Post-stroke seizures and epilepsy: Risk factors, neuropsychiatric outcomes, and a management framework

Abstract

In this editorial, we comment on the article by Wang et al published in the recent issue of the World Journal of Psychiatry. Ischemic strokes constitute a substantial proportion of emergency department presentations, and post-stroke seizures represent a clinically significant subset in which clinicians must balance timely stabilization with decisions that influence long-term neurologic and psychiatric outcomes. Recent studies show that late-onset seizure, cortical involvement, and hemorrhagic infarction are independent predictors of recurrence after a first epileptic episode in ischemic stroke, and these features also align with poorer cognition and higher anxiety and depression scores. Translating these signals into practice, this editorial proposes a risk-stratified management framework: (1) Confirm stroke subtype and systematically screen for the three red-flag predictors via history, focused examination, and review of neuroimaging/early electroencephalography when clinically indicated; (2) Address precipitants and comorbidities (electrolytes/glucose abnormalities, medication interactions, sleep deprivation, infection); (3) Avoid routine primary prophylaxis, but consider early anti-seizure medication in high-risk profiles while individualizing agent selection to cerebrovascular comorbidity and drug-drug interactions; (4) Incorporate brief cognitive and mood screening to trigger early referral and follow-up pathways; and (5) Use clear disposition/discharge bundles (safety counseling, rescue plan, and expedited neurology/epilepsy clinic appointments). By centering management on validated risk markers, clinicians can better align acute decisions with long-term seizure control and neuropsychiatric outcomes.

Key Words: Cognition disorders; Electroencephalography; Risk assessment; Seizures; Stroke

Core Tip: Post-stroke seizures require pathways that combine risk stratification, timely therapy, and neuropsychiatric care. We synthesize consistent predictors and translate them into a five-step framework usable in the emergency department, stroke unit, and early follow-up. The approach endorses the use of validated tools, targeted early electroencephalography, correction of precipitants, individualized non-enzyme-inducing antiseizure therapy when indicated, and brief screening for mood and cognition with structured referral. Standardized discharge bundles and pragmatic follow-up are emphasized. Routine primary prophylaxis is discouraged.

This editorial refers to “Seizure recurrence after first epileptic episode in ischemic stroke: Risk factors and their association with cognition and mood” by Wang et al, 2025; https://doi.org/10.5498/wjp.v15.i11.108292.

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INTRODUCTION

Stroke remains a leading global cause of death and disability, with ischemic stroke accounting for the majority of events[1,2]. In 2021, there were an estimated 11.9 million new stroke cases worldwide, 7.3 million stroke-related deaths, and 93.8 million stroke survivors, underscoring the scale of the problem and the enduring burden in clinical practice[1]. Seizures are among the most consequential post-stroke complications and constitute a principal cause of acquired epilepsy in older adults[3-6]. Clinically, post-stroke seizures are conventionally divided into early (≤ 7 days; typically reflecting acute biochemical/metabolic perturbations) and late (> 7 days; denoting structural and network remodeling with heightened recurrence liability); notably, a single late seizure after stroke often suffices for a diagnosis of post-stroke epilepsy due to its high recurrence risk[7-10].

Numerous investigations have scrutinized the clinical, imaging, and electrophysiological factors influencing the risk of seizures following a stroke; however, ambiguities remain concerning the likelihood of recurrence subsequent to an initial epileptic event, particularly with respect to the role of neuropsychiatric factors (such as cognitive function and mood)[5,11,12]. Addressing this gap, Wang et al[13] published a study in the recent issue of the World Journal of Psychiatry analyzed a cohort of 100 ischemic stroke patients with a first seizure, and identified late-onset seizure, cortical involvement, and hemorrhagic infarction as independent predictors of recurrence; these factors also correlated with worse cognition and higher anxiety/depression scores, underscoring the intertwined neurological and psychiatric burden. Although influential, the single-center design and modest sample size may limit generalizability; therefore, confirmation in larger and more heterogeneous cohorts is needed. In another study, Hou et al[14] reported that in adults with newly diagnosed post-stroke epilepsy followed for six months, cognitive impairment was frequent and accompanied by higher rates of anxiety and depression, with diabetes, elevated homocysteine, and the use of multiple antiseizure medications associated with worse cognition.

