Narrative Review

Subacromial impingement syndrome: a

musculoskeletal condition or a clinical
illusion?
Jeremy S. Lewis1,2,3,4
1

Therapy Department, Chelsea and Westminster Hospital, 2Physiotherapy Department, St Georges Hospital,
Musculoskeletal Service, Central London Community Healthcare, 4St Georges University of London, London,
UK

Published by Maney Publishing (c) W. S. Maney & Son Limited

Background: Subacromial impingement syndrome is considered by many to be the most common of the
musculoskeletal conditions affecting the shoulder. It is based on a hypothesis that acromial irritation leads
to external abrasion of the bursa and rotator cuff.
Objectives: The aim of this paper is to review the evidence for the acromial irritation theory and in doing so
challenge the rationale for subacromial decompression.
Major findings: There is a body of evidence that suggests there is a lack of concordance regarding (i) the
area of tendon pathology and acromial irritation, (ii) the shape of the acromion and symptoms, (iii) the
proposal that irritation leads to the development of tendinitis and bursitis, and (iv) imaging changes and
symptoms and the development of the condition. In addition, there is no certainty that the benefit derived
from the surgery is due to the removal of the acromion as research suggests that a bursectomy in isolation
may confer equivalent benefit. It is also possible that the benefit of surgery is due to placebo or simply
enforces a sustained period of relative rest which may allow the involved tissues to achieve relative
homeostasis. It is possible that pathology originates in the tendon and as such surgery does not address
the primary pathoaetiology. This view is strengthened by the findings of studies that have demonstrated no
increased clinical benefit from surgery when compared with exercise. Additionally, exercise therapy is
associated with a substantially reduced economic burden and less sick leave.
Conclusion: As there is little evidence for an acromial impingement model, a more appropriate name may
be subacromial pain syndrome. Moreover, surgery should only be considered after an appropriate period
of appropriately structured rehabilitation.
Keywords: Shoulder, Subacromial impingement syndrome, Subacromial bursa, Acromioplasty, Subacromial decompression, Rotator cuff tendinopathy,
Shoulder posture

Background
The shoulder complex has a range of movement that
exceeds any other joint in the body and its main
function is to position the hand to affect functional
activities ranging from the performance of high
powered explosive activities, such as throwing baseballs, to positioning the hand, often within the field of
vision, to perform highly complex prehensile tasks.
The shoulder is also used to place the hand so that
the upper limb may be used for weight bearing.
Musculoskeletal pathology involving the shoulder is
common, has the potential to adversely affect upper
limb function and is associated with substantial
morbidity that increases with age.13 Of the wide
spectrum of musculoskeletal disorders affecting the
Correspondence to: Dr J S Lewis, Therapy Department, Chelsea and
Westminster Hospital NHS Foundation Trust, 369 Fulham Road, London
SW10 9NH, UK. Email: [email protected]

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DOI 10.1179/1743288X11Y.0000000027

shoulder, subacromial impingement syndrome is

considered to be one of the most common.4,5 This
condition is well recognized clinically, presenting as
antero-lateral shoulder pain experienced when the
arm is elevated.47 Although numerous historic
references to subacromial pathology exist,813 Neer
argued that abrasion by the under surface of the
anterior margin of the acromion onto the soft tissues
located anatomically in the space between the
humeral head and acromion leads to the symptoms
experienced in subacromial impingement syndrome.4
He stated that this compression occurred principally
in forward elevation and described a clinical test, the
(Neer) impingement sign to reproduce the associated symptoms.5 The test involves restricting scapular movement and forcing the arm into flexion
while the shoulder remains internally rotated.5
According to Neer, this manoeuvre causes the greater

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Lewis

tuberosity to impinge against the acromion. He

argued that 95% of rotator cuff tears are initiated
by impingement and that trauma may enlarge a tear
but is rarely the principal factor. Neer described three
stages of the impingement process. The first occurs in
people under 25 years of age and is associated with
tendinous oedema and haemorrhage, and does not
require surgery. The second involves tendinitis and
occurs in people aged 25 to 40 and bursectomy and
coracoacromial ligament division should be considered after 18 months of conservative treatment. Neer
stated that in this group an acromioplasty is not
usually required. The third stage occurs in people
over 40 years of age and is associated with bone spurs
and tendon rupture and requires anterior acromioplasty. Neer stated that the reason rotator cuff tears
develop in some people and not others is principally
due to the shape of the acromion.5 This hypothesis
was supported by Bigliani et al.14 who described three
distinct morphological variations of acromial shape.
Bigliani et al.14 argued that as a result of the shape
and the damage it would cause, those with a Type III
or hooked acromion were more likely to experience
subacromial impingement syndrome and suffer a
rotator cuff tear. Prior to Neer4,5 presenting his
model, surgeons were performing complete acromionectomies and lateral acromioplasties to alleviate the
symptoms. Basing his argument on intra operative
and cadaver observations, Neer4,5 asserted that
removal of the inferior aspect of the anterior
acromion had greater efficacy. To augment the
procedure, he suggested that a partial resection of
the coracoacromial ligament together with surgery to
remove a hypertrophic acromioclavicular joint may
be required to arrest the impingement process.
Neers impingement model has been widely
embraced by surgeons, sports physicians and physical
therapists. So much in fact, that the percentage of
acromioplasties performed in New York State (USA)
alone has increased 254% in the 10 years from 1996 to
2006. The number of procedures has increased from 30
per 100 000 people (5571 operations) to 102 per
100 000 (19 743 operations).15 Ketola et al.16 reported
that the average cost of an acromioplasty and postsurgical rehabilitation in Finland was J2961 (equivalent to GB2479, US$4017). In London, UK, an
average price for a series of quotations for private
subacromial decompression was GB3500. In New
York State, a figure of US$4860 has been given. If this
is a representative amount, then staggeringly, the total
cost of performing acromioplasties in New York State
alone would be in the order of US$95 959 980. These
figures are not definitive and costs in some centres may
be less and in others higher. Nonetheless this is of
substantial economic burden and healthcare concern,
as Ketola et al.16 have stated:

Subacromial impingement syndrome

Arthroscopic acromioplasty provides no clinically

important effects over a structured and supervised
exercise programme alone in terms of subjective
outcome or cost-effectiveness when measured at
24 months. Structured exercise treatment should be
the basis for treatment of shoulder impingement
syndrome, with operative treatment offered judiciously until its true merit is proven.
This begs the question that if surgery aiming to
remove the cause of the impingement irritation (i.e.
the acromion) is no more clinically effective than a
substantially less expensive structured rehabilitation
programme,1618 then is the original hypothesis
correct, is the procedure valid, or is there an
alternative explanation for the symptoms?

Objectives
The aim of this paper is to review the evidence for the
acromial irritation theory and in doing so challenge
the rationale for the surgical removal of the inferior
aspect of the anterior acromion to remove the source
of symptoms.

Objective Findings
Area of pathology
If 95% of rotator cuff failure is caused by mechanical
irritation by the under surface of the acromion or
coracoacromial ligament,5 then this should result in
abrasion to the superior (bursal side) surface of the
rotator cuff, especially the supraspinatus. Published
research disputes this. Payne et al.19 reported that 39
(91%) partial thickness tears in 43 athletes were on
the inferior (articular or joint) side of the supraspinatus tendon with only 4 (9%) on the superior or
bursal side. In this series, 100% of those with nontraumatic shoulder pain had articular side tears.
Fukuda et al.20 reported that in a study of 249
cadavera, 13% (n533) demonstrated partial thickness
tears. Of the partial thickness tears 82% were either
joint side or intra-tendinous (n527) and only 28%
(n56) were isolated to the upper bursal/acromial side.
Ozaki et al.21 examined 200 shoulders from 100
cadavera and reported that a partial thickness tear
was observed in 69 specimens and that the majority
involved the deeper articular side of the tendon. They
argued that the prevalence of tears increased with age
and occurred due to intrinsic degeneration and not
external (acromial) irritation. In a study of 306
rotator cuff specimens (from 153 cadavera) the
prevalence of partial thickness tears was 32%, with
histological and scanning electron microscopy sections demonstrating that the majority were either
intra-substance or occurred on the articular side of
the supraspinatus tendon, near the insertion.22 This
study did not find a correlation between anatomical
bony variations and tendon failure and argued that
mechanical abrasion may not play an important part

