目的:双相情感障碍(BD)对全球健康产生重大影响,然而,它的神经生理学基础仍然知之甚少。常规治疗有局限性,强调需要更好地了解BD的神经生理学,以进行早期诊断和新的治疗策略。
方法:采用PRISMA指南的系统审查方法,这项研究评估了经颅磁刺激(TMS)神经生理学在BD患者中的有效性和有效性。
方法:搜索的数据库包括PubMed、MEDLINE,Embase,和PsycINFO,涵盖1985年1月至2024年1月的研究。
结果:在筛选的6597篇文章中,九项研究符合纳入标准,使用TMS-肌电图和TMS-脑电图方法提供对BD病理生理基础的神经生理学见解。研究结果表明,与健康对照组相比,BD患者的神经生理损伤显著,特别是皮质抑制和兴奋性。特别是,在所有研究中,BD的短间隔皮质抑制(SICI)持续减弱,这表明BD的皮质抑制功能基本受损。本系统综述证实了TMS神经生理学在阐明BD病理生理基础中的潜在用途。具体来说,在BD患者中观察到的SICI范例中皮质抑制减少提示γ-氨基丁酸(GABA)-A受体介导的功能障碍,但其他TMS范例的结果不一致。因此,复杂的神经生理过程可能与BD的病理基础有关。这项研究表明,BD具有涉及GABA能功能受损的神经基础,期待对TMS神经生理学的进一步研究将进一步阐明BD的病理生理学基础。
OBJECTIVE: Bipolar disorder (BD) has a significant impact on global health, yet its neurophysiological basis remains poorly understood. Conventional treatments have limitations, highlighting the need for a better understanding of the neurophysiology of BD for early diagnosis and novel therapeutic strategies.
METHODS: Employing a systematic review approach of the PRISMA guidelines, this study assessed the usefulness and validity of transcranial magnetic stimulation (TMS) neurophysiology in patients with BD.
METHODS: Databases searched included PubMed, MEDLINE, Embase, and PsycINFO, covering studies from January 1985 to January 2024.
RESULTS: Out of 6597 articles screened, nine studies met the inclusion criteria, providing neurophysiological insights into the pathophysiological basis of BD using TMS-electromyography and TMS-
electroencephalography methods. Findings revealed significant neurophysiological impairments in patients with BD compared to healthy controls, specifically in cortical inhibition and excitability. In particular, short-interval cortical inhibition (SICI) was consistently diminished in BD across the studies, which suggests a fundamental impairment of cortical inhibitory function in BD. This systematic review corroborates the potential utility of TMS neurophysiology in elucidating the pathophysiological basis of BD. Specifically, the reduced cortical inhibition in the SICI paradigm observed in patients with BD suggests gamma-aminobutyric acid (GABA)-A receptor-mediated dysfunction, but results from other TMS paradigms have been inconsistent. Thus, complex neurophysiological processes may be involved in the pathological basis underlying BD. This study demonstrated that BD has a neural basis involving impaired GABAergic function, and it is highly expected that further research on TMS neurophysiology will further elucidate the pathophysiological basis of BD.