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04-16-2012, 10:35 PM
Pain / Analgesia
Is medical marijuana an effective treatment for patients suffering from severe / chronic pain?
The National Institutes of Health (NIH) stated the following in a report to the NIH Director titled "Workshop on the Medical Utility of Marijuana," that was compiled by the self-titled Ad Hoc Group of Experts during a two day meeting held Feb. 19-20, 1997: "A number of studies have been conducted on the antinociceptive [increased pain tolerance] or analgesic [pain reducing] effect of tetrahydrocannabinol (THC) or marijuana in both animals and human subjects; the results have been conflicting...Cannabinoids have been shown to be possibly analgesic in animal models of neuropathic pain... Since oral Delta-9-THC has some analgesic activity, it is highly likely that smoked marijuana has some analgesic activity in some kinds of clinical pain...If marijuana is to be a useful analgesic, healthcare providers need to know how it compares in efficacy and safety to at least a few of the standard analgesics that would be used in managing a particular kind of pain...There appear to be no controlled analgesic studies of smoked marijuana in patients with naturally occurring pain."
More on Pro's and Con's
Tetrahydrocannabinol (THC) and some other cannabinoids, either from the Cannabis sativa plant or synthetic, have analgesic properties, although the use of cannabis derivatives is currently illegal in many countries. A recent study finds that inhaled cannabis is effective in alleviating neuropathy and pain resulting from e.g. spinal injury and multiple sclerosis.<sup>[13]</sup> Other psychotropic analgesic agents include ketamine (an NMDA receptor antagonist), clonidine and other a<sub>2</sub>-adrenoreceptor agonists, and mexiletine and other local anaesthetic analogues. wikipedia
"Cananbinoid-induced analgesia appears linked to the same system by which opioids [synthetic narcotics] produce pain relief. But different from opioids, cannabinoids are also effective in a rat model of neuropathic pain, which means pain cased by nerves. For those of us that care for people with HIVwe know about the painful, peripheral neuropathy they getvery painful numb tingling feet. We often start these patients on a trial of drugs that lead ultimately to morphine, because there isnt anything effective." [26]
Dr. Abrams conducted a valuable human study of 50 HIV patients who used smoked marijuana cigarettes three times per day. Subjects showed positive results in daily pain, hyperalgesia, and a 30% reduction in pain. [27]
My link
A research paper fone at Hammersmith Hospital in London confirmed cannabis analgesic effects in the first UK clinical trial. The papers abstract began, Cannabinoids have analgesic and, possibly, anti-inflammatory properties but their clinical use has been restricted by legislation. That same abstract calling for further studies concluded, Cannabis nave patients would tolerate investigations but may generate medicolegal problems. [28]
The use of cannabis for pain relief was widespread in the membership of legitimate medical marijuana groups under attack by the US government. [29] In 1998, federal law enforcers closed San Francisco Bay Area Cannabis Clubs, forcing over 10,000 seriously ill patients to support nefarious street sources and pay outrageous black market prices for non-medical grade marijuana. In the following year, the government sponsored Institute of Medicine report elevated pain relief to the top of the list of marijuanas medical benefits. [30]
Due to cannabis prohibition and the bias of research regulation by the National Institutes on Drug Abuse, human studies of the pain relieving qualities of cannabis are limited. Grotenherman writes: " Few clinical studies of cannabinoids in painful conditions exist. In two trials, oral THC proved to be effective against cancer pain in doses of 15 and 20 mg, respectively. However, some patients experienced intolerable side effects. In a single case double-blind study a patient with familial Mediterranean fever clearly reduced his need for opiates while receiving THC (50 mg per day divided in five doses) in comparison to placebo."[31]
However, the fascinating new view of the body's endocannabinoid systems provide ample scientific evidence to justify the widespread popularity of cannabis as an analgesic, partivcularly in cases of nerve or neurological pain. Consider the following excerpts from a recent paper titled Mechanisms of Cannabinoid Analgesia:
Within the central nervous system, cannabinoids, like opioids, act at both spine (intrathecal) and supraspinal (intracerebroventricular) levels to produce analgesia. Cannabinoid-induced analgesia is not mediated by opioid receptors because it is unaffected by opioid antagonists. However, cannabinoid and opioid agonists have synergistic analgesic affects.
In vivo electrophysiological studies indicate that, like opioids, cannabinoids suppress the activity of neurons involved in the ascending transmission of nociceptive information. Systemic administration of cannabinoid agonists inhibits noxious stimulus-evoked firing in neurons of the spinal cord dorsal horn and thalamus. Cannabinoids also inhibit windup (a neuronal correlate of hyperalgesia), which is the augmentation of the response of spinal neurons to repetitive noxious electrical stimuli.
It is now becoming apparent that, like opioids, cannabinoids act via specific receptors within pain pathways to produce analgesia. The distinct anatomical receptors within pain pathways suggests that they may be useful for management of different pain sites. The distinction between cannabinoids and opioids is emphasized by more recent electrophysiological studies and provides a cellular basis for their synergistic analgesic actions. These findings suggest that cannabinoids warrant urgent study as therapeutic agents, particularly with the emergence of novel cannabinoid drugs.[32]
IN 2008, i nvestigators at the University of California at Davis, in conjunction with the University of California Center for Medical Cannabis Research (CMCR), assessed the efficacy of inhaled cannabis on pain intensity among 38 patients with central and/or peripheral neuropathic pain in a randomized, placebo-controlled, crossover trial. Researchers reported that smoking low-grade (3.5 percent THC) and mid-grade (7 percent THC) cannabis equally reduced patients perception of spontaneous pain.
They concluded: "In the present experiment, cannabis reduced pain intensity and unpleasantness equally. Thus, as with opioids, cannabis does not rely on a relaxing or tranquilizing effect, but rather reduces both the core component of nociception (nerve pain) and the emotional aspect of the pain experience to an equal degree."
