Altered Glutamate and Gamma-Aminobutyric Acid Metabolism in the Thalamus and Prefrontal Cortex of Patients with Lifelong Premature Ejaculation.

PURPOSE: Previous neuroimaging studies have found abnormalities in the brain structure or functional connectivity of patients with lifelong premature ejaculation (LPE), but the differences in neurotransmitters in relevant brain regions remain unclear. This study aimed to explore the correlation between the central main excitatory neurotransmitter glutamate (Glu) and inhibitory neurotransmitter gamma-aminobutyric acid (GABA) with LPE.

MATERIALS AND

METHODS

This cross-sectional study recruited 50 LPE patients and 50 healthy controls (HCs). Proton magnetic resonance spectroscopy measured Glu, GABA, and creatine levels in the right thalamus and prefrontal cortex. Premature ejaculation symptoms were assessed using the premature ejaculation diagnostic tool (PEDT).

RESULTS

After excluding invalid data, 42 LPE patients and 42 HCs were included. LPE patients showed elevated Glu levels (thalamus: 10.32 vs. 8.59, p<0.001; prefrontal cortex: 9.33 vs. 8.02, p<0.01) and Glu/GABA ratios (thalamus: 4.75 vs. 3.25, p<0.001; prefrontal cortex: 5.45 vs. 4.27, p<0.001), along with reduced thalamic GABA (2.28 vs. 2.27, p<0.001). Glu levels and Glu/GABA ratios positively correlated with PEDT scores, while GABA levels negatively correlated with PEDT. Additionally, GABA levels were higher in LPE patients with good sleep quality than in those with poor sleep (thalamus: 2.50 vs. 2.24, p=0.014; prefrontal cortex: 1.84 vs. 1.63, p<0.01).

CONCLUSIONS

This study reveals differences in Glu and GABA levels in the thalamus and prefrontal cortex between LPE patients and HCs. The imbalance in Glu/GABA may be a contributing factor to increased central excitability and rapid ejaculation in LPE patients. These findings provide new potential targets for the etiological exploration and treatment of LPE.