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    Rights statement: This is the author’s version of a work that was accepted for publication in Epilepsy & Behavior. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Epilepsy & Behavior, 104, B, 2020 DOI: 10.1016/j.yebeh.2019.06.039

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Seizures in the context of occult cerebrovascular disease

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Published
Article number106396
<mark>Journal publication date</mark>31/03/2020
<mark>Journal</mark>Epilepsy and Behavior
Issue numberB
Volume104
Number of pages5
Publication StatusPublished
Early online date29/07/19
<mark>Original language</mark>English

Abstract

There is an important bidirectional relationship between seizures and cerebrovascular disease (CVD). Aside from poststroke epilepsy, Occult CVD is an important cause of late-onset seizures (LOS) and late-onset epilepsy (LOE). Late-onset seizures/LOE are associated with a threefold increased risk of subsequent clinical stroke. This relationship exists not only in later life, but with ‘late-onset’ seizures or epilepsy occurring from the fourth decade of life onwards. There is increasing evidence for the importance of hypertension and cerebral small vessel disease (SVD) in epileptogenesis, but there is a considerable need for further work to elucidate underlying mechanisms. There may be a disproportionately increased risk of intracerebral hemorrhage (ICH) after LOS/LOE; this too requires further study. There is also a bidirectional relationship between LOS/LOE and cognitive impairment/dementia: it is likely that there are important interactions between vascular and neurodegenerative pathological processes mediating LOE, stroke, and dementia. There is a pressing need for better epidemiological and natural history data as well as elucidation of epileptogenic mechanisms, in order to progress our understanding and to better inform clinical practice.

Bibliographic note

This is the author’s version of a work that was accepted for publication in Epilepsy & Behavior. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Epilepsy & Behavior, 104, B, 2020 DOI: 10.1016/j.yebeh.2019.06.039