Citation

Lee Y, Syeda K, Maruschak NA, Cha DS, Mansur RB, Wium-Andersen IK, Woldeyohannes HO, Rosenblat JD, McIntyre RS. J. Clin. Psychopharmacol. 2015; 36(1): 50-56.

Affiliation

From the *Mood Disorders Psychopharmacology Unit, University Health Network; †Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada; ‡Psychiatric Center Copenhagen, Department O, Copenhagen, Denmark; and Departments of §Psychiatry and ∥Pharmacology, University of Toronto, Toronto, Ontario, Canada.

Copyright

(Copyright © 2015, Lippincott Williams and Wilkins)

DOI

10.1097/JCP.0000000000000441

PMID

26658082

Abstract

Available evidence indicates that a single, low-dose administration of ketamine is a robust, rapid-onset intervention capable of mitigating depressive symptoms in adults with treatment-resistant mood disorders. Additional evidence also suggests that ketamine may offer antisuicide effects. Herein, we propose that the antidepressant effects reported with ketamine administration are mediated, in part, by targeting neural circuits that subserve cognitive processing relevant to executive function and cognitive emotional processing. Empirical support for the conceptual framework of the cognitive domain as a critical target of ketamine's action is the additional observation that pretreatment cognitive function predicts treatment outcomes with ketamine administration. The proposal that beneficial effects on cognitive function may be, in some individuals, the proximate mechanism mitigating symptom relief in mood disorders exists alongside the well-established deleterious effect of ketamine on cognitive function. During the past 5 years, there have been several reviews and meta-analyses concluding that ketamine has possible clinical benefits in refractory mood disorders. We introduce the conceptual framework that ketamine's salutary effects, notably in suicidality, may in part be via procognitive mechanisms.

Language: en