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Increase in thalamic cerebral blood flow is associated with antidepressant effects of ketamine in major depressive disorder

Matti Gärtner, Mischa de Rover, Lena Václavů, Milan Scheidegger, Matthias J.P. van Osch, Simone Grimm

The World Journal of Biological Psychiatry January 5, 2022 DOI: 10.1080/15622975.2021.2020900 via OpenAlex

Summary

In patients with Major Depressive Disorder, increased blood flow in the thalamus one day after a single low-dose ketamine infusion is linked to greater improvement in depressive symptoms. Lower thalamus blood flow before treatment predicts both a larger increase in flow after ketamine and stronger symptom reduction. The study used arterial spin labelling, a brain imaging technique that directly measures cerebral blood flow, avoiding the ambiguity of standard BOLD imaging. These findings suggest that measuring regional blood flow could help guide ketamine treatment decisions.

Study at a glance

Characteristics Observational cohort Peer reviewed
Sample size 21
Population Patients with Major Depressive Disorder
Intervention Ketamine
Dose subanesthetic
Duration 24-hour follow-up after a single intravenous infusion
Topics Depression Ketamine
Keywords Antidepressant Cerebral blood flow Thalamus
Citations 11
Key finding Increase in thalamus perfusion 24 hours after ketamine administration is associated with greater improvement of depressive symptoms, and lower baseline thalamus perfusion predicts both larger perfusion increases and stronger symptom reduction.

Abstract

Ketamine is a promising treatment option for patients with Major Depressive Disorder (MDD) and has become an important research tool to investigate antidepressant mechanisms of action. However, imaging studies attempting to characterise ketamine's mechanism of action using blood oxygen level-dependent signal (BOLD) imaging have yielded inconsistent results- at least partly due to intrinsic properties of the BOLD contrast, which measures a complex signal related to neural activity. To circumvent the limitations associated with the BOLD signal, we used arterial spin labelling (ASL) as an unambiguous marker of neuronal activity-related changes in cerebral blood flow (CBF). We measured CBF in 21 MDD patients at baseline and 24 h after receiving a single intravenous infusion of subanesthetic ketamine and examined relationships with clinical outcomes. Our findings demonstrate that increase in thalamus perfusion 24 h after ketamine administration is associated with greater improvement of depressive symptoms. Furthermore, lower thalamus perfusion at baseline is associated both with larger increases in perfusion 24 h after ketamine administration and with stronger reduction of depressive symptoms. These findings indicate that ASL is not only a useful tool to broaden our understanding of ketamine's mechanism of action but might also have the potential to inform treatment decisions based on CBF-defined regional disruptions.

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