Given that the majority of patients presenting with suspected strokes and initial seizures are first assessed in the Emergency Department (ED), it is imperative for frontline practitioners (notably neurologists, as well as emergency medicine physicians, psychiatrists, internists, and hospitalists) to promptly identify high-risk phenotypes and initiate appropriate management and follow-up strategies that integrate acute stabilization with long-term prevention and rehabilitation efforts[8]. Building on the current evidence, in this editorial, we frame the global burden and clinical relevance of post-stroke seizures, synthesize risk factors and prognostic criteria with emphasis on these predictors, outline a risk-stratified management and prophylaxis framework across the ED and inpatient care, and discuss neuropsychiatric outcomes and research priorities. We close with concise practice points at the end of the editorial to guide immediate decision-making in the ED and the stroke unit.

EPIDEMIOLOGY AND INCIDENCE

Stroke is the leading cause of acquired epilepsy in older adults, accounting for nearly half of new epilepsy diagnoses[3,4,11]. Post-stroke seizures are reported in 2%-20% of stroke survivors, with variability driven by study design, stroke subtype, and follow-up methodology[6,11,13,15]. Meta-analyses estimate pooled rates of about 7% for early seizures and 5%-10% for post-stroke epilepsy[11,16]. Stroke subtype is an important determinant of seizure risk. After ischemic stroke, early seizures are reported in 2%-6% and post-stroke epilepsy in 1%-6%, whereas intracerebral hemorrhage carries higher risks, with early seizures in 5%-12% and post-stroke epilepsy in 6%-12%[12,17,18].

The risk of epilepsy is most significant within the first year after stroke[10]. Among ischemic stroke survivors, late seizure risk is approximately 4% at one year and 8% at five years[9]. In hemorrhagic stroke, cumulative risk may approach 37% by 10 months and 50% by 20 months[19]. Younger adults are not exempt; among individuals aged 18-49 years, five-year cumulative risk has been reported as 3.7% after ischemic stroke and 7.6% after intracerebral hemorrhage[20].

Importantly, the relationship between stroke and epilepsy is bidirectional[21]. Epidemiological studies indicate that epilepsy itself increases the risk of subsequent stroke, particularly when seizures begin after the age of 60[21]. In population-based cohorts, late-onset seizures were associated with a two- to threefold higher incidence of stroke compared with controls, suggesting that seizures in older adults may sometimes represent the first clinical manifestation of underlying cerebrovascular disease[15,21]. This finding underscores the importance of vascular risk factor screening and management in patients presenting with late-onset seizures[22].

PATHOGENESIS

The pathogenesis of post-stroke seizures is heterogeneous, reflecting distinct mechanisms in the acute and chronic phases of cerebrovascular injury[3,9]. Early seizures, often classified as acute symptomatic seizures, arise as transient responses to the immediate biochemical and metabolic consequences of stroke. By contrast, late seizures lead to enduring structural and functional reorganization of neuronal networks, promoting epileptogenesis[10,18,22].

Early seizures usually occur within the first seven days after stroke and are driven by acute and largely reversible processes[7,23,24]. Key mechanisms include: (1) Excessive glutamate release leading to neuronal hyperexcitability and excitotoxicity[24,25]; (2) Disruption of the blood-brain barrier, with albumin extravasation triggering astrocytic and microglial activation[3,10]; (3) Neuroinflammatory cascades involving cytokines such as interleukin-1 beta and interleukin-6 that lower seizure threshold[10,19]; (4) Metabolic and ionic derangements, such as extracellular potassium accumulation, oxidative stress, and acid-base imbalance[7,24]; and (5) Acute changes in gene expression and channel function[7,10]. These mechanisms explain why early seizures are regarded as provoked and do not invariably lead to epilepsy.

