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The present issue of Acta Psychiatrica Scandinavica contains a very elegant and comprehensive review and meta-analysis by Professor Strejilevich’s emerging group (1) on the state of the art of social cognition in bipolar patients. According to the authors, deficits in theory of mind and emotion processing would occur even in euthymic bipolar disorder (BD) patients, while decision making would be preserved. It is also known that social cognition impairment may lead to poor social functioning (2).

The term ‘social cognition’ is used to refer to various abilities that allow people to process social information, especially its encoding, storage, retrieval, and application to social situations. It comprises several skills. The most widely used social cognition abilities include emotion processing—the ability to identify and appraise the emotions displayed by other people—decision making, or the effect of reward and punishment on behavior selection, and theory of mind—the ability to attribute mental states such as beliefs, desires, and intents to oneself and others. In summary, social cognitive skills allow us to properly understand or judge the world from an interactive, affective, and empathic perspective. Social cognition is known to be affected in neurodevelopmental disorders such as autism and severe psychiatric conditions as schizophrenia and unipolar depression. However, an issue that needs to be clarified concerns to how big is the word ‘social’ in the ‘social cognition’ construct. In other words, is social cognition impairment merely epiphenomena of neurocognitive impairment? Both decision making and theory of mind might be strongly influenced by executive frontal components, and in fact, both seem to be related to gray matter volume reduction in the ventromedial prefrontal cortex (3). As for emotional processing, it has been described how damage to the fusiform gyrus, in the temporal lobe, can lead to the inability to recognize faces and that amygdale, a usual suspect in bipolar disorders’ pathophysiology, strongly influences fusiform gyrus function during face perception (4). To what extent social cognition dysfunctions are merely the clinical expression of soft neurological signs occurring in bipolar disorders remains as something to be further studied. On the other hand, although Samamé and colleagues find social cognition to be independent from mood state, it is also true that subsyndromal symptoms and medications may also play a role. It is well known, for instance, that even low doses of antidepressants during a few days may improve emotional processing and recognition in depressed patients (5).

Social cognition might even be involved in the sensitization phenomena related to bipolar illness. Bipolar individuals with affected social cognition skills may get involved in social stressful events more often due to their inability to ‘read’ what is happening, to weigh the risks involved in a social situation, or to take the right decision deriving from it. Hence, this enhanced likelihood for negative life events would trigger many episodes and, finally, worsen the course of the disorder. Later on, as supported by the kindling models, the disorder itself develops some biological autonomy, progressively allowing for more neurological soft signs, social, and neurocognitive impairment, biological sensitization and outcome worsening in a never-ending cycle.

All this needs to be taken into account in both the pharmacological and psychotherapeutic approaches to bipolar patients.

From a pharmacological perspective, we may hypothesize that an energetic and early treatment with mood-stabilizing agents may even have positive effects on social cognition and stop or slow down the roughening cycle described above.

From a psychological treatments perspective, we should consider both the early implementation of psychoeducational programs and the potential role of cognitive rehabilitation. Newer cognitive rehabilitation programs should include social cognition remediation. The fear of patronizing the patient by using a very directive intervention would be by far counterbalanced by the benefits deriving from prevention of both some life events and episodes. The political nuisance of using ‘cognitive orthopaedics’—such as some functional remediation models—is by far counterbalanced by its daily benefits in our patients’ both functional and clinical prognosis, and quality of life.

All that said, clinicians have to keep in mind the extreme interindividual variability among all bipolar patients regarding social cognition. Some affected individuals really master social cognition and are particularly gifted with social and political leadership abilities, while others show extremely poor social cognition skills. Or, from an evolutionary perspective, some social cognition problems would be apparently rewarded by the group as they allow for a more effective leadership, particularly important when facing a critical situation. At the end of the day, the world did not ask Theodore Roosevelt or Winston Churchill to be empathic, but effective.

A proper assessment of social cognition is needed to determine its possible impairment for all patients given its clinical, prognostic, functional, and therapeutic significance. Samané et al. paper in this issue of Acta Psychiatrica Scandinavica will help us to further understand why.

Acknowledgements

  1. Top of page
  2. Acknowledgements
  3. Declaration of interest
  4. References

Francesc Colom would like to thank the support and funding of the Spanish Ministry of Health, Instituto de Salud Carlos III, CIBER-SAM and of the Generalitat de Catalunya to the Bipolar Disorders Group (2009 SGR 1022). Dr Colom is also funded by the Spanish Ministry of Science and Innovation, Instituto Carlos III, through a ‘‘Miguel Servet’’ postdoctoral contract (CP08/00140) and a FIS (PS09/01044).

Declaration of interest

  1. Top of page
  2. Acknowledgements
  3. Declaration of interest
  4. References

Dr. Francesc Colom has served as advisory or speaker for the following companies: Adamed, Astra Zeneca, Bristol-Myers, Eli-Lilly, Glaxo-Smith-Kline, Lundbeck, MSD-Merck, Otsuka, Pfizer Inc, Sanofi-Aventis, Shire, and Tecnifar. He has received copyright fees from Cambridge University Press, Solal Ed., Ars Médica, Giovani Fioriti Ed., Medipage, La Esfera de Los Libros, Morales i Torres Ed, Panamericana, Mayo Ed. & Columna.

References

  1. Top of page
  2. Acknowledgements
  3. Declaration of interest
  4. References
  • 1
    Samamé C, Matino DJ, Strejilevich S. Social cognition in euthymic bipolar disorder: systematic review and meta-analytic approach. Acta Psychiatr Scand 2012;125:266280.
  • 2
    Solé B, Bonnin CM, Torrent C et al. Neurocognitive impairment and psychosocial functioning in bipolar II disorder. Acta Psychiatr Scand 2011;125:309317.
  • 3
    Hooker CI, Bruce L, Lincoln SH et al. Theory of mind skills are related to gray matter volume in the ventromedial prefrontal cortex in schizophrenia. Biol Psychiatry 2011;70:11691178.
  • 4
    Herrington JD, Taylor JM, Grupe DW et al. Bidirectional communication between amygdala and fusiform gyrus during facial recognition. Neuroimage 2011;56:23482355.
  • 5
    Harmer CJ, O’sullivan U, Favaron E et al. Effect of acute antidepressant administration on negative affective bias in depressed patients. Am J Psychiatry 2009;166:11781184.