Isolated compression or injury to the suprascapular nerve may occur at the spinoglenoid ligament (Fig. 23.5). While the more common site of suprascapular entrapment neuropathy is at the transverse scapular ligament in the suprascapular foramen or notch, clinical presentation and diagnosis of compression at the most distal site have been well recorded (Fig. 23.6). Several mechanisms have been proposed and previously discussed above. While most commonly thought of in the overhead athletes, injury to this nerve may occur from repetitive traction and microtrauma [3, 4, 12–14]. The spinoglenoid ligament has also been demonstrated to tighten when the shoulder is in a position for overhead throwing, resulting in increased pressure on the suprascapular nerve [15] (Fig. 23.7). Early investigators speculated that injury to this nerve occurred by intimal damage from microemboli in the vasa nervorum [16]. While intriguing, there is no firm science to support this contention. A stenotic suprascapular notch, an ossified spinoglenoid ligament, or even superiorly oriented fibers of the subscapularis muscle may cause a suprascapular nerve compression [8, 17]. Compression of the nerve at the spinoglenoid ligament has been noted by many authors to be caused by a soft tissue mass or ganglion cyst as a result of some form of a labral or capsule injury. While previously treatment of a cyst-associated compression was labral repair [18, 19], the senior author recommends decompressing the ganglion from the posterior aspect of the shoulder without labral repair to yield excellent results (Fig. 23.8a–f). Compression by a ganglion cyst or soft tissue mass has been known to occur because of the relatively fixed position of the suprascapular nerve combined with the close proximity of the infraspinatus muscle to the glenohumeral joint. A ganglion cyst may form when the labral-glenoid junction tears and synovial fluid is transported into the soft tissues via a one-way valve effect. This mechanism is very similar to the formation of meniscal cysts in the knee [20].

While rare, a patient may sustain a neuropathy from a parsonage Turner syndrome, although it is more common for this viral neuritis to attack other nerves. Whatever the mechanism, compression or injury to the suprascapular nerve at the spinoglenoid ligament will result in infraspinatus weakness. If sustained long term, atrophy of the infraspinatus muscle will ensue with little if any probability of return to normal muscle strength expected.

Clinical examination often has nonspecific findings in the early stages of this disease process. Symptoms are often less severe with suprascapular neuropathy at the spinoglenoid notch as opposed to more proximal compression. Some athletes present with isolated painless wasting of the infraspinatus. Surprisingly, palpation at the spinoglenoid notch can be very painful. Some patients may describe micro-instability as a part of their complaints although confirmatory physical findings will not be found.

Completion of a cervical spine examination and a standard exam of both shoulders with a full neurological assessment must be completed. The patient, when placed in a shoulder gown with the complete scapula in full view, may demonstrate subtle or severe atrophy to the infraspinatus fossa (Fig. 23.9). Atrophy though in a well-developed individual who participates in a weight-training program may at times be difficult to discern due to the overlying trapezius and large bulk of the deltoid muscle.

Range of motion and strength must be assessed. There may be only a subtle loss of external rotation as well as abduction strength in young, overhead athletes. Strength of external rotation should be tested with the arm at the side, and weakness will often be present without any significant pain. The painless strength deficit is due to the fact that the sensory portion of the suprascapular nerve may be unaffected at the spinoglenoid notch. We have found that in long-standing disease, the teres minor and serratus anterior muscle may hypertrophy as compensation for the loss of the infraspinatus, hiding any strength deficit.

Provocative tests for labral pathology must be performed as labral tears with associated paralabral cysts may be found in conjunction with a suprascapular neuropathy at the spinoglenoid ligament.

A cross-arm adduction test, as described above, must be performed and recorded and correlated with a Zanca view X-ray in order to rule out acromioclavicular (AC) joint arthritis (Fig. 23.10a, b). If cross-body adduction reproduces the patient’s symptoms with the arm extended or internally rotated and the pain is primarily felt in the posterior aspect of the shoulder but the X-ray is negative, then the diagnosis of AC joint arthritis can be ruled out with an injection of lidocaine. A diagnosis of suprascapular nerve entrapment can now be claimed [21].

The differential diagnosis for suprascapular neuropathy at the spinoglenoid notch includes the same conditions considered for compression of the nerve at the transverse scapular ligament, i.e., cervical disc disease, a brachial neuritis, Parsonage–Turner syndrome, rotator cuff tendinopathy, labral pathology with or without a ganglion cyst, mild adhesive capsulitis, osteoarthritis of the glenohumeral joint, subacromial bursitis with or without impingement syndrome, AC degeneration disease, posterior glenohumeral instability, quadrilateral space syndrome, triangular space and interval disease or thoracic outlet syndrome, and the rare Pancoast tumor. The astute clinician recognizes that the lack of reproducible signs on physical exam for other common diagnoses and the overlapping symptoms with other shoulder problems often leads to a correct diagnosis.

Plain radiographs including an anteroposterior (AP), axillary lateral, and the Y or supraspinatus outlet view should always be obtained (Fig. 23.11a–c). Special views such as a Stryker notch view can be ordered when necessary [5]. This plain series will identify any fracture or significant trauma to the scapula, clavicle, coracoid, or glenoid neck.

Magnetic resonance imaging (MRI) and identification of soft tissue masses such as a ganglion cyst are critically important when evaluating compression of the suprascapular nerve at the spinoglenoid ligament (Fig. 23.12). The MRI can identify a true ganglion with a homogenous signal, low T1 intensity, with high T2 intensity and rim enhancement if contrast is utilized [22]. The MRI will also detect labral tears arising from the posterosuperior quadrant of the glenoid with the ganglion cyst attached (Fig. 23.13). Controversy exists as to whether the cyst truly arises from associated labral tears. Those that believe that this is the case insist on treatment to the labrum to minimize recurrence, while others advocate leaving the labrum alone after the cyst has been excised or decompressed.

The presence of a soft tissue mass or ganglion cyst on MRI does not necessarily indicate suprascapular neuropathy. However, abnormal signal intensity within the infraspinatus muscle will indicate significant suprascapular nerve compression at the spinoglenoid notch. Some patients will demonstrate increased signal intensity on T2 fast spin echo with fat saturation with a normal muscle mass implying subacute denervation of the muscle leading to neurogenic edema. Chronic denervation, seen best on T1 spin echo with increased signal intensity within the muscle mass, will demonstrate muscle atrophy with fatty infiltration (Fig. 23.14).

Newer modalities such as ultrasound may be helpful as well to identify ganglion cysts. This operator-dependent test can be very helpful not only in making a diagnosis but in assisting surgeons to complete an ultrasound-guided aspiration of the ganglion cyst. Compression sites can be readily visualized and aid in making a definitive diagnosis.