M u s c u l o s k e l e t a l I m a g i n g R ev i ew

Yanny and Toms

MRI of the Shoulder

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Musculoskeletal Imaging
Review

MR Patterns of Denervation
Around the Shoulder
Sarah Yanny 1,2
Andoni P. Toms 2
Yanny S, Toms AP

OBJECTIVE. The diagnosis of denervation injury as a cause of shoulder pain is conventionally based on clinical findings and electrophysiologic studies. MRI has an important role
in identifying direct and indirect signs of neuropathy and can confirm the presence of nerve
compression, depict space-occupying lesions, and exclude other intrinsic lesions of the shoulder. In this article, the relevant anatomy, causes, clinical features, and MR appearances of
nerve injury and muscle denervation of the shoulder girdle are presented.
CONCLUSION. MRI is commonly performed in patients with shoulder pain of uncertain origin and can determine the morphologic cause, precise location, and duration of nerve
injury and muscle denervation. Knowledge of the relevant anatomy, cause, and clinical and
imaging findings is important in making a potentially treatable diagnosis, avoiding confusion
with inflammatory or neoplastic processes, and obviating biopsy or surgical intervention.

Keywords: denervation, MRI, muscle atrophy, shoulder,

shoulder injuries, sports medicine
DOI:10.2214/AJR.09.4127
Received December 16, 2009; accepted after revision
January 25, 2010.
1

Present address: Nuffield Orthopaedic Centre, Windmill

Rd., Headington, Oxford, Oxfordshire, OX3, United
Kingdom. Address correspondence to S. Yanny
(sarah.yanny@noc.nhs.uk).

2
Department of Radiology, Norfolk and Norwich
University Hospital, Norwich, Norfolk, United Kingdom.

CME
This article is available for CME credit.
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AJR 2010; 195:W157W163
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American Roentgen Ray Society

AJR:195, August 2010

erve injuries of the shoulder are

an unusual cause of shoulder
pain. They can result from a variety of causes including trauma,
infection, neoplasia, neuropathy, autoimmune
disease, and iatrogenic conditions [1]. Traditionally, the diagnosis of muscle denervation
was based on clinical findings, electromyography, and nerve conduction studies. However, electrophysiologic studies do not determine the cause of muscle denervation. MRI
has an important role because it can identify
the exact site of injury depending on the muscle groups involved, provides information
about the duration of denervation, and often
directly depicts the cause. This article discusses the cause and MR characteristics of the
more common causes of muscle denervation
around the shoulder girdle including compressive lesions of the suprascapular nerve,
quadrilateral space syndrome, and acute brachial neuritis.
Isolated Peripheral Nerve
Compression
Suprascapular Nerve Entrapment
Suprascapular nerve anatomyThe suprascapular nerve is a mixed motor and sensory peripheral nerve that arises from the upper trunk of the brachial plexus. It originates
from the roots of C5 and C6, with a variable
contribution from C4, at Erb point. The nerve

passes deep to omohyoid and trapezius before

entering the supraspinatus fossa through the
suprascapular notch. On entering the fossa, the
nerve supplies the supraspinatus and receives
sensory branches from the glenohumeral and
acromioclavicular joints, rotator cuff, and posterior two thirds of the capsule [2]. The superior transverse scapular ligament forms the
roof of the notch over which the accompanying suprascapular vessels pass. The nerve then
courses around the scapular spine and passes
through the spinoglenoid notch to enter the infraspinatus fossa, where it is a pure motor nerve
to the infraspinatus. The presence of an inferior
transverse scapular ligament (spinoglenoid ligament) spanning the roof of the spinoglenoid
notch is variable [3, 4] (Fig. 1).
Cause and clinical featuresAlthough well
described in the literature, suprascapular nerve
compression is a relatively uncommon condition and is infrequently diagnosed [2, 59]. It
usually presents with nonspecific shoulder pain
and weakness. It is part of the differential diagnosis of chronic shoulder pain, which includes
cervical radiculopathy, rotator cuff and labral
tears, calcific tendinitis, glenohumeral and acromioclavicular joint arthritis, instability, bursitis, and adhesive capsulitis [5].
The anatomy of the suprascapular nerve
renders it particularly susceptible to compression even by small space-occupying lesions. This vulnerability reflects its relatively

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Yanny and Toms

Fig. 1Suprascapular nerve anatomy.

