Suprascapular neuropathy …

Jina Rachel Park MD

General Neurology

Updated 11.08.2023
Released 06.01.2001
Expires For CME 11.08.2026

Suprascapular neuropathy

Author: Jina Rachel Park MD

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Editor: Randolph W Evans MD

Suprascapular neuropathy

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Introduction

Overview

Suprascapular neuropathy is an underappreciated cause of shoulder girdle weakness and pain. The clinical and electrophysiologic techniques of diagnosis can be easily learned. Advances in correlation of nerve conduction study results with treatment choices and outcomes provide a motor-based prognostic model for suprascapular neuropathy. Both nonoperative and operative treatments are successful when properly chosen. In this update, new data regarding diagnostic modalities, etiologies, risk factors, and treatments of suprascapular neuropathy are summarized.

Key points

	• Suprascapular neuropathy should be considered in patients with shoulder pain, weakness, and supraspinatus and infraspinatus muscle atrophy.
	• Suprascapular neuropathy could be common in patients with a history of shoulder trauma, rotator cuff tear, and in overhead sports players.
	• The gold standard for the diagnosis of suprascapular neuropathy is electrodiagnostic testing.

Historical note and terminology

Suprascapular neuropathy connotes injury to the suprascapular nerve anywhere in its course, from the origin at the brachial plexus to its termination in the infraspinatus muscle. Suprascapular neuropathy is a more common cause of shoulder pain and weakness than is generally believed. Despite its relatively low prevalence, it must be kept in mind as a potential cause of shoulder pain, particularly in patients where the history, physical examination, and imaging studies do not adequately explain a patient's symptoms or disability (76).

Shoulder girdle neuropathy was reported as early as 1879 (49), and in 1909, isolated "neuritis" of the suprascapular nerve was described (27). In 1926, 16 cases of suprascapular neuropathy were published in a review of war injuries, and an additional case was discussed in 1936 (35; 94).

In Parsonage and Turner's classic publication of Neuralgic Amyotrophy in 1948, four cases of isolated suprascapular neuropathy are described (78).

In the late 1950s, Kopell and Thompson were the first to define suprascapular neuropathy syndrome. In a series of publications, they defined pathophysiology, clinical characteristics, and treatment approaches for suprascapular nerve entrapment at the suprascapular notch (55; 56).

Gassel was the first to publish nerve conduction study techniques for the suprascapular nerve, and Kraft further defined these methods (38; 58). A report of isolated infraspinatus involvement in suprascapular neuropathy was described in 1982 (02). Increasing attention to the importance of the various presentations and treatments of suprascapular neuropathy has continued to the present.

Clinical manifestations

Presentation and course

The clinical history of patients with suprascapular neuropathy often includes shoulder trauma or overuse. The most common presenting symptom is shoulder pain (97.4%) (77), which is often a deep, diffuse, and dull ache. The pain is localized to the posterolateral shoulder girdle, occasionally radiating medially upward to the neck or laterally to the upper arm. The pain is most often gradually progressive. Symptoms are worsened by shoulder movements and may become constant and severe and interrupt sleep (99). On some occasions, complaints of burning or crushing overlay to the pain are reported (85). The pain is likely referred from sensory articular branches to the shoulder joint (33).

Patients with motor involvement of only the infraspinatus muscle often do not have pain, likely due to the sensory articular branches having already diverged before the motor branch to the infraspinatus (32).

Weakness or muscle atrophy may be a prominent presenting complaint in suprascapular neuropathy. On examination, there may be weakness of external rotation (infraspinatus muscle) and initiation of abduction of the upper extremity at the shoulder girdle (supraspinatus muscle), resulting in difficulty with overhead arm movement, which was present in 84% of patients in a case series (77). Visible muscle loss is usually most apparent in the infraspinatus and was present in 78% of patients (77) and occasionally in the supraspinatus. Supraspinatus atrophy may be more difficult to visualize because of the overlying trapezius.

