CASE REPORT
Infraspinatus Atrophy in a Volleyball Player: A Case of a Bennett Lesion Causing Nerve Impingement Katherine M. Pohlgeers, MD, MS and Jonathan A. Becker, MD Introduction Posterior shoulder injuries are particularly common in athletes utilizing repetitive overhead throwing motions (5). The majority of suprascapular nerve injuries are associated with volleyball players, with an estimated 20% of high-level volleyball players showing clinically evident atrophy of the infraspinatus muscle (4,6,8,13). However, identifying the definitive etiology and mechanism is fairly uncommon (8). This report will discuss a 19-year-old division I volleyball player with isolated suprascapular nerve entrapment secondary to a Bennett lesion. Case Report A 19-year-old division I female volleyball player presented for progressively worsening right shoulder pain without an identifiable inciting event, but she did recall having similar pain in high school that resolved spontaneously. She denied neck pain, any numbness or tingling in her arm, or previous shoulder dislocations or subluxations. Physical examination revealed tenderness over the biceps tendon, scapular winging, and multidirectional instability. O’Brien’s test was equivocal and she demonstrated limited external rotation with grade 4 or 5 weakness as compared with the left shoulder. Rotator cuff testing revealed no abnormalities. She had no pain over the acromioclavicular joint or clavicle and had negative Speed’s, Yergason, Scarf, Neer’s, and Hawkin’s tests. On visual inspection, there was obvious infraspinatus muscular atrophy (Fig. 1). A positive Sulcus sign, Rowe test, and jerk test were all elicited indicating multidirectional instability inferiorly, anteriorly, and posteriorly, respectively. A strict, formal rehabilitation and physical therapy regimen ensued for presumed multidirectional instability. Resistance bands were used to isolate internal and external rotation, and Department of Family and Geriatric Medicine, KentuckyOne Health Primary Care Sports Medicine, University of Louisville, Louisville, KY Address for correspondence: Katherine M. Pohlgeers, MD, MS, Department of Family and Geriatric Medicine, KentuckyOne Health Primary Care Sports Medicine, University of Louisville, Louisville, KY; E-mail:
[email protected]. 1537-890X/1306/358Y360 Current Sports Medicine Reports Copyright * 2014 by the American College of Sports Medicine
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kinetic chain exercises were used to strengthen the scapular stabilizers. Additional treatment modalities included cryotherapy, massages, stretching, taping, and hot packs. A magnetic resonance arthrogram was obtained to evaluate for any additional pathology, particularly a HillsYSachs lesion or labral tear. Results showed a diffusely blunted glenoid labrum diminutive in size without a frank tear or detachment as well as an adjacent posterosuperior quadrant capsule that was irregular and frayed along the inner margin. A 13 10-mm low-signal focus abnormality appeared along the posterior rim of the glenoid at the posterior capsular insertion with moderate to markedly isolated atrophy of the infraspinatus muscle. The biceps tendon and anterosuperior labrum were normal (Fig. 2). A computed tomography (CT) scan was performed to evaluate further the deformity of the glenoid, and a Bennett lesion was identified with frank compression of the suprascapular nerve. She was diagnosed as having a suprascapular nerve palsy secondary to a Bennett lesion causing isolated infraspinatus muscle atrophy. Discussion In 1941, Bennett described a posteroinferior glenoid lesion similar to an osteoarthritic deposit (1). Subsequently this was described as an ossification of the posteroinferior glenoid in the proximity of the posterior band of the inferior glenohumeral ligament complex (5). By imaging elite baseball pitchers, they were able to demonstrate associated posterior labral injury and posterior undersurface rotator cuff damage. They suggested that the lesion was calcific in nature, resulting from posterior capsular microtearing producing bleeding and reactive new bone formation (5). Associated secondary internal impingement of the rotator cuff and posterior labral injury are common. This differs from the original hypothesis that lesions were osteoarthritic growths containing bone marrow (2,3). While Bennett suggested that the lesion was related to triceps attachment, Ferrari et al. (5) hypothesized that the mechanism was actually a result of the humeral head being forced posteriorly while in maximum external rotation during the cocking and extension phase, consistent with the overhead swing of volleyball players. Howell et al. 10) and Fronek et al. 9) also support this theory, suggesting that the absence of any anterior injury indicates that the anterior capsule acts as a A Bennett Lesion Causing Nerve Impingement
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Figure 1: Obvious right-sided infraspinatus muscle atrophy.
