Suprascapular Neuropathy

United States statistics

Although the true incidence is unknown, several authors believe that suprascapular neuropathy is underreported. Suprascapular neuropathy was thought to be a diagnosis of exclusion given the similar clinical presentation as glenohumeral joint and rotator cuff pathology. However, increasing awareness and improvement in diagnostic modalities has resulted in increasing diagnosis.[27, 28] The condition has been described in various athletes, including weight lifters and baseball players, although the prevalence of suprascapular neuropathy appears to be highest among volleyball players.[1, 4, 7, 9, 11, 12, 13, 15, 18, 19, 21, 29, 30, 31]  It occurs primarily in persons aged younger than 40 years.[32]

Studies have reported that 13-33% of elite volleyball athletes have signs of suprascapular neuropathy.[27, 7, 9, 11, 12, 13, 15, 18, 19, 31] This observation lends credence to the term “volleyball shoulder.”

In addition to overhead athletes, some other higher risk populations for suprascapular neuropathy include patients with massive rotator cuff tears resulting in fatty infiltration of the muscle. Patients with posterior labral tears resulting in paralabral cysts that can compress the nerve are also a higher risk population.[27]

The suprascapular nerve (SSN) is a mixed nerve that provides the motor innervation of the supraspinatus and infraspinatus muscles and the sensory and proprioceptive innervation of the posterior aspect of the glenohumeral joint, as well as the acromioclavicular joint, subacromial bursa, and scapula.[33, 34, 35, 36] This nerve carries afferents from approximately 70% of the shoulder joint. The nerve arises from the upper trunk of the brachial plexus and is composed predominantly of C5-C6 level fibers. Some authors suggest that the nerve may also receive contributions from the fourth cervical nerve root in as many as 25% of people. Although the suprascapular nerve is a mixed nerve, it typically carries no cutaneous afferent fibers. The SSN is thought to carry cutaneous afferent fibers in only 15-25% of the general population.

In its initial course, the SSN courses posterior and parallel to the inferior belly of the omohyoid muscle and anterior to the trapezius muscle in the posterior triangle of the neck. The nerve then passes dorsally through the suprascapular notch, where it is retained by the transverse scapular ligament, into the suprascapular fossa, where 2 motor branches to the supraspinatus muscle originate. Just proximal to the suprascapular notch, the SSN gives off the superior articular branch, which travels with its fellow nerve through the notch before proceeding laterally to innervate the acromioclavicular joint and its associated bursa and the coracoclavicular and coracohumeral ligaments (see below).

Cadaveric studies reveal that the suprascapular notch may be either U -shaped or V -shaped, and some physicians believe that this anatomic variation may be related to an individual’s predisposition to SSN entrapment at this level. After supplying the supraspinatus, the nerve subsequently travels inferolaterally to wrap around the spine of the scapula at the spinoglenoid notch.

In roughly 15-80% of cadavers studied, the spinoglenoid (inferior transverse scapular) ligament traverses this notch, creating a tunnel through which the nerve travels. Interestingly, the spinoglenoid ligament is reportedly more common in males than in females; this observation may provide an anatomic basis for any possible sex-related predominance in the prevalence of volleyball shoulder. The inferior articular branch, which contains afferents from the posterior glenohumeral joint capsule, joins the suprascapular nerve at the level of the spine of the scapula. After exiting the fibro-osseous tunnel at the spinoglenoid notch the nerve turns inferomedially before arborizing into 3 or 4 terminal branches that supply the infraspinatus muscle.

Suprascapular nerve entrapment or injury can occur at the suprascapular notch or the spinoglenoid notch. The resulting clinical presentation depends on the location of the suprascapular neuropathy. Selective involvement of the suprascapular nerve at the spinoglenoid notch level results in the isolated atrophy and weakness of the infraspinatus muscle that has been described as an infraspinatus syndrome. The available literature suggests that the most common site of entrapment among volleyball athletes is the spinoglenoid notch.[12, 37]

Several mechanisms have been proposed for suprascapular neuropathy. These mechanisms include repeat traction and microtrauma, direct compression of the nerve by surrounding normal anatomy or compression by pathologic space occupying lesions, and ischemia of the nerve from repetitive trauma. However, general agreement is that the suprascapular nerve may be vulnerable to injury due to compressive forces or repetitive distraction.

