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Depression

Why do antidepressants cause emotional blunting and what can be done to resolve it in clinical practice?

Emotional blunting describes an indifferent, unresponsive affect and inability to feel emotions experienced by people with major depressive disorder (MDD) treated with antidepressants.1,2 Dampening of dopaminergic and noradrenergic input to the prefrontal cortex is thought to play an important role,3 and management can be guided by understanding the neuropathophysiology.3

A negative impact on patient outcome

46% of patients on antidepressants report emotional blunting

Emotional blunting is a residual symptom of MDD, which is a symptom experienced by patients with MDD despite antidepressant therapy. Such patients are at risk of relapse.4

Emotional blunting can impact everyday patient function and prevent a full functional recovery.5 More severe emotional blunting is associated with a poorer quality of remission.6

Nearly half of patients on all types of monoaminergic antidepressants report emotional blunting,6 and it is associated with serotonin reuptake inhibitor (SSRI) therapy as follows:2,5

  • among 161 patients, 46% reported a narrowed range of affect, 21% reported an inability to cry, and 19% reported apathy7
  • a cross-sectional study of 117 patients revealed that approximately 30% of patients reported some form of apathy8

 

What causes emotional blunting?

Higher doses of SSRI are more likely to cause emotional blunting9,10

The primary effect of SSRIs is reduced processing of negative stimuli rather than increased positive stimuli.9

Emotional blunting is related to SSRI dose,9,10 and possibly serotonergic effects on the frontal lobes and/or serotonergic modulation of midbrain dopaminergic systems projecting to the prefrontal cortex (PFC).10 By enhancing serotonergic transmission, SSRIs can activate GABA interneurons, thereby dampening the noradrenergic and dopaminergic input.11

Dorsolateral PFC:

  • is primarily associated with “cognitive” or “executive” functions12
  • appears to play a role in regulating negative emotion through reappraisal/suppression strategies13,14
  • lesions are associated with significantly higher MDD scores than for head injuries not involving the PFC12
  • is hypoactive at rest and increases in activity during symptom remission15

Dorsolateral PFC appears to play a critical role in MDD through a defect in regulation of negative affect

Ventromedial PFC:

  • is largely ascribed “emotional” or “affective” functions12
  • lesions are associated with significantly lower MDD scores than for brain injuries not involving the PFC12
  • is hyperactive at rest and decreases in activity during symptom remission13

Imaging studies suggest a critical link between the automatic processing of emotional signals in the amygdala and the regulation of this activity in the frontal cortex.16

Lowering SSRI dose8 or changing antidepressant are therapeutic options

Options to resolve emotional blunting are therefore to:

  • lower the current dose and/or gradual discontinuation of the SSRI8
  • change the antidepressant to one with a different profile that might improve the patient’s emotional response17

Our correspondent’s highlights from the symposium are meant as a fair representation of the scientific content presented. The views and opinions expressed on this page do not necessarily reflect those of Lundbeck.

References
  1. Loas G, et al. Compr Psychiatry 1994;35:366–72.
  2. Price J, et al. J Affect Disord 2012; 140:66–74
  3. Nutt D, et al. J Psychopharmacol 2007:21;461–71.
  4. Conradi HJ, et al. Psychol Med 2011;41:1165–74.
  5. Price J. Br J Psychiatry 2009;195:211–217.
  6. Goodwin GM, et al. J Affect Disord 2017;221:31–35.
  7. Bolling MY, Kohlenberg, RJ. Psychotherapy Psychosomatics 2004;73;380–5.
  8. Fava M, Graves LM, Benazzi F, Scalia MJ et al. Journal of Clinical Psychiatry. 2006:67;1754–9.
  9. Goodwin GM. Medicographia. 2012;34(3):295–9.
  10. Sansone RA, Sansone LA. Psychiatry (Edgmont) 2010;7:14–18.
  11. Blier P. Int J Neuropsychopharmacol. 2014;17:997–1008.
  12. Koenigs M, Grafman J. Behav Brain Res 2009;201:239–43.
  13. Kelley NJ, et al. Front Behav Neurosci 2019;12:337;2.
  14. Morawetz C, et al. Soc Cogn Affect Neur 2017;12:569–85.
  15. Ye M, et al. PLoS ONE 2015;10:e0133775. 
  16. Banks SJ, et al. Soc Cogn Affect Neurosci 2007;2:303–12.
  17. Godlewska BR, Harmer CJ. Psychopharmacol. 2020; doi.org/10.1007/s00213-019-05448-0.
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