NEUROLOGIC CONDITIONS ABOUT THE SHOULDER

Symptoms of neurologic conditions of the shoulder
include pain, weakness, or both. Obtain a complete history and perform
a thorough physical examination; pay particular attention to testing
and grading each muscle about the shoulder girdle and examining for
specific local areas of tenderness. Then decide to what extent the pain
is related to organic pathology. This decision making takes into
consideration the patient’s credibility, whether worker’s compensation
is a factor, and whether litigation is pending.

The diagnosis of shoulder pain is difficult, analogous
to evaluating the source of low back pain. Most often, pathology
resides in the rotator cuff or with intraarticular problems; take care
not to fall into the trap of missing some of the less common diagnostic
entities. The shoulder often is implicated in pain arising from the
neck (1,8). This
chapter does not discuss the qualities of cervical radiculopathy and
arthritic changes about the neck, but I mention them here to remind you
not to have tunnel vision when evaluating the shoulder.

Pain secondary to nerve compression can be caused by
thoracic outlet syndrome, suprascapular nerve compression syndrome, and
quadrilateral space syndrome. See Chapter 61 for a complete discussion of thoracic outlet syndrome.

Pain can also be secondary to weakness or instability

about the shoulder, due to palsies of the suprascapular, axillary, long
thoracic, and spinal accessory nerves, as well as palsy of the upper
brachial plexus. Vague shoulder pain and weakness of the involved
muscle groups are the main symptoms of isolated nerve injuries about
the shoulder (44).

The purpose of this chapter is to review the diagnosis
and treatment of specific nerve entrapments or palsies about the
shoulder that result in pain, weakness, or both. Systemic conditions,
such as arthrogryposis, muscular dystrophies, polio, and stroke, will
not be discussed; instead, see the works of Saha (58) and Scholtstaedt et al. (60). Also see Chapter 67, Chapter 68, and Chapter 178.

Before addressing specific conditions that can be traced
to an isolated nerve insult, one must be aware of a syndrome comprising
pain and flaccid paralysis of the muscles about the shoulder girdle.
Parsonage and Turner first described it in 1948 (50), calling it neuralgic amyotrophy. The syndrome today is more often referred to by their names.

In their series of 136 patients, Parsonage and Turner
were able to identify a precipitating cause in 66 patients. Some of the
causes cited were infection, trauma, or previous vaccination. They
noted that local pain was almost always the presenting symptom,
generally a constant severe ache that lasted for a few hours to a week
or two and then stopped fairly suddenly as muscle paralysis appeared.
Involvement of the long thoracic nerve leading to paralysis of the
serratus anterior was the most common finding. The authors also
reported cases in which the suprascapular nerve, the axillary nerve,
and C-5 and C-6 nerve root were involved. The prognosis for recovery
was related to the amount of initial paralysis. Muscles not completely
paralyzed or those showing some return during the first few weeks
usually recovered completely in 6 months or less. With severe wasting
occurring early and rapidly, the prognosis for useful return of
function was poor. Recovery of voluntary power in completely paralyzed
muscles was found 9 to 12 months after the onset, and recovery
continued up to 2 years or longer. The only treatment recommended was
to move the shoulder joint through its full range of motion on a
regular basis to prevent stiffness.

The pathophysiology of this syndrome is not any better
understood today than it was by Parsonage and Turner in 1948. It is
important to keep this fact in mind when evaluating any nerve palsy
about the shoulder, because early surgical treatment is not indicated (17).
A history of severe pain preceding muscle paralysis or the close timing
of a vaccination forms the basis for this diagnosis. Other than
symptomatic therapy, no specific treatment is available.

The suprascapular nerve may be compressed in the
suprascapular notch, resulting in little more than pain about the
medial aspect of the scapula. The pain is usually diffuse, deep aching
and may be localized to the posterior aspect of the shoulder. Adduction
of the forward-flexed arm across the body produces traction on the
nerve and may increase this pain (53). Deep
palpation over the suprascapular notch may show marked tenderness. With
further compression or traction on this nerve, atrophy and loss of
external rotator function will ensue (Fig. 59.1).
The external rotation deficit limits the patient’s ability to perform
activities with the arm in an overhead position. With prolonged
compression and loss of all external rotator function, posterior
shoulder instability may also result.

