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Thread: naltrexone treatment of neuropathic pain

  1. #1

    naltrexone treatment of neuropathic pain

    Dr Young, care cure nurse, what do you know about Maltrexone? I have been prescribed 3 milligrams a day of this prescription. It will have to be made by a compounding pharmacy for this dose. My Dr thinks it may help with my neuropathy. Thanks for any information.

  2. #2

    low dose naltrexone

    I was mistaken on the drug. ooopps!! I was asking about "low dose Naltrexone".
    Does anyone have any information on this for pain from sci?

  3. #3

    Low dose Naltrexone for pain

    I know this isn't the right forum for pain, but i didn't get any response there, and i really would like some feedback and hopefully awareness if this could benefit someone. I just got prescribed 3 mg per day of Low dose Naltrexone. I can't wait for it to arrive from the compounding pharmacy. I just wanted all sci persons to read up on "Low Dose Naltrexone". They have a homepage that is really interesting and inspiring from people suffering from different ailments. My Dr thinks it may help. I'm pretty excited at this point as i was trying to avoid all traditional pain killers as they don't seem to have a very good track record and lots of side effects. Anyone have any feedback?? I will let anyone interested know if it helps me with the neuropathy once it arrives.

  4. #4
    Quote Originally Posted by Dennis
    I know this isn't the right forum for pain, but i didn't get any response there, and i really would like some feedback and hopefully awareness if this could benefit someone. I just got prescribed 3 mg per day of Low dose Naltrexone. I can't wait for it to arrive from the compounding pharmacy. I just wanted all sci persons to read up on "Low Dose Naltrexone". They have a homepage that is really interesting and inspiring from people suffering from different ailments. My Dr thinks it may help. I'm pretty excited at this point as i was trying to avoid all traditional pain killers as they don't seem to have a very good track record and lots of side effects. Anyone have any feedback?? I will let anyone interested know if it helps me with the neuropathy once it arrives.
    I am moving your topic back the Pain forum. I think that you are not getting a response because nobody with neuropathic pain has received naltrexone.

    I think that I have posted previously on the subject of naltrexone for pain.
    http://sci.rutgers.edu/forum/showthread.php?t=70353

    Likewise, antiquity has posted previously on the subject
    http://sci.rutgers.edu/forum/showthread.php?t=44523

    I did a literature search for naltrexone and neuropathic. Here are some references:

