SELECTIVE VULNERABILITY IN ACUTE ENERGY DEPRIVATION SYNDROMES

The topography and cellular events in the experimental lesions caused by chlorosugars, 6-aminonicotinamide, dinitrobenzene and tribromoimida zole in animals are considered in relation to those features in human acute thiamine deficiency (Wernicke's) encephalopathy and for comparis on in Leigh's disease. The topography and cellular changes when closel y examined are different and particular to each condition, although th ere is a basic cellular process common to all. The pathogenesis of eac h condition must be considered as multifactorial and a search for the factors responsible for the neuronal and cellular selective vulnerabil ity of different regions of the neuraxis will lead us to understanding the pathogenesis of the disease process in each instance. The experim ental models offer much for the understanding of the human conditions, particularly in the search for satisfactory therapeutic strategies.