Cheng Wei, Cornwall Roger, Crouch Dustin L, Li Zhongyu, Saul Katherine R
Department of Mechanical and Aerospace Engineering, North Carolina State University, Raleigh, NC.
Division of Orthopedic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.
J Hand Surg Am. 2015 Jun;40(6):1170-6. doi: 10.1016/j.jhsa.2015.02.025. Epub 2015 Apr 3.
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.
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.
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.
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.
Simulations suggest that treatment strategies emphasizing treatment of impaired longitudinal growth are warranted for reducing deformity after brachial plexus birth palsy.
臂丛神经产瘫后导致肩部姿势和骨性畸形的两个潜在机制是，功能正常的内旋肌与麻痹的外旋肌之间的肌肉失衡，以及麻痹肌肉的纵向生长受损。我们的目标是使用C5 - 6臂丛神经损伤的计算模型，评估这两种机制对肩部横平面力的联合和单独影响。
我们使用计算肌肉骨骼上肢模型对C5 - 6损伤进行建模。预计因C5 - 6损伤而失神经支配的肌肉被归类为受影响肌肉，其余肩部肌肉被归类为未受影响肌肉。为模拟肌肉失衡，受影响肌肉不赋予静息张力，而未受影响肌肉赋予最大激活度30%的静息张力。为模拟生长受损，与正常情况相比，受影响肌肉长度缩短30% , 而未受影响肌肉长度保持正常。模拟了四种情况：正常、仅肌肉失衡、仅生长受损，以及肌肉失衡和生长受损同时存在。评估被动肩部旋转活动范围和盂肱关节反应力，以评估姿势和骨性畸形。
所有受损情况均表现出活动范围受限，以及盂肱关节压缩力增加且向后。单独来看，与肌肉失衡相比，肌肉生长受损导致的活动范围受限更严重，盂肱关节力更高且更向后。肌肉失衡和生长受损同时存在导致所有情况中关节活动范围受限最严重，关节反应力最高。
肌肉失衡和纵向生长受损均导致与临床观察到畸形一致的活动范围和力的变化，尽管最显著的影响来自肌肉生长受损。
模拟结果表明强调治疗纵向生长受损对于减少臂丛神经产瘫后畸形的治疗策略是必要的。
