eMedicine Specialties > Sports Medicine > Neurological

Suprascapular Neuropathy

Jonathan C Reeser, MD, PhD, Department of Physical Medicine and Rehabilitation, Marshfield Clinic

Updated: Apr 16, 2008

Introduction

Background

Athletes who participate regularly in overhead sports frequently report shoulder pain. Sports such as baseball, volleyball, and tennis demand skills that place substantial load on the athlete’s shoulder when the upper limb is in an overhead or abducted and externally rotated position.^{1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21} Epidemiologic studies have demonstrated that athletes who participate in these and other overhead sports are at higher risk for overuse injuries of the upper limb in general and overuse injuries of the shoulder in particular, including rotator cuff tendinopathy and attritional injury to the glenoid labrum.^{6,22,23,24,25,26} One often overlooked cause of shoulder pain among such athletes is infraspinatus syndrome.

Infraspinatus syndrome is defined as a condition of frequently painless atrophy of the infraspinatus muscle caused by suprascapular neuropathy. The syndrome typically causes symptoms that mimic those of rotator cuff tendinopathy, and the diagnosis may be overlooked until the symptomatic athlete fails to have a therapeutic response to a traditional rotator cuff treatment program.

For excellent patient education resources, visit eMedicine's Osteoporosis and Bone Health Center. Also, see eMedicine's patient education article Shoulder and Neck Pain.

Related eMedicine topics:
Nerve Entrapment Syndromes
Overuse Injury
Rotator Cuff Injury
Shoulder Impingement Syndrome

Related Medscape topics:
Resource Center Arthritis
Resource Center Exercise and Sports Medicine

Frequency

United States

Although the true incidence is unknown, several authors believe that infraspinatus syndrome is underreported. Although the condition has been described in a variety of athletes, including weight lifters and baseball players (and has been reported as an occupational injury among newsreel cameramen), the prevalence of infraspinatus syndrome appears to be highest among volleyball players.^{1,4,7,9,11,12,13,15,18,19,21,22,27,28,29}  Studies have reported that 13-45% of elite volleyball athletes have signs of suprascapular neuropathy.^{7,9,11,12,13,15,18,19,21,29} This observation lends credence to the term “volleyball shoulder.”

Functional Anatomy

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.^30,31,32,33 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 Image 1).

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.

Sport-Specific Biomechanics

Anatomic considerations suggest that at least 2 sites of potential SSN entrapment exist: the suprascapular notch and the spinoglenoid notch. Although the distribution of injury at these 2 sites varies in published case series, findings in the available literature suggest that the most common site of entrapment among volleyball athletes is the spinoglenoid notch.^12,34 Selective involvement of the SSN at this level results in the isolated atrophy and weakness of the infraspinatus muscle that characterizes infraspinatus syndrome. Interestingly, no consensus about the precise mechanism of suprascapular neuropathy exists. There is, however, general agreement that the SSN (like other peripheral nerves) may be vulnerable to injury due to compressive forces or repetitive distraction.

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 SSN can be expected to occur at 1 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 SSN 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 SSN 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 SSN via the sling effect.⁶

Demirhan et al reported that the spinoglenoid ligament, when present, inserts into the posterior glenohumeral capsule.³⁵ 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 SSN at the spinoglenoid notch. Other possible mechanisms in which the SSN may be compromised include Sandow and Ilic’s proposal that the SSN 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 SSN 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.^12,15,21

Several studies have reported that the SSN may be compressed in the vicinity of the spinoglenoid notch by ganglion cysts arising from the glenohumeral joint.^{25,34,36,37,38} 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. 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.

The shoulder joint, or glenohumeral joint, is the most mobile joint in the human body.³ Unfortunately, this mobility comes at the cost of stability, of which the bony components in the joint provide little. Ligamentous structures and the fibrocartilaginous glenoid labrum provide additional static stability, particularly at the extremes of glenohumeral motion. The supraspinatus and infraspinatus muscles are part of the rotator cuff, which dynamically stabilizes the shoulder joint through a precise system of force couples and agonist-antagonist coactivation, keeping the humeral head centered in the glenoid socket. SSN dysfunction disturbs this mechanism and could potentially result in proximal migration and elevation of the humeral head, with consequent secondary impingement of the supraspinatus tendon beneath the coracoacromial ligament.

Related eMedicine topics:
Multidirectional Glenohumeral Instability
Nerve Entrapment Syndromes
Shoulder Impingement Syndrome

Related Medscape topics:
Resource Center Arthritis
Resource Center Exercise and Sports Medicine

Clinical

History

• Although knowledge of the clinical symptom complex has improved since Kopell and Thompson first reported shoulder pain as the result of SSN injury in 1959, from a practical standpoint, the diagnosis of infraspinatus syndrome 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 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, but Ferretti et al reported one series of 38 athletes in which the incidence was approximately equal among males and females.¹²
• More often that 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.
• 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 upon anatomic considerations, it is reasonable to predict that athletes with more proximal lesions of the SSN 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.
• 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.

Physical

• Atrophy of the supraspinatus and/or infraspinatus muscles may be present on the physical examination, depending on the site of the nerve entrapment (see Image 1).
• 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 of the ipsilateral upper limb.
• Pressure applied over the suprascapular or spinoglenoid notches may elicit pain.
• Muscle stretch reflexes are unaffected by this condition.
• Rarely, cutaneous appreciation of sensory modalities may be affected in an approximate axillary nerve distribution.