The study is the second clinical trial conducted by CMCR investigators to conclude that inhaled cannabis significantly reduces chronic neuropathy, a condition that is typically unresponsive to both opioids and non-steroidal anti-inflammatory drugs such as ibuprofen.[33]
GW Pharmeceuticals is a company that has isolated canabinoid compounds in arosol sprays for medical use. Another recent study shows that GW's product, Sativex, sowed remarkable value in trating neuropathic pain. Forty-one patients with multiple sclerosis and central neuropathic pain completed the double blind, placebo-controlled "randomized withdrawal" study. Volunteers in the study were administered either Sativex or a placebo daily for four weeks following their long-term use of the cannabis spray. Previous trials of Sativex have reported that patients required fewer daily doses of the drug and reported lower median pain scores the longer they took it.[34]
Recent studies have located and determined exact mechanisms of cannabis analgesia through the body's endocannabinoid receptors. The following is an excert from "Endocannabinoids and pain: spinal and peripheral analgesia in inflammation and neuropathy" from theInperial College of Science in London:
"Local administration, peptide release and electrophysiological studies support the concept of spinally mediated endocannabinoid-induced analgesia. Whilst a proportion of the peripheral analgesic effect of endocannabinoids can be attributed to a neuronal mechanism acting through CB(1) receptors expressed by primary afferent neurones, the antiinflammatory actions of endocannabinoids, mediated through CB(2) receptors, also appears to contribute to local analgesic effects." [35]
Related sections: Addiction, Arthritis, Neuralgia, Psychoactivity, Replacement of Medications
[1] Doctor urges war on pain, more use of opium-based drugs. Miami Hearald, January 29, 1998
[2] Stolberg, Study Finds Elderly Receive Little Pain Treatment in Nursing Homes. June 17, 1998
[3] Doctor urges war on pain, more use of opium-based drugs. Miami Hearald, January 29, 1998
[4] Researchers say many cancer patients suffer needless pain. Associated Press, June 17, 1998
[5] Drug Enforcement Administration, Statement of policy for the use and handling of controlled substances in the treatment of pain. 1998
[6] Kassirer, Federal foolishness and marijuana. Editorial, The New England Journal of Medicine, January 30, 1997
[7] Russo "Cannabinoids in the management of difficult to treat pain" Therapeutics and Clinical Risk Management" 2008-4(1) 245-259
[8] Mikuriya, Marijuana Medical Papers: 1839-1972. Oakland: Medi-comp Press, 1973
[9] Grinspoon, Marijuana Reconsidered. 3<sup>rd</sup> ed. San Francisco: Quick American Archives, 1971
[10] Russo, "The Role of Cannabis and Cannabinoids in Pain Management" Weiner's Pain Mnagement Guide, 7th ed. American Academy of Pain Management 2006
[11] Noyes and Baram, Cannabis analgesia. Comprehensive Psychiatry. Vol. 15, No. 6, 1974
[12] Beltramo and Piomelli, Functional role of high-affinity anandamide transport, as revealed by selective inhibition. Science, Vol. 277, No. 5329, p1094(4), 1997
[13] Russo, "The Role of Cannabis and Cannabinoids in Pain Management" Weiner's Pain Mnagement Guide, 7th ed. American Academy of Pain Management 2006
[14] Formukong, Evans, and Evans, Analgesic and anti-inflammatory activity of constituents of cannabis sativa L. Inflammation, Vol. 12, No. 4, pp.361-371, 1988
[15] Maurer, Henn, Dittrich, and Hoffman, Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double blind trial. European Archive of Psychiatry and Neurological Science. Vol. 240, No. 1, pp. 1-4, 1990
[16] Cannabidiol, Wonder drug of the 21<sup>st</sup> century? Source: Schaffer Library of Drug Policy, www.druglibrary.org
[17] Pre-clinical studies show CT-3 reduces chronic and acute inflammation and reduces destruction of joints. BW HealthWire, January 1998
[18] "Curative Leaf - Compound in marijuana reduces inflammation without the psychological effects", Amy Maxmen, Science News, June 23rd, 2008, www.sciencenews.com
[19] Medical marijuana: Doing the science. Synapse, 1998, www.itsa.ucsf.edu/synapse/
[20] Symposium Syllabus, Functional Role of Cannabinoid Receptors. Press Conference, August 26, 1998, Source: Medical Marijuana Magazine, www.marijuanamagazine.com
[21] Study reveals pot chemicals can relieve serious pain. Los Angeles Times, October 27, 1998
[22] Ibid.
[23] Morin, Research into cannabinoids provides evidence that the use of marijuana to treat pain and nausea should not e so easily dismissed. May 1998, Source: Morin@Brown.edu
[24] Cowen, Science journal reports that cannabinoid receptors located outside the brain and spine are affected when the skin or flesh is cut or hurt. July 16, 1998, www.marijuananews.com
[25] Widener, Study: Marijuana, morphine work on same area of brain. The Seattle Times, September 25, 1998
[26] Diagnosis: Smoke Pot to Relieve Pain. The University of Washington Daily, May 1997
[27] Abrams, Lindesmith Center Lecture, San Francisco, May 17, 1999
[28] Holdcroft et al., Pain relief with oral cannabinoids in familial Mediterranean fever. Anesthesia, Vol. 52, No. 5, pp. 483-486, May 1997
[29] San Francisco Chronicle, San Francisco Examiner, Associated Press, May 1998
[30] Institute of Medicine: Marijuana and Medicine: Assessing the Science Base. Washington DC: National Academy Press
[31] Grotenhermen, Review of Therapeutic Effects. Chapter 11, p. 126-128 (see Absracts and Studies section of this website)
[32] Vaughn and Christie, Mechanisms of Cannabinoid Analgesia. Chapter 8, p. 90-95
[33] Inhaled Cannabis Reduces Central And Peripheral Neuropathic Pain, Study Says, NORML News, May 3rd, 2008 See: www.NORML.org
[34] Cannabis Spray Demonstrates Long Term Efficacy In Neuropathic Pain, Study Says, NORML News, 9/11/08, See: www.NORML.org
[35] Endocannabinoids and pain: spinal and peripheral analgesia in inflammation and neuropathy, Rice AS, Farquhar-Smith WP, Nagy I., Department of Anaesthetics, Pain Research Group, Inperial College of Science, Technology and Medicine, Chelsea and Westminster Hospital Campus, 369 Fulham Road, London SW10 9NH, UK. a.rice@ic.ac.uk
My link
Researchers at University of California Davis examined whether marijuana produces analgesia for patients with neuropathic pain. Thirty-eight patients were examined. They were given either high-dose (7%), low-dose (3.5%) or placebo cannabis.
The authors reported that identical levels of analgesia were produced at each cumulative dose level by both concentrations of the agent. As with opioids, cannabis does not rely on a relaxing or tranquilizing effect, but reduces the core component of nociception and the emotional aspect of the pain experience to an equal degree. There were undesirable consequences observed from cannabis smoking, such as feeing high or impaired, but they did not inhibit tolerability or cause anyone to withdraw from the study. In general, side effects and mood changes were inconsequential.
It was noted by the authors that since high and low dose cannabis produced equal analgesic efficacy, a case could be made for testing lower concentrations to determine if the analgesic profile can be maintained while reducing potential cognitive decline.
In addition, the authors said further research could probe whether adding the lowest effective dose of cannabis to another analgesic drug might lead to more effective neuropathic pain treatment for patients who otherwise are treatment-resistant
n a randomized, double-blinded, placebo controlled, crossover trial in fifteen healthy volunteers, we evaluated the effects of low, medium, and high dose smoked cannabis (respectively 2%, 4%, and 8% 9-delta-tetrahydrocannibinol by weight) on pain and cutaneous hyperalgesia induced by intradermal capsaicin. Capsaicin was injected into opposite forearms 5 and 45 minutes after drug exposure and pain, hyperalgesia, tetrahydrocannibinol plasma levels, and side effects were assessed. Five minutes after cannabis exposure, there was no effect on capsaicin-induced pain at any dose. By 45 minutes after cannabis exposure, however, there was a significant decrease in capsaicin-induced pain with the medium dose and a significant increase in capsaicin-induced pain with the high dose. There was no effect seen with the low dose nor was there an effect on the area of hyperalgesia at any dose. Significant negative correlations between pain perception and plasma delta-9-tetrahydrocannibinol levels were found after adjusting for the overall dose effects. There was no significant difference in performance on the neuropsychological tests.
This study suggests that there is a window of modest analgesia for smoked cannabis with lower doses decreasing pain and higher doses increasing pain.
The full results of this study were published in the journal Anesthesiology.
ABSTRACT:
By every criteria (deterioration in quality of life; loss of work days, and therapy directed dollars) pain is appreciated to be a major medical problem. Recent findings in the molecular biology and the pharmacology of pain transmission have shed light on mechanisms of nociceptive processing and the activity of a variety of "novel therapeutic" modalities that include the cannabinoids. Although the pre-clinical literature suggests that the cannabinoids produce antinociception and anti-hyperalgesic effects, the efficacy of the cannabinoids in the human pain state is unclear. As an experimental variable, clinical pain is a multidimensional phenomenon with few objective physical correlates. Many other factors such as emotional status and coping skills, make "pain" difficult to study in the clinical setting. An important development has been the implementation of well-controlled experimental pain models to investigate the sensory components of pain processing and to use these models in the assessment of analgesic efficacy in normal volunteers. To the degree that human experimental pain models can predict analgesic efficacy of novel agents, the role of mechanisms defined in preclinical studies can be translated to the human experience under well-controlled conditions. Human experimental pain has been used to test a wide range of currently available analgesics. Knowing the effect of these agents on human experimental pain, I now wish to study the effects of cannabis on human experimental pain and how this compares to commonly used analgesics.
