2 -  Mammillary bodies, hippocampus, inferior
olives and cerebellum
The mammillary bodies are part of the hypothalamus,
which the textbooks tell us controls visceral and
drive-related activities [1, 2].  Neurons in the
hippocampal formation of the temporal lobes synapse
with those in the mammillary bodies.  The mammillary
bodies in turn provide neural input to the anterior
thalamus, which relays signals from brainstem sensory
pathways to the cortical area around the corpus
callosum connecting the left and right cerebral
hemispheres.  This grand neural circuit is thought to
mediate emotion as well as to consolidate recent
memory into cortical areas accessed by association
tracts for retrieval months and years in the future.  
How?  This is yet to be fully understood, and is part of
the work-in-progress in neuroscience.  Some of the
answers could well come from research by computer
scientists working on systems for artificial intelligence.

The inferior olives in the brainstem receive afferent
(incoming) signals from diverse subcortical sites and
the spinal cord.  Its efferent (outgoing) neurons are all
to the cerebellum.  So-called "climbing fibers" from the
inferior olivary complex stimulate the Purkinje cells of
the cerebellum.  Purkinje cell loss is one of the most
consistent neuropathological findings in the few brains
available from individuals who were autistic, which
suggests compromise of the inferior olive to cerebellar
circuit as part of the autistic syndrome.

Kemper and Bauman (1998) pointed out that the
climbing fibers appear around the 30th week of
gestation; thus they suggested that some adverse
event that occurs at this stage of prenatal
development could account for anomalies of the
inferior olives and cerebellum observed postmortem
[3}.  It should be noted however that cerebellar
pathology is in no way unique to autism.  Purkinje cell
loss and anomalies of the cerebellum have been
reported in other conditions such as chronic alcohol
intoxication [4, 5], and as a long-term outcome of
asphyxia at birth [6].  Both prenatal exposure to
alcohol and complications at birth are known to be
associated with autism.

Impairment of a particular brain system does not have
to occur at the time of its development.  Sadly, the
brain is vulnerable to damage at any point from
prenatal life to old age.  Protective mechanisms often
act to preserve function in the brainstem nuclei of high
metabolic rate, at the expense of other important
cortical areas of the brain, but the need to sustain
high metabolic rate also makes these nuclei especially
susceptible to impairment in catastrophic situations.

High metabolic rate in brainstem nuclei may be
required for activities similar to those of signal
switching chips within computer systems, to permit
multiplexing of sensory pathways for transmitting
simultaneous impulses.  Ability to see, hear, feel, and
move at the same time must depend upon some such
parallel processing mechanism.  Awareness of sounds
coming from several different directions, events in the
peripheral as well as the central field of vision, and
ability to focus attention on a particular subset of
incoming stimuli rely upon moment to moment control
of neural circuits that process simultaneous signals.

Full References

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References

1. Nolte J and Angevine JB
   (1995) The Human Brain, in
   Photographs and
   Diagrams..
   
2. Truex RC and Carpenter MB
   (1969) Human
   Neuroanatomy, Sixth Edition.
   
3. Kemper TL, Bauman M
   (1998). Neuropathology of
   infantile autism..
   
4. Butterworth RF (1993)
   Pathophysiology of
   cerebellar dysfunction in the
   Wernicke-Korsakoff
   syndrome.
   
5. Cavanagh JB et al. (1997)
   Selective damage to the
   cerebellar vermis in chronic
   alcoholism: a contribution
   from neurotoxicology to an
   old problem of selective
   vulnerability.
   
6. Faro MD & Windle WF
   (1969) Transneuronal
   degeneration in brains of
   monkeys asphyxiated at
   birth.
   

1. Nolte J and Angevine JB (1995) The Human Brain, in Photographs and Diagrams.  
   Mosby, St. Louis.
   
2. Truex RC and Carpenter MB (1969) Human Neuroanatomy, Sixth Edition. Williams &
   Wilkins, Baltimore.
   
3. Kemper TL, Bauman M (1998). Neuropathology of infantile autism. Journal of
   Neuropathology and Experimental Neurology 57:645-652 .
   
4. Butterworth RF (1993) Pathophysiology of cerebellar dysfunction in the Wernicke-
   Korsakoff syndrome. Canadian Journal of Neurological Sciences 20 Suppl 3:S123-
   S126.
   
5. Cavanagh JB, Holton JL, Nolan CC (1997) Selective damage to the cerebellar vermis in
   chronic alcoholism: a contribution from neurotoxicology to an old problem of selective
   vulnerability. Neuropathology and Applied Neurobiology 23:355-363.
   
6. Faro MD & Windle WF (1969) Transneuronal degeneration in brains of monkeys
   asphyxiated at birth.  Experimental Neurology 24:38-53.