Department of Clinical Neurophysiology, Marqués de Valdecilla University Hospital, 39008 Santander, Cantabria, Spain; Department of Physiology and Pharmacology, School of Medicine, University of Cantabria, 39008 Santander, Cantabria, Spain; Biomedical Research Institute (IDIVAL), 39011 Santander, Cantabria, Spain.
Department of Neurology, Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21210, USA.
Epilepsy Behav. 2024 Oct;159:109968. doi: 10.1016/j.yebeh.2024.109968. Epub 2024 Aug 1.
The aim of this article is to answer three relevant issues: i/What epileptic condition is referred to as subacute encephalopathy with seizures in alcoholics (SESA) syndrome; ii/ Why it can be important to distinguish SESA syndrome in clinical practice and iii/ What do we know about its pathophysiology.
We reviewed all cases published in the English language from the initial description of the syndrome to the present. All met the previously established criteria for SESA syndrome were included in our analysis.
We found 34 patients diagnosed with SESA syndrome Fourteen (41.1%) out of 34 patients were over 60 years of age. In 12 (35.2 %), abstinence, and in 4 (11.7 %) excessive consumption of alcohol, were considered precipitating factors, respectively. Triggering causes were unknown in 18 cases (53.0 %). All cases (100 %) presented with altered mental status. Fourteen (41.1 %) subjects had a history of epileptic seizures in the context of alcohol withdrawal syndrome (AWS). Twenty (58.8 %) patients had focal motor seizures (FMSs), 24 (70.5 %) bilateral tonic-clonic seizures (BTCSs), and 15 (44.1 %) focal impaired awareness seizures (FIASs). In 8 (23.5 %), criteria for focal nonconvulsive status epilepticus (NCSE) were met. Twenty-eight (82.3 %) subjects had transient neurological deficits. In 29 (85.2 %) subjects, lateralized periodic discharges (LPDs) were observed on the EEG. Areas of signal hyperintensities and restricted diffusion in neuroimaging were mentioned in 22 subjects (64.7 %). Transfer to the intensive care unit was necessary in 8 (23.5 %) subjects. Thirteen (38.2 %) had recurrent episodes. Enduring brain damage was mentioned in 9 (26.4 %) cases. The most used anti-seizure medication (ASM) was levetiracetam, followed by phenytoin and lacosamide.
SESA syndrome represents a well-defined subtype of focal NCSE in patients with chronic alcoholism. Its prompt recognition can facilitate the initiation of early ASM therapy and help design appropriate video-EEG evaluation and a treatment strategy.
本文旨在回答三个相关问题:i/ 什么是癫痫状态被称为酒精性亚急性脑病伴发癫痫(SESA)综合征;ii/ 在临床实践中区分 SESA 综合征为何重要;iii/ 我们对其病理生理学了解多少。
我们回顾了自该综合征首次描述以来发表的所有英文病例。所有符合 SESA 综合征先前确立标准的病例均纳入我们的分析。
我们发现 34 例诊断为 SESA 综合征的患者,其中 14 例(41.1%)年龄超过 60 岁。12 例(35.2%)患者的诱发因素分别为戒断,4 例(11.7%)患者的诱发因素为过度饮酒。18 例(53.0%)患者的触发原因不明。所有病例(100%)均表现为精神状态改变。14 例(41.1%)患者有酒精戒断综合征(AWS)背景下癫痫发作史。20 例(58.8%)患者有局灶性运动性癫痫发作(FMS),24 例(70.5%)有双侧强直阵挛性癫痫发作(BTCS),15 例(44.1%)有局灶性意识障碍性癫痫发作(FIAS)。8 例(23.5%)符合局灶性非惊厥性癫痫持续状态(NCSE)标准。28 例(82.3%)患者有短暂性神经功能缺损。29 例(85.2%)患者脑电图出现侧化周期性放电(LPD)。22 例(64.7%)患者神经影像学检查提示信号高信号区和弥散受限。8 例(23.5%)患者需要转入重症监护病房。13 例(38.2%)患者有反复发作。9 例(26.4%)患者有持续脑损伤。最常用的抗癫痫药物(ASM)是左乙拉西坦,其次是苯妥英和拉考酰胺。
SESA 综合征代表慢性酒精中毒患者局灶性 NCSE 的明确亚型。及时识别可以促进早期 ASM 治疗的启动,并有助于设计适当的视频脑电图评估和治疗策略。