Department of Psychiatry, Emory University School of Medicine, Atlanta, GA, USA.
Brain. 2012 Feb;135(Pt 2):615-30. doi: 10.1093/brain/awr332. Epub 2012 Jan 16.
Movement disorders of basal ganglia origin may arise from abnormalities in synchronized oscillatory activity in a network that includes the basal ganglia, thalamus and motor cortices. In humans, much has been learned from the study of basal ganglia local field potentials recorded from temporarily externalized deep brain stimulator electrodes. These studies have led to the theory that Parkinson's disease has characteristic alterations in the beta frequency band (13-30 Hz) in the basal ganglia-thalamocortical network. However, different disorders have rarely been compared using recordings in the same structure under the same behavioural conditions, limiting straightforward assessment of current hypotheses. To address this, we utilized subdural electrocorticography to study cortical oscillations in the three most common movement disorders: Parkinson's disease, primary dystonia and essential tremor. We recorded local field potentials from the arm area of primary motor and sensory cortices in 31 subjects using strip electrodes placed temporarily during routine surgery for deep brain stimulator placement. We show that: (i) primary motor cortex broadband gamma power is increased in Parkinson's disease compared with the other conditions, both at rest and during a movement task; (ii) primary motor cortex high beta (20-30 Hz) power is increased in Parkinson's disease during the 'stop' phase of a movement task; (iii) the alpha-beta peaks in the motor and sensory cortical power spectra occur at higher frequencies in Parkinson's disease than in the other two disorders; and (iv) patients with dystonia have impaired movement-related beta band desynchronization in primary motor and sensory cortices. The findings support the emerging hypothesis that disease states reflect abnormalities in synchronized oscillatory activity. This is the first study of sensorimotor cortex local field potentials in the three most common movement disorders.
基底神经节起源的运动障碍可能源于包括基底神经节、丘脑和运动皮层在内的网络中同步振荡活动的异常。在人类中,从通过暂时外部化的深部脑刺激器电极记录的基底神经节局部场电位的研究中已经学到了很多。这些研究导致了帕金森病在基底神经节-丘脑皮质网络中具有特征性改变β频带(13-30 Hz)的理论。然而,很少有不同的疾病在相同的行为条件下使用相同结构中的记录进行比较,这限制了对当前假设的直接评估。为了解决这个问题,我们利用硬膜下皮层电图研究了三种最常见的运动障碍:帕金森病、原发性肌张力障碍和原发性震颤的皮质振荡。我们使用在深部脑刺激器放置过程中临时放置的带状电极,从 31 名受试者的主要运动和感觉皮层的手臂区域记录局部场电位。我们表明:(i)与其他两种情况相比,帕金森病患者在休息和运动任务期间,主要运动皮层宽带伽马功率增加;(ii)帕金森病患者在运动任务的“停止”阶段,主要运动皮层高β(20-30 Hz)功率增加;(iii)运动和感觉皮层功率谱中的α-β峰值在帕金森病患者中比在其他两种疾病中出现更高的频率;(iv)肌张力障碍患者在主要运动和感觉皮层中运动相关β带去同步化受损。这些发现支持了新兴的假说,即疾病状态反映了同步振荡活动的异常。这是在三种最常见的运动障碍中研究感觉运动皮层局部场电位的首次研究。