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in the initial pathogenesis of degenerative rotator cuff

tears. Ellman23 reported that partial thickness tears
were found in 15% (n520) of people undergoing
arthroscopic subacromial decompression (n5130).
He reported that when the findings of his observational work were combined with the findings of five
other studies23 a total sample of 160 partial thickness
tears was produced, and of these the location was
reported in 126 cases. From these 126 cases, 76%
(n596) had articular side tears, 14% (n517) had
bursal side, and 10% (n513) had both. This repeated
and consistent finding that the predominance of
partial thickness tears occurs on the deeper articular
side of the tendon substantially challenges the
hypothesis that 95% of rotator cuff tears are caused
by acromial abrasion. Furthermore, Codman10 already in 1934 observed that the rotator cuff degenerates within the substance of the tendon or
frequently along the inferior margin of the tendon,
the side opposite the acromion, calling partial
thickness tears in this region, rim rents. He stated,
I am confident that these rim rents account for the
great majority of sore shoulders. It is my unproved
opinion that many of these lesions never heal,
although the symptoms caused by them usually
disappear after a few months. The weight of evidence
supports Codmans early observations that although
the acromion may be involved, the tendon may
structurally fail without direct mechanical irritation
from the overlying acromion. Supporting this contention, Hashimoto et al.24 observed diffuse degenerative changes involving tendon thinning, fibre
disorientation, myxoid and hyaline degeneration,
calcification, and chondroid metaplasia to be more
prominent in the middle and deeper rotator cuff
tendon layers, suggesting intrinsic tendon failure.
Variations observed in the morphology of the
supraspinatus tendon support these findings.25 In a
histological and biomechanical investigation of 20
normal rotator cuff tendons, the deeper, nonacromial, side fibres were reported to have a smaller
cross-sectional area than the superior acromial side
fibres.25 In addition, when stretched to the point of
rupture, the deeper fibres were found to be more
vulnerable to tensile load than the bursal side fibres,
with the deeper fibres failing at approximately half
the tensile load of the failure point of the upper
acromial side fibres.25 Supporting this finding, Bey
et al.26 in a study of seven cadaveric shoulders
reported that when placed at 15, 30, 45 and 60u of
glenohumeral abduction, strain within the supraspinatus tendon increased with increasing joint elevation. At 60u elevation there was no significant
difference in strain between the superior, middle
and inferior portions of the tendon. However and
importantly, as the inferior fibres are comparatively

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weaker,25 Bey et al.26 argued that the fibres in the

inferior region are relatively more susceptible to
failure in elevation. This is of clinical relevance as
many vocational activities and sporting pursuits
involve placing the shoulder in elevation for prolonged periods. As significantly more strain is placed
on the inferior fibres at 45 and 60u abduction than at
15 and 30u, and the deeper side fibres are relatively
weaker and fail earlier than the larger acromial side
fibres, it is arguable that the acromion has little or
nothing to do with the failure, which potentially may
result from the deeper side fibres passing their
physiological failure point.
As there is a lack of concordance between the area
of structural failure observed in the supraspinatus
tendon and the area predicted by an acromial
irritation model, others have suggested that the
observed joint side structural pathology is better
explained by external impingement between the
superior aspect of the glenoid fossa and the humeral
head. This alternative external irritation model has
been referred to as superior, postero-superior and
internal impingement.2730 However, robust evidence
required to support this model of impingement is
lacking, and as such it is possible that the deep side
tendon failure described in this model might not
result from external (extrinsic) impingement but may
result because of the heterogeneity of the fibre
distribution of the upper and lower aspects of the
supraspinatus tendon, together with the disparity of
tendon loading patterns during movement.25,26,31
Recent reviews on the rotator cuff exploring these
and related issues have been published.32,33
More than 70 years ago, Lindblom and Palmer34
suggested that during shoulder abduction uneven
loads may be placed on the upper and lower aspects
of the tendon resulting in intratendinous shearing,
which may play a part in rotator cuff degeneration
and tears. This is relevant as the supraspinatus
tendon is made up of structurally independent
parallel fascicles35,36 and movement will potentially
lead to different length tension relationships occurring within and between the different fascicles. For
example, at the extreme of shoulder horizontal
abduction the anterior part of the tendon may be
relatively lengthened and the posterior shortened,
whereas at the extreme of horizontal adduction this
pattern may be reversed. As a greater range of
movement is required of the shoulder than any other
joint in the body it is conceivable that internal tendon
shearing may result that may predispose pathology
without the need for external compression on either
the superior or inferior aspects of the tendon. In
support of this, external irritation, in the form of an
Achilles tendon allograft wrapped around the left
acromion, in rats, did not lead to rotator cuff

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pathology. However, intrinsic overload in the form of

downhill eccentric running for 4, 8 and 16 weeks did.
The rats subject to overuse (running) demonstrated
an increase in cross-sectional area and reduced
maximal strain at all time points. A combination
group (allograft and overload) lead to the greatest
change, suggesting that compression potentiated
overload even though compression alone did not
produce pathology.3739 These findings suggest that
external compression is insufficient to cause pathology unless there is a concomitant history of tendon
overload, suggesting that the primary pathoaetiology
occurs within the tendon. It is accepted that due to
differences in morphology and biomechanics, caution
is necessary with direct translation from animal
studies. Evolution of the human upper limb may
place biomechanical constraints on the modern
shoulder which make it less capable of sustaining
positions of elevation.40 If this is the case, then work,
recreational and sporting activities performed above
90u of elevation may selectively affect the weaker,
more vulnerable joint side fibres without the need for
acromial compression.

Acromial shape
Based on a study of 140 shoulders in 71 cadavers,
Bigliani et al.14 argued that three distinct shapes of
the acromion existed. These morphological variations
included a Type I (flat), Type II (curved) and Type III
or hooked acromion. If the acromion is responsible
for 95% of rotator cuff pathology and is the causative
mechanism of pathology in impingement syndrome,
then a definitive relationship between acromial shape,
pathology and symptoms should exist with a Type II
or III more likely to predispose pathology. However,
research evidence has failed to demonstrate this.
In a study of 59 people without shoulder pain the
association between acromial morphology, age and
rotator cuff tears was investigated.41 For people over
the age of 50 years, a 40% prevalence of asymptomatic full thickness rotator cuff tears was identified in
this investigation. Based on the substantial number of
people with curved and hooked acromia who were
entirely asymptomatic, Worland et al.41 concluded
that, Surgeons should interpret radiologically hooked or curved acromions as well as rotator cuff tears
diagnosed with ultrasound or other modalities with
caution. In a study of 55 people who underwent
arthroscopic subacromial decompression (anterolateral edge of the acromion resected together with
release and resection of the coracoacromial ligament
from the acromion), the association between preoperative pain, clinical signs (Hawkins test, Neer
sign, Copeland impingement test) and satisfaction
with the severity of rotator cuff and acromial lesions
was investigated. At the 6 month follow-up no

