International Meeting for Autism Research: Functional Brain Imaging of Aberrant Social Motivation In Children with Autism Spectrum Disorders

Functional Brain Imaging of Aberrant Social Motivation In Children with Autism Spectrum Disorders

Friday, May 13, 2011
Elizabeth Ballroom E-F and Lirenta Foyer Level 2 (Manchester Grand Hyatt)
10:00 AM
G. Kohls1, S. Faja2, J. M. Taylor1, E. N. Madva1, S. J. Cayless1 and R. T. Schultz1, (1)Center for Autism Research, Children's Hospital of Philadelphia, Philadelphia, PA, (2)Box 357920, University of Washington, Seattle, WA, United States
Background: We and others have hypothesised that the failure to develop better social perceptual and social cognitive skills in children with autism spectrum disorders (ASD) could at least partly be due to a suboptimal reward-based motivation to seek social experiences and learn social information. Decreased social motivation might be due to dysfunction in neural systems implicated in reward processing such as ventral striatum (including nucleus accumbens/NAcc) or orbitofrontal cortex (OFC). Despite the influence of this “social motivation deficit theory” in the field, very few tests of it using brain imaging have been conducted.

Objectives: This study’s central scientific aim is to develop a better understanding of the neural circuitry of reward based social motivation in children with ASD, and to characterize the relationships between brain activity in motivation circuitry and social behavior.

Methods: We conducted a functional magnetic resonance imaging (fMRI) study to investigate the effects of social reward on brain areas associated with reward ‘wanting’ (NAcc) and reward ‘liking’ (OFC) in 20 children with ASD relative to 20 age, gender, and IQ matched typically developing children (TDC). We apply a modified motivation paradigm that has been tested and validated in the normative literature (Spreckelmeyer, Krach, Kohls et al., 2009). To optimize the ecological validity of our social motivation task, we created and validated a new stimulus set by replacing still photos with short video clips of actors showing social approval. In addition, our modified paradigm includes a tracking algorithm of subject task performance.  This is important as it permits adjustment of task difficulty in real time and, thus, individualized reward delivery. FMRI data are collected on a 3T scanner and analyzed with FSL. 

Results: Data collection is ongoing; we plan to have preliminary analyses on 10 participants with ASD and 10 TDCs.  Analyses will focus on the hypothesis that participants with ASD will show reduced neural activations in the NAcc in response to social reward anticipation, reflecting reduced reward ‘wanting’. Moreover, we predict that the diminished neural responsivity in the NAcc to social reward ‘wanting’ will be significantly correlated with the degree of social deficits among individuals with ASD.

Conclusions: An increased understanding of the biological mechanisms causing social deficits in ASD can be used to develop therapeutic (e.g., brain-based pharmacological) interventions and treatment procedures where, for instance, medications support social learning. If social motivation deficits are indeed a fundamental cause of a cascade of events that support the development of ASD, then interventions that increase social motivation could help individuals with ASD and their families.

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