Dyadic Physiological Interdependence and Social Reciprocity in ASD

Poster Presentation
Thursday, May 10, 2018: 11:30 AM-1:30 PM
Hall Grote Zaal (de Doelen ICC Rotterdam)
O. Saunders Wilder1, J. Sullivan2, K. T. Johnson1, R. V. Palumbo2, C. Cumpanasiou2, R. W. Picard3 and M. S. Goodwin2, (1)MIT Media Lab, Cambridge, MA, (2)Northeastern University, Boston, MA, (3)MIT, Cambridge, MA
Background: Converging evidence in the social and affective neuroscience literature suggests that the same brain regions activated while experiencing emotion are also recruited when observing or inferring affective experiences in another person. This offers a potential process by which inferring another’s affective state automatically influences one’s own affective state. Understanding how this underlying process of interpersonal interoceptive inference may be impacted in individuals with social reciprocity impairment is an important step towards developing an etiological understanding of socio-affective impairment in Autism Spectrum Disorder (ASD). Interpersonal physiology may ultimately help further scientific understanding of the underlying etiology of socio-affective impairment in ASD by providing a feasible, sensitive, and interpretable means of measuring these underlying neurophysiological processes in a variety of contexts.

Objectives: In order to investigate the relationship between interpersonal physiology and social reciprocity impairment, we engaged child-parent dyads in semi-structured social-emotion regulation tasks while collecting ambulatory physiology data and a standard informant report measure of social reciprocity. In addition to simultaneous parent-child physiology, we also collected and analyzed physiological data from a researcher and the child in which they interacted with the child independent of the parent while administering several relevant presses from the ADOS-2. This allowed us to examine interpersonal physiological dynamics when a child is interacting with an unfamiliar adult, as is commonly the case in many diagnostic and assessment settings such as the ADOS-2.

Methods: Using ambulatory electrodermal activity (EDA) sensors, we collected interpersonal physiology data from 30 young children who were either typically developing (TD; N=22) or had an ASD diagnosis (N=8), their parent, and a researcher during semi-structured social interaction and emotion regulation tasks (ADOS-2; LABTAB) adapted from social presses in existing validated paradigms for assessing socio-affective functioning in young children. In addition, parents completed the Social Responsiveness Scale 2nd Edition (SRS-2) about their child, a well-validated 65-item informant-report measure of social reciprocity impairments in autism.

Results: To assess dyadic physiological interdependence, we fit a series of hierarchical linear models following the procedure used by Baker et al. (2015) with the child’s EDA as the dependent variable and child movement, time, and adult EDA (either parent or researcher depending on the task being analyzed) and an interaction term consisting of adult EDA ⨉ SRS-2 Total Score as independent variables. Our results for both ASD and TD indicated a statistically significant dependence of child EDA on both adult EDA and adult EDA ⨉ SRS-2 Total Score, suggesting that physiological interdependence between adult and child was partially moderated by the child’s social reciprocity impairment as measured by the SRS-2. Furthermore, a simple slopes decomposition indicated that physiological interdependence diverged significantly for children with different levels of social reciprocity impairment and varied depending on whether the child was interacting with the parent or the researcher.

Conclusions: Our findings suggest that physiological interdependence between a child and parent or unfamiliar adult is related to standard measures of social reciprocity in young children with and without ASD and may differ depending on dyad familiarity.