Abstracts

THE ROLE OF THE ENTORHINAL CORTEX IN THE PATHOGENESIS OF TEMPORAL LOBE EPILEPSY: A QUANTITATIVE MRI STUDY

Abstract number : 1.211
Submission category :
Year : 2003
Submission ID : 1166
Source : www.aesnet.org
Presentation date : 12/6/2003 12:00:00 AM
Published date : Dec 1, 2003, 06:00 AM

Authors :
Mary Fitzsimons, Kevin Murphy, Colin Doherty, Norman Delanty Epilepsy Programme, Beaumont Hospital, Dublin, Ireland

Reciprocal glutamatergic pathways of the entorhinal cortex (EC) connect the hippocampus to the surrounding cortex. Damage to the EC is associated with increased risk of seizure generation. Neuronal loss of layer III of the EC has been reported in surgical specimens from patients with temporal lobe epilepsy (TLE). Similarly, its strategic position and anatomical connections may implicate it in the propagation of seizures from the hippocampus to extrahippocampal areas. Atrophic change may be determined from MRI based volume estimation. We studied a group of patients with TLE to establish the frequency of co-existing EC and hippocampal volume loss.
High resolution 3D brain image data was acquired from 20 normal control subjects and 20 patients with TLE using a SPGR MRI imaging sequence. Standard anatomical landmarks were used to identify boundaries of the hippocampus and entorhinal cortex upon which i[italic]n-vivo [/italic]volumes were estimated from the image data using a computer based stereological technique.
Normal control volumes were estimated at 3.30(+/-0.38)cm3 [mean +/- S.D.] on the right and 3.13 (+/-0.35)cm3 on the left for the hippocampus, 1.06(+/- 0.16)cm3 on the right and 1.04 (+/-0.15)cm3 on the left for the EC. 70% of the TLE patients had ipsilateral hippocampal volume loss. Of these, 60% had co-existing ipsilateral EC volume loss, while the remainder had normal EC volumes.
Results support the existence of a spectrum of changes which range from isolated hippocampal atrophy, isolated EC atrophy, and co-existing hippocampal and EC atrophy. The position on the spectrum may influence seizure frequency and severity and may have implications for treatment. The pattern of atrophy demonstrated raises questions about the role of the EC in the pathogenesis of TLE. Further elucidation of these questions requires larger studies and clinical correlation.