Working hypotheses and rationale for research
The case for investigating perinatal impairment of the inferior colliculi is based on
the following considerations:
(1) Trophic transmitters guide postnatal growth of later maturing areas of the brain
Neurotransmitters produced during early development in brainstem auditory nuclei appear
to promote growth of their later maturing targets in the cerebral cortex [37, 38]. Thus
perinatal loss of neurons in the inferior colliculi might disrupt normal maturation of
language and association tracts of the cerebral cortex. Damage in monkeys subjected to
asphyxia at birth was initially only seen in the inferior colliculi and other brainstem nuclei;
but examination of the brain several months or years later revealed that brain growth had
not progressed normally [39]. Neurons were sparser in structures like the oculomotor
nuclei, reticular formation, mammillary bodies, hippocampus, amygdala, corpus callosum,
cerebellum (Purkinje cells) and cerebral cortex (parietal and frontal) than in normal
monkeys. Many of these structures are thought to be affected in autism.
Myelin formation in the inferior colliculi and other nuclei of the brainstem auditory pathway
occurs earlier in the human fetus than in any other system of the brain. Figure 9 shows
myelination of the auditory pathway at 25 weeks gestation, and figure 10 at 29
gestational weeks, at which time responses to sound are first elicited [40-42]. Myelination
of the language areas of the cerebral cortex on the other hand continues for four to five
years after birth, as can be seen in figure 11 and figure 12 [40, 41]. Thus children
normally learn to speak "by ear" before the cortical language areas are fully developed.