Does Levetiracetam Prevent Post-Traumatic Epilepsy After TBI?

 What is your competent? doctors EXACT PROTOCOL  to prevent post-stroke epilepsy and seizures?

• 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 (24 posts to December 2016) 

Does Levetiracetam Prevent Post-Traumatic Epilepsy After TBI?

Levetiracetam did not prevent late post-traumatic epilepsy and was associated with a higher burden of adverse outcomes despite reducing early epilepsy risk in patients with severe traumatic brain injury.

Prophylactic levetiracetam is associated with reduced risk for early epilepsy after severe traumatic brain injury (TBI) but not with reduced risk for long-term epilepsy, according to study results published in the Annals of Neurology. Patients with TBI are often prescribed ASMs to prevent post-traumatic epilepsy. However, current recommendations are largely based on older phenytoin and valproate trials and do not incorporate large-scale evidence evaluating levetiracetam, the current agent of choice.

Researchers used data from the TriNetX Research Network to examine the effectiveness and safety of prophylactic levetiracetam for preventing post-traumatic epilepsy after TBI. Patients (N=51,263) were assessed on the basis of whether they received levetiracetam (n=14,630) or no ASMs (n=34,226). Mild TBI was defined as a Glasgow Coma Scale (GCS) score of 13 to 15, moderate TBI as a GCS score of 9 to 12, severe TBI as a GCS score of 3 to 8, early epilepsy as onset within 7 days of injury, and late epilepsy as onset between day 7 and 1 year after injury. Our findings challenge widespread use of levetiracetam and suggest that prophylaxis should not be offered indiscriminately.

The levetiracetam and no ASM cohorts comprised 31.0% and 35.8% women (P <.0001), had a mean (SD) age of 53.9 (20.5) and 47.9 (20.5) years (P <.0001), included 28.9% and 31.2% non-White patients (P <.0001), and included 34.7% and 17.9% of patients with severe TBI, respectively (P <.0001).

Overall, epilepsy occurred in 6.7% of participants, and 14.1% died within 1 year of injury. Epilepsy within 1 year of injury was more frequent among patients with moderate (12.1%) and severe (11.3%) TBI than among those with mild TBI (4.8%; P <.001). Similarly, mortality was higher among patients with severe (39.0%) and moderate (15.7%) TBI than among those with mild TBI (4.7%; P <.001).

After adjustment for potential confounders, levetiracetam was associated with reduced risk for early epilepsy among patients with severe TBI (hazard ratio [HR], 0.545; 95% CI, 0.306-0.969; P =.039). Independent predictors of early epilepsy in this cohort included traumatic subdural hemorrhage, left cerebral contusion or laceration, craniectomy or craniotomy, and routine electroencephalography (EEG).

The researchers observed no significant association between prophylactic levetiracetam and late epilepsy overall or among patients with mild or severe TBI (HR range, 0.897-1.001). Levetiracetam was associated with lower risk for mortality through 1 year in the overall cohort (HR, 0.826; 95% CI, 0.787-0.867; P <.001) and among individuals who survived longer than 7 days after injury (HR, 0.881; 95% CI, 0.815-0.952; P =.001). However, in a sensitivity analysis limited to patients who survived longer than 7 days after injury, levetiracetam was not associated with a reduced risk for early epilepsy, including among patients with severe TBI.

Across 5 years of follow-up, patients who received levetiracetam had higher rates of mortality (difference, 2.2%; P <.0001), impaired memory or awareness (difference, 5.4%; P <.0001), migraine and headache (difference, 4.3%; P <.0001), metabolic disorders (difference, 2.6%; P <.0001), and malaise and fatigue (difference, 2.0%; P <.0001), among other adverse outcomes.

Study limitations include the inability of the TriNetX dataset to determine the sequence of events on the day of injury, preventing investigators from establishing whether levetiracetam was administered before seizure onset.

The researchers concluded, “In this large, severity-stratified cohort study, prophylactic levetiracetam reduced the risk of early seizures only in patients with severe TBI, without preventing late posttraumatic epilepsy and while conferring a substantial burden of adverse outcomes.” They continued, “Our findings challenge widespread use of levetiracetam and suggest that prophylaxis should not be offered indiscriminately.”

