[运动障碍的动态活动模型:理解其病理生理学的统一观点]。

Q4 Medicine
Clinical Neurology Pub Date : 2024-06-27 Epub Date: 2024-05-30 DOI:10.5692/clinicalneurol.cn-001957
Atsushi Nambu, Satomi Chiken, Hiromi Sano, Nobuhiko Hatanaka, José A Obeso
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引用次数: 0

摘要

基底节功能失调会导致帕金森病、肌张力障碍、亨廷顿病、运动障碍和半球症等运动障碍,但其潜在的病理生理学仍存在争议。为了统一理解这些疾病的病理生理学,我们提出了 "动态活动模型",其基础是大脑皮层诱导的基底节单个核团反应的改变。在正常状态下,运动皮层受到电刺激时,模仿大脑皮层在自主运动开始时的活动,会在猴子、啮齿动物和人类的基底神经节输出站引起三相反应,包括早期兴奋、抑制和晚期兴奋。在这三个部分中,大脑皮层诱导的抑制由直接通路介导,通过解除丘脑和大脑皮层活动的抑制,在适当的时候释放适当的运动;而由超直接和间接通路介导的早期和晚期兴奋则分别复位正在进行的大脑皮层活动和停止运动。在各种运动障碍模型中,大脑皮层诱导的三相反应模式会发生系统性改变,这可以很好地解释其运动症状的病理生理学。在帕金森病的猴子和小鼠模型中,大脑皮层诱导的抑制作用减弱,阻止了运动的释放,从而导致运动障碍/运动迟缓。另一方面,在肌张力障碍的小鼠模型中,大脑皮层诱导的抑制作用增强,释放出无意运动,诱发肌肉不自主收缩。此外,在帕金森病的猴子模型中,阻断丘脑下核的活动后,大脑皮层诱导的抑制得到恢复,并能进行自主运动,这解释了立体定向手术改善帕金森病运动症状的内在机制。动态活动模型 "让我们对运动障碍症运动症状的病理生理学有了更全面的认识,并为运动障碍症的新疗法提供了线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Dynamic activity model of movement disorders: a unified view to understand their pathophysiology].

Malfunction of the basal ganglia leads to movement disorders such as Parkinson's disease, dystonia, Huntington's disease, dyskinesia, and hemiballism, but their underlying pathophysiology is still subject to debate. To understand their pathophysiology in a unified manner, we propose the "dynamic activity model", on the basis of alterations of cortically induced responses in individual nuclei of the basal ganglia. In the normal state, electric stimulation in the motor cortex, mimicking cortical activity during initiation of voluntary movements, evokes a triphasic response consisting of early excitation, inhibition, and late excitation in the output stations of the basal ganglia of monkeys, rodents, and humans. Among three components, cortically induced inhibition, which is mediated by the direct pathway, releases an appropriate movement at an appropriate time by disinhibiting thalamic and cortical activity, whereas early and late excitation, which is mediated by the hyperdirect and indirect pathways, resets on-going cortical activity and stops movements, respectively. Cortically induced triphasic response patterns are systematically altered in various movement disorder models and could well explain the pathophysiology of their motor symptoms. In monkey and mouse models of Parkinson's disease, cortically induced inhibition is reduced and prevents the release of movements, resulting in akinesia/bradykinesia. On the other hand, in a mouse model of dystonia, cortically induced inhibition is enhanced and releases unintended movements, inducing involuntary muscle contractions. Moreover, after blocking the subthalamic nucleus activity in a monkey model of Parkinson's disease, cortically induced inhibition is recovered and enables voluntary movements, explaining the underlying mechanism of stereotactic surgery to ameliorate parkinsonian motor signs. The "dynamic activity model" gives us a more comprehensive view of the pathophysiology underlying motor symptoms of movement disorders and clues for their novel therapies.

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来源期刊
Clinical Neurology
Clinical Neurology Medicine-Neurology (clinical)
CiteScore
0.30
自引率
0.00%
发文量
147
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