    • Huang EY, Chen CM and Tao PL (2004). Supraspinal anti-allodynic and rewarding effects of endomorphins in rats. Peptides 25: 577-83. Two potent endogenous opioid peptides, endomorphin-1 (EM-1) and -2 (EM-2), which are selective micro-opioid agonists, have been identified from bovine and human brain. These endomorphins were demonstrated to produce a potent anti-allodynic effect at spinal level. In the present study, we further investigated their supraspinal anti-allodynic effects and rewarding effects. In a neuropathic pain model (sciatic nerve crush in rats), EM-1 and -2 (15 microg, i.c.v.) both showed significant suppressive effects in the cold-water allodynia test, but EM-1 showed a longer duration than EM-2. Naltrexone (NTX; 15 microg) and naloxonazine (NLZ; 15 microg) were both able to completely block the anti-allodynic effects of EM-1 and -2. In the tests of conditioned place preference (CPP), only EM-2 at the dose of 30 microg showed significant positive rewarding effect, whereas both endomorphins did not induce any reward at the dose of 15 microg. Due to the low solubility and the undesired effect (barrel rotation of the body trunk), EM-1 was not tested for the dose of 30 microg in the CPP tests. It was also found that acute EM-2 (30 microg) administration increased dopamine turnover in the shell of nucleus accumbens in the microdialysis experiments. From these results, it may suggest that EM-1 and -2 could be better supraspinal anti-allodynic agents compared with the other opioid drugs, although they may also induce rewarding. Department of Pharmacology, National Defense Medical Center 161, Min-Chuan East Road, Sec. 6, Nei-Hu, Taipei 114, Taiwan, ROC. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15165712
    • Whiteside GT, Harrison JE, Pearson MS, Chen Z, Fundytus ME, Rotshteyn Y, Turchin PI, Pomonis JD, Mark L, Walker K and Brogle KC (2004). DiPOA ([8-(3,3-diphenyl-propyl)-4-oxo-1-phenyl-1,3,8-triazaspiro[4.5]dec-3-yl]-a cetic acid), a novel, systemically available, and peripherally restricted Mu opioid agonist with antihyperalgesic activity: II. In vivo pharmacological characterization in the rat. J Pharmacol Exp Ther 310: 793-9. Mu opioid receptors are expressed throughout the central and peripheral nervous systems. Peripheral inflammation leads to an increase in mu receptor present on the peripheral terminals of primary sensory neurons. Activation of peripheral mu receptors produces potent antihyperalgesic effects in both humans and animals. Here, we describe the in vivo pharmacological properties of the structurally novel, highly potent, systemically available yet peripherally restricted mu opioid agonist, [8-(3,3-diphenyl-propyl)-4-oxo-1-phenyl-1,3,8-triaza-spiro[4.5]dec-3-yl]-a cetic acid (DiPOA). DiPOA administered i.p. produced naltrexone-sensitive, dose-dependent reversal of Freund's complete adjuvant-induced inflammatory mechanical hyperalgesia (1-10 mg/kg). Maximum percent reversal (67%) was seen 1 h postadministration at 10 mg/kg (the highest dose studied). DiPOA also proved antihyperalgesic in a model of postsurgical pain with a maximum percent reversal of 85% 1 h postadministration at 30 mg/kg i.p. (the highest dose studied). DiPOA administered i.p. had no effect in the tail flick assay of acute pain (0.1-10 mg/kg), produced no ataxia as measured by latency to fall from an accelerating rotarod (3-30 mg/kg), and was not antihyperalgesic in the Seltzer model of neuropathic pain (1-10 mg/kg). This is the first report of a peripherally restricted, small-molecule mu opioid agonist that is nonsedating, antihyperalgesic, and effective against inflammatory and postsurgical pain when administered systemically. Departments of Molecular Pharmacology and Neuropharmacology, Purdue Pharma Discovery Research, 6 Cedarbrook Drive, Cranbury, NJ 08512, USA. Garth.Whiteside@pharma.com http://www.ncbi.nlm.nih.gov/entrez/q..._uids=15054116
    • Yeomans DC, Jones T, Laurito CE, Lu Y and Wilson SP (2004). Reversal of ongoing thermal hyperalgesia in mice by a recombinant herpesvirus that encodes human preproenkephalin. Mol Ther 9: 24-9. Herpesvirus-mediated transfer of the human preproenkephalin gene to primary afferent nociceptors prevents phasic thermal allodynia/hyperalgesia in mice. It is not known, however, whether similar viral treatments would reverse ongoing or chronic pain and allodynia/hyperalgesia. To this end, mice were given intrathecal injections of pertussis toxin (PTX), which produces a weeks-long thermal hyperalgesia apparently by uncoupling certain G proteins from inhibitory neurotransmitter receptors. This treatment produced profound thermal hyperalgesia in both Adelta and C-fiber thermonociceptive tests lasting at least 6 weeks. However, treatment of skin surfaces with an enkephalin-encoding herpesvirus, but not control virus or vehicle, completely reversed this hyperalgesia. This profound anti-hyperalgesia was observed for both Adelta- and C-fiber-mediated responses. Interestingly, however, while the anti-hyperalgesic effect of the enkephalin-encoding virus on C-fiber-mediated responses was reversed by intrathecal application of micro or delta opioid antagonists, only delta antagonists reversed the effect of this virus on Adelta hyperalgesia. Thus, virus-mediated delivery of the proenkephalin cDNA reverses thermal hyperalgesia produced by PTX-induced ribosylation of inhibitory G proteins by an opioid-mediated mechanism. These results suggest that herpesvirus vectors encoding analgesic peptides may be useful in attenuating centrally mediated, ongoing neuropathic pain and/or hyperalgesia. Department of Anesthesia, Stanford University, Stanford, CA 94305, USA. dcyeomans@stanford.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=14741774
