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Stress-induced seizure susceptibility ("Psychoepileptogenesis"): From psychological trauma to epileptogenic network reorganization.

PMID: 41688328 · DOI: 10.1016/j.neurol.2026.01.007 · Revue neurologique, 2026 · F Bartolomei, L Soncin, A McGonigal, C Bernard
📄 Abstract

Stress exposure, whether acute or chronic, is now recognized to be a determinant of epileptogenic vulnerability. Psychological stress or trauma may not only precipitate seizures but also actively contribute to the development of epilepsy, a concept that in the clinical setting could be termed "psychoepileptogenesis". Recent evidence from both animal models and clinical studies supports the role of emotional stress in facilitating epileptogenesis, particularly within limbic structures such as the amygdala and hippocampus. In rodent models, chronic stress has been shown to lower seizure thresholds and promote epileptogenesis through mechanisms involving brain-derived neurotrophic factor (BDNF) and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. Human studies reinforce these findings: individuals exposed to trauma or suffering from post-traumatic stress disorder (PTSD) exhibit an elevated risk of developing epilepsy, especially temporal lobe epilepsy (TLE), with structural and functional neuroimaging revealing changes in limbic and paralimbic circuits. These converging lines of evidence suggest that psychoepileptogenesis is a plausible, albeit complex, phenomenon. Further research is needed to identify biomarkers of vulnerability and evaluate whether early interventions targeting stress pathways might alter the course of epileptogenesis.

Confidence: 0.04 · 2 полей извлечено
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Rodent models of chronic stress lowering seizure thresholds and promoting epileptogenesis via BDNF and HPA axis dysregulation
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