Infraspinatus muscle atrophy (photograph)

Muscle loss is apparent in this photograph of infraspinatus muscle atrophy. (Contributed by Dr. Sudhir Kothari.)

Prognosis and complications

Early recognition and treatment of suprascapular neuropathy may prevent the development of muscle atrophy. When suprascapular neuropathy is not recognized or treated, the course may be prolonged, and shoulder pain and weakness can become disabling; as a consequence, suprascapular neuropathy can lead to altered shoulder girdle biomechanics and secondary shoulder pathology (ie, rotator cuff dysfunction) (72). An investigation using an in vitro model of suprascapular neuropathy revealed substantial glenohumeral impairments and lingering functional shoulder deficits (69). Furthermore, isolated infraspinatus atrophy from suprascapular nerve injury could lead to deficient afferent proprioceptive information and impaired shoulder sensorimotor control. Studies have shown that there is an impaired sense of position leading to a higher hand position error with overhead volleyball players with isolated infraspinatus atrophy due to deficient afferent proprioceptive information, leading to poor accuracy in motor commands and impaired shoulder functional stability, which can further increase risk of injury (19).

A review of all prior outcome reports showed that 77% of patients surgically treated for suprascapular neuropathy and 92% of patients nonsurgically treated had good to excellent outcomes (33). Specifically, 95.2% of athletes who underwent decompression of the suprascapular nerve were able to return to sports, with 88% returning to preinjury level (77). The authors are quick to point out that nonoperative treatment should not be considered necessarily "better," in that most patients who were treated surgically had failed a prior course of nonoperative treatment. A retrospective review of pretreatment nerve conduction study findings revealed that pretreatment EMG findings did not reveal statistically significant prognostic indicators on self-assessment measures. Granted, they may connote highly accurate or consistent prognosis, and the findings may help frame operative versus nonoperative treatment recommendations (93).

Another review of 53 patients revealed that best outcomes with surgical management of suprascapular neuropathy were achieved when there was a compressive etiology including a cyst, whereas microtrauma due to overuse injuries did not improve with operative treatment. Traction and direct closed traumatic injuries responded equally to surgical or nonsurgical management, but overall had worse final outcomes (04). Almost all patients who are diagnosed with suprascapular neuropathy and treated surgically or nonsurgically had good-to-excellent results and returned to full activity, including professional competition levels (95; 24).

Clinical vignette

A 20-year-old, left-handed woman had left shoulder pain and weakness for a year. In her training and competition as a Division I National Collegiate Athletic Association swimmer, she gradually developed left posterolateral shoulder girdle deep aching, particularly noticeable to her during freestyle and backstroke. Over several months, comments were made to her by teammates that she had "less muscle" over the posterior left shoulder girdle. Previous evaluation and treatment by team physicians and trainers resulted in no clear diagnosis and no sustained relief. The remainder of her history was otherwise noncontributory.

Physical examination revealed abnormalities only in the left shoulder girdle. There was marked weakness in external rotation. Despite an apparently normal contraction of the left deltoid, weakness was also noted on initiation of abduction. There was possible mild left infraspinatus atrophy. No abnormal involuntary movements or fasciculations were observed.

X-rays and MRI with contrast of the shoulder and cervical spine were normal.

EMG of the left arm, shoulder girdle, and cervical paraspinal muscles revealed positive sharp waves and fibrillations as well as decreased recruitment patterns in the left supraspinatus and infraspinatus muscles.

Nerve conduction studies were performed with surface stimulation at Erb point and with surface and concentric needle recording from the supraspinatus and infraspinatus muscles. On the left, the latency to supraspinatus was 6.4 ms compared to 2.3 ms on the right. The latency to the left infraspinatus was 8.7 ms compared to 3.2 ms on the right. Compound motor action potential amplitudes on the left were 55% and 65% lower on the left compared to the right. The remainder of the nerve conduction studies were normal and symmetric.

