2 – Diminished growth of structures within the
cerebral cortex
Faro and Windle (1969) noted that the frontal and
parietal cortex, "recognized as locations normally
receiving the terminations of tracts destroyed by the
primary lesions" exhibited neuronal loss over time.  
Neuronal loss was a descriptive term indicating
reduced neuronal density in the frontal and parietal
target areas for neural transmission from the
thalamus.  In other words, full maturation of these
cortical areas was curtailed in the monkeys
asphyxiated at birth.

Reduction of white matter (myelinated tracts) in the
corpus callosum was also a primary finding.  Reduced
size of the corpus callosum has been reported in
several investigations of brains from individuals with
autism (Egaas et al. 1995, Piven et al. 1997).  The
corpus callosum is the major connection between the
left and right sides of the cerebral cortex.

Enlargement of the ventricles was another indication
that diminished growth of the cortex had also been a
long-term consequence of asphyxia at birth.  Growth
and maturation begin with the embryonic neural tube
to differentiation of brainstem structures; development
and myelination of the cerebral cortex continue for
years and decades after birth.  Full development of
the cortex is dependent upon integrity of brainstem
pathways that terminate and provide input to specific
functional areas of the cortex.

It is of interest that Faro and Windle reported, "Parts
of the cerebral cortex escaped primary damage and
showed little or no secondary changes.  The occipital
lobes of the cerebrum contained no lesions, and we
could detect no atrophy; the geniculocalcarine tracts
appeared to be intact."  The geniculocalcarine tracts
are the thalamic radiations for visual input.  Thus the
visual system appears to have been spared, in
contrast to the auditory system and sensory systems
required for full development of the parietal and
frontal cortex.

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