The association of stroke and late-onset epilepsy (LOE) is discussed with special regard to its diagnosis, pathogenesis, and prevention. In addition to epidemiological data, including those from different age groups, the mechanisms for the development of acute symptomatic and remote symptomatic seizures are reviewed. The risk factors associated with seizures and post-stroke epilepsy (PSE) are considered, along with the methodological limitations of the study. For future research, the distinction between acute and remote symptomatic seizure before or after seven days from stroke onset should be reviewed because different acute symptomatic seizures (ASSs) themselves can entail a variable PSE risk. The definition of LOE by age is hitherto inconsistent. Comparing adult lifespan epochs, it is evident that stroke and seizures exhibit similar prevalence profiles. Young adulthood, old adulthood, and elderly epochs may be relevant for the differentiation of LOE subtype by age, vascular comorbidity, and other characteristics. A step-scheme strategy as a possible contribution to cerebrovascular prevention approaches is proposed.

Stroke is the fifth most common cause of death in the United States, and projections suggest that its incidence will increase in the coming decade. Of all stroke cases, 85% are caused by vascular occlusion, resulting in infarction to the brain, in a condition more specifically known as acute ischemic stroke (AIS). The American Heart Association (AHA)/American Stroke Association (ASA) guideline addresses early management of AIS for providers' use in ensuring rapid evaluation and imaging for patients suspected to be affected. The guideline also aids providers in determining and delivering the most appropriate interventions upon AIS diagnosis. This article reviews the AHA/ASA AIS guideline and highlights key components of care, such as patient evaluation, criteria for fibrinolysis and mechanical thrombectomy, postacute care, and hospital discharge with secondary prevention measures.

Background/Objectives: Cerebral cavernous malformations (CCMs) are neurological disorders that increase the risk of hemorrhagic stroke. The Mexican Hispanic population has a higher prevalence of both CCMs and metabolic syndrome (MetS), defined by the presence of three or more of the following: central obesity, elevated triglycerides, low HDL, dyslipidemia, hypertension, or elevated fasting glucose. MetS is also associated with an increased risk of hemorrhagic stroke. However, the connection between MetS and hemorrhagic stroke in Hispanic CCM patients remains uncertain. Additionally, it is unclear if Hispanic CCM patients have different cardiometabolic profiles compared to controls. Methods: We analyzed a retrospective cohort of Mexican Hispanic adult CCM patients, including age- and gender-matched controls from the NHANES database. Fisher's exact test or an unpaired Student's t-test was used to compare risk factors between the CCM cohort and controls. Additionally, we conducted relative risk regression analysis to assess the adjusted association of MetS with hemorrhagic stroke. Results: The CCM cohort showed higher rates of epilepsy (24.6% vs. 1.6%, p < 0.001) and hemorrhagic stroke (36.6% vs. 3.6%, p < 0.001), but a lower prevalence of MetS (14% vs. 54.8%, p < 0.001) compared to age- and gender-matched Mexican Hispanic controls. The adjusted analysis revealed that among CCM patients in the older age group (age ≥ 50 years), MetS was associated with hemorrhagic stroke (RR = 2.38, 95%CI: 1.40-4.02, p = 0.001). Conclusions: This study reveals distinct features of CCMs in the Mexican Hispanic population, indicating a higher risk of hemorrhagic stroke and epilepsy compared to other ethnic groups. To mitigate the risk of hemorrhagic stroke, controlling blood pressure and managing comorbidities like metabolic syndrome (MetS) and epilepsy are essential, particularly in CCM patients aged 50 years and above.

Electroencephalography (EEG) has become an indispensable tool in stroke research for real-time monitoring of neural activity, prognosis prediction, and rehabilitation support. In recent decades, EEG applications in stroke research have expanded, particularly in areas like brain-computer interfaces (BCI) and neurofeedback for motor recovery. However, a comprehensive analysis of research trends in this domain is currently unavailable.

The study collected data from the Web of Science Core Collection database, selecting publications related to stroke and EEG from 2005 to 2024. Visual analysis tools such as VOSviewer and CiteSpace were utilized to build knowledge maps of the research field, analyzing the distribution of publications, authors, institutions, journals, and collaboration networks. Additionally, co-occurrence, clustering, and burst detection of keywords were analyzed in detail.

A total of 2,931 publications were identified, indicating a consistent increase in EEG research in stroke, with significant growth post-2017. The United States, China, and Germany emerged as the leading contributors, with high collaboration networks among Western institutions. Key research areas included signal processing advancements, EEG applications in seizure risk and consciousness disorder assessment, and EEG-driven rehabilitation techniques. Notably, recent studies have focused on integrating EEG with machine learning and multimodal data for more precise functional evaluations.

The findings reveal that EEG has evolved from a diagnostic tool to a therapeutic support platform in the context of stroke care. The advent of deep learning and multimodal integration has positioned EEG for expanded applications in personalized rehabilitation. It is recommended that future studies prioritize interdisciplinary collaboration and standardized EEG methodologies in order to facilitate clinical adoption and enhance translational potential in stroke management.

Post-stroke seizures and epilepsy can affect patients' quality of life, increase mortality in stroke patients, affect patient outcomes, and are associated with higher medical expenditures. However, little is known about the risk factors that influence the onset post-stroke seizures and epilepsy.

We aimed to summarize and assess the credibility of evidence of potential risk factors for seizures and epilepsy after stroke.

Qualitative synthesis in random-effects model and evidence appraisal using Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) approach.

Pubmed, Embase, and the Cochrane Library were searched from inception to March 31, 2023. Random-effects models were used to estimate the pooled crude or adjusted relative risks (RRs) with 95% confidence intervals (CIs).

We screened 51 991 citations, selecting 15 publications with 82 829 stroke survivors encompassing 6970 seizures and epilepsy events. Risk factors assessed included patient demographic factors, stroke characteristics, medical pre-existing history, and other clinical factors. Independent risk factors identified from pooled analyses included imaging indicators of cortical location (RR, 1.62; 95% CI, 1.23-2.12), cortical involvement (RR, 3.34; 95% CI, 1.67-6.66), early seizure (RR, 4.84; 95% CI, 2.16-10.85), and stroke severity (Scandinavian Stroke Scale [SSS]-score: <30 vs. >30. RR, 5.45; 95% CI, 2.42-12.24). Based on the quality of the evidence or GRADE criteria, there was high (Class I) to very low (Class IV) confidence in the pooled effect estimates.

This meta-analysis identifies several risk factors for post-stroke seizures and epilepsy among stroke survivors. The findings enhance clinical awareness for early identification of high-risk individuals and may guide interventions to improve outcomes.

