Abstract

Abstract Introduction Ejaculatory dysfunction is common male sexual dysfunction, which is a conceptual continuum, and premature ejaculation (PE) and delayed ejaculation (DE) anchor the opposite ends of this conceptual continuum, and normal ejaculation is in the center. The pathogenesis of PE and DE is still not fully elucidated, and the studies on the central nervous mechanisms are highly lacking, and the differences in brain function between PE and DE are unclear. Objective We try to use a high-density electroencephalogram (HDEEG) to explore the differences in brain function to compensate for the deficiency of previous studies based on functional magnetic resonance Imaging (fMRI) and provide a theoretical foundation for future studies exploring the treatment methods. Methods We included 12 lifelong premature ejaculation (LPE) patients and 11 lifelong delayed ejaculation (LDE) patients, and all of them are right-handed. We evaluated the conditions of all subjects, who reported estimated intravaginal ejaculation latency time (eIELT). We used the premature ejaculation diagnostic tool (PEDT), the abridged international index of erectile function (IIEF-6), and erection hardness score (EHS) to quantify the sexual function and sexual arousal. EEG signals were recorded in patients with LDE and LPE during two segments of resting and watching an erotic video, respectively. The duration of the recording was about five minutes and fifteen minutes, respectively. The subjects whose EEG signals were less than 30 segments were excluded from the final analysis. The power spectral density was analyzed based on fast Fourier transform (FFT). Differences in the power spectral density during resting and sexual arousal between the two groups were compared. We analyzed changes in the power spectral density of β oscillation with sexual arousal in each group. Results There were no statistical differences in the general clinical characteristics. The mean eIELT of LPE patients was 0.8 ± 0.4 minutes. The scores of EHS were not statistically different during watching an erotic video between the two groups. There were no significant differences in δ, θ, and α oscillations between the LDE group and the LPE group during resting, but the LDE group had significantly higher power of β1, β2, and β3 oscillations. The power of β1, β2, and β3 oscillations was significantly higher in the LDE group during watching an erotic video, and other oscillations were not significantly different. The power of β1, β2, and β3 oscillations significantly increased in the LDE group during sexual arousal, and β2 and β3 oscillations significantly increased in the LPE group. Conclusions Based on the previous literature and our results, we proposed a scientific hypothesis to explain the increase of β oscillation in LDE patients. The increase of β oscillation is associated with the activation of the inhibitory brain area. The over-activation of the inhibitory brain area leads to LDE and the under-activation leads to LPE. The activation of the inhibitory brain area may be associated with gamma-aminobutyric, which is an inhibitory neurotransmitter. Disclosure No

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