Authors
Minshew NJ, Payton JB.
Institution
Department of Psychiatry, Western Psychiatric Institute and Clinic,
University of Pittsburgh, Pennsylvania.
Title
New perspectives in autism, Part II: The differential diagnosis and
neurobiology of autism.
Source
Curr Probl Pediatr 1988 Nov;18(11):613-94
Abstract
The clinical spectrum of autism spans a broad range of functions, but
the core symptoms remain the same regardless of the intelligence of the
child: the autistic type of social deficit that ranges from a lack of inclination
to relate to extreme difficulty with the mechanics of social interactions,
a global communication deficit that involves both verbal and nonverbal modes,
and a severe cognitive deficit involving concept formation (abstraction)
that is combined with an exceptional memory for factual information. These
symptoms may vary dramatically in severity, but the basic deficits are identifiable
regardless of IQ. Under-recognition of autism is a major problem at all
IQs, but especially in patients with IQs above 50. No drugs have been found
to significantly improve the core deficits in autism. Antipsychotics should
be avoided except for short-term use. Antidepressants, anxiolytics, and
anticonvulsants are important in the treatment of depression, affective
modulation, situation-related stress, and seizures. Intensive social skills
training is assuming a prominent role in behavior modification programs,
and success with higher-functioning autistic children suggests that outcome
can be improved by intensive training. The neurobiology of autism has also
undergone dramatic changes. The psychogenic theories of etiology have been
completely invalidated. Autism is now considered to be a neurological disorder
resulting from an error in brain development. The precise location and nature
of this deficit are still being actively debated and investigated. One theory
emphasizes a dysfunction of the limbic system that results in an impairment
in the acquisition of information. A second theory proposes a primary role
for dysfunction of the cortical association network responsible for the
processing of information.