期刊
JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY
卷 36, 期 1, 页码 50-56出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/JCP.0000000000000441
关键词
cognition; ketamine; suicidality; major depressive disorder; NMDA antagonist; antisuicide; procognitive
资金
- FAPESP, Brazil
- Lundbeck, Canada
- Eli Lily
- AstraZeneca
- Pfizer
- Lundbeck
- Otsuka
- Sunovion
- Shire
- Bristol-Myers Squibb
- Takeda
- Forest
- Merck
- Allergan
- Janssen-Ortho
- Stanley Medical Research Institute
- National Institutes of Mental Health
- National Alliance for Research on Schizophrenia and Depression
- Canadian Institutes of Health Research
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.
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