Differential Diagnosis of Buttock Pain
Differential Diagnosis of Buttock Pain
Differential Diagnosis of Buttock Pain
DIAGNOSIS
OF BUTTOCK
PAIN
d r a l©i Dr
s oAlison
n g rGrimaldi
i m a l d2021
i.com
DIFFERENTIAL DIAGNOSIS
OF BUTTOCK PAIN
dralisongrimaldi.com
We all need some sort of framework that contains a virtual directory of the
potential sources of local nociception and more remote sources of pain
referral, and a road map for how we might recognise these conditions.
Often the best approach is to simply think of what structures are in the
area or are likely to refer into the area, then look for the mechanisms.
Clarity around diagnostic terms can come later.
0
Radicular Discs & Joints Soft Local Bone
& Stenotic Facet joints Tissues Nerves
SIJ Hip
0
Ligaments Muscles Tendons Bursae Fascia
Ha
First step is what structure/s and then, why – biopsychosocial drivers. The patient is a goldmine of information for directing
your physical examination and ultimately informing your differential diagnosis. The following information can all be gathered
from the patient interview, so listen carefully for the patterns that might assist in differentiating local and remote sources of
nociception associated with buttock pain.
The lumbar spine is a frequent source of buttock pain and should always be in the
LUMBAR starting mix of diagnostic possibilities in your differential diagnosis of buttock pain.
Buttock pain of lumbar origin is most commonly either related to neuro-compressive
RELATED processes, such as radicular pain or stenosis or somatic referred pain from the lumbar
intervertebral discs or facet (zygapophyseal) joints.
Bilateral symptoms may be due to central stenosis or mirror-pain in radicular presentations associated with immune-
inflammatory response in the contralateral dorsal root ganglion and dorsal horn
Facet related pain may extend down the posterior thigh but is generally more focal than neuropathic pain
Disc and facet pain do not generally refer below the knee
The 2 major joints within the pelvis that may give rise to buttock pain associated with local
JOINT nociception, are the sacroiliac joints and the hip joints. Unfortunately, sacroiliac joint
dysfunction still appears to be grossly overdiagnosed and beliefs that are transferred to
RELATED patients about instability and pelvic malposition are generally unhelpful. However, it is also
important not to ignore the sacroiliac joint and especially its associated ligaments as
sources of nociception.
Associated Symptoms:
Feeling of instability in single leg standing
Feeling of heaviness of the leg when lifting the leg, particularly the whole leg in supine
May report difficulty with initial weightbearing through affected side when rising to stand
Aggravating Factors:
Pain and difficulty with load transfer through SIJ – moving from sit – stand, stance phase of gait, lifting into hip
flexion, rolling in bed
Wide leg, split lunge or single leg function
Pain with sustained sitting
Supine leg loading tasks e.g. abdominal leg loading exercise may be provocative
Easing Factors:
Sometimes eased by sacroiliac belt, but this may also increase local pain
History of Onset
During pregnancy or post-partum, particularly with a history of a traumatic natural delivery
History of pelvic trauma – fall onto the ischium or a heavy impact through one leg, traction force through one leg
(e.g. fall from horse and dragged via stirrup), slip into splits (forward or lateral)
Patient Characteristics
More common in females, particularly where trauma has not been involved
Those with connective tissue disorders such as hypermobile Ehlers Danlos Syndrome, may present with difficulties
on load transfer across the pelvis, particularly in perinatal females
HIP JOINT hip joint condition in your differential diagnosis of buttock pain. Hip osteoarthritis (OA) is
more readily recognised in the older patient with an antalgic limp, associated groin pain
RELATED and difficulty reaching their foot due to gradually progressive range restriction. However,
younger patients or those with earlier disease may present with more subtle symptoms
of intra-articular joint pathology.
