Social Cognition Network Research Articles

Part VI Introduction

Emerging research over the last decade has shown that long-term music training and skill learning can be a strong stimulator for neuroplastic changes in the developing as well as adult brain. Making music places unique demands on the nervous system, leading to strong coupling of perception and action mediated by sensory, motor, and multimodal integrative regions distributed throughout the brain. Furthermore, listening to music and making music (“musicking”) provokes motion, improves and increases between-subject communication and interaction, and is considered to be and experienced as a joyous and rewarding activity. Several reports in this volume have now shown that listening to music and musicking may have the power to make rehabilitation processes not only more enjoyable, but also possibly more effective. Why is music so special and how does listening to and making music achieve its rehabilitative effects? Music is a strong multimodal stimulus that simultaneously transmits visual, auditory, and motoric information to a specialized brain network consisting of frontotemporo-parietal regions whose components are also part of the putative human mirrorneuron system. Among other functions, this system might support the coupling between perceptual events (visual or auditory) and motor actions (leg, arm/hand, or vocal/articulatory actions). Music might be a special vehicle to engage components of this mirror-neuron system. Furthermore, music might also provide an alternative entry point into a “broken” brain system to remediate impaired neural processes or neural connections by engaging and linking up brain centers that would otherwise not be engaged or linked with each other. The chapters in this section will demonstrate several music-based experimental interventions whose effectiveness in clinical populations is demonstrated and whose underlying neurobiological mechanisms are being examined. These neurologically based music therapies are grounded in specific effects on brain networks involved in listening to and making music and on the effects of music on emotion, perception-action mediation, and social cognition networks. Using an instrument or using one’s own voice alone or within a group involves, in a unique way, a feed-forward and feedback circuit in the brain that connects sensory and motor regions. Training-induced and use-dependent plastic changes within the nodal points of these networks and in the fiber bundles connecting these regions might underlie effects that outlast the duration of the actual intervention. Nevertheless, the gold standard of proving the efficacy of an intervention will be a randomized clinical trial (RCT), in which participants are randomly assigned and a new music-based intervention is tested against a gold standard or an established intervention. Having a scientific basis for the interventions and obtaining evidence from RCTs are the most important steps in establishing neurologically based music therapies as accepted interventions. Thus, listening to and making music, including singing, if used appropriately and based on a neurobiological understanding of how music is processed in the brain and what brain regions are active in music making (“musicking”), can serve as a powerful and engaging treatment modality that can enhance brain recovery processes and neuroplasticity in general as shown in the following chapters.

Prefrontal social cognition network dysfunction underlying face encoding and social anxiety in fragile X syndrome

Individuals with fragile X syndrome (FXS) commonly display characteristics of social anxiety, including gaze aversion, increased time to initiate social interaction, and difficulty forming meaningful peer relationships. While neural correlates of face processing, an important component of social interaction, are altered in FXS, studies have not examined whether social anxiety in this population is related to higher cognitive processes, such as memory. This study aimed to determine whether the neural circuitry involved in face encoding was disrupted in individuals with FXS, and whether brain activity during face encoding was related to levels of social anxiety. A group of 11 individuals with FXS (5 M) and 11 age- and gender-matched control participants underwent fMRI scanning while performing a face encoding task with online eye-tracking. Results indicate that compared to the control group, individuals with FXS exhibited decreased activation of prefrontal regions associated with complex social cognition, including the medial and superior frontal cortex, during successful face encoding. Further, the FXS and control groups showed significantly different relationships between measures of social anxiety (including gaze-fixation) and brain activity during face encoding. These data indicate that social anxiety in FXS may be related to the inability to successfully recruit higher level social cognition regions during the initial phases of memory formation.

Social cognitive neural networks during in-group and out-group interactions

Several functionally connected networks of activity have now been identified in the resting human brain that may be amplified or attenuated by specific goal-directed tasks. However, it is not known whether there exists a particular network that becomes more active when a person is engaged in a social interaction. fMRI was used to measure brain activity in subjects as they completed a social interactive task and a non-social control task sharing many of the same features. Comparison across the two tasks revealed a network of functionally connected areas that was consistently more active in the social task. This network included default mode network areas, raising the possibility that activity previously observed in default mode regions at rest is related to social cognition. Within this network, information appears to flow from regions involved in salience detection (e.g. anterior insula) to regions involved in mentalizing (dorsomedial prefrontal cortex) to regions involved in executive control (dorsolateral prefrontal cortex). In a second experiment, subjects played the same social interactive task with alleged members of both an experimentally induced in-group and out-group. The default mode network was again active during the task, and several noteworthy differences distinguished interactions with in-group and out-group partners, providing a potential neural substrate for the human tendency to more readily identify with in-group members and more readily distrust, fear and discriminate against out-group members.