    • Bertorelli R, Bastia E, Citterio F, Corradini L, Forlani A and Ongini E (2002). Lack of the nociceptin receptor does not affect acute or chronic nociception in mice. Peptides 23: 1589-96. The peptide nociceptin/orphanin FQ (N/OFQ) and its receptor ORL-1, also designated opioid receptor 4 (OP(4)) are involved in the modulation of nociception. Using OP(4)-knockout mice, we have studied their response following opioid receptor stimulation and under neuropathic conditions.In vas deferens from wild-type and OP(4)-knockout mice, DAMGO (mu/OP(3) agonist), deltorphine II (delta/OP(1) agonist) and (-)-U-50488 (kappa/OP(2) agonist) induced similar concentration-dependent inhibition of electrically-evoked contractions. Naloxone and naltrindole (delta/OP(1) antagonists) shifted the curves of DAMGO (pA(2)=8.6) and deltorphine II (pA(2)=10.2) to the right, in each group. In the hot-plate assay, N/OFQ (10 nmol per mouse, i.t.) increased baseline latencies two-fold in wild-type mice while morphine (10mg/kg, s.c.), deltorphine II (10 nmol per mouse, i.c.v.) and dynorphin A (20 nmol per mouse, i.c.v.) increased hot-plate latencies by about four- to five-fold with no difference observed between wild-type and knockout mice. Furthermore, no change was evident in the development of the neuropathic condition due to chronic constriction injury (CCI) of the sciatic nerve, after both thermal and mechanical stimulation.Altogether these results suggest that the presence of OP(4) receptor is not crucial for (1) the development of either acute or neuropathic nociceptive responses, and for (2) the regulation of full receptor-mediated responses to opioid agonists, even though compensatory mechanisms could not be excluded. Schering-Plough Research Institute, San Raffaele Science Park, Via Olgettina 58, Milan, Italy. rosalia.bertorelli@spcorp.com http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12217419
    • Singh VP, Jain NK and Kulkarni SK (2001). On the antinociceptive effect of fluoxetine, a selective serotonin reuptake inhibitor. Brain Res 915: 218-26. Antidepressant drugs are reported to be used as co-analgesics in clinical management of migraine and neuropathic pain. The mechanism through which they alleviate pain remains unknown. The present study explores the possible mechanism of a selective serotonin reuptake inhibitor (SSRI) fluoxetine-induced antinociception in animals. Acetic acid-induced writhing, hot plate and tail-flick test were used to assess fluoxetine-induced antinociception. Fluoxetine (5-20 mg kg(-1), i.p.) produced a significant and dose-dependent antinociceptive effect against acetic acid-induced writhing in mice. Fluoxetine (20 mg kg(-1)) also exhibited antinociceptive effect in tail flick as well as hot plate assays. Further, i.c.v. administration of fluoxetine showed significant antinociception against writhing test in rats. However, fluoxetine (1 microg/10 microl/rat, i.c.v.) did not exhibit any antinociceptive effect in serotonin-depleted animals. Further, pindolol (10 mg kg(-1), i.p.) enhanced fluoxetine-induced antinociceptive effect. The antinociceptive effect of fluoxetine was sensitive to blockade by naloxone (5 mg kg(-1), i.p.) and naltrexone (5 mg kg(-1), i.p.). These data suggest that fluoxetine-induced antinociception involves both central opioid and the serotoninergic pathways. Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, 160 014, Chandigarh, India. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11595211
    • Porreca F, Burgess SE, Gardell LR, Vanderah TW, Malan TP, Jr., Ossipov MH, Lappi DA and Lai J (2001). Inhibition of neuropathic pain by selective ablation of brainstem medullary cells expressing the mu-opioid receptor. J Neurosci 21: 5281-8. Neurons in the rostroventromedial medulla (RVM) project to spinal loci where the neurons inhibit or facilitate pain transmission. Abnormal activity of facilitatory processes may thus represent a mechanism of chronic pain. This possibility and the phenotype of RVM cells that might underlie experimental neuropathic pain were investigated. Cells expressing mu-opioid receptors were targeted with a single microinjection of saporin conjugated to the mu-opioid agonist dermorphin; unconjugated saporin and dermorphin were used as controls. RVM dermorphin-saporin, but not dermorphin or saporin, significantly decreased cells expressing mu-opioid receptor transcript. RVM dermorphin, saporin, or dermorphin-saporin did not change baseline hindpaw sensitivity to non-noxious or noxious stimuli. Spinal nerve ligation (SNL) injury in rats pretreated with RVM dermorphin-saporin failed to elicit the expected increase in sensitivity