Late seizures emerge months to years after the index event and represent acquired epileptogenesis[8,24]. Persistent changes include gliotic scar formation, aberrant axonal sprouting, and rewiring of cortical networks that favor hypersynchronous discharges[7,19]. Chronic inflammation perpetuates excitability by continuously activating glial cells[7,24]. In hemorrhagic stroke or ischemic lesions with hemorrhagic transformation, deposition of blood products (particularly hemosiderin and iron) exacerbates oxidative stress and ferroptosis, thereby fostering epileptogenic foci. Cortical superficial siderosis has recently been recognized as a strong predictor of post-stroke epilepsy, particularly in the context of cerebral amyloid angiopathy[19,24]. Additional contributors include selective neuronal apoptosis, mitochondrial dysfunction, maladaptive plasticity of gamma-aminobutyric acid (GABA) signaling, and impaired clearance of metabolites due to dysfunction of the glymphatic system[10,18].

Across both early and late phases, cortical involvement emerges as a unifying substrate that magnifies vulnerability to seizures[11]. The cortex’s high density of excitatory pyramidal neurons and its susceptibility to glutamatergic toxicity, inflammatory cascades, and maladaptive plasticity render cortical injury disproportionately epileptogenic compared with subcortical regions[26].

CLINICAL MANIFESTATIONS

Most post-stroke seizures present with localization-related semiology. Roughly two-thirds are focal and about one-third generalize to bilateral tonic-clonic seizures[12]. Status epilepticus occurs in a minority but carries significant prognostic weight[22]. Semiological patterns correspond to the symptomatic zone, though rapid propagation may cause clinical signs to diverge from the primary lesion location. Many events are subtle or nonconvulsive and require electroencephalography (EEG) confirmation; a proportion are purely electrographic[12].

Several bedside features should raise suspicion in the ED. Fluctuating awareness or behavior, aphasia that waxes and wanes, new gaze deviation, rhythmic facial or limb twitching, automatisms, eye blinking spells, and unexplained agitation are common clues[18]. Unexplained encephalopathy after stroke, especially with stepwise fluctuations, should prompt urgent EEG and consideration of nonconvulsive status epilepticus. Early laboratory checks for glucose and electrolytes are essential because metabolic derangements can precipitate or mimic seizures. When uncertainty persists, short-interval neurological re-examination and continuous or prolonged EEG increase diagnostic yield[18,22].

Timing at presentation has clinical implications[7]. Within the first 24 hours, seizures are more often focal or focal to bilateral tonic-clonic. Impaired-awareness focal events become more common beyond 24 hours. Early status epilepticus signals higher mortality and a greater likelihood of subsequent epilepsy. Brief cognitive and mood screening at presentation is functional because anxiety, depression, and cognitive impairment frequently co-occur and influence recovery trajectories[7,18,24].

Common pitfalls and differentials deserve explicit attention[12]. Postictal Todd paresis can be mistaken for a new ischemic event[10,21]. Transient focal neurological episodes associated with cortical superficial siderosis may represent focal seizures or closely mimic them. Other mimics include transient ischemic attack, migraine with aura, syncope, psychogenic seizures, movement disorders, and delirium[8]. When history suggests syncope, look for prodrome, orthostatic triggers, rapid recovery, and absence of postictal confusion. When an epileptic event is likely, typical markers include witnessed focal onset, head version, an ictal cry, lateral tongue biting, postictal confusion, and a transient rise in serum lactate[10,12]. Clinicoradiologic concordance between semiology and cortical involvement on imaging strengthens the diagnosis and should guide EEG strategy and disposition[18,22].

Neuropsychiatric manifestations at the time of presentation warrant careful consideration[13]. Cognitive and mood disturbances often accompany post-stroke seizures, and this comorbid condition significantly influences recovery and overall quality of life[14,25]. Literature reviews indicate that anxiety impacts approximately 18%-34% of individuals who have experienced a stroke during the initial year and may persist for as long as five years, frequently co-occurring with cognitive impairment and depression, thereby exacerbating adverse outcomes[25]. In alignment with this extensive body of research, Wang et al[13] found that the clinical characteristics associated with increased seizure recurrence were also correlated with diminished cognitive performance and heightened anxiety and depressive symptoms, suggesting that the risk of seizures and the neuropsychiatric load frequently co-occur. Beyond the burden of symptoms, recent reviews highlight that post-stroke epilepsy is associated with inferior functional and cognitive outcomes, underscoring the importance of considering cognitive and mood factors in conjunction with traditional neurological benchmarks when assessing patients suspected of having post-stroke seizures[18].

