1 -  Natsume et al. (1995) and Roland et al. (1988)
Natsume et al (1995) investigated neurological signs
and neuropathology in a female infant born at 37
weeks gestation by emergency cesarean section.  
Absence of fetal movements for one day during the
week preceding birth had been reported by the
mother [1].  Spontaneous respirations occurred at
birth, but were weak.  Movements of body, facial
muscles, and eyes were absent.  She was flaccid at
birth and reflex responses were absent.  She lapsed
into respiratory failure, was placed on a respirator,
and fed by tube because oral intake was not
possible.  Throughout her short life of five months her
eyes were “fixed.”

Her electroencephalogram (EEG) was normal but
brainstem auditory evoked potentials (BAEP) were
not; no responses were obtained for sounds less than
85 dB and only two waves with prolonged latency
were evoked with stimuli above 110 dB.

Neuroimaging before death revealed dilation of
cerebral ventricles, abnormalities of the thalamus and
putamen, and atrophy of dorsal brainstem and corpus
callosum.  No abnormalities of the cerebral cortex
were found on examination of the brain after death.  
But neuronal loss was marked in the superior and
inferior colliculi, facial motor nuclei, vestibular nuclei,
and inferior olivary nuclei of the brainstem.  Natsume
et al. noted the similarity of the neuropathology found
to the brainstem damage caused by asphyxia at birth
in monkeys reported by Myers (1972), and several
earlier descriptions of human cases [2-8].

Natsume et al’s paper appears to be the most recent
referring to the investigations of experimental
asphyxia carried out by Myers and Windle [2, 9].  The
findings presented in earlier papers are summarized
below.  With the exception of the account by Roland
et al., neuroimaging was not yet available.

Roland et al. (1988) described a case (gender not
specified) with similarities to that of Natsume et al. [8].
The infant was full-term, weighing 4300 grams (9.5
pounds), suffered severe slowing of the heart rate
during the last 15 minutes before delivery, and was
pale and flaccid at birth.  Resuscitation was required
and seizures occurred during the first hour of life.  
The child remained comatose with minimal
spontaneous movements and minimal withdrawal of
limbs to painful stimuli.  There was marked facial
diplegia and limited eye movements.  A CT scan
made at five days of age appeared normal; at one
month of age there was no evidence of cortical
atrophy, but enlargement of the third ventricle and
abnormalities of tissue adjacent to the third ventricle
were evident.  The infant died at four months of age
from pneumonia.

Post mortem examination of the brain revealed
symmetrical pallor and scarring of brainstem
structures with a minor degree of neuronal loss in
parietal and hippocampal areas of the cerebral
cortex.  Roland et al. noted the similarity of this
pattern of brain damage to that observed by Myers
and Ranck & Windle (1959) [2, 10].
References
  1. Natsume J, Watanabe K, Kuno K, Hayakawa F, Hashizume Y (1995) Clinical,
    neurophysiologic, and neuropathological features of an infant with brain
    damage of total asphyxia type (Myers).  Pediatric Neurology 13:61-64.
  2. Myers RE. Two patterns of brain damage and their conditions of occurrence.
    Am J Obstet Gynecol 1972; 112:246-76.
  3. Norman MG. Antenatal neuronal loss and gliosis of the reticular formation,
    thalamus and hypothalamus. A report of three cases. Neurology 1972;22:
    910-6.
  4. Schneider H, Baliowitz L, Schachinger H, Hanefeld F, Droszus J.-U. Anoxic
    encephalopathy with predominant involvement of basal ganglia, brain stem
    and spinal cord in the perinatal period. Acta Neuropathol 1975;32:287-98.
  5. Wilson ER, Mirra SS, Schwartz JF. Congenital diencephalic and brain stem
    damage: Neuropathologic study of three cases. Acta Neuropathol (Berl)
    1982;57:70-4.
  6. Smith JF, Rodeck C. Multiple cystic and focal encephalomalacia in infancy
    and childhood with brain stem damage. J Neurol Sci 1975; 25:377-88.
  7. Leech RW, Alvord EC Jr. Anoxic-ischemic encephalopathy in the human
    neonatal period. The significance of brain stem involvement. Arch Neurol
    1977;34:109-13.
  8. Roland EH, Hill A, Norman MG, Flodmark O, MacNab AJ. Selective brain stem
    injury in an asphyxiated newborn. Ann Neurol 1988;23:89-92.
  9. Windle WF (1969) Brain damage by asphyxia at birth.  Scientific American
    221(#4):76-84.
  10. Ranck JB Jr. Windle WF. Brain damage in the monkey, Macaca mulatta, by
    asphyxia neonatorum. Exp Neurol 1959;1:130-154
Full References
top
  1. Natsume J et al. (1995)
    Clinical, neurophysiologic,
    and neuropathological
    features of an infant with
    brain damage of total
    asphyxia type (Myers).  
  2. Myers RE (1972) Two
    patterns of brain damage
    and their conditions of
    occurrence.
  3. Norman MG (1972)
    Antenatal neuronal loss and
    gliosis of the reticular
    formation, thalamus and
    hypothalamus. A report of
    three cases.
  4. Schneider H et al. (1975).
    Anoxic encephalopathy with
    predominant involvement of
    basal ganglia, brain stem
    and spinal cord in the
    perinatal period.
  5. Wilson ER et al. (1982)
    Congenital diencephalic and
    brain stem damage:
    Neuropathologic study of
    three cases
  6. Smith JF, Rodeck C (1975)
    Multiple cystic and focal
    encephalomalacia in infancy
    and childhood with brain
    stem damage.
  7. Leech RW, Alvord EC Jr.
    (1977) Anoxic-ischemic
    encephalopathy in the
    human neonatal period. The
    significance of brain stem
    involvement.
  8. Roland EH et al (1988).
    Selective brain stem injury in
    an asphyxiated newborn.
  9. Windle WF (1969) Brain
    damage by asphyxia at birth.
  10. Ranck JB Jr. Windle WF
    (1959). Brain damage in the
    monkey, Macaca mulatta, by
    asphyxia neonatorum.