Neural bases for impaired social cognition in schizophrenia and autism spectrum disorders

Schizophrenia and autism both feature significant impairments in social cognition and social functioning, but the specificity and mechanisms of these deficits remain unknown. Recent research suggests that social cognitive deficits in both disorders may arise from dysfunctions in the neural systems that underlie social cognition. We explored the neural activation of discrete brain regions implicated in social cognitive and face processing in schizophrenia subgroups and autism spectrum disorders during complex social judgments of faces. Twelve individuals with autism spectrum disorders (ASD), 12 paranoid individuals with schizophrenia (P-SCZ), 12 non-paranoid individuals with schizophrenia (NP-SCZ), and 12 non-clinical healthy controls participated in this cross sectional study. Neural activation, as indexed by blood oxygenation level dependent (BOLD) contrast, was measured in a priori regions of interest while individuals rated faces for trustworthiness. All groups showed significant activation of a social cognitive network including the amygdala, fusiform face area (FFA), superior temporal sulcus (STS), and ventrolateral prefrontal cortex (VLPFC) while completing a task of complex social cognition (i.e. trustworthiness judgments). ASD and P-SCZ individuals showed significantly reduced neural activation in the right amygdala, FFA, and left VLPFC as compared to controls and in the left VLPFC as compared to NP-SCZ individuals during this task. These findings lend support to models hypothesizing well-defined neural substrates of social cognition and suggest a specific neural mechanism that may underlie social cognitive impairments in both autism and paranoid schizophrenia.

An Investigation of the Relationship Between Activation of a Social Cognitive Neural Network and Social Functioning

Previous work examining the neurobiological substrates of social cognition in healthy individuals has reported modulation of a social cognitive network such that increased activation of the amygdala, fusiform gyrus, and superior temporal sulcus are evident when individuals judge a face to be untrustworthy as compared with trustworthy. We examined whether this pattern would be present in individuals with schizophrenia who are known to show reduced activation within these same neural regions when processing faces. Additionally, we sought to determine how modulation of this social cognitive network may relate to social functioning. Neural activation was measured using functional magnetic resonance imaging with blood oxygenation level dependent contrast in 3 groups of individuals--nonparanoid individuals with schizophrenia, paranoid individuals with schizophrenia, and healthy controls--while they rated faces as either trustworthy or untrustworthy. Analyses of mean percent signal change extracted from a priori regions of interest demonstrated that both controls and nonparanoid individuals with schizophrenia showed greater activation of this social cognitive network when they rated a face as untrustworthy relative to trustworthy. In contrast, paranoid individuals did not show a significant difference in levels of activation based on how they rated faces. Further, greater activation of this social cognitive network to untrustworthy faces was significantly and positively correlated with social functioning. These findings indicate that impaired modulation of neural activity while processing social stimuli may underlie deficits in social cognition and social dysfunction in schizophrenia.

An Investigation of the Relationship Between Activation of a Social Cognitive Neural Network and Social Functioning

An Investigation of the Relationship Between Activation of a Social Cognitive Neural Network and Social Functioning

Anatomical Differences in the Mirror Neuron System and Social Cognition Network in Autism

Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with impaired social and emotional skills, the anatomical substrate of which is still unknown. In this study, we compared a group of 14 high-functioning ASD adults with a group of controls matched for sex, age, intelligence quotient, and handedness. We used an automated technique of analysis that accurately measures the thickness of the cerebral cortex and generates cross-subject statistics in a coordinate system based on cortical anatomy. We found local decreases of gray matter in the ASD group in areas belonging to the mirror neuron system (MNS), argued to be the basis of empathic behavior. Cortical thinning of the MNS was correlated with ASD symptom severity. Cortical thinning was also observed in areas involved in emotion recognition and social cognition. These findings suggest that the social and emotional deficits characteristic of autism may reflect abnormal thinning of the MNS and the broader network of cortical areas subserving social cognition.

A voxel-based investigation of brain structure in male adolescents with autistic spectrum disorder

Autistic spectrum disorder (ASD) has been associated with abnormal neuroanatomy in many imaging and neuropathological studies. Both global brain volume differences and differences in the size of specific neural structures have been reported. Here, we report a voxel-based morphometric whole brain analysis, using a group specific template, on 16 individuals of normal intelligence with autistic spectrum disorder (ASD), and a group of 16 age-, sex- and IQ-matched controls. Total grey matter volume was increased in the ASD group relative to the control group, with local volume increases in the right fusiform gyrus, the right temporo-occipital region and the left frontal pole extending to the medial frontal cortex. A local decrease in grey matter volume was found in the right thalamus. A decrease in global white matter volume in the ASD group did not reach significance. We found the increase in grey matter volume in ASD subjects was greatest in those areas recognised for their role in social cognition, particularly face recognition (right fusiform gyrus), mental state attribution: ‘theory of mind’ (anterior cingulate and superior temporal sulcus) and perception of eye gaze (superior temporal gyrus). The picture as a whole may reflect an abnormally functioning social cognitive neural network. We suggest that increased grey matter volume may play a pivotal role in the aetiology of the autistic syndrome.

