Abstract
Post-stroke Epilepsy (PSE) is one of the most common forms of acquired epilepsy, especially in the elderly population. As people get increasingly older, the number of stroke patients is expected to rise and concomitantly the number of people with PSE. Although many patients are affected by post-ischemic epileptogenesis, not much is known about the underlying pathomechanisms resulting in the development of chronic seizures. A common hypothesis is that persistent neuroinflammation and glial scar formation cause aberrant neuronal firing. Here, we summarize the clinical features of PSE and describe in detail the inflammatory changes after an ischemic stroke as well as the chronic changes reported in epilepsy. Moreover, we discuss alterations and disturbances in blood-brain-barrier leakage, astrogliosis, and extracellular matrix changes in both, stroke and epilepsy. In the end, we provide an overview of commonalities of inflammatory reactions and cellular processes in the post-ischemic environment and epileptic brain and discuss how these research questions should be addressed in the future.
Highlights
Ischemic strokes are among the most common causes of death and account for a large proportion of disabilities in Western societies (Deuschl et al, 2020)
Good descriptions and reviews of current clinical knowledge of post-stroke epilepsy (PSE) are available (Pitkänen et al, 2016; Feyissa et al, 2019; Xu, 2019; Zelano et al, 2020; Galovic et al, 2021), surprisingly little is known about the underlying pathomechanism that leads to PSE
PSE is one of the most common forms of acquired epilepsy in the elderly, surprisingly little is known about the underlying pathomechanisms
Summary
Ischemic strokes are among the most common causes of death and account for a large proportion of disabilities in Western societies (Deuschl et al, 2020). Seizure-like brain activity during ischemia increases the infarct size and negatively impacts functional recovery (Williams and Tortella, 2002) This suggests that post-ischemic pathological changes and seizure generation are reciprocal processes which influence each other (Feyissa et al, 2019). There are some clinical tools available to determine the risk of developing PSE after ischemic, hemorrhagic, or both stroke types (Strzelczyk et al, 2010; Haapaniemi et al, 2014; Galovic et al, 2018; Lekoubou et al, 2021), an measurable biomarker would ameliorate early diagnosis and facilitate preventive treatment even before the first seizure has occurred. A better understanding of these processes would help to search for possible biomarker candidates in accessible compartments such as the blood and could identify patients at risk of developing PSE in a paraclinical setting
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