Low-dose ketamine modulates brain entropy in treatment-resistant depression: Results from two neuroimaging clinical trials.
Ying-Jay Liou, Li-Kai Cheng, Wei-Chen Lin et al.
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In 30 seconds
This analysis of resting-state functional MRI data from two randomized clinical trials examined whether low-dose ketamine changes brain entropy in patients with treatment-resistant depression. Scans were assessed at baseline and 3 days after a single infusion. In Trial 1, entropy increased after ketamine in several regions, including the gyrus rectus, cerebellar vermis, substantia nigra, red nucleus, and bilateral locus coeruleus. In Trial 2, the ketamine group had higher left-amygdala entropy than the midazolam group. The findings suggest rapid changes in brain signal complexity, but do not establish that these changes mediate clinical improvement.
Key findings
- In Trial 1, brain entropy increased after ketamine in the gyrus rectus, cerebellar vermis I/II, substantia nigra, red nucleus, and bilateral locus coeruleus.
- In Trial 2, the ketamine group showed higher left-amygdala entropy than the midazolam group.
- Imaging was assessed at baseline and 3 days after a single infusion.
Why it matters
The results identify frontolimbic, cerebellar, and neuromodulatory regions in which brain entropy may change soon after ketamine in treatment-resistant depression. This offers a potential neuroimaging correlate of ketamine’s rapid antidepressant and antianhedonic effects, while underscoring that the relationship between entropy changes and clinical response remains uncertain.
What to keep in mind
The abstract does not report whether entropy changes were linked to measured clinical outcomes; their relationship to antidepressant or antianhedonic effects requires further investigation.