The suprascapular nerve is a mixed peripheral nerve that arises from the upper trunk of the brachial plexus (C-4 to C-6) (Fig. 59.2).
It courses laterally, deep to the trapezius and omohyoid muscles, and
enters the supraspinous fossa passing under the transverse
suprascapular ligament. The suprascapular artery and vein course with
the nerve, but they pass above the transverse suprascapular ligament.
The sensory component supplies the posterior capsule of the shoulder
joint and has no cutaneous distribution (57).
The suprascapular nerve courses deep to the supraspinatus muscle,
innervating this muscle with two branches. The nerve continues to the
lateral edge of the spine of the scapula, curving around it medially
into the infraspinous fossa, deep to the infraspinatus muscle. As the
nerve courses under the edge of the spine of the scapula, it commonly
passes through an inferior transverse scapula ligament (the
spinoglenoid ligament) that inserts at the lateral border of the
scapular spine and the scapular neck.

More commonly, the site of entrapment is found to be
underneath the transverse suprascapular ligament; isolated atrophy and
weakness of the infraspinatus muscle, however, have been attributed to
compressions underneath the inferior transverse scapular ligament (63,65). Dermirhan et al. studied the anatomy and morphology

in cadavers to determine the role of entrapment in the suprascapular
nerve. They found the spinoglenoid ligament to be present in 60.8% of
shoulders, and that it was wider at the superior entrance of the tunnel
and fanned and twisted toward the inferior aspect (9).
In all their specimens, the fibers inserted into the posterior shoulder
capsule. During cross-body adduction and internal rotation of the
glenohumeral joint, the suprascapular nerve moved laterally and
stretched underneath the spinoglenoid ligament. In this position, the
interaction of the spinoglenoid ligament and the posterior capsule
resulted in stretching of the nerve (9).

Electromyography is critical for the diagnosis of
compression of the suprascapular nerve. Diagnostic are denervation
potentials in the supraspinatus and infraspinatus muscles and prolonged
conduction time from Erb’s point to the supraspinatus and infraspinatus
muscles in the absence of involvement of other peripheral nerves (37).
Root compression at the C-5 level can mimic suprascapular nerve
entrapment syndrome; if C-5 root compression is the cause, however,
electrodiagnostic studies of the deltoid and rhomboids will demonstrate
abnormalities in these muscles. Magnetic resonance imaging is also
useful not only for the detection of ganglion cysts but also for
assessing the stage of paralysis (26).

Suprascapular nerve palsy can result from direct trauma such as fracture of the scapula or a blow to the shoulder region (70). It has been reported as well to result from compression by a ganglion cyst (26,47,54,62,65) or from a bone cyst (61).
Rengachary et al. studied the anatomy of the suprascapular notch in
cadavers and concluded that certain configurations might contribute to
nerve entrapment (56). Ticker et al. found the ligament to be partially ossified in 18% of cadavers (66).
It is debatable whether this entity is an actual nerve entrapment
syndrome or a situation in which the nerve is fixed at a given point
and the dysfunction is actually caused by traction.

Ferretti et al. studied 96 top-level volleyball players
and in 12 found isolated paralysis of the infraspinatus on the dominant
side (16). They attributed this denervation to
the athlete’s repeated stressing and stretching of the nerve when
serving (with the arm cocked) and following through. Sandow and Ilic
proposed that the infraspinatus branch of the suprascapular nerve can
be directly compressed between the lateral border of the scapular spine
and the medial margin of the rotator cuff during the extremes of
shoulder motion during sports such as volleyball and baseball; they
treat these athletes with a “notchplasty” in addition to release of
both the superior and inferior suprascapular ligaments (59).

Most authors recommend decompression of the
suprascapular nerve for severe pain or atrophy. Martin et al., however,
reviewed their experience with nonsurgical treatment and concluded that
“in the absence of a well-defined lesion producing mechanical
compression of the suprascapular nerve, suprascapular neuropathy should
be treated non-operatively” (43). Twenty
percent of the patients in their study failed conservative treatment,
however, and no predictors were found that would indicate the need for
operative versus nonoperative care. For exposure of the nerve,
posterior, anterior, and superior approaches have all been described (45,48,53,64).
Most authors have abandoned the anterior approach because it is a more
difficult dissection and has a higher risk of complications.

