Abstract
Once considered a diagnosis of exclusion, suprascapular neuropathy (SN) is now becoming a well-recognized condition stemming from traction or compression of the suprascapular nerve. The indirect course of the nerve, as well as its passage through two notches, makes it particularly vulnerable to injury from anatomic variation or local pathology. Dynamic forms of SN are often seen with overhead athletes such as volleyball players and throwing athletes. Patients typically complain of shoulder pain, weakness, paresthesia, and decreased range of motion. Physical examination may reveal atrophy of the supra- and infraspinatus muscles, and weakness of abduction and external rotation. Functional limitations will vary significantly depending on the patient’s activity level. Electrodiagnostic studies are the gold standard test for confirming the diagnosis of SN and grading the injury severity, but an image-guided diagnostic suprascapular nerve block can also assist with diagnosis. Treatment initially focuses on physical therapy to strengthen scapular stabilizers and rotator cuff. Surgery can be considered if conservative measures fail. Overall, SN has a positive prognosis with the majority of patients improving with conservative or operative treatment.
Keywords
Injury, rotator cuff, shoulder pain, Suprascapular nerve
Synonyms | |
| |
ICD-10 Codes | |
G56.80 | Other mononeuritis of unspecified upper limb |
G56.81 | Other mononeuritis of right upper limb |
G56.82 | Other mononeuritis of left upper limb |
G56.90 | Unspecified mononeuritis of unspecified upper limb |
G56.91 | Unspecified mononeuritis of right upper limb |
G56.92 | Unspecified mononeuritis of left upper limb |
Definition
Suprascapular neuropathy (SN) is defined as a demyelinating or axonal injury to the suprascapular nerve. Once considered a diagnosis of exclusion, SN is now becoming a well-recognized condition stemming from traction or compression of the nerve at some point along its course. Epidemiologic data is limited, but the prevalence of SN in overhead athletes is reportedly between 12% and 33%, and 8% to 100% in patients with massive rotator cuff tears.
To understand the pathophysiology, 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 superior transverse scapular ligament (STSL), which connects the two borders of the suprascapular notch, to enter the supraspinous fossa. In 18% to 60% of the population, the anterior coracoscapular ligament (ACSL) lies deep within the anterior portion of the suprascapular notch. Commonly, the suprascapular nerve and vein pass together superior to the ACSL and inferior to the STSL within the suprascapular notch, with the suprascapular artery passing above the STSL. 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, the subacromial bursa, the coracohumeral and coracoacromial ligaments, and the overlying skin. 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.
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 STSL or ACSL can hypertrophy or ossify. Risk of SN is also increased with variations of the suprascapular region such as a bifid or trifid STSL, ACSL, or a small, narrow or shallow suprascapular notch. At the spinoglenoid notch, compression is most frequently due to a space occupying paralabral cyst that develops as a result of a labral tear, and less often from a benign tumor (e.g., lipoma) or hypertrophied spinoglenoid (inferior transverse scapular) ligament.
Dynamic forms of SN are often seen in overhead athletes due to tightening of the spinoglenoid ligament during the overhead motion. This leads to the so-called “infraspinatus syndrome” since only the infraspinatus is affected. In addition, repetitive overhead movements may lead to muscle and tendon microtrauma (the “sling effect”), causing nerve inflammation and compression. This is most apparent in volleyball players, overhead pitchers, weight lifters, and those who do repetitive overhead motions for their occupation.
Less commonly, SN may result from shoulder girdle trauma, glenohumeral joint dislocation, brachial neuritis, iatrogenic injury as a complication of surgery, or large rotator cuff tears. Three-dimensional mapping of operatively treated scapular fractures has shown extension of the fracture to the spinoglenoid notch in 22% of patients.
Symptoms
A range of symptoms may be associated with SN. Patients’ complaints are often similar to those seen with other pathology about the shoulder, including pain, weakness, paresthesia, decreased range of motion, or functional impairment. Some patients, however, may present only after recognizing painless atrophy of the scapular musculature. SN is therefore difficult to diagnose based on history alone. The pain, when present, can be poorly localized but is often located along the posterolateral shoulder and described as a deep, dull, and burning ache with variable radiation to the arm that is worsened with overhead activity or when sleeping on the affected side. 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. For non-traumatic injuries, the onset is typically insidious and night pain is variable. Although less common, trauma can cause SN, and in this case, symptom onset is rapid.
Clinicians should have a high index of suspicion in athletes engaged in sports with repetitive overhead motions, particularly volleyball, baseball, tennis, basketball, and swimming. These repetitive overhead motions can lead to suprascapular nerve injury through the previously described mechanism, and can exacerbate symptoms. Furthermore, throwing athletes may experience a decline in throwing velocity or overhead swing (hitting) speed. Athletes may also describe weakness and a sense of fatigue during these activities.
Physical Examination
A complete physical exam of the shoulder is critical to identify a suprascapular nerve lesion and its underlying etiology. Inspection may demonstrate atrophy in the supraspinatus or infraspinatus fossae. Atrophy of the supraspinatus may be difficult to visualize given the bulk of the overlying trapezius. Isolated atrophy of the infraspinatus suggests compression of the nerve at the spinoglenoid notch. Palpation may elicit tenderness along the course of the nerve, particularly at the level of the suprascapular notch, within the supraspinous fossa or at the spinoglenoid notch. The tenderness may be enhanced with horizontal shoulder adduction, which tightens the spinoglenoid ligament. Strength testing may demonstrate weakness in abduction or external rotation. Weakness may be subtle due to compensatory muscle action. Other special tests should be performed to evaluate for labral pathology, given its association with spinoglenoid notch cysts that can compress the suprascapular nerve. The examiner should also perform a thorough upper extremity neurovascular examination and evaluate the cervical spine and contralateral shoulder.