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Dr. Youg - oral ketamine for pain

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    Dr. Youg - oral ketamine for pain

    Dr. Young, in one of your past posts you mentioned that oral ketamine has been tried for neuropathic pain. Do you know at what dosage? That's something I haven't tried yet.
    Alan

    Proofread carefully to see if you any words out.

    #2
    Alan

    I have seen several abstracts in Medline that indicated that ketamine seemed to help neuropathic pain. I have often wondered if the researchers would follow up and try it on human SCI. I would like to know if Dr. Young has heard anything new.

    By the way, have you tried Arginine-L? It is a precursor to ketamine.(I'm told) Its available through most nutrition centers or drugstores. I felt it gave me more endurance not so much pain relief per se but better ability to deal with pain.

    i get some relief through a combination of baclofen/valium/neurontin. I used to take Elavil but it eventually affected my short term memory and I had to stop. I will still take some Elavil on bad days. If nothing else it makes me sleep like a log.

    Joe

    Joe B
    C6-7
    1988
    Joe B
    C6-7
    1988

    Comment


      #3
      Are we talking Ketamine as in cat tranquilizer and children's anestesia? Isnt this stuff highly hallucinagenic in adults...as in what is known as a K-Hole? I would imagine it would kill the pain, but you wouldnt be too funtioning during its effects. Might be wrong though,

      Andy

      Comment


        #4
        Joe, I never heard of Arginine-L, but I'll check it out.

        Vicki, I have no clue. I simply read an old post of Dr. Young's. It didn't mention tranquilized cats.
        Alan

        Proofread carefully to see if you any words out.

        Comment


          #5
          At a pain clinic I was told Ketamine is injected into the spine via a pump similar to Baclofen.

          Pops

          Comment


            #6
            The dose of oral ketamine is variable and ranges from 20-60 mg. It is a glutamate receptor blocker and some evidence suggests that this drug is more effective for neuropathic pain than for noxious pain. You will have to get prescription. Wise.

            Comment


              #7
              I have tried oral Ketamine for neuropathic pain. It was an extremely bad experience even though I only took half the dose recommended. Experienced paranoia and whole body was pins and needles. Just my experience though.

              Comment


                #8
                So ketamine comes in pill form, I gather? And that's 20-60 mg per day, or per dose?
                Alan

                Proofread carefully to see if you any words out.

                Comment


                  #9
                  Bump.
                  Alan

                  Proofread carefully to see if you any words out.

                  Comment


                    #10
                    I currently take oral ketamine for neuropathic pain. I take 20mgs daily (5 mgs 4x daily). It seems to work well for me but I'm still waiting to hear from Dr. Young to see if it is safe to move up my dosage.

                    Comment


                      #11
                      So do you take ketamine pills? If so, where do you get them (a local pharmacy?)

                      My docs haven't heard of oral ketamine. [img]/forum/images/smilies/frown.gif[/img]
                      Alan

                      Proofread carefully to see if you any words out.

                      Comment


                        #12
                        cdues and alan, here are recent abstracts of papers on the subject. As you can see, a wide variety of doses are used and often in combination with other drugs. Because ketamine has effects on memory and other cerebral function, you should always use the lowest dose possible. Oral doses have lower and variable bioavailability than injected ketamine, of course. Wise.

