A region of the brain known as the amygdala may play a key role in predicting symptom improvement after ketamine treatment in patients with treatment-resistant anxiety depression Affective Disorders Diary.
“Since the antidepressant effects of ketamine in patients with anxiety depression remain uncertain, there is a need to investigate potential biomarkers predicting the antidepressant efficacy of ketamine in patients with anxiety depression,” said the study author Bin Zhang of Guangzhou Medical University Brain Affiliated Hospital. .
“Previous studies have highlighted that differences in functional connectivity in the amygdala are related to improvement in depression after ketamine treatment in depressed patients, but their role in anxious depressed patients is uncertain. Therefore, we investigated the correlation between improvement in depression after ketamine treatment and functional amygdala connectivity in patients with anxious depression.
For their study, the researchers looked at neuroimaging data from 31 patients with anxiety depression and 18 patients with non-anxiety depression.
The researchers only included participants who had been diagnosed with major depression without comorbid psychotic symptoms, had a score greater than 17 on the Hamilton Depression Rating Scale, had failed to improve after at least two antidepressant treatments, had fMRI brain scans done and had six ketamine infusions.
Among patients with anxiety depression, approximately 60% (20 patients) experienced clinically significant reductions in symptoms of depression after their sixth infusion of ketamine. The other 11 patients with anxious depression were classified as non-responders.
The researchers found that prior to ketamine infusions, those who responded to treatment tended to have greater functional connectivity between the left lateral basal amygdala and the left precuneus compared to non-responders. Additionally, connectivity between the two brain regions was significantly reduced after treatment in responders.
Patients with anxiety depression also tended to have reduced connectivity between the right centriomedial agydala and the right middle temporal gyrus compared with patients with non-anxiety depression, which predicted treatment response.
“Corresponding to the crucial role of the amygdala in emotion regulation, particularly in negative emotions, our study showed that functional connectivity of the amygdala is associated with amelioration of depression to ketamine infusions in patients suffering from anxious depression,” Zhang told PsyPost.
“The most surprising finding of the current study was that the baseline amygdala-precuneus hyperconnectivity found in responders versus non-responders was significantly reduced at day 13 from baseline after six infusions This may indicate an underlying neural potential through which ketamine exerts its antidepressant effect in patients with anxiety depression.
The results provide new insights into the mechanisms underlying the antidepressant effects of ketamine. But as with any study, the new research has limitations. The researchers noted that their sample size was relatively small. Future research with larger samples should be conducted to validate the results.
“Although the results of our study may suggest that amygdala functional connectivity is a significant predictor of treatment response to ketamine infusions in patients with anxiety depression, further validation is needed,” Zhang said. “Furthermore, further studies exploring the potential antidepressant mechanisms of ketamine may aid in the treatment of patients with anxiety depression.”
The study, “Differences in functional connectivity in the amygdala are linked to the antidepressant efficacy of ketamine in patients with anxiety depressionwas written by Shiqi Yuan, Xin Luo, Xiaoyu Chen, Mingqia Wang, Yiru Hu, Yanling Zhou, Yuping Ning, and Bin Zhang.