Autism, Viewpoint on the Brain Disorder

2 - Wernicke's (alcoholic) encephalopathy
Reports of autistic behaviors among children exposed
during gestation to alcohol and other drugs began to
appear in the 1990s [1-3]. The finding of autism
among children with fetal alcohol syndrome should be
considered alongside the finding of autism in children
exposed to rubella infection during pregnancy [45.
Most important, the question should be raised as to
what areas of the brain are affected both by infections
and alcohol or other toxic substances, especially
during gestation, and how this might lead to autism in
some cases. Autism has also been found in children
of mothers taking valproic acid (Depakote) during
pregnancy [4, 6]. Autism has also been reported in
some victims of severe deformities caused by
maternal use of thalidomide during pregnancy [7].

It has been known for over a century how the brain is
affected by alcohol [8]. Wernicke (1881) first reported
the characteristic pattern of bilaterally symmetric
hemorragic lesions within the brainstem caused by
chronic alcohol intoxication. This pattern of selective
brainstem damage now bears the name Wernicke's
encephalopathy and its association with alcoholism
has been confirmed many times over. This pattern of
damage can be compared to the ischemic lesions
caused by brief total asphyxia at birth [9]. The inferior
colliculi are affected in most cases whether by
alcoholism or asphyxia, but the most predictable
lesions caused by alcohol abuse are in the mammillary
bodies [10, 11].
.
Figure 11 is from a paper by Kant (1933) and shows
petechial (pinpoint-size hemorrhagic spots) in the
inferior colliculi and surrounding areas of the midbrain,
which are characteristic of the damage in Wernicke's
encephalopathy [12]. The early papers, written in
German, describe the damage as small "flea-bite" size
hemorrhages that result from engorgement then
bursting of capillary vessels, similar to the "whiskey
nose" of many alcoholics.

The mammillary bodies are among the brainstem
nuclei of high metabolic rate, slightly less active than
the inferior colliculi (see tables 3 and 5, which are
discussed further in chapter xx). Protective
biofeedback mechanisms that spare the inferior
colliculi may make the mammillary bodies more
vulnerable to damage, just as motor areas become
more susceptible to damage in hypoxic situations.
The mammillary bodies are part of the limbic system,
in which Kemper and Bauman (1998) found signs of
disrupted prenatal development in brains from some
autistic individuals [13].

Figure 10a shows myelin stain in a midline (or sagittal)
section of the brainstem of a human fetus at 25
gestational weeks (gw) from Yakovlev and Lecours
(1967); this can be compared with the transverse
section in figure 10b [14]. Figure 10a shows the
greater degree of myelination in the superior olive
(SOl) and trapezoid body (TzB) of the auditory
pathway compared for example with the lesser degree
of myelination in the superior colliculus (SCol) of the
visual system.

Figure 12 is a diagram of a sagittal view showing the
location of brainstem structures of high metabolic rate
that are vulnerable to damage from alcohol
intoxication and other factors that impair aerobic
metabolism. Structures shown in figure 9 can be
compared to degrees of prenatal myelination of those
in figure 6a. Greater detail and orientation can be
found by studying diagrams (transverse, sagittal, and
coronal) given in textbooks of neuroanatomy, like that
of Nolte and Angevine [15].

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GH (1989) The Wernicke-
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