Parenting stress and child behavior problems have been posited to have a transactional effect on each other across development. However, few studies have tested this model empirically. The authors investigated the relationship between parenting stress and child behavior problems from ages 3 to 9 years old among 237 children, 144 of whom were typically developing and 93 who were identified as developmentally delayed. Behavior problems and parenting stress covaried significantly across time for both groups of children. Cross-lagged panel analyses generally supported a bidirectional relationship between parenting stress and child behavior problems for mothers and fathers.

IMPORTANCE More than half of youth with autism spectrum disorders (ASDs) have sensory overresponsivity (SOR), an extreme negative reaction to sensory stimuli. However, little is known about the neurobiological basis of SOR, and there are few effective treatments. Understanding whether SOR is due to an initial heightened sensory response or to deficits in regulating emotional reactions to stimuli has important implications for intervention.OBJECTIVE To determine differences in brain responses, habituation, and connectivity during exposure to mildly aversive sensory stimuli in youth with ASDs and SOR compared with youth with ASDs without SOR and compared with typically developing control subjects. DESIGN, SETTING, AND PARTICIPANTS Functional magnetic resonance imaging was used to examine brain responses and habituation to mildly aversive auditory and tactile stimuli in 19 high-functioning youths with ASDs and 19 age-and IQ-matched, typically developing youths (age range, 9-17 years). Brain activity was related to parents' ratings of children's SOR symptoms. Functional connectivity between the amygdala and orbitofrontal cortex was compared between ASDs subgroups with and without SOR and typically developing controls without SOR. The study dates were March 2012 through February 2014. MAIN OUTCOMES AND MEASURESRelative increases in blood oxygen level-dependent signal response across the whole brain and within the amygdala during exposure to sensory stimuli compared with fixation, as well as correlation between blood oxygen level-dependent signal change in the amygdala and orbitofrontal cortex. RESULTSThe mean age in both groups was 14 years and the majority in both groups (16 of 19 each) were male. Compared with neurotypical control participants, participants with ASDs displayed stronger activation in primary sensory cortices and the amygdala (P < .05, corrected). This activity was positively correlated with SOR symptoms after controlling for anxiety. The ASDs with SOR subgroup had decreased neural habituation to stimuli in sensory cortices and the amygdala compared with groups without SOR. Youth with ASDs without SOR showed a pattern of amygdala downregulation, with negative connectivity between the amygdala and orbitofrontal cortex (thresholded at z > 1.70, P < .05). CONCLUSIONS AND RELEVANCEResults demonstrate that youth with ASDs and SOR show sensorilimbic hyperresponsivity to mildly aversive tactile and auditory stimuli, particularly to multiple modalities presented simultaneously, and show that this hyperresponsivity is due to failure to habituate. In addition, findings suggest that a subset of youth with ASDs can regulate their responses through prefrontal downregulation of amygdala activity. Implications for intervention include minimizing exposure to multiple sensory modalities and building coping strategies for regulating emotional response to stimuli.

This report focuses on the emergence of and bidirectional effects between anxiety and sensory over-responsivity (SOR) in toddlers with autism spectrum disorders (ASD). Participants were 149 toddlers with ASD and their mothers, assessed at 2 annual time points. A cross-lag analysis showed that anxiety symptoms increased over time while SOR remained relatively stable. SOR positively predicted changes in anxiety over and above child age, autism symptom severity, NVDQ, and maternal anxiety, but anxiety did not predict changes in SOR. Results suggest that SOR emerges earlier than anxiety, and predicts later development of anxiety.

Anxiety disorders and sensory over-responsivity (SOR) are common in children with autism spectrum disorders (ASD), and there is evidence for an association between these two conditions. Currently, it is unclear what causal mechanisms may exist between SOR and anxiety. We propose three possible theories to explain the association between anxiety and SOR: (a) SOR is caused by anxiety; (b) Anxiety is caused by SOR; or (c) SOR and anxiety are causally unrelated but are associated through a common risk factor or diagnostic overlap. In this paper, we examine support for each theory in the existing anxiety, autism, and neuroscience literature, and discuss how each theory informs choice of interventions and implications for future studies.