PROSPERO (CRD42023434348). Key Messages What is already known on this topic  Post-stroke seizures and epilepsy are common neurological complications of stroke, significantly affecting survivors' quality of life and clinical outcomes. Although several studies have suggested potential risk factors, including stroke severity, cortical involvement, and early seizures, no comprehensive systematic review or meta-analysis has previously been conducted to summarize and appraise the strength of evidence for these factors. What this study adds  This study provides the first comprehensive synthesis of evidence, identifying significant risk factors for post-stroke epilepsy and seizures among stroke survivors. Key findings include that cortical involvement, imaging indicators of cortical location, early seizures, and stroke severity are associated with increased risk. The study also evaluates the strength of evidence for each factor using GRADE criteria, offering a clearer understanding of their clinical relevance. How this study might affect research, practice, or policy  The findings can guide clinicians in identifying stroke survivors at high risk for seizures and epilepsy, allowing for earlier interventions and personalized care strategies. This study underscores the need for further high-quality prospective research to refine our understanding of modifiable risk factors, potentially influencing preventive strategies and healthcare policies related to stroke rehabilitation.

The risk of developing epilepsy substantially increases after the age of 60 years (late-onset epilepsy [LOE]), particularly in people with cognitive decline ([PWCD] ie, dementia and/or mild cognitive impairment). Epilepsy is associated with worse cognitive and mortality outcomes in PWCD. Identifying PWCD at risk for developing LOE can facilitate early screening and treatment of epilepsy.

To investigate factors associated with LOE in PWCD.

This longitudinal, multicenter study is based on participants from 39 US Alzheimer's Disease Research Centers from September 2005 through December 2021. Of 44 713 participants, 25 119 PWCD were identified. Of these, 14 685 were included who did not have epilepsy at enrollment, had 2 or more visits, and were 60 years or older at the most recent follow-up.

The association between various factors and LOE development in PWCD was investigated.

The primary outcome was LOE, defined as seizures starting at or after 60 years of age. Those who did not develop LOE but were 60 years or older at follow-up served as controls. A multivariable Cox regression analysis assessed the association between various factors and LOE. Independent variables included age, sex, and socioeconomic factors (education, race, ethnicity), cardiovascular risks (hypertension, diabetes, hyperlipidemia), cerebrovascular disease (stroke or history of transient ischemic attack [TIA]), other neurologic comorbidities (Parkinson disease [PD], traumatic brain injury), cognition (age at dementia onset, dementia severity, type of dementia [Alzheimer disease (AD) vs non-AD]), genetics (apolipoprotein E4 [APOE4] status), lifestyle (alcohol misuse, smoking), and depression.

Of the 14 685 participants (7355 female [50%] and 7330 male [50%]; mean [SD] age, 73.8 [8.5] years) who met the inclusion criteria, 221 participants (1.5%) developed LOE during follow-up. After adjusting for demographics, cardiovascular risks, neurologic comorbidities, genetics, cognitive factors, and depression, the following were associated with a higher risk of developing LOE: APOE4 allele (adjusted hazard ratio [aHR], 1.39; 95% CI, 1.04-1.86; P = .03), dementia onset before age 60 years (aHR, 2.46; 95% CI, 1.53-3.95; P < .001), worse cognition (aHR, 2.35; 95% CI, 1.97-2.79; P < .001), AD dementia subtype (aHR, 1.68; 95% CI, 1.13-2.49; P = .01), stroke/TIA (aHR, 2.03; 95% CI, 1.37-3.01; P < .001), and PD (aHR, 2.53; 95% CI, 1.08-5.95; P = .03). In sensitivity analysis, using an alternative LOE definition of epilepsy onset after age 65 years revealed the same factors associated with LOE.

This study showed that the APOE4 allele, dementia onset before age 60 years, AD dementia subtype, worse cognition, stroke/TIA, and PD are associated with LOE development in PWCD. PWCD with these risk factors may be considered for routine screening with an electroencephalogram for early identification of LOE.

Pregabalin, gabapentin, and carbamazepine, a potent inducer of cytochrome P450 (CYP) 3A4 and P-glycoprotein, are frequently used antiepileptic drugs that are often administered together with factor Xa inhibitors (FXaI). We aimed to investigate whether potentially clinically relevant drug-drug interactions occur with these combinations.

In an open-label fixed-sequence trial in 36 healthy volunteers, we evaluated the pharmacokinetics of 60 mg edoxaban and of a microdosed FXaI cocktail (25 µg apixaban, 50 µg edoxaban, and 25 µg rivaroxaban) before and during treatment with carbamazepine (12 evaluable volunteers, individually dosed to therapeutic concentrations), gabapentin (11 volunteers, titrated to 3 × 400 mg/d), and pregabalin (12 volunteers, titrated to 2 × 300 mg/d). The antiepileptics were dosed to steady-state and the CYP3A activity was evaluated by assessing the pharmacokinetics of microdosed midazolam (30 µg).

Carbamazepine reduced the area under the plasma concentration-time curve (AUC ∞ ) of 60 mg edoxaban by a factor of 0.48 (geometric mean ratio (GMR) with 90% CI (0.41-0.56); p < 0.0001) and Cmax by a factor of 0.47 (0.34-0.66) and reduced the exposure of the edoxaban metabolite M-4 to a similar extent. Carbamazepine also decreased the exposure (AUC ∞ ) of microdosed apixaban, edoxaban, and rivaroxaban by a factor of 0.66, 0.59, and 0.56, respectively. Gabapentin and pregabalin did neither affect the exposure of 60 mg edoxaban nor the exposure of any microdosed FXaI.

Carbamazepine decreased FXaI exposure to a clinically relevant extent and dose adjustment may be required to maintain an adequate anticoagulant effect, whereas gabapentin and pregabalin do not require dose adjustment of FXaI.

Ischemic stroke, brain tissue infarction following obstructed cerebral blood flow, leads to long-term neurological deficits and death. While neocortex is a commonly affected region with established preclinical models, less is known about deeper brain strokes, despite having unique neurological outcomes. We induced focal ischemic stroke while simultaneously monitoring neuronal activity in awake behaving Thy1-GCaMP6f mice by delivering and collecting light through bilateral fiberoptic implants. Unilateral hippocampal stroke resulted in atypical wandering behavior coincident with ipsilesional terminal spreading depolarization (sustained increase in GCaMP6f fluorescence). Ischemia induced seizures that propagated to the contralesional hippocampus triggering a transient spreading depolarization, predominantly in females. Hippocampal stroke impaired contextual fear conditioning acquired pre-stroke. Yet, 7 days post-stroke, contextual fear conditioning was only improved in mice with contralesional spreading depolarization. Blunting peri-stroke contralesional spreading depolarization prevented recovery of hippocampus-dependent learning. Together, we show that regionally isolated deleterious and beneficial spreading depolarizations can occur concurrently in the murine brain during acute stroke.

The Global Burden of Disease Study (GBD) produces prevalence estimates for 'idiopathic epilepsy' (ie, of unknown aetiology) and 'secondary epilepsy' (ie, with known aetiology) but does not report prevalence by underlying aetiologies for 'secondary epilepsy'.

We used nationwide, population-based register data from Denmark to identify underlying causes of epilepsy and their contribution to prevalence of 'secondary epilepsy' and compared with global prevalence data from GBD 2019. We identified all persons with a hospital-based epilepsy diagnosis and a filled prescription for antiseizure medication between 1 January 2009 and 31 December 2018. Epilepsy was categorised into 'idiopathic' or 'secondary' and 'total epilepsy' as the sum of the two epilepsy categories.

