Anatomy

The SSN arises from the upper trunk of the brachial plexus, usually from the ventral fibers of the C5 and C6 nerve roots. The nerve then takes a course through the posterior triangle accompanied by the suprascapular artery and vein, passing inferior and parallel to the posterior belly of the omohyoid and deep to the trapezius. It enters the supraspinous fossa deep to the supraspinatus. As these neurovascular structures approach the suprascapular notch, their courses become briefly divergent so that the nerve takes a path deep to the transverse scapular ligament (TSL), whereas the artery remains superficial to this (Fig. 24-1). Variations have been reported in this arrangement, with the artery passing beneath the ligament in up to 2.5% of shoulders.¹⁰

FIGURE 24-1 Three-dimensional representation of SSN and suprascapular artery and their relationship with the TSL.

The transverse scapular ligament spans the suprascapular notch, extending from the base of the coracoid and creating the suprascapular foramen. Because it is a ligament that connects two parts of the same bone, it is considered by some to represent a continuation of the coracoclavicular ligaments.¹⁰ Variable degrees of ossification have been reported in the ligament, with complete ossification in 3.7% in one series¹⁴ and partial ossification seen in 18%.¹⁵ It has also been seen to be bifid or trifid in 3% of cases in the same cadaveric series. It is important to remember, therefore, that in up to 25% of cases, the TSL is represented by an ossified variant or one with multiple bands.

As the nerve passes beneath the TSL, it gives two motor branches to supraspinatus, with the first branch generally being the larger of the two. It has been reported that one of these motor branches can pass superficial to the TSL.¹⁶ According to Hilton’s law, the SSN gives articular branches to the acromioclavicular and glenohumeral joints.¹⁰ On a microscopic level, it can be seen that the superficial part of the nerve carries afferent fibers (i.e., proprioception, pain), whereas the deeper fibers are responsible for motor innervation.¹⁷

The nerve then descends around the lateral margin of the scapular spine (Fig. 24-2) to split into three or four terminal motor branches supplying the infraspinatus. In doing so, it passes beneath the spinoglenoid ligament, forming the soft tissue boundary of the spinoglenoid notch. This quadrangular ligament extends from the posterior glenoid neck and capsule to insert onto the scapular spine.¹⁸

FIGURE 24-2 Three-dimensional view of distal SSN passing around the spine of the scapula.

A cutaneous branch has been found in 14.7% of cadaveric specimens examined, which supplies the skin overlying the proximal lateral third of the arm.^17,19 These cutaneous and articular branches may in part explain the nature and location of pain in some patients with SSN dysfunction.

Pathoanatomy

The most recognized site of entrapment of the SSN occurs at the suprascapular notch. Compression here results in weakness of the infraspinatus and supraspinatus. It is important to differentiate this from compression at the spinoglenoid notch, where only the innervation to the infraspinatus is affected. Both these sites represent areas of relative constraint of the nerve, whereby it does not have the freedom to be easily displaced to avoid local injury from compression or sudden motion from traction.

Rengachary and associates²⁰ have described six different types of suprascapular notches of varying depths and profiles, ranging from a wide depression on the superior border of the scapula to complete osseous enclosure. The morphology of these notches may predispose some patients to developing SSN pathology by virtue of having a narrower and therefore more constrictive notch, or one that is entirely osseous. They also offered a second mechanism to explain local nerve trauma through the principle of the sling effect. They proposed that this is caused by the change in angulation of the nerve as it passes through the foramen, especially with the arm in hyperabduction or depression combined with retraction. Kopell and Thompson² preferred a traction friction mechanism of injury to the nerve as it passes through the notch.

Compression by space-occupying lesions has been the subject of numerous case reports and series. These lesions include lipomas, osteochondromas, and malignant tumors. Because of the relative immobility of the nerve at the suprascapular and spinoglenoid notches, it is vulnerable to the mass effect of relatively small space-occupying lesions. Ganglion cysts probably represent the most common of these lesions (incidence, 1% to 4.2%) and, although their cause is not clear, the presence of cysts is strongly associated with capsulolabral pathology.^{2,15,21,22-24}

Repetitive overuse is postulated to result in chronic irritation of the SSN, particularly in those who regularly engage in overhead activities.¹² This is because these activities exacerbate traction on the sites of nerve fixation and expose the nerve to compressive and frictional forces on any sharp turns made by the nerve. Movements involving scapular depression and retraction, hyperabduction, or cross-arm adduction with forward flexion^20,25 all place increased tension on the nerve in the notch.

Glenohumeral joint dislocations, scapular fractures, and penetrating injuries can all result in direct or indirect traumatic injuries to the SSN. Iatrogenic injuries have been reported in surgery for distal clavicle resection, shoulder stabilization, and positioning of spinal patients for procedures.¹²

Finally, rotator cuff tears represent a unique pathology in that the tear itself and the accompanying retraction may lead to SSN dysfunction. The reduction of a chronic massive cuff tear may also result in similarly harmful effects to the nerve (see later).