Darryl C. DeVivo

TL;DR: It is speculated that the increased brain ATP/ADP ratio is central to most, if not all, the observed metabolic perturbations and may account for the increased neuronal stability that accompanies chronic ketosis.

TL;DR: Enzymological observations point to an in vivo defect in the activation mechanism of the pyruvate dehydrogenase complex as the biochemical disturbance in SNE, and suggest that dichloroacetate may be beneficial in treating SNE.

TL;DR: No clear etiologic association could be established between the severity of the neuropathologic alterations and the following actors: age at death, duration of illness, elevated intracranial pressure, or treatment regimens, but the reported case demonstrated the most severe parenchymatous changes at autopsy and received the most intensive treatment of the CNS.

TL;DR: Blood and tissue metabolic perturbations and analysis of hepatic tissue obtained by open biopsy suggest that pyruvate carboxylase is important in modulating the fractional distribution of intracellular acetyl-CoA between the tricarboxylic acid cycle, the beta-hydroxy-beta-methyl-glutaryl-Co a cycle (and the synthesis of cholesterol and ketone bodies), and fatty acid synthesis.

TL;DR: Chronic ketosis effects cerebral metabolism like certain anticonvulsant drugs by slowing brain phosphofructokinase, pyruvate dehydrogenase, and α-ketoglutarate dehydrogenases and it is suggested that each of these metabolic effects contributes to the anticonVulsant action of the ketogenic diet.