Subacromial impingement syndrome

significant correlation between pain and satisfaction and the severity of structural pathology was
identified.42 Confirming this, after a study of 523
people undergoing arthroscopic or open shoulder
surgery, Gill et al.43 reported no significant association between acromial shape and rotator cuff pathology in people over 50 years of age (n5192). A
highly significant correlation between age and rotator
cuff pathology existed and the researchers argued that
a Type III hooked acromial represents a degenerative
process rather than a morphological variation as
described by Bigliani.14,44 Although a relationship
between rotator cuff tears and acromial degeneration
appears to exist, this should be seen as an association,
rather than the acromion being implicated in (i.e. the
cause of) rotator cuff pathology.
An alternative explanation for the observed acromial spurs is possible. Edelson and Taitz45 observed
degenerative spur formation on the acromial insertion
of the coracoacromial ligament but not on the
coracoid side in 18% of 200 scapulae. When compared
with shoulder adduction, increasing ranges of shoulder elevation increase subacromial pressure.46,47 The
coracoacromial ligament is more trapezoid in shape
with a smaller area of insertion on the acromial side
than the coracoid side. It is therefore possible that
superiorly directed pressure from below the ligament
will lead to relatively more tension on the acromial
insertion of the ligament than on the coracoid side due
to the smaller surface area of insertion on the former.
This potential increased stress on the bone may lead to
osteophyte formation. Supporting this hypothesis,
Chambler et al.47 demonstrated in vivo (n55) that
tension in the coracoacromial ligament increased as
the arm was abducted. In an additional study48
analysis of acromial bone spurs (n515) suggested that
the development of the spurs was a secondary
phenomenon. These studies suggest that tension in
the coracoacromial ligament is the probable mechanism of acromial bone spur formation and that
acromial Type II (curved) and Type III (hooked) as
described by Bigliani14,44 may not be inherited, but
may result from increased strain in the ligament
disproportionally affecting the acromial side.
Chronic strain in the coracoacromial ligament may
result from changes in the rotator cuff tendons that
may involve increased tendon volume, as well as from
failure of the rotator cuff to stop superior translation
of the humeral head during arm elevation.4953
Evidence for chronic strain exists, with free nerve
endings and neovascularity observed in coracoacromial ligament samples from people undergoing
subacromial decompression.54 This suggests that the
ligament may be a potential source of symptoms. The
coracoacromial ligament limits superior translation
of the humeral head5557 and as acromioplasty has

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been associated with increased anterosuperior translation of the humeral head,52,5759 the procedure itself
may be an iatrogenic cause of ligament strain.
Ligaments are structures that stabilize joint movement and if disrupted they are replaced in an attempt
to recreate stability. Examples of this include patellar
tendon and hamstrings tendon grafts for anterior
cruciate knee ligament failure.60 It is therefore
surprising that the coracoacromial ligament, which
provides a stabilization role by preventing superior
translation of the humeral head,61 has been extensively sacrificed to retard or stop the subacromial
impingement, due to the belief that it is of relative
structural unimportance, when there is no conclusive
evidence to support the existence of primary external
impingement from this structure. It would be hard to
imagine that a surgeon would suggest, or a patient
would agree to, having the anterior cruciate ligament
removed to treat knee pain.

Posture and muscle imbalance

Physical therapists have also embraced the acromial
irritation model6265 and have argued that an
increased kyphosis, a change in scapular position
due to poor posture, uncontrolled scapular movement (dyskinesis), or an imbalance in muscle activity
leads to subacromial impingement syndrome.63,6668
Even though concepts relating to posture and muscle
imbalance have existed for more than half a century it
is surprising how little evidence there is to support (i)
the existence of an ideal posture of the head, neck,
thorax, (ii) the existence of an ideal scapular position
(i.e. the basis for scapular setting exercises), (iii) that
uncontrolled scapular movement and dyskinesis is
always a primary problem, (iv) that postural deviations and muscle length tension changes alter
scapular position in a consistent manner and significantly lead to a detrimental effect of movement
and provoke impingement symptoms, (v) that rehabilitation can correct posture that is considered
abnormal, and (vi) the idea that this correction
leads to an improvement in function and a reduction in pain. There is evidence to challenge these
concepts6976 which suggests that the certainty with
which this aspect of clinical practice is taught to
undergraduate and postgraduate students and
imparted to patients and clients requires robust
research enquiry. In addition, it is arguably inappropriate to suggest that an increased thoracic
kyphosis leads to restricted shoulder movement and
impingement based on studies that have unnaturally
restricted thoracic spine movement.66,68 An assumption implicit within the postural-muscle imbalance
model of assessment is that a forward head posture and increased thoracic kyphosis observed during static posture has a direct correlation with

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dynamic movement, and that all scapulae have the

same geometric proportions and move in the same
way on the same shaped rib cage and thorax. This is
simply not correct45,70,77,78 and as such, a one size fits
all approach is unlikely to be appropriate. Variations
in shoulder function may be dictated by variations in
structure, and the differences observed between
people with impingement syndrome may reflect a
range of normal values and not deviations from one
idealized normal posture. If this is correct it would
not be possible to identify postural deviations that
lead to subacromial impingement. Based on the
uncertainty of the current models of postural and
clinical assessment alternative models of assessment
have been proposed;69 however, these also require
clinical validation.

Tendinitis
Implicit within the three-stage impingement model
presented by Neer4,5 is the association between the
mechanical abrasion caused by the acromion and the
ensuing microtrauma within the tendon leading to
tendon inflammation (tendinitis). The issue of tendon
inflammation is controversial. Although histological
studies have demonstrated substantial differences
between normal tendon and pathological tendon,
the evidence for the presence of cells classically
associated with inflammation is not robust. No
infiltration of neutrophils, lymphocytes or plasma
cells were identified in specimens taken from 12
subjects with rotator cuff disease during surgery.79
Similarly, no inflammatory cells were identified in
bursal specimens (n58) also taken during surgery for
rotator cuff tendinopathy.80 In another small study,
people with constant shoulder pain were more likely
to have lymphocyte infiltration in bursal tissue in
comparison to people with pain only on movement
who did not exhibit evidence of bursal inflammatory
cells.81 There is distinct need for robust evidence from
appropriately designed research to better understand
if inflammation is part of the continuum of pathoaetiology of tendon and bursal pathology.33 Without
this research an argument that acromial irritation and
the ensuring microtrauma leads to bursal and tendon
inflammation remains unsubstantiated.

The subacromial bursa

The subacromial bursa (SAB) separates the coracoacromial arch and deltoid above, and the rotator
cuff tendons below. Together with the other bursae
in the region, whose reported numbers range from
7/8 to 12, the SAB acts to reduce friction during
movement.13,82 The SAB is innervated anteriorly by
the lateral pectoral nerve and posteriorly by the
suprascapular nerve.83 The identification of mechanoreceptors and free nerve endings (Ad and C) in
bursal tissue suggests the SAB has a role in

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proprioception and nociception.84 The presence of

nociceptors is highly relevant as high concentrations
of pro-inflammatory cytokines, pain mediating substances and matrix modifying proteins have been
identified in bursal tissue of people whose shoulder pain is exacerbated by shoulder elevation.8591
Higher shoulder pain scores were reported by those
found to have higher concentrations of the cytokine
interleukin-1beta and the neuropeptide, substance P,
in their bursal tissue.86
One clinical trial randomized people diagnosed
with subacromial impingement syndrome (n557,
mean age 47 years), to Group I: arthroscopic acromioplasty and bursectomy or Group 2: arthroscopic subacromial bursectomy alone. Good results
were reported in both groups with no significant
differences identified between the two groups at a
mean follow-up of 2.5 years.92 These findings clearly
suggest that the bursa is a significant pain generator
and that the addition of an acromioplasty may be
superfluous. Henkus et al.92 argued that subacromial
impingement syndrome is largely an intrinsic degenerative condition rather than an extrinsic mechanical
disorder. The importance of the SAB as a source of
shoulder pain is reinforced by studies that have
shown that injections reaching the SAB reduced pain
while injections targeting other structures increased
or did not change pain.93 This may be a reason why
ultrasound guided injections appear to produce better
outcomes than non-guided injections.94,95
It is also unclear whether treatment with corticosteroid and lidocaine is any more advantageous than
lidocaine in isolation.9699 Using analgesic injections
as a control, systemic (gluteal) corticosteroid injections have been reported to be as effective as locally
guided corticosteroid injections99 in the treatment of
impingement syndrome. However, the certainty of
this conclusion is questioned by studies that have
shown no added long term effect of analgesic over
steroid,96,97 and no one has yet shown the added
benefit of the pharmacological substance injected
over the mechanical stimulation of the dry needle,
which in itself is frequently painful. The science
supporting the use of injection therapy for impingement syndrome (timing, volume, medications used,
direction of injection, post-injection advice, histological effect on tissues) is not robust and requires
ongoing investigation. In the UK, many physical
therapists perform injections and an increasing
number are performing ultrasound guided injections.
Alongside this change to scope of practice is a
requirement for further research, which is essential to
understand the histological and biochemical nature
of bursal pathology and pain and the relationship
between bursal pathology, tendon pathology and
shoulder pain.