PUBLICATIONS:
Type:
Title:
Journal Article Wallace M, Schulteis G, Atkinson JH, Wolfson T, Lazzaretto D, Bentley H, Gouaux B, Abramson I. Dose-dependent Effects of Smoked Cannabis on Capsaicin-induced Pain and Hyperalgesia in Healthy Volunteers. Anesthesiology. 107(5):785-796, November 2007.
The most frequent complaint that patients look for medical help with is pain. There are several different types of pain, and unfortunately none of the currently-prescribed pharmacological treatments for pain work completely for certain types. A particular example is that of pain caused by damaged nerves (such as that which causes phantom limb pain), which does not respond well to existing medications.
Severe chronic pain is usually treated with opiates, but these are addictive, and tolerance develops so that the dose has to be increased. The risk of severe side effects such as nausea is great, and additionally the user feels drugged, and finds it difficult to function properly. Family life may suffer as patients find it hard to relate to other people, and even reading to children is difficult. Synthetic analgesics are non-addictive but they are not powerful enough.
Cannabis has fewer side effects than other analgesics, and users report it "rounds off" the pain quickly after smoking. An Institute of Medicine report contains a minimal list of 5 situations in which cannabis-based medicines are of use in treating pain:
Some people have used cannabis to control pain for 20 years or more, and many report that they were able to kick their addiction to opiates with small amounts of cannabis. One strange fact is that more experienced users get a greater pain-relieving effect from cannabis than novices. Experienced users also are able to function normally and ignore the psychoactive effects. Cannabis may be better at controlling the different types of pain.
Cannabis has had a long history of use as an analgesic, and was widely used in 19th century Britain, including in the royal household. Dr. J. Russell Reynolds, Fellow of the Royal Society and Physician to Queen Victoria reported in the Lancet in 1890 that he had been prescribing cannabis for 30 years and considered it "one of the most valuable medicines we possess". According to Reynolds indian hemp remained effective as an analgesic for months and even years without an increase in the dose.
It seems that cannabis shares some method of action with opioids, but the mechanism with which it accomplishes its analgesic effects differs. This indicates that they may produce an additive effects when used in conjunction with current medicines. In addition they might provide help to patients who do not react satisfactorily to other treatments. Much anecdotal evidence seems to indicate that this is the case.
Indeed, the British Medical Association has gone on record as stating that 'the prescription of nabilone, THC and other cannabinoids...should be permitted for patients with intractable pain'. Other official bodies have found similar results. A House of Lords report summed up the situation stating that 'there is scientific evidence that cannabinoids possess painrelieving properties, and some clinical evidence to support their medical use in this indication'. In a press conference on October 26th 1997, the US Society for Neuroscience claimed that 'substances similar to or derived from marijuana...could benefit the more than 97 million Americans who experience some form of pain each year'.
Patients' testimonies
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Date
Amanda
Mon 01 Nov 2010
Annon
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Mund
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Mr Dmoore
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Anonymous
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Anonymous
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Anonymous
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Stephen Livingston
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Anonymous
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Roger Pigott
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GC
Mon 31 Oct 2005
Eleanor
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Terry
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vanessa
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gruf
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Nicolas
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Sonia
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Bob
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John
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Anonymous
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Winston Matthews
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Stacey H
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Carl
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Steven
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Nigel Pearson
Sat 09 Dec 2000
Anonymous
Thu 07 Dec 2000
Anonymous
Thu 07 Dec 2000
For the complete collection of testimonies from medical users of cannabis, see our
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Despite the long history of use of cannabis as an analgesic, and the obvious problems with synthetic drugs, the War on Drugs prevented people from reconsidering cannabis until the mid-seventies, when several studies were published.
Patients suffering from cancer usually suffer from severe pain. This can be for a number of reasons, such as the invasion of their bones, inflammation or damage caused to nerves. It is a form of pain which is notoriously hard to treat effectively.
At the University of Iowa Noyes et al (1975a) gave oral THC or a placebo at random to hospitalised cancer patients who were in severe pain. The THC relieved pain for several hours at very low doses and longer periods at higher doses (15 - 20 mg). It also acted as a sedative at the higher dose. It had fewer physical side effects than other commonly used analgesics. There was no incidence of nausea or vomiting unlike many other analgesics - indeed more than half of the patients had an increased appetite.
Then Noyes et al conducted another study (1975b). This time they gave codeine, THC and placebo to 36 patients with advanced cancer. Codeine and cannabis were equally effective, but some patients found the psychoactive effects of THC uncomfortable. However these people did not know they were going to take a psychoactive drug and were obviously frightened. If they had been told beforehand perhaps they would not have been uncomfortable. Many of the patients however felt they generally had a sense of well-being that was absent before. As a result of this experiment, the researchers estimated that 10mg of THC was roughly equivalent to 60mg of codeine.
A study revealing potential additive effects of THC on standard medication was done by Holdcroft et al (1997). It centred on a patient who had severe chronic pain of gastrointestinal origin. The patient used morphine as an analgesic.It was found that the patient required a substantially lower amount of morphine when they were treated with oral THC in the form of cannabis oil.
The differing mechanism of analgesic action cannabis uses compared to existing (mainly opioid) medications means that not only are additive effects likely, but it could be useful in patients resistant to existing medications, and be useful in treating pain which existing medications fail to deal with adequately. The National Institutes of Health suggested that 'Neuropathic pain represents a treatment problem for which currently available analgesics are, at best, marginally effective. ...THC...may be useful in this inadequately treated type of pain'. The findings of Growing et al (1998) concurred with this conclusion, and suggested that this might be the area of greatest medical potential.
Maurer et al (1990) found that a paraplegic patient, who suffered leg pain, gained pain-relief after taking a single dose of THC.
Staquet et al (1978) did a trial using a nitrogen analogue of THC. This too showed significant analgesic effects, and was effective as both codeine and secobarbital. A further study using the synthetic THC analogue Levonantradol was done by Jain et al (1981). The trial population was patients who had moderate to severe post-operative pain. They were administered Levonantrodol by injection, and found significant pain relief as a result.
In Canada, Milstein et al (1975) studied the analgesic effect of smoked cannabis in normal subjects. Half of them had used cannabis before. The researchers caused pain by pressing onto the subjects thumbnails. The subjects were able to withstand more pressure after they had smoked cannabis. Strangely, the analgesic effect was greater in the experienced users.
A article by Noyes and Baram (1974) showed that cannabis relieved the pain of a headache in three patients with an equivalent or better efficacy than aspirin or ergotamine tartrate. Petro (1980) found that two patients suffering pain from a muscle spasticity disorder had a reduction in their discomfort after inhaling cannabis.
Recently, it has been found that the body's natural cannabinoid, anandamide is involved in the control of pain. Calignano et al (1998) found that rats release anandamide when cells are damaged. This then causes seemingly pain-relieving effects in the areas of the brain and spinal cord that process pain stimuli. An ACM bulletin in 1998 demonstrated that when anandamide is used with another naturally occuring compound in the body, palmitylethanolamide, pain was reduced by up to 100 times.
Calignano A. et al (1998) Control of pain by endogenous cannabinoids,
Nature
394
: 277-281.
Growing L et al (1998) Therapeutic use of cannabis: clarifying the debate,
Drug and Alcohol Review
17
: 445-452.
Holdcroft A et al (1997) Pain relief with oral cannabinoids in familial Mediterranean fever.
Anaesthesia,
52
: 483
House of Lords Select Committee on Science and Technology (1998)
Science and Technology - Ninth report
. Science and Technology Committee Publications, UK.
