Lattanzi Simona, Orlandi Niccolò, Giovannini Giada, Brigo Francesco, Trinka Eugen, Meletti Stefano
Neurological Clinic, Department of Experimental and Clinical Medicine, Marche Polytechnic University, Ancona, Italy.
Neurology Unit, OCB Hospital, AOU Modena, Modena, Italy.
Epilepsia. 2024 Apr;65(4):1006-1016. doi: 10.1111/epi.17912. Epub 2024 Feb 10.
Status epilepticus (SE) may lead to long-term consequences. This study evaluated the risk and predictors of seizure occurrence after SE, with a focus on SE due to acute symptomatic etiologies.
Prospectively collected data about adults surviving a first non-hypoxic SE were reviewed. The outcome was the occurrence of unprovoked seizures during the follow-up. Kaplan-Meier survival curve analysis and log-rank test were used to analyze the time to seizure occurrence and determine the statistical significance between etiological groups. Three subcategories within acute etiology were considered according to the presence of the following: (1) structural lesion (acute-primary); (2) brain involvement during systemic disorders (acute-secondary); and (3) drug or alcohol intoxication/withdrawal (acute-toxic). Cox proportional hazards model was adopted to estimate hazard ratios (HRs) with the 95% confidence intervals (CIs).
Two hundreds fifty-seven individuals were included. Fifty-four subjects (21.0%) developed seizures after a median of 9.9 (interquartile range 4.3-21.7) months after SE. The estimated 1-, 2-, and 5-year rates of seizure occurrence according to acute SE etiologies were 19.4%, 23.4%, and 30.1%, respectively, for acute-primary central nervous system (CNS) pathology; 2.2%, 2.2%, and 8.7%, respectively, for acute-secondary CNS pathology; and 0%, 9.1%, and 9.1%, respectively, for acute-toxic causes. Five-year rates of seizure occurrence for non-acute SE causes were 33.9% for remote, 65.7% for progressive, and 25.9% for unknown etiologies. In multivariate Cox regression model, progressive etiology (adjusted HR [HR] 2.27, 95% CI 1.12-4.58), SE with prominent motor phenomena evolving in non-convulsive SE (HR 3.17, 95% CI 1.38-7.25), and non-convulsive SE (HR 2.38, 95% CI 1.16-4.90) were independently associated with higher hazards of unprovoked seizures. Older people (HR .98, 95% CI .96-.99) and people with SE due to acute-secondary CNS pathology (HR .18, 95% CI .04-.82) were at decreased risk of seizure occurrence.
SE carries a risk of subsequent seizures. Both the underlying cause and epileptogenic effects of SE are likely to contribute.
癫痫持续状态(SE)可能导致长期后果。本研究评估了SE后癫痫发作的风险及预测因素,重点关注急性症状性病因导致的SE。
回顾前瞻性收集的首次非缺氧性SE存活成人的数据。结局为随访期间无诱因癫痫发作的发生情况。采用Kaplan-Meier生存曲线分析和对数秩检验分析癫痫发作时间,并确定病因组之间的统计学意义。根据以下情况将急性病因分为三个亚类:(1)结构性病变(急性原发性);(2)全身性疾病期间脑受累(急性继发性);(3)药物或酒精中毒/戒断(急性中毒性)。采用Cox比例风险模型估计风险比(HRs)及其95%置信区间(CIs)。
纳入257例个体。54例受试者(21.0%)在SE后中位数9.9(四分位间距4.3 - 21.7)个月后出现癫痫发作。根据急性SE病因,急性原发性中枢神经系统(CNS)病变的癫痫发作估计1年、2年和5年发生率分别为19.4%、23.4%和30.1%;急性继发性CNS病变分别为2.2%、2.2%和8.7%;急性中毒性病因分别为0%、9.1%和9.1%。非急性SE病因的癫痫发作5年发生率,既往病变为33.9%,进行性病变为65.7%,病因不明为25.9%。在多变量Cox回归模型中,进行性病因(调整后HR [HR] 2.27,95% CI 1.12 - 4.58)、在非惊厥性SE中演变为显著运动现象的SE(HR 3.17,95% CI 1.38 - 7.25)和非惊厥性SE(HR 2.38,95% CI 1.16 - 4.90)与无诱因癫痫发作的较高风险独立相关。老年人(HR 0.98,95% CI 0.96 - 0.99)和急性继发性CNS病变导致SE的患者(HR 0.18,95% CI 0.04 - 0.82)癫痫发作风险降低。
SE有后续癫痫发作的风险。SE的潜在病因和致痫作用可能都起作用。