Social Cognition Deficits Among Individuals at Familial High Risk for Schizophrenia

Schizophrenia is a chronic and disabling disorder that is characterized by significant impairments in social and nonsocial cognition. Individuals with schizophrenia have for some time been shown to have marked neurocognitive deficits in attention, working memory, and executive functioning;1 and growing evidence indicates that deficits are also prominent in such social cognitive domains as emotion perception,2 social cue recognition,3 interpersonal attribution,4 and perspective taking and theory of mind.5 Longitudinal studies have shown that many of these domains of cognitive impairment are stable over time and are present even after the remission of psychotic symptoms.6,7 Recent investigations have not only highlighted the presence and stability of deficits in social and nonsocial cognition in schizophrenia but also underscored the centrality of these impairments in schizophrenic illness by showing consistent and robust relations between cognition and functional outcome in this population.8,9 The frequency, pervasiveness, and stability of cognitive impairment in schizophrenia have led investigators to posit endophenotypic models of the illness with neurobiologically based impairments in cognitive function as a core component.10,11 Support has been garnered for such models in recent years from studies documenting the presence of similar cognitive deficits in patients with schizophrenia and their unaffected relatives,12 although cognitive dysfunction in unaffected relatives appears to be milder than in schizophrenia.13 Unfortunately, the majority of these investigations have focused primarily on the heritability of neurocognitive impairments in attention, working memory, and executive functioning, whereas deficits in social cognition have received little attention in the endophenotyping literature. Although impairments in social cognition have been increasingly recognized as separate, but related to neurocognitive dysfunction,14,15 and convincing theoretical and empirical models suggest that social cognitive impairment may underlie the development of schizophrenic symptoms and disability,16,17 little is known about the degree to which impairments in social cognitive functioning represent endophenotypic markers of the illness. To date, only a few studies have examined the heritability of social cognitive impairment in schizophrenia through the use of samples at heightened genetic risk for the illness. One study by Kee et al18 found that siblings of patients with schizophrenia performed moderately worse on a series of emotion perception tasks (particularly in facial emotion perception tasks) than healthy controls but slightly better than their affected relatives. Another study of unaffected siblings of patients with schizophrenia by Leppanen et al19 was consistent with these findings, where these investigators demonstrated significant performance impairments in the recognition of facial displays of anger in unaffected siblings relative to healthy controls, further supporting social cognitive deficits in emotion perception as a potential endophenotype for schizophrenia. Recently, Addington et al20 extended this line of investigation to the schizophrenia prodrome, where they found that individuals at clinical high risk for developing schizophrenia performed as poorly as first-episode schizophrenia patients on an emotion identification task. Taken together, these findings increasingly suggest that impairments in perhaps the most widely studied domain of social cognition in schizophrenia, emotion perception, may be a marker of genetic liability for the disorder and eventually portend who will develop the illness. While these studies have provided promising results pointing to social cognitive impairment in emotion perception as a potential endophenotype for schizophrenia, several critical questions remain that preclude firm conclusions from these findings. Perhaps, most importantly, none of these investigations have evaluated the independence of this finding relative to the well-replicated deficits in neurocognitive functioning seen between unaffected relatives and healthy controls.12 Although research has supported the notion that social cognition and neurocognition are distinct constructs,15,21 a clear relationship does exist in individuals with the illness.15 The extent of this relationship in unaffected relatives is largely unknown, but if present, it is possible that neurocognitive impairment alone could account for the sometimes subtle poorer performance of unaffected relatives on social cognitive tasks. Further, even if social cognitive impairment exists independent of deficits in neurocognition among genetically predisposed samples, little is known about the degree to which these impairments are associated with manifestations of schizophrenia-spectrum symptoms in at-risk samples. Answers to these 2 questions are critical for solidifying social cognitive impairment as a robust and independent endophenotypic marker of schizophrenia. To begin to address these questions, we conducted a study of social cognitive impairment in relatives of schizophrenia probands and healthy controls to identify the presence of deficits in social cognition, their independence from neurocognitive dysfunction, and their relation to schizophrenia-spectrum psychopathology. Specifically, we aimed to determine whether individuals at familial high risk for schizophrenia would display impairments in social cognition that were independent of neurocognitive dysfunction and, if present, determine whether such impairments would be associated with schizophrenia psychopathology. We hypothesized that at-risk individuals would display impairments in social cognition that were independent of neurocognitive function and that such impairments would be significantly related to prodromal psychopathology portending the development of schizophrenia.