McPherson Laura M, Dewald Julius P A
Program in Physical Therapy, Washington University School of Medicine, St. Louis, MO, United States.
Department of Neurology, Washington University School of Medicine, St. Louis, MO, United States.
Front Neurol. 2022 Oct 10;13:934670. doi: 10.3389/fneur.2022.934670. eCollection 2022.
Individuals with moderate-to-severe post-stroke hemiparesis cannot control proximal and distal joints of the arm independently because they are constrained to stereotypical movement patterns called flexion and extension synergies. Accumulating evidence indicates that these synergies emerge because of upregulation of diffusely projecting brainstem motor pathways following stroke-induced damage to corticofugal pathways. During our recent work on differences in synergy expression among proximal and distal joints, we serendipitously observed some notable characteristics of synergy-driven muscle activation. It seemed that: paretic wrist/finger muscles were activated maximally during contractions of muscles at a different joint; differences in the magnitude of synergy expression occurred when elicited via contraction of proximal vs. distal muscles; and associated reactions in the paretic limb occurred during maximal efforts with the non-paretic limb, the strength of which seemed to vary depending on which muscles in the non-paretic limb were contracting. Here we formally investigated these observations and interpreted them within the context of the neural mechanisms thought to underlie stereotypical movement patterns. If upregulation of brainstem motor pathways occurs following stroke-induced corticofugal tract damage, then we would expect a pattern of muscle dependency in the observed behaviors consistent with such neural reorganization. Twelve participants with moderate-to-severe hemiparetic stroke and six without stroke performed maximal isometric torque generation in eight directions: shoulder abduction/adduction and elbow, wrist, and finger flexion/extension. Isometric joint torques and surface EMG were recorded from shoulder, elbow, wrist, and finger joints and muscles. For some participants, joint torque and muscle activation generated during maximal voluntary contractions were lower than during maximal synergy-induced contractions (i.e., contractions about a different joint), particularly for wrist and fingers. Synergy-driven contractions were strongest when elicited via proximal joints and weakest when elicited via distal joints. Associated reactions in the wrist/finger flexors were stronger than those of other paretic muscles and were the only ones whose response depended on whether the non-paretic contraction was at a proximal or distal joint. Results provide indirect evidence linking the influence of brainstem motor pathways to abnormal motor behaviors post-stroke, and they demonstrate the need to examine whole-limb behavior when studying or seeking to rehabilitate the paretic upper limb.
患有中度至重度中风后偏瘫的个体无法独立控制手臂的近端和远端关节，因为他们受限于称为屈曲和伸展协同运动的刻板运动模式。越来越多的证据表明，这些协同运动的出现是由于中风导致皮质传出通路受损后，广泛投射的脑干运动通路上调所致。在我们最近关于近端和远端关节协同运动表达差异的研究中，我们偶然观察到了协同驱动肌肉激活的一些显著特征。似乎是：在不同关节的肌肉收缩过程中，患侧手腕/手指肌肉被最大程度地激活；通过近端肌肉与远端肌肉收缩引发协同运动时，协同运动表达的幅度存在差异；在非患侧肢体进行最大用力时，患侧肢体出现关联反应，其强度似乎取决于非患侧肢体中哪些肌肉正在收缩。在此，我们正式研究了这些观察结果，并在被认为是刻板运动模式基础的神经机制背景下对其进行了解释。如果中风导致皮质传出束损伤后脑干运动通路上调，那么我们预计在观察到的行为中会出现一种与这种神经重组一致的肌肉依赖模式。12名患有中度至重度偏瘫性中风的参与者和6名未患中风的参与者在八个方向上进行了最大等长扭矩生成：肩关节外展/内收以及肘关节、腕关节和手指的屈曲/伸展。记录了肩关节、肘关节、腕关节和手指关节及肌肉的等长关节扭矩和表面肌电图。对于一些参与者，最大自主收缩期间产生的关节扭矩和肌肉激活低于最大协同运动诱导收缩期间（即围绕不同关节的收缩），特别是对于腕关节和手指。通过近端关节引发协同运动时收缩最强，通过远端关节引发时最弱。腕关节/手指屈肌的关联反应比其他患侧肌肉更强，并且是唯一其反应取决于非患侧收缩是在近端关节还是远端关节的肌肉。结果提供了间接证据，将脑干运动通路的影响与中风后的异常运动行为联系起来，并且它们表明在研究或寻求恢复患侧上肢功能时，需要检查整个肢体的行为。