Subacromial impingement syndrome

Alternative explanations for the potential benefit

of surgery
Success rates of 8090% following subacromial decompression for impingement have been reported.100103
Neer5 and those embracing his model argue that
removing the acromion removes the source of irritation. Henkus et al.92 has clearly demonstrated this may
not be the case, as isolated removal of the bursa has
comparable effects to removing the acromion and
bursa. However, in addition to the suggestion that
bursectomy is more relevant than acromioplasty,92
other, additional explanations for the beneficial results
reported following acromioplasty are entirely feasible.
In Australia, non-manual workers take on average
6 weeks to return to work following an acromioplasty
and 85% of manual workers take 3 months to return to
employment, with driving commencing at 29 days
post-surgery.104 Comparable findings from the UK
suggest that non-manual workers return to work after
9 days, manual workers after 3 weeks and driving
recommences after 13 days.105 These data clearly
demonstrate that there is a prolonged period of
substantial relative rest following the procedure and
to date no study has compared surgery and the ensuing
relative rest with comparable relative rest alone. This
highly relevant issue of relative rest was suggested by
Lewis33 as an essential component of treatment for
rotator cuff tendinopathy in a reactive stage. This will
be referred to again later in this paper. In addition, it is
possible that subacromial decompression is a placebo.
Moseley et al.106 reported that 180 people with painful
knee osteoarthrosis randomized to either (i) arthroscopic lavage, or (ii) arthroscopic debridement or (iii)
placebo surgery (skin incisions) reported the same
improvement at 2 year follow-up. This strongly
suggests that the benefit reported for people undergoing arthroscopic surgery for painful degenerative
knees may be entirely attributable to the placebo effect.
This is not the first time that the benefit of surgery has
been attributed to placebo.107,108 Additionally, to
reduce the economic burden on healthcare systems, it
would be very appropriate to recommend an appropriately structured period of relative rest and a
supervised and graduated exercise programme before
surgery is considered as non-surgical care is at least of
equivalent clinical benefit.1618

Clinical diagnosis
A diagnosis of subacromial impingement syndrome is
initially made on the basis of clinical tests. Neer5
introduced the Neer impingement sign and others
have proposed other tests to confirm or exclude
impingement under the acromion.109,110 The clinical
tests are often supported by imaging investigations.
However, the ability for clinical tests and imaging
investigations to enable a clinician to confirm a
diagnosis of subacromial impingement syndrome is

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contentious,69,111113 as imaging investigations have

consistently demonstrated structural pathology in a
high percentage of people without symptoms.
As discussed earlier there is a poor correlation between acromial radiological changes and
symptoms.4143 In a study of 96 people without
shoulder symptoms 28% or those aged between 40
and 60 years and 54% of those aged above 60 years
had MRI evidence of a partial or full thickness rotator
cuff tear.114 Milgrom et al.115 reported in a study of 90
people (age range 30 to 99 without shoulder symptoms) that the incidence of full thickness rotator cuff
tears identified by ultrasound increased with advancing age and that after the 5th decade approximately
50% of people had asymptomatic full thickness tears
that did not affect function. In a study that compared
42 people with impingement syndrome with 31 age
matched symptom free controls, Frost et al.116
reported that 55% of the symptomatic group and
52% of the asymptomatic group had evidence of
rotator cuff pathology on imaging. They also reported
that pathology related to age and did not correlate
with symptoms. Professional baseball pitchers have
been reported to pitch up to 165 km/hour and
demonstrate internal rotation velocities during pitching of 6100 to 6940u/second.117,118 These examples of
extremely high levels of function may be achieved
even in the presence of structural pathology. Miniaci
et al.119 reported that 14 professional baseball pitchers
without shoulder symptoms demonstrated rotator cuff
changes in their throwing (79%) and non-throwing
(86%) shoulders and labral changes (79%) in both
shoulders. Professional baseball pitchers and tennis
players without symptoms demonstrated partial and
full thickness tears (40%), glenohumeral joint effusions
(90%) and excess subacromial fluid (48%) in their
dominant shoulder and remained asymptomatic at a
5 year follow-up.120 In addition, the sourcil (eyebrow)
sign observed radiologically as sclerosis on the under
surface of the acromion and considered to be an
indictor of rotator cuff pathology due to increased
pressure (impingement) was found not to correlate
with clinical signs of impingement, rotator cuff tears,
or age, and did not aid diagnosis in 175 people with
shoulder pain.121 Lewis et al.122 demonstrated that
neovascularity may be present in both the symptomatic and asymptomatic shoulders of people diagnosed with unilateral rotator cuff pathology.
These imaging studies demonstrate that high percentages of people without symptoms will have evidence of
structural failure and at present there is no clinical
certainty that imaging abnormalities are the cause of
the presenting impingement symptoms. Observation of
structural pathology identified in radiographs, ultrasound, MRI and arthroscopy are frequently employed
as the gold standard comparator in studies designed to

394

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test the diagnostic accuracy, sensitivity, specificity,

positive and negative predictive values, and positive
and negative likelihood ratios. However, if the gold
standard is not robust (i.e. people without shoulder
symptoms have structural failure114116,119,122) then a
concomitant high percentage of false positives would
not provide the confidence required by a clinician to
make a diagnosis with any certainty.
This is of major concern as surgery may be
recommended to people diagnosed with impingement
syndrome based on clinical tests and supported by
imaging findings that are currently incapable of
conclusively confirming such a diagnosis.69,111,112
The consequence of this is that for a substantial
percentage of people the surgery may be unnecessary,
inappropriate and unwarranted. This is clearly highlighted by the number of studies that do not show
added benefit of surgery over non-surgical care.1618 In
addition, surgery carries risks, such as infections, and
is substantially more expensive.16,123 Therefore, an
appropriate and defensible argument is that until a
robust method of confirming a diagnosis is obtainable,
and until clear evidence concerning the pathology is
available, surgery should only be offered after an
appropriate period of appropriate non-surgical care.

Tendinopathy
Shalabi et al.50 performed an MRI investigation of the
Achilles tendon (n544 from 22 people, 30 symptomatic and 14 asymptomatic tendons) immediately
before and within 30 minutes of an intense bout of
concentric (bilateral heel raises) and/or eccentric (6 sets
of 15 repetitions) gastrosoleus exercises. They reported
a 12% increase in tendon volume in the eccentrically
loaded symptomatic Achilles tendons and a 17%
increase in the concentrically loaded (mixed symptomatic and asymptomatic) Achilles tendons. There was
a 20% increase in tendon volume in the concentrically
loaded asymptomatic Achilles tendons. Rats subject to
a tendon overload programme have also demonstrated
an increase in rotator cuff cross-sectional area.37
Increased rotator cuff tendon volume as a result of
unaccustomed activity or activity at an intensity that
surpasses the physiological limit of the tendon (which
will be highly variable between and within individuals)
may lead to increased upward pressure on the acromion and coracoacromial ligament. This increased
strain in the ligament is a possible aetiological mechanism for acromial spur formation and as such the
acromial osteophyte may not be the primary problem
but secondary to the increased tendon volume. If the
increased volume and resulting ligamentous strain
occurs at a subclinical level from bursts of activity or
sport a spur may develop over time but may remain
asymptomatic over a lifetime and explain the poor
correlation between acromial shape and symptoms.4143