Because the patient had already had treatment with rest, antiinflammatory drugs and analgesics, and extensive physical therapy for over 6 months without benefit, she was referred for surgical consultation. She underwent surgical section of the superior transverse scapular ligament at the suprascapular notch. She described immediate relief of pain following surgery.

At a 10-month postoperative follow-up, she was asymptomatic and had normal strength. Muscle bulk had improved substantially, with only subtle reduction of infraspinatus muscle mass compared to the right. EMG was normal. Latency to the left supraspinatus was 3.0 ms compared to 2.6 ms on the right. Latency to the left infraspinatus was 4.0 ms compared to 3.7 ms on the right. CMAP amplitudes were 5% to 10% lower on the left compared to the right.

She resumed training and competition as a collegiate swimmer and had considerable success.

At follow-up 2.5 years after surgery, she was asymptomatic.

Biological basis

Etiology and pathogenesis

The suprascapular nerve provides motor innervation to the supraspinatus and infraspinatus muscles. Although it was predominantly recognized as a motor nerve, several anatomical studies have shown that it has sensory innervation of the coracohumeral ligament, the coracoclavicular ligament, the subacromial bursa, and the posterior shoulder capsule (102).

The suprascapular nerve is a branch of the upper trunk of the brachial plexus. It is derived from components from the ventral rami of C5 and C6 roots and sporadically from the C4 root (92). The nerve courses laterally through the posterior cervical triangle, then travels posterior to the clavicle, and finally comes across the superior border of the scapula into the suprascapular notch (57).

The nerve runs most frequently through the suprascapular notch underneath the transverse scapular ligament, whereas the suprascapular artery and vein pass over it. Rengachary and colleagues reported six types of anatomical variations of the suprascapular notch as follows (87):

• Type 1 depression (8%)
• Type 2 shallow V-shaped (31%)
• Type 3 U-shaped (48%)
• Type 4 deep V-shaped (3%)
• Type 5 type 3 with partial ossification of the ligament (6%)
• Type 6 complete ossification of the ligament (4%)

The nerve passes through the suprascapular notch 3 cm medially to the supraglenoid tubercle. On exiting the notch, it crosses the supraspinous fossa, providing motor branches for the supraspinatus muscle (103). The motor branch then passes through the spinoglenoid notch under the spinoglenoid ligament, where it supplies motor branches to the infraspinatus muscle. The suprascapular nerve sensory branch is a direct branch from the main nerve at or before the transverse scapular ligament and runs superior to the supraspinatus muscle towards the acromioclavicular joint (25). The sensory innervation of the suprascapular nerve is the posterior shoulder capsule and joins with the lateral pectoral nerve in supplying sensory innervation to the acromioclavicular joint, coracoclavicular ligament, and the subacromial bursa, with no cutaneous sensory function.

The susceptibility of the suprascapular nerve to injury is based on anatomic aspects of the shoulder and possible entrapment sites. Evolutionarily, humans have sacrificed stability in the shoulder girdle for mobility of the upper extremity at the shoulder. "Shoulder joint" is a misnomer in that the shoulder girdle includes four joints: (1) acromioclavicular, (2) sternoclavicular, (3) scapulothoracic, and (4) glenohumeral. The muscles acting across these joints act synchronously as "force couples" in order to help compensate for the instability (47).

In a series of studies, Rengachary and colleagues have demonstrated that due to the relative fixation of the suprascapular nerve at its origin at the brachial plexus and termination in the infraspinatus, the nerve is particularly susceptible to angulation at the suprascapular notch. This results in a "sling" effect of entrapment at the suprascapular notch (87b). Isolated motor branch injury to the supraspinatus muscle is rare (03). Isolated infraspinatus involvement is postulated to be related to entrapment at the spinoglenoid notch, perhaps in association with excessive shoulder mobility (108).

