Traditionally, assessment and diagnosis of psychiatric disorders have focused on affective, cognitive, and somatic symptoms. However, interpersonal problems and abnormal social behaviors are often the first indication than an individual is experiencing mental health difficulties. Recent advances in the field of social neuroscience have been instrumental in showing that abnormalities in social cognition are an important aspect of the clinical profile of many psychiatric disorders, and that some interpersonal problems associated with psychopathology are caused by dysfunctions in the social brain (Brüne et al. Reference Brüne, Ribbert and Schiefenhövel2003). In line with this new approach to defining the clinical phenotypes of psychiatric disorders, Crespi & Badcock (C&B) focus on social brain functioning in autism and psychosis. After reviewing an impressive amount of clinical, behavioral, and neurological data, C&B conclude that these two conditions represent opposites along a spectrum from underdeveloped to hyperdeveloped social cognition, with normality at the center, and hypothesize that the development of these disorders is mediated by genomic imprinting.

Whereas it is undisputed that patients with autism display deficits in a wide range of social cognition tasks, the idea that psychosis (and schizophrenia in particular) is associated with a hyperdeveloped social brain is likely to leave many clinicians perplexed. In fact, it seems to go against the prevailing consensus that patients with schizophrenia show defective (rather than enhanced) abilities in the domain of social cognition (Burns Reference Burns2006b). However, before considering C&B's view of schizophrenia as heretical, we should pay attention to the methodological problems that complicate the study of social brain dysfunctions in psychiatric disorders.

First, psychiatric diagnoses in general, and the diagnosis of schizophrenia in particular, lack validity. Patients with the same diagnosis may have different diseases, and these different diseases (or subsyndromes) may involve different abnormalities of the social brain. For example, in the schizophrenia population, social cognition abilities seem to vary with the presence of violent behavior (Abu-Akel & Abushua'leh Reference Abu-Akel and Abushua'leh2004), paranoid features (Langdon et al. Reference Langdon, Coltheart, Ward and Catts2002), and negative symptoms (Corcoran & Frith Reference Corcoran and Frith1996). Second, tasks designed for studying social cognition in psychiatric patients tend to have dubious ecological validity. For example, McCabe et al. Reference McCabe, Leudar and Antaki(2004) showed that individuals with schizophrenia demonstrate intact theory-of-mind abilities when tested in real life during conversational interactions. Third, the term “social cognition” is a broad concept, incorporating all aspects of social functioning from perceiving social emotional stimuli to attributional style and theory of mind. Not distinguishing between the different capacities that allow an individual to navigate the social environment may confound the interpretation of the data deriving from studies of the relationship between psychiatric disorders and the social brain. Here, I will focus in further detail on this last methodological problem.

A promising approach to dissecting the various components of social cognition is to distinguish the capacity to represent other people's intentions and beliefs (referred to as theory of mind or mentalizing) and the capacity to share the feelings of others (referred to as empathy) (Singer Reference Singer2006). Although C&B do not pay much attention to such a distinction in their target article, there is preliminary evidence that the capacities to mentalize and to empathize are differentially impaired in schizophrenia. Discussing these data, Shamay-Tsoory et al. Reference Shamay-Tsoory, Shur, Barcai-Goodman, Medlovich, Harari and Levkovitz(2007) have argued that the conflicting evidence in the literature concerning schizophrenic patients' ability to perform on theory-of-mind tasks is due to the dissociation between cognitive and affective components of social cognition. According to these authors, such dissociation would also explain the puzzling finding that the schizophrenic population includes both individuals who “undermentalize” and individuals who “overmentalize” (C. D. Frith Reference Frith2004). However, probably schizophrenia is not the best model to illustrate the necessity to distinguish between cognitive and affective components of social cognition. In this regard, psychopathy and Williams syndrome are much better.

Psychopathy is a pervasive pattern of disregard for the rights of others associated with distinctive emotional and behavioral features. Individuals with this personality disorder are frequently deceitful and manipulative in order to gain personal profit. Even though they may display a glib, superficial charm, these people tend to be callous, cynical, and contemptuous of the feelings, rights, and suffering of others. The emotional deficits associated with psychopathy interfere with the development of moral reasoning and put the individual at risk for developing high levels of antisocial behavior. In other words, an absence of empathy is what characterizes psychopaths who hurt others without feeling guilt or remorse (Blair Reference Blair2003). Interestingly, the empathic deficit is associated with no other deficit of social cognition. Persons with this disorder are capable of accurately assessing the costs and benefits of short-term social interactions, accurately reading others' behavior rules, utilizing self-monitoring information to alter their strategies, and successfully disguising their intentions (Troisi Reference Troisi2005). Confirming this, experimental studies have found no indications of impairment with theory of mind among individuals with a diagnosis of psychopathy (Richell et al. Reference Richell, Mitchell, Newman, Leonard, Baron-Cohen and Blair2003).

Williams syndrome (WS) is a rare neurodevelopmental disorder caused by hemizygous microdeletion of about 28 genes on chromosome 7q11.23 and characterized by many cardiovascular, endocrine, gastrointestinal, and orthopedic problems. WS is associated with mild to moderate mental retardation and a unique combination of social-emotional and social-cognitive abnormalities. A striking feature of children with WS is their high sociability and empathy for others. Increased interest in social interaction is evident from infancy onwards, and fascination with faces, positive interpersonal bias, and overfriendliness extend into adulthood. Intriguingly, this remarkable hypersociability is coupled with a deficit in the ability to interpret people's behavior in terms of their mental states. Therefore, despite their increased empathy and social gregariousness, individuals with WS encounter problems in everyday interactions because of their inability to detect and understand others' beliefs and intentions (Meyer-Lindenberg et al. Reference Meyer-Lindenberg, Mervis and Berman2006). In short, the social brain dysfunctions observed in psychopathy and WS appear to be distinct and selective. Individuals with psychopathy show a profound empathic dysfunction but no indications of impairment with theory of mind. In contrast, individuals with WS show abnormally high levels of empathy combined with a defective theory of mind.

The distinction between cognitive and affective components of social cognition exemplified by psychopathy and WS may apply to other psychiatric disorders. Future studies in different diagnostic groups will have to clarify when impaired abilities of mentalizing (understanding the propositional attitudes of others) and empathizing (sharing the affects of others) play unique roles and when they play common roles in causing social disability.

The relationship between psychiatric disorders and the social brain is likely to be multiformed. In some psychiatric disorders, abnormalities in social cognition may be a vulnerability factor that gets transformed into full-blown psychopathology in the face of significant stressors. In other disorders, the experience of psychiatric symptoms may produce temporary abnormalities in social cognition in individuals with effective and appropriate capacities for navigating the social environment. Progress in this area of research requires not only refining methods for assessing the various aspects of social cognition, but also developing theoretical models for generating new explicative hypotheses. In this regard, C&B's target article is an important contribution.