Institute of Medicine (1999)
Marijuana and medicine: Assessing the science base
. National Academy Press
Jain AK, Ryan JR, McMahon FG, Smith G. (1981) Evaluation of intramuscular levonantradol
and placebo in acute postoperative pain.
Journal of Clinical Pharmacology
21
:320S-326S.
Maurer M. et al. (1990) Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double-blind trial.
European Archives of Psychiatry and Clinical Neuroscience
240
: 1-4.
Milstein S.L., MacCannell K., Karr, G. and Clark S. (1975) Marijuana-produced changes in pain tolerance: Experienced and non-experienced subjects.
International Pharmacopsychiatry
10
: 177-182.
National Institutes of Health (1997)
Workshop on the Medical Utility of Marijuana: Report to the Director
. Washington, D.C.
Noyes R., Baram D. (1974) Cannabis analgesia.
Compr. Psychiatry
15
: 531.
Noyes R., Brunk S.F., Baram D.A. and Canter A. (1975a) Analgesic effect of delta-9-tetrahydrocannabinol.
Journal of Clinical Pharmacology
15
: 139-143.
Noyes R., Brunk S.F., Avery D.H. and Canter A. (1975b) The analgesic properties of delta-9-tetrahydrocannabinol and codeine.
Clinical Pharmacology and Therapeutics
18
: 84-89.
Petro D. (1980) Marihuana as a therapeutic agent for muscle spasm and spasticity. Psychosomatics 21: 81-85.
Reynolds J.R. (1890) Therapeutic uses and toxic effects of Cannabis indica.
Lancet
1
: 637
Science: Cannabinoid/anandamide-receptor systems involved in peripheral control of pain
, ACM Bulletin, July 26, 1998.
Staquet M, Gantt C, Machin D. (1978) Effect of a nitrogen analog of tetrahydrocannabinol on cancer pain.
Clinical Pharmacology and Therapeutics
23
:397401.
For a large collection of research materials, see our
research
page.
Use of Marijuana in Neurological
<strong>and Movement Disorders</strong>
Medical Marijuana
Use of Marijuana in Neurological and Movement Disorders
1. What research has been done and what is known about the possible medical uses of marijuana? There have been numerous studies both in animals and in various clinical states on the use of cannabinoids on neurological and various movement disorders. These results range from anecdotal reports to surveys and clinical trials. Marijuana or tetrahydrocannabinol (THC) is reported to have some antispasticity, analgesic, antitremor, and antiataxia actions, as well as some activity in multiple sclerosis (MS) and in spinal cord injury patients.
The spasticity and nocturnal spasms produced by MS and partial spinal cord injury have been reported to be relieved by smoked marijuana and to some extent by oral THC in numerous anecdotal reports. The effect seems to appear rapidly with smoked marijuana; patients are able to titrate the dose by the amount they smoke. No large-scale controlled studies or studies to compare either smoked or oral THC with other available therapies have been reported. Several relatively good therapeutic alternatives exist. There is no published evidence that the cannabinoid drugs are superior or even equivalent.
Substantial experimental animal literature exists showing that various cannabinoids, given primarily by parenteral routes, have a substantial anticonvulsant effect in the control of various models of epilepsy, especially generalized and partial tonic-clonic seizures. Scant information is available about the human experience with the use of marijuana or cannabinoids for the treatment of epilepsy. This is an area of potential value, especially for cannabis therapies by other than the smoked route.
Several single case histories have been reported indicating some benefit of smoked marijuana for dystonic states. It must be remembered that dystonia is a clinical syndrome with numerous potential causes, and the information available now does not differentiate which causes are most likely to be improved. Smoked marijuana and oral THC have been tested in the treatment of Parkinson's disease and Huntington's chorea without success.
The cannabinoids also have been used as experimental immunologic modifiers to treat such conditions as the animal models of experimental allergic encephalomyelitis (EAE) and neuritis. Parenteral cannabinoids have been successful in modifying EAE in animals, suggesting that cannabinoids may be of value in a more fundamental way by altering the root cause of a disease such as MS rather than simply treating its symptoms. Smoked marijuana would not be acceptable for such a role because of the variability of dose with the smoked route.
2. What are the major unanswered scientific questions?
The discovery of dedicated systems of central nervous system (CNS) neurons approximately 8 years ago, which express receptors specific for the cannabinoids, is of major scientific interest and importance. The distribution of these cannabinoid receptor-bearing neurons corresponds well with the clinical effects of smoked marijuana; for instance, their presence in the forebrain may relate to adverse changes in short-term memory, but perhaps positively in the control of epilepsy. Cannabinoid receptors in the brainstem and cerebellum may relate to the recognized incoordination that accompanies smoked marijuana use. The discovery of intrinsic ligands for these receptors in the mammalian brain is also of great importance. This system of cannabinoid receptors and ligands may be analogous to the discovery of opiate receptors and endorphins, which linked various opium derivatives (heroin and morphine) to an intrinsic system of neurons in the CNS. That discovery was of major importance for pain research.
The major unanswered scientific questions are:
* How useful is smoked marijuana of known specific potency in controlling various neurologic conditions?
* In comparative studies, how useful is smoked marijuana in altering objective abnormalities such as spasticity versus current standard therapies that have already been approved for human use?
* Can alternative delivery systems (other than the oral route) be developed to provide rapidity of action with more safety than smoked marijuana?
* Can available or newly developed synthetic cannabinoids be used more effectively to stimulate or block receptor activity in the cannabinoid system of the CNS?
* What are the immune-modulating characteristics of the cannabinoids and can they be used for therapeutic human benefit?
* Can the long-term risks of daily smoked marijuana be quantified so that useful risk versus benefit ratios can be determined, especially when considering treatment of long-term conditions such as spasticity or epilepsy?
3. What are the diseases or conditions for which marijuana might have potential as a treatment and which merit further study?
Marijuana or the use of other cannabinoids as human therapies might be considered for treating spasticity and nocturnal spasms complicating MS and spinal cord injury, for various active epilepsy states, for some forms of dystonia, and perhaps most interestingly, for treating neuropathic pain (Zeltser et al. 1991). (Also see the chapter titled Analgesia.) Neuropathic pain complicates many CNS diseases. Few available therapies provide even partial relief.
Reference
Zeltser, R.; Seltzer, Z.; Eisen, A.; Feigenbaum, J.J.; and Mechoulam, R. Suppression of neuropathic pain behavior in rats by a non-psychotropic synthetic cannabinoid with NMDA receptor-blocking properties. Pain 47(1):95-103, October 1991.
source: http://www.onlinepot...l/article44.htm
Is medical marijuana an effective treatment for patients suffering from severe / chronic pain?
The National Institutes of Health (NIH) stated the following in a report to the NIH Director titled "Workshop on the Medical Utility of Marijuana," that was compiled by the self-titled Ad Hoc Group of Experts during a two day meeting held Feb. 19-20, 1997: "A number of studies have been conducted on the antinociceptive [increased pain tolerance] or analgesic [pain reducing] effect of tetrahydrocannabinol (THC) or marijuana in both animals and human subjects; the results have been conflicting...Cannabinoids have been shown to be possibly analgesic in animal models of neuropathic pain... Since oral Delta-9-THC has some analgesic activity, it is highly likely that smoked marijuana has some analgesic activity in some kinds of clinical pain...If marijuana is to be a useful analgesic, healthcare providers need to know how it compares in efficacy and safety to at least a few of the standard analgesics that would be used in managing a particular kind of pain...There appear to be no controlled analgesic studies of smoked marijuana in patients with naturally occurring pain."
