1 – Sudden total cutoff of respiration
This is the report of brain damage found in five
monkeys subjected to asphyxia at birth.  The method
was to deliver the monkey fetuses by hysterotomy –
retaining the fetus within its intact membranes.  
Asphyxia was timed from the moment of placental
separation and lasted for 11 to nearly 16 minutes.  
Resuscitation was accomplished by positive pressure
oxygen or 95 percent oxygen and 5 percent carbon
dioxide through a tracheotomy.  The monkeys were
killed at 2 to 9 days of life for examination of the brain.

The most severely affected monkey (monkey C)
remained in what appeared to be a deep coma
throughout its 9 days of life.  The other 4 recovered
but displayed developmental impairments.  
Comparisons were made with 2 non-asphyxiated
monkeys.  The non-asphyxiated monkeys exhibited a
strong grasp, could right themselves when placed on
their backs or side, used coordinated movements for
progression, reacted to loud sounds, and sucked and
swallowed without difficulty.

The asphyxiated monkeys had difficulty righting
themselves, sucked poorly, and were inactive and
hypo-responsive; but they could be hyper-irritable or
display a marked startle to loud sounds.  Sounds
invoked mass motor movements in two animals lasting
up to 20 seconds; one monkey was described as
being unable to localize sound.  Ranck and Windle
commented that "Hyperreactivity to loud sound during
the first 12 hours followed by hyporeactivity or
complete absence of responses later on may have
been related to the massive destruction the central
acoustic pathways."

In the brain it was noted, "Major lesions were confined
to nuclei of both sides of the brain stem" and
"Changes were distributed in a bilaterally symmetrical
pattern."  Destruction of nuclei of both inferior colliculi
was most striking.  Lesions of other subcortical nuclei
were described as equally constant but less dramatic
and included structures like the oculomotor and
vestibular nuclei, mammillary bodies, hippocampal
formation, roof nuclei of the cerebellum, and loss of
cerebellar Purkinje cells.

1. Ranck JB, Windle WF (1959).
   Brain damage in the
   monkey, Macaca mulatta, by
   asphyxia neonatorum.
   
2. Wernicke C (1881a) Die
   acute, haemorrhagische
   Poliencephalitis superior.
   
3. Brody IA, Wilkins RH. (1968)
   Wernicke's encephalopathy.
   
4. Victor M et al (1971) The
   Wernicke-Korsakoff
   syndrome; a clinical and
   pathological study of 245
   patients, 82 with post-
   mortem examinations.
   
5. Rosenblum WI, Feigin I.
   (1965) The hemorrhagic
   component of Wernicke's
   encephalopathy.
   

Concluding paragraph, p 153:
"The human neuropathologic entity most closely resembling the effects
of asphyxia neonatorum in the monkey is kernicterus. There are similarities
in the distribution and type of nerve cell changes in both conditions.
Major differences between the findings in the monkey and those in human
infants with kernicterus are absence in the former of the usual history of
erythroblastosis fetalis, lack of clinical jaundice, lack of pigment in the
lesions, frequent presence of neuroglia cell damage, and presence of
marked astrocytic and phagocytic reactions."

Citation to work in progress by A Pentschw and C Margoles:
Margoles C, Katami K, Moloney Wc, Pentschew A, Sutow Ww, Haymaker W.
Kernicterus in Japanese infants. II. Pathologic data in 25 cases of kernicterus and
in 20 cases of systemic icterus without kernicterus. World Neurol. 1960
Sep;1:254-71.