                        • Danilova EI, Grafova VN and Reshetniak VK (1997). [The role of the NMDA-receptor blocker and stimulator ketamine and glycine in the development of a neuropathic pain syndrome]. Eksp Klin Farmakol 60:10-3. Summary: The effect of glycine, ketamine, and their combination in chronic oral administration was studied on a model of the neuropathic pain syndrome. Glycine failed to prevent the pain syndrome but had a therapeutic effect. Ketamine possessed a marked preventive and therapeutic effect. In combined administration the drugs mutually potentiated their action. The effect of glycine and ketamine is based on intensification of spinal glycinergic inhibition, differently directed effect on the NMDA receptors, and intensification of monoaminergic inhibition.
                        • Enarson MC, Hays H and Woodroffe MA (1999). Clinical experience with oral ketamine. J Pain Symptom Manage 17:384-6. Summary: Ketamine is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist used recently for analgesia in patients with chronic pain. Twenty one patients with chronic neuropathic pain were treated with oral ketamine starting at a divided dose of 100 mg/day and titrating upwards by 40 mg/day until efficacy was reached, or until side effects became limiting. A retrospective chart review was conducted to evaluate the analgesic efficacy and side effects of the treatment. Nine patients discontinued ketamine because of intolerable side effects, four patients experienced few or no side effects but had no discernible benefit, four others had equivocal responses. Four patients have continued oral ketamine for long periods. One patient has had no significant benefit or side effects but continues to use ketamine 500 mg/day and three people have used doses ranging from 100-240 mg day for over 1 year duration and have reported improvements in pain and decreased use of analgesics. The analgesic benefits of ketamine appeared to be most pronounced in, but not limited to, patients with pain histories of less than 5 years. Department of Family Medicine, University of Alberta, Edmonton, Canada.
                        • Fisher K and Hagen NA (1999). Analgesic effect of oral ketamine in chronic neuropathic pain of spinal origin: a case report. J Pain Symptom Manage 18:61-6. Summary: Ketamine is an injectable anesthetic induction agent that has been reported to have analgesic activity in pain from a variety of mechanisms, but predominantly in neuralgic and dysesthetic neuropathic pain. In this case report we illustrate the effectiveness of ketamine in a patient with neuropathic pain resulting from cauda equina trauma. Among the issues addressed are the role of pretreatment with haloperidol to prevent ketamine-induced psychomimetic effects, the potential for fewer side effects and a need for lower doses when ketamine is administered orally, and the need for further study regarding appropriate monitoring parameters during the titration phase. Oral ketamine can be effective in treatment refractory chronic neuropathic pain of spinal origin. Department of Oncology, University of Calgary, Canada.
                        • Fitzgibbon EJ, Hall P, Schroder C, Seely J and Viola R (2002). Low dose ketamine as an analgesic adjuvant in difficult pain syndromes: a strategy for conversion from parenteral to oral ketamine. J Pain Symptom Manage 23:165-70. Summary: Ketamine is a non-competitive N-methyl D-aspartate (NMDA) receptor antagonist with analgesic and dissociative anesthetic properties. Low dose or sub-anesthetic doses of ketamine have been used effectively as either a primary analgesic or analgesic adjuvant in a variety of pain syndromes. In this paper, three patients with difficult to treat, predominantly neuropathic pain syndromes will be described. Their pain syndromes were initially managed successfully with the addition of low dose parenteral ketamine as an analgesic adjuvant. The strategy of concurrently starting ketamine at a low dose, i.e., 40-60 mg over 24 hours, with a benzodiazepine proved effective in preventing psychotomimetic side effects. An unavoidable shortage of ketamine prompted a literature search, which suggested that the equianalgesic dose of oral ketamine could be lower than the parenteral dose. Subsequently the patients were converted to oral ketamine at doses 30 to 40% of the previous parenteral dose. Their pain syndromes remained controlled on the lower dose of oral ketamine with remarkably few side effects. The implications of this warrant further discussion and study. University of Ottawa Institute of Palliative Care, Ottawa, Ontario, Canada.
                        • Haines DR and Gaines SP (1999). N of 1 randomised controlled trials of oral ketamine in patients with chronic pain. Pain 83:283-7. Summary: Anecdotal reports suggest that the general anaesthetic drug ketamine, taken orally in low doses, can give rise to some extra analgesia in patients with refractory neuropathic pain. This study was designed to determine the proportion of patients with chronic neuropathic pain responding to oral ketamine, and then to separate the true treatment effect from non-specific effects by means of an n of 1 randomised controlled trial. Twenty-one patients gave informed consent and completed daily pain diaries and continued on their usual treatments (drug and non-drug) for the duration of the study. After a 'baseline' week, oral ketamine was taken once a day for 1 week. The dose of 20 mg was increased each day until an analgesic effect was noticed or adverse effects occurred, or until a maximum of 100 mg was reached. Those patients responding to oral ketamine were then entered into the n of 1 randomised trial which consisted of three treatment/placebo week pairs. Twelve patients did not progress to the n of 1 trial because of no benefit and/or intolerable adverse effects (dizziness, drowsiness etc.). Nine patients completed the n of 1 trial; there was no difference between the ketamine and placebo weeks in six patients; one patient demonstrated effective analgesia with ketamine, but it was of short duration and marred by unpleasant adverse effects; two patients showed some evidence of a beneficial response to ketamine, and continued with the oral ketamine after the trial. We conclude that oral ketamine only gave rise to an extra analgesic response in three out of 21 patients with chronic neuropathic pain (14%). Adverse effects limited the use of the drug in almost half of the patients. The n of 1 trial was useful in demonstrating no true therapeutic effect for the ketamine in two thirds of the patients progressing to that part of the trial. Department of Anaesthesia, Royal Hull Hospitals NHS Trust, Hull Royal Infirmary, Anlaby Road, Kingston on, Hull, UK. drhaines@davav.demon.co.uk
