Involuntary Movement: Physiological Analysis

这个项目的目标是了解不同非自愿运动障碍的潜在生理机制。我们使用的工具包括临床神经生理学方法，如脑电、肌电和经颅磁刺激，以及正电子发射断层扫描和功能磁共振成像的神经成像。该科目前正在进行的项目包括对震颤、抽搐、心理性运动障碍和阵发性运动障碍的研究。 治疗特发性震颤需要新药。用震颤加速计量法和临床震颤试验表明，正辛醇单次给药是安全的(最高可达mg/kg)，对良性特发性震颤有显著的减震作用。我们现在已经开始了一项研究，使用辛醇的时间更长。我们还计划研究辛醇的药代动力学。 我们一直在以许多不同的方式研究抽搐的生理学。使用BOLD功能磁共振成像，我们正在检测抽动和抽动模拟抽动时，抽动综合征和慢性抽动障碍患者大脑中哪些区域被激活。以前的研究已经使用神经成像来显示抽搐过程中的大脑激活以及抽动抑制。通过研究患者的自然抽动以及患者对抽搐的自愿模仿，我们希望发现大脑中哪些区域可能被激活，以产生抽搐的冲动和随后的自动运动。我们还使用血流正电子发射计算机断层扫描来确定抽动的解剖结构。在这种情况下，我们使用睡眠状态作为基线，这样我们就可以拥有一个基本上没有抽搐和抽搐冲动的状态。 我们对阵发性运动性肌张力障碍患者进行了一项研究，以更好地在临床上描述这种情况。与此同时，一位校外合作者试图找到负责的突变基因。 我们已经开始探索心因性运动障碍的病理生理学，包括震颤和肌阵挛。我们正在进行脑电和神经成像研究，试图确定大脑中负责启动运动的部分。

The goal of this project is to understand the underlying physiological mechanisms of different involuntary movement disorders. The tools we use include clinical neurophysiological methods such as electroencephalography, electromyography, and transcranial magnetic stimulation and neuroimaging with positron emission tomography and functional magnetic resonance imaging. Currently active projects in the Section include studies of tremor, tic, psychogenic movement disorders and paroxysmal movement disorders. New drugs are needed for treatment of essential tremor. Using tremor accelerometry and clinical tremor testing we have shown that 1-octanol, as a single dose, can be safely used (up to 64 mg/kg) and that it significantly reduces tremor in benign essential tremor. We have now started a study using octanol for longer periods of time. We are also planning to study the pharmacokinetics of octanol. We have been approaching the physiology of tics in many different ways. Using BOLD fMRI, we are examining what brain regions are activated during tics and tic imitations in patients with Tourette's syndrome and chronic tic disorder. Previous studies have used neuroimaging to show brain activation during tics as well as tic suppression. By studying both the patient's natural tics as well as the patient's voluntary imitation of the tic, we hope to find what brain areas may be activated in generating the urge to tic and the automatic movement that follows. We are also using blood flow PET to try to define the anatomy for tic generation. In this situation, we are using a sleep state for baseline so that we can have a state largely free of both tics and urge to tic. We have conducted a study looking at persons with paroxysmal kinesiogenic dystonia to characterize the condition better clinically. Simultaneously, there are attempts by an extramural collaborator to find the responsible mutated gene. We have begun to explore the pathophysiology of psychogenic movement disorders including tremor and myoclonus. We are doing EEG and neuroimaging studies trying to identify the parts of the brain responsible for movement initiation.