1 – How damage to the cerebral cortex occurs
Myers (1972) discusses the effects of "prolonged
partial asphyxia," as opposed to acute total asphyxia
produced by the method of Ranck and Windle [1].  
Myers also repeated the experiments on acute total
asphyxia, with careful physiological measurements.

The method of Ranck and Windle (in which newborn
monkeys were subjected to sudden and total
interruption of respiration) did not produce the animal
model of cerebral palsy that had been anticipated [2].  
Cerebral palsy results from damage of the motor
cortex, and Myers set out to determine how cortical
damage occurs.

Miller and Myers (1972) found the brainstem pattern
of damage also in adult monkeys when circulation to
the brain was blocked [3].  The finding of brainstem
damage in adult monkeys also had not been
anticipated.  Brainstem damage in infant monkeys
had been thought to be possibly a sign of lesser
vulnerability of the infant brain to oxygen
insufficiency.  In the adult monkeys, a pattern of injury
involving the cerebral cortex resulted only when
severe hypotension occurred as a complicating factor
during recovery from the experimental procedure.

Clinical reports of damage caused by circulatory
arrest had almost always emphasized involvement of
the cortex.  Perhaps circulatory insufficiency is part of  
recovery from cardiac arrest, because cardiac
damage is permanent in adults.

Neubuerger (1954) described brainstem damage in a
patient who survived for two weeks following
resuscitation from cardiac arrest during surgery [4].  
Gilles (1963) noted the similarity of brainstem damage
in a child resuscitated after drowning to that found by
Ranck and Windle in asphyxiated monkeys and, in
1969, the same pattern in a child who died following
resuscitation from suffocation [5, 6].  Total asphyxia
or cardiac arrest is more often fatal than not and only
when the person survives for a week or more
following resuscitation does the damage become
detectable.

Landau et al. (1955) published the results of using
radioactive tracers to determine differences in blood
flow in different structures of the brain [7].  This data
is still not sufficiently appreciated.  That the brain is a
collection of different sensory, motor, and association
circuits with differing metabolic activities is not
commonly recognized (but should be, before drugs
are described in daily newspapers as "selective
serotonin re-uptake inhibitors" etc).
  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. Miller JR, Myers RE
    (1972) Neuropathology of
    systemic circulatory arrest
    in adult monkeys.
  4. Neubuerger KT (1954)
    Lesions of the human
    brain following circulatory
    arrest.
  5. Gilles FH (1963) Selective
    symmetrical neuronal
    necrosis of certain brain
    stem tegmental nuclei in
    temporary cardiac
    standstill
  6. Gilles FH (1969)
    Hypotensive brain stem
    necrosis: selective
    symmetrical necrosis of
    tegmental neuronal
    aggregates following
    cardiac arrest.
  7. Landau WM et al (1955)
    The local circulation of
    the living brain; values in
    the unanesthetized and
    anesthetized cat.