Social Cognition in Schizophrenia

Amy E. Pinkham, PhD

Social cognition is often defined as the cognitive processes that allow people to perceive, interpret, and respond to the intentions, dispositions, and behaviors of others. This definition highlights a link between social cognition and behavior that may be crucial for understanding the social impairments that are among the defining features of schizophrenia.

The 4 Domains of Social Cognition

Current consensus among experts in the field identifies 4 core domains of social cognition: (1) emotion processing, (2) social perception, (3) theory of mind/mental state attribution (ToM), and (4) attributional style/bias.1 Emotion processing is broadly defined as perceiving and using emotional information and encompasses both simple and complex behavior. Social perception is defined as decoding and interpreting social cues in others. ToM refers to the ability to represent human mental states and/or make inferences about others’ intentions and beliefs. Finally, attributional style pertains to the ways in which individuals explain positive and negative social events in their lives.1

Social Cognition and Schizophrenia

Social cognition represents a significant area of impairment for individuals with schizophrenia that spans all of the domains detailed above. Specifically, patients show large deficits in emotion recognition, social cue perception, and ToM, and when explaining events, individuals with schizophrenia tend to blame others, rather than situational factors, for negative outcomes.2-5 These difficulties are evident early in the course of the disorder, including the prodromal phase, and are stable over time.6-11 Further, although there is clearly overlap between social cognition and neurocognitive abilities such as memory, attention, and executive function, social cognition appears to be largely independent from neurocognition.4 Most importantly, social cognition impacts real-world outcomes.12 Treatment programs targeted toward improving social cognitive abilities have also resulted in improved outcomes including social adjustment, social functioning, social relationships, and social skills.1

The Social Cognitive Neural Network

Social cognitive abilities are linked to specific neural circuits that show functional abnormalities in individuals with schizophrenia.13,14 Patients tend to show abnormal activation of a network including fusiform gyrus, superior temporal sulcus, amygdala, ventrolateral prefrontal cortex, and medial prefrontal cortex when processing social stimuli (AV 1). Investigations of these neural networks in patients have also demonstrated that brain activation is significantly and positively correlated with social functioning, which suggests that abnormal activation in social cognitive networks may serve as a mechanism for social dysfunction in schizophrenia.15-17 Findings such as these highlight the potential importance of treating social cognitive impairments and pursuing remediation strategies that will normalize these neural processes.

AV 1. A Neural Basis of Social Cognition (00:48)

Future Implications

Despite the promise of social cognition for contributing to our understanding of social impairment in schizophrenia, there are many challenges in this area moving forward, and among them is the issue of measurement. There is disagreement about which tasks best measure social cognition, and many existing measures show poor psychometric properties. A recent project, the Social Cognition Psychometric Evaluation (SCOPE) study, aims to address these problems by providing the field with a well-validated battery of social cognitive tasks that can be used in treatment outcome trials.1

In summary, social cognition is an exciting area of research that offers promise for better understanding the social dysfunction seen in schizophrenia. Research is honing in on the potential mechanisms of social cognitive impairment in patients, and with improved measurement, there is promise for optimizing behavioral and pharmacologic interventions and remediation strategies.

  1. Pinkham AE, Penn DL, Green MF, et al. Schizophr Bull. doi:10.1093/schbul/sbt081 PubMed
  2. Brüne M. Schizophr Bull. 2005;31(1):21–42. doi:10.1093/schbul/sbi002 PubMed
  3. Penn DL, Sanna LJ, Roberts DL. Schizophr Bull. 2008;34(3):408–411. doi:10.1093/schbul/sbn014 PubMed
  4. Pinkham AE. In: Harvey PD, ed. Cognitive Impairment in Schizophrenia: Characteristics, Assessment, and Treatment. New York, NY: Cambridge University Press; 2013:126–141. doi:10.1017/CBO9781139003872.009
  5. Pinkham AE, Gur RE, Gur RC. Expert Rev Neurother. 2007;7(7):807–816. doi:10.1586/14737175.7.7.807 PubMed
  6. Pinkham A, Penn D, Wangelin B, et al. Schizophr Res. 2005;79(2–3):341–343. doi:10.1016/j.schres.2005.07.012 PubMed
  7. Green MF, Bearden CE, Cannon TD, et al. Schizophr Bull. 2012;38(4):854–864. doi:10.1093/schbul/sbq171 PubMed
  8. Horan WP, Green MF, DeGroot M, et al. Schizophr Bull. 2012;38(4):865–872. doi:10.1093/schbul/sbr001 PubMed
  9. Addington J, Penn D, Woods SW, et al. Br J Psychiatry. 2008;192(1):67–68. doi:10.1192/bjp.bp.107.039784 PubMed
  10. Chung YS, Kang DH, Shin NY, et al. Schizophr Res. 2008;99(1–3):111–118. doi:10.1016/j.schres.2007.11.012 PubMed
  11. Phillips LK, Seidman LJ. Schizophr Bull. 2008;34(5):888–903. doi:10.1093/schbul/sbn085 PubMed
  12. Fett AK, Viechtbauer W, Dominguez MD, et al. Neurosci Biobehav Rev. 2011;35(3):573–588. doi:10.1016/j.neubiorev.2010.07.001 PubMed
  13. Pinkham AE. In: Roberts DL, Penn DL, eds. Social Cognition in Schizophrenia: From Evidence to Treatment. New York, NY: Oxford University Press; 2013:263–284.
  14. Pinkham AE, Penn DL, Perkins DO, et al. Am J Psychiatry. 2003;160(5):815–824. doi:10.1176/appi.ajp.160.5.815 PubMed
  15. Pinkham AE, Hopfinger JB, Ruparel K, et al. Schizophr Bull. 2008;34(4):688–697. doi:10.1093/schbul/sbn031 PubMed
  16. Pinkham AE, Loughead J, Ruparel K, et al. Am J Psychiatry. 2011;168(3):293–301. doi:10.1176/appi.ajp.2010.10060832 PubMed
  17. Dodell-Feder D, Tully LM, Lincoln SH, et al. Neuroimage Clin. 2013;4:154–163. doi:10.1016/j.nicl.2013.11.006 PubMed
Amy E. Pinkham, PhD

Amy E. Pinkham, PhD

Department of Psychology, Southern Methodist University, and the Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas

This Brief Report is derived from the roundtable meeting “Understanding the lifetime course of schizophrenia: a longitudinal perspective on neurobiology to promote better outcomes and recovery,” which was held October 15, 2013. The author acknowledges Healthcare Global Village for editorial assistance in developing the manuscripts.

The meeting, manuscript preparation, and dissemination of this brief report were supported by Otsuka America Pharmaceutical, Inc., and Lundbeck. All faculty received a fee for service from Otsuka America Pharmaceutical, Inc., and Lundbeck for participation in the meeting and preparation of the manuscripts.

Faculty Disclosure

Dr Pinkham received a fee for service from Otsuka America Pharmaceutical, Inc., and Lundbeck for participation in the meeting and preparation of this manuscript and, in the last year, has received consulting fees from Otsuka America Pharmaceutical, Inc.


The opinions expressed herein are those of the authors and do not necessarily reflect the opinions of the publisher, the American Society of Clinical Psychopharmacology, Healthcare Global Village, or the commercial supporters.

doi: 10.4088/JCP.13065br5

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