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Background: Neurosyphilis (NS) lacks specificity in clinical and imaging features, and patients are frequently misdiagnosed as viral encephalitis when they present with seizures. This study aimed to compare electroencephalography (EEG) in patients with seizures resulting from the two diseases and provide guidance for differential diagnosis. Methods: A retrospective study on patients diagnosed with neurosyphilis and viral encephalitis with seizures in the Department of Neurology, Zhongshan Hospital, Xiamen University from 2012 to 2020. Results: A total of 39 patients with seizures caused by neurosyphilis and 40 patients with seizures caused by viral encephalitis were included. Chi-square test analysis showed that compared with patients with viral encephalitis, patients with neurosyphilis mainly developed in middle-aged and elderly people (p < 0.001), were more likely to have temporal epileptiform discharges (p < 0.001), and less likely to have status epilepticus (SE) (p = 0.029). There was difference between two groups in the EEG performance of lateralized periodic discharges (LPDs) (p = 0.085). The two groups were matched for age and sex by case-control matching, and 25 cases in each group were successfully matched. Patients with neurosyphilis were more likely to have temporal epileptiform discharges than those with viral encephalitis (p = 0.002), and there were no significant differences in LPDs (p = 0.077) and SE (p = 0.088) between two groups. Conclusion: When EEG shows temporal epileptiform discharges, especially in the form of LPDs, we should consider the possibility of neurosyphilis.
RESUMO
OBJECTIVE: To observe the expression of Nav1.1 and the effect of electroacupuncture therapy (ET) on it after acute cerebral ischemia. METHODS: Focal acute cerebral ischemic model was established by occluding right middle cerebral artery. One hundred and forty-five male adult Sprague-Dawley rats were randomly divided into four groups: sham operation group, middle cerebral artery occlusion (MCAO) group, ET group and riluzole group. Double immunofluorescence and real-time PCR were used to observe Nav1.1 expression, and TTC staining was used to detect infarct volume at 6 hours, 1 day, 2 days, 3 days and 7 days after ischemia. RESULTS: The expression of Nav1.1 in sham operation group had no change. After ischemia, the expression of Nav1.1 was up-regulated evidently at 6 hours compared with sham operation group, down-regulated at 1 day and up-regulated again from 2 to 7 days after ischemia; the expression at 7 days was lower than that at 6 hours. In ET group and riluzole group, Nav1.1 expression were down-regulated compared with that in MCAO group after ischemia, the infarct volume was smaller than that in MCAO group at the same time point, and the difference is significant (p<0.05); however, the difference between ET group and riluzole group is not significant (p>0.05). CONCLUSION: ET and riluzole could regulate the expression of Nav1.1 after ischemia, decrease the infarction volume and reduce cerebral ischemic injury. One of the important mechanisms for ET's cerebral protective function may be that it could regulate the expression of Nav1.1 after ischemia.