Evans et al. (1942) investigated the illness of foxes raised for fur on the
Chastek fox farm in Minnesota, and found brain lesions that resembled
those of Wernicke’s encephalopathy. The diet the foxes were fed was
found to be thiamine deficient; it consisted of raw fish which additionally
was found to contain a thiamine deactivating enzyme. Rinehart et al.
(1949) reported neuropathology caused by thiamine deficiency in
monkeys.
DeJong (1944) is an early report of the dangers of methyl bromide, a
toxic substance that produces Wernicke-encephalopathy-like damage of
brainstem nuclei. Methyl bromide at that time was used as a refrigerant,
herbicide, pesticide, and fire extinguisher.
Bini and Bollea (1947) described clinical features of two pressers in a
dry-cleaning establishment poisoned by fumes from cleaning fluids and
the brain damage found following their deaths. Delirium reminiscent of
alcoholic intoxication preceded coma and death in both victims. The
characteristic lesions of Wernicke’s encephalopathy were found at
autopsy. Call and Gunn (1949) described brainstem lesions caused by
arsenic compounds, which were used to treat syphilis until penicillin
came into use.
Barnhart et al. (1948) and Bodian (1949) described brainstem patterns
of damage caused by the poliovirus.
From
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4- Brainstem damage