Beauchamp James A, Hassan Altamash S, McPherson Laura M, Negro Francesco, Pearcey Gregory E P, Cummings Mark, Heckman C J, Dewald Julius P A
Department of Physical Therapy and Human Movement Sciences, Northwestern University, Chicago, IL.
Department of Biomedical Engineering, Northwestern University, Chicago, IL.
medRxiv. 2023 Nov 22:2023.11.22.23298905. doi: 10.1101/2023.11.22.23298905.
Following a hemiparetic stroke, individuals exhibit altered motor unit firing patterns during voluntary muscle contractions, including impairments in firing rate modulation and recruitment. These individuals also exhibit abnormal muscle coactivation through multi-joint synergies (e.g., flexion synergy). Here, we investigate whether motor unit firing activity during flexion synergy-driven contractions of the paretic biceps brachii differs from that of voluntary contractions and use these differences to predict changes in descending motor commands. To accomplish this, we characterized motor unit firing patterns of the biceps brachii in individuals with chronic hemiparetic stroke during voluntary isometric elbow flexion contractions in the paretic and non-paretic limbs, as well as during contractions driven by voluntary effort and by flexion synergy expression in the paretic limb. We observed significant reductions in motor unit firing rate modulation from the non-paretic to paretic limb (non-paretic - paretic: 0.14 pps/%MVT, 95% CI: [0.09 0.19]) that were further reduced during synergy-driven contractions (voluntary paretic - synergy driven: 0.19 pps/%MVT, 95% CI: [0.14 0.25]). Moreover, using recently developed metrics, we evaluated how a stroke-induced reliance on indirect motor pathways alters the inputs that motor units receive and revealed progressive increases in neuromodulatory and inhibitory drive to the motor pool in the paretic limb, with the changes greatest during synergy-driven contractions. These findings suggest that an interplay between heightened neuromodulatory drive and alterations in inhibitory command structure may account for the observed motor unit impairments, further illuminating underlying neural mechanisms involved in the flexion synergy and its impact on motor unit firing patterns post-stroke.
偏瘫性中风后，个体在自主肌肉收缩期间表现出运动单位放电模式的改变，包括放电频率调制和募集方面的损伤。这些个体还通过多关节协同作用（如屈曲协同）表现出异常的肌肉共同激活。在此，我们研究在协同驱动的患侧肱二头肌屈曲收缩过程中，运动单位的放电活动是否与自主收缩不同，并利用这些差异来预测下行运动指令的变化。为实现这一目标，我们对患有慢性偏瘫性中风的个体在患侧和非患侧肢体进行自主等长肘屈曲收缩时，以及在患侧肢体由自主努力和屈曲协同表达驱动的收缩过程中，肱二头肌的运动单位放电模式进行了特征描述。我们观察到从非患侧肢体到患侧肢体，运动单位放电频率调制显著降低（非患侧 - 患侧：0.14次/秒/%MVT，95%置信区间：[0.09 0.19]），在协同驱动的收缩过程中进一步降低（自主患侧 - 协同驱动：0.19次/秒/%MVT，95%置信区间：[0.14 0.25]）。此外，使用最近开发的指标，我们评估了中风引起的对间接运动通路的依赖如何改变运动单位接收的输入，并揭示了患侧肢体运动神经元池的神经调节和抑制驱动逐渐增加，在协同驱动的收缩过程中变化最大。这些发现表明，增强的神经调节驱动与抑制性指令结构改变之间的相互作用可能解释了观察到的运动单位损伤，进一步阐明了参与屈曲协同及其对中风后运动单位放电模式影响的潜在神经机制。
