Chronic epilepsy and cognition

CE Elger, C Helmstaedter, M Kurthen - The Lancet Neurology, 2004 - thelancet.com
The Lancet Neurology, 2004thelancet.com
Cognitive profiles in epilepsy are as heterogenous as the epileptic syndromes themselves;
causes, topography of epileptogenic areas, pathogenetic mechanisms, and the diverse
features characterising the clinical course all contribute to the effect on cognition. Chronic
epilepsy generally impairs cognition, but it also induces processes of functional
reorganisation and behavioural compensation. In most idiopathic epilepsies, cognition is
only mildly deteriorated or even normal by clinical standards. Localisation-related …
Summary
Cognitive profiles in epilepsy are as heterogenous as the epileptic syndromes themselves; causes, topography of epileptogenic areas, pathogenetic mechanisms, and the diverse features characterising the clinical course all contribute to the effect on cognition. Chronic epilepsy generally impairs cognition, but it also induces processes of functional reorganisation and behavioural compensation. In most idiopathic epilepsies, cognition is only mildly deteriorated or even normal by clinical standards. Localisation-related cryptogenic and symptomatic epilepsy disorders are accompanied by focal deficits that mirror the specific functions of the respective areas. Poor cognitive outcome is generally associated with an early onset and a long duration of the disease and with poor seizure control. There is evidence that cognitive functions are already impaired at the onset of the disease, and that the maturation of cognitive functions in children is susceptible to the adverse influence of epilepsy. In adults, cognitive decline progresses very slowly over decades with an age regression similar to that of people without epilepsy. Successful epilepsy surgery can stop or partly reverse the unfavourable cognitive development, but left-temporal resections in particular have a high risk of additional postoperative verbal memory impairment. Cognitive recovery in the adult brain after successful surgery indicates functional compensation and, to some degree, functional reorganisation or a reactivation of functions previously suppressed by influence from distant but connected epileptogenic areas.
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