Dr. Dimitrakov says that almost everything has a quick fix once you know
what you are trying to fix. I don't suppose that he means things like
cancer, kidney failure, heart disease, etc., but stuff like we are
concerned with here.
Obviously, we usually don't know what we are trying to fix.
That points to diagnosis as the main problem.
But how can you diagnose something whose cause is not understood?
Maybe etiology is the main problem.
Where should we start looking for clues to the etiology?
Well, there are lots of places to look. Mostly people seem to be looking
at biochemistry (including molecular biology) and bacteriology.
An argument can be made that the place to start looking is the pudendal
nerve system.
The reason that I say this is that all of our symptoms (pain, urinary
dysfunction, and sexual dysfunction) can be caused by impaired pudendal
nerve function (according to Dr. Antolak).
Indeed, pain *must* involve nerves, and so I think must the other two.
Therefore a working hypothesis can be
"All prostatitis symptoms result from impaired function of the pudendal nerve."
Now the question becomes
"What impairs the function of the pudendal nerve?"
Can trauma do it?
Can infection do it?
Can immune dysfunction do it?
If the answer is no to any of these, then under the working hypothesis,
that can be ruled out as the fundamental etiology.
If none can be ruled out on this basis, then the question for each
possiblity becomes, "What is the mechanism by which this impairs the
function of the pudendal nerve?" If no one can come up with a reasonable
mechanism for one of these possible causes of nerve impairment, then that
cause is placed under a cloud of suspicion (but it cannot be struck off
the list).
After reasonable mechanisms are generated, they can, in principle, be
tested experimentally.
It seems to me that this would be a logical approach to prostatitis research.
> Can trauma do it?
======Yes.
> Can infection do it?
======Yes (like in MS) - so more appropriately the question is "Can
inflammation do it?"
> Can immune dysfunction do it?
=======Yes.
>
> If the answer is no to any of these, then under the working
hypothesis,
> that can be ruled out as the fundamental etiology.
>
> If none can be ruled out on this basis, then the question for each
> possiblity becomes, "What is the mechanism by which this impairs the
> function of the pudendal nerve?" If no one can come up with a
reasonable
> mechanism for one of these possible causes of nerve impairment, then
that
> cause is placed under a cloud of suspicion (but it cannot be struck
off
> the list).
==========Actually, if you remember Dr. Nyberg's words on Wednesday
morning) we all see and hear patients here when they have converged to
a common pathway of nerve damage. We don't know what initiated this but
we have the result and don't know what caused it.
> After reasonable mechanisms are generated, they can, in principle, be
> tested experimentally.
=====That's what people in IC research are doing.
>
> It seems to me that this would be a logical approach to prostatitis
research.
=====You need to get a lot of basic science people interested in that -
studying neurogenic inflammation, for example.
--
This communication is intended to provide general information, and in
no way is a substitute for face-to-face medical care. No implication
of a
doctor-patient relationship should be assumed by the reader.
Best regards,
Jordan Dimitrakov, MD, PhD
Sent via Deja.com http://www.deja.com/
Before you buy.
"John Garst" <ga...@chem.uga.edu> wrote in message
news:garst-31100...@garst.chem.uga.edu...
> If the prostate gland is inflammed and the swollen gland is constricting the
> urethra thereby causing urinary dysfunction, then what role would the
> pudendal nerve play in terms of urinary dysfunction?
I can only comment that Dr. Antolak stated that pudendal nerve trauma
could cause urinary dysfunction (as well as pain and sexual dysfunction).
One possibility:
nerve trauma => PSA increase in prostate => autoimmune response and inflammation