Attribution and social cognitive neuroscience: a new approach for the "online-assessment" of causality ascriptions and their emotional consequences

Attribution theory plays a central role in understanding cognitive processes that have emotional consequences; however, there has been very limited attention to its neural basis. After reviewing classical studies in social psychology in which attribution has been experimentally manipulated we developed a new approach that allows the investigation of state attributions and emotional consequences using neuroscience methodologies. Participants responded to the Erikson Flanker Task, but, in order to maintain the participant's beliefs about the nature of the task and to produce a significant number of error responses, an adaptive algorithm tuned the available time to respond such that, dependent on the subject's current performance, the negative feedback rate was held at chance level. In order to initiate variation in attribution participants were informed that one and the same task was either easy or difficult. As a result of these two different instructions the two groups differed significantly in error attribution only on the locus of causality dimension. Additionally, attributions were found to be stable over a large number of trials, while accuracy and reaction time remained the same. Thus, the new paradigm is particularly suitable for cognitive neuroscience research that evaluates brain behaviour relationships of higher order processes in ‘simulated achievement settings’.     

Toward socially inspired social neuroscience

Social neuroscience, often viewed as studying the neural foundations of social cognition, has roots in multiple disciplines. This paper argues that it needs a firmer base in social psychology. First, we outline some major opportunities from social psychology--the power of social context and social motives in shaping human behavior. Second, as the social cognition field moves away from studying only deliberate, explicit processes to studying also automatic, implicit processes, adopting a dual-process perspective, social neuroscience also lends itself to both automatic and controlled processes. Finally, social neuroscience is especially suited to study the efficiency and spontaneity of social judgments. All this brings social behavioral grounding to cognitive neuroscience. Among the implications for social neuroscience: Social cognition intrinsically evokes affect, so social cognitive affective neuroscience glues together a variety of fields in psychological and neurosciences.     

Social neuroscience: The social brain,oxytocin, and health

Complex social behaviors allow various social organisms to create emergent organizations that extend beyond the individual. Social neuroscience is a burgeoning field that strives to understand the genetic, hormonal, and neural mechanisms responsible for these social structures and behaviors. Consequently, social neuroscience is highly interdisciplinary in nature and embraces the application of methods ranging from the molecular to the molar to investigate the reciprocal interactions between biological, cognitive, and social levels of analysis. The broad scope of such an endeavor introduces particular challenges associated with the integration of multiple levels of analysis. In the present mini-review, we highlight some recent findings in the field of social neuroscience and demonstrate the potential benefits of applying multilevel integrative analysis to the study of social behavior and its influence on physiology and health.     

Finding faults: How moral dilemmas illuminate cognitive structure

Philosophy is rife with intractable moral dilemmas. We propose that these debates often exist because competing psychological systems yield different answers to the same problem. Consequently, philosophical debate points to the natural fault lines between dissociable psychological mechanisms, and as such provides a useful guide for cognitive neuroscience. We present two case studies from recent research into moral judgment: dilemmas concerning whether to harm a person in order to save several others, and whether to punish individuals for harms caused accidentally. Finally, we analyze two features of mental conflict that apparently contribute to philosophical discord: the insistence that one answer to a problem must be correct (“non-negotiability”) and the absence of an independent means of determining the correct answer (“non-adjudicability”). Fiery Cushman thanks the Mind/Brain/Behavior Initiative for its generous support during the preparation of this work.      