More on Pro's and Con's
Tetrahydrocannabinol (THC) and some other cannabinoids, either from the Cannabis sativa plant or synthetic, have analgesic properties, although the use of cannabis derivatives is currently illegal in many countries. A recent study finds that inhaled cannabis is effective in alleviating neuropathy and pain resulting from e.g. spinal injury and multiple sclerosis.<sup>[13]</sup> Other psychotropic analgesic agents include ketamine (an NMDA receptor antagonist), clonidine and other a<sub>2</sub>-adrenoreceptor agonists, and mexiletine and other local anaesthetic analogues. wikipedia
"Cananbinoid-induced analgesia appears linked to the same system by which opioids [synthetic narcotics] produce pain relief. But different from opioids, cannabinoids are also effective in a rat model of neuropathic pain, which means pain cased by nerves. For those of us that care for people with HIVwe know about the painful, peripheral neuropathy they getvery painful numb tingling feet. We often start these patients on a trial of drugs that lead ultimately to morphine, because there isnt anything effective." [26]
Dr. Abrams conducted a valuable human study of 50 HIV patients who used smoked marijuana cigarettes three times per day. Subjects showed positive results in daily pain, hyperalgesia, and a 30% reduction in pain. [27]
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A research paper fone at Hammersmith Hospital in London confirmed cannabis analgesic effects in the first UK clinical trial. The papers abstract began, Cannabinoids have analgesic and, possibly, anti-inflammatory properties but their clinical use has been restricted by legislation. That same abstract calling for further studies concluded, Cannabis nave patients would tolerate investigations but may generate medicolegal problems. [28]
The use of cannabis for pain relief was widespread in the membership of legitimate medical marijuana groups under attack by the US government. [29] In 1998, federal law enforcers closed San Francisco Bay Area Cannabis Clubs, forcing over 10,000 seriously ill patients to support nefarious street sources and pay outrageous black market prices for non-medical grade marijuana. In the following year, the government sponsored Institute of Medicine report elevated pain relief to the top of the list of marijuanas medical benefits. [30]
Due to cannabis prohibition and the bias of research regulation by the National Institutes on Drug Abuse, human studies of the pain relieving qualities of cannabis are limited. Grotenherman writes: " Few clinical studies of cannabinoids in painful conditions exist. In two trials, oral THC proved to be effective against cancer pain in doses of 15 and 20 mg, respectively. However, some patients experienced intolerable side effects. In a single case double-blind study a patient with familial Mediterranean fever clearly reduced his need for opiates while receiving THC (50 mg per day divided in five doses) in comparison to placebo."[31]
However, the fascinating new view of the body's endocannabinoid systems provide ample scientific evidence to justify the widespread popularity of cannabis as an analgesic, partivcularly in cases of nerve or neurological pain. Consider the following excerpts from a recent paper titled Mechanisms of Cannabinoid Analgesia:
Within the central nervous system, cannabinoids, like opioids, act at both spine (intrathecal) and supraspinal (intracerebroventricular) levels to produce analgesia. Cannabinoid-induced analgesia is not mediated by opioid receptors because it is unaffected by opioid antagonists. However, cannabinoid and opioid agonists have synergistic analgesic affects.
In vivo electrophysiological studies indicate that, like opioids, cannabinoids suppress the activity of neurons involved in the ascending transmission of nociceptive information. Systemic administration of cannabinoid agonists inhibits noxious stimulus-evoked firing in neurons of the spinal cord dorsal horn and thalamus. Cannabinoids also inhibit windup (a neuronal correlate of hyperalgesia), which is the augmentation of the response of spinal neurons to repetitive noxious electrical stimuli.
It is now becoming apparent that, like opioids, cannabinoids act via specific receptors within pain pathways to produce analgesia. The distinct anatomical receptors within pain pathways suggests that they may be useful for management of different pain sites. The distinction between cannabinoids and opioids is emphasized by more recent electrophysiological studies and provides a cellular basis for their synergistic analgesic actions. These findings suggest that cannabinoids warrant urgent study as therapeutic agents, particularly with the emergence of novel cannabinoid drugs.[32]
IN 2008, i nvestigators at the University of California at Davis, in conjunction with the University of California Center for Medical Cannabis Research (CMCR), assessed the efficacy of inhaled cannabis on pain intensity among 38 patients with central and/or peripheral neuropathic pain in a randomized, placebo-controlled, crossover trial. Researchers reported that smoking low-grade (3.5 percent THC) and mid-grade (7 percent THC) cannabis equally reduced patients perception of spontaneous pain.
They concluded: "In the present experiment, cannabis reduced pain intensity and unpleasantness equally. Thus, as with opioids, cannabis does not rely on a relaxing or tranquilizing effect, but rather reduces both the core component of nociception (nerve pain) and the emotional aspect of the pain experience to an equal degree."
The study is the second clinical trial conducted by CMCR investigators to conclude that inhaled cannabis significantly reduces chronic neuropathy, a condition that is typically unresponsive to both opioids and non-steroidal anti-inflammatory drugs such as ibuprofen.[33]
GW Pharmeceuticals is a company that has isolated canabinoid compounds in arosol sprays for medical use. Another recent study shows that GW's product, Sativex, sowed remarkable value in trating neuropathic pain. Forty-one patients with multiple sclerosis and central neuropathic pain completed the double blind, placebo-controlled "randomized withdrawal" study. Volunteers in the study were administered either Sativex or a placebo daily for four weeks following their long-term use of the cannabis spray. Previous trials of Sativex have reported that patients required fewer daily doses of the drug and reported lower median pain scores the longer they took it.[34]
Recent studies have located and determined exact mechanisms of cannabis analgesia through the body's endocannabinoid receptors. The following is an excert from "Endocannabinoids and pain: spinal and peripheral analgesia in inflammation and neuropathy" from theInperial College of Science in London:
"Local administration, peptide release and electrophysiological studies support the concept of spinally mediated endocannabinoid-induced analgesia. Whilst a proportion of the peripheral analgesic effect of endocannabinoids can be attributed to a neuronal mechanism acting through CB(1) receptors expressed by primary afferent neurones, the antiinflammatory actions of endocannabinoids, mediated through CB(2) receptors, also appears to contribute to local analgesic effects." [35]
Related sections: Addiction, Arthritis, Neuralgia, Psychoactivity, Replacement of Medications
[1] Doctor urges war on pain, more use of opium-based drugs. Miami Hearald, January 29, 1998
[2] Stolberg, Study Finds Elderly Receive Little Pain Treatment in Nursing Homes. June 17, 1998
[3] Doctor urges war on pain, more use of opium-based drugs. Miami Hearald, January 29, 1998
[4] Researchers say many cancer patients suffer needless pain. Associated Press, June 17, 1998
[5] Drug Enforcement Administration, Statement of policy for the use and handling of controlled substances in the treatment of pain. 1998
[6] Kassirer, Federal foolishness and marijuana. Editorial, The New England Journal of Medicine, January 30, 1997
[7] Russo "Cannabinoids in the management of difficult to treat pain" Therapeutics and Clinical Risk Management" 2008-4(1) 245-259
[8] Mikuriya, Marijuana Medical Papers: 1839-1972. Oakland: Medi-comp Press, 1973
[9] Grinspoon, Marijuana Reconsidered. 3<sup>rd</sup> ed. San Francisco: Quick American Archives, 1971
[10] Russo, "The Role of Cannabis and Cannabinoids in Pain Management" Weiner's Pain Mnagement Guide, 7th ed. American Academy of Pain Management 2006
[11] Noyes and Baram, Cannabis analgesia. Comprehensive Psychiatry. Vol. 15, No. 6, 1974
[12] Beltramo and Piomelli, Functional role of high-affinity anandamide transport, as revealed by selective inhibition. Science, Vol. 277, No. 5329, p1094(4), 1997
[13] Russo, "The Role of Cannabis and Cannabinoids in Pain Management" Weiner's Pain Mnagement Guide, 7th ed. American Academy of Pain Management 2006
[14] Formukong, Evans, and Evans, Analgesic and anti-inflammatory activity of constituents of cannabis sativa L. Inflammation, Vol. 12, No. 4, pp.361-371, 1988
[15] Maurer, Henn, Dittrich, and Hoffman, Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double blind trial. European Archive of Psychiatry and Neurological Science. Vol. 240, No. 1, pp. 1-4, 1990
[16] Cannabidiol, Wonder drug of the 21<sup>st</sup> century? Source: Schaffer Library of Drug Policy, www.druglibrary.org
[17] Pre-clinical studies show CT-3 reduces chronic and acute inflammation and reduces destruction of joints. BW HealthWire, January 1998
[18] "Curative Leaf - Compound in marijuana reduces inflammation without the psychological effects", Amy Maxmen, Science News, June 23rd, 2008, www.sciencenews.com
[19] Medical marijuana: Doing the science. Synapse, 1998, www.itsa.ucsf.edu/synapse/
[20] Symposium Syllabus, Functional Role of Cannabinoid Receptors. Press Conference, August 26, 1998, Source: Medical Marijuana Magazine, www.marijuanamagazine.com
[21] Study reveals pot chemicals can relieve serious pain. Los Angeles Times, October 27, 1998
[22] Ibid.