                        • Kannan TR, Saxena A, Bhatnagar S and Barry A (2002). Oral ketamine as an adjuvant to oral morphine for neuropathic pain in cancer patients. J Pain Symptom Manage 23:60-5. Summary: To evaluate the role of oral ketamine as an adjuvant to oral morphine in cancer patients experiencing neuropathic pain, 9 cancer patients (5 men, 4 women) taking maximally tolerated doses of either morphine, amitriptyline, sodium valproate, or a combination of these drugs for intractable neuropathic pain, and reporting a pain score of >6 on a 0-10 scale, were studied prospectively to evaluate analgesia and adverse effects. Ketamine in the dose of 0.5 mg/kg body weight three times daily was added to the existing drug regimen. Patients were taught to maintain a pain diary wherein they daily recorded their pain, sedation, and vomiting scores, and other side effects. A decrease of more than 3 from the baseline in the average pain score, or a score of < or =3 was taken as a successful response. Seven patients exhibited a decrease of more than 3. Four patients experienced nausea, of which one had vomiting. Two developed loss of appetite. Eight patients reported drowsiness during the first two weeks of therapy [P = 0.001), and this gradually improved over the next two weeks in 5 of these 8 patients. Three patients withdrew from the study, two owing to excessive sedation and another due to a "feeling of unreality." None of the patients reported visual or auditory hallucinations. This experience suggests that low dose oral ketamine is beneficial and effective in the management of intractable neuropathic pain in patients with advanced cancer. However, its utility is limited in some patients by the adverse effects that accompany its use. Department of Anesthesiology, Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi, India.
                        • Kingery WS (1997). A critical review of controlled clinical trials for peripheral neuropathic pain and complex regional pain syndromes. Pain 73:123-39. Summary: The purpose of this review was to identify and analyze the controlled clinical trial data for peripheral neuropathic pain (PNP) and complex regional pain syndromes (CRPS). A total of 72 articles were found, which included 92 controlled drug trials using 48 different treatments. The methods of these studies were critically reviewed and the results summarized and compared. The PNP trial literature gave consistent support (two or more trials) for the analgesic effectiveness of tricyclic antidepressants, intravenous and topical lidocaine, intravenous ketamine, carbamazepine and topical aspirin. There was limited support (one trial) for the analgesic effectiveness of oral, topical and epidural clonidine and for subcutaneous ketamine. The trial data were contradictory for mexiletine, phenytoin, topical capsaicin, oral non-steroidal anti-inflammatory medication, and intravenous morphine. Analysis of the trial methods indicated that mexiletine and intravenous morphine were probably effective analgesics for PNP, while non-steroidals were probably ineffective. Codeine, magnesium chloride, propranolol, lorazepam, and intravenous phentolamine all failed to provide analgesia in single trials. There were no long-term data supporting the analgesic effectiveness of any drug and the etiology of the neuropathy did not predict treatment outcome. Review of the controlled trial literature for CRPS identified several potential problems with current clinical practices. The trial data only gave consistent support for analgesia with corticosteroids, which had long-term effectiveness. There was limited support for the analgesic effectiveness of topical dimethylsulfoxyde (DMSO), epidural clonidine and intravenous regional blocks (IVRBs) with bretylium and ketanserin. The trial data were contradictory for intranasal calcitonin and intravenous phentolamine and analysis of the trial methods indicated that both treatments were probably ineffective for most patients. There were consistent trial data indicating that guanethidine and reserpine IVRBs were ineffective, and limited trial data indicating that droperidol and atropine IVRBs were ineffective. No placebo controlled data were available to evaluated sympathetic ganglion blocks (SGBs) with local anesthetics, surgical sympathectomy, or physical therapy. Only the capsaicin trials presented data which allowed for meta-analysis. This meta-analysis demonstrated a significant capsaicin effect with a pooled odds ratio of 2.35 (95% confidence intervals 1.48, 3.22). The methods scores were higher (P < 0.01) for the PNP trials [66.2 +/- 1.5, n = 66) than the CRPS trials [57.6 +/- 2.9, n = 26). The CRPS trials tended to use less subjects and were less likely to use placebo controls, double-blinding, or perform statistical tests for differences in outcome measures between groups. There was almost no overlap in the controlled trial literature between treatments for PNP and CRPS, and treatments used in both conditions [intravenous phentolamine and epidural clonidine) had similar results. Physical Medicine and Rehabilitation Service, Veterans Affairs Palo Alto Health Care System, CA 94304, USA. ma.kin@forsythe.stanford.edu