Smartwatch seizure detection app achieves near-perfect sensitivity in trial

 With your risk of seizures post stroke, will your competent? doctor prescribe this for you? 

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 (7 posts to December 2016)

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

You've been wearing a smartwatch containing this for years already because of your risk of Parkinsons, right?

Parkinson’s Disease May Have Link to Stroke March 2017 

Smartwatches Able to Detect Very Early Signs of Parkinson's July 2023 

The latest here:

Smartwatch seizure detection app achieves near-perfect sensitivity in trial

The EpiWatch seizure detection app identified tonic-clonic seizures with 98% sensitivity and an exceptionally low false alarm rate of just 1 false alert every 12.4 days in a multicentre phase 3 study, published in the journal Neurology.

The findings suggest the wearable technology could improve safety for patients with epilepsy -- particularly those at risk for sudden unexpected death in epilepsy (SUDEP) -- while addressing major barriers to adoption seen with existing seizure detection devices.

“For people who have uncontrolled tonic-clonic seizures, which can include a loss of muscle tone and airway obstruction, the risk of SUDEP is high, particularly for those who sleep alone,” said James W. Wheless, MD, Le Bonheur Children’s Hospital, Memphis, Tennessee. “Wearable seizure detection devices can alert caregivers so they can provide first aid, but some devices have high false alarm rates that can discourage use and timely intervention. Our study found the EpiWatch smartwatch app detected nearly all tonic-clonic seizures in participants and had a lower rate of false alarms.”

The study was conducted across 6 epilepsy monitoring units between September 2021 and October 202, enrolling 242 children and adults aged ≥5 years with a history or risk of tonic-clonic seizures who underwent inpatient video-EEG monitoring. Participants wore the smartwatch on the wrist opposite their seizure focus, and seizure detections generated by EpiWatch were compared against independently verified seizure events reviewed by a blinded panel of epileptologists. 

The study’s co-primary endpoints were seizure detection sensitivity and false alarm rate per 24 hours, with additional analyses assessing detection speed and night-time performance.

EpiWatch detected 46 of 47 verified tonic-clonic seizures, yielding an overall sensitivity of 98%. The single missed seizure occurred when a caregiver physically restrained the participant’s arm during the event. Across more than 16,000 hours of monitoring, only 56 false alarms were recorded, corresponding to a false alarm rate of 0.08 per 24 hours -- approximately 1 false alert every 12.4 days and roughly one-tenth the rate reported for other seizure detection devices. 

Median detection latency was 31.5 seconds, and all tonic-clonic seizures occurring during sleep were successfully identified. 

No adverse events were reported. 

“Wearing some seizure monitoring devices may carry a stigma, but using a common smartwatch with an app does not, which is important for encouraging regular use,” said Dr. Wheless. “Being prescribed an app with fewer false alarms can encourage long-term use and provide reliable caregiver alerts to help reduce sudden unexpected deaths and other risks associated with tonic-clonic seizures.”

A limitation of the study was that all seizures occurred in the controlled environment of an epilepsy monitoring unit and may not represent the variety of conditions in which people experience seizures.

Funding for the study was provided by EpiWatch.

Reference: https://www.neurology.org/doi/10.1212/WN9.0000000000000111

SOURCE: American Academy of Neurology

Functional Seizures Linked to Increased Mortality and Physical Comorbidities

 Have your doctor guarantee they can prevent post stroke seizures!

• 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:

Functional Seizures Linked to Increased Mortality and Physical Comorbidities

Individuals with functional seizures have a higher mortality risk than the general population but a lower risk than those with epileptic seizures, with substantial comorbidity burden and persistent survival disparities across matched cohorts.

Risk for death among individuals with functional seizures is higher than in the general population but remains lower than that observed in epileptic seizures, according to study results published in Epilepsia.To compare mortality risk across seizure type, researchers analyzed data from the TriNetX Research Network, including individuals with functional seizures (n=32,854), epileptic seizures (n=1,916,787), and no seizure disorder (n=21,053,667). To reduce cohort differences, 32,711 patients with functional seizures were matched 1:1 with patients with epileptic seizures, and a separate cohort of 32,274 patients with functional seizures was matched 1:1 with control participants.