Gaining insight into adolescent vulnerability for social anxiety from developmental cognitive neuroscience

Social anxiety disorder (SAD) markedly impairs daily functioning. For adolescents, SAD can constrain typical development precisely when social experiences broaden, peers’ opinions are highly salient, and social approval is actively sought. Individuals with extreme, impairing social anxiety fear evaluation from others, avoid social interactions, and interpret ambiguous social cues as threatening. Yet some degree of social anxiety can be normative and non-impairing. Furthermore, a temperament of behavioral inhibition increases risk for SAD for some, but not all adolescents with this temperament. One fruitful approach taken to understand the mechanisms of social anxiety has been to use neuroimaging to link affect and cognition with neural networks implicated in the neurodevelopmental social reorientation of adolescence. Although initial neuroimaging studies of adolescent SAD and risk for SAD underscored the role of fear-processing circuits (e.g., the amygdala and ventral prefrontal cortex), recent work has expanded these circuits to include reward-processing structures in the basal ganglia. A growing focus on reward-related neural circuitry holds promise for innovative translational research needed to differentiate impairing from normative social anxiety and for novel ways to treat adolescent SAD that focus on both social avoidance and social approach.     

Orienting to social stimuli differentiates social cognitive impairment in autism and schizophrenia

Both autism and schizophrenia feature deficits in aspects of social cognition that may be related to amygdala dysfunction, but it is unclear whether these are similar or different patterns of impairment. We compared the visual scanning patterns and emotion judgments of individuals with autism, individuals with schizophrenia and controls on a task well characterized with respect to amygdala functioning. On this task, eye movements of participants are recorded as they assess emotional content within a series of complex social scenes where faces are either included or digitally erased. Results indicated marked abnormalities in visual scanning for both disorders. Controls increased their gaze on face regions when faces were present to a significantly greater degree than both the autism or schizophrenia groups. While the control and the schizophrenia groups oriented to face regions faster when faces were present compared to when they were absent, the autism group oriented at the same rate in both conditions. The schizophrenia group, meanwhile, exhibited a delay in orienting to face regions across both conditions, although whether anti-psychotic medication contributed to this effect is unclear. These findings suggest that while processing emotional information in social scenes, both individuals with autism and individuals with schizophrenia fixate faces less than controls, although only those with autism fail to orient to faces more rapidly based on the presence of facial information. Autism and schizophrenia may therefore share an abnormality in utilizing facial information for assessing emotional content in social scenes, but differ in the ability to seek out socially relevant cues from complex stimuli. Impairments in social orienting are discussed within the context of evidence suggesting the role of the amygdala in orienting to emotionally meaningful information.     

Efficacy and specificity of social cognitive skills training for outpatients with psychotic disorders

Psychosocial interventions that target social cognition show promise for enhancing the functional outcomes of people with psychotic disorders. This randomized controlled trial evaluated the efficacy and treatment-outcome specificity of a 24-session Social Cognitive Skills Training (SCST) that targets emotional processing, social perception, attributional bias, and mentalizing (or Theory of Mind). Sixty-eight stable outpatients with primary psychotic disorders were randomly assigned to one of four time- and group format-matched treatment conditions: (1) SCST, (2) computerized neurocognitive remediation, (3) standard illness management skills training, or (4) a Hybrid treatment that combined elements of SCST and neurocognitive remediation. The SCST group demonstrated greater improvements over time than comparison groups in the social cognitive domain of emotional processing, including improvement on measures of facial affect perception and emotion management. There were no differential benefits among treatment conditions on neurocognitive or clinical symptom changes over time. Results indicate that a targeted social cognitive intervention led to improvements in social cognition among outpatients with psychosis. Findings provide guidance for continued efforts to maximize the benefits of social cognitive interventions.     

Computational approaches to the neuroscience of social perception

Across multiple domains of social perception—including social categorization, emotion perception, impression formation and mentalizing—multivariate pattern analysis (MVPA) of functional magnetic resonance imaging (fMRI) data has permitted a more detailed understanding of how social information is processed and represented in the brain. As in other neuroimaging fields, the neuroscientific study of social perception initially relied on broad structure–function associations derived from univariate fMRI analysis to map neural regions involved in these processes. In this review, we trace the ways that social neuroscience studies using MVPA have built on these neuroanatomical associations to better characterize the computational relevance of different brain regions, and discuss how MVPA allows explicit tests of the correspondence between psychological models and the neural representation of social information. We also describe current and future advances in methodological approaches to multivariate fMRI data and their theoretical value for the neuroscience of social perception.     

