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EP thanks the NRF of South Africa (grant number 142142) and SA MRC (self-initiated research (SIR) grant)
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It has long been recognized that ictal cerebral hypermetabolism is characteristic of seizure disorders, where increased cerebral oxygen (Meyer et al., 1966) and glucose consumption (Ingvar and Siesj, 1983) are observed during seizure activity in experimental epilepsy models and in humans (Guo et al., 2009) and mitochondrial metabolic deficits resulting from inhibition of mitochondrial enzyme complexes in animal and human epilepsies (Kunz et al., 2000, 1999)
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Understanding the central role that glutathione plays in this biochemical struggle provides not only validation for your symptoms but also a clear, scientifically grounded target for therapeutic intervention
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