2018, Number 2
Next >>
Rev Invest Clin 2018; 70 (2)
Ketamine for Treatment-Resistant Depression: a New Advocate
Pérez-Esparza R
Language: English
References: 14
Page: 65-67
PDF size: 59.59 Kb.
ABSTRACT
Current alternatives for the treatment of major depressive disorder lack efficacy and have a delayed onset of action. Recently,
the glutamatergic neurotransmission system has been noted to play an important role in the pathophysiology of this disorder.
Ever since the first report of the antidepressant effects of the N-methyl-D-aspartate receptor antagonist, ketamine, research
has been redirected to novel therapeutic targets. With this rapidly growing evidence of a fast-acting antidepressant such as
ketamine, as well as its efficacy in treatment-resistant cases of depression, off-label use has become popular in certain settings.
In this article, the clinical antidepressant properties of ketamine in relation to the glutamate hypothesis of depression are discussed,
to highlight the breakthrough of these findings in the development of novel therapeutic strategies and provide a
clearer view of its benefits and potential harms.
REFERENCES
GBD 2016 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990-2016: a systematic analysis for the global burden of disease study 2016. Lancet. 2017; 390:1211-59.
Rush AJ, Trivedi MH, Wisniewski SR, et al. Acute and longerterm outcomes in depressed outpatients requiring one or several treatment steps: a STAR*D report. Am J Psychiatry. 2006; 163:1905-17.
Boku S, Nakagawa S, Toda H, Hishimoto A. Neural basis of major depressive disorder: beyond monoamine hypothesis. Psychiatry Clin Neurosci. 2018;72:3-12.
Harmer CJ, Duman RS, Cowen PJ. How do antidepressants work? New perspectives for refining future treatment approaches. Lancet Psychiatry. 2017;4:409-18.
Kupfer DJ, Frank E, Phillips ML. Major depressive disorder: new clinical, neurobiological, and treatment perspectives. Lancet. 2012;379:1045-55.
Lener MS, Niciu MJ, Ballard ED, et al. Glutamate and gammaaminobutyric acid systems in the pathophysiology of major depression and antidepressant response to ketamine. Biol Psychiatry. 2017;81:886-97.
Berman RM, Cappiello A, Anand A, et al. Antidepressant effects of ketamine in depressed patients. Biol Psychiatry 2000;47: 351-4.
Kishimoto T, Chawla JM, Hagi K, et al. Single-dose infusion ketamine and non-ketamine N-methyl-d-aspartate receptor antagonists for unipolar and bipolar depression: a meta-analysis of efficacy, safety and time trajectories. Psychol Med. 2016; 46:1459-72.
Scheuing L, Chiu CT, Liao HM, Chuang DM. Antidepressant mechanism of ketamine: perspective from preclinical studies. Front Neurosci. 2015;9:249.
Yang Y, Cui Y, Sang K, et al. Ketamine blocks bursting in the lateral habenula to rapidly relieve depression. Nature. 2018; 554:317-22.
Ryan CJ, Loo C. The practicalities and ethics of ketamine for depression. Lancet Psychiatry. 2017;4:354-5.
Nutt DJ, King LA, Phillips LD, Independent Scientific Committee on Drugs. Drug harms in the UK: a multicriteria decision analysis. Lancet. 2010;376:1558-65.
Wan LB, Levitch CF, Perez AM, et al. Ketamine safety and tolerability in clinical trials for treatment-resistant depression. J Clin Psychiatry. 2015;76:247-52.
Singh I, Morgan C, Curran V, et al. Ketamine treatment for depression: opportunities for clinical innovation and ethical foresight. Lancet Psychiatry. 2017;4:419-26.