One mechanism is a traction injury that overhead athletes can be susceptible to, given the great amount of motion at the shoulder. The importance of the scapula in the throwing motion and other overhead sport-specific skills is now well appreciated. As the scapula protracts and retracts with functional use of the upper limb, some traction of the suprascapular nerve can be expected to occur at one or both notches through which it traverses. This concept forms the basis of the “sling effect," which proposes that, in certain functional positions of the upper limb, the suprascapular nerve is exposed to damaging sheer stress in the suprascapular notch. Similar reasoning leads to the prediction that the nerve is vulnerable to traction injury as it bends around the spine of the scapula at the spinoglenoid notch.

Some authors have proposed that individuals in whom the suprascapular nerve angles sharply around the spinoglenoid notch may be particularly prone to this mechanism of injury. The so-called "SICK scapula" (defined by Burkhart et al as scapular protraction, inferior border prominence, coracoid tightness, and scapular dyskinesis) that occurs in adaptive response to chronic shoulder overuse and functional instability may also theoretically contribute to the increased tension on the suprascapular nerve via the sling effect.[6]

Demirhan et al reported that the spinoglenoid ligament, when present, inserts into the posterior glenohumeral capsule.[38] They also observed that the ligament becomes taut when the ipsilateral upper limb is adducted across the body or internally rotated; this motion results in traction of the suprascapular nerve at the spinoglenoid notch. Other possible mechanisms in which the suprascapular nerve may be compromised include Sandow and Ilic’s proposal that the suprascapular nerve nerve is vulnerable to direct compression by the medial border of the spinatus tendons at the spinoglenoid notch when the upper limb is abducted and externally rotated.[18] This mechanism would appear to be a further manifestation of posterior (or internal) impingement.

Ferretti, who has written extensively about volleyball shoulder, hypothesized that the mechanism of selective injury to the terminal portion of the suprascapular nerve in volleyball players is traction on the nerve due to repetitive, sudden, eccentric activation of the infraspinatus during the deceleration phase of the floater serve.[12, 15]

Another mechanism of injured is due direct compression on the nerve by a space-occupying lesion. Several studies have reported that the suprascapular nerve may be compressed in the vicinity of the spinoglenoid notch by ganglion cysts arising from the glenohumeral joint.[24, 37, 39, 40, 41] These ganglion cysts, like Baker cysts that occur in the popliteal fossa after meniscal degeneration or injury, are likely to be the consequence of an injury to the posterior glenoid labrum with resultant leakage of synovial fluid.[42]

Finally, some investigators have also proposed that suprascapular neuropathy can result from ischemia caused by migration of posttraumatic microemboli from the suprascapular artery (which generally follows a course parallel to the companion nerve) to the vasa nervorum.

Sports that place a substantial load on the athlete’s shoulder when the upper limb is in an overhead or abducted and externally rotated position may precipitate this condition. The site of suprascapular neural entrapment determines whether the infraspinatus muscle alone or both the supraspinatus and infraspinatus muscles are affected.

Although sports-related overuse mechanisms of suprascapular nerve injury are the most common causes, the SSN can also be damaged as a result of direct trauma as well as iatrogenic factors. The relationship of the nerve to the clavicle makes it vulnerable to injury after a clavicular fracture occurs. Surgical procedures involving the shoulder (eg, Bankhart repair) can place the nerve at risk for either direct injury or indirect injury. Interestingly, suprascapular neuropathy has also been reported to occur after positioning patients for spinal surgery.

Other diagnoses should be considered. Most commonly, the clinician diagnoses rotator cuff tendinopathy and prescribes a conservative treatment program. Because the rehabilitation programs for rotator cuff tendinopathy and infraspinatus syndrome are similar, in many (perhaps most) instances, the patient's condition improves, and the correct diagnosis goes unrecognized. Delayed-onset muscular soreness may be present, but this soreness is not expected to progress over 3 weeks. Rather, symptoms of delayed-onset muscular soreness tend to spontaneously resolve over 7-10 days.

As discussed earlier, the prognosis for a favorable clinical outcome is good. At the time of diagnosis, affected athletes report surprisingly little functional limitation. According to the literature, most cases respond favorably to either conservative treatment programs or, when indicated, surgical intervention. Furthermore, most athletes were able to return to their previous level of sports participation following therapeutic intervention.