The functional seizure, epileptic seizure, and control cohorts comprised 24.9%, 50.6%, and 45.6% men, respectively. Mean (SD) ages were 34.7 (19.5), 40.4 (25.2), and 35.2 (25.0) years, and 58.5%, 56.7%, and 56.4% of participants were White.

 

Although the causes of death are not explained by these data, and would benefit from future elucidation, they should provide further motivation for clinicians and services to improve engagement and therapies for people with [functional seizures].

Patients with functional seizures had higher rates of most mental and physical comorbidities compared with those with epileptic seizures. The most prevalent comorbid conditions among individuals with functional seizures, compared with those with epileptic seizures, included diseases of the nervous system (37.0% vs 24.6%; P <.001); musculoskeletal and connective tissue diseases (34.4% vs 23.3%; P <.001); endocrine, nutritional, and metabolic diseases (28.6% vs 24.8%; P <.001); digestive diseases (27.2% vs 20.8%; P <.001); and respiratory diseases (26.8% vs 21.3%; P <.001). Compared with control participants, individuals with functional seizures had higher rates of all measured comorbid mental and physical health conditions (all P <.001).

Mortality occurred among 1040 patients with functional seizures, 217,193 patients with epileptic seizures, and 627,756 control participants. Risk for mortality was higher among patients with epileptic seizures compared with those with functional seizures (hazard ratio [HR], 2.99; 95% CI, 2.81-3.18), and remained elevated after matching (HR, 2.07; 95% CI, 1.92-2.24). In contrast, control participants had a lower risk for mortality compared with patients with functional seizures (HR, 0.56; 95% CI, 0.53-0.59), including after matching (HR, 0.48; 95% CI, 0.44-0.53).

The lower mortality risk among control participants was most pronounced in the year following functional seizure diagnosis (HR, 0.39; 95% CI, 0.33-0.47). In age-stratified analyses of matched cohorts, the greatest disparity in mortality risk was observed among individuals aged 40 to 49 years (HR, 0.379; 95% CI, 0.274-0.525), with significantly lower risk also observed across other adult age groups.

Study limitations include incomplete mortality capture within the TriNetX database, lack of cause-specific mortality data, absence of socioeconomic variables, potential diagnostic misclassification, and differences in follow-up duration between cohorts.The study investigators concluded, “Although the causes of death are not explained by these data, and would benefit from future elucidation, they should provide further motivation for clinicians and services to improve engagement and therapies for people with [functional seizures].”

Disclosures: Some study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.

Ketogenic Diet May Reduce Epileptic Seizures by Changing Brain Signals: Study

 

We've known of this problem a long time. Is this a guaranteed solution?

• 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:

Ketogenic Diet May Reduce Epileptic Seizures by Changing Brain Signals: Study

Video: Post-Stroke Epilepsy — AES 2025 Expert Insights

 So nothing that will prevent post stroke epilepsy. Here's all the things you need to worry about since your doctor is doing nothing to prevent or fix the problem!

Massive incompetence shown here!

Let's see how long you've known of the problem and HAVEN'T SOLVED IT!

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

• 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 (17 posts to December 2016)

Video: Post-Stroke Epilepsy — AES 2025 Expert Insights

Neurology Advisor: “Can you describe your work in the epilepsy space?”

Dr Mishra: “I am a stroke doctor, a stroke neurologist, and as you know, stroke patients—with the advancement in the way we offer care(NOT RECOVERY!) to them—are surviving much longer, which is a great thing. But they also suffer from various post-stroke complications like post-stroke fatigue, dementia, and cognitive impairment. One of the complications they suffer from is post-stroke epilepsy.

Late seizures, or post-stroke epilepsy, are associated with poor functional outcomes and increased mortality. Therefore, my interest has been in bringing together colleagues from around the world to tackle this question together. This is essentially aimed at drug development to prevent epileptogenesis after stroke in this population. By understanding the mechanism of epileptogenesis, we may even be able to translate that knowledge to epilepsy from other causes, like tumors or post-traumatic [causes]. So the mission is really to understand the mechanism and to prevent epileptogenesis and thereby late seizures.”

