Nerve Entrapment

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. 54.1 ). The suprascapular notch is most commonly U -shaped (48% to 84%) but varies in morphology from flat to enclosed within bone. A study of over 200 scapulas described six types of scapular notches and their incidence as follows: (1) absent (8%), (2) shallow V -shape (31%), (3) U -shaped with parallel margins (48%), (4) deep- V shape (3%), (5) type III with partial ossification of the transverse scapular ligament (6%), (6) complete ossification of the ligament. Together, the suprascapular notch and the overlying ligament form the suprascapular fossa. The suprascapular notch has been shown to be approximately 4.5 cm from the posterolateral acromion, a relationship that becomes important in arthroscopic decompression.

The nerve traverses the deep surface of supraspinatus, innervating it with two motor branches. Sensory branches innervate the glenohumeral and acromioclavicular joints, and as recent anatomic studies show additional sensory innervation to the coracohumeral ligament, the coracoclavicular ligament, subacromial bursa, and posterior shoulder capsule. 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%), although 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, putting it at risk for traction injuries and multiple predictable sites of compression. 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. This has been well described in volleyball players. 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 in throwing or serving, 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 and enters the spinoglenoid notch, sparing the supraspinatus. Ganglion cysts are a common cause of compressive injury to the suprascapular nerve. These cysts are thought to result from superior labral tears, which are very common in overhead athletes, 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. 54.2 ), although cysts at the suprascapular notch have been described. Other etiologies of neuropathy are more rare but have also been described. Suprascapular nerve palsy has been reported after distal clavicular 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. 54.3 ). Scapular body fractures are also associated with suprascapular nerve palsy. Injury to the axillary or suprascapular artery in overhead athletes can result in microemboli and microvascular infarct of the suprascapular nerve as well. Suprascapular nerve injury has also been reported with acute shoulder dislocation in a cyclist.

Recent attention has been given to the association of suprascapular neuropathy and retracted rotator cuff tears. A cadaveric study showed increased tension on the first motor branch of the suprascapular nerve with medial retraction of the supraspinatus muscle. Clinical studies have suggested that predominant infraspinatus fatty degeneration in the context of a massive rotator cuff tear may be secondary to suprascapular nerve compression at the spinoglenoid notch. Repair of the rotator cuff with appropriate tension, however, has been shown to reverse a significant proportion of suprascapular nerve symptoms in the setting of massive tears.

Clinical Evaluation

Suprascapular nerve injury may present after specific trauma acutely or more commonly chronically. The presentation may be painful range of motion (ROM) or shoulder weakness or involve insidious painless muscle atrophy. Athletes who perform repetitive overhead activities—such as baseball players, volleyball players, and swimmers—should be treated with a heightened suspicion for compressive neuropathy. During the history-taking portion of the exam, all recent upper-extremity and neck injuries, sports-related or not, should be reviewed. 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.

The physical exam should begin with general inspection of both shoulders and scapula, concentrating on symmetry of musculature. Scars from trauma or previous surgical incisions should be noted. Active, passive, and resisted ROM is tested, looking for motions that elicit symptoms, the presence of instability, compromised strength, and labral pathology. Tenderness at the suprascapular notch may be elicited with palpation. The inconsistent finding of pain often localizes in the posterior shoulder and radiates to the arm; it may be worse with adduction of the shoulder. An additional physical exam maneuver, the suprascapular nerve stress test, will worsen compression at the suprascapular notch and produce posterior shoulder pain in patients with compressive pathology. Bilateral symptoms should raise suspicion for cervical pathology, and the exam should always include a c-spine exam.

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 a gradual onset of vague posterior shoulder discomfort and weakness. Pain is thought to arise from the articular branches to the acromioclavicular and glenohumeral joints.

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. 54.4 ) and should be compared with the contralateral side. 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. When the diagnosis is in question, an injection of local anesthetic at the level of the spinoglenoid notch can be helpful to distinguish suprascapular nerve pathology from other causes of shoulder pain.