Pathophysiology. The mechanism of suprascapular nerve injury or compression can be classified as traumatic (including repetitive microtrauma) and nontraumatic. Traumatic causes include direct trauma or repetitive overuse. Direct trauma may occur anywhere along the course of the suprascapular nerve, from the origin to the termination (104). The suprascapular nerve may be indirectly traumatized, such as in association with proximal humeral fractures (100). In a review of over 150,000 Finnish military conscripts focusing on backpack shoulder compression, suprascapular neuropathy was found in 7, which is approximately one-third the incidence of the more commonly expected long thoracic neuropathy in backpack carriers (70). Scapular winging may impose traction on the soft tissues of the shoulder region, including the suprascapular nerve (34), which could contribute to shoulder pain in these patients.

Overuse may result in entrapment at either the suprascapular or spinoglenoid notches (33). The classic example of micro-traumatic pathology is the suprascapular neuropathy found in overhead sports like volleyball, baseball, and swimming that can cause dynamic compression to the suprascapular nerve (21; 62). The same mechanism was attributed in a paraplegic patient with suprascapular neuropathy (29). LiBrizzi and colleagues reported that paddle sports such as kayaking can cause similar entrapment of the suprascapular nerve. Although kayaking does not typically involve overhead movement, repetitive cross-body adduction and internal rotation of the upper extremity are mechanisms for distal nerve entrapment or subacromial space impingement (65).

It has been suggested that isolated infraspinatus atrophy in overhead sports athletes is due to nerve traction during repeated overhead motions. One explanation is that the infraspinatus generates a component force that compresses the lateral aspect of the suprascapular nerve against the edge of the scapular spine. In this theory, the angle of the suprascapular nerve against the scapular spine is the key anatomical feature and is related to the scapular notch type (28).

Iatrogenic injury and suprascapular neuropathy were reported after repair of labral tears (11), repair of massive rotator cuff tears (110), arthroscopic repair of a superior labral tear from anterior to posterior (53), arthroscopic decompression of paralabral cyst around suprascapular notch (40), and other procedures. Bilateral suprascapular neuropathy was described following coronary artery bypass surgery, surmised to be due to surgical positioning (42).

Possible ischemic injury to the suprascapular nerve may occur from microemboli, originating from intimal damage in the axillary or suprascapular arteries, becoming trapped in the vasa nervorum of the suprascapular nerve (89). A case of brachial plexopathy associated with COVID-19 in a patient never placed in the prone position was reported, and a similar mechanism of nerve ischemia due to microthrombi from a hypercoagulable state in COVID-19 was proposed (41).

Nontraumatic causes include compression or entrapment, inflammation, and hereditary. The nerve can be compressed or injured in the suprascapular notch and the spinoglenoid notch. Studies from India and Japan have shown that suprascapular notch type 2 has a lower chance of suprascapular nerve entrapment compared to the other narrower types of suprascapular notch as in Rengachary types 3, 4, and 5 due to their anatomy (59). Narrowing of suprascapular notch occurs with aging (109). In some cases, the variation in the suprascapular notch is accompanied by a variation of the superior transverse scapular ligament.

Compression at the spinoglenoid notch, can be caused by cysts, neoplasms, and metastasis. Ganglion cysts are usually associated with posterior capsulolabral injury, lipomas, or varicose veins (30; 98). Cogar and colleagues have also reported a rare anatomic variant—the subclavius posticus muscle, which courses from the rib posterolaterally to the superior border of the scapula, causing suprascapular nerve compression (15).

Compression at the spinoglenoid notch can lead to more atrophy of the infraspinatus than supraspinatus (54). In patients with massive rotator cuff tears, suprascapular neuropathy induced more pronounced denervation and fatty degeneration of infraspinatus muscle than the supraspinatus muscle, partly due to the entrapment at the spinoglenoid notch, which is distal to the branch point to the supraspinatus (54).

Suprascapular nerve entrapment may be caused by supporting ligaments or blood vessels. Polguj and colleagues suggested a classification system of four types regarding the arrangement of the suprascapular nerve, artery, and vein at the suprascapular notch (82).

