Social deficits in autism spectrum disorder: A perspective from the social motivation theory

Impairment in social motivation (SM) has been suggested as a key mechanism underlying social communication deficits observed in autism spectrum disorder (ASD). However, the factors accounting for variability in SM remain poorly described and understood. The current study aimed to characterize the relationship between parental and proband SM. Data from 2,759 children with ASD (Mage = 9.03 years, SDage = 3.57, 375 females) and their parents from the Simons Simplex Collection (SSC) project was included in this study. Parental and proband SM was assessed using previously identified item sets from the Social Responsiveness Scale (SRS). Children who had parents with low SM scores (less impairments) showed significantly lower impairments in SM compared to children who had either one or both parents with elevated SM scores. No parent-of-origin effect was identified. No significant interactions were found involving proband sex or intellectual disability (ID) status (presence/absence of ID) with paternal or maternal SM. This study establishes that low SM in children with ASD may be driven, in part, by lower SM in one or both parents. Future investigations should utilize larger family pedigrees, including simplex and multiplex families, evaluate other measures of SM, and include other related, yet distinct constructs, such as social inhibition and anhedonia. This will help to gain finer-grained insights into the factors and mechanisms accounting for individual differences in sociability among typically developing children as well as those with, or at risk, for developing ASD.

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Social Behavior and Characteristics of Autism Spectrum Disorder in Angelman, Cornelia de Lange, and Cri du Chat Syndromes

American Journal on Intellectual and Developmental Disabilities ◽

10.1352/1944-7558-118.4.262 ◽

2013 ◽

Vol 118 (4) ◽

pp. 262-283 ◽

Cited By ~ 26

Author(s):

Joanna Moss ◽

Patricia Howlin ◽

Richard Patrick Hastings ◽

Sarah Beaumont ◽

Gemma M. Griffith ◽

...

Keyword(s):

Autism Spectrum Disorder ◽

Social Behavior ◽

Social Communication ◽

Social Motivation ◽

Autism Spectrum ◽

Spectrum Disorder ◽

Genetic Syndromes ◽

The Social ◽

Cornelia De Lange ◽

Behavior Profiles

Abstract We evaluated autism spectrum disorder (ASD) characteristics and social behavior in Angelman (AS; n = 19; mean age = 10.35 years), Cornelia de Lange (CdLS; n = 15; mean age = 12.40 years), and Cri du Chat (CdCS, also known as 5 p-syndrome; n = 19; mean age = 8.80 years) syndromes. The proportion of individuals meeting the ASD cutoff on the Social Communication Questionnaire was significantly higher in the AS and CdLS groups than in the CdCS group (p < .01). The groups demonstrated divergent social behavior profiles during social conditions in which adult availability, adult familiarity, and social demand were manipulated. Social enjoyment was significantly heightened in AS, whereas social approaches were heightened in individuals with CdCS. Social motivation, social communication, and enjoyment were significantly lower in CdLS. The findings highlight the importance of detailed observation when evaluating ASD and social behavior in genetic syndromes.

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The mirror neuron system compensates for amygdala dysfunction-associated social deficits in individuals with higher autistic traits

10.1101/2021.05.17.444574 ◽

2021 ◽

Author(s):

Lei Xu ◽

Xiaoxiao Zheng ◽

Shuxia Yao ◽

Jialin Li ◽

Meina Fu ◽

...

Keyword(s):

Autism Spectrum Disorder ◽

Mirror Neuron System ◽

Mirror Neuron ◽

Autistic Traits ◽

Autism Spectrum ◽

Spectrum Disorder ◽

Social Deficits ◽

Neuron System ◽

Therapeutic Benefits ◽

The Social

The amygdala is a core node in the social brain which exhibits structural and functional abnormalities in Autism spectrum disorder and there is evidence that the mirror neuron system (MNS) can functionally compensate for impaired emotion processing following amygdala lesions. In the current study, we employed an fMRI paradigm in 241 subjects investigating MNS and amygdala responses to observation, imagination and imitation of dynamic facial expressions and whether these differed in individuals with higher as opposed to lower autistic traits. Results indicated that individuals with higher compared to lower autistic traits showed reduced left amygdala responses to imitation and enhanced responses in the left superior temporal sulcus (STS) of the MNS to observation, imagination and imitation. Additionally, functional connectivity between the left amygdala and the left STS as well as some other MNS regions was increased in individuals with higher autistic traits, especially during imitation of fearful expressions. The amygdala-MNS connectivity significantly moderated autistic group differences on recognition memory for fearful faces and real-life social network indices, indicating that increased amygdala-MNS connectivity could diminish the social behavioral differences between higher and lower autistic trait groups. Overall, findings demonstrate decreased imitation-related amygdala activity in individuals with higher autistic traits in the context of increased cortical MNS activity and amygdala-MNS connectivity which may functionally compensate for amygdala dysfunction and social deficits. Training targeting the MNS may capitalize on this compensatory mechanism for therapeutic benefits in Autism spectrum disorder.