                        • MacPherson RD (2000). The pharmacological basis of contemporary pain management. Pharmacol Ther 88:163-85. Summary: Pain management has become an increasingly well researched area in medicine over recent years, and there have been advances in a number of areas. While opioids remain an integral part of pain-management strategies, there is now an emphasis on the use of adjuvant drugs, such as paracetamol and anti-inflammatory agents, which through physiological or pharmacological synergism, both enhance pain control and reduce opioid use. The management of neuropathic pain continues to be a challenge. Anti-epileptics and antidepressants, together with clonidine and ketamine, provide the foundations for treatment. Another area of interest has been the widespread use of patient-controlled analgesia and the administration of some drugs, especially opioids, by means other than traditional oral and parenteral routes. The number of new drugs that have reached the stage of clinical trials has been small, yet they offer exciting possibilities. The epibatidine analogue ABT-594 and zinconitide both offer novel approaches to the management of neuropathic pain states, while selective cyclo-oxygenase-2 inhibitors and nitroaspirins may see advances in the management of nociceptive pain states. Department of Anaesthesia and Pain Management, Royal North Shore Hospital, St. Leonards, NSW 2065, Australia. macpher@doh.health.nsw.gov.au
                        • Rabben T and Oye I (2001). Interindividual differences in the analgesic response to ketamine in chronic orofacial pain. Eur J Pain 5:233-40. Summary: The analgesic effect of the N-methyl-D-aspartate (NMDA) receptor blocker ketamine in 17 patients (13 females and four males, age 32-88 years) who had suffered neuropathic orofacial pain for time periods ranging from 6 months to 28 years was examined. The patients were given an i.m. test-dose of 0.4 mg/kg ketamine combined with 0.05 mg/kg midazolam. Four patients did not experience any analgesic effect of the i.m. test dose. The remaining 13 patients experienced an analgesic effect which lasted for less than 1 h (transient effect) in seven and for several hours (long-term effect) in six. One week later they were given 4 mg/kg ketamine to be taken orally in combination with a hypnotic drug for three consecutive nights. All patients who reported a long-term analgesic effect after i.m. ketamine also reported reduced pain intensity on days after taking ketamine at night. The findings of this open study are in accord with the results from a previous double-blind randomized investigation. In order to evaluate the role of age and pain duration for the analgesic effect of ketamine, we pooled the data from the two studies and performed a correlation analysis of 43 patients. We found a positive correlation between a long pain-history and lack of analgesic effect and also between a short pain-history and a long-term analgesic effect of low-dose ketamine. The apparent relationship between patient age and ketamine response was, however, not statistically significant. Further, patients with pain following a nerve lesion and patients without a known lesion of peripheral nerves were equally distributed between the three response groups. These results indicate that pain mechanisms are subject to alterations with time and that these alterations involve transition from NMDA to non-NMDA receptor mediated transmission in central pain pathways. Department of Pharmacology, Oslo University School of Medicine, Box 1057 Blindern, N-0316 Oslo, Norway. Toril.Rabben@studmed.uio.no
                        • Rabben T, Skjelbred P and Oye I (1999). Prolonged analgesic effect of ketamine, an N-methyl-D-aspartate receptor inhibitor, in patients with chronic pain. J Pharmacol Exp Ther 289:1060-6. Summary: We examined the role of N-methyl-D-aspartate (NMDA) receptors in chronic (pathological) pain in humans by using the NMDA receptor antagonist ketamine as a probe. Thirty patients with neuropathic pain in the trigeminal area were given an i.m. injection of ketamine 0.4 mg/kg combined with midazolam 0.05 mg/kg. Pethidine 1.0 mg/kg served as a control. Three different response patterns were observed. Ketamine caused a long-term (6-24 h) analgesic effect partly dissociated from the mental side effects in 8 of the 26 patients who completed the study; these patients also had a slight analgesic effect of pethidine. In nine patients, ketamine caused a short-lasting (<2 h) analgesic effect closely associated with the mental side effects, whereas pethidine caused little or no analgesia. The remaining nine patients did not experience any reduction of pain after either drug in spite of characteristic side effects. One week after the i.m. challenge the patients received either 4.0 mg/kg ketamine hydrochloride or placebo capsules to be taken orally as a nightly dose for three consecutive nights. Five of the eight patients who had a long-term analgesic effect of the i.m. challenge reported decreased pain on days after ketamine. None of the others reported an analgesic effect. The phenomenon of long-term depression of pain in a subgroup of patients was thus confirmed when ketamine was given p.o. These findings indicate that NMDA receptors are involved in the perception and maintenance of pathological pain in some patients. In others, pain appears to be mediated by NMDA receptor-independent mechanisms. We suggest that NMDA receptor-independent transmission in central pain pathways may contribute to the reduced efficiency of analgesic drugs often seen in chronic pain states. Section of Dental Pharmacology and Pharmacotherapeutics, Faculty of Dentistry, I.O.), University of Oslo, Oslo, Norway.
                        • Vick PG and Lamer TJ (2001). Treatment of central post-stroke pain with oral ketamine. Pain 92:311-3. Summary: Case report of 68 year old female with central post-stroke pain successfully treated with oral ketamine. The patient's pain was refractory to conventional pain treatments and she had persistent right hemi-body neuropathic pain with allodynia and hyperalgesia. An intravenous ketamine trial, followed by oral ketamine with titration to 50mg three times a day was beneficial in decreasing allodynia and hyperalgesia, as well as improving functional capabilities. Known side effects including dysphoria, hallucinations, and paranoid feelings were attenuated with benzodiazepines. Department of Anesthesiology, University of North Carolina at Chapel Hill, Campus Box # 7010, Chapel Hill, NC 27599-7010, USA. pvick@aims.unc.edu

