Motor cortex plasticity in Parkinson's disease and levodopa-induced dyskinesias
Motor cortex plasticity in Parkinson's disease and levodopa-induced dyskinesias
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DOI：
10.1093/brain/awl031
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发表时间：
2006-04-01
期刊：
影响因子：
14.5
通讯作者：
Chen, R
中科院分区：
文献类型：
--
作者：
Morgante, F;Espay, AJ;Chen, R
帕金森氏病的实验模型已经证明了皮质纹状体系统中异常的突触可塑性，可能与左旋多巴诱导的运动障碍（LID）的发展有关。我们检验了帕金森病的LID与人类运动皮层（M1）异常可塑性相关的假设。我们采用配对联想刺激（PAS）协议，实验干预，涉及经颅磁刺激（TMS）和正中神经刺激能够产生长时程增强（LTP）的变化，在人类的感觉运动系统。我们研究了16例中度受累的帕金森病患者（9例运动障碍，7例非运动障碍）和9例年龄匹配的健康对照者的优势侧。运动诱发电位（MEP）的幅度和皮质沉默期（CSP）的持续时间进行了测量，在PAS前的基线和PAS后长达60分钟（T0，T30和T60）在拇短展肌（APB）和小指展肌（ADM）肌肉。PAS显著增加了对照组的MEP大小（T30时为基线的+74.8%），但在停药患者中没有增加（T30：非运动障碍组为基线的+0.07%，运动障碍组为+27%）。左旋多巴恢复了非运动障碍组（T30：基线MEP的+64.9%）中PAS的MEP幅度增强，但在运动障碍组（T30：基线的-9.2%）中没有恢复。PAS延长对照组CSP持续时间。在停药的非运动障碍组中有CSP延长的趋势，但在运动障碍组中没有。在运动障碍组中，左旋多巴不能恢复PAS的CSP延长。我们的研究结果表明，LTP样可塑性是缺乏帕金森氏病的药物治疗和恢复左旋多巴在非运动障碍，但不是在运动障碍患者。运动皮层突触可塑性异常可能在LID的发生发展中起一定作用。
Experimental models of Parkinson's disease have demonstrated abnormal synaptic plasticity in the corticostriatal system, possibly related to the development of levodopa-induced dyskinesias (LID). We tested the hypothesis that LID in Parkinson's disease is associated with aberrant plasticity in the human motor cortex (M1). We employed the paired associative stimulation (PAS) protocol, an experimental intervention involving transcranial magnetic stimulation (TMS) and median nerve stimulation capable of producing long-term potentiation (LTP) like changes in the sensorimotor system in humans. We studied the more affected side of 16 moderately affected patients with Parkinson's disease (9 dyskinetic, 7 non-dyskinetic) and the dominant side of 9 age-matched healthy controls. Motor-evoked potential (MEP) amplitudes and cortical silent period (CSP) duration were measured at baseline before PAS and for up to 60 min (T0, T30 and T60) after PAS in abductor pollicis brevis (APB) and abductor digiti minimi (ADM) muscles. PAS significantly increased MEP size in controls (+74.8% of baseline at T30) but not in patients off medication (T30: +0.07% of baseline in the non-dyskinetic, +27% in the dyskinetic group). Levodopa restored the potentiation of MEP amplitudes by PAS in the non-dyskinetic group (T30: +64.9% of baseline MEP) but not in the dyskinetic group (T30: -9.2% of baseline). PAS prolonged CSP duration in controls. There was a trend towards prolongation of CSP in the non-dyskinetic group off medications but not in the dyskinetic group. Levodopa did not restore CSP prolongation by PAS in the dyskinetic group. Our findings suggest that LTP-like plasticity is deficient in Parkinson's disease off medications and is restored by levodopa in non-dyskinetic but not in dyskinetic patients. Abnormal synaptic plasticity in the motor cortex may play a role in the development of LID.