Clinical factors driving the development of epilepsy from viral encephalitis to post-encephalitis epilepsy

doi:10.11817/j.issn.1673-9248.2021.05.008

Abstract

Abstract:

Objective

Analyze the clinical factors driving the evolution of viral encephalitis (VE) seizures to post-encephalitis epilepsy (PE).

Methods

80 patients with VE seizures were included who were hospitalized from January 2018 to November 2019 in the Brain Hospital of Wuhan, General Hospital of the Yangtze River Shipping. According to whether they evolved into PE, the patients who evolved into PE were selected as the observation group (32 cases) while the patients who did not evolve into PE were used as the control group (48 cases). Chi-square test was used to compare gender, age, abnormal CT, abnormal EEG in the acute phase, increase in the cell number of cerebrospinal fluid, type of encephalitis, and disorder of consciousness in the acute phase of encephalitis, nervous defects, mental disorders in the acute phase of encephalitis, no continued use of antiepileptic drugs after the acute phase, seizures＞10 times, and differences in epilepsy in the acute phase of encephalitis. The independent sample t test was used to compare the continuous variables between the two groups. The Logistic multivariate regression were used to analyze the driving factors of VE seizures to PE.

Results

Univariate analysis showed that there was no difference between the two groups in gender, age, abnormal CT, abnormal electroencephalogram in the acute phase, increased cell number of cerebrospinal fluid, type of attack, disturbance of consciousness in the acute phase of encephalitis, neurological deficit, mental disorder in the acute phase of encephalitis, and peripheral blood. There was no statistically significant difference in WBC, serum sodium, and cerebrospinal fluid pressure (all P＞0.05). Differences were significant in taking antiepileptic drugs after the acute phase (31.25% vs 68.75%, χ²=10.861, P=0.001), over 10 seizure attacks (75.00% vs 27.08%, χ²=17.733, P＜0.001), and the acute encephalitis seizures (68.75% vs 25.00%, χ²=15.038, P＜0.001). Multivariate analysis showed that after the acute phase, antiepileptic drugs were not continued to be taken (OR=1.405, P=0.003), over 10 seizure attacks (OR=1.395, P=0.004), and epilepsy in the acute phase of encephalitis (OR=1.388, P=0.001) were independent risk factors for development of VE seizures to PE.

Conclusion

The evolution of VE seizures to PE is closely related to the failure to continue taking antiepileptic drugs after the acute phase, over 10 seizure attacks, and the acute phase of encephalitis seizure epilepsy. Clinically, targeted treatment should be given according to the specific conditions of the patient to minimize PE.

Key words: Viral encephalitis, Seizures, Epilepsy after encephalitis

Meina Feng, Yuanmin Du, Wenxian Tu. Clinical factors driving the development of epilepsy from viral encephalitis to post-encephalitis epilepsy[J]. Chinese Journal of Cerebrovascular Diseases(Electronic Edition), 2021, 15(05): 314-318.

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URL: https://zhnxgbzz.cma-cmc.com.cn/EN/10.11817/j.issn.1673-9248.2021.05.008

