Ocular signs in thiamine-deficient monkeys and in Wernicke's disease in humans
D. G. Cogan, E. D. Witt and P. S. Goldman-Rakic
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.
