Zyp Czyk's List: Cannabis - Medical

• Everything points towards these compounds having been evolved by the plants as antimicrobial defenses that specifically target bacterial cells,” says Gibbons. “But the actual mechanism by which they kill the bugs is still a mystery.
• “The most practical application of cannabinoids would be as topical agents to treat ulcers and wounds in a hospital environment, decreasing the burden of antibiotics,”
• Mark Rogerson of GW Pharmaceuticals, a U.K.-based company that develops cannabinoid-based drugs to treat severe pain caused by multiple sclerosis and cancer, says that the discovery that cannabinoids kill MRSA “really underlines the potentially great diversity of medical applications that cannabis-based medicine can have. You can almost think of the cannabis plant as a mini pharma industry in its own right.”

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• Marijuana extracts kill antibiotic-resistant MRSA without a high.
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  •   By Nora Schultz on September 12, 2008
   
           
• Substances harvested from cannabis plants could soon outshine conventional antibiotics in the escalating battle against drug-resistant bacteria. The compounds, called cannabinoids, appear to be unaffected by the mechanism that superbugs like MRSA use to evade existing antibiotics
• Cannabis has long been known to have antibacterial properties and was studied in the 1950s as a treatment for tuberculosis and other diseases. But research into using cannabis as an antibiotic has been limited by poor knowledge of the plant’s active ingredients and by the controversy surrounding its use as a recreational drug
• MRSA, short for methicillin-resistant Staphylococcus aureus, is a bacterium that can cause difficult-to-treat infections since it does not respond to many antibiotics.
• But when Appendino, Gibbons, and their colleagues applied extracts from five major cannabinoids to bacterial cultures of six strains of MRSA, they discovered that the cannabinoids were as effective at killing the bugs as vancomycin and other antibiotics.
• “The cannabinoids even showed exceptional activity against the MRSA strain that makes extra amounts of the proteins that give the bugs resistance against many antibiotics,” says Gibbons. These proteins, he explains, allow the bacteria to “hoover up unwanted things from inside the cell and spit them out again.”

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• Importance   Opioid analgesic overdose mortality continues to rise in the United States, driven by increases in prescribing for chronic pain. Because chronic pain is a major indication for medical cannabis, laws that establish access to medical cannabis may change overdose mortality related to opioid analgesics in states that have enacted them.
• Objective   To determine the association between the presence of state medical cannabis laws and opioid analgesic overdose mortality.
• Main Outcomes and Measures   Age-adjusted opioid analgesic overdose death rate per 100 000 population in each state. Regression models were developed including state and year fixed effects, the presence of 3 different policies regarding opioid analgesics, and the state-specific unemployment rate.
• Results   Three states (California, Oregon, and Washington) had medical cannabis laws effective prior to 1999. Ten states (Alaska, Colorado, Hawaii, Maine, Michigan, Montana, Nevada, New Mexico, Rhode Island, and Vermont) enacted medical cannabis laws between 1999 and 2010. States with medical cannabis laws had a 24.8% lower mean annual opioid overdose mortality rate (95% CI, −37.5% to −9.5%; P = .003) compared with states without medical cannabis laws. Examination of the association between medical cannabis laws and opioid analgesic overdose mortality in each year after implementation of the law showed that such laws were associated with a lower rate of overdose mortality that generally strengthened over time: year 1 (−19.9%; 95% CI, −30.6% to −7.7%; P = .002), year 2 (−25.2%; 95% CI, −40.6% to −5.9%; P = .01), year 3 (−23.6%; 95% CI, −41.1% to −1.0%; P = .04), year 4 (−20.2%; 95% CI, −33.6% to −4.0%; P = .02), year 5 (−33.7%; 95% CI, −50.9% to −10.4%; P = .008), and year 6 (−33.3%; 95% CI, −44.7% to −19.6%; P < .001). In secondary analyses, the findings remained similar.
• Conclusions and Relevance   Medical cannabis laws are associated with significantly lower state-level opioid overdose mortality rates. Further investigation is required to determine how medical cannabis laws may interact with policies aimed at preventing opioid analgesic overdose.