	• In type I, the artery runs above the superior transverse scapular ligament, whereas the nerve and the vein pass beneath the ligament.
	• In type II, only the nerve passes under the ligament, whereas both vessels cross over it.
	• In type III, the suprascapular artery, vein, and nerve pass under the ligament.
	• In type IV, all other variants of these structures are involved.

In a cadaveric study of 812 specimens, band-shaped ossification of the superior transverse scapular ligament was suggested as a potential cause of neuropathy, as it was associated with reduced cavity size below the ligament (83). Another cadaveric study of 31 specimens demonstrated that compression of the nerve is more likely to occur when the suprascapular artery, vein, and nerve pass through the notch (type III), rendering the suprascapular notch to become narrower (96). Podgorski and colleagues conducted a cadaveric dissection of 60 shoulders and suggested increased diameter of the suprascapular vein that occurs in addition to the suprascapular vein as a potential etiology of nerve compression (80). It has also been postulated that varicose veins result from hypertrophy of the superior transverse scapular ligament and obstruction at the suprascapular notch. This obstruction of the drainage of the suprascapular vein results in varicosities, which push the infraspinatus muscle posteriorly (52).

Podgórski and colleagues showed that suprascapular nerve injury can also be caused by the anterior coracoscapular ligament (ACSL), which extends below the superior transverse scapular ligament on the anterior side of the suprascapular notch (81). This ligament can reduce the available space for the suprascapular nerve and lead to nerve compression (05; 06). Alternatively, it has also been proposed that both the suprascapular notch vein and the anterior coracoscapular ligament can provide a mechanical barrier from the subscapular nerve and protect the nerve from compression against the STSL and from irritation by the bone borders of the notch (60). The suprascapular vein can also act as support for the nerve and protect it against hypermobility and microtrauma.

Lastly, disagreement exists regarding the presence or absence of the inferior transverse scapular ligament (spinoglenoid ligament) and its relationship to possible entrapment of the suprascapular nerve motor branch to the infraspinatus. Estimates of the presence of a spinoglenoid ligament range as low as 3% in men and women (23) to as high as 50% in women and 87% in men (51). In addition, a case of an ossified spinoglenoid ligament causing suprascapular entrapment at the spinoglenoid notch specifically after a scapular fracture and open reduction and internal fixation was described (17). These attributes may contribute to isolated infraspinatus suprascapular neuropathy occurring more frequently in men than in women.

Further potential sites of entrapment include (1) the level of the upper trunk of the brachial plexus in scalene muscle fascia, (2) in the fascia of the subclavius and omohyoid muscle, and (3) between the coracoid process and supraspinatus muscle. The suprascapular nerve may also be injured in full-thickness rotator cuff tears (97; 71; 20) and distal clavicle fractures (46). The association between rotator cuff tears and suprascapular neuropathy, however, has remained debatable. In a review of 49 shoulders with massive rotator cuff tears, Collin and colleagues revealed low chance of association of suprascapular neuropathy with rotator cuff tears (18). This showed redundancy of performing suprascapular nerve release when rotator cuff tears repair is performed.

Inflammation has been reported as one of the most common causes of isolated suprascapular nerve palsy. The study found that the majority of the patients presented with additional affected nerves, suggesting a more diffuse pattern of involvement. In many cases, the data support an inflammatory pathophysiology based on electrodiagnostic studies and MRI (63). In neuralgic amyotrophy or acute brachial neuritis, the suprascapular nerve was found to be involved in 97% of the cases studied by MRI (37). The axillary nerve was involved in 50% of the cases.

A relationship with both hereditary shoulder girdle neuropathy and hereditary neuropathy with liability to pressure palsies that have been genetically mapped to chromosome 17 has been reported (105).

Diagnostic workup

The diagnosis of suprascapular neuropathy can be difficult. Patients are often not diagnosed or treated until after a prolonged period, as evidenced by a mean time of 19 months from symptom onset to decompression (77).