Published by Maney Publishing (c) W. S. Maney & Son Limited

Lewis

Overuse tendinopathies involving the lateral epicondyle, patellar, adductor and Achilles tendons may
occur without impingement from external structures
such as adjacent bony surfaces, and this may also be the
case for the rotator cuff. It is possible that the external
irritation accentuates the tendon failure 3739,124 but it is
unlikely that it is the primary cause. The failure is
likely to be due to a combination of factors including:
relative overload, genetics, nutritional and life style
variables,32 and the rotator cuff tendon failure may
be seen as a continuum of pathology.33 The initial
symptomatic stage of the continuum of pathology has
been termed a reactive tendon,33,125 which may be
characterized by increased tenocyte numbers.126 Increased expression of the large negatively charged
proteoglycan aggrecan is observed in painful overuse
tendinopathy.127,128 Due to its negative charge aggrecan attracts and retains water, which explains the
swelling observed in acute Achilles tendinopathy.50
The non-steroidal anti-inflammatory drug, ibuprofen,
appears to inhibit the synthesis of aggrecan129 and
may be an appropriate treatment at this stage.
Additionally, glucocorticoids have been shown to
inhibit tenocyte proliferation,130 which may explain
the benefit ascribed to corticosteroid injections for the
shoulder in some people.98 However as stated, the
long term efficacy and potential detrimental effects of
corticosteroid injections for the shoulder require ongoing investigation.
The other pathological stages associated with rotator cuff tendinopathy (disrepair and degeneration)33
may have an associated element of reactivity. When
reactivity is present tendon thickening and swelling
is possible. If this pathoaetiology is accurate and if
the pathology is correctly explained by intrinsic
tendon failure as a consequence of relative overload
then it simply may be the swollen tendon pushing up
and not the acromion pushing down that is the cause
of the problem. If this hypothesis is correct, then an
acromioplasty will not treat the primary problem (i.e.
intrinsic tendon failure) or provide appropriate initial
management for the condition. If relative rest and
appropriate reloading strategies are principal factors in
tendon rehabilitation it is possible that a major benefit
of an acromioplasty is enforced relative rest.104,105 If
this is correct, the associate expense, potential risks and
lack of appropriately targeted treatment question its
utility as a first line treatment option.

Surgery versus non-surgical management

As mentioned, reports of 8090% success following
subacromial decompression for impingement have
been published.100102 When acromioplasty was compared with conservative care (physiotherapy exercises
and pain relief) surgery appeared to be no more
beneficial clinically at 6, 12 or 48 months.1618 As

Subacromial impingement syndrome

elucidated earlier there is no certainty that the benefit

relates directly to the stated aim of the surgery (i.e.
removal of the acromion) and benefit may be derived
from the bursectomy, the period of post-surgical
relative rest, and potentially placebo. Relative rest is
of relevance as Cook and Purdam125 in a generic
model of overuse tendinopathy, have suggested that
tendon load management and reduction in frequency
and/or intensity of tendon load is important during
the reactive phase. Relative rest may also be
important in the reactive stage of rotator cuff
tendinopathy.33 Relative rest may allow the tendon
to attain relative homeostasis, by reducing the up
regulation of tenocytes that may be characteristic of a
reactive tendon and thereby reduce the associated
swelling before a graduated and appropriately constructed rehabilitation programme is instigated. It
may be possibly to enhance the exercise prescription
that has been utilized in clinical trials by more
effectively targeting the stage of the rotator cuff
tendinopathy.33,131 In addition, consideration of the
varying effects exercise may have on subacromial
pressure46 is relevant. To further reduce upward
humeral head translation and tendon compression,
avoidance of internal rotation in the early stages of
rehabilitation may be appropriate. Although uncertainty exists,132 it may be possible to enhance the
effect of exercise by including manual therapy in the
treatment package.133,134 These issues relating to
rehabilitation need to be appropriately scrutinized
through robust research investigations.

Conclusion
Subacromial impingement syndrome is considered by
many to be the most common of the musculoskeletal
conditions affecting the shoulder. It is based on a
hypothesis that acromial irritation leads to external
abrasion of the bursa and rotator cuff. Subacromial
decompressive surgery aims to remove the source of
this irritation. There is however a body of evidence that
suggests there is a lack of concordance regarding (i) the
area of tendon pathology and acromial irritation, (ii)
the shape of the acromion and symptoms, (iii) the
proposal that the irritation leads to the development of
tendinitis and bursitis, and (iv) imaging changes and
symptoms and the development of the condition. In
addition, there is no certainty that any benefit derived
from the surgery is due to the removal of the acromion
as research suggests that a bursectomy in isolation may
confer equivalent benefit. It is also possible that the
benefit of surgery is that it simply enforces a sustained
period of relative rest which may allow the involved
tissues to achieve relative homeostasis. It is possible
that pathology originates in the tendon and as such
surgery does not address the primary problem. This
view is strengthened by the findings of studies that have

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Subacromial impingement syndrome

demonstrated no increased clinical benefit from surgery

when compared with exercise, with exercise therapy
being associated with a substantially reduced economic
burden and less sick leave. Evidence based healthcare
involves the integration of clinical expertise, patient
values and best research evidence. To provide the
research evidence required, surgeons performing acromioplasties need to demonstrate that it is the acromioplasty that is beneficial and not the enforced reduction
in activity or the possibility of placebo. As there is little
evidence for an acromial impingement model a more
appropriate name may be subacromial pain syndrome. Moreover, surgery should only be considered
after an appropriate period of appropriately structured
conservative treatment.

Acknowledgements
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References
1 Brox JI. Regional musculoskeletal conditions: shoulder pain.
Best Pract Res Clin Rheumatol 2003;17:3356.
2 van der Heijden GJ. Shoulder disorders: a state-of-the-art
review. Baillieres Best Pract Res Clin Rheumatol 1999;13:287
309.
3 Taylor W. Musculoskeletal pain in the adult New Zealand
population: prevalence and impact. NZ Med J 2005;118:U1629.
4 Neer CS, 2nd. Anterior acromioplasty for the chronic
impingement syndrome in the shoulder: a preliminary report.
J Bone Joint Surg Am 1972;54:4150.
5 Neer CS, 2nd. Impingement lesions. Clin Orthop Relat Res
1983;173:707.
6 Bigliani LU, Levine WN. Subacromial impingement syndrome. J Bone Joint Surg Am 1997;79:185468.
7 Michener LA, Walsworth MK, Doukas WC, Murphy KP.
Reliability and diagnostic accuracy of 5 physical examination
tests and combination of tests for subacromial impingement.
Arch Phys Med Rehabil 2009;90:1898903.
8 Adam R, Todd, RB. Shoulder joint. In: Todd RB, editor.
Cyclopaedia of anatomy and physiology. Vol. 4. London:
Longman; 1852. p. 571621.
9 Meyer A. The minuter anatomy of attrition lesions. J Bone
Joint Surg Am 1931;13:34160.
10 Codman E. The shoulder: rupture of the supraspinatus tendon
and other lesions in or about the subacromial bursa. Boston:
Thomas Todd Company; 1934. p.1831, , 65107.
11 Bosworth D. Analysis of 28 consecutive cases of incapacitating
shoulder lesions radically explored and repaired. J Bone Joint
Surg Am 1940;22:36992.
12 McLaughlin H, Asherman EG. Lesions of the musculotendinous cuff of the shoulder. IV. Some observations based upon the
results of surgical repair. J Bone Joint Surg Am 1951;33:7686.
13 Diamond B. The obstructing acromion: underlying diseases,
clinical development, and surgery. Springfield: Charles C.
Thomas; 1964. p. 53120.
14 Bigliani LU, Morrison DS, April EW. The morphology of the
acromion and its relationship to rotator cuff tears. Ortho
Trans 1986;10:228.
15 Vitale MA, Arons RR, Hurwitz S, Ahmad CS, Levine WN.
The rising incidence of acromioplasty. J Bone Joint Surg Am
2010;92:184250.
16 Ketola S, Lehtinen J, Arnala I, Nissinen M, Westenius H,
Sintonen H, et al. Does arthroscopic acromioplasty provide
any additional value in the treatment of shoulder impingement

Physical Therapy Reviews

18

23

Aspects of the information contained in this paper

were presented as a key note lecture entitled
Subacromial impingement syndrome. A musculoskeletal condition or a clinical illusion? at the 11th
International Conference of Shoulder and Elbow
Surgeons, Edinburgh, Scotland, UK, 58 September
2010.

396

17

2011

VOL .

16

NO .

