The pathological substrate of limbic epilepsy: Neuronal loss in the medialdorsal thalamic nucleus as the consistent change

Citation
Eh. Bertram et C. Scott, The pathological substrate of limbic epilepsy: Neuronal loss in the medialdorsal thalamic nucleus as the consistent change, EPILEPSIA, 41, 2000, pp. S3-S8
Citations number
42
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EPILEPSIA
ISSN journal
00139580 → ACNP
Volume
41
Year of publication
2000
Supplement
6
Pages
S3 - S8
Database
ISI
SICI code
0013-9580(2000)41:<S3:TPSOLE>2.0.ZU;2-Z
Abstract
Purpose: The focus of research in limbic epilepsy has been the hippocampus because of its well-known pathology of hippocampal atrophy and sclerosis as well as the strong propensity for this structure to seize under a variety of circumstances. There is ample evidence, however, for pathological altera tions in other regions of the limbic system in limbic/mesial temporal lobe epilepsy, including the amygdala, the entorhinal cortex, and, in some cases , the thalamus. In this preliminary evaluation of the pathological substrat e for limbic epilepsy, we wished to determine if there was consistent anato mic change at extrahippocampal sites. Methods: We compared paraffin sections of brains from rats with chronic spo ntaneous limbic epilepsy and age-matched controls to determine the consiste ncy of the pathology at five sites: the hippocampus, amygdala, entorhinal c ortex, piriform cortex, and medial dorsal thalamus. Results: In a qualitative evaluation of these sections taken from standardi zed positions, we found that the medial dorsal thalamic nucleus in the epil eptic animals was the site that was consistently involved with neuronal los s. With all other sites, at least several animals had qualitatively normal tissue. Conclusions: This finding suggests that neuronal loss in the medial dorsal thalamus may be the consistent pathology in limbic epilepsy, at least in an animal model of the disorder. The presence of a structurally abnormal subc ortical region with broad connections to the limbic sites involved with chr onic epilepsy may have implications for our understanding of the pathophysi ology of this disorder.