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      Comparing biobehavioral profiles across two social stress paradigms in children with and without autism spectrum disorders

      , 1 , 2 , 3

      Molecular Autism

      BioMed Central

      Cortisol, Autism, Stress, Novelty, Peer, Age

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          Abstract

          Background

          Autism spectrum disorders (ASD) are defined by impairment in reciprocal social interaction and flexible adaptation to the environment. This study compared physiological stress in children with and without ASD exposed to two social stress protocols. We hypothesized that the ASD group would show heightened initial and enduring cortisol levels to the social stressors, which would be moderated by age and intelligence.

          Methods

          Twenty-seven children with ASD and 32 with typical development (TYP) completed a standardized social-evaluative performance task and a validated paradigm of social play with peers. Physiological stress was measured by salivary cortisol at nine time points. Statistical approaches included repeated-measures linear mixed models and correlation analyses.

          Results

          The average cortisol level of both groups during initial exposure to social situations was significantly greater than baseline levels (ASD, P = 0.018; TYP, P = 0.006). Stress responsivity was significantly different between the groups; the TYP group showed a significant reduction in cortisol over time ( P = 0.023), whereas the ASD group maintained an elevated cortisol level ( P >0.05). The ASD group evidenced greater variability in between-group, within-group and intra-individual analyses. Age was a positive moderator of stress for the ASD group ( P = 0.047), whereas IQ was a negative moderator for the TYP group ( P = 0.061).

          Conclusions

          Initial stress to novel social scenarios is idiosyncratic and predictive of subsequent exposure. Amidst significant variability in cortisol, children with ASD show enhanced and sustained social stress that increases with age. Developmental and cognitive factors differentially moderate stress in children with ASD and TYP, respectively. A model of neuroendocrine reactivity is proposed.

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          Most cited references 42

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          A self-report measure of pubertal status: Reliability, validity, and initial norms.

          Puberty is a central process in the complex set of changes that constitutes the transition from childhood to adolescence. Research on the role of pubertal change in this transition has been impeded by the difficulty of assessing puberty in ways acceptable to young adolescents and others involved. Addressing this problem, this paper describes and presents norms for a selfreport measure of pubertal status. The measure was used twice annually over a period of three years in a longitudinal study of 335 young adolescent boys and girls. Data on a longitudinal subsample of 253 subjects are reported. The scale shows good reliability, as indicated by coefficient alpha. In addition, several sources of data suggest that these reports are valid. The availability of such a measure is important for studies, such as those based in schools, in which more direct measures of puberty may not be possible.
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            Neurocircuitry of stress: central control of the hypothalamo-pituitary-adrenocortical axis.

            Integration of the hypothalamo-pituitary-adrenal stress response occurs by way of interactions between stress-sensitive brain circuitry and neuroendocrine neurons of the hypothalamic paraventricular nucleus (PVN). Stressors involving an immediate physiologic threat ('systemic' stressors) are relayed directly to the PVN, probably via brainstem catecholaminergic projections. By contrast, stressors requiring interpretation by higher brain structures ('processive' stressors) appear to be channeled through limbic forebrain circuits. Forebrain limbic sites connect with the PVN via interactions with GABA-containing neurons in the bed nucleus of the stria terminalis, preoptic area and hypothalamus. Thus, final elaboration of processive stress responses is likely to involve modulation of PVN GABAergic tone. The functional and neuroanatomical data obtained suggest that disease processes involving inappropriate stress control involve dysfunction of processive stress pathways.
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              Neuron number and size in prefrontal cortex of children with autism.

              Autism often involves early brain overgrowth, including the prefrontal cortex (PFC). Although prefrontal abnormality has been theorized to underlie some autistic symptoms, the cellular defects that cause abnormal overgrowth remain unknown. To investigate whether early brain overgrowth in children with autism involves excess neuron numbers in the PFC. DESIGN, SETTING, AND CASES: Postmortem prefrontal tissue from 7 autistic and 6 control male children aged 2 to 16 years was examined by expert anatomists who were blinded to diagnostic status. Number and size of neurons were quantified using stereological methods within the dorsolateral (DL-PFC) and mesial (M-PFC) subdivisions of the PFC. Cases were from the eastern and southeastern United States and died between 2000 and 2006. Mean neuron number and size in the DL-PFC and M-PFC were compared between autistic and control postmortem cases. Correlations of neuron number with deviation in brain weight from normative values for age were also performed. Children with autism had 67% more neurons in the PFC (mean, 1.94 billion; 95% CI, 1.57-2.31) compared with control children (1.16 billion; 95% CI, 0.90-1.42; P = .002), including 79% more in DL-PFC (1.57 billion; 95% CI, 1.20-1.94 in autism cases vs 0.88 billion; 95% CI, 0.66-1.10 in controls; P = .003) and 29% more in M-PFC (0.36 billion; 95% CI, 0.33-0.40 in autism cases vs 0.28 billion; 95% CI, 0.23-0.34 in controls; P = .009). Brain weight in the autistic cases differed from normative mean weight for age by a mean of 17.6% (95% CI, 10.2%-25.0%; P = .001), while brains in controls differed by a mean of 0.2% (95% CI, -8.7% to 9.1%; P = .96). Plots of counts by weight showed autistic children had both greater total prefrontal neuron counts and brain weight for age than control children. In this small preliminary study, brain overgrowth in males with autism involved an abnormal excess number of neurons in the PFC.
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                Author and article information

                Journal
                Mol Autism
                Mol Autism
                Molecular Autism
                BioMed Central
                2040-2392
                2012
                17 November 2012
                : 3
                : 13
                Affiliations
                [1 ]Department of Psychiatry, Vanderbilt University, Vanderbilt Kennedy Center, PMB 40, 230 Appleton Place, Nashville, TN, 37203, USA
                [2 ]Cancer Prevention Institute of California, 2201 Walnut Avenue, Suite 300, Fremont, CA, 94538, USA
                [3 ]Veterans Affairs Northern California Healthcare System, 10535 Hospital Way, Building 649, Mather, CA, 95655, USA
                Article
                2040-2392-3-13
                10.1186/2040-2392-3-13
                3533919
                23158965
                Copyright ©2012 Corbett et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Research

                Neurosciences

                autism, age, novelty, stress, peer, cortisol

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