Jiaming Lu1, Xin Zhang1, and Bing Zhang1
1The Affiliated Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China
Synopsis
Keywords: Head & Neck/ENT, Metabolism
In this study, we using non invasion GABA-edited MEGA-PRESS MRS and
NODDI model to measure the GABA content in bilateral thalamus and the water
diffusion pattern in premature ejaculation patient.
The PE patients have more dispersed neurites in the right putamen, more hindered
water, and less space within axons in the orbitofrontal cortex. The
bilateral thalamus GABA content in PE group is significantly lower than NC
group. These findings
may help us have a better neuroimage upstanding of PE from micro-structure to metabolism
level.
INTRODUCTION
Premature ejaculation (PE) is a major component of male sexual disfunction[1]. The pathology of PE was original considered to be related to hyperesthesia of the glans penis or psychosomatic disturbance, while the studies on neurotransmitters and intra neuro cellular component are still vacancy[2-4]. This study aims are to explore the alterations of the fiber microenvironment and the GABA level in the lifelong PE.METHODS
Nine right-handed
patients with LPE (mean age: 28.89 ± 2.47 years) and seven healthy control(HC) subjects (mean age: 28.14 ± 1.46 years) were recruited. All
MRI data were collected on the Phillps Ingenia 3.0T CX MR scanner. Neurite orientation dispersion and density imaging (NODDI) and
GABA-edited MEGA-PRESS magnetic resonance spectroscopy were acquired. The group
difference in Thalamus GABA was compared with two-sample t test. Different NODDI metrics were evaluated
their spatial covariance within subjects across whole brain using DPABI[5] toolbox to determine the spatial
distribution.RESULTS
We found that
the bilateral thalamus GABA in PE group is significantly lower than HC group
(p<0.05). The orientation dispersion index was significantly lower in the
right putamen in PE patients, and the intracellular volume fraction and the volume
fraction of Gaussian isotropic diffusion were decreased in the orbitofrontal
cortex (p < 0.01, GRF corrected). Moreover, the GABA
level in the thalamus (r = 0.729, p = 0.002) and the NODDI metrics were
significantly correlated with the intravaginal ejaculatory latency time (ODI: r = 0.768, p = 0.001; ICVF: r =
0.847, p < 0.001; IsoVF: r = 0.882, p < 0.001).DISCUSSION and CONCLUSION
In this
study, we using non invasion GABA-edited MEGA-PRESS MRS and NODDI model to
measure the GABA content in bilateral thalamus and the water diffusion pattern.
These findings revealed that brain fiber micro-structural and the inhibit
neurotransmitter GABA were altered, which may help us have a better neuroimage
upstanding of PE from structure and metabolism level.Acknowledgements
No acknowledgement found.References
1. Serefoglu, E.C., et al., An evidence‐based unified definition of lifelong and acquired premature ejaculation: Report of the second International Society for Sexual Medicine Ad Hoc Committee for the Definition of Premature Ejaculation. The journal of sexual medicine, 2014. 11(6): p. 1423-1441.
2. Lu, J., et al., Short-and long-range synergism disorders in lifelong premature ejaculation evaluated using the functional connectivity density and network property. NeuroImage: Clinical, 2018. 19: p. 607-615.
3. Zhang, B., et al., Functional insights into aberrant brain responses and integration in patients with lifelong premature ejaculation. Scientific Reports, 2017. 7(1): p. 460.
4. Lu, J., et al., Brain Cortical Complexity and Subcortical Morphometrics in Lifelong Premature Ejaculation. Frontiers in Human Neuroscience, 2020. 14: p. 283.
5. Yan, C.-G., et al., DPABI: Data Processing & Analysis for (Resting-State) Brain Imaging. Neuroinformatics, 2016: p. 1-13.