Neurology Advisor: “How do outcomes differ between those with post-stroke epilepsy and those without seizures after stroke?”

Dr Mishra: “As I said, there are greater odds of mortality and greater odds of poor functional outcomes in patients who suffer from post-stroke seizures. We actually published a paper in JAMA Neurology a couple of years ago that included data from several papers published previously. We pulled them together and looked at the risk for decline: worsening modified Rankin Scale, the mean/median score, and also the outcomes associated with dementia. That paper revealed that the outcomes are worse on all 3 counts.”

Neurology Advisor: “What is the prevention strategy for first seizure after stroke?”

Dr Mishra: “Unfortunately, we currently lack a drug that has been proven to be associated with anti-epileptogenesis. What that means is that we currently do not have a medication that prevents the epileptogenic pathways from getting started after the brain injury—in this context, stroke. So, what is really missing is that information.

As far as strategies are concerned, we do know that individuals with greater cardiovascular risk are at greater risk of having seizures. Therefore, the strategies include tight control of cardiovascular risk. For instance, there are data—secondary data, secondary analyses of existing datasets—suggesting that the use of statins, for example, is associated with reduced seizure risk. Statins are [3-hydroxy-3-methylglutaryl-coenzyme A] reductase inhibitors; they reduce [low-density lipoprotein] and also have pleiotropic effects, such as stabilizing the blood–brain barrier. There are also some data—for instance, a paper on the use of losartan—showing that it stabilizes the blood–brain barrier and has been proposed to reduce the risk for epileptogenesis.

There are a few trials ongoing or recently finished. One is on eslicarbazepine, for example, which is an agent that may have anti-epileptogenic effects. The study is not yet published, so I don’t know the results. Similarly, there is another study from Monash University, led by Patrick Kwan and John-Paul Nicolo, called PEPSTEP, which is about perampanel as an anti-epileptogenic agent. Once we have these data, we will know if there is a signal of benefit in reducing the risk for late seizures in this population.”

Neurology Advisor: “What is the recommended approach for secondary prophylaxis?”

Dr Mishra: “For secondary prophylaxis, we currently lack a strongly worded guideline on which drugs are optimal for secondary prevention. By that, I mean that the patient has already had a seizure, and we want to reduce the risk for recurrent seizures. There are some papers, including 1 that my group published, suggesting that lamotrigine may be a reasonable agent. My colleague Johan Zelano from the University of Gothenburg also mentioned work from his group where lamotrigine appears to have a better profile for secondary seizure prevention.”

Neurology Advisor: “Do you have any takeaways for clinicians treating patients with post-stroke epilepsy?”

Dr Mishra: “We know there is a lack of strong, high-quality data to recommend 1 agent over another. But there are certain patient populations at higher risk for late seizures—for example, those with early seizures or acute symptomatic seizures. When we are confronted with patients with those features, or others known to be associated with late seizures, we should be more vigilant about their late-seizure risk and offer prophylactic treatment in a more personalized manner.

We also lack data on how long to offer antiseizure medications and which ones. But I think that is the approach. Some institutions have what we call a ‘PASS clinic’—Post-Acute Symptomatic Seizures. With this kind of methodical approach, you can follow these patients over time and manage their post-stroke seizure risk. This also helps generate data so we can move the field forward: how long to treat, which agents to use, which features are linked to greater seizure recurrence risk, and how to target that population more specifically.”

For People With Seizures, It May Be Better to Be Old

 Don't let your doctor use this excuse in not preventing seizures post stroke!

Let's see how long your doctor has known of the problem and HASN'T SOLVED IT!

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 (17 posts to December 2016)

For People With Seizures, It May Be Better to Be Old

ATLANTA -- In health matters it's not often that older people do better than their younger peers, but seizure disorders may be an example, suggested a cross-sectional study.

Liverpool Seizure Severity Scale (LSSS) scores, which are based on patients' self-evaluations of their seizure experiences both during and immediately after, were negatively correlated with increasing age, according to Negin Badihian, MD, of the Cleveland Clinic -- meaning that older age was associated with less overall severity. The study was conducted among more than 8,000 patients seen at the clinic from 2007 through early 2025.

