Brain Stimulation Therapy for Central Post-Stroke Pain from a Perspective of Interhemispheric Neural Network Remodeling.

Brain Stimulation Therapy for Central Post-Stroke Pain from a Perspective of Interhemispheric Neural Network Remodeling.
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DOI:
10.3389/fnhum.2016.00166
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发表时间:
2016
影响因子:
2.9
通讯作者:
Inoue T
Inoue T
中科院分区:
医学3区
文献类型:
--
作者:
Morishita T;Inoue T

文献摘要

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中枢性卒中后疼痛(CPSP)是一种影响患者生活质量的严重疾病。由于CPSP是难治性的药物,各种治疗方式已尝试边际结果。自从首次报道硬膜外运动皮层(M1)电刺激(MCS)治疗CPSP以来,许多研究者对M1的电刺激机制进行了研究。CPSP目前被认为是脑卒中后的一个适应不良的网络重组问题,最近的研究表明,脑卒中后受损半球的活动可能受到对侧半球的抑制。尽管这种半球间抑制(IHI)理论最初被提出来解释中风患者的运动恢复过程,我们认为IHI也可能有助于CPSP机制。基于IHI理论和电刺激M1抑制CPSP的事实,我们假设来自对侧半球的抑制信号可能抑制同侧半球的M1活动,因此CPSP患者的疼痛抑制机制可能发生故障。在这种情况下,经颅直流电刺激(tDCS)被认为是解决半球间不平衡的合理程序,因为双侧M1可以同时使用阳极(兴奋性)和阴极(抑制性)刺激。在这篇文章中,我们回顾了潜在的机制,并提出了一个新的模型CPSP。我们还报告了两例CPSP与tDCS一起处理的病例,讨论了tDCS在治疗CPSP中的潜在作用,并对未来的研究提出了建议。
Central post-stroke pain (CPSP) is a debilitating, severe disorder affecting patient quality of life. Since CPSP is refractory to medication, various treatment modalities have been tried with marginal results. Following the first report of epidural motor cortex (M1) stimulation (MCS) for CPSP, many researchers have investigated the mechanisms of electrical stimulation of the M1. CPSP is currently considered to be a maladapted network reorganization problem following stroke, and recent studies have revealed that the activities of the impaired hemisphere after stroke may be inhibited by the contralesional hemisphere. Even though this interhemispheric inhibition (IHI) theory was originally proposed to explain the motor recovery process in stroke patients, we considered that IHI may also contribute to the CPSP mechanism. Based on the IHI theory and the fact that electrical stimulation of the M1 suppresses CPSP, we hypothesized that the inhibitory signals from the contralesional hemisphere may suppress the activities of the M1 in the ipsilesional hemisphere, and therefore pain suppression mechanisms may be malfunctioning in CPSP patients. In this context, transcranial direct current stimulation (tDCS) was considered to be a reasonable procedure to address the interhemispheric imbalance, as the bilateral M1 can be simultaneously stimulated using an anode (excitatory) and cathode (inhibitory). In this article, we review the potential mechanisms and propose a new model of CPSP. We also report two cases where CPSP was addressed with tDCS, discuss the potential roles of tDCS in the treatment of CPSP, and make recommendations for future studies.