Benicar -- neuropathic pain?

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newbie04

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Does Benicar have any use in the tx of neuropathic pain? I haven't found much in regard to its use in this realm except for mention of its use in the Marshall Protocol.

Has anyone used this successfully in pts with neuropathic pain?

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an ARB for pain?? can't imagine it does anything...except a general lower of BP that may theoretically spare the vaso nervosum.

clonidine at least has some sort of autonomic effect to somehow explain it's use for neuropathic pain.
 
Thanks for the reply. That's what I kept thinking. It doesn't make any sense to me.:confused:
 
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There are clinical trials showing efficacy for ARBs in migraine prophylaxis
 
There are clinical trials showing efficacy for ARBs in migraine prophylaxis

Like this one (thanks).

Prophylactic Treatment of Migraine With an Angiotensin II Receptor Blocker
A Randomized Controlled Trial

Erling Tronvik, MD; Lars J. Stovner, PhD; Grethe Helde, RN; Trond Sand, PhD; Gunnar Bovim, PhD


JAMA. 2003;289:65-69.

Context There is a paucity of effective, well-tolerated drugs available for migraine prophylaxis.

Objective To determine whether treatment with the angiotensin II receptor blocker candesartan is effective as a migraine-prophylactic drug.

Design and Setting Randomized, double-blind, placebo-controlled crossover study performed in a Norwegian neurological outpatient clinic from January 2001 to February 2002.

Patients Sixty patients aged 18 to 65 years with 2 to 6 migraine attacks per month were recruited mainly from newspaper advertisements.

Interventions A placebo run-in period of 4 weeks was followed by two 12-week treatment periods separated by 4 weeks of placebo washout. Thirty patients were randomly assigned to receive one 16-mg candesartan cilexetil tablet daily in the first treatment period followed by 1 placebo tablet daily in the second period. The remaining 30 received placebo followed by candesartan.

Main Outcome Measures The primary end point was number of days with headache; secondary end points included hours with headache, days with migraine, hours with migraine, headache severity index, level of disability, doses of triptans, doses of analgesics, acceptability of treatment, days of sick leave, and quality-of-life variables on the Short Form 36 questionnaire.

Results In a period of 12 weeks, the mean number of days with headache was 18.5 with placebo vs 13.6 with candesartan (P = .001) in the intention-to-treat analysis (n = 57). Some secondary end points also favored candesartan, including hours with headache (139 vs 95; P<.001), days with migraine (12.6 vs 9.0; P<.001), hours with migraine (92.2 vs 59.4; P<.001), headache severity index (293 vs 191; P<.001), level of disability (20.6 vs 14.1; P<.001) and days of sick leave (3.9 vs 1.4; P = .01), although there were no significant differences in health-related quality of life. The number of candesartan responders (reduction of 50% compared with placebo) was 18 (31.6%) of 57 for days with headache and 23 (40.4%) of 57 for days with migraine. Adverse events were similar in the 2 periods.

Conclusion In this study, the angiotensin II receptor blocker candesartan provided effective migraine prophylaxis, with a tolerability profile comparable with that of placebo.


Worth a try, but nothing to make me excited.
 
great article steve. and on the other forum question about UDS, i love the idea of a pre-UDS listing of all meds/drugs taking and last time took a dose/"hit".
 
Is this how it works? Angiotensin induces synthesis of PGs. Thus, blocking AGII receptors would reduced PG (and pain) levels. In addition, with the autoregulation of (CBF) cerebral blood flow (as systemic MAP increases, cerebral vessels dilate to increase CBF). Thus, by blocking AGII and lowering blood pressure, cerebral vessels constrict to maintain CBF--presto new migraine prophylaxis med.
 
Is this how it works? Angiotensin induces synthesis of PGs. Thus, blocking AGII receptors would reduced PG (and pain) levels. In addition, with the autoregulation of (CBF) cerebral blood flow (as systemic MAP increases, cerebral vessels dilate to increase CBF). Thus, by blocking AGII and lowering blood pressure, cerebral vessels constrict to maintain CBF--presto new migraine prophylaxis med.

If you lower systemic BP then cerebral vessels have to DILATE to maintain CBF.

P = QR (P = pressure, Q = flow, R = resistance)

If you keep Q (CBF) constant and lower P, then R has to drop, i.e., vasodilation.
 
Thanks, thought I might have it backwards.
Cerebral blood vessels constrict when systemic blood pressure is raised and dilate when it is lowered
CBF = CPP / CVR

CPP = MAP &#8722; ICP (if ICP is higher than JVP) or
CPP = MAP &#8722; JVP (if JVP is higher than ICP).
 
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