A, Drawing shows posterior perspective of suprascapular nerve. Acromion is represented as transparent to allow visualization of suprascapular notch. Nerve enters
suprascapular notch (arrowhead) and passes under superior transverse scapular ligament, giving branches to supraspinatus (ss) and infraspinatus. Inferior to
suprascapular notch is spinoglenoid notch (arrow), which contains only nerve to infraspinatus (is). Curved arrows = supracapsular nerve branches.
B and C, Coronal oblique (B) and axial (C) T1-weighted images in healthy 30-year-old man show normal appearances of suprascapular nerve (arrows) in suprascapular
and spinoglenoid notches, respectively.

fixed position beneath the superior transverse scapular and spinoglenoid ligaments
and its close proximity to the glenohumeral
joint. The suprascapular notch and spinoglenoid notch and their respective spanning ligaments form narrow fibroosseous tunnels
that predispose the suprascapular nerve to
entrapment neuropathy.
Entrapment of the suprascapular nerve in
the suprascapular notch was first described
by Kopell and Thompson in 1959 [10]. In
1982, suprascapular nerve entrapment at
the spinoglenoid notch by a hypertrophied
spinoglenoid ligament was described by
Aiello et al. [3]. Since then, several causes of
entrapment neuropathy have been identified
including trauma, such as scapular and humeral fractures [11, 12] and anterior shoulder
dislocation [13]; anomalous, thickened, or
calcific superior or inferior transverse scapular ligaments [3, 14]; and iatrogenic injury.
Repetitive overhead activities and forceful rotational movements performed during sports
such as baseball, volleyball, and weight lifting may produce traction or stretching at the
potential sites of fixation [6, 1517].
Extrinsic compression may also be due to
space-occupying lesionsmost commonly,
cystsas well as hematomas, varices (Fig. 2),
lipomas, and malignant neoplasms including
Ewings sarcoma, metastatic renal cell carcinoma, and chondrosarcoma [5]. Paralabral cysts
around the glenohumeral joint are recognized
with increasing frequency. Ticker et al. [9]
found an incidence of 1% in a series of 79 cadaveric shoulders. Most paralabral cysts are associated with labral tears [18]. They are most

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commonly posterior and superior because of

the relative weakness of the posterosuperior
joint capsule, which permits extrusion of synovial fluid into the fibrofatty tissue of the suprascapular and spinoglenoid notches [19, 20].
Most paralabral cysts compress the suprascapular nerve only at the spinoglenoid notch [2],
where the nerve passes within 21 mm of the
glenoid rim [21] (Fig. 3).
Imaging findings and treatmentDiagnosis of suprascapular nerve compression is
based on clinical examination, radiography of
the shoulder and cervical spine, MRI with or
without arthrography, and electrophysiologic
studies. Electromyography may show indirect evidence of suprascapular nerve injury or
dysfunction but will not define the exact morphology or site of entrapment [22]. Conversely, MRI is noninvasive, can precisely locate
extrinsic compressive lesions, and can exclude
more common causes of shoulder pain.
The MRI features of compressive neuropathy include direct signs involving the nerve
and indirect signs related to muscle denervation. The direct signs of peripheral nerve
entrapment include abnormalities in the signal intensity, size, and position of the affected nerve [6]. The morphologic cause may be
shown including space-occupying lesions,
such as ganglia or tumors, or osseous abnormalities, such as bony spurs, fracture fragments, and callous. Ganglia are isointense or
hypointense compared with muscle on T1weighted images depending on proteinaceous
content, are homogenously hyperintense on
T2-weighted sequences, and show thin peripheral enhancement with gadolinium. The