Diagnostic Studies

Radiographic evaluation should include routine shoulder views and, if clinically indicated, a c-spine series. A 30-degree cephalic tilt radiograph to visualize the suprascapular notch is helpful, especially in patients with fractures ( Fig. 54.5 ).

MRI is 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 readily be 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, although it is very operator-dependent. 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 is the gold standard study for suprascapular nerve pathology. Indications include unexplained persistent shoulder pain, atrophy, and weakness without a concomitant rotator cuff tear or MRI evidence of supraspinatus or infraspinatus atrophy without obvious rotator cuff pathology. A complete test should include both needle electromyography (EMG) of the entire shoulder girdle, including the paraspinal muscles, and nerve conduction velocity (NCV) 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 ms to the supraspinatus and 2.4 to 4.2 ms 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. In a study of 79 patients with muscle weakness, EMG and NCV have been shown to have an accuracy of 91% in detecting suprascapular neuropathy. Overall sensitivity and specificity of electrodiagnostic testing is not known and depends on the etiology of the neuropathy. Compression with ganglia may involve only one of the three or four suprascapular nerve branches to the infraspinatus; therefore EMG recordings are performed at more than one location within the muscle.

Decision-Making Principles

Conservative management with activity modification and physical therapy is the treatment of choice for the majority of patients who present with neuropathy secondary to repetitive overhead activities. Depending on the duration of symptoms and the etiology, a comprehensive physical therapy regimen will likely decrease pain and improve function. However, muscle bulk may be irreversible once significant atrophy has occurred, even if surgically decompressed. A patient with a chronic condition (i.e., lasting 6 to 12 months) and well-established atrophy that has failed nonoperative measures 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 structural source of compression, such as a ganglion cyst, also benefit from surgical decompression.

Authors' Preferred Technique

Suprascapular Notch Compression

Traditionally open surgical release methods have been utilized to decompress the suprascapular nerve at the suprascapular notch. This was often difficult to visualize open, as the suprascapular nerve is as small as 2 mm and often required detachment of the trapezius muscle for adequate exposure. As our understanding of the anatomy of the area has improved, along with our arthroscopic techniques, multiple all-arthroscopic surgeries have been described and the all-arthroscopic technique has been reported to be a safe and effective alternative to an open approach; this is now considered the standard of care, and we prefer to utilize an all-arthroscopic technique at our institution.

The patient is placed in the standard beach-chair position. The all-arthroscopic procedure is as described by Lafosse. Standard posterior and lateral subacromial portals are utilized for camera visualization. An anterolateral portal and suprascapular nerve portal are used for instrumentation. The suprascapular nerve portal is made under direct visualization approximately 7 cm medial to the lateral border of the acromion between the clavicle and the scapular spine and 2 cm medial to a standard superior-medial portal. Once the glenohumeral joint has been visualized through the posterior portal, we enter the subacromial space. The coracoacromial (CA) ligament is identified, exposed, and traced back to its insertion on the coracoid. The coracoclavicular (CC) ligaments are then identified as the dissection is continued posteriorly and medially from the CA insertion. The transverse scapular ligament's lateral border is just medial to the base of the CC ligaments. The suprascapular portal is then made under direct visualization from the lateral portal. A combination of shavers and radiofrequency ablation devices are used to isolate the ligament. Care is taken to avoid the suprascapular artery, which runs superior to the ligament. Another portal, 1.5 cm lateral to the suprascapular nerve portal, is used with a biter to release the transverse scapular ligament. Gentle manipulation of the nerve with a probe should suffice to determine the adequacy of decompression. A burr can be used to open up the notch if there is residual compression after the ligament is released.

