The morphology of the suprascapular notch , specifically a reduction in the height of the notch, may play a role in the development of suprascapular nerve entrapment [16]. Rengachary first classified 6 variations of the suprascapular notch [34] (Fig. 33.5). Scapula that do not have a notch, but rather a wide depression from the superior angle of the scapula to the base of the scapula, are classified as type I. A type II suprascapular notch is defined as a wide, blunted “V”-shaped notch that occupies approximately one-third of the superior border of the scapula. Symmetrical, “U”-shaped suprascapular notches, which have nearly parallel lateral margins, are classified as type III. Very small, “V”-shaped notches are classified as type IV. A type V notch is similar in shape to a type III notch with a partial ossification of the medial part of the TSL resulting in a small diameter along the superior border of the scapula. In a type VI notch, the TSL is completely ossified creating a bony foramen which is variable in size. Other classification systems of the suprascapular notch have also been described; Ticker et al. classified the suprascapular notch as either “U”- or “V”-shaped, evaluating the degree of ossification of the TSL separately, whereas, Iqbal and colleagues reported three types of notches including “U”-, “V”-, and “J”-shaped [17, 42].

The TSL attaches the base of the coracoid process and the medial end of the suprascapular notch creating a foramen through which the suprascapular nerve traverses in the majority of individuals. The TSL is thin and flat, being narrower at the middle than at its insertions. Ossification of the TSL has been reported to occur in approximately 25 % of clinical cases [42]. Polguj et al. identified 3 variations of the TSL [30]. The majority of specimens exhibited either a fan-shaped ligament (54.6 %) or band-shaped ligament (41.9 %); however, a bifid ligament was also found in 3.5 % of specimens. The anterior coracoscapular ligament was present in only 51 % of specimens and contributed to a smaller area in the suprascapular notch . The presence of the anterior coracoscapular ligament may be an additional etiologic factor to consider in suprascapular nerve compression at the suprascapular notch .

Classically, the suprascapular nerve traverses under the TSL at the suprascapular notch while the suprascapular artery traverses over the TSL. In a 2014 cadaveric study, the suprascapular nerve and vein traveled below the ligament in 61.3 % of specimens [31]. Other arrangements found included (1) the suprascapular artery and vein traveling above the ligament and the nerve coursing below the ligament (17 %), (2) the suprascapular vessels and nerve all traveling below the ligament (12.3 %), and (3) other variations of the suprascapular neurovascular structures occurred in 9.4 % of specimens.

The SGL is quadrangular in shape and extends from the posterior glenoid neck and posterior glenohumeral joint capsule to insert a bilaminar ligament into the scapular spine [29]. Two types of the SGL have been described: (1) type I, a thin indistinct band of tissue, and (2) type II, a well-formed ligament. The geometric shape has been described as either band-like, triangular, or irregular. Plancher et al. previously described this ligament to be present in 100 % of fresh-frozen specimens.

While many authors have suggested that the diagnosis of suprascapular neuropathy is difficult, as it is a diagnosis of exclusion, an accurate history, detailed physical examination, and appropriate diagnostic imaging can accurately recognize this disease entity and detect any overt neoplastic disease.

Plain radiographs should always be obtained including true (Grashey) anteroposterior (AP), Y or supraspinatus outlet, axillary lateral, and Stryker notch views as well as a Zanca view to inspect the AC joint. An AP scapular view with the beam aimed 15–30° cephalad obliquely at the TSL can aid in identifying any calcifications, exostosis, or previous trauma in the form of callous formation at the notch of osseous notch variants [33, 51]. The goal of this plain film series is to detect any fractures or minute trauma to the scapula, clavicle, coracoid, or glenoid neck.

