Department of Neurology, University of Leipzig, Liebigstr. 20, 04103 Leipzig, Germany.
Neurology. 2010 Mar 2;74(9):728-35. doi: 10.1212/WNL.0b013e3181d31dcf.
To study rapid-onset central motor plasticity, and its relationship to motor impairment and CNS injury in patients with multiple sclerosis (MS).
In this cross-sectional observational study, motor plasticity was examined neurophysiologically and behaviorally in 22 patients with moderately severe (median Expanded Disability Status Scale score 2.5 [0-6]) stable MS and matched healthy controls. First, plasticity was assessed using paired associative stimulation (PAS), a protocol modeling long-term synaptic potentiation in human cortex. PAS combines repetitive electric nerve stimulation with transcranial magnetic stimulation (TMS) of the contralateral motor cortex. Second, motor learning was tested by a force production task. Motor impairment was assessed by functional tests. CNS injury was evaluated by obtaining normalized N-acetyl-aspartate (NAA/Cr) spectra using magnetic resonance spectroscopy and by the corticomuscular latency (CML) to the abductor pollicis brevis muscle as tested by TMS.
Patients with MS performed worse than controls in functional motor tests, CMLs were prolonged, and NAA/Cr was decreased. PAS-induced enhancement of corticospinal excitability and training-induced increments of motor performance were comparable between patients with MS and controls. Neither PAS-induced plasticity nor motor learning performance correlated with motor impairment or measures of CNS injury. Patients with high CNS injury and good motor performance did not differ significantly from those with high CNS injury and poor motor performance with respect to PAS-induced plasticity and motor learning success.
Despite motor impairment and CNS injury in patients with multiple sclerosis (MS), rapid-onset motor plasticity is comparable to that in healthy subjects. Compensation of MS-related CNS injury is unlikely to be constrained by insufficient rapid-onset neuroplasticity.
研究多发性硬化症(MS)患者的快速中枢运动可塑性及其与运动障碍和中枢神经系统损伤的关系。
在这项横断面观察性研究中,我们对 22 名处于中度严重(扩展残疾状况量表评分中位数为 2.5[0-6])稳定 MS 的患者和匹配的健康对照者进行了神经生理学和行为学的运动可塑性检查。首先,使用配对关联刺激(PAS)评估可塑性,这一方案模拟了人类皮质中的长时程突触增强。PAS 结合了重复的电神经刺激和对侧运动皮质的经颅磁刺激(TMS)。其次,通过力产生任务测试运动学习。使用功能测试评估运动障碍。通过磁共振波谱获得标准化的 N-乙酰天冬氨酸(NAA/Cr)谱,并通过 TMS 测试对拇短展肌的皮质-运动潜伏期(CML)评估中枢神经系统损伤。
MS 患者在功能运动测试中的表现差于对照组,CML 延长,NAA/Cr 降低。MS 患者与对照组的皮质脊髓兴奋性的 PAS 诱导增强和运动表现的训练诱导增量相当。PAS 诱导的可塑性和运动学习表现均与运动障碍或中枢神经系统损伤的测量值无关。高中枢神经系统损伤和良好运动表现的患者与高中枢神经系统损伤和运动表现差的患者在 PAS 诱导的可塑性和运动学习成功方面没有显著差异。
尽管多发性硬化症(MS)患者存在运动障碍和中枢神经系统损伤,但快速发生的运动可塑性与健康受试者相当。MS 相关中枢神经系统损伤的代偿不太可能受到快速神经可塑性不足的限制。