causes and Symptoms. Oxford: Butterworths.
Taylor S. (1996) Meta-analysis of cognitive-behavioral treatments for social phobia. Journal of
Behavioral and Experimental Psychiatry, 27, 1–9.
Taylor S, Woody S, Koch WJ, McLean P, Paterson RJ, Anderson KW. (1997) Cognitive
restructuring in the treatment of social phobia. Behavior ModiWcation, 21, 487–511.
Telch MJ, Agras WS, Taylor CB, Roth WT, Gallen C. (1985) Combined pharmacological and
behavioural treatment for agoraphobia. Behaviour Research and Therapy, 23, 325–35.
Telch MJ, Brouillard M, Telch CF, Agras WF, Taylor CB. (1989) Role of cognitive appraisal in
panic-related avoidance. Behaviour Research and Therapy, 27, 373–83.
Telch MJ, Schmidt NB, Jaimez TL, Jacquin KM, Harrington PJ. (1995) Impact of cognitive-
behavioral treatment on quality of life in panic disorder patients. Journal of Consulting and
Clinical Psychology, 63, 823–30.
Tellegen A. (1982) Brief Manual for the Multidimensional Personality Questionnaire. Min-
neapolis, MN: University of Minnesota.
Tennant CC, Andrews G. (1976) A scale to measure the stress of life events. Australian and New
Zealand Journal of Psychiatry, 10, 27–32.
Teusch L, Boehme H. (1999). Is the exposure principle really crucial in agoraphobia? The
inXuence of client-centered ‘‘nonprescriptive’’ treatment on exposure. Psychotherapy Re-
search, 9, 115–23.
Thayer JF, Friedman BH, Borkovec TD. (1996) Autonomic characteristics of generalized anxiety
disorder and worry. Biological Psychiatry, 39, 255–66.
599 References
Thomas SE, Thevos AK, Randall CL. (1999) Alcoholics with and without social phobia: a
comparison of substance use and psychiatric variables. Journal of Studies on Alcohol, 60,
472–9.
Thompson JA, Charlton PFC, Kerry R, Lee D. (1995) An open trial of exposure therapy based on
deconditioning for post-traumatic stress disorder. British Journal of Clinical Psychology, 34,
407–16.
Thyer B, Himle J, Curtis G. (1985a) Blood–injury–illness phobia: a review. Journal of Clinical
Psychology, 41, 451–9.
Thyer BA, Parrish RT, Curtis GC, Nesse RM, Cameron OG. (1985b) Ages of onset of DSM-III
anxiety disorders. Comprehensive Psychiatry, 26, 113–22.
Tollefson GD, Birkett M, Koran L, Genduso L. (1994) Continuation treatment of OCD: double
blind and open label experience with Xuoxetine. Journal of Clinical Psychiatry, 55 (10, Suppl.),
69–76.
Torgersen S. (1979) The nature and origin of common phobic fears. British Journal of Psychiatry,
134, 343–51.
Torgersen S. (1983) Genetic factors in anxiety disorders. Archives of General Psychiatry, 40,
1085–9.
Torgersen S. (1986) Childhood and family characteristics in panic and generalized anxiety
disorders. American Journal of Psychiatry, 143, 630–2.
Tseng W-H. (1973) Psychopathologic study of obsessive–compulsive neurosis in Taiwan.
Comprehensive Psychiatry, 14, 139–150.
Tseng W-S, Asai M, Kitanishi K, McLaughlin DG, Kyomen H. (1992) Diagnostic patterns of
social phobia: comparison in Tokyo and Hawaii. Journal of Nervous and Mental Disease, 180,
380–5.
Turgeon L, Marchand A, Dupuis G. (1998) Clinical features in panic disorder with agoraphobia:
a comparison of men and women. Journal of Anxiety Disorders, 12, 539–53.
Turk CL, Heimberg RG, Orsillo SM, Holt CS, Gitow A, Street LL, Schneier FR, Liebowitz MR.
