Alpha-beta decoupling relevant to inhibition deficits leads to suicide attempt in major depressive disorder

One devastating outcome of major depressive disorder (MDD) is high suicidality, especially for patients with suicide attempt (SA). Evidence indicated that SA may be strongly associated with inhibitory control deficits. We hypothesized that the inhibition function deficits of patient with SA might be underpinned by abnormal neuronal oscillations.

Our study recruited 111 subjects including 74 patients and 37 controls, who performed a GO/NOGO task during magnetoencephalography recording. Time-frequency-representations and phase-amplitude-coupling were measured for the brain circuits involved in the inhibitory function. Phase-slope-indexes were calculated between regions to determine the direction of power flow.

Significant increased reaction time and decreased judgment accuracy were observed in SA group. During the perception stage of GO task (approximately 125 ms), SA group manifested elevated alpha power in ventral prefrontal cortex (VPFC) and attenuated beta power in dorsal anterior cingulate (dACC) compared with other groups (p < 0.01). In the processing stage of NOGO task (approximately 300 ms), they showed decreased beta power in VPFC and increased alpha power in dACC (p < 0.01). Alpha-beta decoupling during both tasks was observed in SA group. Furthermore, the decoupling from VPFC to dACC under NOGO tasks was significantly correlated with suicide risk level.

The number of participants was relatively small, and psychological elements were not involved in current study.

Dysregulated oscillatory activities of dACC and VPFC suggested deficits in execution and inhibition functions triggering high suicide risks. The alpha-beta decoupling from VPFC to dACC could be served as a neuro-electrophysiological biomarker for identifying potential suicide risk.