Evidence map›Paper›PMID 38759128›Full record

ReviewNeurology2024

Pathophysiology, Diagnosis, Prognosis, and Prevention of Poststroke Epilepsy: Clinical and Research Implications.

Tomotaka Tanaka, Masafumi Ihara, Kazuki Fukuma, Nishant K Mishra, Matthias J Koepp, Alla Guekht, Akio Ikeda

Registry-linked trialAbstract readReview
In one paragraph

Review in Neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06922734 (Post-stroke Seizures and EEG Analysis), which is not on this map. Cited by 43 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 3 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06922734 active not recruitingnot on this map

Post-stroke Seizures and EEG Analysis

Typeobservational_patient_registrySponsorUniversity Medical Centre MariborRan2014 to 2026Enrolled602ConditionsStroke, Seizures, EEG Power Spectra, Serum Biomarkers
3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Management of glucocorticoid-induced osteoporosis in rheumatic diseases.Best practice & research. Clinical rheumatology · 2026
    Review
  7. Article
  8. Frequency of seizures in post-cerebrovascular accident patients.Pakistan journal of medical sciences · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Tomotaka TanakaFrom the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.ORCID 0000-0002-6023-236X
Masafumi IharaFrom the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.ORCID 0000-0002-7102-4048
Kazuki FukumaFrom the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.ORCID 0000-0001-8117-8916
Nishant K MishraFrom the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.ORCID 0000-0002-9327-3707
Matthias J KoeppFrom the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.ORCID 0000-0002-4277-8000
Alla GuekhtFrom the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.
Akio IkedaFrom the Department of Neurology (T.T., M.I., K.F.), National Cerebral and Cardiovascular Center, Osaka, Japan; Department of Neurology (N.K.M.), Yale University School of Medicine, New Haven, CT; Department of Clinical & Experimental Epilepsy (M.J.K.), UCL Queen Square Institute of Neurology, London, United Kingdom; Moscow Research and Clinical Center for Neuropsychiatry (A.G.), Pirogov Russian National Research Medical University, Russia; and Department of Epilepsy, Movement Disorders and Physiology (A.I.), Kyoto University Graduate School of Medicine, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poststroke epilepsy (PSE) is associated with higher mortality and poor functional and cognitive outcomes in patients with stroke. With the remarkable development of acute stroke treatment, there is a growing number of survivors with PSE. Although approximately 10% of patients with stroke develop PSE, given the significant burden of stroke worldwide, PSE is a significant problem in stroke survivors. Therefore, the attention of health policymakers and significant funding are required to promote PSE prevention research. The current PSE definition includes unprovoked seizures occurring more than 7 days after stroke onset, given the high recurrence risks of seizures. However, the pathologic cascade of stroke is not uniform, indicating the need for a tissue-based approach rather than a time-based one to distinguish early seizures from late seizures. EEG is a commonly used tool in the diagnostic work-up of PSE. EEG findings during the acute phase of stroke can potentially stratify the risk of subsequent seizures and predict the development of poststroke epileptogenesis. Recent reports suggest that cortical superficial siderosis, which may be involved in epileptogenesis, is a promising marker for PSE. By incorporating such markers, future risk-scoring models could guide treatment strategies, particularly for the primary prophylaxis of PSE. To date, drugs that prevent poststroke epileptogenesis are lacking. The primary challenge involves the substantial cost burden due to the difficulty of reliably enrolling patients who develop PSE. There is, therefore, a critical need to determine reliable biomarkers for PSE. The goal is to be able to use them for trial enrichment and as a surrogate outcome measure for epileptogenesis. Moreover, seizure prophylaxis is essential to prevent functional and cognitive decline in stroke survivors. Further elucidation of factors that contribute to poststroke epileptogenesis is eagerly awaited. Meanwhile, the regimen of antiseizure medications should be based on individual cardiovascular risk, psychosomatic comorbidities, and concomitant medications. This review summarizes the current understanding of poststroke epileptogenesis, its risks, prognostic models, prophylaxis, and strategies for secondary prevention of seizures and suggests strategies to advance research on PSE.

Indexed as

EpilepsyStrokeAnticonvulsantsElectroencephalographyHumansPrognosisAnticonvulsants

Identifiers

PMID38759128
PMCPMC11175639

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.