Thalamic Volume Is Reduced in Temporal Lobe Epilepsy with and without Hippocampal Atrophy.
Abstract number :
1.206
Submission category :
Year :
2001
Submission ID :
2988
Source :
www.aesnet.org
Presentation date :
12/1/2001 12:00:00 AM
Published date :
Dec 1, 2001, 06:00 AM
Authors :
J. Natsume, MD, PhD, Neurology and Neurosurgery, Montreal Neurological Institute, Montreal, QC, Canada; A. Bernasconi, MD, Neurology and Neurosurgery, Montreal Neurological Institute, Montreal, QC, Canada; N. Bernasconi, MD, Neurology and Neurosurgery, Mo
RATIONALE: As part of the limbic system, thalamus has reciprocal anatomical connections with the hippocampus, entorhinal cortex and amygdala. The thalamus has been proposed to be involved in the regulation of cortical excitability and seizure propagation in temporal lobe epilepsy (TLE). Pathological studies in TLE patients (Margerison and Corsellis. Brain 1966;89:499-530) and in animal models of TLE (Bertram. Epilepsia 2000;41:S3-S8) have shown neuronal loss in the thalamus. The purpose of our study was to determine if structural changes of the thalamus are apparent on high-resolution MRI in patients with intractable TLE.
METHODS: MRI volumetric analysis of the thalamus and the hippocampus was performed using a T1-weighted 3D gradient echo sequence in 13 healthy subjects and 30 patients with unilateral TLE. The EEG focus was defined as right or left if more than 70% of seizures were recorded from one side. Twenty patients had left TLE and 10 had right TLE. The left TLE group included 10 patients with left hippocampal atrophy and 10 with normal hippocampal volumes. All 10 patients with right TLE had hippocampal atrophy. Images were registered into a standardized space and corrected for intensity non-uniformity. Group analysis was done using analysis of variance (ANOVA).
RESULTS: In normal controls the volume of the right thalamus was 9382 [plusminus] 698 mm3 (mean [plusminus] SD) and that of the left thalamus was 9632 [plusminus] 819 mm3. The left thalamic volume was significantly smaller than that of normal controls in both left TLE patients with (p=0.03) and without hippocampal atrophy (p=0.04). There was no difference in thalamic volumes between the patients with and without hippocampal atrophy. In the right TLE patients, the right thalamic volume was significantly smaller than that of the normal controls (p=0.04). The thalamic volume contralateral to the EEG focus was not different from normal controls in any TLE group.
CONCLUSIONS: Our results showed volume loss in the thalamus ipsilateral to the seizure focus in patients with TLE with and without hippocampal atrophy. The findings suggest that the thalamus may play a critical role in the limbic network and in the pathogenesis in temporal lobe epilepsy.