Objectives: Sensory over-responsivity (SOR), defined as a negative response to or avoidance of sensory stimuli, is both highly prevalent and extremely impairing in youth with autism spectrum disorders (ASD), yet little is known about the neurological bases of SOR. This study aimed to examine the functional neural correlates of SOR by comparing brain responses to sensory stimuli in youth with and without ASD. Method: Twenty-five high-functioning youth with ASD and 25 age- and IQ-equivalent typically developing (TD) youth were presented with mildly aversive auditory and visual stimuli during a functional magnetic resonance imaging (fMRI) scan. Parents provided ratings of children's SOR and anxiety symptom severity. Results: Compared to TD participants, ASD participants displayed greater activation in primary sensory cortical areas as well as amygdala, hippocampus, and orbital-frontal cortex. In both groups, the level of activity in these areas was positively correlated with level of SOR severity as rated by parents, over and above behavioral ratings of anxiety. Conclusions: This study demonstrates that youth with ASD show neural hyper-responsivity to sensory stimuli, and that behavioral symptoms of SOR may be related to both heightened responsivity in primary sensory regions as well as areas related to emotion processing, and regulation.

Neuroimaging investigations of autism spectrum disorders (ASDs) have advanced our understanding of atypical brain function and structure, and have recently converged on a model of altered network-level connectivity. Traditional task-based functional magnetic resonance imaging (MRI) and volume-based structural MRI studies have identified widespread atypicalities in brain regions involved in social behavior and other core ASD-related behavioral deficits. More recent advances in MR-neuroimaging methods allow for quantification of brain connectivity using diffusion tensor imaging, functional connectivity, and graph theoretic methods. These newer techniques have moved the field toward a systems-level understanding of ASD etiology, integrating functional and structural measures across distal brain regions. Neuroimaging findings in ASD as a whole have been mixed and at times contradictory, likely due to the vast genetic and phenotypic heterogeneity characteristic of the disorder. Future longitudinal studies of brain development will be crucial to yield insights into mechanisms of disease etiology in ASD sub-populations. Advances in neuroimaging methods and large-scale collaborations will also allow for an integrated approach linking neuroimaging, genetics, and phenotypic data.

Objective The salience network, an intrinsic brain network thought to modulate attention to internal versus external stimuli, has been consistently found to be atypical in autism spectrum disorders (ASD). However, little is known about how this altered resting-state connectivity relates to brain activity during information processing, which has important implications for understanding sensory over-responsivity (SOR), a common and impairing condition in ASD related to difficulty downregulating brain responses to sensory stimuli. This study examined how SOR in youth with ASD relates to atypical salience network connectivity and whether these atypicalities are associated with abnormal brain response to basic sensory information. Method Functional magnetic resonance imaging was used to examine how parent-rated SOR symptoms related to salience network connectivity in 61 youth (age 8–17; 28 ASD, 33 IQ-matched typically developing). Correlations between resting-state salience network connectivity and brain response to mildly aversive tactile and auditory stimuli were examined. Results SOR in youth with ASD was related to increased resting-state functional connectivity between salience network nodes and brain regions implicated in primary sensory processing and attention. Further, the strength of this connectivity at rest was related to extent of brain activity in response to auditory and tactile stimuli. Conclusion Results support an association between intrinsic brain connectivity and specific atypical brain responses during information processing. Additionally, findings suggest that basic sensory information is overly salient to individuals with SOR, leading to over-attribution of attention to this information. Implications for intervention include incorporating sensory coping strategies into social interventions for individuals with SOR.

Sensory over-responsivity (SOR) is a common condition in autism spectrum disorders (ASD) that is associated with greater social impairment. However, the mechanisms through which sensory stimuli may affect social functioning are not well understood. This study used fMRI to examine brain activity while interpreting communicative intent in 15 high-functioning youth with ASD and 16 age- and IQ-matched typically-developing (TD) controls. Participants completed the task with and without a tactile sensory distracter, and with and without instructions directing their attention to relevant social cues. When completing the task in the presence of the sensory distracter, TD youth showed increased activity in auditory language and frontal regions whereas ASD youth showed decreased activation in these areas. Instructions mitigated this effect such that ASD youth did not decrease activation during tactile stimulation; instead, the ASD group showed increased medial prefrontal activity. SOR severity modulated the effect of the tactile stimulus on social processing. Results demonstrate for the first time a neural mechanism through which sensory stimuli cause disruption of social cognition, and that attentional modulation can restore neural processing of social cues through prefrontal regulation. Findings have implications for novel, integrative interventions that incorporate attentional directives to target both sensory and social symptoms.