Antiseizure medications for primary and secondary seizure prevention after stroke

What protocol will prevent these seizures from happening? The correct way to solve this secondary problem is to prevent it! Where is the research doing that? Medication is NOT the answer!

We've known of this problem a long time. Provide solutions you blithering idiots!

10% seizures post stroke (19 posts to April 2017)

5% epileptic seizures after stroke (10 posts to April 2021)

epileptic seizures (6 posts to December 2015)

post-stroke epilepsy (14 posts to December 2016) 

The latest here:

 Antiseizure medications for primary and secondary seizure prevention after stroke

Zoe C. WolcottBrin E. FreundWilliam O. TatumAnteneh M. Feyissa^*

• Department of Neurology, Mayo Clinic Florida, Jacksonville, FL, United States

Post-stroke seizures (PSS) and post-stroke epilepsy (PSE) are serious complications of cerebrovascular disease, contributing to morbidity, delayed recovery, cognitive decline, and mortality. PSS are classified as early (within 7 days) or late (after 7 days), with late-onset seizures often signaling the development of PSE. As stroke survival improves, the incidence of PSS continues to rise. Risk factors include cortical involvement, large or severe strokes, and early seizures. Although antiseizure medications (ASMs) are central to management(You want these prevented from the start, medications are not the answer.), their use is limited by a lack of high-quality trials and reliable predictive tools. Routine primary prophylaxis is generally discouraged, except in high-risk patients—such as those with hemorrhagic stroke or severe cortical damage—while secondary prophylaxis after unprovoked seizures remains standard. Evidence supporting specific ASMs is limited, but lamotrigine and levetiracetam are considered reasonable first-line options. ASM selection should be individualized, particularly in older adults or those with cardiovascular or cognitive comorbidities, for whom older, enzyme-inducing ASMs carry greater risks. Withdrawal is often recommended after early seizures, but managing established PSE remains challenging without validated biomarkers. High-quality trials are urgently needed to evaluate the efficacy, safety, and tolerability of ASMs in post-stroke seizure prevention. Advancing the field also requires robust validation studies, improved prediction models, and personalized treatment strategies. This minireview summarizes current approaches to ASM use in PSS, with an emphasis on clinical decision-making for initiation and discontinuation.

1 Introduction

Post-stroke seizures (PSS) are classified as early (within 7 days) or late (after 7 days). Early seizures, or acute symptomatic seizures (ASS), result from transient neurochemical changes post-stroke and are not typically epileptic. Late seizures, or unprovoked seizures, stem from lasting structural brain changes and signify post-stroke epilepsy (PSE). The 7-day cutoff is widely accepted and aligns with underlying pathophysiology (1). Early seizures occur in 3–6% of stroke patients, more commonly in hemorrhagic (10–16%) than ischemic strokes (2–4%) (2, 3). Stroke causes 73% of acute symptomatic seizures in adults. Late seizures affect 3–5% using the 7-day definition, with incidence up to 12%. According to the International League Against Epilepsy (ILAE), PSE can be diagnosed after a single unprovoked seizure, as it reflects an enduring brain change with a high recurrence risk (>60% over 10 years) (1). Redefining PSE to include single late seizures has raised incidence estimates to 8–12% (1).

Risk factors for PSS include cortical involvement, severe or large strokes, and early seizures (2, 4, 5). Hemorrhagic strokes carry a higher PSE risk (12.4%) than ischemic ones (6.4%). Additional predictors include ICH volume, younger age, hyponatremia, alcohol use, and premorbid disability (4). Stroke treatments, including decompressive craniectomy, craniotomy, intravenous alteplase, or endovascular treatment, are also considered risk factors (3). Routine scalp electrocephalograpm (EEG) has not reliably predicted PSE, but focal epileptiform discharges and lateralized periodic patterns may carry prognostic value (6). Prediction models like the SeLECT score exist but need further validation before widespread use (7).

Studies indicate that PSS is associated with worse functional outcomes and increased disability. Patients with PSS have significantly higher modified Rankin Scale scores and greater odds of poor outcome (3). PSE also contributes to long-term morbidity. There is growing evidence linking PSE with increased dementia risk. A 2.5-fold higher dementia incidence was reported in young stroke survivors with seizures, and pooled analyses confirm that PSS is independently associated with dementia (8). This suggests a feed-forward relationship among stroke, PSS, and neurodegeneration (8).

This minireview discusses antiseizure medication (ASM) therapies for managing PSS, including clinical considerations for initiating and discontinuing treatment.

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