Wei Cheng1, Roger Cornwall2, Dustin L Crouch3, Zhongyu Li4, Katherine R Saul5. 1. Department of Mechanical and Aerospace Engineering, North Carolina State University, Raleigh, NC. 2. Division of Orthopedic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, OH. 3. Department of Biomedical Engineering, North Carolina State University, Raleigh, NC. 4. Department of Orthopaedic Surgery, Wake Forest School of Medicine, Winston-Salem, NC. 5. Department of Mechanical and Aerospace Engineering, North Carolina State University, Raleigh, NC. Electronic address: ksaul@ncsu.edu.
Abstract
PURPOSE: Two potential mechanisms leading to postural and osseous shoulder deformity after brachial plexus birth palsy are muscle imbalance between functioning internal rotators and paralyzed external rotators and impaired longitudinal growth of paralyzed muscles. Our goal was to evaluate the combined and isolated effects of these 2 mechanisms on transverse plane shoulder forces using a computational model of C5-6 brachial plexus injury. METHODS: We modeled a C5-6 injury using a computational musculoskeletal upper limb model. Muscles expected to be denervated by C5-6 injury were classified as affected, with the remaining shoulder muscles classified as unaffected. To model muscle imbalance, affected muscles were given no resting tone whereas unaffected muscles were given resting tone at 30% of maximal activation. To model impaired growth, affected muscles were reduced in length by 30% compared with normal whereas unaffected muscles remained normal in length. Four scenarios were simulated: normal, muscle imbalance only, impaired growth only, and both muscle imbalance and impaired growth. Passive shoulder rotation range of motion and glenohumeral joint reaction forces were evaluated to assess postural and osseous deformity. RESULTS: All impaired scenarios exhibited restricted range of motion and increased and posteriorly directed compressive glenohumeral joint forces. Individually, impaired muscle growth caused worse restriction in range of motion and higher and more posteriorly directed glenohumeral forces than did muscle imbalance. Combined muscle imbalance and impaired growth caused the most restricted joint range of motion and the highest joint reaction force of all scenarios. CONCLUSIONS: Both muscle imbalance and impaired longitudinal growth contributed to range of motion and force changes consistent with clinically observed deformity, although the most substantial effects resulted from impaired muscle growth. CLINICAL RELEVANCE: Simulations suggest that treatment strategies emphasizing treatment of impaired longitudinal growth are warranted for reducing deformity after brachial plexus birth palsy.
PURPOSE: Two potential mechanisms leading to postural and osseous shoulder deformity after brachial plexus birth palsy are muscle imbalance between functioning internal rotators and paralyzed external rotators and impaired longitudinal growth of paralyzed muscles. Our goal was to evaluate the combined and isolated effects of these 2 mechanisms on transverse plane shoulder forces using a computational model of C5-6 brachial plexus injury. METHODS: We modeled a C5-6 injury using a computational musculoskeletal upper limb model. Muscles expected to be denervated by C5-6 injury were classified as affected, with the remaining shoulder muscles classified as unaffected. To model muscle imbalance, affected muscles were given no resting tone whereas unaffected muscles were given resting tone at 30% of maximal activation. To model impaired growth, affected muscles were reduced in length by 30% compared with normal whereas unaffected muscles remained normal in length. Four scenarios were simulated: normal, muscle imbalance only, impaired growth only, and both muscle imbalance and impaired growth. Passive shoulder rotation range of motion and glenohumeral joint reaction forces were evaluated to assess postural and osseous deformity. RESULTS: All impaired scenarios exhibited restricted range of motion and increased and posteriorly directed compressive glenohumeral joint forces. Individually, impaired muscle growth caused worse restriction in range of motion and higher and more posteriorly directed glenohumeral forces than did muscle imbalance. Combined muscle imbalance and impaired growth caused the most restricted joint range of motion and the highest joint reaction force of all scenarios. CONCLUSIONS: Both muscle imbalance and impaired longitudinal growth contributed to range of motion and force changes consistent with clinically observed deformity, although the most substantial effects resulted from impaired muscle growth. CLINICAL RELEVANCE: Simulations suggest that treatment strategies emphasizing treatment of impaired longitudinal growth are warranted for reducing deformity after brachial plexus birth palsy.
Authors: Raveena M Doshi; Monique Y Reid; Nikhil N Dixit; Emily B Fawcett; Jacqueline H Cole; Katherine R Saul Journal: J Orthop Res Date: 2021-09-05 Impact factor: 3.102
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