28
29
30
31
32
33
34
35
36
37

38

39

40
41

syndrome? a two-year randomised controlled trial. J Bone

Joint Surg Br 2009;91:132634.
Haahr JP, Ostergaard S, Dalsgaard J, Norup K, Frost P,
Lausen S, et al. Exercises versus arthroscopic decompression
in patients with subacromial impingement: a randomised,
controlled study in 90 cases with a one year follow up. Ann
Rheum Dis 2005;64:7604.
Haahr JP, Andersen JH. Exercises may be as efficient as
subacromial decompression in patients with subacromial stage
II impingement: 48-years follow-up in a prospective,
randomized study. Scand J Rheumatol 2006;35:2248.
Payne LZ, Altchek DW, Craig EV, Warren RF. Arthroscopic
treatment of partial rotator cuff tears in young athletes. A
preliminary report. Am J Sports Med 1997;25:299305.
Fukuda H, Mikasa M, Yamanaka K. Incomplete thickness
rotator cuff tears diagnosed by subacromial bursography. Clin
Orthop Relat Res 1987;223:518.
Ozaki J, Fujimoto S, Nakagawa Y, Masuhara K, Tamai S.
Tears of the rotator cuff of the shoulder associated with
pathological changes in the acromion. A study in cadavera.
J Bone Joint Surg Am 1988;70:122430.
Loehr JF, Uhthoff HK. The pathogenesis of degenerative
rotator cuff tears. Orthop Trans 1987;11:237.
Ellman H. Diagnosis and treatment of incomplete rotator cuff
tears. Clin Orthop Relat Res 1990;254:6474.
Hashimoto T, Nobuhara K, Hamada T. Pathologic evidence
of degeneration as a primary cause of rotator cuff tear. Clin
Orthop Relat Res 2003;415:11120.
Nakajima T, Rokuuma N, Hamada K, Tomatsu T, Fukuda H.
Histological and biomechanical characteristics of the supraspinatus tendon. J Shoulder Elbow Surg 1994;3:7987.
Bey MJ, Song HK, Wehrli FW, Soslowsky LJ. Intratendinous
strain fields of the intact supraspinatus tendon: the effect of
glenohumeral joint position and tendon region. J Orthop Res
2002;20:86974.
Walch G, Boileau P, Noel E, Donell ST. Impingement of the
deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder
Elbow Surg 1992;1:23845.
Jobe CM, Sidles JA. Evidence for a superior glenoid
impingement upon the rotator cuff [abstract]. J Shoulder
Elbow Surg 1993;2(Suppl):S19.
Riand N, Levigne C, Renaud E, Walch G. Results of
derotational humeral osteotomy in posterior glenoid impingement. Am J Sports Med 1998;26:4539.
Edelson G, Teitz C. Internal impingement in the shoulder.
J Shoulder Elbow Surg 2000;9:30815.
Nakajima T, Hughes RE, An KN. Effects of glenohumeral
rotations and translations on supraspinatus tendon morphology. Clin Biomech (Bristol, Avon) 2004;19:57985.
Lewis JS. Rotator cuff tendinopathy. Br J Sports Med
2009;43:23641.
Lewis JS. Rotator cuff tendinopathy: a model for the
continuum of pathology and related management. Br J
Sports Med 2010;44:91823.
Lindblom K, Palmer I. Ruptures of the tendon aponeurosis of
the shoulder joint. Acta Chir Scand 1939;82:13342.
Clark JM, Harryman DT, 2nd. Tendons, ligaments, and
capsule of the rotator cuff. Gross and microscopic anatomy.
J Bone Joint Surg Am 1992;74:71325.
Fallon J, Blevins FT, Vogel K, Trotter J. Functional
morphology of the supraspinatus tendon. J Orthop Res 2002;
20:9206.
Soslowsky LJ, Thomopoulos S, Tun S, Flanagan CL, Keefer
CC, Mastaw J, et al. Neer Award 1999. Overuse activity
injures the supraspinatus tendon in an animal model: a
histologic and biomechanical study. J Shoulder Elbow Surg
2000;9:7984.
Perry SM, McIlhenny SE, Hoffman MC, Soslowsky LJ.
Inflammatory and angiogenic mRNA levels are altered in a
supraspinatus tendon overuse animal model. J Shoulder
Elbow Surg 2005;14(Suppl):S7983.
Carpenter JE, Flanagan CL, Thomopoulos S, Yian EH,
Soslowsky LJ. The effects of overuse combined with intrinsic
or extrinsic alterations in an animal model of rotator cuff
tendinosis. Am J Sports Med 1998;26:8017.
Lewis J, Green A, Yizhat Z, Pennington D. Subacromial
impingement syndrome: Has evolution failed us? Physiother
2001;87:1918.
Worland RL, Lee D, Orozco CG, SozaRex F, Keenan J.
Correlation of age, acromial morphology, and rotator cuff

Lewis

42
43

44
45
46

47

Published by Maney Publishing (c) W. S. Maney & Son Limited

48
49
50
51
52
53

54
55

56
57
58

59
60

61
62
63
64

65

tear pathology diagnosed by ultrasound in asymptomatic

patients. J South Orthop Assoc 2003;12:236.
Snow M, Cheong D, Funk L. Subacromial impingement: is
there correlation between symptoms, arthroscopic findings
and outcomes? Shoulder Elbow 2009;1:8992.
Gill TJ, McIrvin E, Kocher MS, Homa K, Mair SD, Hawkins
RJ. The relative importance of acromial morphology and age
with respect to rotator cuff pathology. J Shoulder Elbow Surg
2002;11:32730.
Bigliani LU, Ticker JB, Flatow EL, Soslowsky LJ, Mow VC.
The relationship of acromial architecture to rotator cuff
disease. Clin Sports Med 1991;10:82338.
Edelson JG, Taitz C. Anatomy of the coraco-acromial arch.
Relation to degeneration of the acromion. J Bone Joint Surg
Br 1992;74:58994.
Werner CM, Blumenthal S, Curt A, Gerber C. Subacromial
pressures in vivo and effects of selective experimental
suprascapular nerve block. J Shoulder Elbow Surg 2006;
15:31923.
Chambler AF, Bull AM, Reilly P, Amis AA, Emery RJ.
Coracoacromial ligament tension in vivo. J Shoulder Elbow
Surg 2003;12:3657.
Chambler AF, Pitsillides AA, Emery RJ. Acromial spur
formation in patients with rotator cuff tears. J Shoulder Elbow
Surg 2003;12:31421.
Sarkar K, Taine W, Uhthoff HK. The ultrastructure of the
coracoacromial ligament in patients with chronic impingement
syndrome. Clin Orthop Relat Res 1990 254:4954.
Shalabi A, Kristoffersen-Wiberg M, Aspelin P, Movin T.
Immediate Achilles tendon response after strength training
evaluated by MRI. Med Sci Sports Exerc 2004;36:18416.
Sharkey NA, Marder RA. The rotator cuff opposes superior
translation of the humeral head. Am J Sports Med
1995;23:2705.
Lazarus MD, Yung SW, Sidles JA, Harryman DT.
Anterosuperior humeral head displacement: limitation by the
coracoacromial arch. J Shoulder Elbow Surg 1996;5:S7.
Thompson WO, Debski RE, Boardman ND, 3rd, Taskiran E,
Warner JJ, Fu FH, et al. A biomechanical analysis of rotator
cuff deficiency in a cadaveric model. Am J Sports Med
1996;24:28692.
Tamai M, Okajima S, Fushiki S, Hirasawa Y. Quantitative
analysis of neural distribution in human coracoacromial
ligaments. Clin Orthop Relat Res 2000;373:12534.
Flatow EL, Wang VM, Kelkar R. The coracoacromial
ligament passively restrains anterosuperior humeral subluxation in the rotator cuff deficient shoulder. Orthop Trans
1996;21:229.
Fagelman M, Sartori M, Freedman KB, Patwardhan AG,
Carandang G, Marra G. Biomechanics of coracoacromial
arch modification. J Shoulder Elbow Surg 2007;16:1016.
Chen J, Luo CF, Luo ZP. Initiatory biomechanical study on
humeral head migration after coracoacromial ligament cut.
Arch Orthop Trauma Surg 2009;129:1337.
Harryman DT, 2nd, Lazarus MD, Yung SW, Sidles JA,
Matsen FA. Anterosuperior humeral displacement: limitation
by the coracoacromial arch. J Shoulder Elbow Surg
1996;5:S29.
Su WR, Budoff JE, Luo ZP. The effect of coracoacromial
ligament excision and acromioplasty on superior and anterosuperior glenohumeral stability. Arthroscopy 2009;25:138.
Samuelsson K, Andersson D, Karlsson J. Treatment of
anterior cruciate ligament injuries with special reference to
graft type and surgical technique: an assessment of randomized controlled trials. Arthroscopy 2009;25:113974.
Hockman DE, Lucas GL, Roth CA. Role of the coracoacromial ligament as restraint after shoulder hemiarthroplasty.
Clin Orthop Relat Res 2004;419:802.
Ayub E. Posture and the upper quarter. In: Donatelli R,
editor. Physical therapy of the shoulder. 2nd ed. Melbourne:
Churchill Livingstone; 1991. p. 8190.
Grimsby O, Gray J. Interrelation of the spine to the shoulder
girdle. In: Donatelli R, editor.Physical therapy of the shoulder.
3rd ed. New York: Churchill Livingstone; 1997. p. 95129.
Gray J, Grimsby O. Interrelationship of the spine, rib cage,
and shoulder. In: Donatelli R, editor. Physical therapy of the
shoulder. 4th ed. Edinburgh: Churchill Livingston; 2004.
p. 13385.
Ludewig PM, Cook TM. Alterations in shoulder kinematics
and associated muscle activity in people with symptoms of
shoulder impingement. Phys Ther 2000;80:27691.