On 31 December 2018, a total of 5 784 284 individuals (49.7% males) were living in Denmark including 40 336 with epilepsy (51.5% males). Perinatal conditions, traumatic brain injury, brain tumours and stroke were prominent underlying causes of 'secondary epilepsy'. The prevalence of 'total epilepsy' in Denmark was 697 (95% CI 691 to 704) per 100 000 population (264 (95% CI 260 to 269) for 'secondary epilepsy' and 433 (95% CI 428 to 438) for 'idiopathic epilepsy'). In the GBD 2019 Study, the prevalence of 'total epilepsy' in 2018 was 682 (95% uncertainty interval (UI) 586 to 784) per 100 000 population (359 (95% UI 324-397) for 'secondary epilepsy' and 324 (95% UI 249 to 404) for 'idiopathic epilepsy').

Prevalence estimates of 'total epilepsy', 'idiopathic epilepsy' and 'secondary epilepsy' in Denmark align with the GBD 2019 estimates. In future studies, it is suggested to explicitly include all types of epilepsy, including 'secondary epilepsy', which is currently estimated as sequelae (consequences) of underlying diseases.

This study investigated the clinical predictive value of cerebrospinal fluid (CSF) γ-aminobutyric acid (GABA) and serum neuron-specific enolase (NSE) and microRNA-155 (miR-155) for post-stroke epilepsy (PSE) in patients with cerebral infarction (CI). A total of 69 CI patients with PSE and 84 with non-post-stroke epilepsy (N-PSE) were retrospectively enrolled, with their clinical baseline data (CI type) and the National Institute of Health Stroke Scale (NIHSS) score collected. CSF GABA and serum NSE and miR-155 expression levels were determined, with their clinical value further assessed. The results showed that the proportions of patients with cardiogenic CI, multiple infarcts, and cortical involvement and NIHSS score in PSE patients were higher than those in N-PSE patients. CSF GABA was lowly expressed and serum NSE and miR-155 were highly expressed in PSE patients. The NIHSS score negatively correlated with GABA and positively correlated with NSE and miR-155. GABA [area under the curve (AUC) = 0.906], NSE (AUC = 0.908), miR-155 (AUC = 0.862) and their combined detection (AUC = 0.963) all had certain value in the occurrence of PSE in CI patients, with their combined detection showing higher AUC than that of single detection. Briefly, CSF GABA was reduced while serum NSE and miR-155 were elevated in PSE patients. GABA and NSE combined with miR-155 had high diagnostic value for PSE occurrence in CI patients. Lowly-expressed GABA or highly-expressed NSE and miR-155 were independent risk factors for PSE in CI patients, which could provide effective guidance for the clinical diagnosis and management of PSE.

Acute symptomatic seizures, occurring shortly after a central nervous system insult, constitute nearly half of all seizure cases. However, there is a conspicuous absence of clear, comprehensive, and cohesive guidelines for the management of these seizures with antiseizure medications, especially their duration of use. This lack of consensus on the optimal duration of therapy leads to prolonged treatments that may carry adverse consequences. The primary objective of this narrative review is to present the existing evidence-based literature on the management of acute symptomatic seizures within the context of the underlying pathologies that trigger them. We explore the risk of developing epilepsy for each specific etiology and identify the factors that influence this risk. Finally, to facilitate decision-making regarding treatment duration, we categorize acute seizures based on the temporal characteristics of hyperexcitability as acute, subacute, and prolonged. Such a rubric may offer clarity in an area where consensus and guidelines are lacking.

The lack of specific guidelines for seizure treatment after acute ischemic stroke (AIS), makes the choice of an appropriate anti-seizure medication choice a challenge for providers because each drug may have different adverse effects and outcomes.

In this retrospective matched cohort study, we analyzed a 20% sample of U.S. Medicare beneficiaries aged 65 and over hospitalized for a first acute ischemic stroke (AIS) between 2009-2021 who were discharged home. We included individuals who were enrolled in Medicare hospital, medical and prescription drug insurance for 12 months prior to hospitalization and were not taking epilepsy-specific anti-seizure medication (ESM) prior to hospitalization. We matched individuals on days from discharge to ESM initiation. Individuals who initiated ESMs other than Levetiracetam, i.e. Lamotrigine, Carbamazepine, Oxcarbazepine within 30 days of discharge (N = 229) were matched to Levetiracetam initiators (N =687). We investigated the time to seizure-like events, emergency department (ED) visits, and re-hospitalizations with a follow-up of 180 days after initiation using a semi-competing risk framework. We estimated the average treatment effect among the treated i.e. those who received other ESMs.

The matched cohort of 916 ESM initiators had a median age of 74 (IQR 69, 82) and was 57% female and 71% Non-Hispanic White. Using the semi-competing risk framework, those who received other ESM had a 37% lower hazard of seizure-like events compared to receiving LEV, given that death had not occurred, hazard ratio 0.63 (95% CI: 0.43, 0.91). Among those who initiated ESMs other than Levetiracetam, the hazard of ED visits and hospitalizations, given that death had not occurred, did not different significantly from initiating Levetiracetam; hazard ratios 1.00 (95% CI: 0.80, 1.25) and 0.98 (95% CI: 0.75, 1.28), respectively.

In a sample of Medicare beneficiaries hospitalized for acute ischemic stroke and discharged home, initiating Levetiracetam in the outpatient setting was associated with a higher risk of seizure-like events compared to other ESMs. However, no significant differences were observed in the incidence of ED visits or hospitalizations, suggesting comparable safety profiles in these broader clinical outcomes.

Epilepsy is a frequent consequence of acute brain injuries, such as stroke, brain tumors, and traumatic brain injury (TBI). Accurate prediction of epilepsy is essential for early intervention and improved patient outcomes. This review evaluates the best-established prognostic models, including the SeLECT and CAVE scores, which estimate the risk of developing seizures and epilepsy following these injuries. The review highlights their clinical applicability, predictive accuracy, and limitations for different etiologies. In addition to providing practical tables for risk estimation, we also offer user-friendly online calculators for these models at www.predictepilepsy.com to facilitate clinical implementation. These tools help identify high-risk patients and support decision-making for follow-up and treatment. Furthermore, we discuss the potential of integrating electrophysiological data, including EEG biomarkers, to further enhance prediction accuracy and patient care. These insights highlight the need for further refinement and validation of predictive models, enabling more personalized treatment strategies and better patient care.

This study evaluated the therapeutic effects of open and minimally invasive surgeries in patients with drug-resistant epilepsy.

This study systematically searched electronic databases, including PubMed, Web of Science, Embase, and the Cochrane Library, for randomized controlled trials, subsequent open-label expansion studies, prospective studies and retrospective studies on surgical procedures for patients with drug-resistant epilepsy. The main outcome was seizure-free status. A one-arm meta-analysis integrating data from all studies was performed to evaluate the treatment outcomes at multiple time points.

A total of 62 studies were included, representing 5958 individuals who received five treatment regimens. The analysis results indicate that anterior temporal lobectomy (ATL) and selective amygdalohippocampectomy is still the best choice for treating drug-resistant mesial temporal lobe epilepsy in adult epilepsy patients. During the overall follow-up period, the seizure free rates for ATL, selective amygdalohippocampectomy, laser interstitial thermal therapy, radiofrequency thermocoagulation, and gamma knife surgery were 62%, 70%, 58%, 47%, and 57%, respectively.