(1998) An investigation of gender diVerences in social phobia. Journal of Anxiety Disorders,
12, 209–23.
Turner SM, Beidel DC. (1989) Social phobia: clinical syndrome, diagnosis, and comorbidity.
Clinical Psychology Review, 9, 3–18.
Turner SM, Beidel DC, Dancu CV, Keys DJ. (1986) Psychopathology of social phobia and
comparison of avoidant personality disorder. Journal of Abnormal Psychology, 95, 389–94.
Turner SM, McCanna M, Beidel DC. (1987) Validity of the Social Avoidance and Distress and
Fear of Negative Evaluation scales. Behaviour Research and Therapy, 25, 113–15.
Turner SM, Beidel DC, Dancu CV, Stanley MA. (1989) An empirically derived inventory to
measure social fears and anxiety: the social phobia and anxiety inventory. Psychological
Assessment: A Journal of Consulting and Clinical Psychology, 1, 35–40.
Turner SM, Beidel DC, Borden JW, Stanley MA, Jacob RG. (1991) Social phobia: axis I and II
correlates. Journal of Abnormal Psychology, 100, 102–6.
Turner SM, Beidel DC, Stanley MA. (1992a) Are obsessional thoughts and worry diVerent
cognitive phenomena? Clinical Psychology Review, 12, 257–70.
Turner SM, Beidel DC, Townsley RM. (1992b) Social phobia: a comparison of speciWc and
600 References
generalized subtypes and avoidant personality disorder. Journal of Abnormal Psychology, 101,
326–31.
Turner SM, Beidel DC, Jacob RG. (1994) Social phobia: a comparison of behavior therapy and
atenolol. Journal of Consulting and Clinical Psychology, 62, 350–8.
Turner SM, Beidel DC, WolV PL, Spaulding S, Jacob RG. (1996) Clinical features aVecting
treatment outcome in social phobia. Behavior Research and Therapy, 34, 795–804.
Tweed JL, Schoenbach VJ, George LK, Blazer DG. (1989) The eVects of childhood parental death
and divorce on six-month history of anxiety disorders. British Journal of Psychiatry, 154,
823–8.
Uhde TW, Boulenger JP, Roy-Byrne PP, Geraci MP, Vittone BJ, Post RM. (1985) Longitudinal
course of panic disorder: clinical and biological considerations. Progressive Neuro-Psycho-
pharmacology and Biological Psychiatry, 9, 39–51.
Üstün TB, Von KorV M. (1995) Primary mental health services: access and provision of care. In
Ustun TB, Sartorius N. (Eds), Mental Illness in General Health Care: An International Study.
New York: Wiley.
Vaillant GE. (1971) Theoretical hierarchy of adaptive ego mechanisms. Archives of General
Psychiatry, 24, 107–18.
Van Ameringen M, Mancini C, Streiner D. (1994) Sertraline in social phobia. Journal of AVective
Disorders, 31, 141–5.
Van Ameringen M, Mancini C, Oakman JM. (1998) The relationship of behavioural inhibition
and shyness to anxiety disorder. Journal of Nervous and Mental Disease, 186, 425–31.
van Balkom AJLM, Bakker A, Spinhoven P, Blaauw BMJW, Smeenk S, Ruesink B. (1997) A
meta-analysis of the treatment of panic disorder with or without agoraphobia: a comparison
of psychopharmacological, cognitive-behavioral, and combination treatments. Journal of
Nervous and Mental Disease, 185, 510–16.
van Balkom AJLM, de Haan E, van Oppen P, Spinhoven P, Hoogduin KAL, van Dyck R. (1998)
Cognitive and behavioral therapies alone and in combination with Xuvoxamine in the
treatment of obsessive–compulsive disorder. Journal of Nervous and Mental Disease, 186,
492–9.
van dam-Baggen R, Kraaimaat F. (2000) Group social skills training or cognitive group therapy
as the clinical treatment of choice for generalized social phobia? Journal of Anxiety Disorders,
14, 437–51.
van der Kolk BA, Dreyfuss D, Michaels M, Shera D, Berkowitz R, Fisler R, Saxe G. (1994)
Fluoxetine in posttraumatic stress disorder. Journal of Clinical Psychiatry, 55, 517–22.
van Oppen P, de Haan E, van Balkom AJL, Spinhoven P, Hoogduin K, van Dyck R. (1995)
Cognitive therapy and exposure in vivo in the treatment of obsessive–compulsive disorder.
