J Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, Florida, USA.
Department of Neurology, University of Florida, Gainesville, Florida, USA.
J Neurol Neurosurg Psychiatry. 2020 May;91(5):533-539. doi: 10.1136/jnnp-2019-321973. Epub 2020 Mar 5.
Tourette syndrome is a neurodevelopmental disorder commonly associated with involuntary movements, or tics. We currently lack an ideal animal model for Tourette syndrome. In humans, clinical manifestation of tics cannot be captured via functional imaging due to motion artefacts and limited temporal resolution, and electrophysiological studies have been limited to the intraoperative environment. The goal of this study was to identify electrophysiological signals in the centromedian (CM) thalamic nucleus and primary motor (M1) cortex that differentiate tics from voluntary movements.
The data were collected as part of a larger National Institutes of Health-sponsored clinical trial. Four participants (two males, two females) underwent monthly clinical visits for collection of physiology for a total of 6 months. Participants were implanted with bilateral CM thalamic macroelectrodes and M1 subdural electrodes that were connected to two neurostimulators, both with sensing capabilities. MRI scans were performed preoperatively and CT scans postoperatively for localisation of electrodes. Electrophysiological recordings were collected at each visit from both the cortical and subcortical implants.
Recordings collected from the CM thalamic nucleus revealed a low-frequency power (3-10 Hz) increase that was time-locked to the onset of involuntary tics but was not present during voluntary movements. Cortical recordings revealed beta power decrease in M1 that was present during tics and voluntary movements.
We conclude that a human physiological signal was detected from the CM thalamus that differentiated tic from voluntary movement, and this physiological feature could potentially guide the development of neuromodulation therapies for Tourette syndrome that could use a closed-loop-based approach.
妥瑞氏综合征是一种神经发育障碍，通常与不自主运动或抽搐有关。我们目前缺乏妥瑞氏综合征的理想动物模型。在人类中，由于运动伪影和有限的时间分辨率，功能性成像无法捕捉抽搐的临床表现，而电生理研究仅限于手术室内环境。本研究的目的是确定中央（CM）丘脑核和初级运动（M1）皮层中的电生理信号，这些信号可将抽搐与自主运动区分开来。
该数据是作为美国国立卫生研究院赞助的一项更大规模的临床试验的一部分收集的。四名参与者（两名男性，两名女性）每月进行一次临床就诊，以收集生理学数据，总共进行了 6 个月。参与者接受了双侧 CM 丘脑内电极和 M1 硬脑膜下电极的植入，这些电极与两个都具有感应功能的神经刺激器相连。在术前进行 MRI 扫描，术后进行 CT 扫描以定位电极。在每次就诊时，从皮质和皮质下植入物收集电生理记录。
从 CM 丘脑核收集的记录显示，低频功率（3-10 Hz）增加与不自主抽搐的发作时间锁定，但在自主运动时不存在。皮质记录显示 M1 中的β功率下降，在抽搐和自主运动时存在。
我们得出的结论是，从 CM 丘脑检测到了一种人类生理信号，可将抽搐与自主运动区分开来，这种生理特征可能有助于开发妥瑞氏综合征的神经调节疗法，这些疗法可能使用基于闭环的方法。
