Nerve Entrapment in the Shoulder
Entrapment neuropathies involving the shoulder are rare but potentially debilitating conditions. Their presentation is often subtle and insidious in onset. Injuries resulting from direct trauma, such as in blunt or penetrating mechanisms or from traction across a tethered segment, may present more acutely. A thorough understanding of neurovascular anatomy prompts early clinical suspicion. Appropriate advanced imaging and electrodiagnostic examination serve to confirm the diagnosis. Evidence-based decision-making principles guide operative and nonoperative efforts to return the athlete to competition. This chapter outlines several of the more commonly encountered compressive neuropathies of the shoulder girdle.
Suprascapular Nerve Palsy
Anatomy and Biomechanics
The suprascapular nerve arises from the C5 and C6 nerve roots at the upper trunk of the brachial plexus. It passes deep to the trapezius and the omohyoid muscles to enter the supraspinatus fossa through the suprascapular notch beneath the transverse scapular ligament ( Fig. 58-1 ). The suprascapular notch is most commonly U-shaped (48% to 84%) but varies in morphology from flat to enclosed within bone. Together, the suprascapular notch and the overlying ligament form the suprascapular fossa.
The nerve continues on the deep surface of supraspinatus, innervating it with two motor branches. Sensory branches innervate the glenohumeral and acromioclavicular joints. No cutaneous sensory distribution occurs from the suprascapular nerve. Upon reaching the lateral edge of the spine of the scapula, the nerve descends through the spinoglenoid notch, entering the infraspinatus fossa and innervating the infraspinatus. The spinoglenoid ligament passes from the spine of the scapula to the glenoid neck and posterior shoulder capsule. Its attachment into the posterior capsule results in tightening of the spinoglenoid ligament with cross-body adduction and internal rotation. The ligament is present in 14% to 100% of patients. It may appear as a thin fibrous band, known as type I (60%), or a distinct ligament, known as type II (20%), or it may be absent (20%). The spinoglenoid ligament has been reported to be present more commonly in men (64% to 36%), and in another study, it has been reported to be present in equal proportions in men and women. The average distance from the supraglenoid tubercle to the nerve at the suprascapular notch is 3 cm. The distance from the glenoid rim to the spinoglenoid notch is 1.8 to 2.1 cm.
The suprascapular nerve is relatively fixed at its origin in the brachial plexus and at its terminal branches into the infraspinatus, resulting in several possible sites of injury. Nerve contact with the suprascapular ligament is accentuated with depression, retraction, or overhead abduction of the shoulder. Extremes of scapular motion also place the nerve under tension. Overhead abduction of the shoulder with simultaneous eccentric contraction of the infraspinatus may result in compression of the suprascapular nerve at the spinoglenoid notch. Nerve compression against the lateral margin of the spine of the scapula by supraspinatus and infraspinatus tendons at their point of juncture is also thought to result in nerve injury.
“Athletic stress,” especially throwing, produces a backward and forward rotation of the scapula and suprascapular nerve compression at the suprascapular notch. The nerve is often injured in athletes as it passes around the lateral spine of the scapula, sparing the supraspinatus. Ganglion cysts are a common cause of compressive injury to the suprascapular nerve. These cysts result from superior labral tears, with the cyst expanding into the posterior scapular region, which is devoid of overlying muscle or tendon. Compression of the infraspinatus branch typically occurs as the nerve passes through the spinoglenoid notch ( Fig. 58-2 ), although cysts at the suprascapular notch have been described. Suprascapular nerve palsy has also been reported after distal clavicle fractures and resection of the distal clavicle. The nerve is located within 1.5 cm posterior to the clavicle and within 2 to 3 cm of the acromioclavicular joint ( Fig. 58-3 ). Fractures of the scapula are also associated with suprascapular nerve palsy.
Clinical Evaluation
Suprascapular nerve injury may present after specific trauma, with chronic onset of pain or weakness or with insidious, painless muscle atrophy. Injury to the suprascapular nerve as a result of compression or traction most commonly occurs at either the suprascapular notch or the spinoglenoid notch. Suprascapular neuropathy has been reported in many types of athletes who perform repetitive overhead activities. It has also been reported with acute shoulder dislocation in a cyclist and with sudden onset after a hard throw in a professional baseball player. A direct blow or forceful scapular protraction may cause traction on the nerve at the root level or kinking at either the suprascapular or spinoglenoid notch.
When the injury occurs at the suprascapular notch, pain and motor weakness of both the supraspinatus and infraspinatus muscles may result. The complaint is most often an insidious onset of vague posterior shoulder discomfort and weakness. Pain is thought to arise from the articular branches to the acromioclavicular and glenohumeral joints. Suprascapular notch tenderness may be elicited. The inconsistent finding of pain often localizes in the posterior shoulder and radiates to the arm, and it may be worse with adduction of the shoulder.