Behaviour Research and Therapy, 33, 379–90.
van Velzen CJM, Emmelkamp PMG, Scholing A. (1997) The impact of personality disorders on
behavioral treatment outcome for social phobia. Behaviour Research and Therapy, 35, 889–
900.
van Zijderveld GA, Veltman DJ, van Dyck R, van Doornen LJP. (1999) Epinephrine-induced
panic attacks and hyperventilation. Journal of Psychiatric Research, 33, 73–8.
Vermilyea BB, Barlow DH, O’Brien GT. (1984) The importance of assessing treatment integrity:
601 References
attempts in panic disorder and attacks. New England Journal of Medicine, 321, 1209–14.
Welkowitz LA, Papp LA, Cloitre M, Liebowitz MR, Martin LY, Gorman JM. (1991) Cognitive-
behavior therapy for panic disorder delivered by pharmacologically oriented clinicians.
Journal of Nervous and Mental Disease, 179, 473–7.
Wells A. (1994). A multi-dimensional measure of worry: development and preliminary valida-
tion of the anxious thoughts inventory. Anxiety, Stress and Coping, 6, 289–99.
Wells A, Carter K. (1999) Preliminary tests of a cognitive model of generalized anxiety disorder.
Behaviour Research and Therapy, 37, 585–94.
Wells A, Papageorgiou C. (1998) Social phobia: eVects of external attention on anxiety, negative
beliefs, and perspective taking. Behavior Therapy, 29, 357–70.
Wells A, Papageorgiou C. (1999) The observer perspective: biased imagery in social phobia,
agoraphobia, and blood/injury phobia. Behaviour Research and Therapy, 37, 653–8.
Wells A, Papageorgiou C. (2001) Social phobic interoception: eVects of bodily information on
anxiety, beliefs and self-processing. Behaviour Research and Therapy, 39, 1–11.
Whisman MA. (1990) The eYcacy of booster maintenance sessions in behavior therapy: review
and methodological critique. Clinical Psychology Review, 10, 155–70.
White J, Keenan M. (1990) Stress control: a pilot study of large group therapy for generalized
anxiety disorder. Behavioural Psychotherapy, 18, 143–6.
Whitehead WE, Robinson A, Blackwell B, Stutz R. (1978) Flooding treatment of phobias: does
chronic diazepam increase eVectiveness? Journal of Behavior Therapy and Experimental
Psychiatry, 9, 219–25.
WHO (World Health Organization). (1990) International ClassiWcation of Diseases, 10th revision
(ICD-10). Geneva: World Health Organization.
WHO (World Health Organization). (1993) The ICD-10 ClassiWcation of Mental and Behav-
ioural Disorders: Diagnostic Criteria for Research. Geneva: World Health Organization.
Wilhelm S, Otto MW, Zucker BG, Pollack MH. (1997) Prevalence of body dysmorphic disorder
in patients with anxiety disorders. Journal of Anxiety Disorders, 11, 499–502.
Williams JMG, Watts FN, MacLeod C, Mathews A. (1997). Cognitive Psychology and the
Emotional Disorders, 2nd Edition. New York: Wiley.
Williams SL, Falbo J. (1996) Cognitive and performance-based treatments for panic attacks in
people with varying degrees of agoraphobic disability. Behaviour Research and Therapy, 34,
253–64.
