James Peters1, Nirosen Vijiaratnam2, Heather Angus-Leppan3,4. 1. Department of Neurology, St. Vincent's Hospital, Sydney, NSW, Australia. 2. Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, University College London, London, UK. 3. Epilepsy Initiative Group, Department of Clinical Neurosciences, Royal Free London NHS Foundation Trust, London, UK. heather.angus-leppan@nhs.net. 4. Epilepsy Division, UCL Queen Square Institute of Neurology, University College London, London, UK. heather.angus-leppan@nhs.net.
Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. SIGNIFICANCE: 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.
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. SIGNIFICANCE: 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.
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