%0 Journal Article
%T Occult Cerebrovascular Disease and Late-Onset Epilepsy: Could Loss of Neurovascular Unit Integrity Be a Viable Model?
%A Lorna M. Gibson
%A Stuart M. Allan
%A Laura M. Parkes
%A Hedley C. A. Emsley
%J Cardiovascular Psychiatry and Neurology
%D 2011
%I Hindawi Publishing Corporation
%R 10.1155/2011/130406
%X Late-onset epilepsy (LOE) first occurs after 60 years of age and may be due to occult cerebrovascular disease (CVD) which confers an increased risk of stroke. However, patients with late-onset epilepsy are not currently consistently investigated or treated for cerebrovascular risk factors. We discuss how abnormalities of neurovascular unit function, namely, changes in regional cerebral blood flow and blood brain barrier disruption, may be caused by occult cerebrovascular disease but present clinically as late-onset epilepsy. We describe novel magnetic resonance imaging methods to detect abnormal neurovascular unit function in subjects with LOE and controls. We hypothesise that occult CVD may cause LOE as a result of neurovascular unit dysfunction. 1. Introduction Late-onset epilepsy (LOE) is defined as epilepsy that first occurs after 60 years of age, and is considered by family doctors to be rare [1], despite the fact that it accounts for over a third of all incident epilepsy [2]. LOE occurs in approximately 4% of stroke patients [3], but importantly, LOE can present without a history of overt cerebrovascular disease (CVD), yet LOE confers a subsequent threefold increased risk of stroke [4]. It is widely assumed that LOE is often attributable to otherwise occult CVD. However, at least in the UK, patients with LOE tend to be prescribed anticonvulsant medication, but the opportunity that LOE presents as a marker of increased stroke risk may be lost if a presentation of LOE does not prompt clinicians to screen for other vascular risk factors and initiate appropriate vascular secondary prevention measures, for which there is a strong case [4, 5]. Occult CVD may be detected on brain imaging but by definition does not manifest otherwise clinically. Structural imaging markers of occult CVD are thought to include cortical or subcortical infarcts, white matter hyperintensities, leukoaraiosis (LA), cerebral atrophy, and brain microbleeds (BMBs) which are a marker particularly of cerebral microangiopathy, and strongly associated with hypertension [6]. However, between 72 and 94% of occult infarcts are subcortical, yet epilepsy derives from the cortex. If occult CVD is aetiologically important in LOE then markers of CVD would be expected to have a more diffuse anatomical distribution than described previously. Subcortical lesions in isolation would not be expected to cause the disruption of corticocortical or subcorticocortical circuits that would be a necessary substrate for epileptogenesis. Markers of functional rather than structural integrity may then be
%U http://www.hindawi.com/journals/cpn/2011/130406/