Front Matter

(Rick Simeone) #1

40 Introduction to Autism Spectrum Disorders


Diagnostic and Statistical Manual of Mental Disorders (DSM‐5) [111] has
dropped the category of Asperger syndrome; its characteristics are now
included in the more encompassing category of ASD. Children with Asperger
syndrome may show varying combinations of symptoms, with different degrees
of severity, but these children are now included under the ASD definitional
umbrella.
While the precise causes of the ASD “spectrum” remain enigmatic, charac­
teristics in typical fetal brain development vary significantly from those seen in
children with ASD, including Asperger’s. Here we elaborate on why there is a
“spectrum” in autism and what potential causes have been suggested by health
care providers and researchers.
The pre‐DSM‐5 category of Asperger syndrome shared some basic charac­
teristics of autism, including restricted personal interests, inadequate recog­
nition of emotions in other people, and general social awkwardness. Children
with Asperger’s, however, display no significant intellectual disability or
meaningful delay in speech development, although they may at times speak in
unusual ways and act socially clumsy. Children with Asperger’s may be
extremely brilliant and turn out to be modern Einsteins, Jeffersons, and
Mozarts, individuals capable of inspiring paradigm shifts in science, politics,
and the arts. The use of male examples is particularly appropriate since
Asperger’s is ten times more common in males than females.
The development of the human fetal brain occurs via a remarkably complex
interplay of precisely orchestrated fetal brain progenitor cell differentiation
influenced by environmental factors. Every developmental stage is comparable
with a tiny acorn that grows into an imposing oak tree. Each branch begins
with a germinal center as its node, and this center is guided by specialized
progenitor cells. Each mother cell, in turn, bears its own gifts and faces its own
vulnerabilities. Most ASD children who also have psychiatric disorders experi­
ence the onset of ASD symptoms prior to 3 years old. These neurodevelop­
mental syndromes in classical autism and ASD have likely arisen due to the
specific neuronal degenerations that occurred when they were exposed to
harmful chemicals that depleted certain specialized types of progenitor cells.
If  this harmful chemical exposure occurred between gestation weeks 8–15,
then depletion or significant reduction of the olfactory cells or oxytocin‐ or
arginine vasopressin‐receptor bearing progenitor cells may, after three years,
produce a tree of neuronal connections that is lopsided in shape and inade­
quate in function. This lopsided tree can be compared with a real tree that was
pruned on a specific side or area and in the spring the pruned area grew faster
and larger. The evidence of such lopsided growth is visible early on by using
magnetic resonance imaging, as reported by Eric Courchesne and his cowork­
ers at the University of California, San Diego Autism Center of Excellence.
These scientists compared ASD and normotypic infants from birth through
age 5 and concluded that two phases of abnormal brain development precede
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