Barry Alexander J, Kamper Derek G, Stoykov Mary Ellen, Triandafilou Kristen, Roth Elliot
Shirley Ryan AbilityLab, Arms + Hands Lab, Chicago, Illinios, USA.
Department of Physical Medicine & Rehabilitation, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Top Stroke Rehabil. 2022 Apr;29(3):181-191. doi: 10.1080/10749357.2021.1894660. Epub 2021 Mar 3.
Diminished sensorimotor control of the hand is one of the most common outcomes following stroke. This hand impairment substantially impacts overall function and quality of life; standard therapy often results in limited improvement. Mechanisms of dysfunction of the severely impaired post-stroke hand are still incompletely understood, thereby impeding the development of new targeted treatments.
To identify and determine potential relationships among the mechanisms responsible for hand impairment following stroke.
This cohort study observed stroke survivors (n = 95) with severe, chronic hand impairment (Chedoke-McMaster Hand score = 2-3). Custom instrumentation created precise perturbations and measured kinematic responses. Muscle activation was recorded through electromyography. Strength, spasticity, muscle relaxation time, and muscle coactivation were quantified.
Maximum grip strength in the paretic hand was only 12% of that achieved by the nonparetic hand, and only 6 of 95 participants were able to produce any net extension force. Despite force deficits, spastic reflex response of the finger flexor evoked by imposed stretch averaged 90.1 ± 26.8% of maximum voluntary activation, relaxation time averaged 3.8 ± 0.8 seconds, and coactivation during voluntary extension exceeded 30% of maximum contraction, thereby resulting in substantial net flexion. Surprisingly, these hypertonicity measures were not significantly correlated with each other.
Survivors of severe, chronic hemiparetic stroke experience profound weakness of both flexion and extension that arises from increased involuntary antagonist activation and decreased voluntary activation. The lack of correlation amongst hypertonicity measures suggests that these phenomena may arise from multiple, potentially independent mechanisms that could require different treatments.
手部感觉运动控制能力下降是中风后最常见的后果之一。这种手部损伤严重影响整体功能和生活质量；标准治疗往往只能带来有限的改善。中风后严重受损手部功能障碍的机制仍未完全明确，这阻碍了新的靶向治疗方法的开发。
识别并确定中风后导致手部损伤的机制之间的潜在关系。
这项队列研究观察了95名患有严重慢性手部损伤（Chedoke-McMaster手部评分=2-3）的中风幸存者。定制仪器产生精确的扰动并测量运动学反应。通过肌电图记录肌肉激活情况。对力量、痉挛、肌肉放松时间和肌肉共同激活进行量化。
患侧手的最大握力仅为健侧手的12%，95名参与者中只有6人能够产生任何净伸展力。尽管存在力量缺陷，但施加拉伸诱发的手指屈肌痉挛反射反应平均为最大自主激活的90.1±26.8%，放松时间平均为3.8±0.8秒，自主伸展期间的共同激活超过最大收缩的30%，从而导致明显的净屈曲。令人惊讶的是，这些张力亢进指标之间没有显著相关性。
严重慢性偏瘫性中风幸存者经历了由非自主拮抗肌激活增加和自主激活减少导致的屈伸功能严重减弱。张力亢进指标之间缺乏相关性表明，这些现象可能源于多种潜在独立的机制，可能需要不同的治疗方法。