Thorough history and examination are the key first steps in evaluating suprascapular neuropathy. A history of shoulder trauma or repetitive overuse resulting in posterolateral shoulder girdle pain should raise suspicion of suprascapular neuropathy. Examination findings of weakness of external rotation and initiation of abduction point to the possibility of suprascapular neuropathy. A cross-arm adduction test may indicate suprascapular neuropathy. The test is elicited by resting the hand of the affected extremity on top of the opposite shoulder indicated, which may result in localized pain over the acromioclavicular joint or tenderness over the suprascapular notch (99; 07).

Injection of the area of entrapment with local anesthetic or steroids for diagnostic purposes has been useful in suprascapular neuropathy (33).

Shoulder girdle x-rays may be helpful if bone or joint pathology is suspected. Standard shoulder girdle views may miss the suprascapular notch; angling the tube caudally helps fully visualize the suprascapular notch (26). CT scan can show a scapular fracture if it is not demonstrated on the plain film (10).

MRI is useful not only in delineating rotator cuff tears, but also in defining ganglion cysts, tumors, hematomas, schwannomas, or other clinically unsuspected masses (36; 91). A retrospective analysis indicated that muscle edema represented by increased muscle signal on T2-weighted fast fat-suppressed MRI images in the infraspinatus or supraspinatus was the most significant MRI sign of suprascapular neuropathy when compared to the “gold standard” EMG results (68). MRI evaluation of the spinoglenoid notch for distension can aid in the diagnosis of suprascapular neuropathy (52). A study compared the distance between the glenoid and the infraspinatus at the spinoglenoid notch (spinoglenoid notch distension size) as an indirect marker of venous engorgement in patients with suprascapular neuropathy (confirmed on EMG and treated with arthroscopic release) to normal shoulder controls and found that spinoglenoid notch distension is increased in patients with suprascapular neuropathy (52).

3T magnetic resonance neurography (MRN) has been proposed as a valuable diagnostic tool in clinically suspected cases of suprascapular neuropathy because it can directly demonstrate the nerve abnormality, as well as secondary denervation changes in muscles (09). Abnormalities were detected in the suprascapular nerve in 11 of 13 cases, and denervation findings were detected in the supraspinatus or infraspinatus muscles in 12 of 13 cases. Direct visualization and characterization of abnormalities in the nerve by MRI neurography require further optimization prior to routine clinical use. Currently, MRI muscle changes due to denervation are much more sensitive indicators of suprascapular neuropathy than MRI neurography. MRN, however, further helps distinguish the brachial plexus, rotator cuff, and cervical spine from suprascapular nerve pathologies by allowing concurrent assessment (01). Techniques using ferumoxytol in T2-weighted brachial plexus MR neurography provided robust vascular suppression and aided visualization of the suprascapular nerve in subjects without neuropathy (86).

A review of ultrasonography with broadband transducers of high frequency (greater than 10 MHz) and improved near-field resolution suggests this technique may also prove to be a useful adjunct in the diagnostic evaluation of suprascapular neuropathy (73). The suprascapular nerve can be visualized in the bottom of the suprascapular notch below the superior transverse scapular ligament, along with suprascapular artery and vein complex. With ultrasound in the coronal plane, one can visualize not only the presence but also the shape of the suprascapular notches, with high specificity for type 1 (depressed) and high sensitivity in recognizing type 3 (U-shaped) suprascapular notch (84).

Suprascapular neuropathy can be diagnosed by electrophysiologic testing in a subset of patients with specific clinical and radiographic findings (07). Electrodiagnostic evaluation is helpful in diagnosing suprascapular neuropathy in that it may reveal patterns of abnormality that not only help localize the lesion but also differentiate from more widespread processes and help to define acuity (95). Electromyography (EMG) and nerve conduction studies can be used for the following:

	• Confirm the diagnosis of suprascapular neuropathy in the setting of a suggestive history, physical examination, and imaging studies.
	• Test nerve function in a patient with supraspinatus or infraspinatus atrophy.
	• Evaluate for neuropathy when there is lingering shoulder pain of unclear cause.
	• Monitor nerve function before, during, and after the treatment of any of the causes of suprascapular neuropathy.

