Aberrant default mode network and auditory network underlying the sympathetic skin response of the penis (PSSR) of patients with premature ejaculation: A resting-state fMRI study.

INTRODUCTION

Hyperactivity of the sympathetic nervous system is considered as an important component involved in the pathological mechanisms of premature ejaculation (PE). However, the neural mechanisms of PE with high sympathetic activity are still not well understood.

METHODS

The activity of the sympathetic innervations in the penis was evaluated by the sympathetic skin response of the penis (PSSR) with an electromyograph and evoked potential equipment. Resting-state functional magnetic resonance imaging (fMRI) data were acquired from 18 PE patients with high sympathetic activity (sPE), 17 PE patients with normal sympathetic activity (nsPE), and 24 healthy controls (HC). We investigated the neural basis of sPE based on the measure of regional homogeneity (ReHo). Moreover, the correlations between brain regions with altered ReHo and PEDT scores and PSSR latencies in the patient group were explored.

RESULTS

Altered ReHo values among three groups were found in the temporal, cingulated, and parietal cortex in the default mode network (DMN), as well as the temporal cortex in the auditory network (AUD). Compared with HC, Patients with sPE had increased ReHo values of brain regions in DMN, AUD, and decreased ReHo values of brain regions in DMN. In addition, increased ReHo values were found in DMN of patients with nsPE, while decreased ReHo values were found in DMN and the attention network (AN). Moreover, sPE patients had increased ReHo values in AUD and decreased ReHo values in DMN when compared with nsPE patients. Finally, altered ReHo values of brain regions in DMN and AUD were associated with PEDT scores and PSSR latencies in the patient group.

CONCLUSION

Our results suggested that PE patients had abnormal ReHo values in DMN, AUD, and AN. Patients with sPE were characterized by increased neuronal activity in AUD and decreased activity in DMN. This highlighted the significances of DMN, AUD, and AN in the pathophysiology of PE and also provided potential neuroimaging biomarkers for distinguishing sPE from nsPE and HC.