Magnetic resonance imaging (MRI) is the best imaging modality in suspected suprascapular nerve pathology because of its soft tissue resolution. Visualization of the course of the suprascapular nerve is possible with T2-weighted sagittal oblique images. Identification of soft tissue masses such as ganglion cysts has also become increasingly important when making the diagnosis of suprascapular neuropathy. The MRI will help to identify their presence, location, and size (Fig. 33.6a, b). Fritz has described the characteristic findings in asymptomatic patients with a ganglion cyst, as a homogenous signal, low T1 signal intensity with high T2 signal intensity, and rim enhancement if contrast is placed [14]. Concomitant pathologies such as labral tears which may produce secondary impingement on the suprascapular nerve , rotator cuff tendinopathy, neoplastic processes whether nerve in origin or not, and glenohumeral joint osteoarthritis can also be detected with this imaging modality. Muscle atrophy and fatty infiltration of both supraspinatus and infraspinatus, more common in chronic cases, should also be evaluated as well as the presence of muscle edema which some have suggested to be one of the earliest signs of suprascapular nerve entrapment [20] (Fig. 33.7a, b).

Lastly, computed tomography (CT) and ultrasound can be valuable tools in making the diagnosis of suprascapular neuropathy. CT can detect or confirm notch variants as described by Rengachary (see 33.​2.​1 Adjacent Structures and Variation – Suprascapular Notch), fractures of the clavicle or scapula, and evidence of an ossified TSL [35]. Diagnostic ultrasound may also be helpful in identifying ganglion cysts in the office. In addition, ultrasound can be used to perform ultrasound-guided aspirations of a ganglion cyst.

A 1 % lidocaine anesthetic injection can be immensely helpful to accurately make the diagnosis of suprascapular nerve entrapment at either the TSL or the SGL. The authors routinely use a 25-guage, 1½-inch needle with great success. Ultrasound can be used as an adjunct to guide the needle to ensure accuracy.

When performing the diagnostic injection for compression at the TSL, it is important to understand the relationship of the artery to the nerve as previously described. The needle should be placed into the suprascapular notch from a posterosuperior approach, 3 cm medial to Nevaiser’s portal, and aiming anteriorly and aspirating first (Fig. 33.8a, b).

Injection at the spinoglenoid notch is simpler than at the TSL. When injecting into the spinoglenoid notch, the needle should be placed 4 cm medial to the posterolateral corner of the acromion (Fig. 33.9). When the injector feels the spine of the scapula, they should drop inferior to it by 1–2 cm and aspirate, and then they should easily fall into the spinoglenoid notch.

Patients should be questioned regarding their pain profile immediately following the injection; pain relief can be dramatic and almost immediate. No different than when using a diagnostic injection for confirmation of impingement syndrome, the cross arm adduction test should be performed both before and after the injection to confirm the diagnosis. If previously positive, the test should now be a non-provocative maneuver. The patient may describe the absence of pain at the AC joint after this intervention, once again helping the physician in ascertaining a definite diagnosis of a suprascapular nerve compression.

A negative test, however, does not rule out the disease in those patients who have a type 4–6 notch as the ability to deliver the lidocaine is quite difficult in those situations. Patients with a negative response when there is no atrophy, a negative EMG, and no evidence of a labral tear or ganglion cyst yet present with weakness and pain require a 3-month course of nonoperative treatment before considering any type of operative intervention.

Electrodiagnostic testing with myography and nerve conduction studies can be helpful, if positive, when there is a suspicion of the diagnosis by physical exam, imaging studies are negative (i.e., no soft tissue mass is seen), and atrophy is not present. The suprascapular nerve , as mentioned previously, is a mixed motor and sensory nerve which makes detection of a partial compression extremely difficult. Though evaluation of the sensory velocities is less useful as the sensory innervation of the suprascapular nerve is not as well defined, EMG and nerve conduction velocity testing have been shown to have 91 % accuracy in detecting nerve injury associated with muscle weakness [26, 32]. However, suprascapular nerve dysfunction can still be present with a normal EMG and nerve conduction study, making the diagnosis of suprascapular neuropathy a challenging disease entity.