[23] Morin, Research into cannabinoids provides evidence that the use of marijuana to treat pain and nausea should not e so easily dismissed. May 1998, Source: Morin@Brown.edu
[24] Cowen, Science journal reports that cannabinoid receptors located outside the brain and spine are affected when the skin or flesh is cut or hurt. July 16, 1998, www.marijuananews.com
[25] Widener, Study: Marijuana, morphine work on same area of brain. The Seattle Times, September 25, 1998
[26] Diagnosis: Smoke Pot to Relieve Pain. The University of Washington Daily, May 1997
[27] Abrams, Lindesmith Center Lecture, San Francisco, May 17, 1999
[28] Holdcroft et al., Pain relief with oral cannabinoids in familial Mediterranean fever. Anesthesia, Vol. 52, No. 5, pp. 483-486, May 1997
[29] San Francisco Chronicle, San Francisco Examiner, Associated Press, May 1998
[30] Institute of Medicine: Marijuana and Medicine: Assessing the Science Base. Washington DC: National Academy Press
[31] Grotenhermen, Review of Therapeutic Effects. Chapter 11, p. 126-128 (see Absracts and Studies section of this website)
[32] Vaughn and Christie, Mechanisms of Cannabinoid Analgesia. Chapter 8, p. 90-95
[33] Inhaled Cannabis Reduces Central And Peripheral Neuropathic Pain, Study Says, NORML News, May 3rd, 2008 See: www.NORML.org
[34] Cannabis Spray Demonstrates Long Term Efficacy In Neuropathic Pain, Study Says, NORML News, 9/11/08, See: www.NORML.org
[35] Endocannabinoids and pain: spinal and peripheral analgesia in inflammation and neuropathy, Rice AS, Farquhar-Smith WP, Nagy I., Department of Anaesthetics, Pain Research Group, Inperial College of Science, Technology and Medicine, Chelsea and Westminster Hospital Campus, 369 Fulham Road, London SW10 9NH, UK. a.rice@ic.ac.uk
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Researchers at University of California Davis examined whether marijuana produces analgesia for patients with neuropathic pain. Thirty-eight patients were examined. They were given either high-dose (7%), low-dose (3.5%) or placebo cannabis.
The authors reported that identical levels of analgesia were produced at each cumulative dose level by both concentrations of the agent. As with opioids, cannabis does not rely on a relaxing or tranquilizing effect, but reduces the core component of nociception and the emotional aspect of the pain experience to an equal degree. There were undesirable consequences observed from cannabis smoking, such as feeing high or impaired, but they did not inhibit tolerability or cause anyone to withdraw from the study. In general, side effects and mood changes were inconsequential.
It was noted by the authors that since high and low dose cannabis produced equal analgesic efficacy, a case could be made for testing lower concentrations to determine if the analgesic profile can be maintained while reducing potential cognitive decline.
In addition, the authors said further research could probe whether adding the lowest effective dose of cannabis to another analgesic drug might lead to more effective neuropathic pain treatment for patients who otherwise are treatment-resistant
n a randomized, double-blinded, placebo controlled, crossover trial in fifteen healthy volunteers, we evaluated the effects of low, medium, and high dose smoked cannabis (respectively 2%, 4%, and 8% 9-delta-tetrahydrocannibinol by weight) on pain and cutaneous hyperalgesia induced by intradermal capsaicin. Capsaicin was injected into opposite forearms 5 and 45 minutes after drug exposure and pain, hyperalgesia, tetrahydrocannibinol plasma levels, and side effects were assessed. Five minutes after cannabis exposure, there was no effect on capsaicin-induced pain at any dose. By 45 minutes after cannabis exposure, however, there was a significant decrease in capsaicin-induced pain with the medium dose and a significant increase in capsaicin-induced pain with the high dose. There was no effect seen with the low dose nor was there an effect on the area of hyperalgesia at any dose. Significant negative correlations between pain perception and plasma delta-9-tetrahydrocannibinol levels were found after adjusting for the overall dose effects. There was no significant difference in performance on the neuropsychological tests.
This study suggests that there is a window of modest analgesia for smoked cannabis with lower doses decreasing pain and higher doses increasing pain.
The full results of this study were published in the journal Anesthesiology.
ABSTRACT:
By every criteria (deterioration in quality of life; loss of work days, and therapy directed dollars) pain is appreciated to be a major medical problem. Recent findings in the molecular biology and the pharmacology of pain transmission have shed light on mechanisms of nociceptive processing and the activity of a variety of "novel therapeutic" modalities that include the cannabinoids. Although the pre-clinical literature suggests that the cannabinoids produce antinociception and anti-hyperalgesic effects, the efficacy of the cannabinoids in the human pain state is unclear. As an experimental variable, clinical pain is a multidimensional phenomenon with few objective physical correlates. Many other factors such as emotional status and coping skills, make "pain" difficult to study in the clinical setting. An important development has been the implementation of well-controlled experimental pain models to investigate the sensory components of pain processing and to use these models in the assessment of analgesic efficacy in normal volunteers. To the degree that human experimental pain models can predict analgesic efficacy of novel agents, the role of mechanisms defined in preclinical studies can be translated to the human experience under well-controlled conditions. Human experimental pain has been used to test a wide range of currently available analgesics. Knowing the effect of these agents on human experimental pain, I now wish to study the effects of cannabis on human experimental pain and how this compares to commonly used analgesics.
PUBLICATIONS:
Type:
Title:
Journal Article Wallace M, Schulteis G, Atkinson JH, Wolfson T, Lazzaretto D, Bentley H, Gouaux B, Abramson I. Dose-dependent Effects of Smoked Cannabis on Capsaicin-induced Pain and Hyperalgesia in Healthy Volunteers. Anesthesiology. 107(5):785-796, November 2007.
The most frequent complaint that patients look for medical help with is pain. There are several different types of pain, and unfortunately none of the currently-prescribed pharmacological treatments for pain work completely for certain types. A particular example is that of pain caused by damaged nerves (such as that which causes phantom limb pain), which does not respond well to existing medications.
Severe chronic pain is usually treated with opiates, but these are addictive, and tolerance develops so that the dose has to be increased. The risk of severe side effects such as nausea is great, and additionally the user feels drugged, and finds it difficult to function properly. Family life may suffer as patients find it hard to relate to other people, and even reading to children is difficult. Synthetic analgesics are non-addictive but they are not powerful enough.
