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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)
Rosenthal, S
F.GordonJ
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R., Lewington, A
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