Compression of the suprascapular nerve by a ganglion at the spinoglenoid notch is a well-known clinical entity. If the lesion is at the spinoglenoid notch, distal to the acromioclavicular and glenohumeral branches, the presentation may be one of painless atrophy of the infraspinatus and external rotation weakness. Posterior shoulder atrophy, especially in the infraspinatus fossa, is an important finding ( Fig. 58-4 ). Supraspinatus atrophy may be difficult to observe because of the overlying trapezius. Likewise, supraspinatus weakness is not as easily elicited as that of the infraspinatus. Patients with clinical signs suggestive of a labral tear and wasting of the infraspinatus muscle warrant further diagnostic workup, including magnetic resonance imaging (MRI) and electrodiagnostic nerve studies.
Diagnostic Studies
Radiographic evaluation should include routine shoulder views and, if clinically indicated, a cervical spine series. A 30-degree cephalic tilt radiograph to visualize the suprascapular notch is helpful, especially in patients with fractures ( Fig. 58-5 ).
MRI may be useful in the evaluation of patients with suprascapular nerve palsy. Acute entrapment may be differentiated from chronic injury on T2-weighted images based on increased signal in the affected supraspinatus and/or infraspinatus muscles. The high signal intensity of affected muscle returns to normal after recovery, as noted on clinical and electrodiagnostic examination. Chronic compression appears as typical denervation changes, including decreased bulk and fatty infiltration of the muscles. Ganglion cysts in the supraspinatus fossa causing compression of the suprascapular nerve can be readily identified on MRI, as can associated pathology such as superior labrum, anterior to posterior (SLAP) and rotator cuff tears. Less common causes of suprascapular nerve palsy such as schwannoma and interneural ganglion have also been identified on MRI.
Ultrasound is also reported to be an effective diagnostic tool for the identification of paralabral cysts and associated rotator cuff tears. This modality has the added benefit of facilitating guided aspiration of paralabral cysts, with symptomatic improvement in 86% of patients in one series.
Electrodiagnostic evaluation should include both needle electromyography (EMG) of the entire shoulder girdle, including the paraspinal muscles, and nerve conduction studies from Erb’s point (2.5 cm superior to the clavicle, representing the convergence of the C5 and C6 nerve roots) to the supraspinatus. Normal conduction latency is 1.7 to 3.7 msec to the supraspinatus and 2.4 to 4.2 msec to the infraspinatus. EMG abnormalities may also be present with brachial neuritis, cervical root compression, and incomplete brachial plexopathies. Conversely, findings of EMG studies may be normal with an obvious clinical suprascapular nerve deficit, confirming the need for the nerve conduction examination. Compression with ganglia may involve only one of the three or four suprascapular nerve branches to the infraspinatus, and therefore EMG recordings are performed at more than one location within the muscle.
Decision-Making Principles
Treatment of a patient with a closed, acute suprascapular nerve injury is initially conservative, with follow-up of the problem (including electrical studies) at frequent intervals. A patient with a chronic condition (i.e., lasting 6 to 12 months) and well-established atrophy requires surgical exploration and decompression, as does a patient with suprascapular nerve palsy associated with an acute scapular fracture in the area of the suprascapular notch. Symptomatic patients who have a ganglion cyst compressing the suprascapular nerve also benefit from surgical decompression.
When nonoperative treatment fails to relieve compression of the suprascapular nerve at the suprascapular notch, the patient may benefit from decompression. Open surgical decompression of the suprascapular nerve at the suprascapular notch is performed with the patient in the lateral decubitus position. A skin incision parallel to the spine of the scapula and subperiosteal removal of the trapezius attachment to the spine exposes the superior border of the supraspinatus. The upper border of the supraspinatus is carefully retracted inferiorly and posteriorly to expose the superior surface of the scapula and the suprascapular notch and ligament. The suprascapular artery crosses above the ligament and the nerve below. Ligament excision and appropriate bony resection are performed with a laminectomy rongeur. In thin persons, a less extensile trapezius-splitting approach can be used through an incision across the spine of the scapula 2 cm medial to the acromioclavicular joint. The trapezius is split 5 cm in length, in line with its fibers, centered under the skin incision.
Spinoglenoid Notch Compression
Suprascapular nerve palsy associated with a spinoglenoid ganglion can be treated with arthroscopic techniques to repair or débride associated labral lesions and decompress the labral cyst. The cyst may be decompressed arthroscopically through a preexisting labral tear; however, if no labral tear is present, a capsulotomy is performed with an electrocautery device or a shaver. The cyst is visualized with the arthroscope in the posterior portal. A blunt probe is placed in the labral tear or capsulotomy until the characteristic amber-colored cyst fluid is visualized. Decompression is achieved by placing a shaver within the cyst and evacuating the fluid. The cyst wall may be removed with use of the shaver, but care must be taken to avoid iatrogenic injury to the suprascapular nerve. The shaver is pointed at the glenoid neck during removal, and dissection should not extend more than 1 cm medial to the posterior labral attachment to the glenoid. Associated labral pathology is then addressed.