Although knowledge of the clinical symptom complex has improved since Kopell and Thompson first reported shoulder pain as the result of suprascapular nerve injury in 1959, from a practical standpoint, the diagnosis of suprascapular neuropathy remains largely a diagnosis of exclusion unless the clinician remains alert to the diagnostic possibility when the affected athlete initially presents for treatment.

The typical patient is a young overhead athlete who reports vague posterior shoulder pain. Although, the athlete can have painless atropy presenting as supraspinatus and/or infraspinatus weakness, depending on the location of the suprascapular nerve.

Because of the anatomy (see Functional Anatomy), more distal nerve injuries are often relatively painless. In particular, nerve injuries at the spinoglenoid notch that result in selective denervation of the infraspinatus muscle may be insidious in their onset due to the relative lack of pain. In Ferretti et al's series, elite volleyball players with isolated atrophy of the infraspinatus generally did not report any pain or sports-related functional disability.[12]

Based on anatomic considerations, athletes with more proximal lesions of the suprascapular nerve that affect both the supraspinatus and infraspinatus muscles are more likely to have pain and symptom-limited function than are individuals with distal nerve lesions that affect only the infraspinatus.

Although case reports of bilateral involvement exist, symptoms are typically unilateral and involve the dominant side.

Male athletes account for most of the cases reported in the literature; however, Ferretti et al reported one series of 38 athletes in which the incidence was approximately equal among males and females.[12]

More often than not, the pain (when present) is described as a deep, dull, aching discomfort.

Activities that involve overhead motions or sport-specific skills may exacerbate symptoms. Diagnostic signs may include weakness and compromised endurance in performing overhead, sport-specific skills.

Genetic factors undoubtedly play a role in the predisposition and susceptibility of individual athletes to suprascapular neuropathy, but the specific factors that are involved have yet to be elucidated.

Atrophy of the supraspinatus and/or infraspinatus muscles may be present on the physical examination, depending on the site of the nerve entrapment (see below).

Note that supraspinatus involvement may be frequently overlooked because of the bulk of the overlying trapezius.

Manual muscle testing may reveal relative weakness of ipsilateral shoulder abduction (a function of the supraspinatus muscle in addition to the deltoid muscle) and/or weakness of external rotation (a function of the infraspinatus muscle in addition to the teres minor muscle).

The athlete may report worsening pain with cross-body adduction or internal rotation[28]  of the ipsilateral upper limb.

Pressure applied over the suprascapular or spinoglenoid notches may elicit pain. Tenderness may between the clavicle and the spine of the scapula or deep and posterior to the acromioclavicular joint.[27]

Muscle stretch reflexes are unaffected by this condition.

Rarely, cutaneous appreciation of sensory modalities may be affected in an approximate axillary nerve distribution.

When suprascapular neuropathy is suspected, radiography should be performed. In addition to standard views, suprascapular notch and Stryker views can be ordered.[27, 28] In suprascapular neuropathy, conventional radiographic findings in the shoulder girdle are typically unremarkable in the absence of bony trauma that may account for the condition (eg, fractured clavicle). Conventional radiography of the cervical spine is warranted if concern exists about a possible radicular etiology for the patient’s symptoms.

Shoulder MRI may reveal supraspinatus or infraspinatus muscle edema in acute cases and atrophy with fatty replacement in more chronic cases.[43]

MRI may also reveal a ganglion cyst or other mass such as a paralabral cyst with resultant suprascapular nerve compression.[29, 44, 45]

3T magnetic resonance neurography has been shown to be a valuable diagnostic tool in clinically suspected suprascapular neuropathy. It can demonstrate the nerve abnormality and any secondary muscle denervation changes.[46, 47]

Ultrasonography is a reasonable, less expensive initial imaging option.[43] The suprascapular nerve can be identified under ultrasound, and can be used to screen for parascapular ganglia or masses.[41] Spinoglenoid notch cysts can be identified with ultrasound, particularly in a lean athletic population.[42]

The clinical diagnosis may be confirmed with electrodiagnostic testing and has been the criterion standard for diagnosis of suprascapular neuropathy. Electromyography and nerve conduction velocity tests have from 70% to more than 90% sensitivity in detecting muscle fiber denervation.[32, 48]

The normal distal motor latencies to the supraspinatus muscles during stimulation at the Erb point are 2.7 msec ± 0.5 and and to the infraspinatus muscles, 3.3 msec ± 0.5.

