Are There Differences in Brain Morphology in Patients with Lifelong Premature Ejaculation?

Introduction Even though lifelong premature ejaculation (PE) is highly prevalent, few studies have investigated the neural mechanisms underlying PE. Aim This study aimed to investigate whether patients with lifelong PE exhibit macrostructural or microstructural alterations of the parts of the brain involved in the male sexual response. Materials and Methods We enrolled 42 healthy participants and 54 lifelong PE patients. Lifelong PE was diagnosed according to the Premature Ejaculation Diagnostic Tool (PEDT) and intravaginal ejaculation latency time (IELT). We compared measures of cortical morphology, such as volumes of gray matter, white matter, cerebellum volumes, and subcortical structures (ie, amygdala, caudate, hippocampus, globus pallidus, putamen, and thalamus) between the groups using a voxel-based morphometry method from whole-brain T1-weighted magnetic resonance imaging. Moreover, we evaluated the relationships between the relevant cerebral alterations and the severity of symptoms obtained from participants via self-reported questionnaires. Main Outcome Measures Cerebral macrostructural and microstructural alterations were assessed in PE patients and controls, along with the correlation of caudate nucleus changes in PE patients with clinical data (including the PEDT and the IELT). Results The mean volume of the caudate nucleus was significantly larger in the lifelong PE patients compared with healthy controls (P = .048). Moreover, caudate nucleus volume was positively correlated with PEDT score (r = 0.621; P = .0179) and negatively correlated with the IELT (r = −0.592; P = .0101). However, cortex morphology and the other subcortical volumes were not significantly different between the 2 groups (P > .05). Clinical Implications Microstructural alterations in deep gray matter nuclei might be a useful parameter for studying the mechanism of the neurobiology underlying PE. Strengths and Limitations There are few studies examining microstructural changes in PE patients. This study furthers our understanding of the etiology of PE. Limitations include the small sample, which limits our ability to make an absolute determination as to whether such subcortical changes are the cause or the consequence of lifelong PE. Conclusions We found a significant difference in caudate nucleus volume between patients with PE and healthy controls. In addition, the caudate nucleus volume was positively associated with the severity of PE symptoms. More extensive and possibly longitudinal studies are needed to improve our understanding of the mechanism of the neurobiology underlying PE.