Sharples Simon A, Almeida Quincy J, Kalmar Jayne M
Department of Kinesiology, Wilfrid Laurier University, Waterloo, ON, Canada.
Department of Kinesiology, Wilfrid Laurier University, Waterloo, ON, Canada Sun Life Financial Movement Disorders Research & Rehabilitation Centre, Wilfrid Laurier University, Waterloo, ON, Canada.
J Parkinsons Dis. 2014;4(3):437-52. doi: 10.3233/JPD-130316.
Mirror movements are often reported in the early stages of Parkinson's disease (PD) and have been attributed to bilateral activation of the primary motor cortex; however, the precise cortical mechanisms are still unclear. Subclinical mirror activation (MA) that accompanies mirror movement has also been reported in healthy aging adults.
To characterize mirror activation and determine the cortical mechanisms of MA in individuals with PD who demonstrate mirror movements.
5 Hz rTMS to the supplementary motor area (SMA) will reduce MA by increasing interhemispheric inhibition (IHI) of the ipsilateral motor cortex.
MA was assessed using surface electromyography during maximal and submaximal unimanual contractions of the first dorsal interosseous in 7 individuals with PD with mirror movements (PD-MM: 70.9 ± 13.9 years; UPDRS III: 28.0 ± 8.2), 7 individuals with PD without mirror movements (PD-NM: 71 ± 10.1 years; UPDRS III: 27.8 ± 6.7) and 7 healthy controls (74.4 ± 6.0 years). IHI of the ipsilateral motor cortex was assessed using paired-pulse transcranial magnetic stimulation.
MA was enhanced in both PD groups during submaximal contractions, with the latest onset of activation in PD-NM. Ipsilateral motor cortex excitability was the highest in PDMM; however, IHI did not differ between PD and controls. 5 Hz rTMS to the SMA reduced IHI in PD-NM; however, did not affect MA.
IHI may not be the sole contributor to the expression of overt mirror movements in PD. Expression of overt mirror movement may be due to the combination of enhanced ipsilateral motor cortex excitability and an earlier onset of electromyographic activation in the mirror hand (mirror activation) in PDMM.
帕金森病(PD)早期常出现镜像运动,这被认为是初级运动皮层双侧激活所致;然而,确切的皮层机制仍不清楚。健康老年人中也有伴随镜像运动的亚临床镜像激活(MA)的报道。
描述PD患者出现镜像运动时的镜像激活情况,并确定MA的皮层机制。
对辅助运动区(SMA)进行5Hz重复经颅磁刺激(rTMS)将通过增加同侧运动皮层的半球间抑制(IHI)来减少MA。
在7例有镜像运动的PD患者(PD-MM:70.9±13.9岁;统一帕金森病评定量表第三部分[UPDRS III]评分:28.0±8.2)、7例无镜像运动的PD患者(PD-NM:71±10.1岁;UPDRS III评分:27.8±6.7)和7名健康对照者(74.4±6.0岁)中,使用表面肌电图在第一背侧骨间肌最大和次最大单手收缩期间评估MA。使用配对脉冲经颅磁刺激评估同侧运动皮层的IHI。
在次最大收缩期间,两个PD组的MA均增强,PD-NM组的激活开始时间最晚。PD-MM组同侧运动皮层兴奋性最高;然而,PD组与对照组之间的IHI没有差异。对SMA进行5Hz rTMS可降低PD-NM组的IHI;然而,对MA没有影响。
IHI可能不是PD中明显镜像运动表达的唯一因素。明显镜像运动的表达可能是由于PD-MM组同侧运动皮层兴奋性增强以及镜像手肌电图激活提前(镜像激活)共同作用的结果。