The relationship of social cognition to ward behavior in chronic schizophrenia

The relationship between social cognition (i.e., cognition for social stimuli) and ward behavior among individuals with chronic schizophrenia was investigated. Twenty-seven inpatients completed a battery of cognitive and social-cognitive tasks and were rated by staff on various indices of ward behavior. Overall, there was a relationship between the measures of social cognition and behavior on the ward. Social cognition contributed unique variance beyond cognition to maladaptive behavior on the ward (i.e., irritability). Implications for assessemnt and future research are discussed.     

Do patients with high-functioning autism have similar social cognitive deficits as patients with a chronic cause of schizophrenia?

Objective: There is substantial evidence that both patients with schizophrenia and patients with autism spectrum disorders (ASD) have impaired social cognition including theory of mind (ToM) deficits. However, it remains unclear if both verbal (explicit) and non-verbal (implicit) ToM as well as social perception are similarly affected in both disorders.

Methods: Twenty-one patients diagnosed with schizophrenia and 11 patients diagnosed with ASD were matched one-to-one to healthy controls based on gender, age, and educational level. Social functioning was measured by Personal and Social Performance (PSP) scale. Neurocognition was measured using Brief Assessment of Cognition in Schizophrenia (BACS-DK), and four subtests from Wechsler Adult Intelligence (WAIS-IV) scale were applied to estimate IQ. The Animated Triangles Task was used to measure implicit ToM, while explicit ToM and social perception were measured by The Awareness and Social Inference Test (TASIT).

Results: Patients with schizophrenia had deficits in implicit ToM and complex social perception compared to their matched controls, but no problems with explicit ToM. Surprisingly, patients with ASD solely had deficits with regard to complex social perception compared to their matched controls. The two patient groups were similar regarding estimated IQ, social functioning and years of education, but differed in age and neurocognition. When adjusting the p-values for age and neurocognitive deficits, both patients groups had similar social cognitive deficits.

Conclusions: Results imply that we compared schizophrenia patients with substantial neurocognitive deficits to a group of high-functioning patients with ASD. However, these two subgroups may have the same level of social cognitive deficits.     

Anthropology in the cognitive sciences: the value of diversity

Beller, Bender, and Medin (this issue) offer a provocative proposal outlining several reasons why anthropology and the rest of cognitive science might consider parting ways. Among those reasons, they suggest that separation might maintain the diversity needed to address larger problems facing humanity, and that the research strategies used across the disciplines are already so diverse as to be incommensurate. The present paper challenges the view that research strategies are incommensurate and offers a multimethod approach to cultural research that can help to establish common ground while maintaining diversity.     

Theory of mind ability in the behavioural variant of frontotemporal dementia: An analysis of the neural, cognitive, and social levels

The paper reviews convergent evidence on the ability to attribute mental states to one's self and to others (i.e., theory of mind, ToM) in patients affected by the behavioural variant of frontotemporal dementia (bv-FTD). This disease represents a particular challenge for researchers and clinicians, due to its insidious onset and ambiguous clinical features, which frequently render difficult a precise and timely diagnosis. The paper proposes a way to shed new light on the hypothesis that the neuropsychiatric profile of individuals with bv-FTD can be at least partially explained by a deficit in ToM ability. We examined both neuroimaging data on the neural correlates of ToM ability in healthy participants and studies investigating the progressive cerebral atrophy in patients with bv-FTD. Our findings suggest a link between the progressive degeneration of the anterior regions of medial frontal structures characterising the early stages of the bv-FTD and the ToM deficit these patients show. They also suggest the importance of using ToM tests during the diagnostic process of bv-FTD.     

