The experimental work is promising from the standpoint of the similarities between the behavioral syndrome seen in infant monkeys with neonatal damage to the amygdalohippocampal complex and autistic children. They have in common the symptoms of abnormalities in social interactions, changes in facial and body expressions as well as the development of Stereotypic behaviors. There is an early onset of symptoms in both cases, though in early infancy the complete syndrome is not apparent. Both disorders (at least for low-functioning autistic subjects) are characterized by memory deficits despite normal abilities in certain kinds of learning tasks. Thus, the time course as well as the nature of the socioemotional disturbances and the cognitive impairment observed in monkeys with early damage to the medial temporal lobe structures strongly suggest that autism too may result from early dysfunction of the medial temporal lobe structures. Indeed, an attractive feature of this animal analog of autism is that it can account for a range of apparently unrelated symptoms, that is, social and motivational deficits and motor stereotypies and self-directed behaviors. It is also of interest that, like autistic children, monkeys with early amygdalohippocampal damage exhibited considerable variability of specific symptoms, suggesting that autism too may result from a common locus of pathology that produces multiple phenotypic displays, rather than resulting from multiple pathologies that each yield a particular subset of autistic symptoms. Finally, the extent of damage to the medial temporal lobe could explain some of the heterogeneity of behavioral disturbances in autism. Indeed, the severe learning and memory deficits shown in more developmentally delayed autistic subjects could result from bilateral involvement of amygdala, hippocampal, and adjacent cortex, but, perhaps, in the case of higher functioning subjects with relative preserved cognitive abilities, the amygdala could be affected but the hippocampal and adjacent cortical areas relatively spared, resulting in social impairment but more intact learning capacity. The validity of this animal model may become more apparent as future research defines more specifically the role of each of the medial temporal lobe structures in the development of social skills, emotion, and memory. Together with the neuropathological changes found in the medial temporal lobe region, experimental data are providing incentive to further investigate this fascinating, complex, and devastating disorder of the immature brain.