Among the five surgical methods included in this study, ATL and selective amygdala hippocampal resection seem to have more advantages in postoperative epilepsy control compared to laser interstitial hyperthermia, radiofrequency thermocoagulation, and gamma knife surgery. Each surgical treatment method has its unique focus, and when choosing a specific method, it is necessary to consider the patient's specific situation, the type and location of epileptic seizures, and possible side effects. Treating physician will develop personalized treatment plans based on these factors to maximize treatment effectiveness and reduce risks.

The most effective antiseizure medications (ASMs) for poststroke seizures (PSSs) remain unclear. We aimed to determine outcomes associated with ASMs in people with PSS.

We systematically searched electronic databases for studies on patients with PSS on ASMs. Our outcomes were seizure recurrence, adverse events, drug discontinuation rate, and mortality. We assessed the risk of bias using Cochrane Risk of Bias tool for randomized controlled trials and Risk Of Bias In Non-randomized Studies of Interventions tools. Using levetiracetam as the reference treatment, we conducted a frequentist network meta-analysis and determined the certainty of evidence using the Grading of Recommendations Assessment, Development, and Evaluation methodology.

Our search yielded 15 studies (3 randomized, 12 nonrandomized, N = 18,676 patients (121 early and 18,547 late seizures), 60% male, mean age 69 years) comparing 13 ASMs. Three studies had moderate and 12 had high risk of bias. Seizure recurrence was 24.8%. Compared with levetiracetam, very low-certainty evidence suggested that phenytoin was associated with higher seizure recurrences (odds ratio [OR] 7.3, 95% CI 3.7-14.5) and more adverse events (OR 5.2, 95% CI 1.2-22.9). Low-certainty evidence suggested that carbamazepine (OR 1.8, 95% CI 1.5-2.2) and phenytoin (OR 1.9, 95% CI 1.4-2.8) were associated with high drug discontinuation rates. Moderate to high-certainty evidence suggested that valproic acid (OR 4.7, 95% CI 3.6-6.3) and phenytoin (OR 8.3, 95% CI 5.7-11.9) were associated with higher mortality rates. Considering all treatments and using the GRADE approach for treatment ranking, very low-certainty evidence suggested that eslicarbazepine, lacosamide, and levetiracetam had the fewest seizure recurrences. Low to very low-certainty evidence suggested that lamotrigine had the fewest adverse events and drug discontinuations, whereas lamotrigine and levetiracetam exhibited low mortality rates with moderate-certainty evidence.

We found that levetiracetam and lamotrigine may be safe and tolerable ASMs for PSS. Despite ASM use, the seizure recurrence rate remains high in the PSS population. Owing to bias and confounding risks, these findings should be interpreted cautiously.

PROSPERO: CRD42022363844.

Seizure is a relatively common neurological consequence after spontaneous intracerebral hemorrhage (SICH). This study aimed to investigate risk factors of early, late, and overall seizures in patients with SICH. Retrospective analysis was performed on all patients with SICH who completed two years of follow-up. The variables collected were obtained from demographic, clinical, radiographic and treatment data, in-hospital complications, and follow-up results. Univariate and multivariate analyzes were used to identify risk factors for post-hemorrhagic stroke seizure. Of 400 SICH patients recruited, 30 (7.5%) and 40 (10%) developed early and late seizures during the 2-year follow-up period, respectively. In the final result of the multivariate analysis, factors associated with the occurrence of the early seizure included lobar location of hematoma (p = 0.018), and GCS ≤ 12 on initial clinical presentation (p = 0.007). Factors associated with the occurrence of the late seizure included lobar location of hematoma (p = 0.001), volume of hematoma greater than 10 ml (p = 0.009), and midline shift on initial cranial CT (p = 0.036). Risk factors of the overall seizure after SICH included lobar location of hematoma (p < 0.001), volume of hematoma greater than 10 ml (p < 0.001), and craniotomy with evacuation of hematoma (p = 0.007). Furthermore, seizure was also associated with a poor functional outcome 2 years after the onset of SICH. Several factors associated with the appearance of post-ICH seizures were revealed. In patients with increased risk of post-SICH seizures, appropriate surveillance and management of seizures should be carried out.

Post-stroke epilepsy (PSE) is a major complication of stroke. However, data about the predictors of PSE in patients with acute ischemic stroke (AIS) undergoing mechanical thrombectomy are limited.

To evaluate the relationship between intraoperative angiographic signs and PSE risk in patients with anterior circulation AIS who underwent mechanical thrombectomy.

We conducted a retrospective study. A total of 800 patients with AIS who underwent mechanical thrombectomy were classified into case and control groups based on the occurrence of PSE. Propensity score matching (PSM) (1:4) was applied using covariates such as age, sex, National Institutes of Health Stroke Scale score at admission, and baseline modified Rankin Scale score. Conditional logistic regression and mediation analysis were performed. Subgroup analyses were conducted to assess the effect of modification. A diagnostic model based on the angiographic signs and clinical characteristics was developed.

After PSM, 67 and 234 patients with and without PSE, respectively, were selected. The PSE group had significantly higher incidences of hemorrhagic transformation, early seizures, early venous filling (EVF) sign, inferior frontal gyrus (IFG), hippocampus, basal ganglia blush sign, and larger infarct size. After adjusting for hypertension, diabetes, hemorrhagic transformation, infarct size, early seizure, IFG, and hippocampus involvement, EVF remained independently associated with PSE. Hemorrhagic transformation mediated 14.87% of the EVF-PSE associations. Comparison of the evaluation metrics of each model showed that model 3 exhibited the best overall performance.

Hemorrhagic transformation mediates the EVF-PSE association. EVF signs are key predictors of PSE following mechanical thrombectomy.

Allogeneic modified bone marrow-derived human mesenchymal stromal/stem cells (hMSC-SB623 cells) are in clinical development for the treatment of chronic motor deficits after traumatic brain injury and cerebral ischemic stroke. However, their exact mechanisms of action remain unclear. Here, we investigated the effects of this cell therapy on cortical network excitability, brain tissue, and peripheral blood at a chronic stage after ischemic stroke in a rat model. One month after focal cortical ischemic stroke, hMSC-SB623 cells or the vehicle solution were injected into the peri-stroke cortex. Starting one week after treatment, cortical excitability was assessed ex vivo. hMSC-SB623 cell transplants reduced stroke-induced cortical hyperexcitability, restoring cortical excitability to control levels. The histology of brain tissue revealed an increase of factors relevant to neuroregeneration, and synaptic and cellular plasticity. Whole-blood RNA sequencing and serum protein analyses showed that intra-cortical hMSC-SB623 cell transplantation reversed effects of stroke on peripheral blood factors known to be involved in stroke pathophysiology. Our findings demonstrate that intra-cortical transplants of hMSC-SB623 cells correct stroke-induced circuit disruptions even at the chronic stage, suggesting broad usefulness as a therapeutic for neurological conditions with network hyperexcitability. Additionally, the transplanted cells exert far-reaching immunomodulatory effects whose therapeutic impact remains to be explored.

