Display options
Share it on

Neuropsychiatr Dis Treat. 2015 Nov 11;11:2875-82. doi: 10.2147/NDT.S92795. eCollection 2015.

The ability of early changes in motivation to predict later antidepressant treatment response.

Neuropsychiatric disease and treatment

Philip Gorwood, Guillaume Vaiva, Emmanuelle Corruble, Pierre-Michel Llorca, Franck J Baylé, Philippe Courtet

Affiliations

  1. Centre Hospitalier Sainte-Anne (CMME), Paris, France ; Centre of Psychiatry and Neuroscience, INSERM U894, University Paris-Descartes, Paris, France.
  2. Pôle de Psychiatrie, CHRU de Lille, Hôpital Michel-Fontan, Université Lille-Nord de France, Lille, France.
  3. Psychiatry Department of Bicêtre, University Hospital, INSERM U669, Paris XI University, Le Kremlin Bicêtre, France.
  4. CHU Clermont-Ferrand, Clermont Université, Université d'Auvergne, Clermont-Ferrand, France.
  5. Department of Emergency Psychiatry, CHU Montpellier, Montpellier, France.

PMID: 26635476 PMCID: PMC4646593 DOI: 10.2147/NDT.S92795

Abstract

INTRODUCTION: Baseline values and early changes of emotional reactivity, cognitive speed, psychomotor function, motivation, and sensory perception have not been studied to any extent in unipolar depression, although they could help to characterize different dimensions of illness that are harder to capture by clinicians, give new insights on how patients improve, and offer new early clinical markers for later treatment response.

METHODS: About 1,565 adult outpatients with major depressive disorder receiving agomelatine completed the clinician-rated 16-item quick inventory of depressive symptoms, Clinical Global Impression, and Multidimensional Assessment of Thymic States (MAThyS) rating scales at inclusion, Week 2 and Week 6. The MAThyS includes a 20-item self-rated visual analog scale (from inhibition [0] to activation [10], with [5] representing the usual state) leading to five a priori dimensions (emotional reactivity, cognitive speed, psychomotor function, motivation, and sensory perception).

RESULTS: All MAThyS dimension scores increased from inclusion to Week 2 and from inclusion to Week 6 (P<0.001). Improvement was around 2 points (out of 10) for motivation, 1.5 points for psychomotor function, and 0.5 points for other dimensions. Motivation showed a trend to being more severely impaired at inclusion in future nonresponders (t=1.25, df=1,563, P=0.10). Its improvement at Week 2 was the most discriminating MAThyS dimension between future responders and nonresponders, and represents the best predictor of future response, with the highest area under the receptor operating characteristic curve (area under curve =0.616, 95% confidence interval [0.588-0.643], P<0.001). Finally, improvements in motivation correlated the most strongly with clinician-rated 16-item quick inventory of depressive symptoms improvement (r=-0.491, df=1,563, P<0.001).

CONCLUSION: Motivation had the most capacity for early improvement, the best predictive value for response, and the largest global margin of progress in depressed outpatients. Assessing the evolution of self-reported motivation over time in major depressive disorder could offer an interesting complementary approach to predict response.

Keywords: agomelatine; depression; dimension; motivation; treatment response

References

  1. J Affect Disord. 2010 Dec;127(1-3):300-4 - PubMed
  2. J Affect Disord. 2004 Dec;83(2-3):233-6 - PubMed
  3. J Affect Disord. 2007 Aug;101(1-3):35-41 - PubMed
  4. Neuropsychopharmacology. 2011 Jan;36(1):183-206 - PubMed
  5. Eur Psychiatry. 2013 Aug;28(6):362-71 - PubMed
  6. BMC Psychiatry. 2013 Mar 13;13:79 - PubMed
  7. Can J Psychiatry. 2006 Jan;51(1):3-5 - PubMed
  8. Am J Psychiatry. 2009 Jun;166(6):702-10 - PubMed
  9. Dialogues Clin Neurosci. 2015 Mar;17(1):89-97 - PubMed
  10. Biol Psychiatry. 2010 Jul 15;68(2):118-24 - PubMed
  11. Psychiatry Res. 2013 Aug 30;209(1):50-4 - PubMed
  12. J Abnorm Psychol. 2007 Feb;116(1):95-104 - PubMed
  13. J Affect Disord. 2013 Feb 15;145(1):36-41 - PubMed
  14. Encephale. 2007 Oct;33(5):768-74 - PubMed
  15. Trends Cogn Sci. 2009 Nov;13(11):479-87 - PubMed
  16. J Psychiatry Neurosci. 2014 Jan;39(1):60-5 - PubMed
  17. Front Hum Neurosci. 2013 Jun 11;7:261 - PubMed
  18. Biol Psychiatry. 2003 Sep 1;54(5):573-83 - PubMed
  19. BMC Psychiatry. 2008 Sep 19;8:82 - PubMed
  20. Neuropsychobiology. 2007;56(2-3):73-85 - PubMed
  21. Br J Clin Psychol. 2010 Nov;49(Pt 4):529-45 - PubMed
  22. J Clin Psychiatry. 2010 Jan;71(1):e01 - PubMed
  23. Int Clin Psychopharmacol. 1996 Jun;11 Suppl 3:89-95 - PubMed
  24. Am J Psychiatry. 2006 Oct;163(10):1784-90 - PubMed
  25. Int Clin Psychopharmacol. 2013 May;28(3):121-6 - PubMed
  26. J Abnorm Psychol. 2012 Aug;121(3):553-8 - PubMed
  27. J Comp Neurol. 2005 Dec 5;493(1):115-21 - PubMed
  28. Psychopharmacology (Berl). 1980;71(2):173-9 - PubMed
  29. PLoS One. 2009 Aug 12;4(8):e6598 - PubMed
  30. Br J Pharmacol. 2014 Aug;171(15):3604-19 - PubMed
  31. Psychiatry Res. 2014 Dec 30;220(3):874-82 - PubMed
  32. J Clin Psychopharmacol. 2012 Aug;32(4):487-91 - PubMed
  33. J Biol Regul Homeost Agents. 2011 Jan-Mar;25(1):109-14 - PubMed
  34. Neuropsychopharmacology. 2013 Jan;38(2):275-84 - PubMed
  35. J Pharmacol Exp Ther. 2003 Sep;306(3):954-64 - PubMed
  36. Curr Psychiatry Rep. 2010 Dec;12(6):505-11 - PubMed
  37. Annu Rev Clin Psychol. 2014;10:393-423 - PubMed
  38. PLoS One. 2011;6(8):e23178 - PubMed

Publication Types