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Research Review: Constraining heterogeneity: the social brain and its development in autism spectrum disorder

Pelphrey, Kevin A. ; Shultz, Sarah ; Hudac, Caitlin M. ; Vander Wyk, Brent C.

Journal of child psychology and psychiatry, 2011-06, Vol.52 (6), p.631-644 [Periódico revisado por pares]

Oxford, UK: Blackwell Publishing Ltd

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Título:
Research Review: Constraining heterogeneity: the social brain and its development in autism spectrum disorder
Autor: Pelphrey, Kevin A. ; Shultz, Sarah ; Hudac, Caitlin M. ; Vander Wyk, Brent C.
Assuntos: Amygdala - physiopathology ; Autism ; Autism Spectrum Disorders ; Brain ; Brain - physiopathology ; Brain Hemisphere Functions ; Brain Mapping ; Child ; Child development ; Child Development Disorders, Pervasive - diagnosis ; Child Development Disorders, Pervasive - genetics ; Child Development Disorders, Pervasive - physiopathology ; Child Development Disorders, Pervasive - psychology ; Cognitive Processes ; Communication Strategies ; Diagnostic Tests ; Emotions - physiology ; Endophenotypes ; Facial Expression ; Female ; functional neuroimaging ; Genetic Predisposition to Disease - genetics ; Genetics ; Humans ; Information Processing ; Intention ; Interpersonal Competence ; Longitudinal Studies ; Magnetic Resonance Imaging ; Male ; Medical imaging ; Nerve Net - physiopathology ; Neurology ; Pattern Recognition, Visual - physiology ; Personal Construct Theory ; Pervasive Developmental Disorders ; social brain ; social cognition ; Social Life ; Social perception ; Social skills ; Socialization ; Temporal Lobe - physiopathology ; Theory of Mind ; Young Children
É parte de: Journal of child psychology and psychiatry, 2011-06, Vol.52 (6), p.631-644
Notas: istex:7E3EF04D2CB46B207A820A8019755C840AE0C0CF
ArticleID:JCPP2349
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Conflict of interest statement: No conflicts declared.
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Descrição: The expression of autism spectrum disorder (ASD) is highly heterogeneous, owing to the complex interactions between genes, the brain, and behavior throughout development. Here we present a model of ASD that implicates an early and initial failure to develop the specialized functions of one or more of the set of neuroanatomical structures involved in social information processing (i.e., the ‘social brain’). From this early and primary disruption, abnormal brain development is canalized because the individual with an ASD must develop in a highly social world without the specialized neural systems that would ordinarily allow him or her to partake in the fabric of social life, which is woven from the thread of opportunities for social reciprocity and the tools of social engagement. This brain canalization gives rise to other characteristic behavioral deficits in ASD including deficits in communication, restricted interests, and repetitive behaviors. We propose that focused efforts to explore the brain mechanisms underlying the core, pathognomic deficits in the development of mechanisms for social engagement in ASD will greatly elucidate our understanding and treatment of this complex, devastating family of neurodevelopmental disorders. In particular, developmental studies (i.e., longitudinal studies of young children with and without ASD, as well as infants at increased risk for being identified with ASD) of the neural circuitry supporting key aspects of social information processing are likely to provide important insights into the underlying components of the full‐syndrome of ASD. These studies could also contribute to the identification of developmental brain endophenotypes to facilitate genetic studies. The potential for this kind of approach is illustrated via examples of functional neuroimaging research from our own laboratory implicating the posterior superior temporal sulcus (STS) as a key player in the set of neural structures giving rise to ASD.
Editor: Oxford, UK: Blackwell Publishing Ltd
Idioma: Inglês

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Research Review: Constraining heterogeneity: the social brain and its development in autism spectrum disorder

Pelphrey, Kevin A. ; Shultz, Sarah ; Hudac, Caitlin M. ; Vander Wyk, Brent C.

Oxford, UK: Blackwell Publishing Ltd

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