Feinberg School of Medicine, Department of Physical Therapy and Human Movement Sciences, Northwestern University, 645 N Michigan Ave, Suite 1100, Chicago, IL, 60611, USA.
Department of Biomedical Engineering, Florida International University, 10555 West Flagler Street, EC 2600, Miami, FL, 33174, USA.
J Physiol. 2018 Apr 1;596(7):1211-1225. doi: 10.1113/JP274968. Epub 2018 Feb 19.
Activation of the shoulder abductor muscles in the arm opposite a unilateral brain injury causes involuntary increases in elbow, wrist and finger flexion in the same arm, a phenomenon referred to as the flexion synergy. It has been proposed that flexion synergy expression is related to reduced output from ipsilesional motor cortex and corticospinal pathways. In this human subjects study, we provide evidence that the magnitude of flexion synergy expression is instead related to a progressive, task-dependent recruitment of contralesional cortex. We also provide evidence that recruitment of contralesional cortex may induce excessive activation of ipsilateral reticulospinal descending motor pathways that cannot produce discrete movements, leading to flexion synergy expression. We interpret these findings as an adaptive strategy that preserves low-level motor control at the cost of fine motor control.
A hallmark of hemiparetic stroke is the loss of fine motor control in the contralesional arm and hand and the constraint to a grouped movement pattern known as the flexion synergy. In the flexion synergy, increasing shoulder abductor activation drives progressive, involuntary increases in elbow, wrist and finger flexion. The neural mechanisms underlying this phenomenon remain unclear. Here, across 25 adults with moderate to severe hemiparesis following chronic stroke and 18 adults without neurological injury, we test the overall hypothesis that two inter-related mechanisms are necessary for flexion synergy expression: increased task-dependent activation of the intact, contralesional cortex and recruitment of contralesional motor pathways via ipsilateral reticulospinal projections. First, we imaged brain activation in real time during reaching motions progressively constrained by flexion synergy expression. Using this approach, we found that cortical activity indeed shifts towards the contralesional hemisphere in direct proportion to the degree of shoulder abduction loading in the contralesional arm. We then leveraged the post-stroke reemergence of a developmental brainstem reflex to show that anatomically diffuse reticulospinal motor pathways are active during synergy expression. We interpret this progressive recruitment of contralesional cortico-reticulospinal pathways as an adaptive strategy that preserves low-level motor control at the cost of fine motor control.
在单侧脑损伤的对侧手臂中激活肩外展肌会导致同侧手臂的肘部、手腕和手指弯曲不由自主地增加，这种现象称为弯曲协同作用。有人提出，弯曲协同作用的表达与同侧运动皮层和皮质脊髓束的输出减少有关。在这项人体研究中，我们提供了证据表明，弯曲协同作用表达的幅度与对侧皮质的逐渐、任务依赖性募集有关。我们还提供了证据表明，对侧皮质的募集可能会导致过度激活同侧网状脊髓下行运动通路，从而无法产生离散运动，导致弯曲协同作用的表达。我们将这些发现解释为一种适应性策略，以牺牲精细运动控制为代价来维持低水平的运动控制。
偏瘫性中风的一个标志是对侧手臂和手失去精细运动控制，并受到一种称为弯曲协同作用的分组运动模式的限制。在弯曲协同作用中，增加肩外展肌的激活会导致肘部、手腕和手指弯曲的逐渐、不由自主的增加。这种现象的神经机制尚不清楚。在这里，我们在 25 名患有慢性中风后中度至重度偏瘫的成年人和 18 名没有神经损伤的成年人中进行了测试，以检验以下总体假设：两个相互关联的机制是弯曲协同作用表达所必需的：对完整的、对侧皮质的任务依赖性激活增加和通过同侧网状脊髓投射对对侧运动通路的募集。首先，我们在实时成像中，在通过弯曲协同作用表达逐渐限制的伸展运动期间，我们发现大脑活动确实朝着对侧半球转移，与对侧手臂中肩外展的负荷成直接比例。然后，我们利用中风后重新出现的一种发育性脑干反射来表明，解剖上弥散的网状脊髓运动通路在协同作用表达期间是活跃的。我们将这种对侧皮质-网状脊髓通路的逐渐募集解释为一种适应性策略，以牺牲精细运动控制为代价来维持低水平的运动控制。