to non-noxious mechanical or noxious thermal stimuli applied to the paw. RVM dermorphin or saporin did not alter SNL-induced experimental pain, and no pretreatment affected the responses of sham-operated groups. This protective effect of dermorphin-saporin against SNL-induced pain was blocked by beta-funaltrexamine, a selective mu-opioid receptor antagonist, indicating specific interaction of dermorphin-saporin with the mu-opioid receptor. RVM microinjection of dermorphin-saporin, but not of dermorphin or saporin, in animals previously undergoing SNL showed a time-related reversal of the SNL-induced experimental pain to preinjury baseline levels. Thus, loss of RVM mu receptor-expressing cells both prevents and reverses experimental neuropathic pain. The data support the hypothesis that inappropriate tonic-descending facilitation may underlie some chronic pain states and offer new possibilities for the design of therapeutic strategies. Departments of Pharmacology and Anesthesiology, University of Arizona, Tucson, Arizona 85724, USA. frankp@u.arizona.edu http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11438603
    • Mika J, Przewlocki R and Przewlocka B (2001). The role of delta-opioid receptor subtypes in neuropathic pain. Eur J Pharmacol 415: 31-7. A large body of evidence suggests an important role of delta-opioid receptor agonists in antinociception at the level of the spinal cord. Our study was undertaken to analyse the spinal antinociceptive and antiallodynic effects of delta(1)- and delta(2)-opioid receptor agonists and antagonist after their acute and chronic intrathecal administration in a neuropathic pain model in the rat. In rats with a crushed sciatic nerve, the delta(1)-opioid receptor agonist [D-Pen(2), D-Pen(5)]enkephalin (DPDPE, 5-25 microg i.t.) and the delta(2)-opioid receptor agonist deltorphin II (1.5-25 microg i.t.) dose dependently antagonized the cold-water allodynia which developed after sciatic nerve injury. These effects of DPDPE were antagonized by 7-benzylidenenaltrexon (BNTX, 1 microg i.t.) while the effects of deltorphin II were antagonized by 5'naltrindole izotiocyanate (5'NTII, 25 microg i.t.). Both agonists had a dose-dependent, statistically significant effect on the tail-flick latency in two tests, with focused light and cold water. Chronic administration of DPDPE (25 microg i.t.) and deltorphin II (15 microg i.t.) resulted in significant prolongation of the reaction time determined on days 2, 4 and 6 post-injury. In conclusion, our results show an antiallodynic and antinociceptive action of DPDPE and deltorphin II at the spinal cord level, which suggests that both delta-opioid receptor subtypes play a similar role in neuropathic pain. This indicates that not only delta(1)- but also delta(2)-opioid receptor agonists can be regarded as potential drugs for the therapy of neuropathic pain. Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343 Cracow, Poland. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=11245849
    • Courteix C, Coudore-Civiale MA, Privat AM, Zajac JM, Eschalier A and Fialip J (1999). Spinal effect of a neuropeptide FF analogue on hyperalgesia and morphine-induced analgesia in mononeuropathic and diabetic rats. Br J Pharmacol 127: 1454-62. 1DMe, a neuropeptide FF (NPFF) analogue, has been shown to produce antinociception and to enhance morphine analgesia in rats after intrathecal administration. To determine whether 1DMe could correct hyperalgesia and restore morphine efficacy in mononeuropathic (MN) and diabetic (D) rats we examined the spinal effect of 1DMe in MN and D rats without and after spinal blockade of mu- and delta-opioid receptors with CTOP and naltrindole, respectively. The influence of 1DMe on morphine-induced antinociception was assessed in the two models using isobolographic analysis. Whereas 1DMe intrathecally injected (0.1, 1, 7.5 microg rat(-1)) was ineffective in normal (N) rats, it suppressed mechanical hyperalgesia (decrease in paw pressure-induced vocalisation thresholds) in both MN and D rats. This effect was completely cancelled by CTOP (10 microg rat(-1)) and naltrindole (1 microg rat(-1)) suggesting that it requires the simultaneous availability of mu- and delta-opioid receptors. The combinations of morphine: 1DMe (80.6:19.4% and 99.8:0.2%, in MN and D rats, respectively) followed by isobolographic analysis, showed a superadditive interaction, relative to the antinociceptive effect of single doses, in D rats only. In N rats, the combination of morphine: 1DMe (0.5 mg kg(-1), i.v.: 1 microg rat(-1), i.t., ineffective doses) resulted in a weak short-lasting antinociceptive effect. These results show a different efficacy of 1DMe according to the pain model used, suggesting that the pro-opioid effects of the NPFF in neuropathic pain are only weak, which should contribute to hyperalgesia and to the impaired efficacy of morphine. Equipe NPPUA, INSERM E9904, Laboratoire de Pharmacologie, Faculte de Pharmacie, Clermont-Ferrand, France. http://www.ncbi.nlm.nih.gov/entrez/q..._uids=10455296
