The ability to indicate a failure to understand a message is a critical pragmatic (social) language skill for managing communication breakdowns and supporting successful communicative exchanges. The current study examined the ability to signal noncomprehension across different types of confusing message conditions in children and adolescents with fragile X syndrome (FXS), Down syndrome (DS), autism spectrum disorder (ASD), and typical development (TD). Controlling for nonverbal mental age and receptive vocabulary skills, youth with comorbid FXS and ASD and those with DS were less likely than TD controls to signal noncomprehension of confusing messages. Youth with FXS without ASD and those with idiopathic ASD did not differ from controls. No sex differences were detected in any group. Findings contribute to current knowledge of pragmatic profiles in different forms of genetically-based neurodevelopmental disorders associated with intellectual disability, and the role of sex in the expression of such profiles. Learning Outcomes Upon completion of this article, readers will have learned about: (1) the social-communicative profiles of youth with FXS, DS, and ASD, (2) the importance of signaling noncomprehension in response to a confusing message, and (3) the similarities and differences in noncomprehension signaling in youth with FXS (with and without ASD), DS, idiopathic ASD, and TD.

Background Fragile X syndrome (FXS) and non‐syndromic autism spectrum disorder (ASD) are distinct disorders with overlapping behavioral features. Both disorders are also highly associated with anxiety with abnormal physiological regulation implied mechanistically. Some reports suggest atypical hypothalamus‐pituitary‐adrenal (HPA) axis function, indexed via aberrant cortisol reactivity, in both FXS and non‐syndromic ASD. However, no study has compared cortisol reactivity across these two disorders, or its relationship to ASD symptom severity. Methods Cortisol reactivity (prior to and following a day of assessments) was measured in 54 adolescent/young adult males with FXS contrasted to 15 males with non‐syndromic ASD who had low cognitive abilities. Results Greater ASD symptom severity was related to increased cortisol reactivity and higher levels at the end of the day, but only in the non‐syndromic ASD group. Elevated anxiety was associated with increased HPA activation in the group with FXS alone. Conclusions Taken together, findings suggest a unique neuroendocrine profile that distinguishes adolescent/young adult males with FXS from those with non‐syndromic ASD. Severity of ASD symptoms appears to be related to cortisol reactivity in the non‐syndromic ASD sample, but not in FXS; while anxiety symptoms are associated with HPA activation in the FXS sample, but not in ASD despite a high prevalence of ASD, anxiety and physiological dysregulation characteristic in both populations.

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