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