Post-stroke seizures present a global challenge, yet its frequency and factors associated with its incidence are poorly documented, particularly in the Middle East. Thus, this study aims to investigate post-stroke seizure frequency and stroke-associated factors among ischemic stroke patients in Saudi Arabia, addressing demographic, clinical, and comorbid aspects to improve prognosis, diagnosis, prevention, and management. A multicenter, cohort observational study included eligible ischemic stroke patients who were categorized into those who developed seizures after injury and those who did not. Additionally, the study assessed the association between post-stroke seizure and 12-month mortality, 12-month stroke recurrence, and the occurrence of hemorrhagic transformation (HT) within 30 days. The study involved 1235 ischemic stroke patients, in which 13.5% developed post-stroke seizures. Patients with post-stroke seizures had more extended hospital stays, higher intensive care unit (ICU) admission rates, and a higher prevalence of comorbidities. Factors independently associated with post-stroke seizures included previous stroke history (OR = 1.93; 1.35-2.75), ICU admission (OR = 1.7; 1.15-2.5), and depression (OR = 2.1; 1.38-3.30). Logistic regression revealed associations between post-stroke seizures and HT (OR = 2.61; 1.70-4.00), stroke recurrence (OR = 2.30; 1.58-3.36), and mortality (OR = 1.89; 1.33-2.68). However, after adjusting for covariates, post-stroke seizures were significantly associated with stroke recurrence only (aOR = 1.7; 1.11-2.63). Our study identifies notable associations and risk factors for post-stroke seizures in ischemic stroke patients. This underscores the importance of adopting a comprehensive approach to stroke care to enhance the prediction, prevention, and management of post-stroke seizures. Further research is warranted to validate these findings, enhance the understanding of post-stroke seizure mechanisms, and guide management strategies.

Epilepsy is highly heritable, with numerous known genetic risk loci. However, the genetic predisposition's role in poststroke epilepsy (PSE) remains understudied. This study assesses whether a higher genetic predisposition to epilepsy raises poststroke survivor's risk of PSE.

We conducted a case-control genetic association study nested within the UK Biobank, a large UK-based prospective cohort. Our exposures of interest were 2 distinct polygenic risk scores-generalized and focal epilepsy-modeled as deciles and constructed using genetic variants identified in the latest International League Against Epilepsy genome-wide association study meta-analysis. We aimed to evaluate the association between these polygenic risk scores and their corresponding subtype of PSE-generalized and focal. In sensitivity analyses, we evaluated participants of European ancestry separately and considered focal and generalized epilepsy outcomes in participants without a history of stroke. In secondary analyses, we evaluated the polygenic risk of PSE by stroke subtype (ischemic, hemorrhagic, or any stroke). Multivariable logistic regression models were fitted, adjusting for age, sex, genetic ancestry, and the first 5 principal genetic components.

Among 17 549 UK Biobank stroke survivors with available genetic information (mean age, 61; 43% female), 185 (1%) developed generalized PSE, while 124 (0.7%) developed focal PSE. Multivariable logistic regression results showed that, when compared against the lowest decile, participants within the highest PRS decile for generalized PSE had 5-fold higher odds of developing generalized PSE (OR, 5.05 [95% CI, 2.37-12.5]; P trend<0.001). Similarly, when compared against the lowest decile, participants within the highest polygenic risk score decile for focal PSE had 3-fold higher odds of developing focal PSE (OR, 3.20; [5% CI, 1.25-9.82]; P trend=0.024). Sensitivity analyses among participants of European ancestry yielded similar results.

Our findings suggest that, like other forms of epilepsy, genetic predisposition plays an essential role in PSE. These results underscore the need for future studies to elucidate the mechanisms underlying PSE development and to identify novel therapeutic avenues.

Older adults constitute a large proportion of people with epilepsy (PWE) due to the changing demographics worldwide and epilepsy's natural history. Aging-related pathophysiological changes lower the tolerance and increase our vulnerability to stressors, which manifests as frailty. Frailty is closely associated with adverse health outcomes. This narrative review examines the interplay between frailty and epilepsy, especially in older adults, emphasizing its clinical implications, including its role in managing PWE. Mechanistically, frailty develops through complex interactions among molecular and cellular damage, including genomic instability, mitochondrial dysfunction, and hormonal changes. These contribute to systemic muscle mass, bone density, and organ function decline. The concept of frailty has evolved from a primarily physical syndrome to include social, psychological, and cognitive dimensions. The "phenotypic frailty" model, which focuses on physical performance, and the "deficit accumulation" model, which quantifies health deficits, provide frameworks for understanding and assessing frailty. PWE are potentially more prone to developing frailty due to a higher prevalence of risk factors predisposing to frailty. These include, but are not limited to, polypharmacy, higher comorbidity, low exercise level, social isolation, low vitamin D, and osteoporosis. We lack commercial biomarkers to measure frailty but can diagnose it using self- or healthcare provider-administered frailty scales. Recent attempts to develop a PWE-specific frailty scale are promising. Unlike chronological age, frailty is reversible, so its management using multidisciplinary care teams should be strongly considered. Frailty can affect antiseizure medication (ASM) tolerance secondary to its impact on pharmacokinetics and pharmacodynamics. While frailty's effect on seizure control efficacy of ASM is poorly understood, its undoubted association with overall poor outcomes, including epilepsy surgery, behooves us to consider its presence and implication while treating older PWE. Incorporation of frailty measures in future research is essential to improve our understanding of frailty's role in PWE health. PLAIN LANGUAGE SUMMARY: Frailty is the declining state of the human body. People with epilepsy are more prone to it. It should be factored into their management.

To examine the efficacy and safety of perampanel (PER) in patients with post-stroke epilepsy (PSE), brain tumor-related epilepsy (BTRE), and post-traumatic epilepsy (PTE) using Japanese real-world data.

The prospective post-marketing observational study included patients with focal seizures with or without focal to bilateral tonic-clonic seizures who received PER combination therapy. The observation period was 24 or 52 weeks after the initial PER administration. The safety and efficacy analysis included 3716 and 3272 patients, respectively. This post hoc analysis examined responder rate (50% reduction in seizure frequency), seizure-free rate (proportion of patients who achieved seizure-free), and safety in patients included in the post-marketing study who had PSE, BTRE, and PTE in the 4 weeks prior to the last observation.

Overall, 402, 272, and 186 patients were included in the PSE, BTRE, and PTE subpopulations, and 2867 controls in the "Other" population (etiologies other than PSE, BTRE, or PTE). Mean modal dose (the most frequently administered dose) values at 52 weeks were 3.38, 3.36, 3.64, and 4.04 mg/day for PSE, BTRE, PTE, and "Other," respectively; PER retention rates were 56.2%, 54.0%, 52.6%, and 59.7%, respectively. Responder rates (% [95% confidence interval]) were 82% (76.3%-86.5%), 78% (70.8%-83.7%), 67% (56.8%-75.6%), and 50% (47.9%-52.7%) for PSE, BTRE, PTE, and "Other," respectively, and seizure-free rates were 71% (64.5%-76.5%), 62% (54.1%-69.0%), 50% (40.6%-60.4%), and 28% (25.8%-30.1%), respectively. Adverse drug reactions tended to occur less frequently in the PSE (14.7%), BTRE (16.5%), and PTE (16.7%) subpopulations than in the "Other" population (26.3%).