Cannabis has fewer side effects than other analgesics, and users report it "rounds off" the pain quickly after smoking. An Institute of Medicine report contains a minimal list of 5 situations in which cannabis-based medicines are of use in treating pain:
- There are medical conditions or patients in which they are more effective than any currently available medication.
- They have a broad clinical spectrum of efficacy and a unique side effect profile that differs from other analgesics.
- They have synergistic interactions with other analgesics.
- They exhibit "side effects" which are considered useful in certain clinical situations.
- Their efficacy is enhanced in patients who have developed tolerance to opioids.
Some people have used cannabis to control pain for 20 years or more, and many report that they were able to kick their addiction to opiates with small amounts of cannabis. One strange fact is that more experienced users get a greater pain-relieving effect from cannabis than novices. Experienced users also are able to function normally and ignore the psychoactive effects. Cannabis may be better at controlling the different types of pain.
Cannabis has had a long history of use as an analgesic, and was widely used in 19th century Britain, including in the royal household. Dr. J. Russell Reynolds, Fellow of the Royal Society and Physician to Queen Victoria reported in the Lancet in 1890 that he had been prescribing cannabis for 30 years and considered it "one of the most valuable medicines we possess". According to Reynolds indian hemp remained effective as an analgesic for months and even years without an increase in the dose.
It seems that cannabis shares some method of action with opioids, but the mechanism with which it accomplishes its analgesic effects differs. This indicates that they may produce an additive effects when used in conjunction with current medicines. In addition they might provide help to patients who do not react satisfactorily to other treatments. Much anecdotal evidence seems to indicate that this is the case.
Indeed, the British Medical Association has gone on record as stating that 'the prescription of nabilone, THC and other cannabinoids...should be permitted for patients with intractable pain'. Other official bodies have found similar results. A House of Lords report summed up the situation stating that 'there is scientific evidence that cannabinoids possess painrelieving properties, and some clinical evidence to support their medical use in this indication'. In a press conference on October 26th 1997, the US Society for Neuroscience claimed that 'substances similar to or derived from marijuana...could benefit the more than 97 million Americans who experience some form of pain each year'.
Patients' testimonies
The medical testimonies database contains 51 testimonies from cannabis users with pain
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Name
Date
Amanda
Mon 01 Nov 2010
Annon
Mon 01 Nov 2010
Mund
Mon 01 Nov 2010
jimmy
Mon 01 Nov 2010
Mr Dmoore
Mon 02 Nov 2009
Anonymous
Mon 02 Nov 2009
Anonymous
Sun 06 Dec 2009
Anonymous
Wed 02 Dec 2009
Anonymous
Wed 02 Dec 2009
Anonymous
Sun 02 Nov 2008
Annamarie Grogan
Tue 02 Dec 2008
Anonymous
Thu 02 Nov 2006
Stephen Livingston
Sat 09 Dec 2006
Ian Lunar Module
Wed 06 Dec 2006
Anonymous
Sat 02 Dec 2006
Roger Pigott
Fri 01 Dec 2006
GC
Mon 31 Oct 2005
Eleanor
Sun 04 Dec 2005
Ronald Roberson
Sat 03 Dec 2005
Maggie Froud
Fri 02 Dec 2005
Terry
Sun 05 Dec 2004
vanessa
Fri 03 Dec 2004
gruf
Sun 02 Nov 2003
J. Gribbin
Sat 01 Nov 2003
Welshstoner
Fri 31 Oct 2003
Nicolas
Tue 09 Dec 2003
George Lister
Sun 07 Dec 2003
Sonia
Fri 05 Dec 2003
Bob
Mon 01 Dec 2003
John
Sat 02 Nov 2002
Anonymous
Sat 02 Nov 2002
Winston Matthews
Fri 01 Nov 2002
Stacey H
Thu 31 Oct 2002
Carl
Thu 31 Oct 2002
Steven
Mon 09 Dec 2002
Garry Pearson
Sat 07 Dec 2002
Missi
Fri 06 Dec 2002
Hugh
Tue 03 Dec 2002
Russ Points
Fri 02 Nov 2001
Puffs
Thu 01 Nov 2001
Phil James
Thu 01 Nov 2001
Anonymous
Sun 09 Dec 2001
Anonymous
Mon 03 Dec 2001
Anonymous
Sun 02 Dec 2001
Sybil
Sun 02 Dec 2001
Anonymous
Sun 02 Dec 2001
Anonymous
Tue 31 Oct 2000
Anonymous
Sat 09 Dec 2000
Nigel Pearson
Sat 09 Dec 2000
Anonymous
Thu 07 Dec 2000
Anonymous
Thu 07 Dec 2000
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Scientific evidence
Despite the long history of use of cannabis as an analgesic, and the obvious problems with synthetic drugs, the War on Drugs prevented people from reconsidering cannabis until the mid-seventies, when several studies were published.
Patients suffering from cancer usually suffer from severe pain. This can be for a number of reasons, such as the invasion of their bones, inflammation or damage caused to nerves. It is a form of pain which is notoriously hard to treat effectively.
At the University of Iowa Noyes et al (1975a) gave oral THC or a placebo at random to hospitalised cancer patients who were in severe pain. The THC relieved pain for several hours at very low doses and longer periods at higher doses (15 - 20 mg). It also acted as a sedative at the higher dose. It had fewer physical side effects than other commonly used analgesics. There was no incidence of nausea or vomiting unlike many other analgesics - indeed more than half of the patients had an increased appetite.
Then Noyes et al conducted another study (1975b). This time they gave codeine, THC and placebo to 36 patients with advanced cancer. Codeine and cannabis were equally effective, but some patients found the psychoactive effects of THC uncomfortable. However these people did not know they were going to take a psychoactive drug and were obviously frightened. If they had been told beforehand perhaps they would not have been uncomfortable. Many of the patients however felt they generally had a sense of well-being that was absent before. As a result of this experiment, the researchers estimated that 10mg of THC was roughly equivalent to 60mg of codeine.
A study revealing potential additive effects of THC on standard medication was done by Holdcroft et al (1997). It centred on a patient who had severe chronic pain of gastrointestinal origin. The patient used morphine as an analgesic.It was found that the patient required a substantially lower amount of morphine when they were treated with oral THC in the form of cannabis oil.
The differing mechanism of analgesic action cannabis uses compared to existing (mainly opioid) medications means that not only are additive effects likely, but it could be useful in patients resistant to existing medications, and be useful in treating pain which existing medications fail to deal with adequately. The National Institutes of Health suggested that 'Neuropathic pain represents a treatment problem for which currently available analgesics are, at best, marginally effective. ...THC...may be useful in this inadequately treated type of pain'. The findings of Growing et al (1998) concurred with this conclusion, and suggested that this might be the area of greatest medical potential.
Maurer et al (1990) found that a paraplegic patient, who suffered leg pain, gained pain-relief after taking a single dose of THC.
Staquet et al (1978) did a trial using a nitrogen analogue of THC. This too showed significant analgesic effects, and was effective as both codeine and secobarbital. A further study using the synthetic THC analogue Levonantradol was done by Jain et al (1981). The trial population was patients who had moderate to severe post-operative pain. They were administered Levonantrodol by injection, and found significant pain relief as a result.
In Canada, Milstein et al (1975) studied the analgesic effect of smoked cannabis in normal subjects. Half of them had used cannabis before. The researchers caused pain by pressing onto the subjects thumbnails. The subjects were able to withstand more pressure after they had smoked cannabis. Strangely, the analgesic effect was greater in the experienced users.
