The article presents a case study of a 22 year-old female college athlete with multidirectional instability (MDI) of the glen-humeral (GH) joint. The athlete participated in overhead sports activities such as softball, basketball and swimming, and her presenting symptoms included decreased function, crepitus and spontaneous subluxation. Clinical management and range of motion (ROM) measurement are also discussed

Freeman, T.

Maurer-Starks, Suanne

Wise, K. A.

Ziaks, L. J.

Virtual Commons - Bridgewater State University

Bridgewater State UniversityVirtual Commons - Bridgewater State UniversityMovement Arts, Health Promotion and LeisureStudies Faculty PublicationsMovement Arts, Health Promotion and LeisureStudies Department2010Severe multidirectional instability of the gleno-humeral jointL. J. ZiaksT. FreemanK. A. WiseSuanne Maurer-StarksBridgewater State University, suanne.maurer@bridgew.eduThis item is available as part of Virtual Commons, the open-access institutional repository of Bridgewater State University, Bridgewater, Massachusetts.Virtual Commons CitationZiaks, L. J.; Freeman, T.; Wise, K. A.; and Maurer-Starks, Suanne (2010). Severe multidirectional instability of the gleno-humeral joint.In Movement Arts, Health Promotion and Leisure Studies Faculty Publications. Paper 34.Available at: http://vc.bridgew.edu/mahpls_fac/34Athletic therApy todAy  jAnuAry 2010  45 © 2010 Human Kinetics - ATT 15(1), pp. 45-49ULTIDIRECTIONAL instability (MDI) of the gleno-humeral (GH) joint is defined as symptomatic instability in two or more directions. This condition is pri-marily diagnosed on the basis of clinical findings, which requires a thorough patient history and physical examination.1-3 MDI typically presents one of three distinct patterns: (a) antero-inferior dislocation with posterior subluxation,( b) postero-inferior dislocation with anterior subluxation, and (c) antero-postero-inferior dislocation.1-4 Patients with MDI often pres-ent GH laxity, symptomatic multi-planar translation, and impingement syndrome.3,5 The chief complaint is often generalized shoulder pain that is exacerbated by overhead activities and specific arm positions. The GH joint is generally asymptomatic at rest in the anatomical position.1-3 Clinical findings may include (a) a positive sulcus sign (at least 2mm), (b) positive anterior and posterior apprehension tests, (c) a posi-tive Neer or Hawkins-Kennedy test, and (d) joint glide hypermobility.3,6,7MDI lacks a consistent definition in the literature, which complicates interpretation of epidemiologic studies.1-4,8,9 Owens et al.9 reported that females had a greater incidence of MDI events than males had. This difference is likely due to differences in joint laxity between men and women.10Initial management of MDI consists of activity modification and rehabilitation that is focused on strengthening the rotator cuff (RTC) and scapular stabilizers and improvement of GH joint propriocep-tion.1,3,7,11,12 As many as 89% of patients with MDI may respond favorably to rehabilitation and thereby avoid a surgical intervention.1,13 This report reviews the clinical presentation of a patient who had prolonged neurological and functional impairments associated with undiagnosed MDI. The cause of dysfunction was confirmed to be GH laxity, rather than psychosomatic or neurological factors. The patient was diagnosed with severe MDI in all three planes. An open inferior capsular shift was performed to address capsular redundancy.1,7,11 This surgical proce-dure has been reported to have an 86% success rate at 38 months postsurgery.1 The patient was able to return to asymptomatic activities of daily living (ADLs). Background A 22 year-old female college athlete, who had left hand dominance, presented symptoms in the right upper extremity. She reported an extensive history of overhead sports activities that included softball, basketball, swimming, and diving. She was found to have congenital GH laxity without any other abnormal clinical examination findings.The patient experienced progressively greater symptoms of decreased function, pain, spontaneous subluxation, crepitus, and parasthesia that was dis-tributed throughout the brachial plexus dermatomes (C5-T1).14-16 The terms “numbing, burning, aching, and shooting” were used to describe the nature of pain experienced when sleeping or performing overhead Joe J. Piccininni, BA, BEd, MSc, ATM, CAT(C), Report