The axillary nerve contains fibers from C-5 and C-6 and
is a terminal branch of the posterior cord. It lies on the
subscapularis muscle behind the axillary artery and dips posteriorly
just inferior to the glenohumeral joint before emerging in the
quadrilateral space (Fig. 59.5). It innervates
the teres minor and the deltoid muscles. The axillary nerve enters the
quadrilateral space together with the posterior humeral circumflex
artery.

The quadrilateral space is bounded anteriorly by the
subscapularis fascia, superiorly by the teres minor, inferiorly by the
teres major, laterally by the humerus and joint capsule, and medially
by the long head of the triceps (49). The
axillary nerve is tethered in this space by muscular fascia, joint
capsule, and periosteum. At the time of surgery, normally this space
will admit an index finger along the neurovascular pedicle; the arm is
in a relaxed position at the side. In abduction, this space is narrowed
by the scissorlike effect of the triceps and the teres major, and the
nerve is placed under tension by its distal site of innervation. Full
forward flexion of the arm puts the subscapularis, teres major, and
triceps muscles under tension, and it causes the humeral head to
impinge on the axillary nerve. Abduction and external rotation further
narrow the tunnel (49).

Idiopathic axillary nerve compression (the quadrilateral
space syndrome) is a rare condition, and the diagnosis is often delayed
(7). One case caused by a ganglion has been reported (27).
Pain usually is described as being diffuse and anterior; extreme
movements of the shoulder involving abduction and external rotation,
however, exacerbate the symptoms. Typically, examination reveals
tenderness over the posterior aspect of the quadrilateral space. Rarely
is there any weakness of the deltoid or sensory deficit over the
distribution of the axillary nerve. Electromyographic examinations are
often normal and patients are often labeled neurotic.

Arteriography was once deemed necessary to confirm the diagnosis (3,4).
This invasive procedure should be performed to document this syndrome
only if surgery is contemplated. Perform a subclavian arteriogram by
using the Seldinger technique with the humerus at the side and in
abduction and external rotation (Fig. 59.6).
Follow the dye distally to visualize the posterior humeral circumflex
artery. In a positive arteriogram, the posterior humeral circumflex
artery is patent with the arm at the side and occludes with the arm in
external rotation and abduction. In normal extremities, the posterior
humeral artery does not occlude in this position.

Francel et al. have found that arteriography is
unnecessary and make the diagnosis on the basis of tenderness over the
quadrilateral space, paresthesia over the lateral shoulder and upper
posterior arm, and deltoid weakness associated with decreased shoulder
abduction in the presence of a history of trauma (18).
In addition, I have found that a diagnostic nerve block is more
valuable in confirming the diagnosis than are any radiologic or
electrodiagnostic studies. I inject 10 ml of 1% plain lidocaine into
the quadrilateral space. If the injection produces numbness in the
distribution of the axillary nerve, and the shoulder pain resolves in
spite of provocative maneuvers, the diagnosis is more likely.

Conservative therapy consists of avoiding aggravating
movements, administration of antiinflammatory medication, steroid
injections, and range-of-motion exercises. When this therapy has failed
and diagnosis is confirmed, surgical decompression is recommended.

The long thoracic nerve is formed from the roots of C-5
to C-7. It passes posterior to the brachial plexus and lies on or
penetrates the anterior surfaces of the scalenus medius, then angulates
over the first or second ribs as it courses along the lateral thoracic
wall downward and branches to supply the digitations of the serratus
anterior muscle (30).

To avoid injury to the long thoracic nerve, it is
important to be aware that it courses obliquely in an anterosuperior to
posteroinferior direction as it progresses to the posterior angle of
the second rib (14). Traction on the nerve is
exerted when the shoulder is depressed or when the cervical spine is
bent in a contralateral direction. Kauppila’s autopsy study suggests
that the potential site for damage is anterior to the lower part of the
scapula, where the nerve may be exposed to both compression and
traction (32).

