Department of Medical Sciences, Infectious Diseases, Uppsala University, Uppsala 75185, Sweden.
Department of clinical neuroscience, Institute of neuroscience and physiology, Sahlgrenska Academy, University of Gothenburg, Sweden; Department of Neurology, Sahlgrenska University Hospital, Blå stråket 7, Gothenburg 41345, Sweden; Wallenberg Center for Molecular and Translational Medicine, University of Gothenburg, Sweden.
Seizure. 2022 Oct;101:11-14. doi: 10.1016/j.seizure.2022.07.005. Epub 2022 Jul 9.
We aimed to investigate whether SARS-CoV-2 infection was associated with an increased risk of incident epilepsy.
National register-based matched study. Verified cases of SARS-CoV-2 infection were acquired from the system for communicable disease surveillance in Sweden (SmiNet) and linked to data from the National Patient Register (NPR) and Cause of Death register in Sweden. Cases and non-infected controls were compared using a Cox proportional hazards model.
A total of 1,221,801 SARS-CoV-2 infected patients and 1,223,312 controls were included. Infection was not associated with an increased risk of epilepsy on a whole population level (HR 1.01, 95% CI 0.92-1.12). Statistically significant effects were observed in patients between 61 and 80 years (HR 1.66, 95% CI 1.37-2.02), also when adjusting for stroke, traumatic brain injury, tumours (same age group HR 1.50, 95% CI 1.24-1.82) and mechanical ventilation (HR 1.28, 95% CI 1.05-1.57). In patients 81-100 years, a similar significant difference was observed (HR 1.77, 95% CI 1.30-2.42), which remained after adjustment for stroke, traumatic brain injury and tumours (HR 1.51, 95% CI 1.10-2.05) but not when mechanical ventilation was included as a covariate (HR 1.34, 95% CI 0.97-1.84).
On a whole population level, SARS-CoV-2 infections is not associated with an increased risk of epilepsy. In patients above 60 years, a moderately increased risk of epilepsy was observed. However, considering potential non-controllable bias and that Covid-19 patients in intensive care present with a lower risk than the general ICU population, the virus-induced epileptogenic effect is likely very small.
我们旨在探究 SARS-CoV-2 感染是否与癫痫发病风险增加相关。
基于全国登记的匹配研究。从瑞典传染病监测系统(SmiNet)获取确诊的 SARS-CoV-2 感染病例,并与瑞典全国患者登记处(NPR)和死因登记处的数据相链接。使用 Cox 比例风险模型对病例组和未感染对照组进行比较。
共纳入了 1221801 例 SARS-CoV-2 感染患者和 1223312 例对照组。在全人群水平上,感染并未增加癫痫发病风险(HR 1.01,95%CI 0.92-1.12)。在 61-80 岁患者中观察到统计学显著的效应(HR 1.66,95%CI 1.37-2.02),当调整了中风、创伤性脑损伤、肿瘤(同年龄段 HR 1.50,95%CI 1.24-1.82)和机械通气(HR 1.28,95%CI 1.05-1.57)后仍存在这种效应。在 81-100 岁患者中,也观察到了类似的显著差异(HR 1.77,95%CI 1.30-2.42),这种关联在调整中风、创伤性脑损伤和肿瘤后仍然存在(HR 1.51,95%CI 1.10-2.05),但当将机械通气作为协变量纳入分析时,这种关联则不显著(HR 1.34,95%CI 0.97-1.84)。
在全人群水平上,SARS-CoV-2 感染与癫痫发病风险增加无关。在 60 岁以上患者中,观察到癫痫发病风险略有增加。然而,考虑到潜在的不可控偏倚以及重症监护病房中的新冠患者比一般 ICU 患者的风险更低,病毒引起的致痫效应可能非常小。