pattern of muscle denervation provides information about the duration of entrapment

and can identify the site of neurologic compromise. Acute denervation presents as hyperintensity of the supraspinatus and infraspinatus or infraspinatus muscle alone on
fluid-sensitive sequences. Chronic compression is shown as a reduction in muscle bulk
and fatty infiltration of the involved muscles.
Involvement of both the supra- and infraspinatus muscles reflects proximal compression
at the suprascapular notch, whereas isolated
infraspinatus denervation suggests compression at the spinoglenoid notch [6] (Fig. 4).
The treatment of suprascapular nerve compression depends on the duration of symptoms
and the location and cause of the entrapment.
Spontaneous recovery can occur with conservative therapy and cessation of exacerbating
activities [23]. Suprascapular neuropathy related to entrapment at the suprascapular notch
may be treated by excision of the superior
transverse scapular ligament [24]. Similarly,
with isolated infraspinatus dysfunction, excision of the spinoglenoid ligament may be performed [23]. Removal of masses and repair
or reduction of a fracture may be necessary.
Symptomatic ganglia may be treated using an
arthroscopic or open procedure with repair of
associated labral tears and cyst decompression or excision. Recurrence may merit further investigation for untreated labrocapsular
tears or other intraarticular abnormalities.
Quadrilateral Space Syndrome
Axillary nerve anatomyThe axillary
nerve (C5, C6) originates from the posterior

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MRI of the Shoulder

Fig. 2Suprascapular notch varices in 36-year-old
woman. Sagittal oblique fast spin-echo T2 images
with fat suppression (left and right images) and
coronal oblique T1 image (middle image) show
varices in suprascapular notch (arrows, left and
middle images) are high signal on T2-weighted
and intermediate signal on T1-weighted images.
There is resulting denervation edema and atrophy
of supraspinatus (arrowhead, right image) and
infraspinatus (arrow, right image) due to compression
of the suprascapular nerve. Arrowheads in left image
show denervation edema in supraspinatus and
infraspinatus.

Fig. 3Suprascapular nerve compression from paralabral cyst in 27-year-old

woman. Coronal oblique fast spin-echo (left image) and sagittal oblique (right
image) T2 images of shoulder with fat saturation show septated paralabral cyst
(arrow, left image) arising from tear in superior labrum. Resulting denervation
edema of infraspinatus is due to compression at level of spinoglenoid notch. ss =
supraspinatus, is = infraspinatus, sub = subscapularis.

cord of the brachial plexus in the axilla. It descends inferolaterally, anterior to subscapularis, before passing through the quadrilateral
space accompanied by the posterior humeral
circumflex artery. This space is located inferoposterior to the glenohumeral joint and is
bounded superiorly by the teres minor muscle,
inferiorly by the teres major muscle, medially
by the long head of the triceps, and laterally
by the humeral neck [25] (Fig. 5). After passing through the quadrilateral space, the axillary nerve divides into anterior and posterior trunks. The branches of the anterior trunk
supply the anterior and middle parts of the
deltoid muscle. The posterior trunk supplies
the posterior part of the deltoid and teres minor muscles before terminating as the superior lateral brachial cutaneous nerve. Branches
also supply the glenohumeral joint and surgical neck of the humerus.
Cause and clinical featuresQuadrilateral space syndrome is a rare condition referring to an isolated compressive neuropathy
of the axillary nerve. The syndrome was first
described by Cahill and Palmer [26] in 1983
in which the neurovascular bundle, comprising the axillary nerve and posterior humeral
circumflex artery, is compressed by fibrous

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Fig. 4Suprascapular nerve compression from ganglion cyst in 50-year-old man.

