Hippocampal Cell Density and Subcortical Metabolism in Temporal Lobe Epilepsy
Version of Record online: 2 AUG 2005
Volume 40, Issue 4, pages 408–413, April 1999
How to Cite
Dlugos, D. J., Jagg, J., O'Connor, W. M., Ding, X.-S., Reivich, M., O'Connor, M. J. and Sperling, M. R. (1999), Hippocampal Cell Density and Subcortical Metabolism in Temporal Lobe Epilepsy. Epilepsia, 40: 408–413. doi: 10.1111/j.1528-1157.1999.tb00734.x
- Issue online: 2 AUG 2005
- Version of Record online: 2 AUG 2005
- Temporal lobe epilepsy;
- Epilepsy surgery;
- Positron emission tomography;
- Basal ganglia;
Summary: Purpose: Correlations between hippocampal cell density and subcortical metabolism in patients with temporal lobe epilepsy (TLE) were studied to explore possible links between subcortical function and the regulation of hippocampal excitability.
Methods: Resected hippocampal cell densities were correlated with cortical and subcortical regional cerebral metabolic rate for glucose (CMRglu), as measured by [18F]-fluorodeoxyglucose positron emission tomography (18-FDGPET), in 39 patients with intractable TLE who underwent anterior temporal lobectomy (ATL). CMRglu was measured ipsilateral and contralateral to the resected temporal lobe. Linear regression techniques were used for statistical analysis.
Results: Hilar cell densities correlated positively and significantly with CMRglu in the bilateral thalamus, putamen and globus pallidus, and the ipsilateral caudate. Dentate granule cell densities correlated positively and significantly with CMRglu in the bilateral thalamus and putamen. There was no significant correlation between cell densities and CMRglu in any cortical region, including the hippocampus.
Conclusions: We postulate that hippocampal cell loss results in decreased efferent synaptic activity to the thalamus and basal ganglia, causing decreased neuronal activity in these structures with consequent hypometabolism. This synaptic activity has a significant bilateral component. Subcortical hypometabolism in patients with TLE may reinforce the epileptogenic potential of mesial temporal lobe discharges.