While anterior bony impingement is now well recognised, posterior femoroacetabular impingement (FAI) and associated
chondrolabral pathology are often overlooked. In addition, posterior laxity or instability of the hip joint remains
underrecognised, particularly in those with ‘hip stiffness’ associated with anterior FAI. Anterior impingement at end range
flexion and internal rotation results in a levering of the femoral head from the posterior aspect of the acetabulum. Focal
instability and overload may also be related to bony undercoverage posteriorly associated with acetabular retroversion.
More global hypermobility is usually due to some form of collagen disorder (Hypermobile Spectrum Disorder or
hypermobile Ehlers Danlos Syndrome).
Associated Symptoms:
Hip stiffness is a key sign of hip OA - difficulty reaching the foot of the painful side when
dressing/difficulty manipulating shoes and socks
Painful limp
Posterior instability - giving way, lack of stability or confidence when weightbearing in flexion
+/- internal rotation
Aggravating Factors:
Deep flexion-squatting and sitting - mediated by depth of chair/amount of hip flexion – worse in low seats *car
Start-up pain and stiffness in hip OA– pain that occurs immediately on rising to stand and walk, but eases with
continued walking (compared with lumbar stenotic pain that is less likely to occur on immediate standing/walking
but tends to increase with time in standing/walking1)
Pain on weightbearing tasks - buttock pain usually on impact/loading phase, associated with anterior pain that occurs
in hip extension, at end stance phase
Pain on weightbearing rotation - getting in/out of the car (stance leg), change of direction
Pain lifting the leg in/out of car
Posterior FAI symptoms may be aggravated by hip extension +/- external rotation.
Easing Factors:
Eased by changing hip loads – reducing hip flexion – sitting on higher seats, on edge of chair with knee hanging
down, reducing impact activity and reducing hip extension e.g. reducing stride length in walking
History of Onset
May be associated with a single acute trauma involving impact through the foot or knee, hyperflexion or
rapid/forceful rotation
More often gradual onset or associated with an increase in volume or intensity of activity
Patient Characteristics
Older age groups - suspect hip OA especially if accompanied by gradually increasing stiffness
Risk of hip OA increased with family history of OA, previous trauma, childhood hip disorders (Perthes, Slipped Capital
Femoral Epiphysis, Dysplasia) and known Cam morphology (FAIS)
Posterior instability - increased risk in those with known acetabular dysplasia, collagen disorders (hypermobility), or
anterior bony impingement.
RELATED innervated, particularly in more superficial fascial sheets and should be considered as a
possible source of nociception.
Associated Symptoms:
May be accompanying stiffness or weakness
Aggravating Factors:
Pain aggravated by activity/ loading of the specific tissue
usually on initial loading after rest and
on loading of the tissue beyond its level of load tolerance (dependent on local and
central factors)
Pain at rest usually only if
acute/inflammatory condition or
positional - relating to direct loading of tissues e.g. ischial pain in sitting with proximal hamstring tendinopathy
Easing Factors:
Common to experience pain on initial activity that eases during warm-up and then may return if load tolerance level is
reached during activity, or after cool-down.
