Ocular signs in thiamine-deficient monkeys and in Wernicke's disease in humans.

Thiamine deficiency in the monkey is the animal counterpart of Wernicke's disease in humans. In the present study, thiamine deficiency was induced in 11 monkeys while three monkeys were given paired feedings supplemented by thiamine hydrochloride and three monkeys were maintained on regular chow. The typical clinical symptoms were apathy, inattention to peripheral stimuli, ataxia, ptosis, mydriasis progressing to pupillary areflexia, nystagmus, and ophthalmoparesis progressing to total ophthalmoplegia. With thiamine treatment, recovery was prompt and complete in mild to moderate cases but delayed and incomplete in severe cases. The animals were killed six or more months after discontinuance of the experiments to determine the chronic effects of treated thiamine deficiency. The significant abnormalities in the brain stem were symmetric gliosis and neuronal loss in the inferior colliculi, the regions of the third and sixth nerve nuclei, and the medial vestibular nuclei. White matter was characteristically spared. With the exception of the inferior colliculi, the target sites for neuropathologic changes were the centers for ocular motor control.

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.

Intermittent thiamine deficiency in the rhesus monkey. II. Evidence for memory loss.

Thiamine-deprived rhesus monkeys exhibited a pattern of impairments in spatial-reversal learning and in recognition of highly familiar items reminiscent of certain memory deficits shown by Wernicke-Korsakoff patients. Postmortem examination in these experimental animals showed neuronal degeneration in the basal ganglia, the parafascicular nucleus of the thalamus, and discrete nuclei of the brainstem and cerebellum. No abnormalities were found in the mammillary bodies and mediodorsal nucleus of the thalamus, structures that have been incriminated in the genesis of the memory impairment of the Wernicke-Korsakoff syndrome of man.