Suprascapular Neuropathy
- Author: Jonathan C Reeser, MD, PhD; Chief Editor: Sherwin SW Ho, MD more...
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 (see image below).[1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21]
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. 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, 27] 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.
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Epidemiology
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, 28, 29, 30] Studies have reported that 13-45% of elite volleyball athletes have signs of suprascapular neuropathy.[7, 9, 11, 12, 13, 15, 18, 19, 21, 30] 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.[31, 32, 33, 34] 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).
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. 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.
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, 35] 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.[36] 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, 35, 37, 38, 39] 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.
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