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Aim Children with special health care needs (CSHCN) are those who require more care for their physical, developmental, or emotional differences than their typically developing peers. Among a wide range of burdens that caregivers of CSHCN experience, the mental burden of caregivers is still not well investigated. This study aimed at examining the relationship between caring for CSHCN and mothers' anxiety/depression. Methods This study used data from the Tokyo Early Adolescence Survey, a population-based cross-sectional survey. Using screening questionnaires, we evaluated the prevalence of CSHCN and identified their primary caregivers. Focusing on mothers as caregivers, we analyzed the relationship between having CSHCN and mothers' anxiety/depression, and between the severity of children's condition and mothers' anxiety/depression. We further determined what mediates these relationships using path analyses. Results Among 4003 participants, we identified 502 CSHCN (12.5%), and 93% of responding caregivers were mothers. We found that mothers with CSHCN were significantly more anxious/depressed than those without CSHCN, which was closely related to the severity of children's condition. The mediation effect of social support on the relation between CSHCN and mothers' anxiety/depression was statistically significant. Conclusion Mothers of CSHCN were more anxious/depressed than other mothers in this study. Social support was indicated to have a significant mediating effect on the relationship between CSHCN and mothers' anxiety/depression. Our results suggest that considering ways to offer social support may effectively relieve the mental stress experienced by mothers of CSHCN. This article is protected by copyright. All rights reserved.

AIM Although advanced parental age holds an increased risk for autism spectrum disorder (ASD), its role as a potential risk factor for an atypical white matter development underlying the pathophysiology of ASD has not yet been investigated. The current study was aimed to detect white matter disparities in ASD, and further investigate the relationship of paternal and maternal age at birth with such disparities. METHODS Thirty-nine adult males with high-functioning ASD and 37 typically developing (TD) males were analyzed in the study. The FMRIB Software Library and tract-based spatial statistics were utilized to process and analyze the diffusion tensor imaging data. RESULTS Subjects with ASD exhibited significantly higher mean diffusivity (MD) and radial diffusivity (RD) in white matter fibers, including the association (inferior fronto-occipital fasciculus, right inferior longitudinal fasciculus, superior longitudinal fasciculi, uncinate fasciculus, and cingulum), commissural (forceps minor), and projection tracts (anterior thalamic radiation and right corticospinal tract) compared to TD subjects (Padjusted

Aim: Although inconsistencies in neuropsychological impairments in Tourette's syndrome (TS) have been discussed with respect to comorbid disorders, such as obsessive–compulsive disorder, few studies have focused on the specific dimensions of obsessive–compulsive symptoms (OCS) related to TS, such as aggression and symmetry. The aim of this study was to explore the impact of specific TS-related OCS on neuropsychological performance. Methods: A series of neuropsychological tasks examining attention and executive functioning were performed in groups of 33 TS participants and 18 healthy controls. The neuropsychological performance of TS with Aggression OCS (n = 11) were compared to TS without Aggression OCS (n = 22) and controls by using mancova controlling for age. In the same way as Aggression, we compared the performance of three groups by Symmetry: TS with Symmetry OCS (n = 14), TS without Symmetry OCS (n = 19) and controls. Results: TS participants with Aggression OCS tended to make more perseverative errors than those without. Global OCS severity and tic severity did not correlate with any neuropsychological performances. No significant differences were detected between TS participants with and without Symmetry OCS. Conclusion: Neuropsychological deficits in TS might be affected not by global OCS severity but by specific TS-related OCS.

The common features of autism spectrum disorder, a highly heritable representative pervasive developmental disorder with significant heterogeneity and multiple-genetic factors, are severe dysfunction in social reciprocity, abnormalities in social brain regions, and disproportionately low probability in the female gender. Concomitantly, certain domains of mental function, such as emotional memory and social reciprocity, show a significant sex difference. In addition, recent neuroimaging studies have shown significant sexual dimorphisms in neuroanatomical correlates of social cognition. Recently, some sexually dimorphic factors, including oxytocin, vasopressin, and genes linked with the x-chromosome, have received attention because of their possible contribution to mental development especially in the social cognitive domain. Taking this evidence together, it is hypothesized that a sexually dimorphic factor associated with social reciprocity could affect characteristics of autism spectrum disorder including dysfunction in social reciprocity, abnormalities in social brain regions, and disproportionately low probability in female gender. This review article overviews sexual dimorphisms in clinical features of autism spectrum disorder, in normal social cognition, and in social brain function and structure. The association of oxytocin with sexual dimorphisms, social reciprocity, neural correlates of social cognition, and the pathogenesis of autism spectrum disorder were further summarized. Recent studies have suggested that oxytocin plays a role in social attachment in experimental animals, in enhancing social interactive ability in human adults, and in the pathogenesis of autism spectrum disorder. Thus, the ongoing accumulated evidence suggests that oxytocin deserves to be examined as a candidate that causes the sexually dimorphic aspect of human social reciprocity, social brain development and the pathogenesis of autism spectrum disorder.

Although inconsistencies in neuropsychological impairments in Tourette's syndrome (TS) have been discussed with respect to comorbid disorders, such as obsessive-compulsive disorder, few studies have focused on the specific dimensions of obsessive-compulsive symptoms (OCS) related to TS, such as aggression and symmetry. The aim of this study was to explore the impact of specific TS-related OCS on neuropsychological performance.A series of neuropsychological tasks examining attention and executive functioning were performed in groups of 33 TS participants and 18 healthy controls. The neuropsychological performance of TS with Aggression OCS (n = 11) were compared to TS without Aggression OCS (n = 22) and controls by using MANCOVA controlling for age. In the same way as Aggression, we compared the performance of three groups by Symmetry: TS with Symmetry OCS (n = 14), TS without Symmetry OCS (n = 19) and controls.TS participants with Aggression OCS tended to make more perseverative errors than those without. Global OCS severity and tic severity did not correlate with any neuropsychological performances. No significant differences were detected between TS participants with and without Symmetry OCS.Neuropsychological deficits in TS might be affected not by global OCS severity but by specific TS-related OCS.

The common features of autism spectrum disorder, a highly heritable representative pervasive developmental disorder with significant heterogeneity and multiple-genetic factors, are severe dysfunction in social reciprocity, abnormalities in social brain regions, and disproportionately low probability in the female gender. Concomitantly, certain domains of mental function, such as emotional memory and social reciprocity, show a significant sex difference. In addition, recent neuroimaging studies have shown significant sexual dimorphisms in neuroanatomical correlates of social cognition. Recently, some sexually dimorphic factors, including oxytocin, vasopressin, and genes linked with the x-chromosome, have received attention because of their possible contribution to mental development especially in the social cognitive domain. Taking this evidence together, it is hypothesized that a sexually dimorphic factor associated with social reciprocity could affect characteristics of autism spectrum disorder including dysfunction in social reciprocity, abnormalities in social brain regions, and disproportionately low probability in female gender. This review article overviews sexual dimorphisms in clinical features of autism spectrum disorder, in normal social cognition, and in social brain function and structure. The association of oxytocin with sexual dimorphisms, social reciprocity, neural correlates of social cognition, and the pathogenesis of autism spectrum disorder were further summarized. Recent studies have suggested that oxytocin plays a role in social attachment in experimental animals, in enhancing social interactive ability in human adults, and in the pathogenesis of autism spectrum disorder. Thus, the ongoing accumulated evidence suggests that oxytocin deserves to be examined as a candidate that causes the sexually dimorphic aspect of human social reciprocity, social brain development and the pathogenesis of autism spectrum disorder.