Abstracts

Extrahippocampal Abnormalities in Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

Abstract number : 3.123
Submission category : Clinical Epilepsy-Adult
Year : 2006
Submission ID : 6808
Source : www.aesnet.org
Presentation date : 12/1/2006 12:00:00 AM
Published date : Nov 30, 2006, 06:00 AM

Authors :
1,2,3Dami[aacute]n E. Consalvo, 1Marcelo Kauffman, 1Pablo A. Salgado, and 1,3Kochen S. Silvia

In patients with the syndrome of mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS), extrahippocampal abnormalities (EHA) are frequently described on MRI studies.
The aim of the study was to evaluate the frequency of EHA in patients with MTLE-HS, and to correlate these findings with some of its clinical characteristics., MTLE-HS patients, diagnosed by electro-clinical and high resolution MRI findings were examined. The presence of temporal lobe atrophy (TLA), parahippocampal gyrus atrophy (PHA), fornix atrophy (FA) and mammillary bodies atrophy (MBA) on MRI studies were considered EHA by visual analysis.
The variables studied were age, age at the beginning of the epilepsy, time of evolution, history of febrile convulsions (FC), familial epilepsy, status epilepticus, secondary generalization of the seizures and response to the pharmacological treatment., Fifty four patients were included. Fifty of them (92.5%) showed EHA on MRI studies. They were divided in 4 groups. Group 1: TLA patients, 18 cases (33.3%); Group 2: PHA patients, 44 cases (81.4%); Group 3: FA patients, 29 cases (53.7%); and Group 4: MBA patients, 23 cases (42.5%). EHA were found in 14 of 17 (82.3%) normal controls. Anyone showed TLA or PHA. Three controls showed FA (p[lt] 0.02) and 2 MBA (p[lt] 0.04). A strong association between PHA and the history of FC was observed (p= 0,002). There were no differences in the rest of the variables analyzed., The presence of EHA suggests that the causal noxa of the syndrome of MTLE-HS also affects other areas widely connected with the hippocampus. The association between PHA and FC introduce a hypothesis of a physiopathological mechanism of common affectation.,
Clinical Epilepsy