Among the many areas of functioning that are impaired in patients with major depressive disorder (MDD), interpersonal difficulties are common. For example, researchers have linked depression to low relationship quality and social isolation.1,2 These impairments may be attributed in part to deficits in social cognitive function. Social cognition is “broadly defined as the way in which humans identify, perceive and interpret socially salient information. … [and] therefore encompasses a wide range of verbal and nonverbal information, including facial expressions, prosody, body language and theory of mind,” according to a new review by Weightman et al, published in Psychiatry Research.3

The authors examined 107 studies published between 1990 and 2018 to elucidate the effects of social cognitive deficits on psychological functioning, as well as treatment approaches that may improve these deficits. Selected findings from the review are summarized here.

Social performance. In a 2012 study of older patients who are depressed, those with poor facial affect recognition showed greater hostility and smaller social networks compared with patients who have better affect recognition.4 Another study found greater sensitivity to the detection of fearful emotions and increased withdrawal from emotional stimuli in this population.5 In addition, worse social decision-making ability has been noted in depressed patients vs control patients; this was mediated by the facial affective expressions of others.6

Emotional and empathic performance. People with depression “have greater difficulty than controls at ignoring the emotional dimension of facial expressions, suggesting increased sensitivity to emotional social cues,” according to the review.3 These patients are also more likely to act fearfully (freezing or tensing) in response to these cues, and to rate facial expressions as untrustworthy. “These reactions likely lead to reduced desire for social interaction and reduce the quality of interpersonal relationships, underscoring the need for more research in this domain.” Other findings suggest reduced levels of empathy in depressed vs individuals who are not depressed, which may negatively influence psychosocial functioning.3

General cognitive functioning. Researchers have linked social cognitive performance to general cognitive ability in depressed patients, as in studies revealing that impaired theory of mind and prosody interpretation were associated with deficits in executive functioning and working memory, even in patients with remitted MDD.3 In one study,7 for example, patients with depression were “quicker than controls at integrating sad content into a working memory task, but slower at linking more complex emotional stimuli into working memory,” wrote Weightman and colleagues.3 Other findings have demonstrated worse performance in facial affect recognition and theory of mind in individuals with lower cognitive flexibility.3

General quality of life. A range of studies have found connections between social cognitive dysfunction and quality of life in patients with MDD, including: lower Global Assessment of Functioning score in those with reduced theory of mind performance; higher self-reported well-being and social functioning in patients with increased facial recognition accuracy for happy expressions; and reduced social and occupational functioning in those with reduced ability to mentalize and interpret prosody.3

Treatment effects

Various pharmacological, psychotherapeutic, and neuromodulation therapies have shown promise for reducing social cognitive dysfunction in MDD.3 Trials have demonstrated improved accuracy of facial expression interpretation after treatment with citalopram, reboxetine, intra-nasal oxytocin, transcranial direct current stimulation (tDCS), and repetitive transcranial magnetic stimulation (rTMS). In a 2009 comparative study, citalopram demonstrated superiority to reboxetine at 2 weeks but not 6 weeks.8 Additionally, both rTMS and inpatient psychiatric treatment have been linked to improved recognition of angry faces.3

Treatment with escitalopram and intranasal oxytocin led to reductions in pretreatment bias toward negative faces, and “more frequent negative interpretations of neutral facial expressions in a treated depressed population were associated with missed anti-depressant doses, suggesting adherence to treatment may be a relevant factor,” as reported in the review.3 Pretreatment bias toward negative faces was also reduced after mindfulness-based cognitive therapy and inpatient psychoanalytic-interactional group therapy.

Numerous results point to the potential utility of functional magnetic resonance imaging (fMRI) in predicting treatment response in MDD.3 For example, greater baseline anterior cingulate activity in response to affective faces has been shown to predict treatment response to both antidepressant medication and cognitive behavioral therapy (CBT), and reduced activity in this area was noted following treatment with sertraline.3,9 “Such findings suggest there could be an opportunity to target treatment to patients with anterior cingulate hyperactivity,” Weightman et al stated.3

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Multiple studies have shown improvements in amygdala hyperactivity in response to affective faces in patients treated with

  • escitalopram,
  • sertraline,
  • venlafaxine-XR,
  • citalopram,
  • fluoxetine,
  • reboxetine, and
  • other agents.

Such improvements were also observed in patients treated with electroconvulsive therapy, CBT, and fMRI-based neurofeedback training.3 Inpatient psychotherapy, behavioral training programs, and deep brain stimulation were found to improve mentalization tasks and negative interpretation bias in patients who are depressed.3

In sum, many of the therapies currently used for depression treatment “appear to have a role in the treatment of social cognitive deficits and the associated psychosocial functional impairments,” the authors concluded.3 “Future developments in personalised medicine could potentially identify neural patterns that either indicate the use of a particular treatment or provide prognostic information about the likelihood of response to intervention.”


1. Teo AR, Choi H, Valenstein M. Social relationships and depression: ten-year follow-up from a nationally representative study. PLoS One. 2013;8(4):e62396.

2. Chou KL, Liang K, Sareen J. The association between social isolation and dsm-iv mood, anxiety, and substance use disorders: wave 2 of the national epidemiologic survey on alcohol and related conditions. J Clin Psychiatry. 2011;72(11):1468-1476.

3. Weightman MJ, Knight MJ, Baune BT. A systematic review of the impact of social cognitive deficits on psychosocial functioning in major depressive disorder and opportunities for therapeutic intervention. Psychiatry Res. 2019;274:195-212.

4. Szanto K, Dombrovski AY, Sahakian BJ, et al. Social emotion recognition, social functioning, and attempted suicide in late-life depression. Am J Geriatr Psychiatry. 2012;20(3):257-265.

5. Derntl B, Seidel EM, Eickhoff SB, et al. Neural correlates of social approach and withdrawal in patients with major depression. Soc Neurosci. 2011;6(5-6):482-501.

6. Radke S, Schäfer IC, Müller BW, de Bruijn ER. Do different fairness contexts and facial emotions motivate ‘irrational’ social decision-making in major depression? An exploratory patient study. Psychiatry Res. 2013;210(2):438-443.

7. Levens SM, Gotlib IH. Updating positive and negative stimuli in working memory in depression. J Exp Psychol Gen. 2010;139(4):654-664.

8. Tranter R, Bell D, Gutting P, Harmer C, Healy D, Anderson IM. The effect of serotonergic and noradrenergic antidepressants on face emotion processing in depressed patients. J Affect Disord. 2009;118(1-3):87-93.

9. Victor TA, Furey ML, Fromm SJ, Öhman A, Drevets WC. Changes in the neural correlates of implicit emotional face processing during antidepressant treatment in major depressive disorder. Int J Neuropsychopharmacol. 2013;16(10):2195-2208.