3 – Diminished growth of the amygdala,
oculomotor nuclei, and cerebellum
In addition to diminished growth of the cerebral cortex,
other subcortical nuclei and the cerebellum also
displayed diminished development.  The amygdala
was a frequent site of secondary involvement, as were
the vestibular nuclei, and the inferior olivary complex
and associated nuclei of the cerebellum; all of these
sites in the brain have been of interest to autism
researchers.

The oculomotor nuclei (for control of eye movements),
mammillary bodies, and hippocampus were variably
involved.  Cell loss in the periaqueductal gray
(between the third and fourth ventricles of the
brainstem) was also prominent.  These areas and
structures are often most prominently affected in
Wernicke's encephalopathy associated with alcoholic
intoxication.  The pattern of "transneuronal
degeneration" observed by Faro and Windle can be
considered to be a variant of Wernicke's
encephalopathy.

Wernicke encephalopathy lesions associated with
alcohol intoxication are most often hemorrhagic.  The
lesions of asphyxia at birth are just the opposite; they
are the result of ischemia, or diminished blood flow.  
Alcohol intoxication leads to increased blood flow as
shown by the deoxyglucose studies of Grünwald et al
(1995); increased blood flow may be the response to
toxic poisoning of aerobic enzymes – a mechanism for
increasing oxygen delivery.  Ischemia is a curtailment
or blockage of blood flow, a non-toxic impairment of
aerobic metabolism.  Lesions of brainstem nuclei of
high metabolic rate can thus be hemorrhagic (if
caused by toxic substances), or non-hemorrhagic (if
caused by ischemia).

So much has been written about the lack of "eye
contact" displayed by children with autism.  
Impairment of the oculomotor nuclei may be involved
as discussed by Rosenhall et al (1988), Miller et al
(1998), and Miller and Stromland (1999).

Faro and Windle reported considerable variability
both in locations affected and extent of damage.  This
is true too of the neuropathology reported in cases of
autism.  The primary lesions were constant and with
time extended up and down the auditory pathway.  
Damage to structures within the basal ganglia were
nearly always found, and in the putamen and globus
pallidus thought to be part of the primary pattern of
damage; involvement of the caudate was more
variable.  Faro and Windle suggested that postnatal
hypoxic episodes during respiratory distress may
have added to the damage caused by the
experimentally induced and timed period of asphyxia
at birth.

1. Faro MD & Windle WF
   (1969) Transneuronal
   degeneration in brains of
   monkeys asphyxiated at
   birth.
   
2. Egaas B et al (1995)
   Reduced size of corpus
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3. Piven J et al (1997) An
   MRI study of the corpus
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4. Grünwald F et al (1993)
   Changes in local cerebral
   glucose utilization in the
   awake rat during acute
   and chronic administration
   of ethanol.
   
5. Rosenhall U et al (1988)
   Oculomotor findings in
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6. Miller MT et al (1998) The
   puzzle of autism: an
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7. Miller MT, Stromland K.
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