Causes

• 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.
  • Suprascapular neuropathy causes infraspinatus syndrome.
  • 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 SSN 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, SSN 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.

Related eMedicine topics:
Clavicle Fractures
Clavicular Injuries
Rotator Cuff Injury

Related Medscape topics:
Resource Center Exercise and Sports Medicine
Resource Center Fracture

Differential Diagnoses

Cervical Disc Injuries
Cervical Radiculopathy
Rotator Cuff Injury
Shoulder Impingement Syndrome
Superior Labrum Lesions

Other Problems to Be Considered

Adhesive Capsulitis
Axillary neuropathy
Degenerative arthritis of the acromioclavicular or glenohumeral joints
Ganglion or cyst from the glenohumeral joint (which may compress the suprascapular nerve)
Idiopathic upper trunk brachial plexopathy (ie, Parsonage-Turner syndrome)
Stinger injury (ie, neurapraxic injury of the C6 nerve root or upper trunk of the brachial plexus)
Stress fractures of the first ribs or scapula
Subacromial bursitis
Tumors (including Pancoast tumor)

Workup

Imaging Studies

• In infraspinatus syndrome, 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 magnetic resonance imaging (MRI) may reveal supraspinatus or infraspinatus muscle edema in acute cases and atrophy with fatty replacement in more chronic cases.
• MRI may also reveal a ganglion cyst or other mass with resultant suprascapular nerve compression.^27,39,40
• Ultrasonography is a reasonable, less expensive initial imaging option that can be used to screen for parascapular ganglia or masses.³⁸

Other Tests

• The clinical diagnosis may be confirmed with electrodiagnostic testing.
• 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 and Other Problems to Be Considered).

Related eMedicine topics:
Electrophysiology
Motor Unit Recruitment in EMG

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

The treatment for infraspinatus syndrome 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 infraspinatus syndrome is recommended. The natural history of idiopathic 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 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.

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. 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 SSN blocks.^41,42,43 Because such blocks have been used to manage perioperative shoulder pain and adhesive capsulitis in addition to other painful shoulder conditions, the diagnostic utility 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 admixture into the suprascapular notch may provide temporary benefit. In select cases, radiofrequency SSN 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 they do not alter or address the underlying mechanism of suprascapular neuropathy.

Recovery Phase

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.

Maintenance Phase

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 )

Medication

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.

Antiepileptics

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).

Dosing

Adult

300 mg PO tid

Pediatric

Not established

Interactions

Antacids may significantly reduce bioavailability (administer at least 2 h after antacids); may significantly increase norethindrone levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in the presence of severe renal disease

Analgesic, Cox-2 Inhibitor

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.

Dosing

Adult

100 mg PO bid or 200 mg PO qd

Pediatric

Not recommended

Interactions

Coadministration with fluconazole may cause an increase in celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause fluid retention and peripheral edema; caution in patients with compromised cardiac function, hypertension, conditions predisposing to fluid retention; caution in the presence of severe heart failure and hyponatremia because circulatory hemodynamics may deteriorate; NSAIDs may mask the usual signs of infection; caution in the presence of existing controlled infections; evaluate therapy when symptoms or laboratory results suggest liver dysfunction

Follow-up

Return to Play

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.

Related Medscape topic:
Resource Center Exercise and Sports Medicine

Prevention

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.

Prognosis

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.

Miscellaneous

Medicolegal Pitfalls

• A thorough examination and a reasonably high degree of clinical suspicion are required to diagnose suprascapular neuropathy.
• Sports medicine practitioners should include suprascapular neuropathy in their differential diagnosis of shoulder pain (see Differentials and Other Problems to Be Considered), particularly in volleyball players or in athletes with rotator cuff tendinopathy in whom the pain fails to respond to initial attempts at treatment.

Related Medscape topic:
Resource Center Medical Malpractice and Legal Issues

Multimedia

Media file 1: Clinically relevant anatomy of the subscapular nerve (SSN) and the structures it innervates. The SSN is vulnerable to entrapment at the superior scapular notch and the spinoglenoid notch, beneath the inferior transverse scapular ligament. The inset depicts the clinical appearance in an individual with predominantly right-sided atrophy of the infraspinatus muscle due to suprascapular neuropathy.

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Keywords

volleyball shoulder, suprascapular neuropathy, shoulder pain, infraspinatus muscle, rotator cuff tendinopathy, suprascapular nerve, infraspinatus syndrome

Contributor Information and Disclosures

Author

Jonathan C Reeser, MD, PhD, Department of Physical Medicine and Rehabilitation, Marshfield Clinic
Jonathan C Reeser, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Sports Medicine, American Medical Association, Association of Academic Physiatrists, Phi Beta Kappa, Physiatric Association of Spine, Sports and Occupational Rehabilitation, and State Medical Society of Wisconsin
Disclosure: Nothing to disclose.

Medical Editor

Leslie Milne, MD, Assistant Clinical Instructor, Department of Emergency Medicine, Harvard University School of Medicine
Leslie Milne, MD is a member of the following medical societies: American College of Sports Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

CME Editor

Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

Chief Editor

Sherwin SW Ho, MD, Associate Professor, Department of Surgery, Section of Orthopedic Surgery and Rehabilitation Medicine, University of Chicago
Sherwin SW Ho, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

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