RISK FACTORS AND PROGNOSTIC CRITERIA

Across various investigations, a consistent array of clinical and imaging parameters is frequently correlated with an increased probability of seizures following a stroke. Cortical involvement is the most reproducible signal in both ischemic and hemorrhagic stroke and reflects the intrinsic epileptogenicity of cortical networks[13]. Greater stroke severity, mostly quantified by National Institutes of Health Stroke Scale, hemorrhagic stroke, and hemorrhagic transformation, and larger lesion burden cluster with risk[15]. Seizures are most common when the infarct or bleeding involves the anterior circulation, particularly in the territory of the middle cerebral artery or the temporal lobe. Larger lesion burden is associated with a higher likelihood of seizures. In a multicenter cohort, Bladin et al[27] reported that lesion volumes greater than 70 mL were linked to an approximately fourfold increase in the odds of post-stroke seizures[24]. In a meta-analysis by Nandan et al[11] encompassing 128 studies, early seizures were more frequent with hemorrhagic stroke [odds ratio (OR): 2.14], severe deficits (OR: 2.68), cortical involvement (OR: 3.09), and hemorrhagic transformation (OR: 2.70). At the same time, the strongest predictors of post-stroke epilepsy were severe stroke (OR: 4.92), cortical involvement (OR: 3.20), anterior-circulation infarcts (OR: 3.28), hemorrhagic transformation (OR: 2.81), and, most notably, the occurrence of an early post-stroke seizure (OR: 7.24).

Age influences these trends without fundamentally altering them. In a prospective cohort study involving young adults aged 18 years to 49 years with neuroimaging-confirmed strokes, the five-year cumulative risk of developing post-stroke epilepsy was 3.7% following ischemic strokes and 7.6% following intracerebral hemorrhages. Within this demographic, the presence of an acute symptomatic seizure and cortical involvement remained the predominant predictors, and established assessment tools demonstrated strong discriminative ability[20].

Reperfusion therapies for acute ischemic stroke (intravenous thrombolysis and/or mechanical thrombectomy) have a heterogeneous and overall inconclusive association with subsequent post-stroke epilepsy. Although some studies report temporally related “reperfusion seizures” and outline plausible mechanisms such as cortical irritability and blood-brain barrier disruption after reperfusion, these observations remain anecdotal and pathophysiological in nature, lacking causal evidence. In contrast, extensive multicenter propensity-matched analyses found no independent association between receiving reperfusion, IV thrombolysis, or mechanical thrombectomy and either acute symptomatic seizures or post-stroke epilepsy; apparent crude signals disappeared after balancing covariates[15,28]. These analyses emphasize treatment-selection confounding; patients offered reperfusion often have greater baseline severity, cortical involvement, and large-artery etiologies, which also raise seizure risk, so unadjusted comparisons are misleading. After matching, secondary hemorrhage did not mediate seizure risk, which suggests the neutral association is not explained by reperfusion-related bleeding. Taken together, the evidence is rated as having low certainty. When guideline syntheses are taken into account, they support a neutral interpretation of the association between reperfusion and post-stroke epilepsy. Although reperfusion improves functional outcomes, adjusted analyses to date do not demonstrate an independent increase or decrease in the risk of subsequent seizures or epilepsy[29].

