I had video urodynamics done in December 2009 that I have subsequently been told by other urologists failed because I did not urinate. The diagnosis of the urologist who did the test was: "In view of long history, he may have bladder neck dysynnergia v. Hinmans syndrome. Plan: Three options: no treatment v. start CIC v. Bladder neck incision."
At the urging of my urologist I did begin catherization before bed and upon waking (that was her recommendation to prevent further bladder decompensation); however, I had five infections if less than four months. Subsequent urologists said that these infections were caused by only using a catheter twice a day while retaining large amounts of urine. CIC is clean, but it is not sterile. A urologist here on "Just Answers" concurred.
I had a cytoscopy in November 2007 with the only reportable findings of: Posterior urethra showed lateral lobe hypertrophy, relative significant. No bladder stones or mucosal lesions identified. Prostate gland approximately 3 cm in size. Uroflo revealed a voiced volume of 296 ml with a flow time of 31 seconds and an average flow of 4 ml per second and a peak flow of 13 ml second. Post void residual was 155 ml."
I also had a cyctoscopy in August 2003 which stated: "There were no strictures encountered. The prostate was hyperemic and obstructive, approximately 10-15 grams in size, tribolar. Benign prostatic hypertrophy with chronic prostatitis, no evidence of urethral stricture, and hypogonadism."
I went an urologist at Stanford a few weeks ago and he wants to do urodyamics again. According to "Urodynamics Made Easy" by Dr. Christopher R Chapple, copyright 2009, "Video urodynamics is necessary to make the diagnosis of bladder neck obstruction. In this condition the bladder neck does not open completely during voiding and there is little or no flow during a well sustained detrusor contraction."
The Stanford urologist said given my age and duration of the condition, 99% of the time the problem is the bladder neck and not the prostate. (I assume he meant if there is a blockage and the problem is not just detrusor underactivity). I showed him a copy of the relevant pages in the book and he pointed to the representation showing a "tight bladder neck".
He warned that if the urodynamics revealed the need for a TUBIN (Transurethral Incision of the Bladder Neck), a possibility exists for retrograde ejaculation and accompanying reduced sensation at orgasm. He said probability was about 20% with single incision and 40% with bilaterial incision. But like every other doctor he said "But if you're one of the 20% it doesn't matter what the odds are". That must be on the final test at medical school! Most urologists cannot give you a percentage for that side effect and the literature goes all the way from zero percent for a single incision to retrograde ejaculation happening "most of the time". I read an article recently that said that a modified TUBIN exists which preserves antegrade ejaculation by preserving a portion of the supramontanal tissue. (Urology International, January 18, 2008)
The doctor told me to try Sudafed to see if that would produce antergrade ejaculation with the Rapiflo. He said that would also show whether antergrade could be produced via Sudafed if I had the TUBIN, and I had the retrograde ejaculation side effect. I am concerned about doing that since I have had tachycardia episodes from mitral valve prolapse, and take Metropopol daily as a result.
Since I wrote the above question, I know have read the following:
Tamsulosin (Flomax) did not cause retrograde ejaculation. It causes
anejaculation (absence of ejaculation) probably due to the drug's
effect on the D2 (dopaminergic) receptors. In addition it seems to
have an effect on the 5HT1a (serotoninergic) receptors. We all know
what fiddling with serotonin does to sexual function from the SSRI
experience. (I know that personally from taking Prozac a decade ago!)
A recent comparative study (ABEJAC Study) of alfuzosin and tamsulosin in young, healthy volunteers has objectively confirmed the increased risk of ejaculatory disorders in patients receiving tamsulosin. This disorder is not due to tamsulosin's effect on the bladder neck and thus is not retrograde ejaculation (Figure 4).
(Well, there goes my thinking that the Rapiflo may be working because it is having the retrograde ejaculation effect on me.)
This effect could be due to differential peripheral effects on the seminal vesicles and/or vas deferens or central actions involving binding to 5HT1A and D2 receptors involved in the ejaculation mechanism. A novel, mechanistic study by Giuliani and colleagues explored the central differences of these 2 agents in adult Wistar rats. A central facilitatory role of 8-OH-DPAT, a 5HT1A agonist, on ejaculation is well documented. Using various inhibitors of 5HT1A and D2-like receptors, which were co-injected intracerebroventrically concurrently with 8-OH-DPAT, these investigators determined that tamsulosin's effect was likely due to interaction with D2 receptors centrally. These and other pioneering studies will help us map out uncharted central pathways involved in many aspects of sexual function (arousal, erection, ejaculation, and orgasm).
The article has graphs that show that alfuzosin has little to no effect on ejaculatory function, even at increased dosages.
Uroxatral worth a try?
Thank you for your assistance.