Figure xx -  Autoradiograph showing blood flow in the brain of a newborn monkey.  The
    greatest blood flow is to the inferior colliculi in the midbrain.  High blood flow is also seen in
    other subcortical structures and inner sulci of the cerebral cortex (with permission from the
    American Medical Association).
7 – Blood flow in the brain
Myers (1972) cited publications by Kety and Sokoloff
on blood flow in the brain and pointed out, "The
inferior colliculus, the structure most outstandingly
vulnerable to total asphyxia, is also the structure most
highly perfused with blood" [1, p254].  Nevertheless,
Myers did not question why this structure should have
such a high rate of blood flow.  On the contrary and on
the same page he states emphatically, "The brainstem
injury pattern produced in the monkey fetus by total
asphyxia bears no relation to the brain pathology
typifying human perinatal damage."

Figure xx is an autoradiograph from Myers' article
showing greatest localization of the radiographic tracer
in the inferior colliculi of a newborn monkey [1, p254].

Myers, unlike Ranck and Windle (1959), did not
mention the neuropathology of kernicterus, but did cite
two symposia presentations (by JB Brierley) reporting
brainstem damage in young children following cardiac
arrest, his own work with Miller on circulatory arrest in
adult monkeys, and a paper describing brainstem
injury caused by exposure to hyperbaric oxygen [4, 5].


According to Myers, it is the infant heart (not the infant
brain) that is resistant to anoxia, "Only the protected
adult heart or the tolerant infant heart is able to
support a sufficient head of blood pressure in the
postarrest period to avert the hemishperal injury
pattern which typifies cerebral malperfusion" (p255).  
Preventing damage to the cerebral cortex was of
overriding interest to Myers.  For some reason Myers,
in this valuable research study, was unable to interpret
the finding of brainstem damage as being important
enough to investigate further.
  1. Myers RE (1972) Two patterns of perinatal brain damage and their conditions of
    occurrence.  
  2. Ranck JB, Windle WF (1959). Brain damage in the monkey, Macaca mulatta, by
    asphyxia neonatorum.
  3. Brierley JB (1965) The influence of brain swelling, age and hypotension upon the
    pattern of cerebral damage in hypoxia. In F.Lüthy & A. Bischoff, eds. Proceedings
    of the Fifth International Congress of Neuropathology, Zürich, 31 August - 3
    September 1965), Excerpta Medica Foundation International Congress Series No
    100, Amsterdam.(Harvard/Countway call # ZW 1 E939 no.100 1965).
  4. Brierley JB (1967) Comment on Windle WF, Progressive degenerative changes in
    brains of monkeys surviving neonatal asphyxia. In LS James, RE  Myers, GE Gaul,
    eds. Brain damage in the fetus or newborn from hypoxia or asphyxia, report of the
    fifty-seventh Ross Conference on Pediatric Research, Columbus, p 26.
    (Harvard/Countway Serial, Report of the Ross Conferences v.30-102,1959-1992).
  5. Miller JR, Myers RE (1972) Neuropathology of systemic circulatory arrest in adult
    monkeys.
  6. Balentine JD. (1968) Pathogenesis of central nervous system lesions induced by
    exposure to hyperbaric oxygen.

In progress
                   -  Autoradiograph
showing blood flow in the brain
of a newborn monkey, showing
greatest blood flow is to the
inferior colliculi in the midbrain.
Figure xx
top
top
  1. Myers RE (1972) Two
    patterns of perinatal
    brain damage and their
    conditions of
    occurrence.  
  2. Ranck JB, Windle WF
    (1959). Brain damage in
    the monkey, Macaca
    mulatta, by asphyxia
    neonatorum.
  3. Brierley JB (1965)
  4. Brierley JB (1967)
  5. Miller JR, Myers RE
    (1972) Neuropathology of
    systemic circulatory
    arrest in adult monkeys.
  6. Balentine JD. (1968)
    Pathogenesis of central
    nervous system lesions
    induced by exposure to
    hyperbaric oxygen.

In progress