Neuroanatomical consequences of thiamine deficiency: a comparative analysis.
In this paper, the neuroanatomical locus of lesions produced by thiamine deficiency was examined. An attempt was made to analyse the relationship between the pattern of development of neuropathological lesions and such experimental variables as length of deficiency, species, and method of deprivation. There is evidence in all species studied that certain structures are selectively vulnerable to thiamine deficiency. Current theories concerning the pathogenesis of lesions, including metabolic, neurophysiological, and genetic mechanisms were also discussed. It was concluded that the selective vulnerability of certain structures to thiamine deficiency is the result of a complex interaction between cellular, neurochemical, and metabolic properties of various brain regions which make them more susceptible to a breakdown in thiamine-dependent systems.
Witt
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D000425:Alcohol Amnestic Disorder / Q000473:pathology; D000818:Animals; D001921:Brain / Q000201:enzymology / Q000473:pathology*; D001933:Brain Stem / Q000473:pathology; D002531:Cerebellum / Q000473:pathology; D004734:Energy Metabolism; D004798:Enzymes / Q000378:metabolism; D006801:Humans; D007031:Hypothalamus / Q000473:pathology; D008326:Mammillary Bodies / Q000473:pathology; D008636:Mesencephalon / Q000473:pathology; D009410:Nerve Degeneration; D018377:Neurotransmitter Agents / Q000378:metabolism; D013787:Thalamic Nuclei / Q000473:pathology; D013832:Thiamine Deficiency / Q000201:enzymology* / Q000473:pathology*; D014899:Wernicke Encephalopathy / Q000201:enzymology / Q000473:pathology*
D004798:Enzymes; D018377:Neurotransmitter Agents