EditorSevere Multidirectional Instability  of the Gleno-Humeral Joint CASE REVIEWLauren J. Ziaks ATC, LAT; Tracey Freeman, ATC; Kimberly A. Wise, EdD (c), MS, ATC •  Northeastern University and Suanne Maurer-Starks, EdD, ATC • Bridgewater State CollegeM46  jAnuAry 2010  Athletic therApy todAyactivities. She reported pain during active shoulder range of motion (AROM) and persistent parasthesia that extended to the palmar surface of her right hand. Over a period of two and one-half years, the patient’s symptoms of pain, weakness, and disability became progressively more disabling.Clinical ManagementThe patient experienced an insidious onset of decreased function (an inability to perform overhead activities or upper extremity weightlifting exercises) and increasing neurological impairment. Her history included a fall on the right upper extremity, with the GH joint in a position of flexion, abduction, and external rotation. Seven months after the traumatic incident, the patient sought care at an emergency room for parasthesia that radiated from the cervical spine to the distal digits of her right upper extremity. She was diagnosed as having an ulnar neuropathy. Subsequently, the patient was evaluated by an orthopedic surgeon, who diagnosed a rhomboid strain. Scapular winging, crepitus, pain, and audible “pop-ping” within the GH joint were noted. She was referred for six months of conservative rehabilitation, which was primarily focused on GH stabilization, postural correction, and RTC strengthening. The patient did not experience any relief from her neurologic symptoms, instability, or pain. Her rehabilitation program was modified to incor-porate mobilizations of the cervical spine, thoracic spine, and first rib, which provided minimal relief of neurological symptoms and a slight improvement in functional abilities. The patient was then referred to a neurologist, who included thoracic outlet syndrome and multiple sclerosis in the differential diagnosis. The existence of a neurologic disorder was ruled out by physical examination findings, nerve conduction velocity testing, electromyography, blood tests for autoimmune disorders, and an MRI of the brain. Functional impairments continued to progress, which ultimately led to the inability to perform ADLs and increasing discouragement. Increased radicular symptoms throughout the distribution of the brachial plexus, audible popping and clicking within the GH joint, and pain restricted the use of the right upper extremity. MRI of the GH joint demonstrated mild RTC inflammation and no evidence of a labrum lesion. The patient was ultimately evaluated by an ortho-pedic surgeon with shoulder subspecialty expertise, who diagnosed MDI. The GH capsular laxity allowed anterior, inferior, and posterior subluxation without anesthesia. The neurological symptoms were exacer-bated by inferior traction, which produced a positive inferior sulcus sign. The physician believed that the neurologic symptoms were caused by the head of the humerus resting on the anterior margin of the gle-noid rim, which was responsible for brachial plexus impingement. He recommended an open inferior capsular shift as the best option to address the GH laxity and restore function. Presurgical ManagementThe patient elected to delay the surgical intervention for personal reasons. During this period, the patient was instructed to refrain from performance of activities that exacerbated symptoms and to begin a scapular strengthening program. Joint mobilizations were per-formed in an effort to relocate the position of the head of the humerus, which produced a transient decrease in pain and parasthesia. Her status continued to dete-riorate, with development of palmar diaphoresis, con-tinuous numbness and pain, crepitus in the GH joint, and recurring spontaneous subluxations. Two cortisone injections in the posterior GH capsule were adminis-tered six weeks apart, which produced a temporary decrease in symptoms and an increase in functional capabilities. Following the injections, the patient was able to move her upper extremity throughout the normal ROM, but audible and palpable clicking and popping were still present. Subsequently, the surgical intervention was performed.Objective Measures of StatusAll ROM measurements were acquired by the same clinician for both an asymptomatic range and the com-plete symptomatic range. AROM was recorded prior to passive ROM (PROM) with the patient in a supine posi-tion and the scapula stabilized to ensure isolation of GH joint motion. End-range PROM was only achieved in forward flexion; the patient could not tolerate extreme GH joint displacement in other planes. The change in values for asymptomatic and symptomatic ROM was substantial (Tables 1 and 2; Figures 1 and 2).Athletic therApy todAy  jAnuAry 2010  47 The patient’s positive postsurgical outcome con-firmed that MDI was the primary cause of dysfunction. The patient’s cervical symptoms might have been attributable to upper trapezius spasms and kyphotic posture. Excessive movement of the humeral head was probably responsible for RTC inflammation. After the surgery, the patient developed bicipital tendonitis and RTC impingement, which may have been due to inadequate strength of the scapular stabilizers. As the rehabilitation program progressed, the patient’s symp-toms resolved and her functional abilities continued to improve.At a 9-month postsurgery follow-up examination, the patient reported a complete resolution of neurologi-cal symptoms and demonstrated normal asymptom-atic ROM. The surgery and rehabilitation led to a 96.7% increase in asymptomatic forward flexion AROM and a 268.4% increase in asymptomatic external rotation AROM. Table 1. ROM Measurements (degrees)Motion PROM AROMPre-Surgery Asymptomatic Full ROM Asymptomatic Full ROM Forward Flexion (supine) 120 196 90 185 Extension (prone) 42 71 41 58 External Rotation (supine @ 90/90) 73 110 19 79 Internal Rotation (supine @ 90/90) 46 71 35 546 Months Post-Surgery  Forward Flexion (supine) 174 182 162 174 Extension (prone) 51 59 34 43 External Rotation (supine @ 90/90) 79 86 72 77 Internal Rotation (supine @ 90/90) 65 70 56 ***9 Months Post-Surgery Forward Flexion (supine) 187* *** 177* *** Extension (prone) 62 *** 54 *** External Rotation (supine @ 90/90) 71 89** 70 79 Internal Rotation (supine @ 90/90) 62 *** 54 ****Stretch anterior, mild parasthesia, discomfort returning**Stretch at end range, weak returning, general feeling of stability***No symptoms presentTable 2. Pre-Post Change  in Asymptomatic ROMMotion PROM (%) AROM (%)Forward flexion (supine) 55.8 96.7Extension (prone) 47.6 31.7External rotation  (supine @ 90/90)* 268.4Internal rotation  (supine @ 90/90)34.8 54.3< 30% changeTreatment OutcomeThe patient reported decreased pain and parasthesia immediately following the surgical procedure. As she progressed through the postsurgical rehabilitation pro-gram, she reported increased stability and function. 48  jAnuAry 2010  Athletic therApy todAyUniqueness of the CaseThe patient’s clinical care was initially based on symptoms, rather than identification of the cause of dysfunction.2,4 The lack of an accurate diagnosis led to a prolonged course of ineffective treatment. The severe loss of function and neurologic symptoms represent an unusual presentation for MDI. The anterior, pos-terior, and inferior subluxations were easily reduced, which was evidence of severe laxity of the GH joint. The patient experienced an immediate decrease in symptoms following the surgical intervention and she was able to perform normal ADLs within 4 months. She was allowed to resume performance of overhead activities at 6 months postsurgery.SummaryThis case emphasizes the importance of careful consid-eration of the patient’s description of symptoms and concerns, and the performance of a thorough physical examination. The postsurgical resolution of symptoms and restoration of function confirmed that the cause of dysfunction was GH instability. Figure  1 AroM asymptomatic.Figure  2 proM asymptomatic.Athletic therApy todAy  jAnuAry 2010  49 AcknowledgmentsMiss Rebecca C. Payne was an investigator for this case report prior to her untimely passing in May of 2008. Becca was an amazing classmate and a won-derful friend. She was an inspiration to all who knew her and we wish to continue to keep her memory alive. A special thank you is expressed to Dan Murray, MS, PT, CSCS, at Sports and PT Associates in Boston, MA for his persistence and continued care and to Dr. Mininder Kocher for accurate assessment of the patient’s condition and performance of a successful surgical intervention.References  1. Bahu MJ, Trentacosta N, Vorys GC, Covey AS, Ahmad CS. Multidirec-tional instability: evaluation and treatment options. Clin Sports Med. 2008;27:671-689.  