Abstract
Hyperactivity of the sympathetic nervous system was considered as one of the factors involved in the pathological mechanisms of premature ejaculation (PE). Sympathetic skin response of the penis (PSSR) was used to evaluate the activity of sympathetic innervations in the penis, which was controlled by the central nervous system (brain). Shorter PSSR was found in PE patients; however, little was known regarding the central neural mechanisms of PE patients with high sympathetic activity. PSSR of PE patients was evaluated, and diffusion tensor images ofparticipants were collected. Graph theoretical analysis was employed to examine the differences of the topological properties of structural brain connectome between PE patients with high sympathetic activity and healthy controls (HCs). Moreover, the relationships between topological characteristics and clinical features in PE patients were also explored. Decreased local efficacy was found in the left amygdala, right pallidum and thalamus in the white matter brain networks of PE when compared with HC (survived false discovery rate (FDR) correction). In addition, PE patients showed decreased global efficacy in the left amygdala and right rolandic operculum, supramarginal gyrus, heschl gyrus, inferior temporal gyrus, pallidum and thalamus; however, these results did not survive FDR correction. Finally, the local efficacy of right thalamus had a positive correlation with the premature ejaculation diagnostic tool (PEDT) scores, while the local efficacy of left amygdala was negatively associated with the state score of the state-trait anxiety inventory (STAI) and penile shaft sensory threshold. The results highlighted the abnormal topological properties of structural brain connectome in PE with high sympathetic activity. We also suggested that the clinical features of PE were related to the abnormality of several brain regions involved in the central control of ejaculation and emotion. This study provided new insights into the central neural mechanisms of PE, which might offer biological markers for understanding the physiopathology of PE.
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