Isolated serratus anterior palsy may follow an injury
such as a direct blow to the shoulder or a sudden jerk of the arm
forward or backward (68). The nerve can be
injured between the coracoid process and the first or second ribs.
Injury to the nerve during surgery has been reported following axillary
approaches for thoracotomy, radical mastectomy, and axillary node
dissection (12,40,51). Repetitive trauma can also cause loss of serratus anterior

function, particularly in laborers who carry heavy objects on their
shoulders. Sustained compression has been described from the downward
strain on the shoulder produced by carrying heavy knapsacks. A sudden
forceful muscular exertion such as lifting a heavy box or pushing with
arms stretched overhead to support a ladder has also been reported as a
cause. The prognosis is favorable if the nerve injury is from chronic
minor trauma, but it seems to be less favorable if the nerve is injured
by a single major episode (67).
Gozna and Harris studied cadavers and showed that, when the underside
of the scapula was coated with graphite and depressed forcefully
downward against the thorax, a graphite imprint was found on the long
thoracic nerve at the level of the second rib (19).
They concluded that this is the site of the nerve injury. Successful
repair of this nerve is hampered by its surgically inaccessible
location. Generally, one should wait for 1 or 2 years before
considering operative treatment, as most patients improve slowly with
time (17,19).

Nerve injury must be differentiated from traumatic
avulsion of the serratus anterior muscle, which also causes winging of
the scapula (21); the latter injury is rare. Electromyography and radiographs are diagnostic.

Paralysis of the serratus anterior muscle causes
scapular instability with attempts to elevate the shoulder. The scapula
pulls away from the chest wall as the extremity moves into forward
flexion or abduction. Normally, to elevate the shoulder fully, the
scapula must remain stable and close to the chest wall; at the same
time, the medial angle must depress and the inferior angle must rotate
laterally and upward. Patients who have serratus anterior muscle palsy
may be able to attain full shoulder motion in a supine position where
the weight of the body supports and stabilizes the scapula; when they
are standing upright, however, they cannot complete full shoulder
flexion and abduction.

The serratus anterior muscle has two functions:
Statically, it stabilizes the scapula to the thorax so that
scapulohumeral muscles can work against a fixed point to achieve arm
elevation; dynamically, it actively rotates the scapula anteriorly and
dorsally to contribute to full arm elevation.

Examine the patient standing, at rest. If he has
serratus anterior muscle paralysis, the medial rim of the scapula
protrudes from the thoracic wall, and the inferior border of the
scapula “wings.” The winging of the scapula is more distinct if the
patient lifts his arm into forward flexion and uses it for some sort of
exertion, such as in doing a pushup against a wall (Fig. 59.9).

Nerve conduction studies and electromyography are both
valuable in determining whether the lesion is partial or complete and
whether regeneration is occurring after Wallerian degeneration. The
rest of the upper brachial plexus requires electrodiagnostic study to
confirm the diagnosis of isolated long thoracic nerve palsy.

Spinal accessory nerve injury leads to trapezius muscle
dysfunction. The trapezius muscle is important in stabilizing the
scapula during forward elevation of the arm, and paralysis of it
results in drooping, lateral displacement, and winging of the scapula,
with weakness of forward elevation and abduction. Patients complain of
pain in the shoulder and axilla. Pain and weakness increase with
exertion of the arm. The pain may result from traction on the brachial
plexus, causing a radiculitis; it has even been demonstrated that
traction on the suprascapular nerve alone can be the cause of pain in
trapezius palsy (46). The pain also may result from a neuroma (see Chapter 53), which is demonstrated by eliciting Tinel’s sign in the posterior cervical triangle.

