Shirley Ryan AbilityLab, Chicago, Illinois, United States.
Department of Physical Medicine and Rehabilitation, Northwestern University, Chicago, Illinois, United States.
J Neurophysiol. 2024 Jul 1;132(1):78-86. doi: 10.1152/jn.00067.2024. Epub 2024 May 1.
Stroke-caused synergies may result from the preferential use of the reticulospinal tract (RST) due to damage to the corticospinal tract. The RST branches multiple motoneuron pools across the arm together resulting in gross motor control or abnormal synergies, and accordingly, the controllability of individual muscles decreases. However, it is not clear whether muscles involuntarily activated by abnormal synergy vary depending on the muscles voluntarily activated when motor commands descend through the RST. Studies showed that abnormal synergies may originate from the merging and reweighting of synergies in individuals without neurological deficits. This leads to a hypothesis that those abnormal synergies are still selectively excited depending on the context. In this study, we test this hypothesis, leveraging the Fugl-Meyer assessment that could characterize the neuroanatomical architecture in individuals with a wide range of impairments. We examine the ability to perform an out-of-synergy movement with the flexion synergy caused by either shoulder or elbow loading. The results reveal that about 14% [8/57, 95% confidence interval (5.0%, 23.1%)] of the participants with severe impairment (total Fugl-Meyer score <29) in the chronic phase (6 months after stroke) are able to keep the elbow extended during shoulder loading and keep the shoulder at neutral during elbow loading. Those participants underwent a different course of neural reorganization, which enhanced abnormal synergies in comparison with individuals with mild impairment ( < 0.05). These results provide evidence that separate routes and synergy modules to motoneuron pools across the arm might exist even if the motor command is mediated possibly via the RST. We demonstrate that abnormal synergies are still selectively excited depending on the context.
中风引起的协同作用可能是由于皮质脊髓束损伤导致对网状脊髓束(RST)的优先使用。RST 分支多个运动神经元池横跨手臂,导致整体运动控制或异常协同作用,因此,个别肌肉的可控性降低。然而,目前尚不清楚由于 RST 下行的运动指令引起的异常协同作用所引起的不自主激活的肌肉是否会因主动激活的肌肉而异。研究表明,异常协同作用可能源自于无神经缺陷个体的协同作用的合并和重新加权。这导致了一个假设,即那些异常协同作用仍然根据上下文选择性地兴奋。在这项研究中,我们利用 Fugl-Meyer 评估来检验这一假设,该评估可以描述具有广泛损伤的个体的神经解剖结构。我们检查了在肩部或肘部加载引起的屈肌协同作用下执行不协调运动的能力。结果表明,大约 14%(8/57,95%置信区间(5.0%,23.1%))的慢性期(中风后 6 个月)严重损伤(总 Fugl-Meyer 评分<29)的参与者能够在肩部加载时保持肘部伸展,并且在肘部加载时保持肩部中立。与轻度损伤(<0.05)的参与者相比,这些参与者经历了不同的神经重组过程,这增强了异常协同作用。这些结果提供了证据,表明即使运动指令可能通过 RST 介导,也可能存在到手臂中运动神经元池的单独途径和协同模块。我们证明了异常协同作用仍然根据上下文选择性地兴奋。