Antiseizure Medication Withdrawal, Risk of Epilepsy, and Longterm EEG Trends in Acute Symptomatic Seizures or Epileptic EEG Patterns.

IF 2.3 Q3 CLINICAL NEUROLOGY Neurology. Clinical practice Pub Date : 2024-12-01 Epub Date: 2024-08-16 DOI:10.1212/CPJ.0000000000200342
Adithya Sivaraju, Alice Tao, Rakesh Jadav, Karen N Kirunda, Nishi Rampal, Jennifer A Kim, Emily J Gilmore, Lawrence J Hirsch
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Abstract

Background and objectives: Patients with acute symptomatic seizures (ASyS) and acute epileptiform findings on EEG are common. They are often prescribed long-term antiseizure medications (ASMs); it is unknown whether or when this is necessary. Primary outcome was late unprovoked seizure occurrence and association with ASM taper. The secondary outcome was EEG pattern evolution over time.

Methods: This is a retrospective cohort study of patients from 2015 to 2021 with ASyS (clinical or electrographic) and/or epileptiform findings on index hospitalization EEGs who were discharged on ASMs and had subsequent follow-up including an outpatient EEG at Yale New Haven Hospital. All patients were seen in our postacute symptomatic seizure (PASS) clinic after hospital discharge. We also developed a simple predictive score, Epilepsy-PASS (EPI-PASS), using variables independently associated with seizure recurrence based on stepwise regression; each of the 3 identified variables was assigned a score of 0 (absent) or 1 (present), for a total score of 0-3.

Results: Of 190 patients screened, 58 were excluded, leaving a final cohort of 112 patients. Twenty-four percent (27/112) patients developed a late unprovoked seizure (i.e., epilepsy). Independent predictors of epilepsy were persistence of epileptiform abnormalities on follow-up EEGs [56% developed epilepsy vs 19% without, 0.002, OR 7.18 (1.36-37.88)], clinical ASyS [32% vs 13%, p = 0.002, OR 7.45 (2.31-54.36)], and cortical involvement on imaging [40% vs 11%, p = 0.003, OR 7.63 (1.96-29.58)]. None of the 23 patients with none of these predictors (0 points on EPI-PASS) developed epilepsy, vs 13% with 1 predictor (EPI-PASS = 1) and 46% with 2 or 3 predictors (EPI-PASS = 2-3) at 1-year follow-up. ASM taper was not associated with seizure recurrence. Abnormal EEG findings in the index hospitalization usually resolved [54/69 (78%) patients] on subsequent EEGs.

Discussion: Most patients with clinical ASyS or acute epileptiform EEG findings do not require long-term ASMs. Index hospitalization EEG findings usually resolve, but if they do not, there is a >50% chance of developing epilepsy. Other predictors of epilepsy are cortical involvement on imaging and clinical ASyS. A simple 4-point scale using these 3 predictors (EPI-PASS) may help predict the risk of developing epilepsy but requires independent validation.

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急性症状性癫痫发作或癫痫脑电图模式中的抗癫痫药物停药、癫痫风险和长期脑电图趋势。
背景和目的:急性症状性癫痫发作(ASyS)和急性脑电图癫痫样发现的患者很常见。他们经常被处方长期抗癫痫药物(ASM),但是否有必要或何时有必要尚不清楚。主要研究结果是晚期无诱因癫痫发作的发生率以及与抗癫痫药物减量的关系。次要结果是脑电图模式随时间的演变:这是一项回顾性队列研究,研究对象是 2015 年至 2021 年期间住院脑电图有 ASyS(临床或电图)和/或癫痫样发现的患者,这些患者在使用 ASM 后出院,随后在耶鲁纽黑文医院接受了包括门诊脑电图在内的随访。所有患者出院后都在我们的急性症状发作后(PASS)门诊就诊。我们还根据逐步回归法,利用与癫痫复发独立相关的变量制定了一个简单的预测性评分--癫痫-PASS(EPI-PASS);3 个已确定的变量中的每个变量都被赋予 0 分(不存在)或 1 分(存在),总分为 0-3:在筛选出的 190 名患者中,有 58 人被排除在外,最后剩下 112 名患者。24%(27/112)的患者在后期出现了无诱因癫痫发作(即癫痫)。癫痫的独立预测因素包括随访脑电图中癫痫样异常的持续性[56%发生癫痫 vs 19%未发生癫痫,0.002,OR 7.18 (1.36-37.88)]、临床 ASyS [32% vs 13%,p = 0.002,OR 7.45 (2.31-54.36)]和影像学中皮质受累[40% vs 11%,p = 0.003,OR 7.63 (1.96-29.58)]。在随访 1 年时,23 名没有上述预测指标(EPI-PASS 为 0 分)的患者中没有一人发展为癫痫,而有 1 项预测指标(EPI-PASS = 1)的患者占 13%,有 2 或 3 项预测指标(EPI-PASS = 2-3)的患者占 46%。ASM 减量与癫痫复发无关。索引住院期间的异常脑电图结果通常在随后的脑电图检查中消失 [54/69 (78%) 名患者]:讨论:大多数临床 ASyS 或急性癫痫样脑电图结果患者不需要长期 ASM。住院索引脑电图结果通常会缓解,但如果没有缓解,则有大于 50% 的几率发展为癫痫。其他预测癫痫的因素包括影像学和临床 ASyS 的皮质受累。使用这 3 个预测指标的简单 4 点量表(EPI-PASS)可能有助于预测罹患癫痫的风险,但需要独立验证。
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Neurology. Clinical practice
Neurology. Clinical practice CLINICAL NEUROLOGY-
CiteScore
4.00
自引率
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发文量
77
期刊介绍: Neurology® Genetics is an online open access journal publishing peer-reviewed reports in the field of neurogenetics. The journal publishes original articles in all areas of neurogenetics including rare and common genetic variations, genotype-phenotype correlations, outlier phenotypes as a result of mutations in known disease genes, and genetic variations with a putative link to diseases. Articles include studies reporting on genetic disease risk, pharmacogenomics, and results of gene-based clinical trials (viral, ASO, etc.). Genetically engineered model systems are not a primary focus of Neurology® Genetics, but studies using model systems for treatment trials, including well-powered studies reporting negative results, are welcome.
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