If open decompression of the nerve at the spinoglenoid notch is necessary with excision of ganglia, a surgical approach to the posterior glenoid is performed. This approach is begun with a deltoid split over the glenohumeral joint with limited deltoid detachment laterally from the acromion. The superior edge of the infraspinatus is identified, and at most, the upper half of that tendon is detached, leaving a humeral side stump for repair. The size of the exposure needed is based on the MRI position of the ganglion and the size of the patient.
Results
Nonoperative
The overall response to conservative management is good, which suggests that traction injury rather than compression may be the cause of the problem in most cases. In the absence of a compressing lesion, rest from sports or other inciting causes may be helpful. The timing of return to activity relies on the judgment of the physician and is based on factors in the course of follow-up, including the extent of the initial paralysis, findings of electrical studies, symptoms, and improvements in the muscle examination with therapy. In persons who have painless infraspinatus muscle palsy without a cyst, function is usually good with nonoperative care. Asymptomatic ganglia without nerve findings may not require treatment.
A program of therapy may allow an elite pitcher with spinoglenoid notch lesions to return to high-level competition, assuming the infraspinatus is not completely denervated. EMG studies have demonstrated that only 30% to 40% of the maximal strength of the infraspinatus is used during overhead throwing, and thus in the case of a partial nerve injury, a return to pitching is possible. In a study of asymptomatic volleyball players, it was found that 12 of 96 players had isolated partial infraspinatus paralysis predominantly in the dominant shoulder. Whereas some players only had electrical abnormalities, others demonstrated muscle atrophy. A 15% to 30% loss of external rotation power was found. The suggested etiology was nerve tension at the spinoglenoid notch when the arm was cocked in maximal external rotation and during follow-through. In a long-term study, subjects with isolated infraspinatus atrophy were reexamined at a mean of 5.5 years. All subjects were still able to play volleyball at a high level with the degree of atrophy unchanged. The incidence of subacromial impingement in this subject population was no higher than in the general population of volleyball players. Surgical exploration of a well-localized lesion should be performed if 3 to 6 months of conservative management has failed to elicit improvement.
Suprascapular Notch Decompression
Most reports show good return of function in selected patients after open surgical decompression. A retrospective review of 42 patients at a mean of 18 months demonstrated measurable improvements in motor strength, with supraspinatus strength improving from grades 0 to 2 to grade 4 in 90% of patients. Infraspinatus strength improved from grades 0 to 2 to grade 3 or better in 32% of patients. Pain symptoms improved almost uniformly.
Spinoglenoid Notch Decompression
Several authors have reported cyst resolution and return of nerve function after arthroscopic decompression of the cyst. Cyst resolution and return of nerve function after repair or debridement of an associated SLAP lesion without attempts at cyst debridement have been reported. In a large series of patients diagnosed with suprascapular nerve compression, 65 patients were found to have spinoglenoid notch ganglion cysts associated with glenoid labral tears. Patients with the highest degree of satisfaction (97%) were treated with labral repair and open or arthroscopic decompression of the cyst. Lower satisfaction rates were reported by persons treated with isolated labral repair (67%) or needle aspiration of the cyst (64%) or in persons treated nonoperatively (53%).
Long Thoracic Nerve Palsy
Anatomy and Biomechanics
The long thoracic nerve arises from ventral rami of roots of C5, C6, and C7, which branch shortly after they exit from the intervertebral foramina. Branches of C5 and C6 form the upper trunk of the nerve, which pierces through the middle scalene muscle. It then joins the lower trunk from C7, which passes anterior to the middle scalene, to form the long thoracic nerve. This pure motor nerve courses posterior to the brachial plexus, with a mean length of 30 cm, to perforate the fascia of the proximal serratus anterior ( Fig. 58-6 ). The nerve supplies a single muscle, the serratus anterior, which covers much of the lateral thorax and acts with the trapezius to position the scapula for elevation. It arises from the upper nine ribs and attaches at the deep surface of the scapula along the vertebral border. Innervation of the upper and intermediate portions of the muscle is supplied by the upper division of the long thoracic nerve, which produces shoulder protraction. The lower portion is primarily responsible for scapular stabilization. These portions typically work together to draw the scapula forward and rotate its inferior angle upward. The serratus anterior also acts as an accessory inspiratory muscle, as is seen in runners who fix their scapulae by holding their thighs to catch their breath after a race.