Beyond routine predictors, advanced biomarkers may refine individual risk estimates; however, their generalizability is constrained by availability and workflow limitations. In unselected stroke cohorts, specialized blood tests are not obtained systematically, and lumbar puncture is not performed in most patients, which limits the use of blood or cerebrospinal fluid biomarkers for universal screening. Nevertheless, where available, signal-bearing candidates have been reported. In a systematic review, higher plasma endostatin and interleukin-1 beta/interleukin-6 transcript levels were correlated with post-stroke epilepsy, whereas lower S100 calcium-binding protein B and heat shock 70kDa protein 8 levels, as well as selected genetic variants in CD40 and transient receptor potential cation channel, subfamily M, member 6, showed differential associations. Combined panels improved discrimination over clinical variables alone[30]. In a single-center cerebral infarction cohort, reduced cerebrospinal fluid GABA and elevated serum neuron-specific enolase and microRNA-155 independently associated with post-stroke epilepsy; each marker demonstrated good discrimination, and the three-marker combination achieved an area under the curve of 0.963; National Institutes of Health Stroke Scale correlated inversely with GABA and positively with neuron-specific enolase and microRNA-155[31]. In parallel, advanced imaging biomarkers enhance risk evaluation beyond mere lesion dimensions. The topographical characteristics of the cortex and the magnitude of lesions remain pivotal, with cortical superficial siderosis emerging as a significant clinical indicator that correlates the by-products of cortical hemorrhage with the development of epilepsy and transient focal neurological events that may resemble focal seizures[15,19].

EEG contributes prognostic and diagnostic value in selected patients after stroke. Beyond cases with overt convulsions, EEG should be obtained when mental status fluctuates, when nonconvulsive seizures or status epilepticus are suspected, or when clinical-imaging correlations are incongruent[15]. In the acute and subacute phases, interictal epileptiform abnormalities and marked background asymmetry are associated with a higher risk of subsequent seizures, whereas nonspecific rhythmic patterns are less informative. These signals refine individual risk estimates when interpreted alongside clinical predictors and neuroimaging, rather than in isolation[9]. Continuous or serial EEG monitoring is reasonable in patients with depressed consciousness or unexplained encephalopathy to detect electrographic events that would otherwise be missed and to guide antiseizure-medication decisions during post-acute care and rehabilitation[7].

Risk assessment scores convert these variables into individualized predictions of late seizures/post-stroke epilepsy. Following ischemic stroke, the SeLECT tool amalgamates factors such as stroke severity, large-artery pathology, occurrence of early seizures, cortical involvement, and the territory of the middle cerebral artery, demonstrating the highest validated efficacy among multivariable assessments[9]. More recently, the same group introduced SeLECT 2.0, which adds the type of acute symptomatic seizure as a predictor, assigning greater weight to status epilepticus and thereby improving the identification of patients at very high risk. The model preserves overall discrimination while extending the upper range of predicted risk and provides updated risk charts and a calculator to support clinical follow-up and decisions about the continuation of antiseizure therapy in selected cases[32]. In the context of intracerebral hemorrhage, the CAVE model incorporates cortical location, age under 65 years, hematoma volume exceeding 10 mL, and early seizures, showcasing notable discriminative capability[9]. A systematic review and meta-analysis have reported pooled areas under the curve of approximately 0.77 for SeLECT and 0.81 for CAVE, while also highlighting prevalent discrepancies in calibration and validation within the existing literature[18,33].

Neuropsychiatric comorbidity is not merely incidental but frequently correlates with an increased risk of seizures[13]. Post-stroke epilepsy that is newly diagnosed often presents alongside cognitive deficits and symptoms of anxiety or depression. These characteristics are essential for guiding patient counseling and follow-up, despite their current absence from standardized risk assessment models[14].

NEUROPSYCHIATRIC OUTCOMES

Neuropsychiatric sequelae are integral to the burden of post-stroke seizures and post-stroke epilepsy, and they shape long-term recovery and quality of life. Compared with stroke survivors without seizures, those with seizures have higher odds of subsequent dementia, mortality, and overall poor functional outcome, and recurrence relates to steeper disability accrual on standard functional scales[18].

Cognition and mood are frequently affected. In a hospital cohort, about two-thirds of patients with post-stroke epilepsy showed cognitive impairment across visuospatial and executive skills, naming, attention, language, and delayed recall, and depression and anxiety were more prevalent in the cognitively impaired subgroup. Diabetes, elevated homocysteine, and polytherapy are independently associated with cognitive impairment[14]. Contemporary syntheses estimate post-stroke depression near one-third and post-stroke anxiety between one-fifth and one-third during the first year, with anxiety often persisting over several years; apathy is also common and has distinct clinical and prognostic features that should not be conflated with depression[14,25].

