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

Abstract

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.

Reduced segregation and integration of structural brain network associated with sympathetic and dorsal penile nerve activity in anejaculation patients: a graph‐based connectome study

“…The phase of expulsion is controlled by the parasympathetic and somatic nervous system, as well as the perineal muscles (Alwaal et al, 2015;Clement & Giuliano, 2016;Ch ehensse et al, 2017a,b). The events of peripheral neural system are under the control of spinal centers including the spinal generator of ejaculation (SGE) (Chehensse et al, 2016;Ch ehensse et al, 2017a,b;de Rodr ıguez-Peña et al, 2017), which is regulated by the excitatory and inhibitory inputs from the brain (Qin et al, 2017;Zhang et al, 2017;Atalay et al, 2019;Xu et al, 2019). Therefore, the brain is also responsible for these two phases and it is especially involved in the pleasant sensation produced by the orgasm reaction (Flannigan et al, 2018;Wise et al, 2017).…”

Is There A Role for Dihydrotestosterone/ Estradiol Ratio in Premature Ejaculation?

“…Increased aromatase activity secondary to the accumulation of adipose tissue may be a plausible explanation because of the significant positive correlation between BMI and E2 in our patients. However, secondary PE showed significantly higher BMI compared to primary PE and the control group that could be explained by the fact that primary PE has been viewed as a neurobiological defect rather than a hormonal dysfunction (34) ; nevertheless; the condition appears to be more complex and may include other significant biological components (35) .…”

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

“…In this study, both the degree and betweenness centrality of ORBmid.R were abnormal in the group of PE with depression when compared with the groups of HC and PE without depression. The prefrontal cortex, especially the orbitofrontal cortex was supposed to play an important role in the occurrence, maintenance, remission of depressive symptom (Frodl et al., 2010; Scheuerecker et al., 2010) and was also considered to be involved in the aetiology of PE (Atalay et al., 2019; Guo et al., 2018). Previous studies had demonstrated that the orbitofrontal cortex, a part of prefrontal cortex was involved in the regulation of cognition, emotion and attention (Rolls & Grabenhorst, 2008; Golkar et al., 2012), as well as the inhibitory control over sexual activity (Cheng et al., 2015).…”

“…In addition, PE is not only a common symptom of depression but also a frequent side‐effect of the selective serotonin reuptake‐inhibitors (SSRIs), which is a first line treatment option of antidepressant medication (Castiglione et al., (2016); Chokka & Hankey, 2018). Therefore, PE is considered as a complex interaction of psychological and biological factors, including depression and abnormal function and structure of certain brain areas (Zhang et al., 2017; Atalay et al., 2019).…”