Non-social Deficits Research Articles

Reward processing in autism spectrum disorder and psychopathy: a systematic review

AimsEmerging research suggests that aberrant reward processing may underpin much of the social dysfunction we see in psychiatric disorders. Two conditions associated with marked social dysfunction are Autism Spectrum Disorder (ASD) and Psychopathy. However, no review to date has directly contrasted reward processing in both conditions and incorporated literature on social and non-social rewards. This systematic review aims to: (i) identify and compare reward processing abnormalities in ASD and Psychopathy as demonstrated in task-based functional magnetic resonance imaging (fMRI) studies; and (ii) identify correlations between fMRI reward processing abnormalities and manifested symptoms, with a focus on those giving rise to social dysfunction.MethodThe electronic databases PubMed, PsycINFO and EMBASE were searched to identify studies satisfying the following criteria: (i) a validated measure was used to assess ASD or Psychopathy; (ii) the study was published in an English language peer review journal; (iii) the age of participants was 18 years or older; (iv) individuals participated in a reward-based experimental paradigm; and (v) the response to the reward was measure using fMRI.ResultA total of 12 articles were identified that satisfied inclusion criteria. Six studies examined reward processing in ASD and six studies examined reward processing in Psychopathy. All studies in both conditions indicated some degree of abnormal reward-related neural response. The most replicated findings were aberrant responses in the Ventral Striatum (VS). Autism Spectrum Disorder was typified by VS hypoactivation to social and non-social reward, while Psychopathy was associated with VS hyperactivation in response to non-social reward anticipation. No studies were identified of social reward in Psychopathy.ConclusionThe reported fMRI findings correlate with clinical observations in both conditions. Reduced reward response in ASD to a range of social and non-social stimuli would provide a parsimonious account of the social and non-social deficits that characterise the condition. Enhanced responses to the anticipation of reward in Psychopathy provides an account of the ruthless and destructive pursuit of reward-driven behaviours not inhibited by immoral or aversive signals. If, as the literature suggests, reward circuitry dysfunction plays a role in the development and manifestation of symptoms in both conditions, reward processing and its underlying neural circuitry may represent important targets for the development of novel treatment strategies.

Multidimensional processing in the amygdala

Brain-wide circuits that coordinate affective and social behaviours intersect in the amygdala. Consequently, amygdala lesions cause a heterogeneous array of social and non-social deficits. Social behaviours are not localized to subdivisions of the amygdala even though the inputs and outputs that carry social signals are anatomically restricted to distinct subnuclear regions. This observation may be explained by the multidimensional response properties of the component neurons. Indeed, the multitudes of circuits that converge in the amygdala enlist the same subset of neurons into different ensembles that combine social and non-social elements into high-dimensional representations. These representations may enable flexible, context-dependent social decisions. As such, multidimensional processing may operate in parallel with subcircuits of genetically identical neurons that serve specialized and functionally dissociable functions. When combined, the activity of specialized circuits may grant specificity to social behaviours, whereas multidimensional processing facilitates the flexibility and nuance needed for complex social behaviour.

Phenotypic characterization of nonsocial behavioral impairment in neurexin 1α knockout rats.

Neurexins are neuronal presynaptic proteins that play a key role in mediation of synapse formation. Heterozygous partial deletions in the neurexin-1 gene (NRXN1, 2p16.3) have been observed in autism spectrum disorder (ASD) patients. NRXN1-α knockout (KO) mice present behavioral impairments that resemble some of the core ASD symptoms of social impairment and inflexibility/stereotypy. At present, a thorough assessment of cognitive function has yet to be completed. Rats, containing a biallelic deletion of the NRNX1-α gene on a Sprague Dawley background were compared to littermate wild types across a range of tasks designed to test functional domains disrupted in ASD and other neurodevelopmental disorders, including sensory perception (prepulse inhibition), attention (latent inhibition), associative learning (instrumental and Pavlovian conditioning), and memory (rewarded alternation T maze and spatial discrimination). NRXN1α KO rats were found to present with large and persistent nonsocial deficits, including hyperactivity, deficits in simple instrumental learning, latent inhibition, and spatial-dependent learning. No deficit in sensorimotor gating was observed, despite the presence of an exaggerated startle response. Although KO animals were also able to learn a simple Pavlovian conditioning discrimination, they did display impaired latent inhibition. The presence of pronounced impairments in several domains in NRXN1α KO rats clearly suggests that nonsocial cognitive deficits can also be measured in an animal model of ASD. Further exploration of those deficits, both clinically and preclinically, as planned in the Innovative Medicines Initiative's European Autism Interventions: A Multicenter Study for Developing New Medications program, may help to better understand the brain circuitry involved in ASD and therefore open new avenues to advance novel therapies.

Social and non-social deficits in children with high-functioning autism and their cooperative behaviors

The persistent deficits in social communication and social interactions of individuals with high-functioning autism (HFA) may impair their cooperative behaviors. This study investigated the relationship between social and non-social deficits in children with HFA and the cooperative behaviors of such children. Theory of mind (ToM), executive function, and central coherence of children with HFA and typically developing (TD) children, aged 6–12 years, were investigated, and the effects of these social and non-social deficits on children's cooperativeness were examined. The classical prisoner's dilemma game (PDG) and cooperative implemental tasks were used to assess children's cooperativeness. ToM was measured using a series of classical false belief tasks and the face test. The Wisconsin Card Sorting Task (WCST) and the Embedded Figures Test (EFT) were administered to assess executive function and central coherence, respectively. The results showed that there was no significant difference in cooperation in PDG between HFA and TD children, while cooperation in children with HFA in the interruption period of the implemental tasks was significantly lower than that of TD children. Children with HFA had social deficits and had more poorly developed ToM than TD children, and executive function in children with HFA was poorer than that in TD children. Different types of deficits were predictive of HFA children's degree of cooperation on different tasks: the social perceptual component of ToM and executive function predicted children's cooperativeness in the PDG, and executive function predicted HFA children's cooperativeness during the interruption period of an implemental task. By contrast, central coherence did not predict either of the two types of cooperation. It might indicate that the two different types of cooperative tasks may require different mental abilities.