The accessory nerve exits the skull through the jugular
foramen and passes inferior to the surface of the sternocleidomastoid
muscle, which it innervates. As it passes underneath or penetrates the
deep head of that muscle, it reappears under its posterior edge between
the upper and middle thirds. It then enters the posterior cervical
triangle, where it lies superficially. The nerve passes beneath the
trapezius and forms a plexus with fibers from the third and fourth
cervical nerves while innervating the trapezius muscle (72).
To delineate the safe limits for muscle-splitting incisions of the
trapezius, Jobe et al. dissected the shoulders of 25 cadavers and found
that the spinal accessory nerve runs a vertical course medial and
parallel to the vertebral border of the scapula (29).
They also found that three to six nerve branches also run a vertical
course lying 33% to 50% of the distance from the tips of the vertebral
spinous processes to the lateral tip of the acromion.

They concluded that muscle-splitting incisions are relatively safe in the lateral half of the muscle (29).

The spinal accessory nerve’s superficial position in the
floor of the posterior cervical triangle renders it vulnerable to
injury. Most commonly, the injury occurs during a surgical procedure
such as surgical lymph node biopsy or removal of a benign tumor (13,71).
It used to be that the nerve was frequently excised during radical neck
dissection for malignant tumor, but more recently it is being spared
when this operation is performed. The nerve may also be injured by
penetrating or blunt trauma to the neck; I explored and grafted one
patient’s nerve that had been divided from a bite in the neck during a
lovers’ quarrel. Spontaneous palsy of the accessory nerve has been
reported, but all known cases were due to heavy, repetitive work or
were related to a particular incident of strenuous activity (41).

On examination, look for signs of surgical scars, and
percuss to elicit Tinel’s sign in the posterior cervical triangle. The
patient may be unable to abduct the shoulder above 80°, and shrugging
of the shoulder produces winging of the superior border of the scapula.
An abduction test has been devised to further demonstrate the flaring
of the vertebral border of the scapula: Hold the patient’s wrist firmly
at his side and ask him to attempt abduction against resistance. The
test is considered positive if there is flaring of the entire vertebral
border of the scapula (69).

Electrodiagnostic testing will confirm trapezius muscle
palsy, help localize the lesion, and rule out other forms of
neuropathy. Initially and up to 1 year, perform exploration of the
nerve with neurolysis, repair, or grafting as necessary. After 1 year,
consider reconstructive substitutions for the trapezius.

Conservative treatment is usually unsuccessful. Before
surgery, however, I give the patient a trial of shoulder immobilization
to see if removing the pull of the weight of the extremity on the
brachial plexus will decrease the pain. If Tinel’s sign is positive in
the posterior cervical triangle, I usually inject 3 or 4 ml of 1%
lidocaine at the site of Tinel’s sign to see if this injection
eliminates the pain. If the pain is diminished by a trial unweighing of
the arm, I find that trapezius muscle substitution reconstruction will
be predictably successful.

Reconstructive options take the form of static or
dynamic scapular stabilizations. Static stabilization procedures using
fascia tend to stretch in time and are more often used in patients who
have neuromuscular disorders and widespread weakness (10,22). The procedure of choice is an operation first described by Eden (15) in 1924, and later by Lange (35) in 1951. The Eden-Lange procedure is a lateral transfer of the levator scapulae and rhomboid major and minor muscles (36).
The trapezius muscle has upper, middle, and lower components: The upper
portion rotates and elevates the scapula, the middle portion stabilizes
and adducts the scapula, and the lower portion downwardly rotates and
depresses the scapula. The lateral transfer of the levator scapulae and
rhomboid muscles allows them to approximate the function of the three
portions of the trapezius muscle by changing the direction of their
pull. The operation is well described by Bigliani et al., whose
technique follows (2).

With C5–C6 brachial plexus palsy, a patient will develop
a flail shoulder. In time, the weight of the shoulder will cause
inferior glenohumeral subluxation and pain. The pain may be secondary
to traction on the brachial plexus or joint incongruity. In general,
the treatment is reconstruction of the brachial plexus or a shoulder
arthrodesis (see Chapter 60 and Chapter 103).

In a C5–C6 brachial plexus palsy, the function of elbow
flexion is also absent. While constructing elbow flexion with either
pectoralis major or latissimus dorsi tendon transfer, the shoulder may
be stabilized if the transfer is performed by rotating the muscle
completely on its neurovascular pedicle. Since the primary function of
these muscle transfers is elbow reconstruction, they will not be
described in this chapter (see Chapter 58 and Chapter 60).