Graph theory analysis reveals premature ejaculation is a brain disorder with altered structural connectivity and depressive symptom: A DTI-based connectome study.

ABSTRACT

Recent research has shown that premature ejaculation (PE) is associated with negative psychological effects (e.g., depression) and the decline of control over ejaculation is accompanied by structural and functional abnormalities in specific brain areas and connections. However, little is known about the alterations of topological organization in the brain network of patients with PE and its relationship with depressive symptom. We acquired diffusion tensor images, sexual function and depression assessment in 16 lifelong PE patients with depressive symptom, 16 lifelong PE patients without depression and 32 age- and education-matched healthy controls (HC). The differences in nodal centrality and different hub regions among the three groups were compared. Correlation analyses were conducted between the nodal centrality of brain regions displaying significant group differences and the clinical parameters of PE patients. PE patients with depression had increased nodal degree in the right middle frontal gyrus (orbital part) (ORBmid.R) (survived FDR-correction) compared with HC and PE without depression. PE patients with depression also had increased nodal degree in the left and right posterior cingulate gyrus (PCG.L; PCG.R) compared with HC. In addition, PE with depression had increased nodal betweenness in ORBmid.R compared with HC and PE without depression. Moreover PE with depression had decreased nodal participation in the right rolandic operculum (ROL.R), postcentral gyrus (PoCG.R) and supramarginal gyrus (SMG.R) compared with HC, and had decreased nodal participation in ROL.R and the right inferior parietal gyrus (IPL.R) compared with PE without depression, while PE without depression had increased nodal participation in the left precuneus (PCUN.L) compared with HC. The degree and betweenness of ORBmid.R were positively correlated with the total scores of Beck depression inventory (BDI) while the participation of IPL.R had a negative association with the total scores of BDI. Different hubs were found among PE patients with and without depression and HC based on nodal degree, betweenness and participation; however, no significant group differences were found in the frequency distribution of high-degree hubs, high-betweenness hubs, provincial hubs and connector hubs. These findings demonstrated that PE was a brain disorder with altered structural connectivity pattern of brain network and depressive symptom, which suggested that altered structural connectivities of the fronto-cingulate-parietal control network were core neurobiological features associated with PE and depression. Together, these alterations could prove helpful for understanding the pathophysiological mechanisms of PE in depression.