Axial fast spin-echo T2 image (left image) of shoulder shows spinoglenoid notch
cyst (arrow, left image) is emanating from posterosuperior labrum. Sagittal oblique
T2 image with fat saturation (right image) shows isolated infraspinatus edema
(arrowhead, right image) due to distal suprascapular nerve compression. ss =
supraspinatus, sub = subscapularis, tm = teres minor.

Fig. 5Quadrilateral
space anatomy in posterior
perspective. Axillary
nerve passes through
quadrilateral space (QLS)
accompanied by posterior
humeral circumflex
artery. Space is bounded
superiorly by teres minor
muscle, inferiorly by teres
major muscle, medially by
long head of triceps, and
laterally by humeral neck.

bands as it passes through the quadrilateral

space. It typically occurs in young athletes
between the ages of 25 and 35 years without a history of significant trauma. The syndrome is characterized clinically by poorly localized anterolateral shoulder pain and
is exacerbated by forward flexion, abduction, and external rotation of the humerus.
This pain is usually associated with point
tenderness over the posterior shoulder, near
the teres minor insertion site. Skin paraesthesia in the sensory distribution of the axil-

lary nerve (overlying the deltoid muscle) and

atrophy or weakness of the teres minor and
deltoid may also occur [27].
The formation of fibrous bands in the
quadrilateral space appears to be related to
microtrauma as a result of repeated overhead movements such as throwing [28, 29].
Although extrinsic compression by fibrous
bands is the most common cause of the syndrome, several other causes have now been
described in the literature. Robinson et al.
[30] were the first to report a case of quad-

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Yanny and Toms

Fig. 6Iatrogenic axillary nerve injury in 60-year-old man.

A and B, Coronal (A) and axial (B) T1 images of left shoulder show atrophy of deltoid (arrowhead, A) caused by axillary nerve (arrows) paresis after internal fixation of
fracture of surgical neck of humerus with plate and screws. Tip of one screw (arrowhead, B) is shown abutting axillary nerve in quadrilateral space. After removal of
screw, patient recovered partial deltoid function.

rilateral space syndrome caused by a paralabral cyst. Juxtaarticular cysts are a common
entity occurring adjacent to large joints and
are a well-documented cause of compressive
suprascapular neuropathy in the shoulder.
Glenoid labral cysts are thought to originate
from extrusion of joint fluid through labrocapsular tears. They occur most commonly in the superior and posterior regions and
are uncommon in the inferior aspect of the
joint [19]. When large, inferior labral cysts

can produce mass effect on the neurovascular bundle in the tightly bound quadrilateral space. Quadrilateral space masses such as
hematomas and soft-tissue tumors also have
been reported to result in this syndrome.
Other described cases of axillary nerve injury include trauma (humeral neck or scapular fractures), acute translational events such
as glenohumeral subluxation or anterior dislocation, and surgical (Fig. 6) or arthroscopic intervention [3133]. The relatively fixed

position of the quadrilateral space makes it

particularly susceptible, and such injuries
usually affect both the teres minor and deltoid muscles because of the level at which the
axillary nerve injury occurs [34].
Imaging findings and treatmentThe diagnosis of quadrilateral space syndrome may
be difficult on the basis of clinical grounds
alone and is usually one of exclusion. Typically poorly localized shoulder pain may be
confused with a rotator cuff injury or im-

Fig. 7Quadrilateral space syndrome in 40-yearold man. Sagittal oblique (left image) and coronal
oblique (middle image) images with fat saturation
of shoulder show teres minor muscle (arrows) is
atrophied and infiltrated with fat, which creates
striated appearance on coronal oblique T1 image
(right image). Axillary nerve (arrowhead, right
image) appears normal. No mass was identified
in quadrilateral space. Denervation injury of teres
minor was thought to be secondary to fibrous bands
compressing axillary nerve.

