fifties2txt

Hicks (1950) described brain lesions caused by a variety of agents that
interfere with energy metabolism, cyanide, insulin hypoglycemia,
asphyxia in nitrogen, and fluroacetate poisoning in rats, and noted that
"... the lesions were nearly always symmetrically bilateral..." (p 119).
This bilaterally symmetric pattern of damage or impairment of the brain
would be recognized later in investigations of toxic substances. Oyanagi
et al. (1989) reported widespread involvement of the auditory system in
fourteen cases of methyl mercury intoxication, including the inferior
colliculus. Bertoni and Sprenkle (1988) found reduced metabolism in
auditory nuclei caused by lead.

Leigh (1951) reported bilateral symmetric brainstem lesions in an infant
whose death was thought to have resulted from an encephalitic process,
but Leigh noted the similarity of the brain damage to that described by
Wernicke and proposed that the child perhaps died of nutritional
deficiency. However, Wernicke (1881) compared the brain damage
caused by alcohol and sulfuric acid to that seen in poliomyelitis, and
effects of the polio virus and other infections have also been found to
cause mainly brainstem damage (Buzzard & Greenfield 1919, Barnhart
et al. 1948, Bodian 1949).

Neubuerger (1954) reported the same pattern of symmetrical bilateral
damage to brainstem nuclei in seven people who were resuscitated after
cardiac arrest but died shortly thereafter. Neubuerger expressed
surprise that the location of lesions showed more variety than expected,
and made special note of one case in which there was, “...involvement of
centers usually affected in Wernicke's disease, especially the mammillary
bodies and posterior colliculi...” This was a person who died, at age 72,
of respiratory failure during surgery. Artificial respiration and heart
massage were performed with spontaneous heart beats obtained after
eight minutes and spontaeous respiration after eighteen minutes. The
patient, however, remained in a coma until death one week later. This
can be regarded as a case of total acute asphyxia, comparable to
asphyxia at birth as produced in the experiments by Ranck and Windle
(1959).

Victor and Yakovlev (1955) translated the article by Korsakoff (1889) on
the psychic disorder that develops with chronic use of alcohol. Malamud
and Skillicorn (1956) presented neuropathological data confirming that
Wernicke’s encephalopathy and Korsakoff syndrome are acute and
chronic forms of the same disorder.

Jubb et al. (1956) discovered a form of Wernicke’s encephalopathy that
occurred in pet cats fed a canned cat food product consisting of raw
fish. They replicated this finding experimentally, and compared their
observations with those of Evans et al. (1942) on foxes fed a diet of raw
fish.

Franken (1959) described striking lesions of the Wernicke encephalitic
type located in both posterior quadrigeminal bodies in a 28-year old man
with chronic exposure to methyl bromide over a two-year period in his
work filling fire extinguishers. During a three-month period before death,
he had displayed transient alterations of consciousness and jerking of
his legs during sleep. He lapsed into a coma following an episode of
acute intoxication with methyl bromide and died two days later. Franken
cited four case reports of deaths caused by methyl bromide in French
medical journals dating back to 1937 that are not readily available, but
they do not seem to describe pathology in the brain as clearly as
Franken did.

Malamud (1959) reported a Wernicke-encephalopathy like pattern of
brain damage in two children with disintegrative disorder possibly caused
by a mitochondrial energy disorder. The children were siblings, one of
whom died at age 13 and her brother at age 11. Malamud reported
symmetric bilateral lesions of the corpus Luysi (subthalamic nucleus),
Mammillary bodies, and mammillo-thalamic tracts.
Ross (1959) discovered a Wernicke-encephalopathy like pattern of
neuropathology in a child with autistic behaviors. This child appeared to
be anorexic and the damage in her brain may have been due to
nutritional deficiencies. She would now be thought of as a child with
disintegrative disorder or early childhood schizophrenia, but her autistic
disinterest in her environment provides an association with this kind of
behavior and Wernicke’s encephalopathy in a child.

Ranck and Windle (1959) reported damage of the inferior colliculi in
monkeys subjected to experimental asphyxia at birth. This pattern of
damage can now be viewed as a Wernicke-encephalopathy type pattern
of damage affecting the brainstem nuclei of highest metabolic rate.