Side-to-side differences greater than 0.4 msec suggest focal entrapment of the SSN or other neural injury.

Electromyography may reveal the following:

• Evidence of denervation, such as positive sharp waves and fibrillation potentials

• Motor unit recruitment abnormalities, such as motor unit dropout in acute cases and polyphasic motor unit action potentials in cases of long-term neuropathy. (This latter finding suggests a degree of reinnervation.)

• The physical examination and electrodiagnostic test results should enable the clinician to rule out underlying cervical radiculopathy, brachial plexopathy, or axillary neuropathy and to localize the site of SSN impairment (see Differentials).

Rehabilitation Program

Physical Therapy

The treatment for suprascapular neuropathy depends on the cause, severity, and duration of the symptoms; degree of functional disability; and patient preference. In the absence of specific compressive lesions, conservative initial treatment for suprascapular neuropathy is recommended. The natural history of suprascapular neuropathy is typically favorable, and most cases respond to conservative care within 6 months.

In athletes without pain or limitations in the performance of sport-specific skills, a simple program of exercises for scapular stabilization/mobilization and rotator cuff strengthening is probably reasonable. Such a program should prevent not only progression of the condition, but also secondary impingement of the rotator cuff.

A similar program is recommended in symptomatic athletes; however, activity modification to limit symptoms during the acute phase is warranted. The athlete should then progress through a series of functionally oriented exercises designed to restore flexibility and proprioception, scapular control, and balanced rotator cuff strength and endurance. This program should culminate in the resumption of sport-specific skills.

The use of passive modalities (eg, superficial or deep heat application, iontophoresis) and/or injection procedures for pain relief (see Other Treatment) may help symptomatic athletes make the transition to such exercise programs.

Surgical Intervention

Should conservative care fail to resolve the symptoms and allow the athlete to return to the sport activity, surgical intervention may be therapeutic. A degree of controversy exists in the literature because some authors believe that early surgical intervention is the treatment of choice.

Described surgical treatment procedures for suprascapular neuropathy unrelated to a space-occupying lesion include simple widening of the spinoglenoid notch or suprascapular notch, depending on the site of nerve injury. In one retrospective review of 3 cases of idiopathic infraspinatus syndrome refractory to conservative care, subsequent surgery was beneficial in 2 cases.

Some authors argue that documented compressive lesions of the SSN (eg, ganglia) should be promptly resected because of the high failure rate of nonsurgical care in this situation. Any accompanying labral pathology can be simultaneously repaired, if indicated. Both open and arthroscopic procedures have been described.[49]

In general, surgical outcomes reported in the literature are good. Patients in whom the condition is diagnosed promptly and treated with early surgical decompression seem to have a better likelihood of regaining full muscular strength and bulk.[50, 51] The patient should participate in a postoperative program of rehabilitation and/or functional restoration to ensure the return of balanced strength and flexibility.

Other Treatment

In addition to the approaches discussed above (see Physical therapy and Surgical intervention), other nonsurgical treatment options include suprascapular nerve blocks.[52, 53, 54] Because such blocks have been used to manage perioperative shoulder pain and adhesive capsulitis in addition to other painful shoulder conditions, the diagnostic use and specificity of such blocks is debatable. Nevertheless, blocks may provide symptomatic relief, thereby permitting the patient to more fully participate in a rehabilitation program.

The injection of an anesthetic and/or corticosteroid mixture into the suprascapular notch may provide temporary benefit. Given the variability in sensitivity and specificity of electromyography and nerve conduction studies,[28] injections can be an important diagnostic tool to confirm that the pain is in fact from suprascapular neuropathy.

Several studies have reported good clinical results with ultrasound-guided paralabral cyst aspiration; thus, it can be considered as an alternative to operative management.[28, 42] However, cyst recurrence rate has been reported between 75-100%.[28]

In select cases, radiofrequency suprascapular neuropathy ablative procedures may provide longer symptomatic relief. Several injection approaches to minimize the inherent risk of pneumothorax are described. However, such interventions are purely palliative and do not alter or address the underlying mechanism of suprascapular neuropathy.

