Social ‘wanting’ dysfunction in autism: neurobiological underpinnings and treatment implications

Abstract

Most behavioral training regimens in autism spectrum disorders (ASD) rely on reward-based reinforcement strategies. Although proven to significantly increase both cognitive and social outcomes and successfully reduce aberrant behaviors, this approach fails to benefit a substantial number of affected individuals. Given the enormous amount of clinical and financial resources devoted to behavioral interventions, there is a surprisingly large gap in our knowledge of the basic reward mechanisms of learning in ASD. Understanding the mechanisms for reward responsiveness and reinforcement-based learning is urgently needed to better inform modifications that might improve current treatments. The fundamental goal of this review is to present a fine-grained literature analysis of reward function in ASD with reference to a validated neurobiological model of reward: the ‘wanting’/’liking’ framework. Despite some inconsistencies within the available literature, the evaluation across three converging sets of neurobiological data (neuroimaging, electrophysiological recordings, and neurochemical measures) reveals good evidence for disrupted reward-seeking tendencies in ASD, particularly in social contexts. This is most likely caused by dysfunction of the dopaminergic–oxytocinergic ‘wanting’ circuitry, including the ventral striatum, amygdala, and ventromedial prefrontal cortex. Such a conclusion is consistent with predictions derived from diagnostic criteria concerning the core social phenotype of ASD, which emphasize difficulties with spontaneous self-initiated seeking of social encounters (that is, social motivation). Existing studies suggest that social ‘wanting’ tendencies vary considerably between individuals with ASD, and that the degree of social motivation is both malleable and predictive of intervention response. Although the topic of reward responsiveness in ASD is very new, with much research still needed, the current data clearly point towards problems with incentive-based motivation and learning, with clear and important implications for treatment. Given the reliance of behavioral interventions on reinforcement-based learning principles, we believe that a systematic focus on the integrity of the reward system in ASD promises to yield many important clues, both to the underlying mechanisms causing ASD and to enhancing the efficacy of existing and new interventions.

Oxytocin enhances brain function in children with autism

“…We speculate that these results may imply that OT makes social stimuli more rewarding and socially salient to children with ASD. Our findings are remarkably consistent with nonhuman animal and human studies that have demonstrated influences on social reward, social attention, and salience following changes to oxytocinergic neuropathways (35)(36)(37)(38)(39)(40).…”

Tracking Social Motivation Systems Deficits: The Affective Neuroscience View of Autism

“…: ''I tend to think about losing loved ones often''). These inter-personal situations may not be particularly distressing for individuals with ASD who do not appear to place as much emphasis on the concern for others (Chevallier et al 2012c;Grove et al 2013;Kohls et al 2012). Interestingly, ASD participants AQ scores were positively associated with BDI-13 scores (r = 0.59, p \ 0.006) but not with SADNESS scores (see Table 3), which is consistent with the suggestion that dysphoric affects emerge secondarily to ASD (Schultz 2005).…”

Investigating emotional impairments in adults with autism spectrum disorders and the broader autism phenotype

“…As the Chapman anhedonia scales tend to contain items relevant to both constructs (their elaboration predate the determination of the neural circuitry of reward responsiveness), our study does not inform the question of whether those with ASD have only poor hedonic experience, or motivation, or both. This is a topic that has recently received increased attention in ASD (e.g., see Kohls et al, 2012), and future studies using instruments that carefully distinguish between these deficits (such as the Clinical Assessment Interview for Negative Symptoms scale; Horan et al, 2011) are needed.…”