Nerve conduction studies for the suprascapular nerve were first described in 1964 and further defined in the early 1970s (38; 58). The techniques are simple to perform and easily added to the electrodiagnostician's armamentarium. Concentric needle electrodes are used to record compound motor action potentials in the infraspinatus and supraspinatus with surface stimulation at Erb point. Normal latency ranges of 1.7 to 3.7 ms for the supraspinatus and 2.4 to 4.2 ms for the infraspinatus.

During needle EMG, both supraspinatus and infraspinatus muscles should be examined to differentiate suprascapular notch lesions (both muscles are abnormal because the motor branches that innervate supraspinatus and infraspinatus muscles were divided proximal to the suprascapular notch) from spinoglenoid lesions (just the infraspinatus muscle is abnormal) (67). The muscles innervated by C5-C6 should also be examined to rule out brachial plexus lesions and radiculopathy. According to Moen and colleagues, the sensitivity and specificity of EMG and nerve conduction studies vary from 74% to 91% (76).

Reports have argued the relative merits of concentric electrode versus monopolar electrode versus surface electrode recordings (45; 67; 12). Most agree that needle electrodes are best for determining latencies. Amplitude data, side-to-side comparisons, and recording electrode placement are well described by Casazza and colleagues (12). Nonetheless, a study found the use of surface electrodes to be a reasonable option because the normal values are comparable to the values of previous studies that used the gold standard method (surface and depth electrodes) (08). In light of the nerve conduction study results and treatment outcome data noted in the prognosis section, it would be advisable to use surface electrode measurements followed by needle electrode nerve conduction studies to maximize the accuracy of latency and amplitude data.

Side-by-side comparison of compound muscle action potential (CMAP) amplitude and latency is a valid approach to determine unilateral abnormalities. Of note, CMAP amplitude difference of up to 50% and distal latency difference of 20% in side-to-side values can be normal (08). These findings imply that a difference of more than 50% in CMAP amplitudes can distinguish the affected from the non-affected side.

Another use of electrodiagnostic testing is to monitor suprascapular nerve recovery after treatment. In a prospective study, pre- and postoperative EMG was performed in nine patients with a paralabral cyst to evaluate nerve regeneration (31). All patients showed complete electrophysiological recovery from axonal regeneration of the suprascapular nerve after surgical decompression.

Management

The first approach to suprascapular neuropathy treatment is nonsurgical if no mass lesions are identified. Counseling is provided to avoid precipitating or aggravating positions and motions. A physical therapy program is initiated, with focus on gradual strengthening of the shoulder girdle, rotator cuff, and periscapular muscles as well as stabilization of the scapula. Supervised exercise and eventual self-care programs are implemented (72). No studies provide evidence of medication utility beyond symptomatic relief.

Blind suprascapular nerve blockade with bupivacaine and methylprednisolone is a treatment option for the management of both acute and chronic pain in suprascapular neuropathy, but the limitations of the procedure include some possible complications such as pneumothorax or injury to the neighboring vascular structures. Ultrasound visualization of the related anatomic part and the needle itself may improve the success of the procedure and lower the complication rates (39). In addition to the suprascapular nerve injection, transcutaneous electrical nerve stimulation or peripheral nerve stimulation, cryoneurolysis, and pulsed radiofrequency are potential minimally invasive treatment options when no structural lesions are identified (66).

Controversy exists regarding the length of time nonoperative treatment is continued. Often, if conservative management has failed or 6 months have passed, then surgical approaches are considered (72; 33; 21). Le Hanneur and colleagues presented a unique case of suprascapular nerve palsy lasting for 2 years. At surgery, the suprascapular nerve was found to be partially sectioned by the transverse scapular ligament. This case highlights the utility of surgical exploration for suprascapular neuropathy of unknown etiology (64).

