3 -  Pathology responsible for autistic traits
The impairment of consciousness, general awareness,
and attention deficits of children with autism are not
the same as the somnolence described in Wernicke’s
encephalopathy.  However, DesLauriers and Carlson
(1969) put forth such an idea in a book titled Your
Child is Asleep [1].  Neurological deficits are not as
conspicuous in autism as they are in Wernicke’s
encephalopathy caused by alcohol intoxication, but
signs of impairment to a lesser degree are evident.

Lack of facial expression and poor eye contact noted
in autistic children could represent impairment of eye
movements though less serious than those observed
in Wernicke’s disease.  Rosenhall et al. (1988) found
decreased eye motor precision and difficulty following
a moving target in a group of autistic children high-
functioning enough to cooperate in the experiments
[2].  Auditory brainstem response (ABR) was
measured as an indicator of brainstem dysfunction.  
Two of the eleven children had measurable hearing
loss and five had abnormal ABR-recordings, which
correlated with impaired oculomotor function.  Miller et
al. (1998) also described varying degrees of
oculomotor dysfunction in children with autism.

The neuropathology described by Bailey et al. (1998),
Kemper and Bauman (1998), and Williams et al.
(1980) in brains from people with autism represent
changes that took place during early development,
and most were retarded which would imply
longstanding difficulty in incorporating experience into
long-term memory.  High functioning children with
autism on the other hand often display excellent
capacity to commit new information to memory.  
Impairment of the mammillary bodies would therefore
be less likely involved in children with preserved
memory function.

The social, shared-attention, and especially the
language disabilities of high-functioning autistic
children would be better explained by deficits in
function of metabolically active auditory nuclei like the
inferior colliculi, medial geniculate nuclei, superior
olives, and nuclei of the lateral lemniscal system.

Kemper and Bauman (1998) pointed out that it is
important to know not only what area of the brain is
damaged but also how this happens.  They proposed
disruption of cell migration during development in the
brains of the autistic subjects they examined.  The
event initiating abnormal cell migration should also be
sought.  Kemper and Bauman reasoned that an event
around the 30th week of gestation would prevent
climbing fibers from the inferior olives to populate the
Purkinje layer of the cerebellum.  This event may well
have begun with an increase in blood flow to the
inferior olives, hyperemia, and small hemorrhages in
response to whatever the damaging factor might have
been.  Abnormal migration of neurons is the long-term
residual finding.

Brain damage in autism is not the same as that in
Wernicke’s encephalopathy; brain damage in autism is
not clear-cut and not usually visible, but visible
abnormalities in some of the same sites were reported
by Kemper and Bauman (1998) and others, and
should be investigated as possibly contributory to the
behavioral features of autism.  The effect of a
damaging factor during early development is different
from that in a mature brain.  But the brainstem nuclei
of high metabolic rate appear to be most vulnerable
even during fetal life and to have been affected in
many individuals with life-long autistic disorders.

1. DesLauriers AM & Carlson CF
   (1969) Your Child is asleep;
   early infantile autism; etiology,
   treatment, parental influences.
   
2. Rosenhall U et al. (1988)
   Oculomotor findings in
   autistic children.
   
3. Miller MT et al. (1998) The
   puzzle of autism: an
   ophthalmologic contribution.
   
4. Bailey A et al. (1998) A
   clinicopathological study of
   autism.
   
5. Kemper TL, Bauman M
   (1998). Neuropathology of
   infantile autism.
   
6. Williams RS et al. (1980)
   Autism and mental
   retardation: Neuropathologic
   studies performed in four
   retarded persons with autistic
   behavior.
   

References

Full References

1. DesLauriers AM & Carlson CF (1969) Your Child is asleep; early infantile autism; etiology,
   treatment, parental influences. Homewood IL, Dorsey Press.
   
2. Rosenhall U, Johansson E, Gillberg C (1988) Oculomotor findings in autistic children.  
   Journal of Laryngology and Otology 102:435-9.
   
3. Miller MT, Stromland K, Gillberg C, Johansson M, Nilsson EW (1998) The puzzle of autism: an
   ophthalmologic contribution. Transactions of the American Ophthalmological Society 96:369-
   387.
   
4. Bailey A, Luthert P, Dean A, Harding B, Janota I, Montgomery M, Rutter M, Lantos P (1998) A
   clinicopathological study of autism.  Brain 121:889-905.
   
5. Kemper TL, Bauman M (1998). Neuropathology of infantile autism. Journal of Neuropathology
   fcand Experimental Neurology 57:645-652 .
   
6. Williams RS, Hauser S, Purpura DP, deLong GR, Swisher CN (1980) Autism and mental
   retardation: Neuropathologic studies performed in four retarded persons with autistic
   behavior.  Archives of Neurology 37:748-753..
   

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