The suprascapular nerve comes off the upper trunk of the brachial plexus, receiving innervation from both the C5 and C6 roots. The nerve runs posteriorly under the trapezius, passing through the suprascapular notch of the scapula to enter the supraspinous fossa. The suprascapular notch is U shaped, located along the superior border of the scapula, and covered by the transverse scapular ligament. The suprascapular nerve first supplies motor fibers to the supraspinatus muscle, a shoulder abductor, before proceeding laterally to supply deep sensory fibers to the glenoacromial and acromioclavicular joints and the coracoacromial ligament. It then wraps around the spinoglenoid notch of the scapular spine under the spinoglenoid ligament to enter the infraspinous fossa, where it supplies motor fibers to the infraspinatus muscle, an external rotator of the shoulder. The suprascapular nerve usually carries no cutaneous sensory fibers, although rare anomalous innervations have been reported. In these rare cases, the suprascapular nerve carries cutaneous sensation to the proximal lateral arm, the area usually supplied by the axillary nerve.
Suprascapular entrapment most commonly occurs at the suprascapular notch, under the transverse scapular ligament. Less frequently, the nerve can also be entrapped distally at the spinoglenoid notch. The suprascapular nerve is relatively immobile both at its origin at the upper trunk and at the suprascapular notch. Because both the shoulder and scapula are quite mobile, movement, especially repetitive movement, results in stretch and nerve injury. Also, like most of the major proximal upper extremity nerves, the suprascapular nerve is often prominently involved in neuralgic amyotrophy. Rare cases of suprascapular nerve entrapment have been reported secondary to a variety of mass lesions, including ganglion cysts, sarcomas, and metastatic carcinomas. Ganglion cysts are especially common at the spinoglenoid notch. In addition, certain activities, positions, and professions are associated with suprascapular entrapment. For example, weightlifting has been implicated in several reports as a provocative factor in suprascapular entrapment, likely as a consequence of repetitive movement of the scapula, especially during lifts that involve shoulder abduction and protraction.
Suprascapular neuropathy has also been reported as a consequence of positioning during surgical procedures, when patients are placed in a knee-chest position with the scapula protracted. Of interest, several professions put patients at risk for suprascapular entrapment. These include professional volleyball players, baseball pitchers, and dancers. In these professions, the clinical and electrophysiologic findings most often suggest a distal lesion at the spinoglenoid notch. In addition, suprascapular neuropathy, which is sometimes confused clinically with a rotator cuff injury, may also accompany a rotator cuff injury. One might initially assume that both have a common traumatic etiology. However, a suprascapular neuropathy may actually occur as a result of a rotator cuff tear, usually a large and full thickness tear. Following a rotator cuff tear, there may be medial retraction of the tendons to the supraspinatus and infraspinatus muscles. This may result in increased tension on the suprascapular nerve both at the suprascapular notch and the spinoglenoid notch.
Symptoms and signs depend on the site of nerve entrapment. At the most common site of entrapment, the suprascapular notch, shoulder pain may be prominent. Indeed, there is anatomic and clinical evidence that the suprascapular nerve supplies the majority of deep sensory fibers (including pain fibers) to the shoulder joint. The pain typically is described as deep and boring, occurring along the superior aspect of the scapula and radiating to the shoulder, but usually not more distally. The pain may be exacerbated by shoulder movements, especially adduction of the extended arm. This movement results in protraction of the scapula, which increases the nerve tethering between the upper trunk and the suprascapular notch. Occasionally, the suprascapular notch may be tender to palpation. Weakness involves shoulder abduction (supraspinatus) and external rotation (infraspinatus). Impairment of these motions may or may not be noticed by the patient, because both functions are subserved by other muscles as well. Atrophy may be recognized, especially over the infraspinatus muscle, which is only partially covered by the trapezius muscle.
