New Onset Focal Seizure Following COVID-19 Vaccination: Case Report

IntroductionAs more novel COVID-19 vaccines are being rolled out in a frantic pace globally, any complication that might be related to COVID-19 vaccines should be highlighted, especially since COVID-19 vaccines are relatively new, and side effects may yet to be fully elucidated. We report a case of a healthy 18-year-old male who presented with new onset focal seizures 5 days after receiving 1st dose of Oxford/AstraZeneca COVID-19 vaccine. Case PresentationThe patient was treated with intravenous phenytoin and oral levetiracetam 250mg twice daily with no further events. There was no documented fever. CT venogram and EEG were unremarkable. MRI brain revealed generalised atrophy including mild bilateral hippocampal atrophy with no evidence of sclerosis. There was no predilection for seizures identified from the patient’s history. The patient was discharged the following day on levetiracetam and advised to proceed with the 2nd dose of Oxford/AstraZeneca COVID-19 vaccination in 3 months’ time.ConclusionSeizures following COVID-19 vaccination have only been reported in a handful of cases. COVID-19 vaccination could lower seizure threshold, or unmask an underlying predisposition for epilepsy. As most COVID-19 vaccines worldwide are given in 2 doses, clinicians should consider maintaining patients on anti-seizure drugs if vaccination was thought to be a provoking factor.

Two Focal Seizure in a Patient Caused by Different Mechanism

Poststroke epilepsy is the most common cause of epilepsy in adult. Acute symptomatic seizure is a provoked seizure usually caused by systemic metabolic disorders. If stroke patient has a seizure, it is very important to discriminate whether it is a poststroke epilepsy or provoked seizure. The reason is that there are differences in the approach to treatment and the continuation of antiepileptic drugs. We report a stroke mimic patient who had two different mechanisms of focal seizures.

Case Report: Migralepsy: The Two-Faced Janus of Neurology

We report three cases of pediatric patients suffering from migraine aura triggered seizures. This entity, also called migralepsy, still does not have a unique definition today. Migraine and epilepsy are both episodic neurological disorders with periods of interictal well-being; this is indicative of similar pathophysiological mechanisms, such as increased neuronal excitation and ion channel dysfunction. The purpose of this paper is to discuss the clinical and instrumental features of migralepsy through the description of three clinical cases in which the symptoms of the usual migraine aura developed into a generalized tonic–clonic or focal seizure.

Spreading depression as an innate antiseizure mechanism

Spreading depression (SD) is an intense and prolonged depolarization in the central nervous systems from insect to man. It is implicated in neurological disorders such as migraine and brain injury. Here, using an in vivo mouse model of focal neocortical seizures, we show that SD may be a fundamental defense against seizures. Seizures induced by topical 4-aminopyridine, penicillin or bicuculline, or systemic kainic acid, culminated in SDs at a variable rate. Greater seizure power and area of recruitment predicted SD. Once triggered, SD immediately suppressed the seizure. Optogenetic or KCl-induced SDs had similar antiseizure effect sustained for more than 30 min. Conversely, pharmacologically inhibiting SD occurrence during a focal seizure facilitated seizure generalization. Altogether, our data indicate that seizures trigger SD, which then terminates the seizure and prevents its generalization.

Dementia, Subtype of Seizures, and the Risk of New Onset Seizures: A Cohort Study of a National U.S. Managed Care Database

Background: Seizure disorders have been identified in patients suffering from different types of dementia. However, the risks associated with the seizure subtypes have not been characterized. Objective: To compare the occurrence and risk of various seizure subtypes (focal and generalized) between patients with and without a dementia diagnosis. Methods: Data from 40.7 million private insured patient individual electronic health records from the U.S., were utilized. Patients 60 years of age or more from the Optum Insight Clinformatics-data Mart database were included in this study. Using ICD-9 diagnoses, the occurrence of generalized or focal seizure disorders was identified. The risk of new-onset seizures and the types of seizures associated with a dementia diagnosis were estimated in a cohort of 2,885,336 patients followed from 2005 to 2014. Group differences were analyzed using continuity-adjusted chi-square and hazard ratios with 95%confidence intervals calculated after a logistic regression analysis Results: A total of 79,561 patient records had a dementia diagnosis, and 56.38%of them were females. Patients with dementia when compared to those without dementia had higher risk for seizure disorders [Hazard ratio (HR) = 6.5 95%CI = 4.4–9.5]; grand mal status (HR = 6.5, 95%CI = 5.7–7.3); focal seizures (HR = 6.0, 95%CI = 5.5–6.6); motor simple focal status (HR = 5.6, 95%CI = 3.5–9.0); epilepsy (HR = 5.0, 95%CI = 4.8–5.2); generalized convulsive epilepsy (HR = 4.8, 95%CI = 4.5–5.0); localization-related epilepsy (HR = 4.5, 95%CI = 4.1–4.9); focal status (HR = 4.2, 95%CI = 2.9–6.1); and fits convulsions (HR = 3.5, 95%CI = 3.4–3.6). Conclusion: The study confirms that patients with dementia have higher risks of generalized or focal seizure than patients without dementia.

Traveling waves reveal a dynamic seizure source in human focal epilepsy

Treatment of patients with drug resistant focal epilepsy relies upon accurate seizure localization. Ictal activity captured in intracranial EEG (iEEG) has traditionally been interpreted to suggest that the underlying cortex is actively involved in seizures. Here, we hypothesize that such activity instead reflects propagated activity from a relatively focal seizure source, even during later time points when ictal activity is more widespread. We use the time differences observed between ictal discharges in adjacent electrodes to estimate the location of the hypothesized focal source. We demonstrate that the seizure source, localized in this manner, closely matches the clinically- and neurophysiologically-determined brain region giving rise to seizures. Moreover, this focal source is a dynamic entity that moves and evolves over the time course of a seizure. Our results offer an interpretation of ictal activity observed in iEEG that challenges the traditional conceptualization of the seizure source.