Several approaches to surgically decompress the suprascapular nerve (including posterior, anterior, and superior) as well as bone resection around the suprascapular or spinoglenoid notch have been described. Most reports indicate a preference for posterior decompression of the suprascapular nerve without bone resection (14; 85; 16).

Most surgical procedures for suprascapular neuropathy involve sectioning the suprascapular or spinoglenoid ligament to decompress the nerve. Surgery is usually followed by rapid postoperative mobilization to tolerance. Suprascapular nerve transfer techniques have also been described (75).

Arthroscopic approaches can be used for suprascapular nerve decompression, especially when cystic entrapment of the nerve is involved (107; 106). Lafosse and colleagues showed that arthroscopic release of the suprascapular nerve can be performed safely and effectively with improvement in electromyographic findings, pain relief, and function (61). Arthroscopic decompression has the benefit of simultaneously diagnosing with superior visualization of the neurovascular structures and addressing intra-articular and/or subacromial pathology with minimizing morbidity and pain (79). Clavert and Thomazeau reported that arthroscopic nerve release for suprascapular nerve entrapment is a preferred procedure in patients with paralabral cysts with favorable outcomes in terms of pain, functionality, mobility, and strength (13). Arthroscopic suprascapular nerve release was then studied on a larger scale. Davis and colleagues retrospectively reviewed 112 patients with confirmed suprascapular neuropathy undergoing suprascapular nerve release and reported that there was a significant reduction in pain and a significant improvement in both supraspinatus and infraspinatus strength on manual muscle test clinically without major complications (22). However, a concurrent review by von Knoch and colleagues indicated that arthroscopic decompression of the suprascapular nerve in the suprascapular notch often does not lead to a complete recovery of the supraspinatus and infraspinatus muscle strength (in 60% of cases) or to a reversal of the structural (fatty) degeneration of the muscle bellies on MRI, especially in the setting of proximal compression (101).

Radiological cyst aspiration was, however, reported to be associated with a failure and recurrence rate as high as 75% to 100%. In a 5-year retrospective review of the outcome of suprascapular neuropathy, Hill and colleagues made an observation that the presence of cyst and rotator cuff tears are important occurrences, indicating surgical treatment (43). When large or massive rotator cuff tears were associated with suprascapular neuropathy, combined arthroscopic release of the superior transverse scapular ligament and rotator cuff repair did not produce statistically significant improved outcomes compared with repair of the rotator cuff alone (90).

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All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Jina Rachel Park MD

Dr. Park of Neurology Group of Bergen County has no relevant financial relationships to disclose.
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Randolph W Evans MD

Dr. Evans of Baylor College of Medicine received honorariums from Abbvie, Amgen, Biohaven, Impel, Lilly, and Teva for speaking engagements.
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Former Authors

Howard W Sander MD
Harold R Smith MD, Syeda Maria Muzammil, Sameera Salman Ghauri MBBS, and Kazim Sheikh MD

Patient Profile

Age range of presentation: 6 to 65+ years
Sex preponderance: Male>female
Heredity: none
Population groups selectively affected: Amateur and professional athletes in baseball, volleyball, weightlifting, swimming, diving, tennis, canoeing, backpacking
Occupation groups selectively affected: Amateur and professional athletes

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Suprascapular neuropathy

Associated Disorders

Shoulder rotator cuff tear
Traumatic shoulder injury

Differential Diagnosis

rotator cuff dysfunction
cervical radiculopathy
brachial plexus problems
diffuse peripheral neuropathy
shoulder girdle pathologies
- acromioclavicular joint disease
- glenohumeral joint disease
- adhesive capsulitis
- biceps tendonitis
- bursitis
- Pancoast tumor

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Epidemiology

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Suprascapular neuropathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

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NF2-related schwannomatosis

Familial dysautonomia

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Toxic and nutritional deficiency optic neuropathies

This is an article preview.
Start a Free Account
to access the full version.