Altered neural reward activation predicts clinical depression improvement after a novel loving-kindness meditation: a...

Major depressive disorder (MDD) has become the second largest risk factor affecting human health, with a progress in its treatment especially non-pharmacological therapies. The loving-kindness meditation (LKM) has been introduced to depression but is not popular due to requirement on awareness and concentration, and its utilization in clinical MDD is absent as well as exploration on neural mechanism. This study aims to develop a more feasible novel therapy-loving-kindness meditation integrating cognition and behavior (LKM-CB), examine its effect on clinical depression, and further explore its neural mechanism by multimodal neuroimaging.

In study 1, the knowledge about love and the behavior of love were integrated into the LKM to form a LKM-CB, to better activate patients with cognitive and behavioral approach. It was further utilized to 30 MDD patients (31 controls). Study 2 further explored the neural mechanism behind the LKM-CB with 16 MDD patients, who underwent a structural MRI, resting-state fMRI, and reward card-guessing task fMRI before and after the LKM-CB.

Study 1 developed a novel 8-week LKM-CB and found that compared with control group, LKM-CB significantly improved clinical depression in intervention group. Study 2 further showed that after LKM-CB intervention, patients showed lower activation in frontal-striatum especially middle orbito-frontal cortex (OFC) and anterior cingulate (AC) and insula for win and neutral outcome and anticipation following a loss feedback, while they showed higher activation in frontal-striatum including medial/middle-OFC and hippocampus for loss outcome and anticipation following a win feedback. Similar increased ALFF activation and grey matter in frontal cortex was also found. In contrast, patients showed higher activation in non-reward temporal-occipital cortex for loss and neutral outcome and anticipation following a loss feedback, while they showed decreased temporal-occipital ALFF activation and grey matter.

This study develops a novel LKM-CB, which is effective in improving clinical depression. After the LKM-CB, there is dissociation in the neural reward activation pattern between reward anticipation (hyperactivation) and reward outcome (hypoactivation), and a hypoactivation in non-reward temporal-occipital cortex. This study provides a new feasible LKM-CB for non-pharmacological therapy of MDD, and to our knowledge, this is the first study to explore the neural mechanism behind the efficacy of LKM in depression therapy.