    • Catheline G, Guilbaud G and Kayser V (1998). Peripheral component in the enhanced antinociceptive effect of systemic U-69,593, a kappa-opioid receptor agonist in mononeuropathic rats. Eur J Pharmacol 357: 171-8. The contribution of a peripheral action of the kappa-opioid receptor agonist U-69,593 (trans-3,4-dichloro-N-methyl-N-[7-(1-pyrrolidinyl) cycloexil] benzene-acetamide methanesulfonate) in the augmented antinociceptive effect of this substance was investigated in a well-established rat model of peripheral unilateral neuropathy (chronic constriction of the common sciatic nerve). Relatively low dose of systemic U-69,593 (0.75 mg/kg intravenous (i.v.)) and intraplantar (i.pl.) low doses of specific antagonists of kappa-(nor-binaltorphimine) or mu-(D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2: CTOP) opioid receptors were used. Vocalization thresholds to paw pressure were used as a nociceptive test. The i.pl. injection of nor-binaltorphimine (10-15 microg injected into the nerve-injured hind paw) had no effect on the antinociceptive effect of U-69,593. Higher doses (20-30 microg i.pl. nor-binaltorphimine) significantly reduced the effect of U-69,593 on this paw but not on the contralateral paw, an effect which plateaued at 30 microg. By contrast, the i.pl. injection of CTOP (1 microg into the nerve-injured paw) had no effect on U-69,593 antinociception, whereas it reduced the effect of systemic morphine in these animals. The doses of nor-binaltorphimine used, injected into the contralateral paw or i.v., failed to modify the antinociceptive effects of U-69,593 on either paw. These results provide evidence for a peripheral component in the enhanced antinociceptive effect of systemic U-69,593 in this model of neuropathic pain. Unite de Recherches de Physiopharmacologie du Systeme Nerveux, I.N.S.E.R.M. U 161, Paris, France. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9797033
    • Jasmin L, Kohan L, Franssen M, Janni G and Goff JR (1998). The cold plate as a test of nociceptive behaviors: description and application to the study of chronic neuropathic and inflammatory pain models. Pain 75: 367-82. A cold plate apparatus was designed to test the responses of unrestrained rats to low temperature stimulation of the plantar aspect of the paw. At plate temperatures of 10 degrees C and 5 degrees C, rats with either chronic constriction injury (CCI) of the sciatic nerve or complete Freund's adjuvant (CFA) induced inflammation of the hindpaw displayed a stereotyped behavior. Brisk lifts of the treated hindpaw were recorded, while no evidence of other nociceptive behaviors could be discerned. The most consistent responses were obtained with a plate temperature of 5 degrees C in three 5-min testing periods, separated by 10-min intervals during which the animals were returned to a normal environment. Concomitantly to cold testing, the rats were evaluated for their response to heat (plantar test) and mechanical (von Frey hairs) stimuli. In both injury models, while responses to heat stimuli had normalized at 60 days post-injury, a clear lateralization of responses to cold was observed throughout the entire study period. Systemic lidocaine, clonidine, and morphine suppressed responses to cold in a dose-related fashion. At doses that did not affect motor or sensory behavior, both lidocaine and its quaternary derivative QX-314 similarly reduced paw lifts, suggesting that cold hyperalgesia is in part due to peripheral altered nociceptive processing. Clonidine was more potent in CCI then in CFA rats in reducing the response to cold. Paradoxically, clonidine increased the withdrawal latencies to heat in the CCI hindpaw at 40 days and thereafter, at a time when both hindpaws had the same withdrawal latencies in control animals. Morphine was also more potent on CCI than CFA cold responses, indicating that, chronically, CFA-induced hyperalgesia might be opiate resistant. Evidence for tonic endogenous inhibition of cold hyperalgesia was obtained for CFA rats, when systemic naltrexone significantly increased the number of paw lifts; this was not found in rats with CCI. At 60 days, neither morphine nor naltrexone affected cold-induced paw lifting in CFA rats, suggesting that the neuronal circuit mediating cold hyperalgesia in these animals had become opiate insensitive. In conclusion, the cold plate was found to be a reliable method for detecting abnormal nociceptive behavior even at long intervals after nerve or inflammatory injuries, when responses to other nociceptive stimuli have returned to near normal. The results of pharmacological studies suggest that cold hyperalgesia is in part a consequence of altered sensory processing in the periphery, and that it can be independently modulated by opiate and adrenergic systems. Department of Neurosurgery, Georgetown University Medical Center, Washington, DC 20007, USA. ljasmi01@gumedlib.dml.georgetown.edu http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9583773
