Pudendal nerve and internal pudendal artery damage may contribute to radiation-induced erectile dysfunction - Abstract

PURPOSE/OBJECTIVES: Erectile dysfunction is common after radiation therapy for prostate cancer; yet, the etiopathology of radiation-induced erectile dysfunction (RI-ED) remains poorly understood.

A novel animal model was developed to study RI-ED, wherein stereotactic body radiation therapy (SBRT) was used to irradiate the prostate, neurovascular bundles (NVB), and penile bulb (PB) of dogs. The purpose was to describe vascular and neurogenic injuries after the irradiation of only the NVB or the PB, and after irradiation of all 3 sites (prostate, NVB, and PB) with varying doses of radiation.

METHODS AND MATERIALS: Dogs were treated with 50, 40, or 30 Gy to the prostate, NVB, and PB, or 50 Gy to either the NVB or the PB, by 5-fraction SBRT. Electrophysiologic studies of the pudendal nerve and bulbospongiosus muscles and ultrasound studies of pelvic perfusion were performed before and after SBRT. The results of these bioassays were correlated with histopathologic changes.

RESULTS: SBRT caused slowing of the systolic rise time, which corresponded to decreased arterial patency. Alterations in the response of the internal pudendal artery to vasoactive drugs were observed, wherein SBRT caused a paradoxical response to papaverine, slowing the systolic rise time after 40 and 50 Gy; these changes appeared to have some dose dependency. The neurofilament content of penile nerves was also decreased at high doses and was more profound when the PB was irradiated than when the NVB was irradiated. These findings are coincident with slowing of motor nerve conduction velocities in the pudendal nerve after SBRT.

CONCLUSIONS: This is the first report in which prostatic irradiation was shown to cause morphologic arterial damage that was coincident with altered internal pudendal arterial tone, and in which decreased motor function in the pudendal nerve was attributed to axonal degeneration and loss. Further investigation of the role played by damage to these structures in RI-ED is warranted.

Written by:
Nolan MW, Marolf AJ, Ehrhart EJ, Rao S, Kraft SL, Engel S, Yoshikawa H, Golden AE, Wasserman TH, LaRue SM.   Are you the author?
Department of Clinical Sciences, and Center for Comparative Medicine and Translational Research, North Carolina State University, Raleigh, North Carolina; Department of Environmental and Radiologic Health Sciences, Colorado State University, Fort Collins, Colorado; Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado; Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado; Department of Radiation Oncology, Washington University, St. Louis, Missouri.  

Reference: Int J Radiat Oncol Biol Phys. 2015 Mar 15;91(4):796-806.
doi: 10.1016/j.ijrobp.2014.12.025

PubMed Abstract
PMID: 25752394

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