Rest generally eases pain, unless the condition is acute/inflammatory condition or the patient adopts a position of
provocative load for the particular tissue
History of Onset
History usually reflects some form of overload
Acute high-load trauma – history of injury or accident
Fatigue overload – Abnormal stresses on normal tissues – increase in training volume or intensity
Insufficiency overload – Normal stresses on insufficient tissues – the overload may not be initially apparent, but in
deconditioned individuals and/or those with significant structural pathology, relatively low loads may result in overload
and nociception
Patient Characteristics
Muscular injury/overload is more common in active individuals
O
Tendon conditions present in both active individuals (e.g proximal hamstring tendinopathy in runners) and older,
deconditioned and/or sedentary individuals
Tendon conditions are common in post-menopausal females
GMed
GMax
Gluteal
Fascia
AM
ST
SM BFLH
Deep
Quadratus Lumborum
Gluteus Medius
Piriformis
Gluteus Minimus
Superior Gemellus
Gluteus Medius &
Minimus Tendons Obturator Internus
Inferior Gemellus
Subgluteus Quadratus Femoris
Maximus & Obturator
Medius Bursae Internus
Proximal hamstring
tendons
Ischiogluteal Bursa Obturator Internus
Bursa (deep to OI)
Local nerves running through the buttock can also be responsible for both local and/or
NERVE remote symptoms. The sciatic nerve is the largest and most recognised source of local
nerve related buttock pain. Entrapment or irritation of the sciatic nerve as it passes
RELATED
through the buttock has been given many names, among them the more well
recognised piriformis syndrome and deep gluteal syndrome
Nature of Pain:
Often described as burning and/or sharp or shooting pain
Also, may experience a deep ache, particularly with nerves within the deep gluteal space
Associated Symptoms:
Dysaesthesia/paraesthesia – tingling, change in sensation, itching/crawling sensations
Altered temperature sensitivity (deficit in cold and/or warm)
Cramping in buttock/posterior thigh and/or sometimes calf
Gluteal weakness – may be pre-existing, pain inhibited or possible gluteal nerve injury
Weakness of external rotators – may be pre-existing, pain inhibited or possible nerve injury
Easing Factors:
Getting up and moving – from sitting and at night
Aggravating Factors:
Sitting – tolerance is often limited to 30 minutes or less
Slump type postures or activities where nerves are on stretch or moving between structures in the buttock
Cluneal nerve pain may be exacerbated by direct pressure (tight belt/pants) or stretch of the thoracodorsal/gluteal
fascia through which the nerves transit to the skin
Night time pain (and/or cramping)
Gluteal and particularly deep rotator exercise (deep gluteal space entrapments)
History of Onset
O May have history of trauma e.g. impact +/- haematoma to buttock, pelvic fracture
Previous surgery or intramuscular injection into the buttock
History of muscular overload of deep rotators – physical labour, gym/sport, trail running on uneven surfaces
Patient Characteristics
Variable
Presentation may be influenced by other general health issues and psychological stressors
Higher rates of neuralgia in those with connective tissue disorders.
SCN's
MCN's
PFCN
ICN's
Deep
SGN
nOI SN
PN
IGN nQF
PR
PFCN
Now that you have a good idea of what structures may be involved in your patient’s buttock pain, you can apply physical
tests to confirm or refute your hypothesis and assess impairments to be addressed within the rehabilitative process.
It is also important to note that systemic causes, non-nociceptive or nociplastic pain states and psychosocial contributors
to any pain presentation should always be considered. There are also other processes that cause nociception within
musculoskeletal structures, such as malignancy or infection, so questioning around general health is mandatory.
While the lumbar spine, SIJ, hip joint, soft tissues and nerves are the most common
OTHER sources of nociception associated with buttock pain, it is important to be aware of those
less common causes. Missing these may have substantial consequences for our
SOURCES patients, so we all need to ensure we listen and assess carefully.
Malignancy, Infection, Nociplastic Pain States and Systemic Causes of Buttock Pain
Systemic causes, nociplastic pain states and psychosocial contributors to any pain presentation should always be
considered. There are also other processes that cause nociception within musculoskeletal structures, such as malignancy
or infection, so questioning around general health is mandatory.
We have focused on nociceptive and neuropathic mechanisms for buttock pain, but I did want to highlight the need for
early identification of spondyloarthropathies such as axial spondyloarthopathy and ankylosing spondylitis (AS). There is
often substantial delay between onset of symptoms, diagnosis and management of AS, particularly in those who are
HLAB27 -ve8. Awareness and screening is key to early diagnosis. Pain onset is usually in the 20's or 30's and patients
report back and buttock pain with morning stiffness that lasts more than 30minutes, isn’t eased with rest but improves
with activity and anti-inflammatory medication. While this diagnosis might come to mind more readily when assessing a
male patient with these symptoms, sometimes it is overlooked in females due to other more common sources of pelvic
pain. Make sure you consider this differential diagnosis in any such presentation, regardless of sex.
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