Central neural mechanisms of lifelong premature ejaculation: a narrative synthesis of neuroimaging and electrophysiological evidence

Introduction Premature ejaculation (PE) is one of the most prevalent male sexual disorders, with lifelong PE (LPE) affecting ~cx3%-5% of men. While peripheral, psychological, and relational factors are well-known contributing factors, accumulating neuroimaging and electrophysiological evidence suggests central neural mechanisms, including serotonergic, dopaminergic, and other neuromodulatory pathways play a role. Objectives To synthesize findings from neuroimaging and electrophysiological (electroencephalography) studies, providing an integrative perspective on the neural substrates of LPE and identifying gaps for future research. Methods A narrative review was conducted based on 43 original studies reporting structural-, functional-, and network-level neural correlates of LPE. The literature search and selection were performed in accordance with the Scale for the Assessment of Narrative Review Articles guidelines to ensure transparency and methodological rigor. Studies were categorized by modality, and findings were qualitatively synthesized to identify convergent patterns, regional alterations, and clinical correlations. Results Structural neuroimaging in LPE patients consistently demonstrates altered gray matter volume, cortical thickness, and white matter microstructure in prefrontal, orbitofrontal, striatal, thalamic, limbic, and temporal regions. Functional analyses reveal reduced top-down inhibitory control from prefrontal regions, hyperconnectivity within limbic–temporal sensory circuits, and dysregulated network dynamics across cortico-striato-thalamic pathways. Electroencephalography studies indicate abnormal cortical excitability and high-beta responses in frontal and temporal regions during sexual arousal. Multimodal studies show these neural alterations correlate with clinical severity, and machine learning models achieve high accuracy in differentiating LPE patients from healthy controls. Conclusions LPE is associated with distributed neural network dysfunction, characterized by impaired inhibitory control, exaggerated sensory processing, and dysregulation of serotonergic, dopaminergic, and other neuromodulatory systems. Although central changes may be both a cause and a consequence of LPE, these findings primarily advance mechanistic understanding and should be considered research-level indicators rather than diagnostic biomarkers.