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Post Stroke Seizures and Epilepsy: From Proteases to Maladaptive Plasticity
Keren Altman1, Efrat Shavit-Stein1, Nicola Maggio1,2,3
1Department of Neurology, The Chaim Sheba Medical Center, Ramat Gan, Israel.
Frontiers in Cellular Neuroscience
|October 15, 2019
Summary
Post-stroke epilepsy (PSE) is common in older adults, but its causes are unclear. Thrombin and its receptor PAR1 may contribute to developing epilepsy after ischemic stroke by causing lasting brain changes.
Area of Science:
- Neurology
- Neuroscience
- Pathophysiology
Background:
- Post-stroke epilepsy (PSE) is the most frequent cause of seizures in the elderly.
- Current understanding of PSE's mechanisms, incidence, prognosis, and treatment lacks consensus.
- Late seizures in PSE, occurring ≥1 week post-stroke, are linked to permanent structural brain changes.
Purpose of the Study:
- To investigate the potential role of the coagulation cascade, specifically thrombin and its receptor PAR1, in the development of post-stroke epilepsy.
- To explore how thrombin and PAR1 might induce structural brain changes leading to epileptic foci.
Main Methods:
- Review of existing literature on stroke pathophysiology and epilepsy.
- Analysis of the known roles of thrombin and PAR1 in coagulation and neuroplasticity.
- Hypothesizing a mechanism linking thrombin/PAR1 activity to PSE development.
Main Results:
- Thrombin is involved in the acute phase of ischemic stroke.
- Thrombin and PAR1 are implicated in maladaptive plasticity.
- This suggests a potential pathway for thrombin and PAR1 in creating permanent structural changes that foster epilepsy post-stroke.
Conclusions:
- Thrombin and PAR1 are proposed as key players in the development of post-stroke epilepsy.
- Further research is needed to elucidate the precise role of thrombin and PAR1 in PSE pathophysiology.
- Understanding this mechanism could lead to targeted therapies for PSE.
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