Theory of mind in autism, schizophrenia, and in-between

2008 ◽  
Vol 31 (3) ◽  
pp. 261-262 ◽  
Author(s):  
Ahmad Abu-Akel

AbstractAutism and schizophrenia are presented as the extremes of disorders affecting the social brain. By viewing human cognition impairment in terms of competence and performance, a variety of social brain disorders can be identified along the autistic-psychotic continuum.

To understand who we are and why we are, we need to understand both modern humans and the ancestral stages that brought us to this point. The core to that story has been the role of evolving cognition — the social brain — in mediating the changes in behaviour that we see in the archaeological record. This volume brings together two powerful approaches — the social brain hypothesis and the concept of the distributed mind. The volume compares perspectives on these two approaches from a range of disciplines, including archaeology, psychology, philosophy, sociology and the cognitive and evolutionary sciences. A particular focus is on the role that material culture plays as a scaffold for distributed cognition, and how almost three million years of artefact and tool use provides the data for tracing key changes in areas such as language, technology, kinship, music, social networks and the politics of local, everyday interaction in small-world societies. A second focus is on how, during the course of hominin evolution, increasingly large spatially distributed communities created stresses that threatened social cohesion. This volume offers the possibility of new insights into the evolution of human cognition and social lives that will further our understanding of the relationship between mind and world.


2018 ◽  
Vol 56 (1) ◽  
pp. 234-264 ◽  
Author(s):  
Carlos Alós-Ferrer

Social neuroscience studies the “social brain,” conceived as the set of brain structures and functions supporting the perception and evaluation of the social environment. This article provides an overview of the field, using the book Social Neuroscience: Brain, Mind, and Society (Russell K. Schutt, Larry J. Seidman, and Matcheri S. Keshavan, editors) as a starting point. Topics include the evolution of the social brain, the concept of “theory of mind,” the relevant brain networks, and documented failures of the social brain. I argue that social neuroscience and economics can greatly benefit from each other because the social brain underlies interpersonal decision making, as studied in economics. (JEL D11, D71, D87, Z13)


2013 ◽  
Vol 13 (1) ◽  
pp. 104-117 ◽  
Author(s):  
A. K. Martin ◽  
G. Robinson ◽  
I. Dzafic ◽  
D. Reutens ◽  
B. Mowry

2007 ◽  
Vol 21 (4/5) ◽  
pp. 353-367 ◽  
Author(s):  
Jeffrey Braithwaite ◽  
Rick A. Iedema ◽  
Christine Jorm

Author(s):  
Robin I. M. Dunbar

Primate societies are unusually complex compared to those of other animals, and the need to manage such complexity is the main explanation for the fact that primates have unusually large brains. Primate sociality is based on bonded relationships that underpin coalitions, which in turn are designed to buffer individuals against the social stresses of living in large, stable groups. This is reflected in a correlation between social group size and neocortex size in primates (but not other species of animals), commonly known as the social brain hypothesis, although this relationship itself is the outcome of an underlying relationship between brain size and behavioral complexity. The relationship between brain size and group size is mediated, in humans at least, by mentalizing skills. Neuropsychologically, these are all associated with the size of units within the theory of mind network (linking prefrontal cortex and temporal lobe units). In addition, primate sociality involves a dual-process mechanism whereby the endorphin system provides a psychopharmacological platform off which the cognitive component is then built. This article considers the implications of these findings for the evolution of human cognition over the course of hominin evolution.


Reading Minds ◽  
2020 ◽  
pp. 113-123
Author(s):  
Henry M. Wellman

This chapter examines how children’s theory of mind springs from their social brains. Neuroscience shows that adults have a theory-of-mind neural network. Children’s developing theory of mind uses some of the same neural regions that are used by adults. But, it also shows considerable neural change over time. Theory of mind is a deeply developmental achievement, driven by experience and learning. Because the brain is plastic, that experience and learning also shape the structure and functioning of the brain. We experience and learn new things, and the brain changes in response. Indeed, theory-of-mind understandings and theory-of-mind brain activations change throughout childhood, together, step by step. There is no simple brain-tells-all story. Mind reading is learned; the social brain is a product of learning as well.


2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Sarah I Mossad ◽  
Marlee M Vandewouw ◽  
Mary Lou Smith ◽  
Margot J Taylor

Abstract Neurodevelopmental difficulties emerge in very preterm born children (<32-week gestation) in infancy and continue to early adulthood but little is known about their social-cognitive development. This study utilized the complementary methodological advantages of both functional MRI and magnetoencephalography to examine the neural underpinnings of Theory of Mind in very preterm birth. Theory of Mind, one of the core social-cognitive skills, is the ability to attribute mental states to others, and is crucial for predicting others’ behaviours in social interactions. Eighty-three children (40 very preterm born, 24 boys, age = 8.7 ± 0.5 years, and 43 full-term born, 22 boys, age = 8.6 ± 0.5 years) completed the study. In functional MRI, both groups recruited classic Theory of Mind areas, without significant group differences. However, reduced Theory of Mind connectivity in the very preterm born group was found in magnetoencephalography in distinct theta, alpha and beta-band networks anchored in a set of brain regions that comprise the social brain. These networks included regions such as the angular gyrus, the medial pre-frontal cortex, the superior temporal gyrus and the temporal poles. Very preterm born children showed increased connectivity compared to controls in a network anchored in the occipital gyri rather than classical social-processing regions. Very preterm born children made significantly more attribution errors and mis-construed the social scenarios. Findings offer novel insight into the neural networks, supporting social cognition in very preterm born children and highlight the importance of multimodal neuroimaging to interrogate the social brain in clinical populations.


2008 ◽  
Vol 31 (3) ◽  
pp. 241-261 ◽  
Author(s):  
Bernard Crespi ◽  
Christopher Badcock

AbstractAutistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum.;>We propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions.


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