As the anatomy of the rotator cuff musculature itself has been covered in detail in prior chapters, this chapter will only focus on the role of the rotator cuff in stability and anatomic discussion of the SSN [11, 12].

The SSN is a mixed sensory – sending fibers to both the glenohumeral and acromioclavicular joint – and motor nerve. It arises from the brachial plexus at the level of the superior trunk with contributions from the fifth to sixth cervical roots, with up to 50% of people receiving contributions from C4 as well [13]. The nerve exits the posterior triangle of the neck between the sternocleidomastoid and trapezius muscles and descends on the anterior aspect of the trapezius. It then descends further along the upper border of the scapula alongside the suprascapular artery toward the suprascapular notch. Upon arrival at the notch, the artery and nerve diverge, with the artery coursing above the transverse scapular ligament, while the nerve maintains its course beneath the ligament. Typically, the first motor branch of the nerve to the supraspinatus arises at this point with some minor variations both just proximal and distal to the notch [14]. After passing through the suprascapular notch, the nerve then passes obliquely beneath the supraspinatus muscle, toward the spinoglenoid notch, passing within 20 mm of the glenoid rim [15]. Above the nerve at the level of the spinoglenoid notch lies the inferior transverse scapular, or spinoglenoid, ligament with fibers extending from the lateral aspect of the scapular spine to the posterior aspect of the glenoid and glenohumeral joint capsule. After making the turn around the scapular spine, the nerve gives off three to four motor branches to the infraspinatus muscle belly.

Understanding of the anatomy of the SSN becomes essential when considering the relationship between RCTs and concomitant SSN injuries. Albritton et al. demonstrated that the acuity of the SSN takeoff at its first motor branch at the level of the suprascapular notch increased from 143° in an intact cuff to 98.7° with as little as 1 cm of retraction. As expected, even further levels of retraction, present in chronic tears, lead to even more dramatic angles with the nerve taking a 47° or 35° turn with cuff retraction of 3 cm and 5 cm, respectively [14]. Retraction beyond 2 cm in this cadaveric study provides a possible explanation for the degree of atrophy and fatty changes in the muscle belly with massively retracted tears [16].

One recent multicenter, prospective study attempted to establish a direct correlation between suprascapular neuropathy and fatty infiltration of cuff musculature. Eighty-seven shoulders suspected of suprascapular neuropathy were enrolled and underwent both electromyography/nerve conduction velocity (EMG/NCV) testing and magnetic resonance imaging (MRI). On MRI, cuff musculature was graded according to the Goutallier system, and notation was made regarding the continuity and quality of the tendons. Of the 87 shoulders tested, 32 were found to have objective findings on EMG/NCV consistent with suprascapular neuropathy. A significant association was found between degree of tendon pathology and fatty degeneration (P value <0.001), with more severe tendon pathologies correlating with an increasing degree of fatty atrophy. Infraspinatus tendon tears were found to be associated with suprascapular neuropathy (P = −.01) [17]. The association seen between infraspinatus tears and suprascapular neuropathy may imply an insult at the level of the spinoglenoid notch, making the spinoglenoid ligament to release a more enticing option in this instance.

Clinical examination, in the setting of instability with suspicion of SSN injury, should assess joint stability, integrity of the cuff musculature, and neurovascular status of the limb, no different than a standard shoulder examination. Findings can be somewhat nebulous when suprascapular neuropathy is expected, especially in the setting of coexisting rotator cuff disease. Periscapular muscle wasting in both the supraspinatus and infraspinatus fossa should prompt consideration for such pathology, though this can also be present in the individual with chronic, massive RTC. Tenderness to palpation might be appreciated either over the suprascapular notch or posterosuperiorly in the region of the spinoglenoid notch. Weakness in external rotation with the arm at the side is often painless, as the sensory portion of the nerve can be unaffected when the pathology originates at the spinoglenoid notch.

The cross-arm adduction test should also be utilized as a means of discerning pathology originating in the area of the spinoglenoid notch. A study published by the senior author demonstrated that the highest pressures measured at the spinoglenoid notch arose in positions of late follow-through or the position of the greatest adduction [18]. Typically patients with positive findings will demonstrate pain in the posterior shoulder in the absence of any findings on plain shoulder imaging, and intra-articular injection of lidocaine into the AC joint can also be used to rule out AC arthralgia.

In the case of uncertain diagnosis without evidence of muscle wasting, diagnostic injections can also be of benefit, as both the suprascapular and spinoglenoid notches can be reached with percutaneous injections in the office setting. The suprascapular notch can be reached via a posterosuperior approach, with an insertion point 3 cm medial to Nevaiser’s portal with a trajectory toward the acromion. The spinoglenoid notch can be approached in a direct, posterior fashion, from a point 4 cm medial to the posterolateral corner of the acromion, just inferior to the scapular spine.