Rehabilitation Program

Physical Therapy

The goal of the recovery phase of a rehabilitation program is to maintain active range of motion in the shoulder girdle while helping the athlete progress through a strengthening program designed to improve scapular stabilization and strengthen the rotator cuff. Interventions include concentric and eccentric isotonic exercises that emphasize sport-specific movement patterns. Eventually, the patient can progress to upper limb plyometric exercises.

Rehabilitation Program

Physical Therapy

On the basis of reports in the available literature, nonsurgical care should result in a satisfactory outcome in most idiopathic cases within 6-8 months. Most reports indicate that patients who are treated conservatively are generally able to resume their previous level of function, including high-level sports participation.

Longitudinal follow-up findings suggest that muscular atrophy is generally not reversible to a significant extent, although symptoms of pain may improve with time. The athlete may return to play when he or she is able to perform appropriate skills without provoking symptoms.

Ideally, the rehabilitation program should extend beyond the mere resolution of symptoms to address the other facets of Kibler's "vicious cycle." This program should include an analysis of the athlete's technique to determine if any flaws or compensatory biomechanical changes need to be corrected to minimize the risk of recurrent injury or overload of other soft tissues further down the kinetic chain. (A formal discussion of the vicious cycle is beyond the scope of this article. For further information, the reader is referred to Kibler WB, Herring SA, Press JM, Lee PA, eds. Functional Rehabilitation of Sports and Musculoskeletal Injuries. Gaithersburg, Md: Aspen Publishers; 1998.[3] )

Most individuals with suprascapular neuropathy are asymptomatic and compete with little to no discernible performance deficit. This observation complicates the issue of how to handle the return-to-play decision in an athlete who is asymptomatic and whose physical examination incidentally reveals suprascapular neuropathy.

In practical terms, elite athletes (in whom the prevalence is highest) can probably continue to compete while they are concurrently participating in a rehabilitation program. However, to minimize the progression of the condition, the extent to which the athlete performs overhead skills during practice should be limited.

In symptomatic athletes, a more restrictive course seems reasonable. Once the athlete can perform sport-specific skills (eg, spiking and blocking in volleyball) in a pain-free manner, he or she can return to play. Athletes who undergo surgical decompression should participate in an appropriate postoperative rehabilitation program to restore their strength, flexibility, and endurance before returning to play.

In patients with dynamic primary compression, the overall outcomes of conservative management are good. Pain relief is achieved in more than 80% of patients, and nearly all can return to sport activities within 3 months.[32]

Ferretti proposed that suprascapular neuropathy in volleyball players is related to performance of the floater serve. If so, the incidence of volleyball shoulder is expected to decrease because, with the advent of the jump serve or spike serve, the floater serve has become less popular.

To the author's knowledge, no definitive study findings implicate specific spiking styles in suprascapular neuropathy; thus, providing technical advice about biomechanics to volleyball athletes with suprascapular neuropathy is difficult. Additional considerations remain unanswered; for example, the duration and magnitude of the load that is sufficient to precipitate volleyball shoulder through chronic overuse is unknown. Furthermore, the extent to which a SICK scapula is associated with the incidence of suprascapular neuropathy deserves further investigation.

To the author's knowledge, enteral pharmaceutical intervention to relieve symptoms associated with infraspinatus syndrome has not been studied or reported in the literature. For individuals with pain, a trial of nonsteroidal anti-inflammatory drugs early in the course of treatment seems reasonable. Alternatively, a trial of the gamma aminobutyric acid (GABA) analogue gabapentin may provide some analgesia.

Class Summary

The use of certain antiepileptics (AEDs), such as the GABA analogue Neurontin (gabapentin), is helpful in some cases of neuropathic pain. Although unstudied, a trial of an AED agent might provide some analgesia in symptomatic athletes with suprascapular neuropathy.

Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, the exact mechanism of action is unknown.

Structurally related to GABA but does not interact with GABA receptors.

Titration to effect can take place over several days (eg, 300 mg on day 1, 300 mg bid on day 2, 300 mg tid on day 3).

Class Summary

Cyclooxygenase (COX)-2 inhibitors have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action may be inhibition of COX activity and prostaglandin synthesis. Others may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Celecoxib (Celebrex)

Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced by pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, the COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased when compared with nonselective NSAIDs. Seek the lowest dose for each patient.

Neutralizes circulating myelin antibodies through anti-idiotypic antibodies; downregulates proinflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; and may increase CSF IgG (10%).

Has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.