Neurology 2001;56:1335-1339
© 2001 American Academy of Neurology
Articles
Entorhinal cortex atrophy in epilepsy patients exhibiting normal hippocampal volumes
N. Bernasconi, MD;,
A. Bernasconi, MD;,
Z. Caramanos, MA;,
F. Dubeau, MD, FRCP(C);,
J. Richardson, MD, FRCP(C);,
F. Andermann, MD, FRCP(C); and
D.L. Arnold, MD, FRCP(C)
From the Departments of Neurology and Neurosurgery (Drs. N. Bernasconi, A. Bernasconi, Dubeau, Andermann, and Arnold, and Z. Caramanos) and Pathology (Dr. Richardson), McGill University, and Montreal Neurological Institute and Hospital, PQ, Canada.
Address correspondence and reprint requests to Dr. N. Bernasconi, Montreal Neurological Hospital and Institute, 3801 University Street, Montreal, PQ, Canada, H3A 2B4.
OBJECTIVE: To determine whether MRI volumetric measurement of the entorhinal cortex could detect structural damage and lateralize the seizure focus in patients with temporal lobe epilepsy in whom no measurable hippocampal abnormalities were found.
BACKGROUND: A reduction in the volume of the entorhinal cortex ipsilateral to the seizure focus in patients with intractable temporal lobe epilepsy and hippocampal atrophy was recently shown.
METHODS: MRI volumetric analysis of the entorhinal cortex was performed using a T1-weighted three-dimensional gradient echo sequence in 24 control subjects and 22 patients with temporal lobe epilepsy and normal hippocampal volumes. Thirteen patients underwent surgery, with a mean postoperative follow-up of 36 months.
RESULTS: Group analysis (multivariate analysis of variance) showed a reduction in the volume of the entorhinal cortex ipsilateral to the seizure focus in patients with left (p < 0.0001) and right temporal lobe epilepsy (p < 0.0001). Lateralization of the seizure focus could be done in 14 of 22 patients (64%) based on entorhinal cortex volumetry.
CONCLUSION: Entorhinal cortex atrophy ipsilateral to the seizure focus supports the presence of structural damage in the mesial temporal lobe in patients with temporal lobe epilepsy and normal hippocampal volumes and emphasizes the participation of the entorhinal cortex in the pathogenesis of this disorder.
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