Fig. 8Malignant brachial plexopathy in 70-year-old woman. Axial CT image

(left image) shows large Pancoast tumor (arrow, left image) at left apex. Sagittal
oblique fast spin-echo T2 image with fat saturation (right image) shows high signal
at tumor site (arrow, right image) as well as diffuse muscle edema of supraspinatus
(ss), infraspinatus (is), and subscapularis (sub) due to indirect injury from brachial
plexus infiltration.

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MRI of the Shoulder

pingement. When an obvious structural lesion such as fibrous bands or a mass is found
on imaging, diagnosis can be relatively
straightforward. However, MRI commonly
shows no structural abnormality within the
quadrilateral space but may reveal secondary features of denervation myopathy (Fig.
7). These features include atrophy of the
teres minor and, less commonly, of the deltoid, which is seen as a reduction in muscle
bulk and fatty infiltration with chronic compression [27]. Fatty infiltration is best seen
on T1-weighted images but also can be seen
as abnormal signal intensity within the muscle belly on T2-weighted sequences.
Cahill and Palmer [26] advocated the use
of subclavian arteriography for the diagnosis of quadrilateral space syndrome, with occlusion of the posterior circumflex humeral artery in the symptomatic extremity that
is abducted and externally rotated (ABER).
However, in subsequent studies, authors have
found this finding to be nonspecific. Mochizuki et al. [35] found stenosis or occlusion
of the artery in the ABER position in both
asymptomatic healthy volunteers and in patients with quadrilateral space syndrome,
thus negating the use of MR angiography as
a diagnostic tool in this condition.
Quadrilateral space syndrome is a potentially reversible cause of shoulder pain. It should
be considered when selective atrophy or a signal change of teres minor with or without involvement of the deltoid is seen in the appropriate clinical setting. Other diagnoses producing
muscle atrophy or neurogenic edema in the absence of a visible cause, such as traumatic injury to the axillary nerve, brachial plexus, or
nerve roots, must also be considered [36].

Surgical decompression of fibrous bands has

proven successful in patients with symptoms refractory to conservative treatment [37]. Of the
18 patients studied by Cahill and Palmer [26],
resection of fibrous bands led to an improvement
of symptoms in 89% of the subjects with quadrilateral space syndrome. Excision of spaceoccupying masses, including paralabral cysts,
with resection and labral repair is curative.
Peripheral Nerve Polyneuropathy
Parsonage-Turner Syndrome
Cause and clinical featuresParsonageTurner syndrome is an uncommon, self-limiting disorder characterized by sudden onset of
nontraumatic shoulder pain associated with
progressive weakness of the shoulder girdle
musculature. It was first recognized in 48 patients by Spillane in 1943 [38] and then by
Parsonage and Turner [39] in 1948 who described the condition in 136 servicemen,
which they named neuralgic amyotrophy or
shoulder-girdle syndrome. Since then, the
condition has generally been referred to as
Parsonage-Turner syndrome or acute brachial
neuritis, although the terms brachial plexus
neuropathy [40], acute brachial radiculitis
[41, 42], and paralytic brachial neuritis [43,
44] have all been used to describe the entity.
Clinical diagnosis may be challenging because symptoms can mimic those of other
more common disorders such as cervical
spondylosis, rotator cuff tears, impingement
syndrome, adhesive capsulitis, and calcific
tendinitis [3840, 45].
The precise cause of Parsonage-Turner
syndrome is unknown, although viral neuritis [40, 46], immunization [43], autoimmune
mechanisms [47], trauma, strenuous exercise,

