Quantitative Neuropathology of the Entorhinal Cortex Region in Patients with Hippocampal Sclerosis and Temporal Lobe Epilepsy
Article first published online: 11 JAN 2005
Volume 46, Issue 1, pages 23–30, January 2005
How to Cite
Dawodu, S. and Thom, M. (2005), Quantitative Neuropathology of the Entorhinal Cortex Region in Patients with Hippocampal Sclerosis and Temporal Lobe Epilepsy. Epilepsia, 46: 23–30. doi: 10.1111/j.0013-9580.2005.21804.x
- Issue published online: 11 JAN 2005
- Article first published online: 11 JAN 2005
- Accepted August 21, 2004.
- Entorhinal cortex;
- Hippocampal sclerosis;
- Temporal lobe epilepsy;
- Neuronal loss
Summary: Purpose: Clinical, radiologic, and experimental evidence indicates that the entorhinal cortex (EC) region may be linked to the pathophysiology of hippocampal sclerosis (HS) in patients with temporal lobe epilepsy. Few neuropathologic studies of this region have been undertaken in patients with HS undergoing surgery, some suggesting preferential loss of layer III neurones.
Methods: We carried out a quantitative analysis in 26 patients with HS, nine patients with lesional temporal lobe epilepsy (LTLE), and eight postmortem controls. We measured neuronal densities in EC by using a three-dimensional cell-counting technique on NeuN immunostained and Nissl-stained sections. We also quantified the density of calretinin-positive interneurones in this region and the density of neurones in adjacent subiculum and CA1 subfields. We also assessed the patterns of gliosis in the EC in the patient groups and the presence of any neocortical neurone loss.
Results: No significant difference was found in the mean neuronal densities in the EC region between HS and LTLE groups or postmortem controls. Laminar gliosis in midcortical layers was seen in a proportion of HS cases but also in the LTLE group. No significant difference was seen in the density of calretinin interneurones and no correlation between the presence of neocortical neuronal loss and EC neuronal densities.
Conclusions: A stereotypical pattern of neuronal loss and gliosis in the EC region in patients with HS is not confirmed that distinguishes this pathologic process from that in patients with lesional TLE.