Intermittent thiamine deficiency in the rhesus monkey. I. Progression of neurological signs and neuroanatomical lesions

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Abstract
Rhesus monkeys were subjected to one, two, or four periods of thiamine deficiency to determine how the number of deprivation episodes affects the development and progression of neurological and neuropathological changes. Recrurent thiamine deprivation produced all major neurological signs and most of the anatomical lesions found in Wernicke‐Korsakoff syndrome. Neither the number and gravity of neurological symptoms nor the extent or location of lesions was related to the number of deprivation periods in a simple way. Thus, some structures, such as the inferior colliculus and medial vestibular nuclei, were affected after only one period of deficiency. Other structures, such as the parafascicular nucleus of the thalamus, were more resistant and exhibited degeneration only after four periods of thiamine deprivation. Severe damage in the basal ganglia was infrequent and was associated with prolonged rather than multiple periods of deprivation. No parenchymal damage was found in the mammillary bodies or mediodorsal nucleus of the thalamus, suggesting that lesions in these prominent sites of damage in Wernicke‐Korsakoff disease develop only in the most advanced stages of thiamine deprivation. As a consequence of individual differences in susceptibility to thiamine deficiency, neurological symptoms and signs were more related to the profile of neural damage than to the number or duration of deprivation episodes.