Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label antiseizure medications. Show all posts
Showing posts with label antiseizure medications. Show all posts

Monday, July 21, 2025

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


  • 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.

More at link.

Wednesday, October 2, 2024

Some Epilepsy Drugs Tied to Cardiovascular Events in Older People

 With your chance of epilepsy and seizures post stroke make sure your competent? doctor is aware of this.


Just maybe you want your doctor to try these solutions.

Cannabidiol May Reduce Seizures by Half in Hard-to-treat Epilepsy

Or maybe the nasal spray referred to in here:

Preventing Seizure-Caused Damage to the Brain

The answers are out there, does your doctor know about them? 

Mozart may reduce seizure frequency in people with epilepsy

 

A dietary supplement dampens the brain hyperexcitability seen in seizures or epilepsy

 The latest here:

Some Epilepsy Drugs Tied to Cardiovascular Events in Older People

Link likely due to enzyme-inducing antiseizure medications

A computer rendering of a transparent body with the heart highlighted.

An association between epilepsy and cardiovascular events (CVEs) in older people was likely largely due to the use of enzyme-inducing antiseizure medications (EIASM), according to a prospective cohort study from Canada.

Among over 27,000 participants, new-onset CVEs were more likely in those with epilepsy than those without (adjusted OR 2.20, 95% CI 1.48-3.27), with the relative contribution to this association highest for "strong" EIASM use (24.6%), reported Mark Keezer, MD, PhD, of Centre de Recherche du Centre Hospitalier de l'Université de Montréal, and colleagues in JAMA Neurology.

"Our study suggests that enzyme-inducing antiseizure medications increase the risk of cardiovascular events," Keezer told MedPage Today. "Future studies will need to study whether this should lead to screening for cardiovascular disease in certain people at greater risk. Our study may also provide healthcare professionals further justification for avoiding enzyme-inducing antiseizure medications, when clinically feasible."

There is a strong association between epilepsy and cardiovascular disease, at least partly because of the overlap in risk factors, Keezer and co-authors noted. Stroke can cause epilepsy, and even in populations without cerebrovascular disease, the risk of developing cardiovascular disease is high, they pointed out. Previous research has suggested that potential damage to the heart and coronary vasculature by repeat seizures may contribute to this connection, along with EIASM use.

For this study, Keezer and team used data from 27,230 participants in the ongoing Canadian Longitudinal Study on Aging (CLSA) with 6 years of follow-up from 2015 to 2021. The CLSA includes adults ages 45 to 85 and excludes residents of long-term care facilities and those with cognitive impairment, among others.

Participants were included in this analysis if they reported no previous history of CVEs (stroke, transient ischemic attack, or myocardial infarction) at baseline. Mean age was 62.3, 52.4% were women, and 94.4% were white. In total, 431 had a lifetime history of epilepsy. Of those included, 86% completed follow-up.

The primary outcome was new-onset CVEs over 6 years, and new-onset strokes, transient ischemic attacks, or myocardial infarctions separately were secondary outcomes. To understand how mediator variables influenced relationships between epilepsy and CVEs, the researchers ran mediation analyses for strong EIASM use, weak EIASM use, Framingham score, Physical Activity Scale for the Elderly (PASE) score, and waist-to-hip ratio.

"Strong EIASM use" included use of carbamazepine, phenytoin, phenobarbital, and primidone, while "weak EIASM use" included use of drugs like oxcarbazepine, eslicarbazepine, topiramate, and rufinamide. Of the CVEs, strong EIASM use appeared to have the largest effect on myocardial infarction, with a proportion-mediated value of 59.1%.

Apart from the mediating effect of strong EIASM use, "more than two-thirds of this association may be due to other factors, such as more prevalent [cardiovascular risk factors] or a direct effect of epilepsy on [cardiovascular disease]," Keezer and colleagues wrote. Weak EIASM use, PASE score, and waist-to-hip ratio also played a role, with proportion-mediated values of 4.0%, 3.3%, and 1.6%, respectively.

The authors noted that they were limited by self-reported data, and by potential effects of the 14% of participants lost to follow-up. They also did not differentiate between ischemic stroke and hemorrhagic stroke, and noted that participants may have begun or stopped EIASM during follow-up, but EIASM data were only available for baseline use.

  • author['full_name']

    Sophie Putka is an enterprise and investigative writer for MedPage Today. Her work has appeared in the Wall Street Journal, Discover, Business Insider, Inverse, Cannabis Wire, and more. She joined MedPage Today in August of 2021. Follow

Disclosures

Data/biospecimens for this study came from the Canadian Longitudinal Study on Aging, which is funded by the Government of Canada through the Canadian Institutes of Health Research and the Canada Foundation for Innovation.

Keezer reported financial relationships with UCB, Eisai, Jazz Pharmaceuticals, and Paladin.

Co-authors reported financial relationships with Fonds de Recherche du Québec-Santé Support, Xenon, Theravance, Novartis, Eisai, Angelini Pharma, LivAssured, UCB, Montreal Heart Institute, and Jazz Pharmaceuticals.

Primary Source

JAMA Neurology

Source Reference: Li J, et al "Antiseizure medications and cardiovascular events in older people with epilepsy" JAMA Neurol 2024; DOI: 10.1001/jamaneurol.2024.3210.

Monday, November 21, 2022

Prophylactic Antiseizure Drugs for Spontaneous Intracerebral Hemorrhage: An Updated Systematic Review and Meta-analysis

So you found a problem but did nothing to solve it. Useless. Nothing on any followup needed or change to the stroke strategy to actually solve this problem. If all I ever did was describe programming problems and not solve them I'd be fired in no time. The same should apply here, going up to the mentors and senior researchers also.

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING?

Prophylactic Antiseizure Drugs for Spontaneous Intracerebral Hemorrhage: An Updated Systematic Review and Meta-analysis

Abstract

Background: 
 
There is concern that recommendations on prophylactic antiseizure drugs (PASDs) for patients with spontaneous intracerebral hemorrhage (sICH) are biased by studies using older drugs and no electrographic monitoring.
 
Aims: 
 
We performed a systematic review and meta-analysis to determine whether PASDs in patients with sICH reduced seizure occurrence and improved functional outcomes. We included analyses of newer trials, newer antiseizure drugs, and effectiveness in patients with consistent electrographic monitoring.
 
Methods: 
 
Medline, Embase, and Cochrane were searched from inception until August 12th, 2022, to identify studies with patients with sICH treated with PASDs, regardless of study design. The studied outcomes were functional status and occurrence of seizures.
 
Results:  
 
14 studies were included, including 6742 patients. Risk of bias was low overall. There was no effect of PASD on seizure occurrence overall (OR 0.73, 95% CI 0.47-1.15) but they were associated with reduced occurrence in studies with electrographic monitoring (OR 0.36, 95% CI 0.18-0.70). There was no effect of PASDs on functional outcomes (OR 1.15; 95% CI 0.91-1.47) or mortality (OR 0.85, 95% CI 0.65-1.11).
 
Conclusions: 
 
Prophylactic antiseizure medications after spontaneous intracerebral hemorrhage reduce seizures in studies with EEG monitoring in high-risk patients. However, this benefit did not reflect in improvement of functional outcomes, even in studies with newer, less toxic, antiseizure drugs.

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