Abstracts

Rationale: Mesial temporal lobe epilepsy (MTLE) is associated with structural and functional abnormalities, such as hippocampal sclerosis, axonal reorganization and hyperexcitable neural networks. The temporal evolution of these changes remains to be determined, and there is a need for in vivo imaging techniques that can uncover the epileptogenic processes at an early stage. In this regard, MEMRI may be useful. The aim of this study was to analyze temporospatial changes in manganese enhancement in the kainate animal model of MTLE.Methods: Status epilepticus was induced in Sprague-Dawley rats by 10mg/kg kainate intraperitoneally. MnCl₂ was given subcutaneously on day two (early phase), day 15 (latent phase), and 11 weeks (chronic phase with spontaneous recurrent seizures) after the initial status epilepticus. Twenty-four hours after MnCl₂ injection T1-weighted 3D MRI was performed followed by analysis of manganese enhancement. Results: In the early phase there was a pronounced decrease in manganese enhancement in medial temporal lobe structures such as the hippocampal subregions CA1 and CA3, dentate gyrus, entorhinal cortex and lateral amygdala. In the latent and chronic phases recovery of the manganese enhancement was observed in all these structures except CA1. A significant increase in manganese enhancement was detected in entorhinal cortex and amygdala in the chronic phase. In the latter phase, the structurally intact cerebellum showed significantly decreased manganese enhancement.Conclusions: This study demonstrates that the epileptogenic process initiated by systemic kainate is associated with a highly differentiated temporospatial pattern of manganese enhancement which can be distinguished using MEMRI. The changes in manganese enhancement cannot be attributed to a single mechanism or to alterations in a single cellular compartment. Rather, the changes are likely to represent the net outcome of a number of pathological and pathophysiological events, including cell loss and changes in neuronal activity. Greater neuronal cell loss in the hippocampal formation than in other medial temporal lobe structures may obscure activity changes in the former structure.