Subacromial impingement syndrome

66 Kebaetse M, McClure P, Pratt NA. Thoracic position effect

on shoulder range of motion, strength, and three-dimensional
scapular kinematics. Arch Phys Med Rehabil 1999;80:94550.
67 Sahrmann S. Diagnosis and treatment of movement impairment syndromes. London: Mosby; 2002. p. 193261.
68 Bullock MP, Foster NE, Wright CC. Shoulder impingement:
the effect of sitting posture on shoulder pain and range of
motion. Man Ther 2005;10:2837.
69 Lewis JS. Rotator cuff tendinopathy/subacromial impingement syndrome: is it time for a new method of assessment? Br
J Sports Med 2009;43:25964.
70 Lewis JS, Green A, Wright C. Subacromial impingement
syndrome: the role of posture and muscle imbalance.
J Shoulder Elbow Surg 2005;14:38592.
71 Lewis JS, Valentine RE. The pectoralis minor length test: a
study of the intra-rater reliability and diagnostic accuracy in
subjects with and without shoulder symptoms. BMC
Musculoskelet Disord 2007;8:64.
72 Grimmer K. An investigation of poor cervical resting posture.
Aust J Physiother 1997;43:716.
73 McClure PW, Bialker J, Neff N, Williams G, Karduna A.
Shoulder function and 3-dimensional kinematics in people
with shoulder impingement syndrome before and after a 6week exercise program. Phys Ther 2004;84:83248.
74 Griegel-Morris P, Larson K, Mueller-Klaus K, Oatis CA.
Incidence of common postural abnormalities in the cervical,
shoulder, and thoracic regions and their association with pain in
two age groups of healthy subjects. Phys Ther 1992;72:42531.
75 Lederman E. The fall of the postural-structural-biomechanical
model in manual and physical therapies: Exemplified by lower
back pain. J Bodyw Mov Ther 2011;15:1318.
76 Raine S, Twomey LT. Head and shoulder posture variations
in 160 asymptomatic women and men. Arch Phys Med
Rehabil 1997;78:121523.
77 Singer KP, Goh S. Anatomy of the thoracic spine. In: Giles
LGF, Singer KP, editors. The clinical anatomy and management of thoracic spine pain. Vol 2. Oxford: Butterworth
Heinemann; 2000. p. 1733.
78 Lewis JS, Valentine RE. Clinical measurement of the thoracic
kyphosis. A study of the intra-rater reliability in subjects with
and without shoulder pain. BMC Musculoskelet Disord
2010;11:39.
79 Fukuda H, Hamada K, Yamanaka K. Pathology and
pathogenesis of bursal-side rotator cuff tears viewed from en
bloc histologic sections. Clin Orthop Relat Res 1990;254:7580.
80 Sarkar K, Uhthoff HK. Ultrastructure of the subacromial
bursa in painful shoulder syndromes. Virchows Arch A Pathol
Anat Histopathol 1983;400:10717.
81 Santavirta S, Konttinen YT, Antti-Poika I, Nordstrom D.
Inflammation of the subacromial bursa in chronic shoulder
pain. Arch Orthop Trauma Surg 1992;111:33640.
82 Standring S. Grays Anatomy. 39th ed. Edinburgh: Elsevier
Churchill Livingstone; 2005. p. 81749.
83 Aszmann OC, Dellon AL, Birely BT, McFarland EG.
Innervation of the human shoulder joint and its implications
for surgery. Clin Orthop Relat Res 1996;330:2027.
84 Ide K, Shirai Y, Ito H, Ito H. Sensory nerve supply in the
human subacromial bursa. J Shoulder Elbow Surg 1996;5:371
82.
85 Gotoh M, Hamada K, Yamakawa H, Yanagisawa K,
Nakamura M, Yamazaki H, et al. Interleukin-1-induced
subacromial synovitis and shoulder pain in rotator cuff
diseases. Rheumatology (Oxford) 2001;40:9951001.
86 Gotoh M, Hamada K, Yamakawa H, Inoue A, Fukuda H.
Increased substance P in subacromial bursa and shoulder pain
in rotator cuff diseases. J Orthop Res 1998;16:61821.
87 Gotoh M, Hamada K, Yamakawa H, Yanagisawa K,
Nakamura M, Yamazaki H, et al. Interleukin-1-induced
glenohumeral synovitis and shoulder pain in rotator cuff
diseases. J Orthop Res 2002;20:136571.
88 Sakai H, Fujita K, Sakai Y, Mizuno K. Immunolocalization
of cytokines and growth factors in subacromial bursa of
rotator cuff tear patients. Kobe J Med Sci 2001;47:2534.
89 Yanagisawa K, Hamada K, Gotoh M, TokunagaT, Oshika Y,
Tomisawa M, et al. Vascular endothelial growth factor
(VEGF) expression in the subacromial bursa is increased in
patients with impingement syndrome. J Orthop Res 2001;
19:44855.
90 Hyvonen P, Melkko J, Lehto VP, Jalovaara P. Involvement of
the subacromial bursa in impingement syndrome of the

Physical Therapy Reviews

2011

VOL .

16

NO .

