A profile of prosodic speech differences in individuals with autism spectrum disorder and first-degree relatives.

Abstract

Impairments in prosody (e.g., intonation, stress) are among the most notable communication characteristics of individuals with autism spectrum disorder (ASD) and can significantly impact communicative interactions. Evidence suggests that differences in prosody may be evident among first-degree relatives of autistic individuals, indicating that genetic liability to ASD is expressed through prosodic variation, along with subclinical traits referred to as the broad autism phenotype (BAP). This study aimed to further characterize prosodic profiles associated with ASD and the BAP to better understand the clinical and etiologic significance of prosodic differences. Autistic individuals, their parents, and respective control groups completed the Profiling Elements of Prosody in Speech-Communication (PEPS-C), an assessment of receptive and expressive prosody. Responses to expressive subtests were further examined using acoustic analyses. Relationships between PEPS-C performance, acoustic measurements, and pragmatic language ability in conversation were assessed to understand how differences in prosody might contribute to broader ASD-related pragmatic profiles. In ASD, receptive prosody deficits were observed in contrastive stress. With regard to expressive prosody, both the ASD and ASD Parent groups exhibited reduced accuracy in imitation, lexical stress, and contrastive stress expression compared to respective control groups, though no acoustic differences were noted. In ASD and Control groups, lower accuracy across several PEPS-C subtests and acoustic measurements related to increased pragmatic language violations. In parents, acoustic measurements were tied to broader pragmatic language and personality traits of the BAP. Overlapping areas of expressive prosody differences were identified in ASD and parents, providing evidence that prosody is an important language-related ability that may be impacted by genetic risk of ASD.