                        [This message was edited by Wise Young on 03-12-03 at 06:26 AM.]

                        [This message was edited by Wise Young on 03-12-03 at 06:27 AM.]

                        Comment


                          #13
                          I sent him the abstracts, but my doc doesn't like the idea of using something so much like angel dust. He prefers intrathecal pump.
                          Alan

                          Proofread carefully to see if you any words out.

                          Comment


                            #14
                            Alan,

                            Ketamine does have abuse potential. However, it has been used for many years as the tranquilizing agent of choice for children before surgery. Because of its rapid onset and short half-life, it has long been used as a tranquilzing agent for young kids in emergency rooms, pediatric intensive care units, and pediatric dentistry.

                            The oral dose (0.2-0.5 mg/kg or 12-24 mg for the average adult, up to four times a day) that is commonly used to treat neuropathic pain is about 10 times lower than doses that cause anesthesia (2 mg/kg IV, 5-10 mg/kg IM). Oral hallucinogenic doses have been reported to be in the range of 300-375 mg.

                            Ketamine has been applied intrathecally in animals and even patients http://www.esraeurope.org/abstracts/...8/errando1.htm but I don't think that there is any reason to go that route when the oral route has been reported to be effective.

                            By the way, we use intramuscular ketamine in rats, typically in doses as high as 50-150 mg/kg to achieve anesthesia for minor surgical procedures. The most commonly anesthetic combination for rat surgery is IP or IM ketamine (100 mg/kg) and Xylazine (15 mg/kg).

                            Wise.

                            Comment


                              #15
                              Want to prescribe it to me, and tell me where to get it in oral form? [img]/forum/images/smilies/smile.gif[/img]
                              Alan

                              Proofread carefully to see if you any words out.

                              Comment

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