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Ketamine-Associated Brain Changes: A Review of the Neuroimaging Literature

Dawn F. Ionescu, J. Felicione, Aishwarya K. Gosai, Cristina Cusin, Philip Shin, Benjamin G. Shapero, Thilo Deckersbach

Harvard Review of Psychiatry February 20, 2018 DOI: 10.1097/hrp.0000000000000179 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Intervention Ketamine
Dose Subanesthetic doses
Topics Esketamine Ketamine
Key findings The authors report that neuroimaging studies of ketamine in treatment-resistant depression repeatedly implicate the subgenual anterior cingulate cortex and suggest ketamine may decrease self-monitoring, increase emotional blunting, and increase reward-processing activity. They conclude that ketamine's antidepressant mechanism remains incompletely understood and requires further study.

Abstract

Abstract Major depressive disorder (MDD) is one of the most prevalent conditions in psychiatry. Patients who do not respond to traditional monoaminergic antidepressant treatments have an especially difficult-to-treat type of MDD termed treatment-resistant depression. Subanesthetic doses of ketamine—a glutamatergic modulator—have shown great promise for rapidly treating patients with the most severe forms of depression. As such, ketamine represents a promising probe for understanding the pathophysiology of depression and treatment response. Through neuroimaging, ketamine’s mechanism may be elucidated in humans. Here, we review 47 articles of ketamine’s effects as revealed by neuroimaging studies. Some important brain areas emerge, especially the subgenual anterior cingulate cortex. Furthermore, ketamine may decrease the ability to self-monitor, may increase emotional blunting, and may increase activity in reward processing. Further studies are needed, however, to elucidate ketamine’s mechanism of antidepressant action.

Comparable studies

Other narrative reviews on ketamine, most cited first.

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