In the study by Wang et al[13] late-onset first seizure, cortical involvement, and hemorrhagic infarction independently predicted seizure recurrence, and these same features aligned with poorer cognitive performance and higher anxiety and depression scores. This pattern supports the view that recurrence risk and neuropsychiatric burden often co-occur.

Taken together, neuropsychiatric outcomes are not ancillary concerns but determinants of prognosis in post-stroke seizure care. Early recognition of cognitive and mood symptoms, systematic follow-up, and selection of antiseizure therapy with attention to neurocognitive tolerability are actionable steps within a psychiatry-informed, multidisciplinary pathway[18]. Accordingly, brief screening for mood and cognition should be considered a key component of post-stroke follow-up care.

SEIZURE MANAGEMENT AND PROPHYLAXIS: A RISK-STRATIFIED FRAMEWORK

This section translates the consistent predictors of post-stroke seizures into a practical, stepwise approach that minimizes overtreatment while prioritizing prevention and timely therapy in high-risk profiles.

Confirm stroke subtype and screen for red-flag predictors

Verify ischemic vs hemorrhagic stroke and review history, focused examination, neuroimaging, and EEG. Treat late onset of the index seizure, cortical involvement, and hemorrhagic infarction or transformation as high-risk signals, since these features independently predict recurrence and often coincide with worse cognitive and mood outcomes[11,13,24].

Address precipitants and comorbidities before committing to long-term therapy

Correct reversible triggers such as electrolyte or glucose abnormalities, acute infection, medication interactions, and sleep deprivation. When mental status fluctuates or nonconvulsive events are suspected, obtain a timely EEG review; interictal epileptiform abnormalities and marked background asymmetry carry prognostic value, whereas nonspecific rhythmic patterns are less informative[7,12,18].

Consider anti-seizure medication in high-risk profiles and individualize selection

Evidence from randomized trials and meta-analyses does not support routine primary prophylaxis in stroke populations[3,22,24,34]. Initial therapy should be considered after a first late unprovoked seizure or in carefully selected high-risk scenarios, and choose agents with attention to vascular comorbidity and drug-drug interactions[7,18,34]. Comparative evidence favors lamotrigine and levetiracetam for tolerability over enzyme-inducing agents, as phenytoin and valproate are associated with more adverse outcomes in pooled analyses[3,15,34,35]. While levetiracetam allows rapid initiation and simple dosing, vigilance for potential mood and behavioral adverse effects is warranted. Lamotrigine is generally well-tolerated and may be beneficial for cognition and mood; however, slow titration is required to minimize the risk of rash. Although evidence is still emerging, brivaracetam, which shares synaptic vesicle protein 2A binding with levetiracetam, may offer improved behavioral tolerability in some patients and can be considered when such effects limit the use of levetiracetam. For pragmatic starting regimens and key cautions (Table 1)[7,22,34-37].

Table 1 Common frontline antiseizure medications in post-stroke care: Pragmatic starting regimens and cautions.