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The Dopamine Hypothesis of Autism Spectrum Disorder Revisited: Current Status and Future Prospects

Developmental Neuroscience ◽

10.1159/000515751 ◽

2021 ◽

pp. 1-11

Author(s):

Denis Pavăl ◽

Ioana Valentina Micluția

Keyword(s):

Autism Spectrum Disorder ◽

Dopaminergic System ◽

Autism Spectrum ◽

Spectrum Disorder ◽

Current Status ◽

Social Deficits ◽

Future Prospects ◽

Autistic Behavior ◽

Stereotyped Behaviors ◽

Dopamine Hypothesis

Autism spectrum disorder (ASD) comprises a group of neurodevelopmental disorders characterized by social deficits and stereotyped behaviors. Despite intensive research, its etiopathogenesis remains largely unclear. Although studies consistently reported dopaminergic anomalies, a coherent dopaminergic model of ASD was lacking until recently. In 2017, we provided a theoretical framework for a “dopamine hypothesis of ASD” which proposed that autistic behavior arises from a dysfunctional midbrain dopaminergic system. Namely, we hypothesized that malfunction of 2 critical circuits originating in the midbrain, that is, the mesocorticolimbic and nigrostriatal pathways, generates the core behavioral features of ASD. Moreover, we provided key predictions of our model along with testing means. Since then, a notable number of studies referenced our work and numerous others provided support for our model. To account for these developments, we review all these recent data and discuss their implications. Furthermore, in the light of these new insights, we further refine and reconceptualize our model, debating on the possibility that various etiologies of ASD converge upon a dysfunctional midbrain dopaminergic system. In addition, we discuss future prospects, providing new means of testing our hypothesis, as well as its limitations. Along these lines, we aimed to provide a model which, if confirmed, could provide a better understanding of the etiopathogenesis of ASD along with new therapeutic strategies.

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Structural neuroimaging correlates of social deficits are similar in autism spectrum disorder and attention-deficit/hyperactivity disorder: analysis from the POND Network

Translational Psychiatry ◽

10.1038/s41398-019-0382-0 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 16

Author(s):

Danielle A. Baribeau ◽

Annie Dupuis ◽

Tara A. Paton ◽

Christopher Hammill ◽

Stephen W. Scherer ◽

...

Keyword(s):

Autism Spectrum Disorder ◽

Attention Deficit Hyperactivity Disorder ◽

Attention Deficit ◽

Autism Spectrum ◽

Spectrum Disorder ◽

Social Deficits ◽

Structural Neuroimaging ◽

Hyperactivity Disorder

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Renaming schizophrenia: 5 × 5

Epidemiology and Psychiatric Sciences ◽

10.1017/s2045796018000586 ◽

2018 ◽

Vol 28 (03) ◽

pp. 254-257 ◽

Cited By ~ 5

Author(s):

Sinan Guloksuz ◽

Jim van Os

Keyword(s):

