Abstracts

RATIONALE: As part of the limbic system, the 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). Previous quantitative MRI studies have shown a decrease in volume of the thalamus in TLE patients. However, the specificity of these findings for TLE has not been established. To determine if thalamic volume changes are specific to TLE, we measured the thalamic volumes on high resolution MRI in groups of patients with TLE, extra-temporal lobe epilepsy (ETE) and idiopathic generalized epilepsy (IGE). We also determined correlation of thalamic volumes with volumes of mesial temporal structures in TLE.
METHODS: Thalamic volume measurements were carried out using T1-weighted 3D gradient echo sequence magnetic resonance imaging (MRI) in 40 patients with TLE (20 with hippocampal atrophy and 20 without hippocampal atrophy), 16 patients with ETE, and 17 with IGE. Each individual[Aring]fs volume measurement was standardized relative to the volume of normal controls using a z-score transformation. Thalamic volumes in patients were compared to those in 21 neurologically normal controls. The correlation among volumes of thalamus, hippocampus, amygdala and entorhinal cortex was also determined in TLE patients and normal controls.
RESULTS: In TLE patients, thalamic volumes ipsilateral to the seizure focus in patients with hippocampal atrophy (mean [plusminus]SD, -0.95 [plusminus] 1.25) and without hippocampal atrophy (-0.88 [plusminus] 0.92) were smaller than the volume in normal controls (p[lt]0.05). There was no significant difference in thalamic volume between patients with HA and without HA. Thalamic volumes contralateral to seizure focus in TLE groups were not significantly different from those in normal controls. Thalamic volumes in patients with ETE and IGE were not significantly different from those of normal controls. There was no correlation of thalamic volumes with the volumes of hippocampus, amygdala and entorhinal cortex in TLE patients nor in normal controls.
CONCLUSIONS: Atrophy of the thalamus is present only in patients with TLE and is not found in patients with ETE or IGE. Thalamic atrophy ipsilateral to the seizure focus exists even in TLE patients who do not demonstrate hippocampal atrophy on MRI. Thalamic atrophy appears to be specific to TLE, probably as a part of the limbic system disorder, and may contribute to the diagnosis and lateralization of the seizure focus in TLE.
[Supported by: Canadian Institutes of Health Research]