2 - Norman (1972)
Norman (1972) reported three cases of brainstem
damage found in infants who died within the neonatal
period, and she compared these findings with those
of Ranck and Windle (1959) in monkeys subjected to
asphyxia at birth [1, 2].
Norman’s first case was a male infant who did not
breathe spontaneously at birth; he was delivered as a
footling breech and weighed 2730 grams (a little over
6 pounds). Intratracheal suction, mechanical
resuscitation, and oxygen were required; his one-
minute Apgar score was 1. He developed pneumonia
and was treated 36 hours after birth with
intramuscular penicillin. He was kept in an upright
position, fed by gavage tube, and maintained for 21
days on oxygen and 24 days on intrvenous fluids. He
was admitted to the hospital at 30 days of age with
spastic limbs and in a position of opisthotonus (spine
arched backwards). He developed seizures five days
later at died at 43 days of age. Microscopic
examination of the brain revealed patchy neuronal
loss in the reticular formation of the medulla and
pons, lateral and medial lesions of the thalamus, and
neuronal loss and astrocytosis within the
hippocampus. Other areas of the brain including
cerebellum and cerebral cortex appeared normal.
Norman’s second case was a female child born to a
woman who had taken an overdose of salicylates
three weeks before the baby was born. The infant
was delivered in breech position and her birth weight
was 1950 grams (about 4 pounds 5 ounces). After
two hours she appeared unconscious, flaccid, and
without reflexes. Petechial hemorrhages covered her
face and head which spread during the first day of
life, and she suffered several episodes of stiffness.
She remained unconscious and
electroencephalogram indicated little and poorly
organized periods of cerebral activity. She died at
one week of age. Her brain appeared grossly normal,
but microscopic examination revealed a bilaterally
symmetric pattern of damage involving primarily the
reticular formation. The lesion involved the inferior
colliculi in the midbrain, patchy damage within the
thalamus, severe damage of the hypothalamus, and
neuronal loss and astrocytosis within the
hippocampus.
Norman’s third case was a male infant who was born
flaccid and white after a pregnancy complicated by
hydramnios (excessive amniotic fluid, which is
frequently associated with birth defects). Birth weight
was 1960 grams (about 4 pounds 5 ounces). Three
hours after birth the child was described as a
“gasping, cyanosed premature infant.” He was flaccid
and unresponsive but after intubation and mechanical
ventilation breathed spontaneously and became
pink. He died at eight days of life. The only
abnormalities found were in the brain; the brain
appeared normal but microscopic examination
revealed a “butterfly-shaped lesion” extending from
the lower medulla up the reticular formation, involved
the inferior colliculi in the midbrain, and included
severe neuronal loss in the thalamus, hypothalamus,
and hippocampus.
Norman commented that in each case the damage
had existed prenatally but appeared in all to have
resulted from a single insult. She noted that the
damage in the inferior colliculus, thalamus, and
hippocampus was similar to that described by Ranck
and Windle (1959) in monkeys asphyxiated at birth.
These three patients succumbed shortly after birth,
but Norman proposed that infants with similar
brainstem damage may survive to form part of the
population of brain-damaged children.
- Norman MG. Antenatal
neuronal loss and gliosis of
the reticular formation,
thalamus and
hypothalamus. A report of
three cases.
- Ranck JB Jr. Windle WF.
Brain damage in the
monkey, Macaca mulatta, by
asphyxia neonatorum.
- Norman MG. Antenatal neuronal loss and gliosis of the reticular formation,
thalamus and hypothalamus. A report of three cases. Neurology 1972;22:
910-6.
- Ranck JB Jr. Windle WF. Brain damage in the monkey, Macaca mulatta, by
asphyxia neonatorum. Exp Neurol 1959;1:130-154