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• 
   THC (Tetrahydrocannabinol) gets a user high, a larger THC content will produce a stronger high. Without THC you don't get high.
• 
   Cannabidiol - CBD also occurs in almost all strains. Concentration range from none, to about 95 percent of the total cannabinoids present. THC and CBD are the two most abundant naturally occurring cannabinoids. CBD is not psychotomimetic in the pure form, although it does have sedative, analgesic, and antibiotic properties.
• 
   Cannabidiol - CBD also occurs in almost all strains. Concentration range from none, to about 95 percent of the total cannabinoids present. THC and CBD are the two most abundant naturally occurring cannabinoids. CBD is not psychotomimetic in the pure form, although it does have sedative, analgesic, and antibiotic properties.
• 
   Cannabidiol - CBD also occurs in almost all strains. Concentration range from none, to about 95 percent of the total cannabinoids present. THC and CBD are the two most abundant naturally occurring cannabinoids. CBD is not psychotomimetic in the pure form, although it does have sedative, analgesic, and antibiotic properties.
• Cannabinol - CBN
• THC (Tetrahydrocannabinol) gets a user high, a larger THC content will produce a stronger high. Without THC you don't get high.
• THC (Tetrahydrocannabinol) gets a user high, a larger THC content will produce a stronger high. Without THC you don't get high.
   
   CBD (Cannabidiol) increases some of the effects of THC and decreases other effects of THC. High levels of THC and low levels of CBD contribute to a strong, clear headed, more energetic high.
• Cannabidiol - CBD
• THC (Tetrahydrocannabinol) gets a user high, a larger THC content will produce a stronger high. Without THC you don't get high.
• CBD (Cannabidiol) increases some of the effects of THC and decreases other effects of THC. High levels of THC and low levels of CBD contribute to a strong, clear headed, more energetic high.
• CBN (Cannabinol) is produced as THC ages and breaks down, this process is known as oxidization.
• Tetrahydrocannabinol - THC
• Delta 9-trans-tetrahydrocannabinol - delta-9 THC is the main psychotomimetic (mindbending) ingredient of marijuana. Estimates state that 70 to 100 percent of the marijuana high results from the delta-9 THC present.
• CBD appears to potentiate the depressant effects of THC and antagonize is excitatory effects. CBD also delays the onset of the high but can make it last considerably longer (as much as twice as long).
• CBN seems to potentiate THC's disorienting qualities. One may feel more dizzy or drugged

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• Cannabis contains a number of natural chemicals called cannabinoids and the brain has the ability to respond to such compounds. Cannabis and synthetically manufactured cannabinoid compounds can relieve pain in animal models of arthritis, but their use has been limited because of undesirable psychological side-effects.

• At present, there are two known types of cannabinoid receptors, termed CB₁ and CB₂,^[1] with mounting evidence of more.^[6] The human brain has more cannabinoid receptors than any other G protein-coupled receptor (GPCR) type.^[7]
• Cannabinoid receptor type 1
• CB₁ receptors are found primarily in the brain, to be specific in the basal ganglia and in the limbic system, including the hippocampus.^[1]
• Cannabinoid receptor type 2
• CB₂ receptors are predominantly found in the immune system, or immune-derived cells^[8] with the greatest density in the spleen.
• CB₂ receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.^[8]
• Cannabidiol
• Cannabidiol (CBD) is not psychoactive
• recent evidence shows that smokers of cannabis with a higher CBD/THC ratio were less likely to experience schizophrenia-like symptoms.^[19]
• Cannabidiol has also been shown to act as a 5-HT_1A receptor agonist,^[23] an action that is involved in its antidepressant,^[24][25] anxiolytic,^[25][26] and neuroprotective^[27][28] effects.
• It appears to relieve convulsion, inflammation, anxiety, and nausea.^[29] CBD has a greater affinity for the CB₂ receptor than for the CB₁ receptor.^[29]
• . CBD apparently plays a role in preventing the short-term memory loss associated with THC in mammals.
• Cannabinol
• Cannabinol (CBN) is the primary product of THC degradation
• Its affinity to the CB₂ receptor is higher than for the CB₁ receptor.^[35]
• Cannabis indica may have a CBD:THC ratio 4–5 times that of Cannabis sativa.

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• After doing a little digging this morning. I came up these magnificent seven medical marijuana strains that represent a wide spectrum of cannabinoids available to help with pain reduction in fibromyalgia patients. These cannabinoids have several well-documented beneficial effects for many aliments.

