Neuromodulation:经颅交流电刺激可减少神经网络同步过强和持续性眩晕

2021-07-23 MedSci原创 MedSci原创

振荡刺激在环境中是丰富的自然和人为的来源。声音、运动、光和电信号有可能通过振荡刺激与神经系统相互作用,即使它们不是有意识感知的。振荡性眩晕被称为Mal de Débarquement综合

振荡刺激在环境中是丰富的自然和人为的来源。声音、运动、光和电信号有可能通过振荡刺激与神经系统相互作用,即使它们不是有意识感知的。振荡性眩晕被称为Mal de Débarquement综合征(MdDS),或“下船病”。MdDS的神经影像学研究表明, 此病会导致神经系统功能的长期变化。MdDS通常发生在暴露于低振幅振荡运动之后,例如来自水、空气或陆地旅行。由此产生的振荡性眩晕,被描述为“摇摆”、“摆动”或“摇摆”,只有在再次暴露于被动运动(如驾驶汽车或恢复初始触发刺激)时才会改善。

内嗅皮质被认为是维持持久性MdDS的重要基质,因为它可以通过周期性刺激进入,在功能上与大片新皮质相连,并且在更新海马体与导航相关的环境特征方面起着关键作用。据报道,MdDS患者左内嗅皮质的高代谢和内嗅皮质与新皮质区域之间静息状态功能连接的改变。在背外侧前额叶皮质进行重复经颅磁刺激(rTMS)后,症状减轻与内嗅皮质和后顶叶感觉联合区(包括默认模式网络)之间的功能连接减少相关,也与前顶叶-枕叶网络之间的功能连接减少相关参与空间注意加工。患有MdDS的人除了眩晕外,还可能经历许多症状,包括头痛、视觉运动不耐受、疲劳、认知迟缓和耳鸣。这可以部分解释为内嗅皮质与前额和感觉相关区域的广泛连接。触发MdDS的相对无害的运动刺激可能因此影响广泛的大脑区域,其影响可以通过跨模态的方式测量。检验了MdDS患者听觉稳态反应(ASSR)测量的超同步性是否与症状状态相关的假设。ASSR测量听觉皮层对周期性声音刺激的神经反应,并代表皮层网络中刺激驱动同步的测量。40 Hz的ASSR已被证明是复杂认知加工、睡眠状态和双相情感障碍和精神分裂症等疾病的潜在生物标记物,因此可作为大脑同步性的一般标记物。

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刺激波形和电场分布

 

为了确定ASSR与MdDS症状状态的关系,将一组MdDS患者与年龄匹配的健康对照组进行了比较,并确定了ASSR变化与经颅交流电刺激(tACS)改变振荡性眩晕知觉之间的关系。应用三种不同的tACS条件以提供生理上的平衡刺激(反相α-tACS、同相α-tACS和反相γ-tACS)。这些刺激在参与者之间以双盲的方式随机给予,方案旨在直接测试α频率(vs.gamma)的反相刺激是否是驱动超同步症状相关正常化的关键范式。研究表明,与MdDS症状改善相关的高α带同步性降低。研究结果表明MdDS是一种由周期性运动输入驱动的多网络疾病,其中使用alpha-tACS降低超同步可能是一种治疗选择。

难治性MdDS至少持续6个月的患者, 接受单次额-顶-枕tACS治疗6个月,采用“n/1”双盲随机设计:α频率同相、α频率反相和γ频率反相对照对比。受试者按随机顺序在这三种情况下各接受一次治疗。三个条件可以排列成六个不同的顺序(1-2-3、3-2-1、2-3-1等)。每个顺序的刺激被给予四个参与者,最终形成一个由24个参与者组成的研究组。研究开始时(2017年7月),由一名未参与数据分析的研究协调员确定任何个体参与者的刺激顺序。

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MdDS参与者和健康对照组的ASSR、治疗反应

24名MdDS患者参与了研究(平均年龄53.0岁) ;平均病程38.6 ± 53.4 月[范围:6–240 月,中位数:18.0 个月)。在基线检查时,与健康对照组相比,MdDS患者的ASSR升高(t11) = 5.95页 < 0.001)。同相和反相α-tACS均能改善症状,但只有反相α-tACS在40- Hz ASSR(t检验,t12 = −9.6页 < 0.001)中有显著降低的作用。为了确定ASSR失同步是否是tACS治疗的一个标志,以及它与症状状态的相关性程度,还需要进一步将ASSR应用于其他临床综合征。超同步被认为是包括抑郁症、癫痫和帕金森氏症在内的脑部疾病的病理特征,有一种假说认为长程超同步限制了内在脑节律的表达。通过脑刺激方法来减少这种超同步现象,也许可以使局部功能恢复到一种自然状态。

总之,这是tACS如何通过减少脑网络中的病理性振荡来改善临床症状的首次研究。但是还需要大量临床实验研究。

Ahn, S., Gleghorn, D., Doudican, B., Fröhlich, F. and Cha, Y.-H. (2021), Transcranial Alternating Current Stimulation Reduces Network Hypersynchrony and Persistent Vertigo. Neuromodulation: Technology at the Neural Interface, 24: 960-968. https://doi.org/10.1111/ner.13389

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