Results

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, with a mean length of 30 cm, courses posterior to the brachial plexus to perforate the fascia of the proximal serratus anterior ( Fig. 54.6 ). 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. In patients with serratus anterior muscle paralysis, shoulder motion is severely limited because of the lack of scapular rotation. The serratus anterior also acts as an accessory inspiratory muscle, as is seen in runners who fix their scapulas by holding their thighs to catch their breath after a race.

The most common site of compression is where the nerve passes through the middle scalene muscle or angulates over the second rib. 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 “bowstrings” 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. Sports and repetitive overhead work 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 swimming, basketball, football, golf, gymnastics, ballet, and wrestling. Occupational injuries are also certainly possible, with reports from household activities such as hedge clipping or car washing to construction jobs and shoveling. Traumatic injuries are typically neuropraxias from sudden depression of the shoulder girdle. 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 is unlikely to cause isolated palsy. Serratus anterior rupture has been reported in patients with rheumatoid arthritis, and injury has been reported as a complication of interscalene blocks administered in the course of regional anesthesia. All of a patient's past surgical procedures should be reviewed as iatrogenic causes for injury have been described as well, including lymph node biopsies, clavicular resections, and any other procedure performed at the head/neck/shoulder junction.

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.

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 ROM 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 to occur.

Paralysis of the serratus anterior results in medial 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. 54.7 ). A shoulder protraction test can identify long thoracic nerve injuries affecting the upper trunk. In this test, the patient is placed in the supine position and asked to forward flex (protract) the shoulder. Ability to protract the shoulder indicates an intact upper trunk of the nerve. Occasionally a Tinel sign over the trajectory of the long thoracic nerve is present.

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.

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 will provide a reliable return to a competitive sport that requires overhead strength.

Authors' Preferred Technique

Long Thoracic Nerve Palsy

Cessation of the activity that is suspected of inciting the injury is important. Shoulder braces cannot begin to normalize rotational balance of the scapula due to the force couple between the serratus anterior and the trapezius. However, in the case of severe serratus winging, braces may prevent progressive attenuation of the trapezius muscle.

Surgical treatment is infrequently indicated. Although pectoralis minor transfer to the lateral inferior scapula for dynamic support has been reported, transfer of the pectoralis major sternal head, with or without augmentation, to the inferior border of the scapula is the currently favored reconstruction owed to its similar line of pull, excursion, and cross-sectional area as compared with the serratus anterior. Indirect transfers with interpositional grafts have been described with equivalent functional results as a direct transfer. The advantage of the interpositional graft is that it avoids overtensioning, which would restrict postoperative ROM and reduce the risk of traction neuropraxia to the medial and lateral pectoral nerves. There is considerable controversy in the literature regarding the most effective surgical technique. A recent study failed to show a consensus among polled shoulder and elbow surgeons regarding the use of the entire tendon or a split tendon technique, direct versus indirect transfers, or regarding graft type.

The patient is placed in the lateral position. A 5-cm incision is made in the inferior deltopectoral groove. The shoulder is abducted to accentuate the interval between the sternal and clavicular heads of the pectoralis major. The sternal head is released sharply from its humeral insertion and bluntly separated from the clavicular head. Care is taken to work medially against the chest wall to avoid the neurovascular structures. Sutures are placed in the tendon to maintain proper orientation during shuttling through the second incision. A second incision is made over the inferior angle of the scapula. The infraspinatus, subscapularis, and serratus anterior are subperiosteally dissected to expose the inferomedial portion of the scapula. A long curved clamp is used to develop a tunnel in the scapulothoracic interval, medial to the coracoid process and conjoined tendon. The transferred pectoral tendon is then secured to the scapula through drill holes with the scapula held in a reduced position. Postoperative immobilization in a sling or scapulothoracic orthosis is emphasized for 6 weeks. Gentle gravity-assisted pendulum exercises and isometrics are allowed during this time. ROM of the shoulder girdle begins 6 weeks after surgery. Return to noncontact athletic activities begins at 12 weeks, but lifting of more than 20 lb is delayed until 6 months after surgery.