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Impaired Growth of Denervated Muscle Contributes to Contracture Formation Following Neonatal Brachial Plexus Injury
Sia Nikolaou, PhD1; Elizabeth Peterson, BS1; Annie Kim2; Christopher Wylie, PhD3; Roger Cornwall, MD1
1 Division of Pediatric Orthopaedic Surgery, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, MLC 2017, Cincinnati, OH 45229. E-mail address for R. Cornwall: roger.cornwall@cchmc.org
2 University of Notre Dame, Notre Dame, IN 46556
3 Division of Developmental Biology, Cincinnati Children's Research Foundation, 3333 Burnet Avenue, MLC 7007, Cincinnati, OH 45229
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Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity.

Investigation performed at the Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio

Copyright © 2011 by The Journal of Bone and Joint Surgery, Inc.
J Bone Joint Surg Am, 2011 Mar 02;93(5):461-470. doi: 10.2106/JBJS.J.00943
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The etiology of shoulder and elbow contractures following neonatal brachial plexus injury is incompletely understood. With use of a mouse model, the current study tests the novel hypothesis that reduced growth of denervated muscle contributes to contractures following neonatal brachial plexus injury.


Unilateral brachial plexus injuries were created in neonatal mice by supraclavicular C5-C6 nerve root excision. Shoulder and elbow range of motion was measured four weeks after injury. Fibrosis, cross-sectional area, and functional length of the biceps, brachialis, and subscapularis muscles were measured over four weeks following injury. Muscle satellite cells were cultured from denervated and control biceps muscles to assess myogenic capability. In a comparison group, shoulder motion and subscapularis length were assessed following surgical excision of external rotator muscles.


Shoulder internal rotation and elbow flexion contractures developed on the involved side within four weeks following brachial plexus injury. Excision of the biceps and brachialis muscles relieved the elbow flexion contractures. The biceps muscles were histologically fibrotic, whereas fatty infiltration predominated in the brachialis and rotator cuff muscles. The biceps and brachialis muscles displayed reduced cross-sectional and longitudinal growth compared with the contralateral muscles. The upper subscapularis muscle similarly displayed reduced longitudinal growth, with the subscapularis shortening correlating with internal rotation contracture. However, excision of the external rotators without brachial plexus injury caused no contractures or subscapularis shortening. Myogenically capable satellite cells were present in denervated biceps muscles despite impaired muscle growth in vivo.


Injury of the upper trunk of the brachial plexus leads to impaired growth of the biceps and brachialis muscles, which are responsible for elbow flexion contractures, and impaired growth of the subscapularis muscle, which correlates with internal rotation contracture of the shoulder. Shoulder muscle imbalance alone causes neither subscapularis shortening nor internal rotation contracture. Impaired muscle growth cannot be explained solely by absence of functioning satellite cells.

Clinical Relevance: 

The current study suggests a primary role for impaired growth of denervated muscle in contracture pathogenesis following neonatal brachial plexus injury. These findings provide a novel avenue for investigation toward development of rational contracture prevention and treatment strategies.

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    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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