The amygdala and development of the social brain.

The amygdala comprises part of an extended network of neural circuits that are critically involved in the processing of socially salient stimuli. Such stimuli may be explicitly social, such as facial expressions, or they may be only tangentially social, such as abstract shapes moving with apparent intention relative to one another. The coordinated interplay between neural activity in the amygdala and other brain regions, especially the medial prefrontal cortex, the occipitofrontal cortex, the fusiform gyrus, and the superior temporal sulcus, allows us to develop social responses and to engage in social behaviors appropriate to our species. The harmonious functioning of this integrated social cognitive network may be disrupted by congenital or acquired lesions, by genetic anomalies, and by exceptional early experiences. Each form of disruption is associated with a slightly different outcome, dependent on the timing of the experience, the location of the lesion, or the nature of the genetic anomaly. Studies in both humans and primates concur; the dysregulation of basic emotions, especially the processing of fear and anger, is an almost invariable consequence of such disruption. These, in turn, have direct or indirect consequences for social behavior.

What Does the Implicit Association Test Measure? A Test of the Convergent and Discriminant Validity of Prejudice-Related IATs

What Does the Implicit Association Test Measure? A Test of the Convergent and Discriminant Validity of Prejudice-Related IATs

Social Network Ties, Self-Efficacy, and Condom Use among Women who Use Crack Cocaine: A Pilot Study

So far, attempts to change the sexual risk behavior of women who use crack cocaine have been less successful than efforts to change the needle risk behavior of injection drug users. Two theoretical areas that have shown some success in predicting behavior change among of out-of-treatment drug users are Bandura's social cognitive theory (self-efficacy theory) and social network theory. According to Bandura, social networks are important sources of social support, and social support is vital to self-efficacy. Social network research also indicates that close bonds with network members may be a protective factor independently of self-efficacy. In order to test the feasibility of collecting such data, a pilot study was conducted with 60 women who used crack cocaine and who were not in treatment. Results of Pearson product-moment correlations indicated that self-efficacy (.7230) and number of very strong ties (.31252994) were positively correlated with condom use for women in the sample. In addition, the number of very strong ties (.3142) was significantly, if modestly, correlated with self-efficacy. Self-efficacy was

Personal Relationships as an Interface between Social Networks and Social Cognitions

The concept of shared knowledge structures is introduced as one way of demonstrating how personal relationships serve as a bridge between collective activity at the level of the social network and cognitive activity at the level of the individual. The field of social cognition has studied how individuals organize information, and social network analysis has studied how information is passed within groups, but both have largely ignored the role that personal relationships play in leading individuals to share the ways they organize and interpret this information. This conceptual framework is applied to two qualitative studies on the production of shared knowledge structures: first, for knowledge about coping with the stresses of recent widowhood, and second, for the organization of knowledge about preventing heart attacks. The results point to the importance of integrating work on social cognition, personal relationships, and social networks.

Informant accuracy in social network data III: A comparison of triadic structure in behavioral and cognitive data

Abstract This paper provides a comparison of the triadic-level structure inherent in behavioral and cognitive social network data taken on the same group, using a variety of groups whose communication could easily be monitored. It is found that many types of structure occur significantly more or less than chance in both behavioral and cognitive data, and providing that these are treated in similar ways, there is good agreement between the two structures. However, there are several ways to treat behavioral data, and these produce at least two essentially different structures. If cognitive and behavioral triads are compared, triad by triad, then there is virtually no agreement between them (even though they may both display the same structure on an overall triad census). Finally, as a demonstration of the dangers of relying solely on cognitive data, an unlikely null hypothesis is proposed. This asserts — for demonstration purposes — that, under many circumstances, behavioral structure never alters. Change in structure over time apparently occurs because of informant error in the reporting of the cognitive data. A pseudo-transition matrix, giving the probability that a triad is reported as one type when data are first taken, and a different type at a later date, is calculated. This compares reasonably with a genuine transition matrix evaluated for longitudinal cognitive data. It is believed that no data currently exist which can disprove this hypothesis, unlikely though it is. Much more accurate data are therefore necessary if any reliable theory of social structure is to be produced.