If the entrapment occurs more distally at the spinoglenoid notch, the syndrome is limited to atrophy and weakness of the infraspinatus muscle. Pain usually is absent because the deep sensory fibers to the shoulder joint have exited more proximally. Several conditions may be confused with suprascapular neuropathy, including cervical radiculopathy, rotator cuff injury and other orthopedic conditions, and neuralgic amyotrophy. In contrast to suprascapular neuropathy, a C5–C6 radiculopathy may have radiating pain from the neck into the shoulder and arm, associated with sensory abnormalities in the lateral arm, forearm, and thumb. Often, the biceps and brachioradialis tendon reflexes are depressed or absent. Higher cervical radiculopathies (e.g., C3 or C4) may have a similar pain distribution to suprascapular neuropathy but are not associated with significant weakness of the shoulder or arm. Local orthopedic conditions may be difficult to differentiate clinically from suprascapular neuropathy. Although weakness should not be present, pain often prevents full muscle activation. Exacerbation of pain by palpation (other than at the suprascapular notch) or by passive shoulder movement (other than protraction of the shoulder) would be unusual for suprascapular entrapment. Lastly, neuralgic amyotrophy often presents with severe proximal arm and shoulder pain and, later, weakness. In some cases, the suprascapular nerve may be primarily involved. However, close clinical and electrophysiologic evaluation usually reveals evidence of more widespread involvement of other nerves.
The goal of electrodiagnosis is to demonstrate abnormalities of the suprascapular-innervated muscles and exclude cervical radiculopathy, brachial plexopathy, or involvement of other proximal nerves. Because the suprascapular nerve has no cutaneous distribution, there is no corresponding sensory nerve to be recorded. However, as the suprascapular nerve originates from the upper trunk of the brachial plexus, studies of the sensory nerves that pass through the upper trunk should be performed to help exclude a more widespread plexus lesion. These studies should include the lateral antebrachial cutaneous nerve and the median and radial sensory nerves, especially when recording from the thumb. Often, comparison with the contralateral asymptomatic side can be useful in identifying a mild abnormality, even if the studies are within normal range on the symptomatic side. Any abnormality present in these sensory studies suggests a more widespread brachial plexopathy. Of course, an abnormality found in the median sensory nerve may indicate a superimposed median neuropathy at the wrist, which may need to be studied further. Motor conduction studies can be performed, stimulating Erb’s point and recording with a monopolar needle electrode in either the supraspinatus or infraspinatus muscle, or both, simultaneously. A surface recording electrode should not be used to record from the spinati muscles, especially the supraspinatus, because they are covered by the trapezius. A surface reference electrode is placed distally over the shoulder joint. Compound muscle action potential (CMAP) amplitude and latency are measured. Comparing amplitude side to side can give an estimate of the amount of axonal loss present. However, these studies generally do not increase the yield over conventional EMG in terms of localizing the lesion and demonstrating axonal loss. Typically, the pathophysiology of these entrapment neuropathies is axonal loss. Thus, although motor nerve conduction studies may show reduced amplitudes and slightly prolonged latencies, there really is no information gained over needle EMG, which more easily demonstrates axonal loss. When Erb’s point stimulation is performed, high stimulating currents often are required, and supramaximal stimulation can be difficult to ensure. During needle EMG, both the supraspinatus and infraspinatus muscles should be sampled. Care must be taken to ensure that the EMG needle is not in the more superficial trapezius muscle, by checking that no motor unit action potentials (MUAPs) are activated with a shoulder shrug. In lesions at the suprascapular notch, both the supraspinatus and infraspinatus are abnormal. With spinoglenoid lesions, however, only the infraspinatus is involved. If either of these muscles is abnormal, it is essential to sample other C5–C6- innervated muscles (e.g., deltoid, biceps, brachioradialis), as well as the cervical paraspinal muscles, to exclude a cervical radiculopathy or more widespread brachial plexus lesion.
NCS:
Sensory: Median - D2, ulnar-D5 radial-Forearm, median-radial to D1, LABC: Check both sides
Motor: Median, ulnar, suprascapular (erbs) to infraspinatus
nEMG: Deltoid, biceps, triceps, brachioradialis, infraspinatus, supraspinatus, C5-C6-C7 paraspinal muscles.