Social cognition in autism. A survey of functional imaging studies

Klinik und Poliklinik für Psychiatrie und Psychotherapie, Zentrum für Nervenheilkunde der Universität Rostock, Gehlsheimer Strasse 20, 18147 Rostock.
Der Nervenarzt (Impact Factor: 0.79). 04/2008; 79(3):261-74. DOI: 10.1007/s00115-008-2409-2
Source: PubMed

ABSTRACT Autism spectrum disorders (autism, Asperger's syndrome, high-functioning autism) are characterized by a common pattern of marked impairments in social interactions. Deficits have been described in face processing, facial emotion recognition, and social attribution ("theory of mind") or generally speaking in social cognition. Some studies have shown that these impairments are already detectable in early childhood, leading to the assumption that the underlying cause is an early disruption of neuronal development. Accordingly, neuroimaging data have revealed alterations of structure and function in the brains of autistic children, adolescents, and adults. The present review gives a systematic overview of the existing literature on functional imaging studies using experimental paradigms of social cognition, i.e. face discrimination, facial emotion recognition, and theory of mind in autistic disorders.

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    • "It stands to be reasoned that such reduced or distorted input, if present during development as it may be assumed in a developmental disorder such as ASD, would have substantial effects on the shaping of capacities emerging from it. Given the behavioral evidence reviewed above, it may thus be argued that aberrant facial processing may lead to dysfunctional mechanisms for mimicry and intention understanding and ultimately deficits in complex social processes such as theory of mind, all of which have been shown to be abnormal in patients with ASD (Domes et al. 2008). Consequently and in synopsis with the earlier discussion of visual processing aberrations, we would argue that aberrant sensory (visual) processing may be a central pathophysiological aspect in ASD, whereas the clinically more prominent deficits in social processing are secondary effects of these. "
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    ABSTRACT: One of the most consistent neuropsychological findings in autism spectrum disorders (ASD) is a reduced interest in and impaired processing of human faces. We conducted an activation likelihood estimation meta-analysis on 14 functional imaging studies on neural correlates of face processing enrolling a total of 164 ASD patients. Subsequently, normative whole-brain functional connectivity maps for the identified regions of significant convergence were computed for the task-independent (resting-state) and task-dependent (co-activations) state in healthy subjects. Quantitative functional decoding was performed by reference to the BrainMap database. Finally, we examined the overlap of the delineated network with the results of a previous meta-analysis on structural abnormalities in ASD as well as with brain regions involved in human action observation/imitation. We found a single cluster in the left fusiform gyrus showing significantly reduced activation during face processing in ASD across all studies. Both task-dependent and task-independent analyses indicated significant functional connectivity of this region with the temporo-occipital and lateral occipital cortex, the inferior frontal and parietal cortices, the thalamus and the amygdala. Quantitative reverse inference then indicated an association of these regions mainly with face processing, affective processing, and language-related tasks. Moreover, we found that the cortex in the region of right area V5 displaying structural changes in ASD patients showed consistent connectivity with the region showing aberrant responses in the context of face processing. Finally, this network was also implicated in the human action observation/imitation network. In summary, our findings thus suggest a functionally and structurally disturbed network of occipital regions related primarily to face (but potentially also language) processing, which interact with inferior frontal as well as limbic regions and may be the core of aberrant face processing and reduced interest in faces in ASD.
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    ABSTRACT: Since its first use in medical literature the meaning of the term autism has constantly changed. An historical overview indicates that in both adult and child psychiatry autism was first used to refer to a symptom of schizophrenia. Later on the use of the term in child psychiatry took a different independent course, which led to present-day conceptualization of autism, mainly due to the work of Leo Kanner and Hans Asperger. Currently autism and autistic disorders are regarded as severe developmental disorders and, due to their stable nature, have gained considerable attention in adult psychiatry. In order to better understand this development, the path from onset to reception is traced via Kanner and Asperger. In the search for central characteristics of autism, one finds restrictions in social communication and interaction, which can be explained by fundamental deficits in social cognition. These restrictions in social cognition can be considered the central characteristic of autism - one which has been a constant since the phenomenon was first described. Our historical review considers to what extent experimental psychopathological research can deepen our understanding of the disorder.
    Der Nervenarzt 08/2009; 81(1):55-65. · 0.79 Impact Factor
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    ABSTRACT: Die stetig steigende Anzahl funktionell und strukturell bildgebender Studien in den letzten 2 Jahrzehnten hat maßgeblich zum Verständnis der neurobiologischen Basis von Autismusspektrumstörungen (,,autism spectrum disorders“ ASD) beigetragen. Der Artikel gibt einen Überblick über Studien zu den neuronalen Grundlagen der Symptomtrias (Störung der sozialen Interaktion und Kommunikation, repetitives und restriktives Verhalten) und zu angenommenen zugrunde liegenden neuropsychologischen Beeinträchtigungen (Theory of Mind, Exekutivfunktionen, zentrale Kohärenz), ergänzt durch konsistente Befunde zu strukturellen Veränderungen des Gehirns. Die Forschungsergebnisse zeigen, dass, obwohl kognitive Funktionen bei ASD generell durch die gleichen Gehirnareale vermittelt werden wie bei typisch entwickelten Menschen, sich das Ausmaß der Aktivierungen, vor allem aber die Aktivierungsmuster unterscheiden. Zunehmend setzt sich daher die Hypothese einer geringeren Konnektivität rekrutierter kortikaler Netzwerke gegen die Annahme durch, dass einzelne Gehirnareale betroffen sind.
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