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关于皮质可塑性的研究是否为使用非侵入性脑刺激治疗帕金森病患者提供了理论依据?

Do studies on cortical plasticity provide a rationale for using non-invasive brain stimulation as a treatment for Parkinson's disease patients?

作者信息

Koch Giacomo

机构信息

Non-Invasive Brain Stimulation Unit, Neurologia Clinica e Comportamentale, Fondazione Santa Lucia IRCCS , Rome , Italy ; Stroke Unit, Policlinico Tor Vergata , Rome , Italy.

出版信息

Front Neurol. 2013 Nov 6;4:180. doi: 10.3389/fneur.2013.00180.

DOI:10.3389/fneur.2013.00180
PMID:24223573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3818583/
Abstract

Animal models of Parkinson's disease (PD) have shown that key mechanisms of cortical plasticity such as long-term potentiation (LTP) and long-term depression (LTD) can be impaired by the PD pathology. In humans protocols of non-invasive brain stimulation, such as paired associative stimulation (PAS) and theta-burst stimulation (TBS), can be used to investigate cortical plasticity of the primary motor cortex. Through the amplitude of the motor evoked potential these transcranial magnetic stimulation methods allow to measure both LTP-like and LTD-like mechanisms of cortical plasticity. So far these protocols have reported some controversial findings when tested in PD patients. While various studies described evidence for reduced LTP- and LTD-like plasticity, others showed different results, demonstrating increased LTP-like and normal LTD-like plasticity. Recent evidence provided support to the hypothesis that these different patterns of cortical plasticity likely depend on the stage of the disease and on the concomitant administration of l-DOPA. However, it is still unclear how and if these altered mechanisms of cortical plasticity can be taken as a reliable model to build appropriate protocols aimed at treating PD symptoms by applying repetitive sessions of repetitive TMS (rTMS) or transcranial direct current stimulation (tDCS). The current article will provide an up-to-date overview of these issues together with some reflections on future studies in the field.

摘要

帕金森病(PD)动物模型表明,诸如长时程增强(LTP)和长时程抑制(LTD)等皮质可塑性的关键机制会受到PD病理的损害。在人类中,非侵入性脑刺激方案,如配对联想刺激(PAS)和theta爆发刺激(TBS),可用于研究初级运动皮质的皮质可塑性。通过运动诱发电位的幅度,这些经颅磁刺激方法能够测量皮质可塑性的LTP样和LTD样机制。到目前为止,这些方案在PD患者中进行测试时报告了一些有争议的结果。虽然各种研究描述了LTP样和LTD样可塑性降低的证据,但其他研究显示了不同的结果,表明LTP样可塑性增加而LTD样可塑性正常。最近的证据支持了这样一种假设,即这些不同的皮质可塑性模式可能取决于疾病阶段以及左旋多巴的联合使用。然而,目前仍不清楚这些改变的皮质可塑性机制如何以及是否可以作为一个可靠的模型,来制定通过重复经颅磁刺激(rTMS)或经颅直流电刺激(tDCS)治疗PD症状的合适方案。本文将提供这些问题的最新概述以及对该领域未来研究的一些思考。

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本文引用的文献

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Paired associative stimulation enforces the communication between interconnected areas.成对联合刺激加强了相互连接区域之间的交流。
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