Screen Media and Autism Spectrum Disorder : A Systematic Literature Review

Autism prevalence in California, based on individuals eligible for state-funded services, rose throughout the 1990s. The extent to which this trend is explained by changes in age at diagnosis or inclusion of milder cases has not been previously evaluated. Autism cases were identified from 1990 through 2006 in databases of the California Department of Developmental Services, which coordinates services for individuals with specific developmental disorders. The main outcomes were population incident cases younger than age 10 years for each quarter, cumulative incidence by age and birth year, age-specific incidence rates stratified by birth year, and proportions of diagnoses by age across birth years. Autism incidence in children rose throughout the period. Cumulative incidence to 5 years of age per 10,000 births rose consistently from 6.2 for 1990 births to 42.5 for 2001 births. Age-specific incidence rates increased most steeply for 2- and 3-year olds. The proportion diagnosed by age 5 years increased only slightly, from 54% for 1990 births to 61% for 1996 births. Changing age at diagnosis can explain a 12% increase, and inclusion of milder cases, a 56% increase. Autism incidence in California shows no sign yet of plateauing. Younger ages at diagnosis, differential migration, changes in diagnostic criteria, and inclusion of milder cases do not fully explain the observed increases. Other artifacts have yet to be quantified, and as a result, the extent to which the continued rise represents a true increase in the occurrence of autism remains unclear.

In an fMRI experiment, participants were exposed to narratives based on true stories designed to evoke admiration and compassion in 4 distinct categories: admiration for virtue (AV), admiration for skill (AS), compassion for social/psychological pain (CSP), and compassion for physical pain (CPP). The goal was to test hypotheses about recruitment of homeostatic, somatosensory, and consciousness-related neural systems during the processing of pain-related (compassion) and non-pain-related (admiration) social emotions along 2 dimensions: emotions about other peoples' social/psychological conditions (AV, CSP) and emotions about others' physical conditions (AS, CPP). Consistent with theoretical accounts, the experience of all 4 emotions engaged brain regions involved in interoceptive representation and homeostatic regulation, including anterior insula, anterior cingulate, hypothalamus, and mesencephalon. However, the study also revealed a previously undescribed pattern within the posteromedial cortices (the ensemble of precuneus, posterior cingulate cortex, and retrosplenial region), an intriguing territory currently known for its involvement in the default mode of brain operation and in self-related/consciousness processes: emotions pertaining to social/psychological and physical situations engaged different networks aligned, respectively, with interoceptive and exteroceptive neural systems. Finally, within the anterior insula, activity correlated with AV and CSP peaked later and was more sustained than that associated with CPP. Our findings contribute insights on the functions of the posteromedial cortices and on the recruitment of the anterior insula in social emotions concerned with physical versus psychological pain.

Several studies support currently the hypothesis that autism etiology is based on a polygenic and epistatic model. However, despite advances in epidemiological, molecular and clinical genetics, the genetic risk factors remain difficult to identify, with the exception of a few chromosomal disorders and several single gene disorders associated with an increased risk for autism. Furthermore, several studies suggest a role of environmental factors in autism spectrum disorders (ASD). First, arguments for a genetic contribution to autism, based on updated family and twin studies, are examined. Second, a review of possible prenatal, perinatal, and postnatal environmental risk factors for ASD are presented. Then, the hypotheses are discussed concerning the underlying mechanisms related to a role of environmental factors in the development of ASD in association with genetic factors. In particular, epigenetics as a candidate biological mechanism for gene × environment interactions is considered and the possible role of epigenetic mechanisms reported in genetic disorders associated with ASD is discussed. Furthermore, the example of in utero exposure to valproate provides a good illustration of epigenetic mechanisms involved in ASD and innovative therapeutic strategies. Epigenetic remodeling by environmental factors opens new perspectives for a better understanding, prevention, and early therapeutic intervention of ASD.