[InHisHands]

I just talked to a girl who became pain free after taking this- anyone else hear of it? Or has anyone tried this?

Thanks!!

[JOAN_M]

DRUG CLASS AND MECHANISM: Terazosin belongs to a class of medications called alpha 1 blockers which relaxes the smooth muscles of the arteries, the prostate, and the bladder neck. Other alpha blockers in the same class of drugs include doxazosin (Cardura), alfuzosin (Uroxatral), tamsulosin (Flomax), and prazosin (Minipress). Relaxing the smooth muscles of the arteries lowers blood pressure. Relaxing the smooth muscles around the bladder neck relieves urinary obstruction caused by an enlarged prostate (prostate hypertrophy)

this is what i know of hytrin's use ... for prostate enlargement. i never hear of it used for RSD! that is something i will have to google!!!
Joan

[JOAN_M]

The involvement of other sympathetic midline connections and plexi such as celiac (abdominal pain, peptic ulcer, nausea, vomiting, and weight loss), superior and inferior mesenteric plexi (diarrhea, abdominal cramps, and weight loss), and cardiac plexus (chest pain, abnormal heart beat, tachycardia, and heart attack), and carotid and vertebral plexi (severe vascular headaches, dizziness, tinnitus, attacks of falling spells, and syncopal attacks), should be identified as such and should be treated with the help of Clonodine Patch, Hytrin, or Dibenzyline as well as proper treatment applied to the source of RSD (definitely avoiding ice, but encouraging exercise, moist heat, epsom salt and hot water, and newer antidepressants as the best analgesics of choice for RSD).

this is from Hooshman's RSD Puzzle #019 .... so there you go.

[tayla4me]

Originally Posted by InHisHands

I just talked to a girl who became pain free after taking this- anyone else hear of it? Or has anyone tried this?

Thanks!!

Hi Vanessa,

As Joan has said it is a drug used mainly for high blood pressure , an Alpha blocker that relaxes the nerves to the blood vessels allowing easier access of blood to the tissue.
I am really happy this girl you spoke to has found a drug that has helped her so much. It seems that the major source of her pain was from the vasoconstriction occuring due to autonomic dysfunction and that the damage was not so great that it couldn't be reversed.
I should imagine that her success will hopefully encourage Doctors to use it in others. I would have given it a try early in the piece but I imagine that once there are major trophic changes that there would be less likelihood of a significant change---but I guess if you don't try we may never know
Lots of good luck Vanessa, you are too young to be dealing with this.
Love Tayla
Would you consider asking for it Vanessa?--wouldn't it be a blessing

[InHisHands]

Originally Posted by tayla4me

Would you consider asking for it Vanessa?--wouldn't it be a blessing

Defintely!! I plan on asking my doctor about this-- even though it might not work, and even though it might only work for the blood vessel constriction (which really makes me wonder if the above mentioned friend only had a disease that mainly caused that -misdiagnosis or not-).

Thanks!

[fmichael]

Dear Vanessa -

Thank you for posting this thread. For an older (Hooshman-era) abstract, see:

"Treatment of sympathetically maintained pain with terazosin, Stevens DS, Robins VF, Price HM, Reg Anesth. 1993 Sep-Oct; 18(5): 318-21.
Department of Anesthesiology, University of Massachusetts Medical Center, Worcester 01655.

BACKGROUND AND OBJECTIVES. alpha-adrenergic antagonists can be effective in the treatment of sympathetically maintained pain. METHODS. Oral terazosin was prescribed to treat sympathetically maintained pain refractory to other therapies. RESULTS. The authors describe a patient whose symptoms could not be controlled with commonly prescribed therapies, who obtained total relief of sympathetically maintained pain and vasospasm with terazosin, a new alpha 1 antagonist. CONCLUSIONS. Terazosin is effective in the treatment of sympathetically maintained pain when given once daily because of a long elimination half-time and a long duration of action. This may encourage better patient compliance than do other alpha antagonists of shorter effective duration.

And for something a little more up to date:

"Alpha1-adrenergic receptors augment P2X3 receptor-mediated nociceptive responses in the uninjured state," Meisner JG, Waldron JB, Sawynok J, J Pain 2007 Jul; 8(7): 556-62. Epub 2007 May 23.

Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada.

In the present study, the adrenergic receptor (AR) subtype mediating adrenergic augmentation of P2X(3) receptor-mediated nociceptive responses on sensory nerve endings was examined by using selective AR receptor agonists and antagonists in Sprague Dawley rats in the uninjured state. Local administration of alphabeta-methyleneATP (ligand for P2X3/P2X2/3 receptors) into the plantar hind paw produced few pain behaviors when given alone in this strain of rats; combination with adrenaline (alpha1- and alpha2-AR agonist) and phenylephrine (alpha1-AR agonist) but not clonidine or UK 14,304 (alpha2-AR agonists) increased flinching behaviors. Flinching produced by noradrenaline (NA)/alphabeta-methyleneATP was suppressed by low doses of prazosin (alpha1-AR antagonist), and this reduction was selective compared with yohimbine (alpha2-AR antagonist). Prazosin also reduced flinching produced by phenylephrine/alphabeta-methyleneATP. Using thermal threshold determinations, adrenaline and phenylephrine but not clonidine or UK 14,304, mimicked the action of NA in augmenting reductions in thermal thresholds produced by alphabeta-methyleneATP. Terazosin (another alpha1-AR antagonist) inhibited hyperalgesia produced by NA/alphabeta-methyleneATP. These results provide evidence for alpha1-AR involvement in adrenergic augmentation of P2X3/P2X2/3 receptor-mediated responses on sensory nerve endings in the uninjured state in Sprague Dawley rats. PERSPECTIVE: This study indicates the alpha1-adrenergic receptor subtype mediates adrenergic augmentation of the activation of sensory nerves by purinergic P2X3 receptors (respond to ATP) in the periphery. Observations are potentially relevant to chronic pain conditions in which sympathetic nerves influence sensory nerves.

So it would seem that there may be something to this. I join everyone in wondering why our doctors haven't mentioned this, and will certainly bring this up with both my neurologist and pm doc at my next appointment(s).

Thanks for the heads up.

Mike

[Sandel]

Wild..
Thanks Ness

[fmichael]

If anyone wants it, I now have a copy of "Alpha1-adrenergic receptors augment P2X3 receptor-mediated nociceptive responses in the uninjured state," Meisner JG, Waldron JB, Sawynok J, J Pain 2007 Jul; 8(7): 556-62. Epub 2007 May 23.

Let me know.