    • Hao JX, Yu W and Xu XJ (1998). Evidence that spinal endogenous opioidergic systems control the expression of chronic pain-related behaviors in spinally injured rats. Exp Brain Res 118: 259-68. We have previously reported that ischemic spinal cord injury in rats leads to chronic pain-related behaviors. Thus, rats exhibited aversive reactions to innocuous mechanical stimuli (mechanical allodynia) applied to a body area at or rostral to the dermatomes innervated by the injured spinal segments. The responses of the rats to cold are also markedly enhanced (cold allodynia). Interestingly, more than 50% of spinally injured rats did not develop these abnormal pain-related behaviors after spinal cord injury. In the present study, we showed that the extent of injury is similar between allodynic and non-allodynic rats. Furthermore, intrathecal (i.t.) naloxone, a broad-spectrum opioid receptor antagonist, reversibly provoked mechanical and cold allodynia-like responses in spinally injured rats that did not develop such behaviors spontaneously. However, naloxone did not elicit such reactions in normal rats and did not alter the tail-flick latency in normal or spinally injured rats. Furthermore, i.t. D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) or naltridole, selective antagonists of mu and delta opioid receptors, respectively, also triggered pain-related behaviors similarly to naloxone. Although norbinaltorphimine (nor-BIN), a selective kappa-receptor antagonist, also elicited such responses, the time course of the effect makes it unlikely that spinal kappa-receptors were involved. These results suggested that the expression of abnormal pain-related behaviors in some spinally injured rats is tonically suppressed by the spinal opioidergic system. Interindividual differences that lead to lack or dysfunction of such inhibition may underly the appearence of pain-related behavior in some, but not all, spinally injured rats. It is suggested that such inhibition is exerted through spinal mu and delta, but not kappa, opioid receptors. The endogenous opioidergic control appears to be only active against abnormal painrelated behaviors in spinally injured rats. Our results are relevant for the clinical observation that only a subgroup of patients with nerve injury suffers from neuropathic pain. Department of Medical Laboratory Sciences and Technology, Karolinska Institute, Huddinge University Hospital, Sweden. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9547096
    • Catheline G, Kayser V and Guilbaud G (1996). Further evidence for a peripheral component in the enhanced antinociceptive effect of systemic morphine in mononeuropathic rats: involvement of kappa-, but not delta-opioid receptors. Eur J Pharmacol 315: 135-43. The contribution of a peripheral action of morphine in the augmented antinociceptive effect of this substance was re-evaluated in a well established rat model of peripheral unilateral mononeuropathy (chronic constriction of the common sciatic nerve), using a relatively low dose of systemic morphine (1 mg/kg i.v.) and local low doses of specific antagonists of kappa- (nor-binaltorphimine) or delta-(naltrindole) opioid receptors. Vocalization thresholds to paw pressure were used as a nociceptive test. Escalating doses of nor-binaltorphimine (10-30 micrograms injected locally into the nerve injured paw) significantly and dose dependently reduced the effect of morphine on this paw but not on the contralateral paw, an effect which plateaued at 30 micrograms. By contrast, the local injection of naltrindole (30-40 micrograms into the nerve injured paw) had no effect on morphine analgesia. The doses of opioid receptor antagonists used, injected i.v., in the contralateral paw, or alone in the nerve injured paw had no significant effect. These results suggest that the peripheral effect of systemic morphine in this model of neuropathic pain could be mediated not only by mu- but also by kappa-opioid receptors. Unite de Recherches de Physiopharmacologie du Systeme Neri eux, I.N.S.E.R.M. U 161, Paris, France. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8960876
    • Desmeules JA, Kayser V and Guilbaud G (1993). Selective opioid receptor agonists modulate mechanical allodynia in an animal model of neuropathic pain. Pain 53: 277-85. This study evaluated the antinociceptive effects of systemically administered selective opioid agonists of mu (DAMGO), delta (BUBU) and kappa (U 69593) receptors on the vocalization threshold to paw pressure in a rat model of peripheral unilateral mononeuropathy produced by loose ligatures around the common sciatic nerve. DAMGO (0.5-2 mg/kg), BUBU (1.5-6 mg/kg) and U 69593 (0.75-3 mg/kg) injected intravenously (i.v.) produced a potent long-lasting antinociceptive effect on both hind paws. The effects on the lesioned paw were clearly and statistically more potent than for the non-lesioned paw. The selective antinociceptive effect of 2 mg/kg DAMGO, 3 mg/kg BUBU and 1.5 mg/kg U 69593 were completely prevented by prior administration of the appropriate antagonists: 0.1 mg/kg naloxone, 1 mg/kg naltrindole and 0.4 mg/kg MR 2266. The present data clearly show that an acute i.v. injection of these selective opioid agonists induces potent antinociceptive effects in a rat model of peripheral neuropathy. These data are discussed with regard to the classical view that there is opioid resistance in neuropathic pain. INSERM (U 161), Unite de Recherches de Physiopharmacologie du Systeme Nerveux, Paris, France. http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=8394563