• (CNN) -- It's been eight months since I last wrote about medical marijuana, apologizing for having not dug deeply into the beneficial effects of this plant and for writing articles dismissing its potential. I apologized for my own role in previously misleading people, and I feel very badly that people have suffered for too long, unable to obtain the legitimate medicine that may have helped them.
• shows and proves what marijuana can do for the body but provides better insights into the mechanisms of marijuana in the brain, helping us better understand a plant whose benefits have been documented for thousands of years. This journey is also about a Draconian system where politics override science and patients are caught in the middle.
• I have sat in labs and personally analyzed the molecules in marijuana that have such potential but are also a source of intense controversy. I have seen those molecules turned into medicine that has quelled epilepsy in a child and pain in a grown adult. I've seen it help a woman at the peak of her life to overcome the ravages of multiple sclerosis.

• I am more convinced than ever that it is irresponsible to not provide the best care we can, care that often may involve marijuana.

   

• Marijuana is classified as a Schedule I substance, defined as "the most dangerous" drugs "with no currently accepted medical use."

   

  Neither of those statements has ever been factual. Even many of the most ardent critics of medical marijuana don't agree with the Schedule I classification, knowing how it's impeded the ability to conduct needed research on the plant.
• the United States already holds a patent on medical marijuana for that very purpose. Patent No. 6630507:
• Cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke or trauma.
• How can the government deny the benefits of medical marijuana even as it holds a patent for those very same benefits? Members of the Food and Drug Administration declined my repeated requests for an interview.
• Yes, I know there is a concern that many people out there will feign ailments just to get marijuana. But withholding legitimate treatment for the needy is a very unjust way of addressing that concern.

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• Might Cannabis reduce neuropathic pain?
• The Journal of Pain’s 4^th most downloaded article in 2013 (Wilsey ey al 2013) is a study of vaporised cannabis for the treatment of neuropathic pain.
• Participants did report more psychoactive side-effects with cannabis than with placebo, but none of these effects was strong enough to be clinically concerning.  Neurocognitive tests showed diminished function with cannabis – particularly in the domains of learning and memory – but, again, these effects were relatively minor.  As expected, low-dose cannabis was associated with less severe side-effects than medium-dose cannabis, yet still performed well for pain relief.
• But within a few months, the Journal of Pain had published a letter from Brett Stacey and Jeffrey Moller that warned readers against getting too excited.
• The psychoactive consequences of cannabis inhalation are a longstanding concern, yet this study found minimal negative psychoactive effects of the cannabis treatment
• Don’t miss the fact that a criterion for participation in this study was previous exposure to cannabis
• As far as I can see, the experiment studied the effects of cannabis for a 6-hour period.  Presumably, patients with neuropathic pain would be looking for pain relief for longer than that

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• Weed reduced pain in five out of five randomized controlled trials of smoked marijuana, TheAnswerPage.com reports today, as part of a controversial, ongoing physician education program sponsored by The Massachusetts Medical Society, publisher of the New England Journal of Medicine.

• Strain Name: Sour Diesel

   

  Grade: A

   

  Type: 90% sativa, 10% indica

   

  Looks: Light green with a lot of orange hairs (10/10)

   

  Smell: Citrus, kinda tangy gas (9/10)

   

  Taste: Complex but smooth (10/10)

   

  Effects: Creeps up and hits you, making you feel very light. Mostly a head head high and very happy. (10/10)

   

  Potency: Super Strong 2-3 hours (10/10)

   

  Reviewed by: Rachel

   

  Good Strain For: Energy, pain relief, nausea, insomnia

   

• Strain Name: Kali Mist

   

  Grade: A

   

  Type: 2 sativa dominant hybrids

   

  Looks: Bright Green

   

  Smell: Sweet and piney

   

  Taste: With Kali Mist you get both sides of the taste range accompanied by a sweet and spicy taste

   

  Effects: True Sativa. Kali Mist’s effects have proven beneficial for medical users with multiple sclerosis, fatigue, and chronic pain. The high from Kali Mist is a great floating cerebral high that doesn’t bog down your mind and lets you focus. Kali Mist has been well-known for its very beneficial medical effects and is a great marijuana strain that you can smoke all day without fail.

   

  Potency: 9/10

   

• The University of Washington has received an 18-month grant of $110,299 from the state Attorney General’s Office to provide training and education for health professionals and the general public on the subject of chronic pain management and cannabis use.
• “Chronic pain is a major public health issue,” Carlini said. “This project will offer non-judgmental, science-based information to clinicians and to the general public on the role of medical marijuana as an option in alleviating intractable pain in our state.”

