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Curr Probl Pediatr. 1988 Nov;18(11):613-94.

New perspectives in autism, Part II: The differential diagnosis and neurobiology of autism.

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  • 1Department of Psychiatry, Western Psychiatric Institute and Clinic, University of Pittsburgh, Pennsylvania.

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.

PMID:
3063439
[PubMed - indexed for MEDLINE]
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