Examining individual items on the LSSS questionnaire indicated that nearly all were less severe in older patients, she reported at the American Epilepsy Society annual meeting. During the ictal phase itself, greater age was associated with shorter duration, less loss of consciousness and falling, and less automotor behaviors such as lip smacking and fidgeting. Afterward, such issues as headache and confusion frequency were less severe with increasing age.

Only two of the scale's 12 items didn't correlate with age: incontinence and confusion duration.

Also surprising was that a greater comorbidity burden had relatively little impact on LSSS scores. It did correlate with greater probability of incontinence, but also with less automotor behavior, Badihian reported.

At the Cleveland Clinic's epilepsy unit, patients complete the LSSS during outpatient visits. The LSSS items are structured as statements about their seizures in general and specific common effects, which patients complete by rating the item's severity. For example,"I feel that my most severe seizures have mostly been..." followed by options ranging from "very severe" to "very mild." Other items cover loss of consciousness, falling, confusion, urinary incontinence, tongue biting, other injuries, post-seizure somnolence, headache, and time to recover full cognition. Most items refer specifically to the person's most severe seizure. Scores range from 0 to 100, increasing with greater severity.

Badihian and colleagues took account of numerous factors in analyzing the data: sex, race, epilepsy type (focal or generalized) and duration, frequency over the previous 4 weeks, whether they had undergone surgery for the seizures, use of anti-seizure medications, and area deprivation index (ADI) for the patient's residence. Analyses were performed on the raw data without adjustment, with adjustments excepting epilepsy duration, and with adjustments for all the listed factors including epilepsy duration.

In that fully adjusted model, the following significant correlations were found:

• Age: -2.69 LSSS points per 10 years
• Male sex: -2.48 points
• Black race: 2.92 points
• ADI national rank: 1.36 points per 10 units
• Seizure frequency: -5.35 points for ≥11 vs 1
• Epilepsy surgery history: -6.89 points

On the other hand, comorbidity burden, as expressed in the Charlson Comorbidity Index, did not correlate with overall LSSS scores, with an increase in 5 units associated with just a -0.10 change (P=0.91). The 10 items other than incontinence and automotor signs all appeared indifferent to comorbidity burden.

"These findings highlight the impacts of aging and comorbidities on seizure-related features," Badihian said, "which are important for patient counseling and management."

Study limitations included the long time period covered in the study, during which the treatment landscape has changed considerably. As a retrospective analysis, unmeasured confounders could have influenced the results. The study also relied on ICD-9/10 codes in patients' records for comorbidity counts, and was conducted among patients seen at one clinic.

Article Commentary: “Association of the Timing and Type of Acute Symptomatic Seizures With Poststroke Epilepsy and Mortality”

 Massive incompetence shown here!

Let's see how long you've known of the problem and HAVEN'T SOLVED IT!

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

• 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 (17 posts to December 2016)

Article Commentary: “Association of the Timing and Type of Acute Symptomatic Seizures With Poststroke Epilepsy and Mortality”

Schubert KM, Zieglgänsberger D, Bicciato G, Abraira L, Santamarina E, Álvarez-Sabín J, Ferreira-Atuesta C, Katan M, Sinka L, Terziev R, et al. Association of the Timing and Type of Acute Symptomatic Seizures With Poststroke Epilepsy and Mortality. Stroke. 2025;56:1748–1757.

Poststroke epilepsy (PSE) represents the most common cause of new-onset epilepsy in older adults.1 Recent research has shown it to be associated with increased morbidity and mortality in patients with stroke, prompting interest in the identification of risk factors and the development of prediction tools for PSE.1,2

(WOW! Prediction; NOT PREVENTION!  I'd have you all fired for cause!)

Acute symptomatic seizures (ASyS), or seizures that occur within 7 days of acute stroke, have been identified as a prominent risk factor for PSE and are included in the SeLECT score, which estimates risk of seizures in the 12 months following acute ischemic stroke.3 In their recently published cohort study, Schubert et al. take the next step by asking whether specific features of ASyS more strongly predict PSE and mortality.

