Nadeau Stephen E, Dobkin Bruce, Wu Samuel S, Pei Qinglin, Duncan Pamela W
Malcom Randall VA Medical Center, Gainesville, FL, USA University of Florida College of Medicine, Gainesville, FL, USA
Geffen/UCLA School of Medicine, Los Angeles, CA, USA.
Neurorehabil Neural Repair. 2016 Aug;30(7):615-25. doi: 10.1177/1545968315613851. Epub 2015 Oct 23.
Background Paresis in stroke is largely a result of damage to descending corticospinal and corticobulbar pathways. Recovery of paresis predominantly reflects the impact on the neural consequences of this white matter lesion by reactive neuroplasticity (mechanisms involved in spontaneous recovery) and experience-dependent neuroplasticity, driven by therapy and daily experience. However, both theoretical considerations and empirical data suggest that type of stroke (large vessel distribution/lacunar infarction, hemorrhage), locus and extent of infarction (basal ganglia, right-hemisphere cerebral cortex), and the presence of leukoaraiosis or prior stroke might influence long-term recovery of walking ability. In this secondary analysis based on the 408 participants in the Locomotor Experience Applied Post-Stroke (LEAPS) study database, we seek to address these possibilities. Methods Lesion type, locus, and extent were characterized by the 2 neurologists in the LEAPS trial on the basis of clinical computed tomography and magnetic resonance imaging scans. A series of regression models was used to test our hypotheses regarding the effects of lesion type, locus, extent, and laterality on 2- to 12-month change in gait speed, controlling for baseline gait speed, age, and Berg Balance Scale score. Results Gait speed change at 1 year was significantly reduced in participants with basal ganglia involvement and prior stroke. There was a trend toward reduction of gait speed change in participants with lacunar infarctions. The presence of right-hemisphere cortical involvement had no significant impact on outcome. Conclusions Type, locus, and extent of lesion, and the loss of substrate for neuroplastic effect as a result of prior stroke may affect long-term outcome of rehabilitation of hemiparetic gait.
中风后瘫痪主要是由于皮质脊髓束和皮质延髓束下行通路受损所致。瘫痪的恢复主要反映了反应性神经可塑性(自发恢复所涉及的机制)以及由治疗和日常经验驱动的经验依赖性神经可塑性对这种白质病变神经后果的影响。然而,理论思考和实证数据均表明,中风类型(大血管分布/腔隙性梗死、出血)、梗死部位和范围(基底节、右半球大脑皮质)以及白质疏松或既往中风的存在可能会影响步行能力的长期恢复。在这项基于中风后运动经验应用(LEAPS)研究数据库中408名参与者的二次分析中,我们试图探讨这些可能性。方法:LEAPS试验中的2名神经科医生根据临床计算机断层扫描和磁共振成像扫描对病变类型、部位和范围进行了特征描述。使用一系列回归模型来检验我们关于病变类型、部位、范围和侧别对2至12个月步态速度变化影响的假设,并对基线步态速度、年龄和伯格平衡量表评分进行控制。结果:基底节受累和既往中风的参与者1年时的步态速度变化显著降低。腔隙性梗死参与者的步态速度变化有降低趋势。右半球皮质受累对结果无显著影响。结论:病变的类型、部位和范围,以及既往中风导致的神经可塑性效应底物丧失可能会影响偏瘫步态康复的长期结果。