1. Christ SE, Kester LE, Bodner KE, Miles JH. {{Evidence for selective inhibitory impairment in individuals with autism spectrum disorder}}. {Neuropsychology};2011 (Jul 4)
Objective: The social and communicative challenges faced by individuals with autism spectrum disorder (ASD) are often compounded by additional difficulties with executive function. It remains unclear, however, to what the extent individuals with ASD experienced impairment in inhibitory control. The objective of the present study was to assess the three main subtypes of executive inhibitory control within a single ASD sample thus providing new insight into the unique ASD-related pattern of sparing and impairment observed across different aspects of inhibitory control. Method: A sample of 28 children with ASD (mean age = 13.1 years) and a comparison group of 49 neurologically uncompromised children (mean age = 13.3 years) participated. A prepotent response inhibition task, a flanker visual filtering task, and a proactive interference memory task were used to evaluate prepotent response inhibition, resistance to distracter interference, and resistance to proactive interference, respectively. Results: After accounting for individual differences in noninhibition abilities (e.g., processing speed) and overall level of functioning, there was no evidence of group-related differences in inhibitory performance on the prepotent response inhibition test or proactive interference test. ASD-related impairments in inhibitory control were evident, however, on the flanker visual filtering task. Conclusions: Taken together, the present findings indicate that ASD is associated with impairments in some, but not all, aspects of inhibitory control. Individuals with ASD appear to have difficulty ignoring distracting visual information, but prepotent response inhibition and resistance to proactive interference are relatively intact. The current findings also provide support for a multitype model of inhibitory control. (PsycINFO Database Record (c) 2011 APA, all rights reserved).
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2. Croen LA, Grether JK, Yoshida CK, Odouli R, Hendrick V. {{Antidepressant Use During Pregnancy and Childhood Autism Spectrum Disorders}}. {Arch Gen Psychiatry};2011 (Jul 4)
CONTEXT: The prevalence of autism spectrum disorders (ASDs) has increased over recent years. Use of antidepressant medications during pregnancy also shows a secular increase in recent decades, prompting concerns that prenatal exposure may contribute to increased risk of ASD. OBJECTIVE: To systematically evaluate whether prenatal exposure to antidepressant medications is associated with increased risk of ASD. DESIGN: Population-based case-control study. Medical records were used to ascertain case children and control children and to derive prospectively recorded information on mothers’ use of antidepressant medications, mental health history of mothers, and demographic and medical covariates. SETTING: The Kaiser Permanente Medical Care Program in Northern California. PARTICIPANTS: A total of 298 case children with ASD (and their mothers) and 1507 randomly selected control children (and their mothers) drawn from the membership of the Kaiser Permanente Medical Care Program in Northern California. MAIN OUTCOME MEASURES: ASDs. RESULTS: Prenatal exposure to antidepressant medications was reported for 20 case children (6.7%) and 50 control children (3.3%). In adjusted logistic regression models, we found a 2-fold increased risk of ASD associated with treatment with selective serotonin reuptake inhibitors by the mother during the year before delivery (adjusted odds ratio, 2.2 [95% confidence interval, 1.2-4.3]), with the strongest effect associated with treatment during the first trimester (adjusted odds ratio, 3.8 [95% confidence interval, 1.8-7.8]). No increase in risk was found for mothers with a history of mental health treatment in the absence of prenatal exposure to selective serotonin reuptake inhibitors. CONCLUSION: Although the number of children exposed prenatally to selective serotonin reuptake inhibitors in this population was low, results suggest that exposure, especially during the first trimester, may modestly increase the risk of ASD. The potential risk associated with exposure must be balanced with the risk to the mother or fetus of untreated mental health disorders. Further studies are needed to replicate and extend these findings.
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3. Hallmayer J, Cleveland S, Torres A, Phillips J, Cohen B, Torigoe T, Miller J, Fedele A, Collins J, Smith K, Lotspeich L, Croen LA, Ozonoff S, Lajonchere C, Grether JK, Risch N. {{Genetic Heritability and Shared Environmental Factors Among Twin Pairs With Autism}}. {Arch Gen Psychiatry};2011 (Jul 4)
CONTEXT: Autism is considered the most heritable of neurodevelopmental disorders, mainly because of the large difference in concordance rates between monozygotic and dizygotic twins. OBJECTIVE: To provide rigorous quantitative estimates of genetic heritability of autism and the effects of shared environment. Design, Setting, and PARTICIPANTS: Twin pairs with at least 1 twin with an autism spectrum disorder (ASD) born between 1987 and 2004 were identified through the California Department of Developmental Services. MAIN OUTCOME MEASURES: Structured diagnostic assessments (Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule) were completed on 192 twin pairs. Concordance rates were calculated and parametric models were fitted for 2 definitions, 1 narrow (strict autism) and 1 broad (ASD). RESULTS: For strict autism, probandwise concordance for male twins was 0.58 for 40 monozygotic pairs (95% confidence interval [CI], 0.42-0.74) and 0.21 for 31 dizygotic pairs (95% CI, 0.09-0.43); for female twins, the concordance was 0.60 for 7 monozygotic pairs (95% CI, 0.28-0.90) and 0.27 for 10 dizygotic pairs (95% CI, 0.09-0.69). For ASD, the probandwise concordance for male twins was 0.77 for 45 monozygotic pairs (95% CI, 0.65-0.86) and 0.31 for 45 dizygotic pairs (95% CI, 0.16-0.46); for female twins, the concordance was 0.50 for 9 monozygotic pairs (95% CI, 0.16-0.84) and 0.36 for 13 dizygotic pairs (95% CI, 0.11-0.60). A large proportion of the variance in liability can be explained by shared environmental factors (55%; 95% CI, 9%-81% for autism and 58%; 95% CI, 30%-80% for ASD) in addition to moderate genetic heritability (37%; 95% CI, 8%-84% for autism and 38%; 95% CI, 14%-67% for ASD). CONCLUSION: Susceptibility to ASD has moderate genetic heritability and a substantial shared twin environmental component.