A tight fascial band has been identified between the inferior aspect of the brachial plexus and the region of the middle scalene insertion on the first rib. The long thoracic nerve “bow-strings” over this band with shoulder abduction and external rotation. Medial and upward rotation of the scapula further compress the nerve. Asynchronous motion between the arm and scapula has been implicated as a cause of internal traction injury to the nerve.
Clinical Evaluation
Isolated serratus anterior palsy may result from acute injury, chronic irritation, or brachial neuritis. Long thoracic nerve palsy may also occur with prolonged recumbency or intraoperative stretch during thoracic surgery. Serratus anterior weakness after transaxillary first rib resection is not uncommon and has a good prognosis, although complete paralysis has a poor outlook. Sports have been implicated as a cause of isolated serratus anterior palsy, with the proposed mechanism being traction injury (either single or repetitive) to the long thoracic nerve. In one series, the repetitive trauma of tennis and archery was thought to be the cause of the lesion in 5 of 20 patients. Other sports implicated in this type of injury are basketball, football, golf, gymnastics, and wrestling. Other causes of nerve palsy include backpacking and shoveling. Proposed traumatic mechanisms include crushing of the nerve between the clavicle and the second rib, tetanic scalenus medius muscle contraction, and nerve stretch with cervical spine flexion or rotation and lateral tilt with ipsilateral arm elevation or backward arm extension. Because the nerve is in a deep location, a direct blow seems unlikely to cause isolated palsy. Serratus anterior rupture has been reported in patients with rheumatoid arthritis.
The long thoracic nerve is often affected by the poorly understood syndrome of brachial neuritis. Parsonage and Turner coined the term neuralgic amyotrophy (brachial neuritis), which they found in 136 military personnel, 30 of whom had isolated serratus anterior paralysis. These investigators also noted a right-sided predominance. Significant pain lasting a variable time, from days to weeks, precedes loss of function in one or more shoulder girdle muscles. Sensory loss does not exclude the syndrome. The prognosis for recovery is good; 36% of patients diagnosed with this syndrome recover by the end of the first year, and 75% recover by the end of the second year. Further improvement may occur beyond 2 years. Recurrent long thoracic nerve palsy is rare.
A patient with early thoracic nerve palsy may present with subtle changes in the ability to perform his or her sport, along with decreased active range of motion of the shoulder and altered scapulohumeral rhythm. The onset may be painful, as in persons with brachial neuritis, or it may be more subtle, involving difficulties with weight lifting or the recognition of pressure from a chair against the “winging” (protruding) scapula while sitting. Scapular winging may not become evident until several weeks after an acute injury, perhaps because a certain amount of time is required for progressive attenuation of the trapezius.
Paralysis of the serratus anterior results in lateral winging and poor scapular stabilization, limiting active shoulder elevation to 110 degrees in patients with complete lesions. Scapular winging as a result of long thoracic nerve palsy is characterized by elevation and retraction of the scapula as it moves toward the midline and slightly superior. The deformity is accentuated by resisted active arm elevation or by performing a push-up maneuver while leaning against a wall ( Fig. 58-7 ). A shoulder protraction test can identify upper trunk long thoracic nerve injuries. In this test, the patient is placed in the supine position and asked to elevate (protract) the shoulder. Ability to protract the shoulder indicates an intact upper trunk of the nerve.
Causes of winging other than serratus anterior palsy include trapezius palsy, painful shoulder conditions resulting in splinting of the glenohumeral joint, winging associated with multidirectional instability, and voluntary winging. The appearance of winging with arm elevation due to serratus anterior palsy differs from that of winging due to trapezius palsy. When the serratus anterior muscle does not function, the inferior tip of the scapula is pulled medially and posteriorly. With trapezius paralysis, the scapular body is held in position, and the medial border merely becomes more prominent, which is a more subtle deformity. In neither type of winging is the scapula rotated laterally to facilitate arm elevation.
Diagnostic Studies
Plain radiographs of the cervical spine and shoulder may identify contributing arthrosis, fracture malunions, or the presence of accessory ribs and osteochondromas. MRI is generally reserved for patients with shoulder instability or cuff tears, although T2-weighted fast-spin echo with fat saturation may demonstrate increased signal intensity consistent with denervation edema. EMG studies confirm the diagnosis of long thoracic nerve palsy. Conduction studies should be performed from Erb’s point to the serratus anterior muscle on the anterolateral chest wall. Repeat nerve studies at 3- to 6-month intervals are helpful to monitor improvement.
Decision-Making Principles
Surgery may be indicated for patients with long thoracic nerve palsy who remain symptomatic and for whom electrodiagnostic studies show no improvement despite 1 to 2 years of nonoperative therapy. Athletes must be counseled that no surgical intervention provides a reliable return to a competitive sport that requires overhead strength.
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