and surgery [48] have all been proposed. Antecedent infection has been reported in up to
25% of cases [40]. The overall incidence has
been estimated at 1.64 per 100,000 individuals in one population [49]. The age range of
affected patients is extremely wide, with most
patients presenting in the third to seventh decades of life [45, 50]. Males are predominantly affected; bilateral involvement is seen in up
to one third of patients [40, 49].
Imaging findings and treatmentNo test
is specific for the diagnosis of ParsonageTurner syndrome. Electromyography, nerve
conduction studies, and MRI must be interpreted in light of the patients clinical history. MRI is the technique of choice in patients
with shoulder pain and weakness. It is sensitive for the detection of signal abnormalities
in the shoulder girdle musculature related to
denervation injury. MRI is also useful in excluding intrinsic shoulder abnormalities that
can produce symptoms similar to ParsonageTurner syndrome such as rotator cuff tears,
impingement syndrome, and labral tears.
MRI can depict structural lesions that may
cause similar denervation changes in the rotator cuff musculature such as cuff tears or
masses impressing the brachial plexus (Fig.
8) or peripheral nerves and other causes of
intramuscular high signal including inflammatory myopathies, myositis, compartment
syndrome, rhabdomyolysis, and tumor involvement of muscle [51, 52].
The studies by Gaskin and Helms [53] and
Scalf et al. [45] are the largest reported series describing the MR features of Parsonage-Turner
syndrome to date. The diagnosis is suggested
when there is an abnormality of the muscles innervated by the brachial plexus in the absence of

Fig. 9Parsonage-Turner syndrome with involvement of suprascapular and axillary nerves in 54-year-old man.
A, Sagittal oblique T1 image (left image) shows fatty atrophy within supraspinatus (ss), infraspinatus (is), and teres minor (tm), giving characteristic striated appearance.
Sagittal oblique fast spin-echo T2 image (right image) with fat saturation shows increased signal intensity within these muscles, which is consistent with denervation
edema.
B, Coronal oblique T2 image (left image) with fat saturation and coronal oblique image T2 image (right image), which is anterior to left image, show diffuse increased
signal intensity within infraspinatus and teres minor (arrow, left image), supraspinatus (arrow, right image), and deltoid muscles; these findings are consistent with
denervation injury of suprascapular and axillary nerves.

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Yanny and Toms

a history of trauma or excessive overhead activity or when a morphologic cause is identified at
MRI. The earliest detectable change in denervated muscles is diffusely increased signal on
fluid-sensitive sequences such as STIR or T2weighted sequences (because of increase in extracellular water content) and normal signal on
T1-weighted images [1]. After a few weeks in
the subacute to chronic phase, the denervated
muscle atrophies, seen as a reduction in muscle
bulk and increased T1 signal due to fatty infiltration [45]. Intramuscular signal may return to
normal several months after the chronic phase;
however, in complete muscle denervation (> 1
year after injury), changes are irreversible [54].
Initially the long thoracic nerve was believed to be the most commonly involved in
Parsonage-Turner syndrome [39]. However,
later studies showed the most commonly involved muscles are those innervated by the suprascapular nerve (supraspinatus and infraspinatus) [50] (Fig. 9), although the entire
brachial plexus can be affected. In their 2006
study of 27 patients with Parsonage-Turner
syndrome, Gaskin and Helms [53] found that
the suprascapular nerve was involved in 97%
of the subjects and the axillary nerve in 50%.
Treatment of patients with Parsonage-Turner syndrome is nonsurgical and consists of
analgesia for pain and physical therapy for
weakness. The long-term prognosis is generally good; however, patients with more severe symptoms initially are predisposed to a
more protracted course. Most patients with
Parsonage-Turner syndrome have resolution
of muscle weakness in the first 23 months
after diagnosis, with 90% of subjects making
a full recovery by 3 years [40, 48]. A low incidence of recurrence has been reported [40].
Summary
Denervation syndromes of the shoulder are an underrecognized but important
cause of shoulder pain and weakness. Diagnosis is conventionally based on clinical
findings and electrodiagnostic tests, which
do not determine the exact cause or anatomic site of denervation. MRI is commonly performed in patients with shoulder pain
of uncertain origin and can determine the
morphologic cause and precise location and
duration of nerve injury and muscle denervation. Knowledge of the relevant anatomy,
cause, and clinical and imaging findings is
important in making a potentially treatable
diagnosis, avoiding confusion with inflammatory or neoplastic processes, and obviating biopsy or surgical intervention.

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