The study population included patients with imaging-confirmed acute ischemic stroke at nine different international centers and was derived from the registry used for the creation of the SeLECT score (n=4552). Investigators focused this study on those patients with ASyS, which represented 5% of the total study population (n=233). The primary outcome measures were the development of PSE, defined by the occurrence of remote symptomatic seizures (RSyS), and mortality.

To answer their research question, Schubert et al. characterized ASyS by seizure type and time from stroke onset and performed statistical analyses a multivariable Cox proportional hazard regression to ascertain hazard ratios for development of PSE and mortality, adjusting for covariates such as demographic and stroke features.  

Timing of ASyS in relation to stroke was defined as days between stroke onset and seizure; as 55% (n=127) were found to have seizures on day 0, timing was dichotomized into day 0 and day 1-7. They found that patients with ASyS on day 0 have an adjusted hazard ratio of 2.3 (95% CI 1.3-4.0, p=0.003) for PSE as compared to those with ASyS on days 1-7.

Types of ASyS were subdivided first by presence of status epilepticus. Those without status epilepticus were characterized as having “short ASyS” and further subdivided by initial seizure into focal aware, focal unaware, and focal to bilateral tonic-clonic (FBTCS). Of these four types, status epilepticus and FBTCS were significantly associated with development of PSE with higher risk for status epilepticus (aHR of 9.6, p<0.001) than FBTCS (aHR of 3.4, p<0.001). Presence of status epilepticus or occurrence of FBTCS on day 0 were also associated with increase in mortality.

In addition to seizure type and timing, Schubert et al. also looked at the role of a handful of other variables associated with the development of PSE within the ASyS population, including age, male sex, stroke severity, location, and cause. Cortical involvement and large artery atherosclerosis as cause of stroke were each statistically associated with increased risk of PSE with hazard ratios of 2.2 and 1.6, respectively.

Finally, the investigators adjusted the current SeLECT score to incorporate these findings, creating the SeLECT-ASyS score to predict risk of recurrent seizure, or RSyS, which would qualify as diagnosis of PSE. Validation of the score was performed using the same three cohorts used for the initial SeLECT score, and results demonstrated its superior discrimination as compared to the existing SeLECT model in predicting PSE. The updated SeLECT-ASyS score has already been integrated into the SeLECT mobile application.

To summarize, this study by Schubert et al. demonstrates the importance of ASyS timing and type to the development of PSE and mortality. In addition, it offers a convenient tool to assist in real-time clinical assessment for this patient population. While assessing risk for PSE is desirable for clinicians, many questions remain about what to do with this knowledge of risk. Should those patients with ASyS at higher risk for PSE be treated empirically with antiseizure medications? If so, how long should they be continued? These are the natural next questions as our knowledge of PSE continues to expand.

Correlation between systemic inflammatory response index and post-stroke epilepsy based on multiple logistic regression analysis

Biomarkers don't prevent this problem! You've known of this for years, solve it you blithering idiots!

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

• 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)

 Correlation between systemic inflammatory response index and post-stroke epilepsy based on multiple logistic regression analysis

Yong Mei Hu¹Hua Huang^2*Yu Ting Chen¹Wen Jin Wang¹Bai Hui Zhang¹

• ¹College of Life and Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, China
• ²Department of Neurology, Dazhou Central Hospital, Dazhou, China

Background: Post-stroke epilepsy (PSE) is an important neurological complication affecting the prognosis of stroke patients. Recent studies have found that the systemic inflammatory response index (SIRI) is a new inflammatory marker, and its mechanism of association with PSE is not yet clear. The purpose of this study was to investigate the correlation between SIRI level and the occurrence of PSE.

