Objective: Stress is a known trigger for seizures in patients with epilepsy (PWE). However, the association between stress and seizures has not been thoroughly investigated. In December 2019, an outbreak of coronavirus disease (COVID-19) occurred in Wuhan, Hubei province, China, causing tremendous collateral stress. This study was designed to evaluate the influence of the COVID-19 outbreak on seizures in PWE in the most severely affected area, Wuhan, and its surrounding cities. Methods: In this single-center, cross-sectional study, PWE were surveyed via online questionnaires between February 23 and March 5, 2020. Collected data included demographic information, epilepsy-related characteristics (seizure type, frequency, antiepileptic drugs [AEDs], and medication management), direct and perceived threat of COVID-19, and changes in seizures during the outbreak. Psychological comorbidities were evaluated by the Patient Health Questionnaire-9, Generalized Anxiety Disorder-7 items, and Insomnia Severity Index (ISI). Multivariate logistic regression was used to identify precipitants for seizure exacerbation. Results: We received 362 completed questionnaires after excluding 12 duplicates (response rate = 63.51%). A total of 31 (8.56%) patients had increased seizures during the outbreak. Exposure history to COVID-19 (P = .001), uncontrolled seizure after AED therapy (P = .020), seizure frequency of two or more times per month before the outbreak (P = .005), change of AED regimen during the outbreak (AED reduction, withdrawal, replacement, skipping altogether; P = .002), and worry about the adverse effect of the outbreak on overall seizure-related issues (severity = moderate to critical; P = .038) were risk factors for increased seizures. Significance: A minority of PWE experienced seizure exacerbation during the outbreak of COVID-19. Stress, uncontrolled seizures, and inappropriate change in AED regimen were associated with increased seizures. Based on these findings, stress might be an independent precipitant for triggering seizures in some PWE.

Background Epileptic seizures can be difficult to distinguish from other etiologies that cause cerebral hypoxia, especially cardiac diseases. Long QT syndrome (LQTS), especially LQTS type 2 (LQT2), frequently masquerades as seizures because of the transient cerebral hypoxia caused by ventricular arrhythmia. The high rate of sudden death in LQTS highlights the importance of accurate and early diagnosis; correct diagnosis of LQTS also prevents inappropriate treatment with anti-epileptic drugs (AEDs). Case presentation We report a case of congenital LQT2 with potassium voltage-gated channel subfamily H member 2 gene (KCNH2) mutation misdiagnosed as refractory epilepsy and treated with various AEDs for 22 years. The possibility of cardiac arrhythmia was suspected after the patient presented to the emergency room and the electrocardiograph (ECG) monitor showed paroxysmal ventricular tachycardia during attacks. Atypical seizure like attacks with prodromal uncomfortable chest sensation and palpitation, triggered by auditory stimulation, and typical ventricular tachycardia monitored by ECG raised suspicion for LQT2, which was confirmed by exome sequencing and epileptic seizure was ruled out by 24-h EEG monitoring. Although the patient rejected implantation of an implantable cardioverter defibrillator, β blocker was given and the syncope only attacked 1–2 per year when there was an incentive during the 5 years follow up. Conclusions Our case illustrates how long LQTS can masquerade convincingly as epilepsy and can be treated wrongly with AEDs, putting the patient at high risk of sudden cardiac death. Careful ECG evaluation is recommend for both patients with first seizure and those with refractory epilepsy.

Background SMASH‐U is a systematic aetiological classification system for intracerebral haemorrhage (ICH) proven to be a predictor of post‐ICH haematoma expansion and mortality. However, its role in predicting functional outcome remains elusive. Therefore, we aimed to investigate whether SMASH‐U is associated with long‐term functional outcome after ICH and improves the accuracy of prediction when added to max‐ICH score. Methods Consecutive acute ICH patients from 2012 to 2018 from the neurology department of Tongji Hospital were enrolled. ICH aetiology was classified according to the SMASH‐U system. The association of SMASH‐U with 12‐month functional outcome after ICH and the predictive value were evaluated. Results Of 1938 ICH patients, the aetiology of 1295 (66.8%) patients were classified as hypertension, followed by amyloid angiopathy (n = 250, 12.9%), undetermined (n = 159, 8.2%), structural lesions (n = 149, 7.7%), systemic disease (n = 74, 3.8%) and medication (n = 11, 0.6%). The baseline characteristics were different among the six aetiologies. In multivariate analysis, SMASH‐U was proven to be a predictor of 12‐month unfavourable functional outcome. When adding the SMASH‐U system, the predictive performance of max‐ICH score was improved (area under the receiver operating characteristic curve from 0.802 to 0.812, p = 0.010) and the predictive accuracy was enhanced (integrated discrimination improvement [IDI]: 1.60%, p < 0.001; continuous net reclassification improvement [NRI]: 28.16%, p < 0.001; categorical NRI: 3.34%, p = 0.004). Conclusions SMASH‐U predicted long‐term unfavourable functional outcomes after acute ICH and improved the accuracy of prediction when added to max‐ICH score. Integrating the aetiology to a score model to predict the post‐ICH outcome may be meaningful and worthy of further exploration.