Siegel Karen Lohmann, Kepple Thomas M, Stanhope Steven J
Physical Disabilities Branch, National Institutes of Health (NIH), Department of Health and Human Services, Bldg 10, CRC, Rm 1-1469, 10 Center Dr, MSC 1604, Bethesda, MD 20892-1604, USA.
Clin Biomech (Bristol). 2007 Mar;22(3):319-26. doi: 10.1016/j.clinbiomech.2006.11.002. Epub 2006 Dec 21.
The purpose of this case series was to quantify different strategies used to compensate in gait for hip muscle weakness.
An instrumented gait analysis was performed of three females diagnosed with idiopathic inflammatory myopathies and compared to a healthy unimpaired subject. Lower extremity joint moments obtained from the gait analysis were used to drive an induced acceleration model which determined each moment's contribution to upright support, forward progression, and hip joint acceleration.
Results showed that after midstance, the ankle plantar flexors normally provide upright support and forward progression while producing hip extension acceleration. In normal gait, the hip flexors eccentrically resist hip extension, but the hip flexor muscles of the impaired subjects (S1-3) were too weak to control extension. Instead S1-3 altered joint positions and muscle function to produce forward progression while minimizing hip extension acceleration. S1 increased knee flexion angle to decrease the hip extension effect of the ankle plantar flexors. S2 and S3 used either a knee flexor moment or gravity to produce forward progression, which had the advantage of accelerating the hip into flexion rather than extension, and decreased the demand on the hip flexors.
Results showed how gait compensations for hip muscle weakness can produce independent (i.e. successful) ambulation, although at a reduced speed as compared to normal gait. Knowledge of these successful strategies can assist the rehabilitation of patients with hip muscle weakness who are unable to ambulate and potentially be used to reduce their disability.
本病例系列的目的是量化在步态中用于补偿髋部肌肉无力的不同策略。
对三名被诊断为特发性炎性肌病的女性进行了仪器化步态分析,并与一名健康未受损受试者进行比较。从步态分析中获得的下肢关节力矩被用于驱动一个诱导加速度模型,该模型确定每个力矩对直立支撑、向前推进和髋关节加速度的贡献。
结果显示,在支撑中期之后,踝关节跖屈肌通常提供直立支撑和向前推进,同时产生髋关节伸展加速度。在正常步态中,髋关节屈肌离心抵抗髋关节伸展,但受损受试者(S1 - 3)的髋关节屈肌过于薄弱,无法控制伸展。相反,S1 - 3改变关节位置和肌肉功能以产生向前推进,同时将髋关节伸展加速度降至最低。S1增加膝关节屈曲角度,以减少踝关节跖屈肌的髋关节伸展效应。S2和S3利用膝关节屈肌力矩或重力来产生向前推进,这具有使髋关节加速屈曲而非伸展的优势,并减少了对髋关节屈肌的需求。
结果表明,尽管与正常步态相比速度降低,但针对髋部肌肉无力的步态补偿如何能够实现独立(即成功)行走。了解这些成功策略可以帮助无法行走的髋部肌肉无力患者进行康复,并有可能用于减轻他们的残疾程度。