Methods: The study retrospectively included 226 stroke patients admitted from July 2021 to October 2024. According to the occurrence of epilepsy, they were divided into PSE group (n = 57) and non-PSE group (n = 169). Multivariate Logistic regression analysis was used to evaluate the correlation strength between SIRI and PSE, and the Restricted Cubic Spline (RCS) model was used to explore the strong nonlinear relationship between SIRI and PSE. At the same time, the stratified analysis method was used to deeply explore the basic disease status and correct the following variables: (1) Demographic characteristics: social demographic indicators such as age, gender, BMI and education level were included; (2) lifestyle factors: including smoking status and drinking habits; (3) complications: clinical diagnosed diseases such as hypertension, diabetes, coronary heart disease and chronic obstructive pulmonary disease; (4) laboratory test parameters: including neutrophils, lymphocytes, monocytes and other blood cell classification counts, as well as biochemical indicators such as platelets, hemoglobin, total protein and total cholesterol.

Results: The baseline SIRI level in the PSE group was significantly higher than that in the non-PSE group (3.43 ± 2.74 vs. 1.79 ± 1.40, p < 0.001). Stratified analysis showed that there was a significant interaction between SIRI and PSE in the subgroup with underlying diseases (p < 0.001). The RCS analysis also suggested that there was a nonlinear positive correlation between SIRI and PSE risk (p = 0.382), and the risk inflection point appeared when SIRI = 1.36.

Conclusion: This study shows that elevated SIRI is associated with the occurrence of PSE, especially in stroke patients with underlying diseases. The results of this study provide a new reference of inflammatory biomarkers for early warning and hierarchical management of PSE.

Prediction of late seizures after ischemic stroke using cognitive scores

 

Are you that blitheringly stupid? Survivors don't want predictions; they want EXACT RECOVERY PROTOCOLS! Right now, stroke rehab is a complete failure; 10% full recovery! Why aren't you solving that problem? Predictions are fucking lazy crapola; YOU'RE FIRED!

You've known of seizures for years, PREVENT THEIR OCCURENCE! At least leaders would do that. I guess you're not leadership material, just a mouse!

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:

Prediction of late seizures after ischemic stroke using cognitive scores

• Hiroya Ohara, 
• Hironori Shimizu, 
• Masami Yamanaka, 
• Nanami Yamada, 
• Naoya Kikutsuji, 
• Ryuhei Miyoshi, 
• Hiromi Kanesaki, 
• Takahiro Kanda, 
• Keisuke Honda, 
• Masako Kinoshita & 
• Kazuma Sugie 

BMC Neurology volume 25, Article number: 410 (2025) Cite this article

Abstract

Background

Late seizures are well-known sequelae after stroke. Previous history of stroke and dementia is common etiology of epilepsy, however, the effect of cognitive impairment on late seizures has not been fully investigated. We investigated the clinical significance of cognitive scores in predicting the occurrence of post-stroke late seizures.

Methods

Adult patients with acute cerebral infarction were analyzed. Their cognitive function was evaluated using the Addenbrooke’s Cognitive Examination (ACE)-III and the Japanese version of Montreal Cognitive Assessment (MoCA-J) within two weeks after stroke. Factors associated with late seizures and accuracy of cognitive scores to predict late seizures were analyzed.

Results

Of 45 patients enrolled (28 males, age 77.2 ± 8.5 years, mean ± SD), eight patients had late seizures within 123.8 ± 126.5 days after cerebral infarction. Cognitive evaluation was performed at 8.0 ± 3.9 days. ACE-III and MoCA-J scores were significantly lower in patients with late seizures than in those without late seizures (ACE-III: 27.5 ± 17.3 vs. 59.1 ± 27.2, MoCA-J: 7.6 ± 5.9 vs. 15.4 ± 8.6, p < 0.05, unpaired t-test). Receiver operating characteristic curve analysis revealed that area under curve of ACE-III was larger than that of MoCA-J and size of cerebral infarction. The optimum cut-off scores of ACE-III were ≤ 58.5 (Sensitivity: 1.00, specificity: 0.62) and ≤ 45.0 (0.88, 0.73). Kaplan-Meier estimates showed that each cut-off score significantly associated with late seizures. Sizes of infarcts and of cortical lesion were not significantly different between patients with and without late seizures. ROC curve and Kaplan-Meier survival analyses showed a significant association between size of infarct and late seizures, however, ACE-III scores more strongly associated with late seizures than the size of infarct did.

Conclusion

Cognitive scores, especially ACE-III, within two weeks after cerebral infarction can be useful for predicting post-stroke late seizures.

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.

More at link.