Williams SL, Turner SM, Peer DF. (1985) Guided mastery and performance desensitization
treatments for severe agoraphobia. Journal of Consulting and Clinical Psychology, 53, 237–47.
Wilson GT. (1996). Manual-based treatments: the clinical application of research Wndings.
Behaviour Research and Therapy, 34, 295–314.
Wilson JP, Keane TM. (1997) Assessing Psychological Trauma and PTSD: New York: Guilford.
Wilson PH. (1992) Relapse prevention: conceptual and methodological issues. In Wilson PH
(Ed), Principles and Practice of Relapse Prevention. New York: Guilford, pp. 1–22.
Wittchen H-U, Robins LN, Cottler N, Sartorius N, Burke JD, Regier D. (1991) Cross-cultural
feasibility, reliability and sources of variance of the Composite International Diagnostic
Interview (CIDI). The Multicentre WHO/ADAMHA Field Trials. British Journal of Psychia-
try, 159, 645–53.
603 References
Wittchen H-U, Kessler RC, Zhao S, Abelson J. (1995) Reliability and clinical validity of
UM-CIDI DSM-III-R generalized anxiety disorder. Journal of Psychiatric Research, 29, 95–
110.
Wittchen H-U, Stein MB, Kessler RC. (1999) Social fears and social phobia in a community
sample of young adults: prevalence, risk factors and comorbidity. Psychological Medicine, 29,
309–23.
Wittchen H-U, Zhao Z, Kessler RC, Eaton WW. (1994) DSM-III-R generalized anxiety disorder
in the National Comorbidity Survey. Archives of General Psychiatry, 51, 355–64.
Wlazlo Z, Schroeder-Hartwig K, Hand I, Kaiser G, Munchau N. (1990) Exposure in vivo vs.
social skills training for social phobia: long-term outcome and diVerential eVects. Behavior
Research and Therapy, 28, 181–93.
Wolpe J. (1958) Psychotherapy by Reciprocal Inhibition. Stanford, CA: Stanford University Press.
Woodman CL, Noyes R, Black DW, Schlosser S, Yagla, SJ. (1999) A 5-year follow-up study of
generalized anxiety disorder and panic disorder. Journal of Nervous and Mental Disease, 187,
3–9.
WoodruV R, Pitts F. (1964) Monozygotic twins with obsessional illness. American Journal of
Psychiatry, 120, 1075–80.
Woody SR, Chambless DL, Glass CR. (1997) Self-focused attention in the treatment of social
phobia. Behaviour Research and Therapy, 35, 117–29.
Yaryura-Tobias JA, Neziroglu FA. (1983) Obsessive–Compulsive Disorders: Pathogenesis, Diag-
nosis, Treatment. Basel: Marcel Dekker.
Yehuda R. (1999) Risk Factors for Posttraumatic Stress Disorder. Washington, DC: American
Psychiatric Press.
Yehuda R, Marshall R, Giller E. (1998) Psychopharmacological treatment of post-traumatic
stress disorder. In Nathan P, Gorman J (Eds), A Guide to Treatments that Work. New York:
Oxford University Press, pp. 377–97.
Yerkes RM, Dodson JD. (1908) The relation of strength of stimulus to rapidity of habit-
formation. Journal of Comparative Neurology and Psychology, 18, 459–82.
Yonkers KA, Warshaw MG, Massion, AO, Keller MB. (1996). Phenomenology and course of
generalized anxiety disorder. British Journal of Psychiatry, 168, 308–13.
Yonkers KA, Zlotnick C, Allsworth J, Warshaw M, Shea T, Keller MB. (1998) Is the course of
panic disorder the same in women and men? American Journal of Psychiatry, 155, 596–602.
Zak J, Miller JA, Sheehan DV, Fanous BSL. (1988) The potential role of serotonin re-uptake
inhibitors in the treatment of obsessive compulsive disorder. Journal of Clinical Psychiatry, 49
(Suppl.), 23–9.
