PATHOGENETIC MECHANISMS OF EPILEPSY DEVELOPMENT IN PATIENTS IN THE ACUTE PERIOD OF ISCHEMIC STROKE
DOI:
https://doi.org/10.32689/2663-0672-2025-1-10Keywords:
post-stroke epilepsy, glutamate excitotoxicity, neuroinflammation, blood-brain barrier, ion channels, pharmacotherapyAbstract
Acute cerebrovascular accidents are one of the factors in the development of acquired epilepsy, especially in the elderly. Approximately one in ten adults has a first epileptic seizure associated with a stroke, and one in four over the age of 65. In middleaged and elderly patients who are newly diagnosed with epilepsy, the risk of developing a stroke in the next 2-3 years increases 2-3 times. Despite numerous studies, the mechanisms of epilepsy development in patients with acute ischaemic stroke have not yet been fully defined. It is known that stroke causes neuroinflammation, blood-brain barrier disruption, gliomas and neurotransmitter imbalance, which can lead to seizures. Further study of the mechanisms of this process is necessary to develop effective treatment and prevention strategies. The aim of the study is to analyse the pathogenetic mechanisms of epilepsy in patients with acute ischaemic stroke. The study focuses on the neurophysiological, biochemical and molecular changes that cause epileptogenesis. Systematisation of these data may help in the development of effective methods of prevention and treatment. Materials and methods. For a systematic review of the literature, we searched PubMed, Scopus, Web of Science, Cochrane, and Google Scholar (2019-2025). The key phrases used were: «epilepsy after acute stroke», «acute ischaemic stroke and seizures», «pathogenesis of epilepsy in acute stroke». Peer-reviewed articles, meta-analyses, systematic reviews, and experimental studies covering the pathophysiological mechanisms of post-stroke epilepsy were selected. The literature review summarises the current understanding of the role of ischaemia, inflammation, neuroplasticity and changes in neurotransmitter systems in the development of epilepsy after acute ischaemic stroke. Conclusion. Epilepsy in patients with acute ischaemic stroke is a serious complication that worsens the recovery of patients. Its development is associated with glutamate excitotoxicity, dysfunction of the GABAergic system, neuroinflammation and blood-brain barrier disruption. Early seizures are caused by acute metabolic changes, while later seizures indicate deeper structural disorders of the brain. Changes in ion channels and excessive activation of NMDA receptors play an important role. Genetic predisposition also increases the risk of epilepsy after stroke. Understanding these mechanisms will help to develop effective approaches to prevention and treatment.
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