Cerebrovascular disease burden in late-onset non-lesional focal epilepsy.


Epilepsy Unit, Neurology Department, Vall d'Hebron University Hospital, Autonomous University of Barcelona, Barcelona, Spain. Electronic address: [Email]


OBJECTIVE : Late-onset non-lesional focal epilepsy, defined as new-onset seizures in patients older than 60 years, is diagnosed increasingly more often in relation to aging of the population. It has been attributed mainly to occult cerebral small vessel disease (SVD), although high levels of evidence to support this notion are lacking. This study aimed to evaluate the burden of leukoaraiosis, a marker of cerebral SVD, and hippocampal atrophy in patients with late-onset epilepsy (LOE).
METHODS : Brain magnetic resonance imaging (MRI) studies were retrospectively analyzed by two blinded radiologists. The Fazekas and Scheltens scales were used to assess the degree of leukoaraiosis and hippocampal atrophy in 33 patients with non-lesional LOE, 41 patients with clinical signs of SVD (eg, recent history of transient ischemic attack [TIA] or lacunar stroke), and 26 healthy controls, all >60 years of age.
RESULTS : Mean age in epilepsy patients was 70.9 (±6.6) years; 57.6% were men. The history of vascular risk factors was similar in all groups. Median (interquartile range) Fazekas score was 1 (0-1) in the epilepsy group, 1 (0-2) in TIA/lacunar stroke patients, and 0 (0-1) in the healthy group. Degree of leukoaraiosis was milder in epilepsy patients compared to the TIA/lacunar stroke group (p = 0.004), and similar to that of healthy controls (p = 0.593). Hippocampal atrophy was significantly greater in patients with epilepsy (p < 0.005).
CONCLUSIONS : These findings suggest that the etiology of LOE is not exclusively related to cerebrovascular disease. Hippocampal atrophy may contribute to the origin of the seizures.



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