Centre for Sensorimotor Performance, The University of Queensland, Brisbane, Australia; Centre for Sports Research, Deakin University, Melbourne, Australia.
Innovations in Health Technology, Menzies Health Institute Queensland, Griffith University, Gold Coast, Australia.
Gait Posture. 2018 Mar;61:169-175. doi: 10.1016/j.gaitpost.2018.01.010. Epub 2018 Jan 12.
Altered neural control of movement and musculoskeletal deficiencies are common in children with spastic cerebral palsy (SCP), with muscle weakness and contracture commonly experienced. Both neural and musculoskeletal deficiencies are likely to contribute to abnormal gait, such as equinus gait (toe-walking), in children with SCP. However, it is not known whether the musculoskeletal deficiencies prevent normal gait or if neural control could be altered to achieve normal gait. This study examined the effect of simulated muscle weakness and contracture of the major plantarflexor/dorsiflexor muscles on the neuromuscular requirements for achieving normal walking gait in children. Initial muscle-driven simulations of walking with normal musculoskeletal properties by typically developing children were undertaken. Additional simulations with altered musculoskeletal properties were then undertaken; with muscle weakness and contracture simulated by reducing the maximum isometric force and tendon slack length, respectively, of selected muscles. Muscle activations and forces required across all simulations were then compared via waveform analysis. Maintenance of normal gait appeared robust to muscle weakness in isolation, with increased activation of weakened muscles the major compensatory strategy. With muscle contracture, reduced activation of the plantarflexors was required across the mid-portion of stance suggesting a greater contribution from passive forces. Increased activation and force during swing was also required from the tibialis anterior to counteract the increased passive forces from the simulated dorsiflexor muscle contracture. Improvements in plantarflexor and dorsiflexor motor function and muscle strength, concomitant with reductions in plantarflexor muscle stiffness may target the deficits associated with SCP that limit normal gait.
运动神经控制的改变和肌肉骨骼缺陷在痉挛型脑瘫（SCP）患儿中很常见，常伴有肌肉无力和挛缩。肌肉无力和挛缩都可能导致 SCP 患儿出现异常步态，如马蹄内翻足（足尖着地）。然而，目前尚不清楚肌肉骨骼缺陷是否会阻止正常步态，或者神经控制是否可以改变以实现正常步态。本研究探讨了模拟主要跖屈/背屈肌的肌肉无力和挛缩对儿童实现正常行走步态的神经肌肉需求的影响。对正常儿童的正常肌肉骨骼特性进行了初始肌肉驱动的行走模拟。然后进行了具有改变的肌肉骨骼特性的额外模拟；通过分别降低选定肌肉的最大等长力和肌腱松弛长度来模拟肌肉无力和挛缩。然后通过波形分析比较所有模拟的肌肉激活和所需力。单独的肌肉无力对正常步态的维持似乎很稳健，增加无力肌肉的激活是主要的代偿策略。对于肌肉挛缩，在站立中期需要减少跖屈肌的激活，这表明被动力的贡献更大。为了抵消模拟背屈肌挛缩引起的增加的被动力，还需要在前胫骨肌中增加摆动时的激活和力。改善跖屈肌和背屈肌的运动功能和肌肉力量，同时降低跖屈肌的僵硬度，可能针对限制正常步态的 SCP 相关缺陷。
