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Article
August 1985

Ocular Signs in Thiamine-Deficient Monkeys and in Wernicke's Disease in Humans

Author Affiliations

From the National Eye Institute (Dr Cogan) and the National Institute of Neurological and Communicative Disorders and Stroke (Dr Witt), National Institutes of Health, Bethesda, Md, and the Section on Neuro-anatomy, Yale University School of Medicine, New Haven, Conn (Dr Goldman-Rakic).

Arch Ophthalmol. 1985;103(8):1212-1220. doi:10.1001/archopht.1985.01050080124032
Abstract

• 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.

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