Dawson and others have proposed a social motivation hypothesis of autism. This hypothesis suggests that some impairment evident in ASDs, such as the well-documented face-processing impairment, are not fundamental, but are secondary to the fundamental impairment in social motivation. As a result of reduced social motivation, the infant at risk for ASD spends less time paying attention to, and socially engaging with, other people. Reduced social engagement with the “world” contributes to a failure to develop expertise in processing face, language and other elements of social information exchange. Because experience drives cortical specialization, reduced attention to “others” results in a failure of specialization and less efficient function of the brain regions that mediate social cognition[54]. Indeed, hypo-activation of the fusiform gyrus and amygdala in autistic individuals during face perception tasks has been repeatedly found in well-designed functional MRI studies[55].

The social motivation hypothesis can also assimilate the results of early deprivation studies into the concept of autism, as well as those of preterm children. All of the factors which negatively interfere with the development of social expertise can be viewed, in a broader sense, as vulnerability factors. One potential lesson stemming from the oxytocin studies is that at least some autistic children may possess latent social skills[27] which can be unmasked and revealed through oxytocin administration. This leads to a cardinal question: wouldn’t this hypothesized subgroup of children be nearly identical to the group of children who experienced “optimal outcomes” in the recovery studies?

Furthermore, it seems plausible to take one further step ahead and consider a broader model of social disorders in psychiatry. Our suggestions are demonstrated in Figure 1. We propose the umbrella term “Social Inhibition Disorders.” Within this proposed concept, we hypothesize that all ASDs, as well as some other social disorders, could generally be viewed as the brain functioning in a “socially reduced mode” or “socially safe mode” (if we may express it symbolically using Microsoft Windows terminology) in response to a variety of more or less specific damaging, overloading and long-lasting conditions. The presentation of the “socially safe mode” state of Social Inhibition Disorders would depend upon age and developmental stage and would manifest in variety of social symptoms that are partially common (e.g. social inhibition and social clumsiness) and partially unique for each diagnosis grouped under the umbrella of “Social Inhibition Disorders.”

Figure 1 Social inhibition disorders. This figure presents the conditions included under this suggested umbrella term as well as the relationships between the included conditions, age and vulnerability factors. VF – vulnerability factors, PDD-NOS - Pervasive Developmental Disorder – Not Otherwise Specified, ASD - autism spectrum disorders, PD - personality disorder. Full size image

The “vulnerability window” for most ASDs, which can be derived from studies on autistic regression, seems to close during the toddler years, given that the average onset of regression is consistently described as being between 14 and 24 months of age[56]. That having been said, rare cases of herpes encephalitis have demonstrated that the “biological vulnerability window” for ASD can be “re-opened” as a repercussion of serious organic brain damage in late childhood, adolescence or even adulthood.

Milder reductions in social motivation and expertise (in terms of Dawson´s social motivation hypothesis), which may be conditioned on a lower grade of biological vulnerability factors, does not lead to true ASD, but could manifest as social phobia or schizoid, schizotypal, or obsessive-compulsive personality disorders at a later age. The connection between these disorders and non-syndromic ASDs could be the concept of continuously distributed autistic traits, which was introduced to autism research by John Constantino and coworkers.

Constantino & Todd[57] examined 788 sets of twins aged 7 to 15 years and found that autistic traits, as measured using the Social Responsiveness Scale, were common, continuously distributed and moderately to highly heritable. Levels of severity of autistic traits at or above the previously published means for patients with PDD-NOS were found in 1.4% of boys and 0.3% in girls. The hypothesis that the variation in autistic traits could be attributed to a single continuously distributed underlying factor was later confirmed in a clinical sample of patients with ASD and other psychiatric disorders[58] and in siblings of children with ASD[59]. Robinson et al.[60] studied 5968 sets of twins aged 12 years using the Childhood Autism Spectrum Test (CAST). Moderate to high heritability was found for autistic traits in the general population (53% for females and 72% for males). There were no differences in heritability between extreme groups and the general population. The data provided support for a continuous risk hypothesis and for conceptualizing ASD as the quantitative extreme of a neurodevelopmental continuum.

To our knowledge, there have yet to be any specific studies focused on autistic traits in patients with schizoid, schizotypal and obsessive-compulsive personality disorders or social phobia. In our opinion, it is an essential issue that deserves intensive research in the near future.

Indirect observations were made by Hallett et al.[61] when the authors studied approximately 6000 sets of twins ages 7 and 8 and again at age 12 using CAST (for identifying autistic-like traits) and the emotional problems subscale of the Strengths and Difficulties Questionnaire (for measurement of internalizing traits). It was found that autistic-like traits at age 7 made a modest but significant contribution to the presence of internalizing traits at age 12. There was also an association between shared environmental influences on the two traits, particularly at ages 7 and 8. It suggests that environmental factors, such as parental and home influences, may be important. The observation supports the role of psychosocial vulnerability factors, which are suggested in our model (see Figure 1).

Heterogeneity within the autism spectrum is, perhaps, the single greatest obstacle to research at all levels[62]. The overlap of ASDs with other social disorders seems to contribute to the confusion in autism research. Our model offers an unambiguous solution to overcome this handicap.