In real-world clinical conditions, efficacy and tolerability for PER combination therapy were observed at low PER doses for the PSE, BTRE, and PTE subpopulations.

To find out how well the medication perampanel works and whether it is safe for people who have epilepsy after having had a stroke, brain tumor, or head injury, we used information from real-life medical situations in Japan. We looked at the data of about 3700 Japanese patients with epilepsy who were treated with perampanel. We found that perampanel was used at lower doses and better at controlling seizures, and had fewer side effects for patients with epilepsy caused by these etiologies than the control group.

In stroke survivors, persistent seizure activity could be associated with poor functional outcomes. At the same time, antiepileptic over-treatment could hamper post-stroke recovery. We systematically investigated the occurrence of seizures, the prevalence of epileptic discharges, and delta slow waves on electroencephalogram (EEG) and anti-seizure medication (ASM) management in relation to clinical manifestations and EEG abnormalities. This was a multi-centre prospective study involving two intensive rehabilitation units (IRUs). Clinical and EEG data were acquired at admission to the IRU, discharge (T1), and six-month follow-up (T2). A total of 163 patients underwent EEG recording upon admission to the IRU, while 149 were available for analysis at discharge from the IRU. Eighteen patients were treated with ASMs upon IRU admission despite only five of these patients having early seizures. Among the 145 patients not treated upon admission to the IRU, eight had late seizures, of which six were during the IRU stay, while two were after discharge from the IRU. During IRU stay, ASMs were generally discontinued in patients with no early seizures reported and were started in patients with late seizures. Among the 18 patients treated with ASMs at admission to the IRU, only six maintained the therapy also at T2. Our results suggest that post-acute inpatient rehabilitation is a proper setting to observe patients treated with ASMs after stroke and provide personalized post-stroke epilepsy management.

Objectives: The multifaceted impact of Traumatic brain injury (TBI) encompasses complex healthcare costs and diverse health complications, including the emergence of Post-Traumatic Seizures (PTS). In this study, our goal was to discern and elucidate the incidence and risk factors implicated in the pathogenesis of PTS. We hypothesize that the development of PTS following TBI varies based on the type and severity of TBI. Methods: Our study leveraged the Nationwide Inpatient Sample (NIS) to review primary TBI cases spanning 2016-2020 in the United States. Admissions featuring the concurrent development of seizures during the admission were queried. The demographic variables, concomitant diagnoses, TBI subtypes, hospital charges, hospital length of stay (LOS), and mortality were analyzed. Results: The aggregate profile of TBI patients delineated a mean age of 61.75 (±23.8) years, a male preponderance (60%), and a predominantly White demographic (71%). Intriguingly, patients who encountered PTS showcased extended LOS (7.5 ± 9.99 vs. 6.87 ± 10.98 days, p < 0.001). Paradoxically, PTS exhibited a reduced overall in-hospital mortality (6% vs. 8.1%, p < 0.001). Notably, among various TBI subtypes, traumatic subdural hematoma (SDH) emerged as a predictive factor for heightened seizure development (OR 1.38 [1.32-1.43], p < 0.001). Conclusions: This rigorous investigation employing an extensive national database unveils a 4.95% incidence of PTS, with SDH accentuating odds of seizure risk by OR: 1.38 ([1.32-1.43], p < 0.001). The paradoxical correlation between lower mortality and PTS is expected to be multifactorial and necessitates further exploration. Early seizure prophylaxis, prompt monitoring, and equitable healthcare provision remain pivotal avenues for curbing seizure incidence and comprehending intricate mortality trends.

Stroke is a major contributor to mortality and morbidity worldwide and the most common cause of epilepsy in the elderly in high income nations. In recent years, it has become increasingly evident that both ischemic and hemorrhagic strokes induce dysfunction of the blood-brain barrier (BBB), and that this impairment can contribute to epileptogenesis. Nevertheless, studies directly comparing BBB dysfunction and poststroke epilepsy (PSE) are largely absent. Therefore, this review summarizes the role of BBB dysfunction in the development of PSE in animal models and clinical studies. There are multiple mechanisms whereby stroke induces BBB dysfunction, including increased transcytosis, tight junction dysfunction, spreading depolarizations, astrocyte and pericyte loss, reactive astrocytosis, angiogenesis, matrix metalloproteinase activation, neuroinflammation, adenosine triphosphate depletion, oxidative stress, and finally cell death. The degree to which these effects occur is dependent on the severity of the ischemia, whereby cell death is a more prominent mechanism of BBB disruption in regions of critical ischemia. BBB dysfunction can contribute to epileptogenesis by increasing the risk of hemorrhagic transformation, increasing stroke size and the amount of cerebral vasogenic edema, extravasation of excitatory compounds, and increasing neuroinflammation. Furthermore, albumin extravasation after BBB dysfunction contributes to epileptogenesis primarily via increased transforming growth factor β signaling. Finally, seizures themselves induce BBB dysfunction, thereby contributing to epileptogenesis in a cyclical manner. In repairing this BBB dysfunction, pericyte migration via platelet-derived growth factor β signaling is indispensable and required for reconstruction of the BBB, whereby astrocytes also play a role. Although animal stroke models have their limitations, they provide valuable insights into the development of potential therapeutics designed to restore the BBB after stroke, with the ultimate goal of improving outcomes and minimizing the occurrence of PSE. In pursuit of this goal, rapamycin, statins, losartan, semaglutide, and metformin show promise, whereby modulation of pericyte migration could also be beneficial.

Stroke is the second leading cause of global deaths. Post-stroke seizures (PSS) can lead to lasting complications, such as prolonged hospitalizations, increased disability rates, and higher mortality. Our study investigates the associated factors that contribute to post-stroke seizures in patients at a local tertiary hospital.

We designed a case-control study where patients admitted with PSS were recruited with consent. Controls admitted for stroke without seizure were then included. Suitability based on exclusion criteria was ensured before recording their sociodemographic and clinical data. An EEG was performed and read by two certified neurologists before the data was analyzed.

We recruited 180 participants, 90 cases and 90 matched controls. Gender (p=0.013), race (p=0.015), dyslipidemia (p<0.001), prior stroke (p<0.031), large artery atherosclerosis (p<0.001), small vessel occlusions (p<0.001), blood pressure on presentation (p<0.028) and thrombolysis administration (p<0.029) were significantly associated with the occurrence of PSS. An increase in odds of PSS was observed in the male gender (1.974), dyslipidemia (3.480), small vessel occlusions (4.578), and in participants with epileptiform changes on EEG (3.630). Conversely, lower odds of PSS were seen in participants with high blood pressure on presentation (0.505), large artery atherosclerosis (0.266), and those who underwent thrombolysis (0.319).

