PSYCHIATRIC DISORDERS AS DISORDERS OF SOCIAL INTERACTION Impairments of social interaction and communication are an important if not essential component of many psychiatric disorders. In the context of psychopathology, one tends to think predominantly of autism spectrum disorders. However,many psychopathologies are to some degree characterized by alterations or impairments of interpersonal functioning in the DSM-5 (American Psychiatric Association, 2013), for instance schizophrenia [even auditory hallucinations have been linked to social cognition; (Bell, 2013)], or personality disorders such as borderline personality disorder (Wright et al., 2013). For different pathologies, the difficulties in social interaction may originate in different impairments; for instance in schizophrenia they may be related to a deficit in context processing (Cohen et al., 1999). Still, irrespective of the specific place that social interaction impairments take within different etiologies, it is clear that the systematic study of interaction patterns could teach us a lot about how they manifest themselves in patients, how healthy people with whom the patients interact engage with these patterns, and how they relate to underlying neurobiology. Here, we argue why this should and how this could be accomplished. One important aspect of social interaction that is increasingly shown to be impaired in psychiatric disorders is the recognition and production gaze behavior, often related to disorder-specific attentional bias (Armstrong and Olatunji, 2012). Schizophrenia has been associated with gaze-related attention deficits (Tso et al., 2012; Dalmaso et al., 2013). A recent study shows that patients with schizophrenia can be distinguished from neurotypical controls with astonishing accuracy on the basis of abnormal eye-tracking patterns on simple tasks such as fixation and smooth pursuit (Benson et al., 2012). Depression and bipolar disorder have been associated with prefrontal and cerebellar disturbances of oculomotor control during episodes of major depression, problems with antisaccade tasks (production of saccades away from a cue), and delayed initiation of saccades made on command (Sweeney et al., 1998). Finally, it is well known that people with autism orient to different kinds of contingencies (Gergely, 2001; Klin et al., 2009). However, most of the experimental paradigms used to establish gaze anomalies are essentially non-interactive and focus on how particular clinical populations differentially perceive stimuli or social scenes, passively. Likewise, the study of social cognition has only in the last decade begun to incorporate social interaction into its explanation of how we come to understand others and how we manage to navigate a complex social world (Schilbach et al., 2013). This “interactive turn” marks a departure from more traditional approaches, which have emphasized the importance of being able to think about the mental states of others. We have argued that the core problem with social interaction in clinical populations may not only lie in passive perception of social cues, but rather in a skewed experience of how one’s own actions influence the social world and in patient’s abilities to automatically and rapidly generate behavioral adjustments in response to social stimuli (Schilbach et al., 2012, 2013). Recently, methodological advances have allowed for the study of real-time dynamic social coordination in for instance children with autism (Fitzpatrick et al., 2013), but while undoubtedly rich, the problem with full-body social interaction is precisely that it is so rich, which makes it most difficult to operationalize so as to be used to quantify aspects of interpersonal coordination. Furthermore, fully interactive approaches become problematic if one wanted to use neuroimaging techniques that can access deeper brain structures, such as fMRI, to investigate the neural correlates of interpersonal coordination in on-going social interactions. Indeed, we have showed that the experience of self-initiated (gaze-based) contingencies is linked to activity in the brain’s reward system, notably the ventral striatum [Pfeiffer et al. (2014); Figure 1A], and it has been suggested that for instance individuals with autism may have difficulties with precisely those rewarding aspects of social interaction (Schmitz et al., 2008; Kohls et al., 2012).
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Jul 1, 2016
Douglas Mclelland + 2
Open Access