  5. #5
    Quote Originally Posted by janacv
    I was mistaken on the drug. ooopps!! I was asking about "low dose Naltrexone".
    Does anyone have any information on this for pain from sci?

    How did the Naltresone treatments work?

    Blessings
    Jo

  6. #6
    I have not personally tried this medicine myself, but I had a friend with MS who swore by it. He claimed that allowed him to greatly reduce his intake of baclofen, marijuana, and other MS related prescriptions that I do not have knowledge of.
    He believed that there was a conspiracy theory against the use of this drug because large drug companies cannot/do not make a profit from it. This is/was just his theory. I would be interested to know if other people with neurological deficiencies have benefited from it though.

  7. #7
    Quote Originally Posted by JoPattson
    How did the Naltresone treatments work?

    Blessings
    Jo
    Natrexone binds onto opiate receptors. Normally in high concentrations, it blocks the receptors and therefore reverses the effects of drugs like heroin. However, it appears that it may bind and somehow affect the receptors when given in very low doses.

    Wise.

  8. #8
    Quote Originally Posted by Wise Young
    Natrexone binds onto opiate receptors. Normally in high concentrations, it blocks the receptors and therefore reverses the effects of drugs like heroin. However, it appears that it may bind and somehow affect the receptors when given in very low doses.

    Wise.
    Oh, I'm so sorry, I wasn't very clear.
    My question was meant to ask if the Natrexone treatment worked for the person who started this thread.

    And if it worked, what did it do specifically, that sort of thing.

    Sorry about that, but thank you for your reply

    Blessings
    Jo

  9. #9
    Quote Originally Posted by Chaz19
    I have not personally tried this medicine myself, but I had a friend with MS who swore by it. He claimed that allowed him to greatly reduce his intake of baclofen, marijuana, and other MS related prescriptions that I do not have knowledge of.
    He believed that there was a conspiracy theory against the use of this drug because large drug companies cannot/do not make a profit from it. This is/was just his theory. I would be interested to know if other people with neurological deficiencies have benefited from it though.
    Don't know why he thinks there is a conspiracy, it's used all over the place and there are lots of studies for it. And it makes tons and tons of money. However, it's FDA approved use is for alcohol and drug addiction. Any other use is off label, and thus the mfger can neither advertize, nor support projects for any such off label use. Other people can though.

    So, it's up to your friend and others like him to spread the word, create web sites, etc.

    I have a friend with Periferal Neuropathy, she tried it for 3 months with no effect at all. She's thinking that maybe she just didn't take it long enough.

    I think it works for MS, and other kinds of pain, but not nerve pain.
    And I think that it's benefit is not towards treatment as some web sites would have you believe, but merely for pain. (not that pain relief is a simple merely, but it's not a cure either)

    That's why I was asking if this treatment worked, if it just relieved pain or did more, and how much of the pain was relieved, for how long.

    Blessings
    Jo

  10. #10
    Quote Originally Posted by JoPattson
    I think it works for MS, and other kinds of pain, but not nerve pain.
    MS pain (at least much of it, I don't know all that much about the condition) IS nerve pain.

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