This study emphasized that identifying post-stroke seizures may be aided by EEGs and recognizing at-risk groups, which include males of Chinese descent in Asia, dyslipidemia, small vessel occlusions, those with low to normal blood pressure on presentation, and epileptiform changes in EEGs.

Insomnia is highly prevalent in stroke patients; however, there is no ideal intervention. This systematic review examined the effect and safety of Chinese herbal medicine (CHM) and acupuncture on sleep in adults with stroke.

Six databases were searched from inception to June 2023 to identify randomised controlled trials (RCTs). The primary outcome was Pittsburgh Sleep Quality Index (PSQI) scores. Risk of bias and evidence quality was assessed. A pairwise random-effect meta-analysis was performed.

A total of 54 RCTs published in 55 articles were finally included in the systematic review, including 35 of CHM and 19 of acupuncture therapies. Compared with placebo/sham procedure, CHM and acupuncture were more effective in improving PSQI scores. The evidence of moderate quality suggested that CHM outperformed benzodiazepine drugs (BZDs) while it presented an effect similar to that of non-BZDs in improving sleep quality. CHM and acupuncture also provided additional benefits to the patients treated with pharmacological agents alone. However, the evidence specific to individual CHM prescriptions lay in various factors and methodological quality, and the evidence on the comparative effectiveness between acupuncture and other therapies was conflicting or limited.

Overall, CHM and acupuncture used alone or in combination with pharmacotherapy can safely improve sleep in stroke patients with insomnia. In the future, RCTs on outstanding CHM prescriptions and the comparative effectiveness research between acupuncture and other therapies are needed.

PROSPERO No. CRD42020194029 and No. CRD42020194030.

Acute large hemispheric infarction (ALHI) is an overwhelming emergency with a great challenge of gastrointestinal dysfunction clinically. Here, we initially proposed delayed bowel movements as the clinical phenotype of strike to gut-brain axis (GBA) in ALHI patients by epidemiological analysis of 499 acute ischemic stroke (AIS) patients. 1H NMR-based metabolomics revealed that AIS markedly altered plasma global metabolic profiling of patients compared with healthy controls. Risk factors of strike on GBA were the National Institutes of Health Stroke Scale (NIHSS) score ≥ 5 and stroke onset time ≤ 24 h. As a result, first defecating time after admission to the hospital ≥2 days could be considered as a potential risk factor for strike on GBA. Subsequently, the ALHI Bama miniature (BM) pig model with acute symptomatic seizure was successfully established by ligation of the left ascending pharyngeal artery combined with local air injection. Clinical phenotypes of brain necrosis such as hemiplegia were examined with brain diffusion-weighted imaging (DWI) and pathological diagnosis. In addition to global brain injury and inflammation, we also found that ALHI induced marked alterations of intestinal barrier integrity, the gut microbial community, and microbiota-derived metabolites including serotonin and neurotransmitters in both plasma and multiple brain tissues of BM pigs. These findings revealed that microbiota-gut-brain axis highly contributed to the occurrence and development of ALHI.

Seizures are a common complication of subarachnoid hemorrhage (SAH) in both acute and late stages: 10-20 % acute symptomatic seizures, 12-25 % epilepsy rate at five years. Our aim was to identify early electroencephalogram (EEG) and computed tomography (CT) findings that could predict long-term epilepsy after SAH.

This is a multicenter, retrospective, longitudinal study of adult patients with aneurysmal SAH admitted to two tertiary care hospitals between January 2011 to December 2022. Routine 30-minute EEG recording was performed in all subjects during admission period. Exclusion criteria were the presence of prior structural brain lesions and/or known epilepsy. We documented the presence of SAH-related cortical involvement in brain CT and focal electrographic abnormalities (epileptiform and non-epileptiform). Post-SAH epilepsy was defined as the occurrence of remote unprovoked seizures ≥ 7 days from the bleeding.

We included 278 patients with a median follow-up of 2.4 years. The mean age was 57 (+/-12) years, 188 (68 %) were female and 49 (17.6 %) developed epilepsy with a median latency of 174 days (IQR 49-479). Cortical brain lesions were present in 189 (68 %) and focal EEG abnormalities were detected in 158 patients (39 epileptiform discharges, 119 non-epileptiform abnormalities). The median delay to the first EEG recording was 6 days (IQR 2-12). Multiple Cox regression analysis showed higher risk of long-term epilepsy in those patients with CT cortical involvement (HR 2.6 [1.3-5.2], p 0.009), EEG focal non-epileptiform abnormalities (HR 3.7 [1.6-8.2], p 0.002) and epileptiform discharges (HR 6.7 [2.8-15.8], p < 0.001). Concomitant use of anesthetics and/or antiseizure medication during EEG recording had no influence over its predictive capacity. ROC-curve analysis of the model showed good predictive capability at 5 years (AUC 0.80, 95 %CI 0.74-0.87).

Focal electrographic abnormalities (both epileptiform and non-epileptiform abnormalities) and cortical involvement in neuroimaging predict the development of long-term epilepsy. In-patient EEG and CT findings could allow an early risk stratification and facilitate a personalized follow-up and management of SAH patients.

To assess the effectiveness and tolerability of brivaracetam (BRV) in adults with epilepsy by specific comorbidities and epilepsy etiologies.

EXPERIENCE/EPD332 was a pooled analysis of individual patient records from several non-interventional studies of patients with epilepsy initiating BRV in clinical practice. Outcomes included ≥ 50% reduction from baseline in seizure frequency, seizure freedom (no seizures within prior 3 months), continuous seizure freedom (no seizures since baseline), BRV discontinuation, and treatment-emergent adverse events (TEAEs) at 3, 6, and 12 months. Analyses were performed for all adult patients (≥ 16 years of age) and stratified by comorbidity and by etiology at baseline (patients with cognitive/learning disability [CLD], psychiatric comorbidity, post-stroke epilepsy, brain tumor-related epilepsy [BTRE], and traumatic brain injury-related epilepsy [TBIE]).

At 12 months, ≥ 50% seizure reduction was achieved in 35.6% (n = 264), 38.7% (n = 310), 41.7% (n = 24), 34.1% (n = 41), and 50.0% (n = 28) of patients with CLD, psychiatric comorbidity, post-stroke epilepsy, BTRE, and TBIE, respectively; and continuous seizure freedom was achieved in 5.7% (n = 318), 13.7% (n = 424), 29.4% (n = 34), 11.4% (n = 44), and 13.8% (n = 29), respectively. During the study follow-up, in patients with CLD, psychiatric comorbidity, post-stroke epilepsy, BTRE, and TBIE, 37.1% (n = 403), 30.7% (n = 605), 33.3% (n = 51), 39.7% (n = 68), and 27.1% (n = 49) of patients discontinued BRV, respectively; and TEAEs since prior visit at 12 months were reported in 11.3% (n = 283), 10.0% (n = 410), 16.7% (n = 36), 12.5% (n = 48), and 3.0% (n = 33), respectively.

BRV as prescribed in the real world is effective and well tolerated among patients with CLD, psychiatric comorbidity, post-stroke epilepsy, BTRE, and TBIE.

