Decreased grey matter volume in dorsolateral prefrontal cortex and thalamus accompanied by compensatory increases in middle cingulate gyrus of premature ejaculation patients

Abstract Introduction The prefrontal–cingulate–thalamic areas are associated with ejaculation control. Functional abnormalities of these areas and decreased grey matter volume (GMV) in the subcortical areas have been confirmed in premature ejaculation (PE) patients. However, no study has explored the corresponding GMV changes in the prefrontal–cingulate–thalamic areas, which are considered as the important basis for functional abnormalities. This study aimed to investigated whether PE patients exhibited impaired GMV in the brain, especially the prefrontal–cingulate–thalamic areas, and whether these structural deficits were associated with declined ejaculatory control. Methods T1‐weighted structural magnetic resonance imaging (MRI) data were acquired from 50 lifelong PE patients and 50 age‐, and education‐matched healthy controls (HCs). The PE diagnostic tool (PEDT) was applied to assess the subjective symptoms of PE. Based on the method of voxel‐based morphometry (VBM), GMV were measured and compared between groups. In addition, the correlations between GMV of brain regions showed differences between groups and PEDT scores were evaluated in the patient group. Results PE patients showed decreased GMV in the right dorsolateral superior frontal gyrus (clusters = 13, peak T ‐values = −4.30) and left thalamus (clusters = 47, T = −4.33), and increased GMV in the left middle cingulate gyrus (clusters = 12, T = 4.02) when compared with HCs. In the patient group, GMV of the left thalamus were negatively associated with PEDT scores ( r = −0.35; P = 0.01). Receiver operating characteristic (ROC) analysis showed that GMV of the right dorsolateral superior frontal gyrus (AUC = 0.71, P < 0.01, sensitivity = 60%, specificity = 78%), left thalamus (AUC = 0.72, P < 0.01, sensitivity = 92%, specificity = 46%) and middle cingulate gyrus (AUC = 0.69, P < 0.01, sensitivity = 50%, specificity = 90%), and the combined model (AUC = 0.84, P < 0.01, sensitivity = 78%, specificity = 80%) all had the ability to distinguish PE patients from HCs. Conclusion Disturbances in GMV were revealed in the prefrontal–cingulate–thalamic areas of PE patients. The findings implied that decreased GMV in the dorsolateral prefrontal cortex and thalamus might be associated with the central pathological neural mechanism underlying the declined ejaculatory control while increased GMV in the middle cingulate gyrus might be the compensatory mechanism underlying PE.