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Evidence from computerized tomography (CT) suggests that schizophrenic patients may have smaller brains than normal subjects. Magnetic resonance imaging (MRI), which produces more clearly defined images than CT, was used to measure T1 and brain size of 24 schizophrenic and 24 normal subjects matched for age and sex but not for education. Two transverse images were obtained: slice 1 at the foramina of Monro and slice 2 at the widest part of the lateral ventricles. Adequate T1 instrumental reliability could not be demonstrated. Schizophrenic subjects had smaller right hemispheres (slice 1) and smaller frontal areas (slice 2) than normal subjects. However, when education was taken into account, only the left frontal area (slice 2) was smaller in schizophrenic than in normal subjects. Larger brain areas were associated with better cognitive test scores and fewer neurological signs. Cranial and body size were similar in both diagnostic groups.

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Decreases in brain serotonin levels have been implicated in the pathogenesis of human depression. While circulating levels of tryptophan (TRP) might possibly reflect concentration of brain serotonin, a more relevant peripheral measure may be the ratio of plasma TRP to five other neutral amino acids (TRP/5aa ratio). In depressed subjects and normal controls, plasma TRP (free and total), phenylalanine (PHE), tyrosine (TYR), leucine, isoleucine, and valine were measured on three days. When depression was most severe, depressed patients had lower TRP/5aa ratios and total TRP levels and higher PHE and TYR levels. After the patients' conditions improved, these differences disappeared. As Hamilton depression scores improved, the plasma TRP/5aa ratios increased significantly. This finding tends to support the idea that changes in brain serotonin level reflect changes in depression severity.

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Progress in the study of infantile autism over the past 10 years was reviewed in terms of classification and diagnosis, relation to other disorders, demographics, parental characteristics, genetics, intelligence, language, perceptual processes, behavioral characteristics, neurobiological, biochemical and pharmacological aspects, behavioral/educational treatment methodologies, prognosis, and theoretical considerations. This decade's research led to the now generally accepted position that infantile autism is a type of developmental disorder accompanied by severe and, to a large extent, permanent intellectual/behavioral deficits. However, its relationship to other forms of developmental disorders and to mental retardation remains to be delineated. Perceptual/cognitive/language defects appear central to the autistic syndrome, but the specific underlying mechanisms are unknown. Most studies indicate that autistic children have more signs of brain dysfunction than do normal children and about the same number as mentally retarded children. The overwhelming evidence suggests that te treatment of choice for maximal benefit to autistic children is a systematic, intrusive behavioral/educational approach. Yet, in spite of significant gains in almost all children treated, the typical prognostic picture is poor in terms of achieving self-supportive adulthood. The parents of autistic children have been found to be essentially similar to parents of children with organic brain disorders, and manifest no psychopathology which conceivably could induce the disorder. The vast majority of theoretical articles appearing in the 1970s proposed some from of neurobiological defect as the causative factor in autism. One of the major goals for future research is to undertake more extensive comparative studies on nonautistic brain dysfunctional children and autistic children that could yield cleared differential behavioral profiles and testable neurobiological hypotheses.

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Three major causation theories of infantile autism were tested during 12 years of research: (i) "nurture," (ii) "nature," and (iii) "nature-nurture" interaction. Data from major studies are presented showing strong support for the nature causation theory. Aut parents, in comparison to two control groups (normal and nonpsychotic abnormal), were appropriately stimulating and warmly relating to their Aut infants. Aut parents had no greater amounts of psychopathology than control parents. Aut children had: (i) more signs of neurobiological pathology than normal children; (ii) a high preponderance (94%) of IQ's in mentally retarded ranges; (iii) central language disorders which precluded development of normal verbal abstraction ability and creative speech; (iv) visual-motor disorders akin to a dyspraxis interfering with normal acquisition of "body language". With a greatly reduced capacity for acquiring both verbal and nonverbal communication skills, the ability of Aut Children to use other humans as helpful interpreters of the environment was also seriously curtailed. Not finding other humans useful in such interpretation, the phenomenon of social withdrawal was the logical end product in Aut Child.

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In previous studies the author and her associates found that the IQs of autistic children can be measured and are also predictive of the child's future functioning. Contrary to earlier opinion, autistic children were found to have subnormal intelligence and more signs of neurological dysfunction than subnormal controls. In this study test data were reviewed to see what subtests differentiated a group of 66 autistic children from a group of 29 children with subnormal intelligence. Results indicated that "high autistic" children were similar to subnormal children on verbal subtests. However, subnormal children were superior to autistic children in some performance areas as in ball play. Findings are interpreted to suggest that autistic children with severe visual/motor disabilities as indicated by low ball play scores may be propelled into emotional withdrawal, even though they are only moderately retarded on verbal subtests.

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