Post-stroke seizure (PSS) is a common considerable complication of acute ischemic stroke (AIS). Early risk assessment can clinical practitioners to plan effective prevention and management. We aimed to determine whether assessing Diffusion-Weighted Imaging-Alberta Stroke Program Early CT Score (DWI-ASPECTS), and neutrophil indices allows for identifying patients at risk of PSS.

This prospective study included AIS patients with cortical involvement admitted to a single academic center between January 2020 to October 2023. For all included subjects, DWI-Brain MRI, blood neutrophils, and platelet counts were obtained and the DWI-ASPECTS score was calculated. Then, the patients were followed up for 6 months in terms of PSS occurrence. Based on the occurrence of PSS, patients were divided into two groups of PSS and non-PSS. For analysis, imaging and laboratory data were compared between two groups. Logistic regression was applied to determine the relationship between DWI-ASPECTS and neutrophil indices, with early PSS. Finally, the sensitivity and specificity of these variables for PSS were estimated.

A total of 309 were included in the final statistical analysis. DWI-ASPECT and neutrophil-to-lymphocyte ratio (NLR) were significantly associated with early PSS with OR of 0.74 and OR of 1.13, respectively (P < 0.05). Further analysis showed that, a combination of DWI-ASPECTS, NLR had an area under the curve (AUC) of 0.72 for predicting the occurrence of early PSS.

DWI-ASPECTS and NLR are associated with the occurrence of early PSS after cortical ischemic stroke. A combination of these predictors had higher sensitivity and specificity for PSS rather than each factor alone. These findings may be helpful for determining the risk of PSS if validated in future studies.

Convulsive (CSE) and non-convulsive (NCSE) Status Epilepticus are a complication in 0.2-0.3% ischemic strokes. Large stroke and cortical involvement are the main risk factors for developing SE. This study evaluates the prevalence of SE in patients treated with endovascular thrombectomy (EVT) through EEG recording within 72- h from admission. Moreover, we compared clinical, radiological, and outcome measures in SE and no-SE patients.

We collected retrospectively demographical and clinical characteristics of acute ischemic stroke patients who underwent EVT, admitted in the Stroke Unit (SU) of the University Hospital of Trieste between January 2018 and March 2020 who underwent EEG recording within 72- h from the symptoms' onset.

Out of 247 EVT patients, 138 met the inclusion criteria, of whom 9 (6.5%) showed SE with median onset time of 1 day (IQR 1-2). No difference was found between the two groups as for age, sex, risk factors, grade of recanalization, etiology of stroke, and closed vessel. The no-SE group presented higher NIHSS improvement rate (p=0.025) compared to the SE group. The sum of the lobes involved in the ischemic lesion was significantly higher in SE group (p=0.048).

SE after EVT in large strokes is a non-rare complication, with most being NCSE. Performing a rapid EEG assessment in a Stroke Unit setting may allow for a prompt recognition and treatment of SE in the acute/hyper-acute phase. SE may be correlated with worse clinical outcomes in patients with large vessel occlusion.

Biomedical research on the brain has led to many discoveries and developments, such as understanding human consciousness and the mind and overcoming brain diseases. However, historical biomedical research on the brain has unique characteristics that differ from those of conventional biomedical research. For example, there are different scientific interpretations due to the high complexity of the brain and insufficient intercommunication between researchers of different disciplines owing to the limited conceptual and technical overlap of distinct backgrounds. Therefore, the development of biomedical research on the brain has been slower than that in other areas. Brain biomedical research has recently undergone a paradigm shift, and conducting patient-centered, large-scale brain biomedical research has become possible using emerging high-throughput analysis tools. Neuroimaging, multiomics, and artificial intelligence technology are the main drivers of this new approach, foreshadowing dramatic advances in translational research. In addition, emerging interdisciplinary cooperative studies provide insights into how unresolved questions in biomedicine can be addressed. This review presents the in-depth aspects of conventional biomedical research and discusses the future of biomedical research on the brain.

Epilepsy is a chronic neurological disorder with recurrent unprovoked seizures, affecting ~ 65 million worldwide. Evidence in patients with epilepsy and animal models suggests a contribution of neuroinflammation to epileptogenesis and the development of epilepsy. Interleukins (ILs), as one of the major contributors to neuroinflammation, are intensively studied for their association and modulatory effects on ictogenesis and epileptogenesis. ILs are commonly divided into pro- and anti-inflammatory cytokines and therefore are expected to be pathogenic or neuroprotective in epilepsy. However, both protective and destructive effects have been reported for many ILs. This may be due to the complex nature of ILs, and also possibly due to the different disease courses that those ILs are involved in. In this review, we summarize the contributions of different ILs in those processes and provide a current overview of recent research advances, as well as preclinical and clinical studies targeting ILs in the treatment of epilepsy.

The occurrence of seizures after aneurysmal subarachnoid hemorrhage (aSAH) is associated with a poorer functional and cognitive prognosis and less favorable quality of life. It would be of value to promptly identify patients at risk of epilepsy to optimize follow-up protocols and design preventive strategies. Our aim was to develop a predictive score to help stratify epilepsy risk in patients with aSAH.

This is a retrospective, longitudinal study of all adults with aSAH admitted to our center (2012-2021). We collected demographic data, clinical and radiologic variables, data on early-onset seizures (EOSs), and data on development of epilepsy. Exclusion criteria were previous structural brain lesion, epilepsy, and ≤7 days' follow-up. Multiple Cox regression was used to evaluate factors independently associated with unprovoked remote seizures (i.e., epilepsy). The best fitting regression model was used to develop a predictive score. Performance was evaluated in an external validation cohort of 308 patients using receiver-operating characteristic curve analysis.

From an initial database of 743 patients, 419 met the inclusion criteria and were included in the analysis. The mean age was 60 ± 14 years, 269 patients (64%) were women, and 50 (11.9%) developed epilepsy within a median follow-up of 4.2 years. Premorbid modified Rankin Score (mRS) (hazard ratio [HR] 4.74 [1.8-12.4], p = 0.001), VASOGRADE score (HR 2.45 [1.4-4.2], p = 0.001), surgical treatment (HR 2.77 [1.6-4.9], p = 0.001), and presence of EOSs (HR 1.84 [1.0-3.4], p = 0.05) were independently associated with epilepsy. The proposed scale, designated RISE, scores 1 point for premorbid mRS ≥ 2 (R), VASOGRADE-Yellow (I, Ischemia), surgical intervention (S), and history of EOSs (E) and 2 points for VASOGRADE-Red. RISE stratifies patients into 3 groups: low (0-1), moderate (2-3), and high (4-5) risk (2.9%, 20.8%, and 75.7% developed epilepsy, respectively). On validation in a cohort from a different tertiary care center (N = 308), the new scale yielded a similar risk distribution and good predictive power for epilepsy within 5 years after aSAH (area under the curve [AUC] 0.82; 95% CI 0.74-0.90).

The RISE scale is a robust predictor of post-SAH epilepsy with immediate clinical applicability. In addition to facilitating personalized diagnosis and treatment, RISE may be of value for exploring future antiepileptogenesis strategies.