buttress forcing the humeral head posteriorly and that posterior subluxation is associated with posterior capsular calcification and posterior glenoid erosions, respectively. By appreciating the mechanism and technique that volleyball players utilize in their sport, it is not surprising that this population has such a propensity for Bennett lesions (8). It is estimated that approximately 20% of high-level volleyball players show clinically evident atrophy of the infraspinatus muscle (6,8). Volleyball players attempt to strike the ball sharply with a sudden retraction and deceleration of the arm in order to impart a ‘‘floating’’ trajectory (8). This sudden retraction requires a much greater degree of shoulder stabilization provided by the external rotators (8). This is in contrast to baseball pitchers that have a consistent follow through with a gradual deceleration. Dynamic electromyography (EMG) analysis demonstrated a more intensely activated infraspinatus muscle that stabilizes the shoulder during this sudden withdrawal. Increasing the distance between the points of origin and termination of the nerve stretches the nerve across the lateral edge of the spine of the scapula (7). The cumulative effects of this proposed mechanism, in addition to the propensity for dynamic shoulder instability in this specific patient population, predisposes these athletes to infraspinatus atrophy (8). The suprascapular nerve originates in the upper trunk of the brachial plexus from the fifth and sixth cervical roots. It runs loosely under the trapezius muscle, forming a concave arch behind the clavicle. It enters the suprascapular notch beneath the superior transverse scapular ligament. It is here that the nerve divides into two branches: the first supplying motor fibers to the supraspinatus muscle and the second receiving sensory branches from the acromioclavicular and glenohumeral joints. The nerve continues to course around the lateral border of the spine of the scapula before passing through the spinoglenoid notch and reaching the infraspinatus muscle, estimated to pass within 8 to 21 mm of the glenoid rim (11). The suprascapular nerve branches at the glenoid notch supplying independent innervation to the supraspinatus and infraspinatus muscles. When there is injury to the suprascapular nerve at or below the spinoglenoid notch, the infraspinatus muscle will show marked atrophy with sparing of the supraspinatus muscle (8). www.acsm-csmr.org
Diagnosis The cross-body adduction test isolates suprascapular nerve entrapment in either the scapular or spinoglenoid notch. Adduction of a forward flexed arm across the body tenses the nerve and elicits pain (8) as the impingement of the nerve on the medial border of the scapula is accentuated (12). When employing simultaneous external rotation of the humerus, the test can be enhanced (8). Thumb pressure over the spinoglenoid notch also may elicit the pain during this test (14). Lesions are best visualized on plain radiographs when utilizing Bennett and Stryker notch views (5). EMG will demonstrate denervation of muscle but is employed rarely. The definitive imaging test of choice is typically an arthrogram in tandem with magnetic resonance or CT. Conservative treatment is recommended for patients experiencing infraspinatus atrophy, including avoidance of activities that result in overuse of the shoulder and strengthening of the external rotators (8). Surgical treatment is indicated only for compression neuropathies, such as compression from a Bennett lesion in this particular case, in which case, neurolysis and enlargement of the notch by shaving the base of the scapular spine are performed (8). Other etiologies for compression neuropathies that also would warrant surgical removal include labral cysts, ganglion from a labral tear, and other mass lesions. Conclusion In this case, surgical intervention was deferred, despite being indicated, because of a reasonable initial response to physical therapy and concerns that her underlying multidirectional instability potentially could compromise the outcome. Her rehabilitation regimen focused on strengthening the external rotators and scapular stabilization. Symptomatic treatment that had been employed earlier was continued, including massage, stretching, and taping. By employing a relatively conservative treatment regimen, focusing on strengthening of the shoulder joint and scapular stabilization exercises, the athlete was able to return to competitive play. Currently she is
Figure 2: Magnetic resonance imaging arthrogram of the right shoulder after fluoroscopic injection of dilute gadolinium contrast. Current Sports Medicine Reports
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experiencing only minimal discomfort and is subjectively and objectively stronger. She does, however, experience continued restriction and fatigue, and she maintains the same degree of infraspinatus muscular atrophy, all symptoms that should be corrected theoretically via surgical intervention (i.e., neurolysis of the Bennett lesion) during her off season.
5. Ferrari JD, Ferrar DA, Coumas J, Pappas AM. Posterior ossification of the shoulder: the Bennett lesion. Am. J. Sports Med. 1994; 22:171Y6. 6. Ferretti A, Cerullo G, Russo G. Suprascapular neuropathy in volleyball players. J. Bone Joint Surg. 1987; 69A:260Y3. 7. Ferretti A, De Carli A, Fontana M. Entrapment of the suprascapular nerve at the spinoglenoid notch. In: Vastama¨ki M, Jalovaara P, editors. Surgery of the Shoulder. Amsterdam: Elsevier Science; 1995, pp. 385Y92. 8. Ferretti A, De Carli A, Fontana M. Injury of the suprascapular nerve at the spinoglenoid notch. Am. J. Sports Med. 1998; 26:759Y63. 9. Fronek J, Warren RF, Bowen MK. Posterior subluxation of the glenohumeral joint. J. Bone Joint Surg. 1989; 71A:205Y16.
The authors declare no conflicts of interest and do not have financial disclosures.
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10. Howell SM, Galinat BJ, Renzi AJ, et al. Normal and abnormal mechanics of the glenohumeral joint in the horizontal plane. J. Bone joint Surg. 1989; 70A:227Y32. 11. Moore TP, Fritts HM, Buss DD. Suprascapular nerve entrapment secondary to supraglenoid cyst compression. J. Shoulder Elbow Surg. 1996; 5:455Y62. 12. Narakas A. Compression syndromes about the shoulder including brachial plexus. In: Szabo RM, editor. Nerve Compression Syndromes: Diagnosis and Treatment. Thorofare (NJ): Slack, 1989, p. 236Y9.
3. Bennett GE. Shoulder and elbow lesions of the professional baseball pitcher. J. Am. Med. Assoc. 1941; 117:510Y4.
13. Ozer D, Baltaci G, Leblebicioglu G. Rehabilitation and shoulder function after suprascapular nerve entrapment operation in a volleyball player. Arch. Orthop. Trauma Surg. 2007; 127:759Y61.
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A Bennett Lesion Causing Nerve Impingement
Copyright © 2014 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.