A article by Noyes and Baram (1974) showed that cannabis relieved the pain of a headache in three patients with an equivalent or better efficacy than aspirin or ergotamine tartrate. Petro (1980) found that two patients suffering pain from a muscle spasticity disorder had a reduction in their discomfort after inhaling cannabis.
Recently, it has been found that the body's natural cannabinoid, anandamide is involved in the control of pain. Calignano et al (1998) found that rats release anandamide when cells are damaged. This then causes seemingly pain-relieving effects in the areas of the brain and spinal cord that process pain stimuli. An ACM bulletin in 1998 demonstrated that when anandamide is used with another naturally occuring compound in the body, palmitylethanolamide, pain was reduced by up to 100 times.
<strong>References
</strong>
</strong>
Calignano A. et al (1998) Control of pain by endogenous cannabinoids,
Nature
394
: 277-281.
Growing L et al (1998) Therapeutic use of cannabis: clarifying the debate,
Drug and Alcohol Review
17
: 445-452.
Holdcroft A et al (1997) Pain relief with oral cannabinoids in familial Mediterranean fever.
Anaesthesia,
52
: 483
House of Lords Select Committee on Science and Technology (1998)
Science and Technology - Ninth report
. Science and Technology Committee Publications, UK.
Institute of Medicine (1999)
Marijuana and medicine: Assessing the science base
. National Academy Press
Jain AK, Ryan JR, McMahon FG, Smith G. (1981) Evaluation of intramuscular levonantradol
and placebo in acute postoperative pain.
Journal of Clinical Pharmacology
21
:320S-326S.
Maurer M. et al. (1990) Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double-blind trial.
European Archives of Psychiatry and Clinical Neuroscience
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: 1-4.
Milstein S.L., MacCannell K., Karr, G. and Clark S. (1975) Marijuana-produced changes in pain tolerance: Experienced and non-experienced subjects.
International Pharmacopsychiatry
10
: 177-182.
National Institutes of Health (1997)
Workshop on the Medical Utility of Marijuana: Report to the Director
. Washington, D.C.
Noyes R., Baram D. (1974) Cannabis analgesia.
Compr. Psychiatry
15
: 531.
Noyes R., Brunk S.F., Baram D.A. and Canter A. (1975a) Analgesic effect of delta-9-tetrahydrocannabinol.
Journal of Clinical Pharmacology
15
: 139-143.
Noyes R., Brunk S.F., Avery D.H. and Canter A. (1975b) The analgesic properties of delta-9-tetrahydrocannabinol and codeine.
Clinical Pharmacology and Therapeutics
18
: 84-89.
Petro D. (1980) Marihuana as a therapeutic agent for muscle spasm and spasticity. Psychosomatics 21: 81-85.
Reynolds J.R. (1890) Therapeutic uses and toxic effects of Cannabis indica.
Lancet
1
: 637
Science: Cannabinoid/anandamide-receptor systems involved in peripheral control of pain
, ACM Bulletin, July 26, 1998.
Staquet M, Gantt C, Machin D. (1978) Effect of a nitrogen analog of tetrahydrocannabinol on cancer pain.
Clinical Pharmacology and Therapeutics
23
:397401.
For a large collection of research materials, see our
research
page.
Use of Marijuana in Neurological
<strong>and Movement Disorders</strong>
Medical Marijuana
Use of Marijuana in Neurological and Movement Disorders
1. What research has been done and what is known about the possible medical uses of marijuana? There have been numerous studies both in animals and in various clinical states on the use of cannabinoids on neurological and various movement disorders. These results range from anecdotal reports to surveys and clinical trials. Marijuana or tetrahydrocannabinol (THC) is reported to have some antispasticity, analgesic, antitremor, and antiataxia actions, as well as some activity in multiple sclerosis (MS) and in spinal cord injury patients.
The spasticity and nocturnal spasms produced by MS and partial spinal cord injury have been reported to be relieved by smoked marijuana and to some extent by oral THC in numerous anecdotal reports. The effect seems to appear rapidly with smoked marijuana; patients are able to titrate the dose by the amount they smoke. No large-scale controlled studies or studies to compare either smoked or oral THC with other available therapies have been reported. Several relatively good therapeutic alternatives exist. There is no published evidence that the cannabinoid drugs are superior or even equivalent.
Substantial experimental animal literature exists showing that various cannabinoids, given primarily by parenteral routes, have a substantial anticonvulsant effect in the control of various models of epilepsy, especially generalized and partial tonic-clonic seizures. Scant information is available about the human experience with the use of marijuana or cannabinoids for the treatment of epilepsy. This is an area of potential value, especially for cannabis therapies by other than the smoked route.
Several single case histories have been reported indicating some benefit of smoked marijuana for dystonic states. It must be remembered that dystonia is a clinical syndrome with numerous potential causes, and the information available now does not differentiate which causes are most likely to be improved. Smoked marijuana and oral THC have been tested in the treatment of Parkinson's disease and Huntington's chorea without success.
The cannabinoids also have been used as experimental immunologic modifiers to treat such conditions as the animal models of experimental allergic encephalomyelitis (EAE) and neuritis. Parenteral cannabinoids have been successful in modifying EAE in animals, suggesting that cannabinoids may be of value in a more fundamental way by altering the root cause of a disease such as MS rather than simply treating its symptoms. Smoked marijuana would not be acceptable for such a role because of the variability of dose with the smoked route.
2. What are the major unanswered scientific questions?
The discovery of dedicated systems of central nervous system (CNS) neurons approximately 8 years ago, which express receptors specific for the cannabinoids, is of major scientific interest and importance. The distribution of these cannabinoid receptor-bearing neurons corresponds well with the clinical effects of smoked marijuana; for instance, their presence in the forebrain may relate to adverse changes in short-term memory, but perhaps positively in the control of epilepsy. Cannabinoid receptors in the brainstem and cerebellum may relate to the recognized incoordination that accompanies smoked marijuana use. The discovery of intrinsic ligands for these receptors in the mammalian brain is also of great importance. This system of cannabinoid receptors and ligands may be analogous to the discovery of opiate receptors and endorphins, which linked various opium derivatives (heroin and morphine) to an intrinsic system of neurons in the CNS. That discovery was of major importance for pain research.
The major unanswered scientific questions are:
* How useful is smoked marijuana of known specific potency in controlling various neurologic conditions?
* In comparative studies, how useful is smoked marijuana in altering objective abnormalities such as spasticity versus current standard therapies that have already been approved for human use?
* Can alternative delivery systems (other than the oral route) be developed to provide rapidity of action with more safety than smoked marijuana?
* Can available or newly developed synthetic cannabinoids be used more effectively to stimulate or block receptor activity in the cannabinoid system of the CNS?
* What are the immune-modulating characteristics of the cannabinoids and can they be used for therapeutic human benefit?
* Can the long-term risks of daily smoked marijuana be quantified so that useful risk versus benefit ratios can be determined, especially when considering treatment of long-term conditions such as spasticity or epilepsy?
3. What are the diseases or conditions for which marijuana might have potential as a treatment and which merit further study?
Marijuana or the use of other cannabinoids as human therapies might be considered for treating spasticity and nocturnal spasms complicating MS and spinal cord injury, for various active epilepsy states, for some forms of dystonia, and perhaps most interestingly, for treating neuropathic pain (Zeltser et al. 1991). (Also see the chapter titled Analgesia.) Neuropathic pain complicates many CNS diseases. Few available therapies provide even partial relief.
Reference
Zeltser, R.; Seltzer, Z.; Eisen, A.; Feigenbaum, J.J.; and Mechoulam, R. Suppression of neuropathic pain behavior in rats by a non-psychotropic synthetic cannabinoid with NMDA receptor-blocking properties. Pain 47(1):95-103, October 1991.
source: http://www.onlinepot...l/article44.htm