• Medicinal cannabis is a better choice than opioids when standard first-line pain medications have failed to relieve chronic pain, according to Gregory T. Carter, MD, MS, clinical professor of medicine at the University of Washington in Seattle. Speaking at a session titled “Medical Marijuana: Science, Practice, Policy, & Ethics,” he noted that medicinal cannabis has fewer drug-drug interactions than opioids and does not cause respiratory suppression or constipation. Cannabis, he noted, decreases inflammation, is neuroprotective, and has anti-tumor properties.
• Some patients cannot tolerate the drug, and some do not experience pain relief from it.
• Adverse effects are mainly seen in new users, and they are short lived and reversible,

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• Endogenous Cannabinoid Receptors
• The biological effects of cannabinoid compounds are mediated by their binding to and further activation of cannabinoid receptors. Four subtypes of these receptors have been identified. Two have been cloned, type 1 (CB₁) and type 2 (CB₂)
• The CB₂ receptor is located mainly in the immune system, but has been found in others sites
• Neuroanatomic Distribution of CB1 Receptors in the Nervous System
• CB₁ receptors are abundant and widely dispersed throughout the brain
• CB₁ receptors are synthesised in neurons of the rat dorsal root ganglia (that express neuropeptide markers found in nociceptive primary afferents) [59], and these receptors are transported both centrally, reaching superficial dorsal horn terminals [59] and peripherally towards peripheral nerve terminals of sensory nerves [58]. Interestingly, these sensory nerves are engaged in the ascent of nociceptive stimuli to the spinal cord

• Endocannabinoids

  The endocannabinoids, or endogenous cannabinoids, are a family of bioactive lipids that activate cannabinoid receptors to exercise their effects, modulating neural transmission. They are present in only small amounts in brain and other tissues and participate in the regulation of various cerebral functions, including pain perception, mood, appetite, and memory.
• CANNABINOID PHARMACOLOGY
• Activation of cannabinoid receptors inhibits GABAergic synaptic transmission in a number of central nervous system regions, including areas participating in nociceptive signalling like the amygdala [93], periaqueductal grey matter [162], rostral ventromedial medulla (RVM) [163], and superficial dorsal horn [72].
• ANALGESIC EFFICACY OF CANNABINOIDS
• Activation of Cannabinoid Receptors
• Cannabinoid receptor agonists effects in the central nervous system (CNS) include disruption of psychomotor behaviour, short-term memory impairment, intoxication, stimulation of appetite, antiemetic effects, and antinociceptive actions [68]. Administration of natural or synthetic cannabinoid receptor agonists has shown therapeutic value for a number of important medical conditions, including pain (particularly against pain of neuropathic origin), anxiety, glaucoma, nausea, emesis, muscle spasms, and wasting diseases. Insofar as pain is concerned, it is well known that cannabinoid receptor agonists have antinociceptive and anti-hyperalgesic effects at the peripheral and central (spinal and supraspinal) levels, as has been demonstrated in acute and chronic pain models [69, 116]. Cannabinoid receptors and endocannabinoids are present in pain circuits from the peripheral sensory nerve endings up to the brain (Fig. ​(Fig.1).1). Cannabinoid receptor agonists modulate nociceptive thresholds by regulating neuronal activity [4], but they also relieve pain by acting on non-nervous tissues
• CB₁ receptor is involved in the attenuation of synaptic transmission, and a proportion of the peripheral analgesic effect of endocannabinoids can be attributed to a neuronal mechanism acting through CB₁ receptors expressed by primary afferent neurons
• However, recent findings suggest that CB₁ receptors are also present in mast cells and may participate in some anti-inflammatory effects.
• activation of peripheral CB₂ receptors generates an antinociceptive response in situations of inflammatory hyperalgesia and neuropathic pain
• Possible mechanisms of this CB₂-mediated effect include the attenuation of NGF-induced mast cell degranulation and of neutrophil accumulation, both of which are processes known to contribute to the generation of inflammatory hyperalgesia
• CB₂ receptors have novel pain control actions. A CB₂-mediated effect exists, consisting in the indirect stimulation of opioid receptors located in primary afferent pathways
• Thus, cannabinoid compounds can modulate hyperalgesia of various origins and they are effective even in inflammatory and neuropathic pain
• Cannabinoids and Opioids Analgesic Synergism
• The opioid system is one of the systems interacting with the cannabinoids that has been most explored
• Cannabinoid and opioid receptors both exist at various levels in the pain circuits and these two systems may operate synergistically. THC and morphine have been shown to act synergistically, mutually potentiating their antinociceptive actions.
• although cannabinoids and opioids both produce analgesia within the dorsal horn, their pharmacologic mechanisms of action differ.
• cannabinoid receptor agonists induce the synthesis and/or release of endogenous opioid peptides
• although the antinociception of morphine is mediated predominately by μ-opioid receptors, it may be enhanced by THC through the activation of kappa and delta opioid receptors.
• new CB₂ locations and mechanisms of action, which are important to pain modulation, have been recently identified
• These CB₂ receptors, when activated, stimulate release of the endogenous opioid β-endorphin, which then acts at μ-opioid receptors on local primary afferent neurons to inhibit nociception.
• Interactions Between Cannabinoids and Prostaglandin Inhibitors and COX-2
• An interaction between cannabinoids and inhibitors of prostaglandin biosynthesis (like NSAIDs) has been reported, and it appears to be due to the similarity in chemical structure of endogenous cannabinoid ligands and prostaglandins (arachidonic acid derivatives
• The enhancement of CB₁ receptors activity by some NSAIDs (indomethacin, fluribuprofen) has been confirmed
• COX-2 exerts a negative influence on endocannabinoids because it catabolises them
• This also suggests that COX-2 inhibitors treatment may produce an indirect enhancement of cannabinoid receptors activity, by increasing endocannabinoid levels.
• THERAPEUTIC USES OF CANNABINOIDS IN PAIN EPISODES
• Studies in experimental models of acute and chronic pain have demonstrated the efficacy of cannabinoid receptor agonists, even in neuropathic or inflammatory pain
• The results to date suggest that cannabinoid receptor agonists are analgesic substances per se whose potency is similar to that of opioids like codeine
• Unfortunately, few clinical trials have been made and they have been carried out with major methodologic limitations.
• cannabinoid receptor agonists have shown to be up to 10 times more potent than morphine in animal models of acute and neuropathic pain
• 

