中风后运动恢复的机制可能涉及存活网络的重组。然而,结构连通性适应性变化的细节还没有得到很好的理解。这里,我们显示了与卒中患者运动恢复相关的白质微结构的长期变化.我们研究了10例皮质下缺血性中风患者,这些患者在最初的临床检查中表现出运动性偏瘫,在最初的弥散加权磁共振成像扫描中,梗死灶位于单侧半球内囊的后肢。参与者在连续三个时间点进行了系列扩散张量成像和运动功能评估;在2周内,发病后1个月和3个月。分析了半球和时间点之间的区域差异的分数各向异性(FA),以及使用基于道的空间统计分析与运动恢复的相关性。结果表明,3个月时,红核和同损侧背桥的FA明显增加,在所有时间点均显着降低了皮损内囊的FA,在大脑花梗中,日冕辐射,3个月时和call体。在相关性分析中,红核中团簇的FA值,背桥,call体的中体,扣带与运动功能恢复呈正相关。我们的研究表明,白质微结构的变化在替代下降的运动束,包括斑纹-脊髓通路,和半球间call骨连接可能在补偿皮质下卒中后的运动障碍中起关键作用。
The mechanism of motor recovery after stroke may involve reorganization of the surviving networks. However, details of adaptive changes in structural connectivity are not well understood. Here, we show long-term changes in white matter microstructure that relate to motor recovery in stroke patients. We studied ten subcortical ischemic stroke patients who showed motor hemiparesis at the initial clinical examination and an infarcted lesion centered in the posterior limb of internal capsule of the unilateral hemisphere at the initial diffusion-weighted magnetic resonance imaging scan. The participants underwent serial diffusion tensor imaging and motor function assessments at three consecutive time points; within 2 weeks, and at 1 and 3 months after the onset. Fractional anisotropy (FA) was analyzed for regional differences between hemispheres and time points, as well as for correlation with motor recovery using a tract-based spatial statistics analysis. The results showed significantly increased FA in the red nucleus and dorsal pons in the ipsi-lesional side at 3 months, and significantly decreased FA in the ipsi-lesional internal capsule at all time points, and in the cerebral peduncle, corona radiata, and corpus callosum at 3 months. In the correlation analysis, FA values of clusters in the red nucleus, dorsal pons, midbody of corpus callosum, and cingulum were positively correlated with recovery of motor function. Our study suggests that changes in white matter microstructure in alternative descending motor tracts including the rubro-spinal pathway, and interhemispheric callosal connections may play a key role in compensating for motor impairment after subcortical stroke.