Department of Neurology, St. Vincent's Hospital, Sydney, NSW, Australia.
Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK.
J Neurol. 2021 Jan;268(1):321-336. doi: 10.1007/s00415-020-10153-6. Epub 2020 Aug 17.
The clinical spectrum of tics induced by antiepileptic drugs (AED), a form of 'secondary Tourettism', is largely unknown. Examining the literature aimed to help clinicians identify, understand and manage these cases. Understanding the mechanism of AED-induced tics could provide valuable insights into why certain patients may be vulnerable to this adverse event.
A pragmatic systematic review, adapted from the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, was performed. Data sources included: PubMed, Medline and Cochrane Library. No lower date restrictions were employed, with December 2019 being the end date. Any tics reported in the presence of an AED were included in the review. Case reports were not excluded due to the scant evidence. Individual patient-level data was extracted from published material and the Naranjo Scale was applied to each case to assess the likelihood of causality.
181 unique papers were identified from the search. 24 manuscripts with a total of 43 subjects met eligibility for analysis. AED with different modes of action: carbamazepine, clonazepam, lacosamide, lamotrigine, levetiracetam, phenytoin and phenobarbital; were identified as causative AEDs. The clinical phenotype was broad, although a neuropsychiatric history characterised by reduced impulse control was more predictive than a previous tic in the adult population, phenomenology had a facial/truncal predominance and most tics resolved or improve with either AED withdrawal or dose reduction.
Multiple AEDs with different modes of action can induce tic disorders, including newer AEDs. The cause is therefore unlikely to be an alteration to a single neurotransmitter, but rather an imbalance of networks, influenced further by individual factors.
抗癫痫药物(AED)引起的抽搐,即“继发性图雷特综合征”,其临床表现谱很大程度上尚未被了解。本研究旨在通过文献回顾帮助临床医生识别、理解和管理这些病例。了解 AED 引起抽搐的机制可能为为何某些患者易发生这种不良反应提供有价值的见解。
采用从系统评价和荟萃分析首选报告项目(PRISMA)指南改编而来的实用系统评价方法。数据来源包括:PubMed、Medline 和 Cochrane Library。没有设定较低的日期限制,截止日期为 2019 年 12 月。在 AED 存在的情况下报告的任何抽搐均包含在本综述中。由于证据不足,并未排除病例报告。从已发表的材料中提取个体患者数据,并对每个病例应用 Naranjo 量表评估因果关系的可能性。
从检索中确定了 181 篇独特的论文。24 篇论文共 43 名患者符合纳入分析的标准。作用机制不同的 AED:卡马西平、氯硝西泮、拉科酰胺、左乙拉西坦、苯妥英钠和苯巴比妥,被确定为致病 AED。临床表现谱广泛,尽管成年人群中存在以减少冲动控制为特征的神经精神病史比既往抽搐更具预测性,但在神经学上存在以面部/躯干为主的表现,并且大多数抽搐在 AED 停药或剂量减少后可缓解或改善。
多种作用机制不同的 AED 可引起抽搐障碍,包括新型 AED。因此,其病因不太可能是单一神经递质的改变,而是网络的失衡,个体因素也会进一步影响这种失衡。