New insights into erectile dysfunction


This article was originally posted on harvardprostateknowledge.org

When erectile function becomes impaired following radical prostatectomy, the problem has traditionally been attributed to nerve damage. The nerves that trigger erections may become damaged during surgery (even during so-called nerve-sparing surgery), leading to a problem known as neuropraxia — a temporary loss of function that theoretically should recover in time. The problem is that it can take as long as two years for the nerves to recover sufficiently to enable a man to have a spontaneous erection, and by then other damage may have occurred.

Recent research suggests that when the penis is flaccid for long periods of time, and therefore deprived of a lot of oxygen-rich blood, the low oxygen level causes some muscle cells in the columns of erectile tissue (corpora cavernosa) to lose their flexibility and gradually change into something akin to scar tissue. This scar tissue, moreover, seems to interfere with the penis’s ability to expand when it’s filled with blood. In fact, imaging studies indicate that blood may drain away from the penis rather than fill it.

Less research has been done about impotence after radiation therapy, but it appears that the underlying cascade of damaging events is similar to what occurs after radical prostatectomy. Radiation damages the lining of the small blood vessels, but this damage may take months or even years to manifest itself.

What all this means is that the traditional advice given to men — essentially to wait for erectile function to return on its own — may not be adequate. Simply put, erections seem to work on a use-it-or-lose-it basis. To prevent the secondary damage that may occur if the penis remains flaccid for a prolonged period, researchers now think that a better approach is to intervene soon after treatment to restore erectile function.

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