Agent	Typical starting regimen	Titration/usual maintenance	Key cautions and interactions	When to favor	When to avoid
Levetiracetam	250-500 mg twice daily	Up-titrate by 500 mg every few days to 500-1500 mg twice daily	Renal dose adjustment; behavioral irritability possible	Polypharmacy, vascular comorbidity, minimal interactions needed	Severe behavioral issues; advanced renal failure without adjustment
Lamotrigine	25 mg daily, slow titration	25 mg → 50 mg daily after 2 weeks, then increase 50 mg every 1-2 weeks; usual 100-200 mg daily	Rash risk; very slow titration; interactions with enzyme inducers or inhibitors	Need for excellent tolerability and low interaction burden	Need for rapid control; history of severe rash
Lacosamide	50 mg twice daily	Increase to 100-200 mg twice daily over 1-2 weeks	PR prolongation and conduction disease; dizziness	Focal seizures in older adults; good tolerability needed	Known conduction abnormalities or significant bradyarrhythmia
Eslicarbazepine	400 mg daily	Increase to 800-1200 mg daily	Hyponatremia; dizziness; fewer interactions than carbamazepine	Alternative to carbamazepine with fewer interactions	Recurrent hyponatremia; severe renal impairment
Brivaracetam	50 mg twice daily	50-100 mg twice daily	Similar to levetiracetam, with fewer behavioral effects; hepatic metabolism	Prior behavioral issues with levetiracetam	Significant hepatic dysfunction
Topiramate	25 mg nightly	Increase by 25-50 mg weekly to 50-100 mg twice daily	Cognitive slowing, weight loss, and kidney stones	Obesity or migraine comorbidity	Cognitive vulnerability after stroke
Carbamazepine	100-200 mg twice daily	200-400 mg twice daily	Enzyme inducer with many interactions; hyponatremia	Limited scenarios with few interactions	Anticoagulants, statins, multiple antihypertensives; older adults
Phenytoin	100 mg three times daily or load per protocol	Level-guided	Narrow therapeutic window; arrhythmia with IV; many interactions	Rescue when IV control is needed and alternatives are unsuitable	Long-term use in older adults: Polypharmacy
Valproate	250-500 mg twice daily	500-1000 mg twice daily; level-guided	Weight gain, tremor, thrombocytopenia; interactions	Limited scenarios where alternatives are unsuitable	Older adults, polypharmacy, stroke with thrombocytopenia risk

Dosing ranges were compiled from Food and Drug Administration or manufacturer labels and standard monographs for adult focal-onset seizures; adjust to renal and hepatic function, co-medications, and local formulary. PR: P-R interval.

Integrate brief cognitive and mood screening into early pathways

Because seizure risk and neuropsychiatric burden often travel together after stroke, include a short bedside check of cognition and mood, for example, Patient Health Questionnaire-2 and Generalized Anxiety Disorder-2 for mood screening and a 5 minutes Montreal Cognitive Assessment or a comparable ultra brief cognitive screen in the ED or stroke unit, and route positive findings into structured follow-up for formal evaluation and specialty referral, alongside seizure-specific management; initiate a standardized care bundle that includes sleep assessment, medication reconciliation/optimization, brief patient-and-caregiver psychoeducation with a written rescue/safety plan, and timely scheduling of neurology, stroke psychiatry/psychology, neuropsychology, and rehabilitation services, with clear documentation of results and next steps[13,25,38,39].

Use clear disposition and discharge bundles tailored by risk

Standardize discharge content: Safety counseling, a written rescue plan, medication titration and monitoring instructions when applicable, and expedited neurology or epilepsy clinic appointments[22,34]. Use validated tools to guide the urgency of follow-up. After ischemic stroke, SeLECT estimates late-seizure risk using severity, large-artery disease, early seizure, cortical involvement, and middle cerebral artery territory; after intracerebral hemorrhage, CAVE uses cortical location, age under 65 years, hematoma volume over 10 mL, and early seizure[33]. External validation and calibration are improving but remain areas for development.

CONCLUSION

Post-stroke seizure care benefits from a focused synthesis of predictors and practical steps. Their impact extends beyond recurrence to neuropsychiatric outcomes that shape recovery and quality of life; therefore, seizure care is most effective when embedded in multidisciplinary pathways that include screening for mood and cognition, as well as coordinated follow-up. A concise roadmap should aim to minimize overtreatment while enabling timely therapy in high-risk profiles, and it supports pragmatic decision-making across the ED, stroke unit, and early outpatient care.

For clinical practice, we encourage the systematic incorporation of validated risk stratification, along with early EEG when clinically indicated, and brief screening for mood and cognition within routine pathways. Clear discharge bundles, which include safety counseling, a written rescue plan, medication reconciliation and optimization, and timely referral to neurology, stroke psychiatry, psychology, neuropsychology, and rehabilitation, improve continuity and promote patient-centered outcomes. Future work should refine and validate the proposed framework, implement studies that pair risk stratification with screening-anchored follow-up, and develop biomarker-augmented prediction models that combine clinical features with advanced neuroimaging and blood or cerebrospinal fluid markers.