https://zhnxgbzz.cma-cmc.com.cn/EN/Y2021/V15/I05/314

Figures/Tables 3

因素	观察组（32例）	对照组（48例）	统计值	P值
性别[例（%）]			χ²=0.868	0.351
男	16（50.00）	29（60.42）
女	16（50.00）	19（39.58）
年龄[例（%）]			χ²=0.755	0.385
≥45岁	23（71.88）	30（62.50）
＜45岁	9（28.13）	18（37.50）
CT异常[例（%）]			χ²=1.222	0.543
皮层	10（31.25）	15（31.25）
皮层下	12（37.50）	13（27.08）
皮层及皮层下	10（31.25）	20（41.67）
急性期脑电图异常[例（%）]			χ²=0.012	0.911
非癫痫波样异常	7（21.88）	10（20.83）
癫痫波样异常	25（78.13）	38（79.17）
脑脊液细胞数增多[例（%）]			χ²=0.079	0.779
是	13（40.63）	18（37.50）
否	19（59.37）	30（62.50）
急性期后未继续服用抗癫痫药物[例（%）]			χ²=10.861	0.001
是	22（68.75）	15（31.25）
否	10（31.25）	33（68.75）
发作次数＞10次[例（%）]			χ²=17.733	＜0.001
是	24（75.00）	13（27.08）
否	8（25.00）	35（72.92）
脑炎急性期发作癫痫[例（%）]			χ²=15.038	＜0.001
是	22（68.75）	12（25.00）
否	10（31.25）	36（75.00）
发作类型[例（%）]			χ²=0.034	0.853
全面性	14（43.75）	20（41.67）
部分性	18（56.25）	28（58.33）
脑炎急性期意识障碍[例（%）]			χ²=1.014	0.314
是	17（53.13）	20（41.67）
否	15（46.88）	28（58.33）
神经系统缺损[例（%）]			χ²=0.149	0.699
是	10（31.25）	17（35.42）
否	22（68.75）	31（64.58）
脑炎急性期精神障碍[例（%）]			χ²=0.222	0.637
是	11（34.38）	19（39.58）
否	21（65.63）	29（60.42）
外周血WBC计数（×10⁹/L， $x ¯$ ±s）	8.92±1.62	8.69±1.59	t=0.629	0.531
血清钠质量浓度（mmol/L， $x ¯$ ±s）	135.26±25.66	137.11±26.04	t=0.313	0.755
脑脊液压力（mmH₂O， $x ¯$ ±s）	238.62±37.62	239.05±37.92	t=0.050	0.960

因素	观察组（32例）	对照组（48例）	统计值	P值
性别[例（%）]			χ²=0.868	0.351
男	16（50.00）	29（60.42）
女	16（50.00）	19（39.58）
年龄[例（%）]			χ²=0.755	0.385
≥45岁	23（71.88）	30（62.50）
＜45岁	9（28.13）	18（37.50）
CT异常[例（%）]			χ²=1.222	0.543
皮层	10（31.25）	15（31.25）
皮层下	12（37.50）	13（27.08）
皮层及皮层下	10（31.25）	20（41.67）
急性期脑电图异常[例（%）]			χ²=0.012	0.911
非癫痫波样异常	7（21.88）	10（20.83）
癫痫波样异常	25（78.13）	38（79.17）
脑脊液细胞数增多[例（%）]			χ²=0.079	0.779
是	13（40.63）	18（37.50）
否	19（59.37）	30（62.50）
急性期后未继续服用抗癫痫药物[例（%）]			χ²=10.861	0.001
是	22（68.75）	15（31.25）
否	10（31.25）	33（68.75）
发作次数＞10次[例（%）]			χ²=17.733	＜0.001
是	24（75.00）	13（27.08）
否	8（25.00）	35（72.92）
脑炎急性期发作癫痫[例（%）]			χ²=15.038	＜0.001
是	22（68.75）	12（25.00）
否	10（31.25）	36（75.00）
发作类型[例（%）]			χ²=0.034	0.853
全面性	14（43.75）	20（41.67）
部分性	18（56.25）	28（58.33）
脑炎急性期意识障碍[例（%）]			χ²=1.014	0.314
是	17（53.13）	20（41.67）
否	15（46.88）	28（58.33）
神经系统缺损[例（%）]			χ²=0.149	0.699
是	10（31.25）	17（35.42）
否	22（68.75）	31（64.58）
脑炎急性期精神障碍[例（%）]			χ²=0.222	0.637
是	11（34.38）	19（39.58）
否	21（65.63）	29（60.42）
外周血WBC计数（×10⁹/L， $x ¯$ ±s）	8.92±1.62	8.69±1.59	t=0.629	0.531
血清钠质量浓度（mmol/L， $x ¯$ ±s）	135.26±25.66	137.11±26.04	t=0.313	0.755
脑脊液压力（mmH₂O， $x ¯$ ±s）	238.62±37.62	239.05±37.92	t=0.050	0.960

组别	危险因素	赋值
X1	急性期后未继续服用抗癫痫药物	否=0，是=1
X2	发作次数＞10次	否=0，是=1
X3	脑炎急性期发作癫痫	否=0，是=1

因素	Wald值	P值	OR值	95%CI
急性期后未继续服用抗癫痫药物	4.614	0.003	1.405	1.091~1.455
发作次数＞10次	4.598	0.004	1.395	1.024~1.468
脑炎急性期发作癫痫	4.571	0.001	1.388	1.011~1.485

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