Suprascapular neuropathy is a demyelinating or axonal injury to the suprascapular nerve. Once considered a diagnosis of exclusion, suprascapular neuropathy is now becoming a well-recognized condition stemming from traction or compression of the nerve at some point along its course. Epidemiologic data are limited, but the prevalence of suprascapular neuropathy is reportedly between 12% and 33% in overhead athletes and between 8% and 100% in patients with massive rotator cuff tears [1].

To understand the pathophysiologic mechanism, it is imperative to have a good knowledge of the anatomy (Fig. 20.1). The suprascapular nerve arises from the upper trunk of the brachial plexus and receives contributions mainly from the fifth and sixth cervical nerve roots, with variable contribution from the fourth cervical nerve root. It courses posterolaterally, deep to the trapezius and clavicle, on its way to the suprascapular notch. Here, it passes beneath the transverse scapular ligament to enter the supraspinous fossa. Within the supraspinous fossa, the suprascapular nerve sends two motor branches to the supraspinatus muscle and receives sensory branches from multiple surrounding structures, including the posterior aspect of the glenohumeral joint, the acromioclavicular joint, and the subacromial bursa. The nerve then courses inferolaterally around the lateral aspect of the scapular spine. This region is referred to as the spinoglenoid notch and is a common area of suprascapular nerve compression. Finally, the nerve enters the infraspinous fossa, where its terminal motor branches innervate the infraspinatus muscle.

f20-01-9781455775774 — FIGURE 20.1 Posterior view of the scapula demonstrating the course of the suprascapular nerve through the suprascapular and spinoglenoid notches.

The indirect course of the nerve as well as its passage through two notches makes it particularly vulnerable to injury. Static forms of compression or traction can stem from anatomic variations, particularly at the suprascapular notch, where the transverse scapular ligament can hypertrophy or ossify. At the spinoglenoid notch, compression is most frequently due to a space-occupying paralabral cyst that develops as a result of a labral tear [1].

Dynamic forms of suprascapular neuropathy are often seen in overhead athletes because of tightening of the spinoglenoid ligament during the overhead motion [2]. This leads to the so-called infraspinatus syndrome because only the infraspinatus is affected. Large rotator cuff tears can also cause a suprascapular neuropathy because the medially retracted muscle belly places a traction force on the nerve [3,4].

Less commonly, suprascapular neuropathy may result from shoulder girdle trauma or from iatrogenic injury as a complication of surgery. Three-dimensional mapping of operatively treated scapular fractures has shown extension of the fracture to the spinoglenoid notch in 22% of patients [5].

Symptoms

A range of symptoms may be associated with suprascapular neuropathy. Patients’ complaints are often similar to those of patients with other pathologic processes about the shoulder, including pain, weakness, and functional impairment. Some patients, however, may present only after recognizing painless atrophy. Suprascapular neuropathy is therefore difficult to diagnose on the basis of history alone. The pain, when it is present, can be poorly localized but is often located along the posterolateral shoulder and described as a deep, dull ache. This pain pattern coincides with the diffuse sensory contribution of the suprascapular nerve, as it carries sensory afferents from up to 70% of the shoulder [6]. For nontraumatic injuries, the onset is typically insidious and night pain is variable. Although it is less common, trauma can cause suprascapular neuropathy, and in this case, symptom onset is rapid.

For athletes, overhead sport-specific motions can intensify typical pain symptoms, and a decline in throwing velocity or hitting speed may be seen. Weakness is often described as a sense of fatigue during these activities.