Assessment of social judgments and complex mental states in the early phases of psychosis

OBJECTIVES: Social cognition plays an important role in the functioning of individuals with psychosis. In this study, we explored two areas of social cognition not previously investigated early in the course of psychosis. METHOD: Eighty-eight clinical high risk participants, 26 participants diagnosed with schizophrenia for less than 5 years, and 41 non-clinical control participants completed two measures of social cognition. RESULTS: Clinical high risk participants demonstrated biased responses to untrustworthy faces compared to both of the other groups. Early schizophrenia participants performed more poorly on an advanced theory of mind task compared to the clinical high risk and control groups. CONCLUSIONS: There are different patterns of performance on social cognitive tasks in these groups, which require further examination in longitudinal studies.     

Cognition in people with Prader-Willi syndrome: Insights into genetic influences on cognitive and social development

We present a mini-review of cognition in Prader-Willi syndrome. Studies cited include findings on general ability (IQ), IQ correlates with family members, strengths and weaknesses in cognitive profiles in genetic subtypes, attainment in literacy and numeracy, language, comprehension, modality preferences, executive functions, and social cognition. The latter includes investigations of theory of mind, emotion recognition, face processing and knowledge of social norms. Results from research on mouse models and brain imaging studies relevant to cognition are briefly discussed.The importance of these studies to understanding and managing education and behaviour in PWS and the limitations of the studies in terms of small numbers, non-representativeness, and lack of replication is also touched upon.     

Introduction: Philosophy in and Philosophy of Cognitive Science

Despite being there from the beginning, philosophical approaches have never had a settled place in cognitive research and few cognitive researchers not trained in philosophy have a clear sense of what its role has been or should be. We distinguish philosophy in cognitive research and philosophy of cognitive research. Concerning philosophy in cognitive research, after exploring some standard reactions to this work by nonphilosophers, we will pay particular attention to the methods that philosophers use. Being neither experimental nor computational, they can leave others bewildered. Thought experiments are the most striking example but not the only one. Concerning philosophy of cognitive research, we will pay particular attention to its power to generate and test normative claims, claims about what should and should not be done.     

Sensorimotor mu rhythm during action observation changes across the lifespan independently from social cognitive processes

The observation of actions performed by another person activates parts of the brain as if the observer were performing that action, referred to as the ‘mirror system’. Very little is currently known about the developmental trajectory of the mirror system and related social cognitive processes. This experimental study sought to explore the modulation of the sensorimotor mu rhythm during action observation using EEG measures, and how these may relate to social cognitive abilities across the lifespan, from late childhood through to old age. Three-hundred and one participants aged 10- to 86-years-old completed an action observation EEG task and three additional explicit measures of social cognition. As predicted, findings show enhanced sensorimotor alpha and beta desynchronization during hand action observation as compared to static hand observation. Overall, our findings indicate that the reactivity of the sensorimotor mu rhythm to the observation of others’ actions increases throughout the lifespan, independently from social cognitive processes.     

The benefit of directly comparing autism and schizophrenia for revealing mechanisms of social cognitive impairment

Autism and schizophrenia share a history of diagnostic conflation that was not definitively resolved until the publication of the DSM-III in 1980. Though now recognized as heterogeneous disorders with distinct developmental trajectories and dissociative features, much of the early nosological confusion stemmed from apparent overlap in certain areas of social dysfunction. In more recent years, separate but substantial literatures have accumulated for autism and schizophrenia demonstrating that abnormalities in social cognition directly contribute to the characteristic social deficits of both disorders. The current paper argues that direct comparison of social cognitive impairment can highlight shared and divergent mechanisms underlying pathways to social dysfunction, a process that can provide significant clinical benefit by informing the development of tailored treatment efforts. Thus, while the history of diagnostic conflation between autism and schizophrenia may have originated in similarities in social dysfunction, the goal of direct comparisons is not to conflate them once again but rather to reveal distinctions that illuminate disorder-specific mechanisms and pathways that contribute to social cognitive impairment.