Zinbard RE, Barlow DH. (1996) Structure of anxiety and the anxiety disorders: a hierarchical
model. Journal of Abnormal Psychology, 105, 181–93.
Zitrin CM, Klein DF, Woerner MG, Ross DC. (1983) Treatment of phobias: I. Comparison of
imipramine hydrochloride and placebo. Archives of General Psychiatry, 40, 125–38.
Zlotnick C, Davidson J, Shea MT, Pearlstein T. (1996) Validation of the Davidson Trauma Scale
in a sample of survivors of childhood sexual abuse. Journal of Nervous and Mental Disease,
184, 255–7.
Index
604
605 Index
Social Interaction Anxiety Scale (SIAS) 157, speciWc phobias, see phobias
158 SSRIs, see selective serotonin reuptake inhibitors
social phobia 148–260 (SSRIs)
assessment instruments 157–8, 179–80 stress inoculation training (SIT) 484, 485
case examples 150–3 Structured Clinical Interview for DSM-IV 20
classiWcation 149 Structured Interview for PTSD (SI-PTSD) 476
clinical description 148–9 structured problem solving 28–9
comorbidity 150, 161–3, 177–9 Subjective Units of Discomfort (SUDs) 263,
course 154–5 499
deWned 18 substance abuse
diVerential diagnosis 39, 156–7 and anxiety treatment 30–1
disability 155–6 associations with anxiety disorders 17
epidemiology 22, 153–4 panic disorder and agoraphobia 53
etiology PTSD 494–5
behavioral inhibition 158–9 suicide
cognitive theories 160–1 panic disorder and agoraphobia 82–3
genetic factors 158 social phobia 161–2
neurobiology 159 surgery, for OCD 353
psychological models 159–60 systematic desensitization 272–3
information processing biases 160–1 see also imaginal exposure
Patient Treatment Manual 197–260
shyness 153, 158 therapists
subtypes 149–50 morale 34–5
treatment, pharmacological motivation of patients 33–4
benzodiazepines 172–3 patient dependency on 33
beta blockers 172 primary roles 32
dropout rates 174 rated by patients 33
long-term outcome 175 see also motivational interviewing principles
monoamine oxidase inhibitors 173 thought–action fusion in OCD 335, 336, 341
selective serotonin reuptake inhibitors threats
173–4 appraisal of 8
treatment, pharmacological vs. psychological processing in GAD 395
174–5 processing in panic attacks 47–8
treatment, psychological Tourette’s syndrome and OCD 335, 336
behavioral techniques 165–6 trait anxiety, see neuroticism
CBT 166–8, 175 traumatic events 466
combination 166–8 traumatic stress
dropout rates 168–9 acute stress disorder (ASD) 471, 491, 492
individual or group 171, 180–1 complex PTSD 471–2
long-term outcomes 169 PTSD, see posttraumatic stress disorder
predictors of outcome 169–71 (PTSD)
research limitations 171–2 trazadone 488
social skills training 164–5 tricyclic antidepressants 60, 61, 62
treatment program twin studies
anxiety management 186 comorbidity and vulnerability factors
assertiveness 195 13–15
assessment 177–80 GAD 388
cognitive restructuring 186–8 neuroticism 10
expected progress 195 OCD 341–2
failure to progress 196 phobias 158, 268
format 180–1
graded exposure 188–95 uncertainty, intolerance of 395, 413
group therapy, see group therapy for social
phobia valproate 488
patient education 185–6 venlafaxine 404
time management 184–5 verbalization strategy in worriers 392
see also avoidant personality disorder voluntary hyperventilation 25, 45
(APD) vulnerability factors 11–13
Social Phobia and Anxiety Inventory (SPAI) and comorbidity 13–15
157, 158 modiWcation by CBT 63
Social Phobia Scale (SPS) 157 PTSD 474–5
social skills training 164–5 vulnerability to panic disorder 42–4, 63
611 Index