Abstract

The article this month in the Journal of Endourology by Kim and associates presents evidence for the potential role of anti-inflammatory intervention to reduce injury and or accelerate recovery of cavernosal nerve function. Surgeons and patients alike have long recognized that after robotic radical prostatectomy, recovery of sexual function essentially always takes months to years. Clearly understanding the physiology of why it takes “2 years” is the key to understanding either how to prevent injury or help accelerate recovery.
In 1943, the neurosurgeon HJ Seddon described the mechanisms for peripheral nerve injury and recovery (Seddon HJ Brain 1943;66:237). When simplified to its most basic components, he demonstrated three levels of injury: neurotmesis or permanent because of transection/resection, axonotmesis, or intermediate (months to years), where the myelin sheath is preserved but the axon is injured requiring regeneration, and neurapraxia or transient (days to weeks) similar to a concussion. 1 Based on Seddon's findings, a surgeon can physically preserve the cavernosal nerve, but because of thermal or traction injury, the axon is injured presumably near the prostatic vascular pedicle, requiring degeneration of the axon and regeneration explaining the axonotmetic injury. The potential to prevent injury or improve recovery logically introduces a role for anti-inflammatory interventions. This study sheds reasonably compelling evidence for a role for an anti-inflammatory intervention. Usually, retrospective nonrandomized consecutive experiences are fatally flawed because of the confounding effect of the “learning curve.” What is unique is that the control group is introduced after the agent eliminated this confounder. The fact that a benefit is seen, in my opinion, warrants and supports publication and additionally further study with a multicentered randomized controlled trial. However, the remaining unknown confounder of individual surgeon skill demands that each individual surgeon must have randomization of the agent to adjust for this confounder.