397

Lewis

Subacromial impingement syndrome

91

92

93

94

95

Published by Maney Publishing (c) W. S. Maney & Son Limited

96

97
98
99

100
101

102
103

104
105

106

107
108
109
110

111

112

398

shoulder as judged by expression of tenascin-C and histopathology. J Bone Joint Surg Br 2003;85:299305.
Voloshin I, Gelinas J, Maloney MD, OKeefe RJ, Bigliani LU,
Blaine TA. Proinflammatory cytokines and metalloproteases
are expressed in the subacromial bursa in patients with rotator
cuff disease. Arthroscopy 2005;21:1076.
Henkus HE, de Witte PB, Nelissen RG, Brand R, van Arkel
ER. Bursectomy compared with acromioplasty in the management of subacromial impingement syndrome: a prospective
randomised study. J Bone Joint Surg Br 2009;91:50410.
Henkus HE, Cobben LP, Coerkamp EG, Nelissen RG, van
Arkel ER. The accuracy of subacromial injections: a prospective randomized magnetic resonance imaging study. Arthroscopy 2006;22:27782.
Naredo E, Cabero F, Beneyto P, Cruz A, Mondejar B, Uson J,
et al. A randomized comparative study of short term response
to blind injection versus sonographic-guided injection of local
corticosteroids in patients with painful shoulder. J Rheumatol
2004;31:30814.
Chen MJ, Lew HL, Hsu TC, Tsai WC, Lin WC, Tang SF,
et al. Ultrasound-guided shoulder injections in the treatment of
subacromial bursitis. Am J Phys Med Rehabil 2006;85:315.
Alvarez CM, Litchfield R, Jackowski D, Griffin S, Kirkley A.
A prospective, double-blind, randomized clinical trial comparing subacromial injection of betamethasone and xylocaine to
xylocaine alone in chronic rotator cuff tendinosis. Am J Sports
Med 2005;33:25562.
Akgun K, Birtane M, Akarirmak U. Is local subacromial
corticosteroid injection beneficial in subacromial impingement
syndrome? Clin Rheumatol 2004;23:496500.
Plafki C, Steffen R, Willburger RE, Wittenberg RH. Local
anaesthetic injection with and without corticosteroids for
subacromial impingement syndrome. Int Orthop 2000;24:402.
Ekeberg OM, Bautz-Holter E, Tveita EK, Juel NG, Kvalheim S,
Brox JI. Subacromial ultrasound guided or systemic steroid
injection for rotator cuff disease: randomised double blind
study. BMJ 2009;338:2736.
Burns TP, Turba JE. Arthroscopic treatment of shoulder
impingement in athletes. Am J Sports Med 1992;20:136.
Checroun AJ, Dennis MG, Zuckerman JD. Open versus
arthroscopic decompression for subacromial impingement. A
comprehensive review of the literature from the last 25 years.
Bull Hosp Jt Dis 1998;57:14551.
Ellman H, Kay SP. Arthroscopic subacromial decompression
for chronic impingement. Two- to five-year results. J Bone
Joint Surg Br 1991;73:3958.
Chin PY, Sperling JW, Cofield RH, Stuart MJ, Crownhart
BS. Anterior acromioplasty for the shoulder impingement
syndrome: long-term outcome. J Shoulder Elbow Surg
2007;16:697700.
McClelland D, Paxinos A, Dodenhoff RM. Rate of return to
work and driving following arthroscopic subacromial decompression. ANZ J Surg 2005;75:7479.
Charalambous CP, Sahu A, Alvi F, Batra S, Gullett TK,
Ravenscroft M. Return to work and driving following
arthroscopic subacromial decompression and acromio-clavicular joint excision. Shoulder Elbow 2010;2:836.
Moseley JB, OMalley K, Petersen NJ, Menke TJ, Brody BA,
Kuykendall DH, et al. A controlled trial of arthroscopic
surgery for osteoarthritis of the knee. N Engl J Med
2002;347:818.
Dimond EG, Kittle CF, Crockett JE. Comparison of internal
mammary artery ligation and sham operation for angina
pectoris. Am J Cardiol 1960;5:4836.
Cobb LA, Thomas GI, Dillard DH, Merendino KA, Bruce
RA. An evaluation of internal-mammary-artery ligation by a
double-blind technic. N Engl J Med 1959;260:11158.
Hawkins RJ, Kennedy JC. Impingement syndrome in athletes.
Am J Sports Med 1980;8:1518.
Zaslav KR. Internal rotation resistance strength test: a new
diagnostic test to differentiate intra-articular pathology from
outlet (Neer) impingement syndrome in the shoulder.
J Shoulder Elbow Surg 2001;10:237.
Lewis JS, Tennent TD. How effective are diagnostic tests for the
assessment of rotator cuff disease of the shoulder? In: MacAuley
D, Best TM, editors. Evidenced based sports medicine. 2nd ed.
London: Blackwell Publishing; 2007. p. 32759.
Hegedus EJ, Goode A, Campbell S, Morin A, Tamaddoni M,
Moorman CT, 3rd, et al. Physical examination tests of the

Physical Therapy Reviews

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128
129

130
131

132

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134

shoulder: a systematic review with meta-analysis of individual

tests. Br J Sports Med 2008;42:8092.
Schellingerhout JM, Verhagen AP, Thomas S, Koes BW. Lack
of uniformity in diagnostic labeling of shoulder pain: time for
a different approach. Man Ther 2008;13:47883.
Sher JS, Uribe JW, Posada A, Murphy BJ, Zlatkin MB.
Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg Am 1995;77:105.
Milgrom C, Schaffler M, Gilbert S, van Holsbeeck M. Rotatorcuff changes in asymptomatic adults. The effect of age, hand
dominance and gender. J Bone Joint Surg Br 1995;77:2968.
Frost P, Andersen JH, Lundorf E. Is supraspinatus pathology
as defined by magnetic resonance imaging associated with
clinical sign of shoulder impingement? J Shoulder Elbow Surg
1999;8:5658.
Dillman CJ, Fleisig GS, Andrews JR. Biomechanics of
pitching with emphasis upon shoulder kinematics. J Orthop
Sports Phys Ther 1993;18:4028.
Feltner M. Three-dimensional interactions in a two-segment
kinetic chain. Part II: application to the throwing arm in
baseball pitching. Int J Sports Biomech 1989;5:42050.
Miniaci A, Mascia AT, Salonen DC, Becker EJ. Magnetic
resonance imaging of the shoulder in asymptomatic professional baseball pitchers. Am J Sports Med 2002;30:6673.
Connor PM, Banks DM, Tyson AB, Coumas JS,
DAlessandro DF. Magnetic resonance imaging of the
asymptomatic shoulder of overhead athletes: a 5-year followup study. Am J Sports Med 2003;31:7247.
Smith C, Deans V, Drew S. The sourcil sign: a useful finding
on plain x-ray? Shoulder Elbow 2010;2:912.
Lewis JS, Raza SA, Pilcher J, Heron C, Poloniecki JD. The
prevalence of neovascularity in patients clinically diagnosed
with rotator cuff tendinopathy. BMC Musculoskelet Disord
2009;10:163.
Brox JI, Staff PH, Ljunggren AE, Brevik JI. Arthroscopic
surgery compared with supervised exercises in patients with
rotator cuff disease (stage II impingement syndrome). BMJ
1993;9:899903.
Soslowsky LJ, Thomopoulos S, Esmail A, Flanagan CL,
Iannotti JP, Williamson JD, 3rd, et al. Rotator cuff tendinosis
in an animal model: role of extrinsic and overuse factors. Ann
Biomed Eng 2002;30:105763.
Cook JL, Purdam CR. Is tendon pathology a continuum? A
pathology model to explain the clinical presentation of loadinduced tendinopathy. Br J Sports Med 2009;43:40916.
Scott A, Cook JL, Hart DA, Walker DC, Duronio V, Khan
KM. Tenocyte responses to mechanical loading in vivo: a role
for local insulin-like growth factor 1 signaling in early
tendinosis in rats. Arthritis Rheum 2007;56:87181.
Corps AN, Robinson AH, Movin T, Costa ML, Hazleman
BL, Riley GP. Increased expression of aggrecan and biglycan
mRNA in Achilles tendinopathy. Rheumatology (Oxford)
2006;45:2914.
Riley G. Tendinopathyfrom basic science to treatment. Nat
Clin Pract Rheumatol 2008;4:829.
Tsai WC, Tang FT, Hsu CC, Hsu YH, Pang JH, Shiue CC.
Ibuprofen inhibition of tendon cell proliferation and upregulation of the cyclin kinase inhibitor p21CIP1. J Orthop Res
2004;22:58691.
Scutt N, Rolf CG, Scutt A. Glucocorticoids inhibit tenocyte
proliferation and Tendon progenitor cell recruitment.
J Orthop Res 2006;24:17382.
Ainsworth R, Lewis JS, Conboy V. A prospective randomized
placebo controlled clinical trial of a rehabilitation programme
for patients with a diagnosis of massive rotator cuff tears of
the shoulder. Shoulder Elbow 2009;1:5560.
Yiasemides R, Halaki M, Cathers I, Ginn KA. Does passive
mobilization of shoulder region joints provide additional
benefit over advice and exercise alone for people who have
shoulder pain and minimal movement restriction? A randomized controlled trial. Phys Ther 2011;91:17889.
Bang MD, Deyle GD. Comparison of supervised exercise with
and without manual physical therapy for patients with
shoulder impingement syndrome. J Orthop Sports Phys Ther
2000;30:12637.
McClatchie L, Laprade J, Martin S, Jaglal SB, Richardson D,
Agur A. Mobilizations of the asymptomatic cervical spine can
reduce signs of shoulder dysfunction in adults. Man Ther
2009;14:36974.