A causal role for the human subthalamic nucleus in non-selective cortico-motor inhibition.
A causal role for the human subthalamic nucleus in non-selective cortico-motor inhibition.
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人类底丘脑核在非选择性皮质运动抑制中的因果作用。
DOI：
10.1016/j.cub.2022.06.067
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发表时间：
2022-09-12
期刊：
影响因子：
9.2
通讯作者：
Greenlee, Jeremy D. W.
中科院分区：
文献类型：
--
作者：
Wessel, Jan R.;Diesburg, Darcy A.;Chalkey, Nathan H.;Greenlee, Jeremy D. W.
韦塞尔等人。人类底丘脑核（STN）与非选择性运动抑制存在因果关系。结合经颅磁刺激和深部脑刺激 (DBS)，他们表明，当通过 DBS 破坏 STN 时，快速停止动作对皮质脊髓兴奋性（存在于 DBS 外和健康对照中）的广泛影响不存在。 常见的运动控制皮质基底节模型表明丘脑底核（STN）在运动抑制中发挥着关键作用。特别是，当已经开始的动作必须突然停止时，据称 STN 会通过超直接途径募集，以广泛的、非选择性的方式净抑制皮质运动系统。事实上，快速动作停止期间皮质脊髓兴奋性（CSE）的抑制超出了停止的肌肉范围，甚至影响与任务无关的运动表征。尽管这种非选择性 CSE 抑制长期以来一直被归因于 STN 对运动系统的广泛抑制影响，但迄今为止缺乏这种关联的因果证据。在这里，20 名接受 STN 深部脑刺激 (DBS) 治疗的帕金森病患者和 20 名匹配的健康对照者执行了口头停止信号任务，同时通过与任务无关的手部肌肉测量 CSE。 DBS 允许对 STN 进行因果操作，而 CSE 则通过初级运动皮层的经颅磁刺激 (TMS) 和同步肌电图来测量。在 OFF-DBS 患者和对照组中，当言语反应成功停止时，手的 CSE 受到非选择性抑制。至关重要的是，当患者组中的 STN 通过 DBS 中断时，这种效应消失了。利用 DBS 和 TMS 在人类行为过程中的独特组合，当前的研究提供了第一个因果证据，表明 STN 可能参与非选择性抑制动作停止期间皮质运动系统的生理兴奋性。这证实了长期以来皮质基底神经节运动回路模型的核心预测。 STN-DBS 期间缺乏皮质运动抑制也可能为了解 STN-DBS 的常见副作用（例如冲动性增加）提供潜在的见解。
Wessel et al. causally link the human subthalamic nucleus (STN) to non-selective motor inhibition. Combining transcranial magnetic stimulation and deep-brain stimulation (DBS), they show that the broad effects of rapid action stopping on cortico-spinal excitability (which are present OFF-DBS and in healthy controls) are absent when STN is disrupted via DBS. Common cortico-basal ganglia models of motor control suggest a key role for the subthalamic nucleus (STN) in motor inhibition. In particular, when already-initiated actions have to be suddenly stopped, the STN is purportedly recruited via a hyperdirect pathway to net inhibit the cortico-motor system in a broad, non-selective fashion. Indeed, the suppression of cortico-spinal excitability (CSE) during rapid action stopping extends beyond the stopped muscle and affects even task-irrelevant motor representations. Although such non-selective CSE suppression has long been attributed to the broad inhibitory influence of STN on the motor system, causal evidence for this association is hitherto lacking. Here, 20 Parkinson’s disease patients treated with STN deep-brain stimulation (DBS) and 20 matched healthy controls performed a verbal stop-signal task while CSE was measured from a task-unrelated hand muscle. DBS allowed a causal manipulation of STN, while CSE was measured using transcranial magnetic stimulation (TMS) over primary motor cortex and concurrent electromyography. In patients OFF-DBS and controls, the CSE of the hand was non-selectively suppressed when the verbal response was successfully stopped. Crucially, this effect disappeared when STN was disrupted via DBS in the patient group. Using this unique combination of DBS and TMS during human behavior, the current study provides first causal evidence that STN is likely involved in non-selectively suppressing the physiological excitability of the cortico-motor system during action stopping. This confirms a core prediction of long-held cortico-basal ganglia circuit models of movement. The absence of cortico-motor inhibition during STN-DBS may also provide potential insights into the common side effects of STN-DBS, such as increased impulsivity.
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