2. Matsen FA, Chebli C, Lippit S. Principles for the evaluation and man-agement of shoulder instability. J Bone Joint Surg Am. 2006;88:648-649.  3. Provencher MT, Romeo AA. Posterior and multidirectional instability of the shoulder: challenges associated with diagnosis and manage-ment. Instr Course Lect. 2008;57:133-152.  4. Darlow B. Neuromuscular retraining for multidirectional instability of the shoulder- a case study. NZ J Physiotherapy. 2006;34(2):60-65.  5. Hambly N. Fitzpatrick P, MacMahon P, Eustace S. Rotator cuff impinge-ment: correlation between findings on MRI and outcome after fluo-roscopically guided subacromial bursography and steroid injection. Am J Roentgenol.  2007;189(5):1179-1184.  6. Magarey ME; Jones MA. Specific evaluation of the function of force couples relevant for stabilization of the glenohumeral joint. Manual Ther. 2003; 8(4):247-53.  7. An, YH, Friedman RJ. Multidirectional instability of the glenohumeral joint. Orthop Clin North Am. 2000;31:275-285.  8. Wong KL, Williams GR. Complications of thermal capsulorrhaphy of the shoulder. J Bone Joint Surg Am. 2001;83:151-155.  9. Owens BD, Duffey ML, Nelson BJ et al. The incidence and character-istics of shoulder instability at the United States Military Academy. Am J Sports Med. 2007;35:1168-73.  10. Huston LJ, Greenfield ML, Wojtys EM. Anterior cruciate ligament injuries in the female athlete: potential risk factors. Clin Orthop Relat Res. 2000;98:50-63. 11. Hayes K, Callanan M, Walton Judie, Paxinos A, Murrell GAC. Shoulder instability: management and rehabilitation. J Orthop Sports Phys Ther. 2002;32(10):1-1. 12. Cordasco FA. Understanding multidirectional instability of the shoul-der. J Athl Train. 2000;35:278-85.  13. Hurley JA, Anderson TE, Dear W, Andrish JT, Bergfeld JA, Weiker GA. Posterior shoulder instability: surgical versus conservative results with evaluation of glenoid version. Am J Sports Med. 1992;20:396-400.  14. Starkey C, Johnson G. Athletic Training and Sports Medicine. In: Berget N, Harmon B, Yocum L, eds. Shoulder Injuries. Sudbury, MA: Jones and Bartlett; 2006: 311.  15. Sieg K. Adams, S. Illustrated Essentials of Musculoskeletal Anatomy. Gainesville, FL: Megabooks Inc; 2002:11-27, 73-78.  16 Moore K. Dalley II, A. Clinically Oriented Anatomy. New York: Lippin-cott, Williams & Wilkins; 2006.Lauren Ziaks graduated in 2009 with a bachelor’s degree in Athletic Training from Northeastern University. While earning her DPT, she is working as an independent contractor LAT in the greater Boston area.Tracey Freeman graduated from Northeastern University with a bach-elors of science in athletic training. She currently resides in Buffalo, NY working as a physician extender and outreach athletic trainer.Kimberly Wise presently teaches and coordinates the clinical educa-tion component for the ATEP at Northeastern University and is complet-ing her doctorate of education. Research interest includes pedagogical development and instructional strategies.Suanne Maurer-Starks is the ATEP Undergraduate Program Coordina-tor at Bridgewater State College. Her research efforts revolve around athletic training pedagogy and issues surrounding diversity within the profession of athletic training.stAteMent of ownership, MAnAgeMent, And circulAtion  of aThLeTic Therapy Today (issn 1078-7895), as required by 39 u.s. code 3685:Athletic Therapy Today (ISSN 1078-7895) is published six times a year. Subscription fees are $52 per year for individuals and $263 per year for institutions (2010). The owner of Athletic Therapy Today is Human Kinetics, Inc., whose office of publication is at 1607 North Market St., Champaign, IL 61820-2200. The editor is Gary Wilkerson, Dept. #6606, UT-Chattanoonga, Chat-tanooga, TN 37403-2598. The publisher is Rainer Martens, P.O. Box 5076, Champaign, IL 61825-5076. There are no bondholders, mortgagees, or other security holders.Average number of copies printed per issue (net press run) during the preceding 12 months is 2,888; number of copies nearest to filing date is 2,595. Average number of copies of each issue distributed after mass mailing to subscribers is 21; number of copies nearest to filing date is 31. Average number of copies of each issue distributed in mass mailing to subscribers 2,411; number of copies nearest to filing date is 2,204. 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Severe multidirectional instability of the gleno-humeral joint

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