MR Spectroscopy in Epilepsy
In the pathogenesis of epilepsies genetic and acquired factors are involved. The elementary electrophysiological phenomenon is the so-called intracellular paroxysmal depolarisation shift (PDS). Spontaneous chronic recurrence of paroxysmal epileptiform activity indicates an epileptogenic process. This epileptogenic process is correlated to biochemical changes in metabolism. The activity on CNS circuits is influenced by dominant excitatory (e.g. glutamate, aspartate, quisqualate) or dominant inhibitory (e.g. gamma-aminobutyric acid (GABA), GAB A agonist) transmitters and neuromodulators. The excitation (paroxysmal depolarisation) is mediated by glutamate receptors. Ion-bound receptors are, for example, of the N-methyl-D-aspartate, Ampa or kainate types. The release of glutamate and the depolarisation of the neuron are closely linked. The result of glutamate release and the binding to the N-methyl-D-aspartate receptor causes an increase of calcium into the neuron. This energy consuming process may be accompanied by an increase of inorganic phosphate and energy depletion with decrease of ATP and phosphocreatine. In addition to the intracellular neuronal release of glutamate, or in the case of inhibition of GABA and reaction with the GABA-receptor complex, metabolic pathways obviously involve glia cells. The uptake of GABA and glutamate in the glial cell is influenced by different enzymes and pharmacological mechanisms. Tetrahydroisoxa-colopyridinol PHPD decreases GABA uptake into the glial cell. Glutamine synthetase decreases uptake of glutamate into the glial cell. Anti-epileptic drugs such as valproate acid or vigabatrin enhance the concentration of GABA in the neurotransmitter pool. Lamotrigine may lead to a decrease of glutamate in the region of the focus. The concentration of glutamate GABA-aspartate and taurine was found to be decreased in the focus centre (van Gelder et al., 1972), whereas Perry and Hansen (1981) found an increase of GABA and glutamate in the focus centre.