Mental Health ◽

Autism Spectrum Disorder ◽

Well Being ◽

Autism Spectrum ◽

Spectrum Disorder ◽

Evidence Based ◽

Long Run ◽

The Social ◽

Technical Features ◽

In The Beginning

AbstractThere had been a long way to go before we felt comfortable about even discussing the issues revolving around the concept of ‘schizophrenia’, let alone reckoning on mere semantic revision. In this editorial, we aim to extend our discussion on the reasons behind the slow death of the concept of ‘schizophrenia’ and the benefits of changing the name and embracing a spectrum approach with an umbrella psychosis spectrum disorder (PSD) category (similar to autism spectrum disorder) that goes further than a mere semantic revision. We attempted to cover the topic of the renaming by providing five most pertinent points categorised under five domains: reasons, signals, challenges, promises and steps for the change. Admittedly, even a modest revision, such as classifying all psychotic disorder categories under an umbrella category of PSD, and abolishing the term schizophrenia requires careful deliberation and some effort in the beginning, but the revision is well worth the effort considering the benefits in the long run. Renaming a particular form of mental suffering should be accompanied by a broader debate of the entire diagnosis-evidence-based-practice (EBP)-symptom-reduction model as the normative factor driving the content and organisation of mental health services that may be detached from patients’ needs and reality, overlooks the trans-syndromal structure of mental difficulties, appraises the significance of the technical features over the relational and ritual components of care, and underestimates the lack of EBP group-to-individual generalisability. Individuals may make great strides in attaining well-being by accommodating to living with mental vulnerabilities through building resilience in the social and existential domains. Changing the name and the concept of ‘schizophrenia’, which goes beyond a mere semantic revision, may become the first step that allows catalysation of the process of modernising psychiatric science and services worldwide.

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Lexical Development in Young Children With Autism Spectrum Disorder (ASD): How ASD May Affect Intake From the Input

Journal of Speech Language and Hearing Research ◽

10.1044/2018_jslhr-l-rsaut-18-0024 ◽

2018 ◽

Vol 61 (11) ◽

pp. 2659-2672 ◽

Cited By ~ 5

Author(s):

Sudha Arunachalam ◽

Rhiannon J. Luyster

Keyword(s):

Autism Spectrum Disorder ◽

Social Communication ◽

Children With Autism ◽

Autism Spectrum ◽

Lexical Representation ◽

Spectrum Disorder ◽

Learning Situation ◽

Lexical Development ◽

The Social ◽

Processing Demands

Purpose Most children with autism spectrum disorder (ASD) have below-age lexical knowledge and lexical representation. Our goal is to examine ways in which difficulties with social communication and language processing that are often associated with ASD may constrain these children's abilities to learn new words and to explore whether minimizing the social communication and processing demands of the learning situation can lead to successful learning. Method In this narrative review of recent work on lexical development in ASD, we describe key findings on children's acquisition of nouns, pronouns, and verbs and outline our research program currently in progress aimed at further elucidating these issues. Conclusion Our review of studies that examine lexical development in children with ASD suggests that innovative intervention approaches that take into account both the social communication and processing demands of the learning situation may be particularly beneficial. Presentation Video https://doi.org/10.23641/asha.7324013

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Prenatal Risk for Autism Spectrum Disorder (ASD): Fetal Cortisol Exposure Predicts Child ASD Symptoms

Clinical Psychological Science ◽

10.1177/2167702618811079 ◽

2018 ◽

Vol 7 (2) ◽

pp. 349-361 ◽

Cited By ~ 1

Author(s):

Sheena Ram ◽

Mariann A. Howland ◽

Curt A. Sandman ◽

Elysia Poggi Davis ◽

Laura M. Glynn

Keyword(s):

Autism Spectrum Disorder ◽

Developmental Disorder ◽

Maternal Plasma ◽

Autism Spectrum ◽

Spectrum Disorder ◽

Sexually Dimorphic ◽

Fetal Exposure ◽

Prospective Longitudinal Study ◽

The Social ◽

Prospective Longitudinal

The etiology of autism spectrum disorder (ASD) is multifactorial, complex, and likely involves interactions among genetic, epigenetic, and environmental factors. With respect to environmental influences, a growing literature implicates intrauterine experiences in the origin of this pervasive developmental disorder. In this prospective longitudinal study, we examined the hypothesis that fetal exposure to maternal cortisol may confer ASD risk. In addition, because ASD is four times more prevalent in males than in females, and because sexually dimorphic responses to intrauterine experiences are commonly observed, we examined whether or not any associations differ by fetal sex. Maternal plasma cortisol was measured at 15, 19, 25, 31, and 37 weeks’ gestation in a sample of 84 pregnant women. ASD symptoms were assessed in their 5-year-old children with the Social Communication Questionnaire (SCQ). Fetal exposure to lower levels of maternal cortisol was associated with higher levels of ASD symptoms only among boys. The observed hypocortisolemic profile exhibited by these mothers may indicate a risk factor that precedes the stress of caregiving for a child with ASD and may not be solely a consequence of the stress of caregiving, as previously thought. These findings confirm the value of examining prenatal hormone exposures as predictors of ASD risk and support the premise that altered prenatal steroid exposures may play a role in the etiology of ASD.

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