  Table 1.

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  Effects of Cannabinoid Receptor Agonists in Healthy Volunteers Submitted to Acute Noxious Stimuli

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  Table 2.

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  Effects of Cannabinoid Receptor Agonists on Acute Postoperative Pain

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  Table 3.

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  Data from Questionnaires / Surveys of Humans, Taking Cannabis as a Medicine to Relief Chronic Non-Cancer Pain of Different Types, Especially as a Symptom of Multiple Sclerosis

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  Table 4.

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  Data from Clinical Trials of Humans Treated with Cannabinoid Receptor Agonists to Relief Chronic Non-Cancer Pain of Different Types, Especially as a Symptom of Multiple Sclerosis or Other Neuropathic Pain
• THC is the substance with the greatest psychoactive potency of the natural cannabinoids, and exhibits the greatest analgesic activity
• THC administered epidurally (intrathecal, intraventricular) produces antinociception similar to that obtained with opioid compounds
• Clinical trials have shown that nonselective cannabinoid receptor agonists are relatively safe and therapeutically efficacious, but they also induce psychotropic side effects
• The THC analogues most often used for preclinical or therapeutic purposes in humans are dronabinol, nabilone, levonantradol, CT-3 (or ajulemic acid), and HU211
• Cannabidiol (CBD) is another major constituent of the Cannabis sativa plant, having the same therapeutic effects than THC (analgesic, anti-inflammatory, and others), but with a different pharmacologic profile
• some of these cannabidiol derivatives did not have central nervous system effects, but maintained their antinociceptive and anti-inflammatory properties.
• Medications have also been developed from extracts of the Cannabis sativa plant containing known amounts of THC and CBD [6, 111, 163, 164]. These medications are being used in clinical trials, and a form dispensed as sublingual spray has just been approved to be marketed in Canada
• the role of CB₂ receptors is fundamental in other cannabimimetic actions, such as immunomodulatory and antiproliferative effects. On the other hand, as mentioned earlier, new CB₂ receptor properties are being discovered, as it has been confirmed that they indirectly stimulate opioid receptors located in primary afferent pathways [67].
• Smoking cannabis remains the most efficient means of drug delivery since absorption is much more rapi
• the effects of natural cannabinoids (plant extracts) seems to be better than those of synthetic cannabinoids.

  • YES YES YES !!!!!!!!!!!!!!!!!!!
• Short-term effects, such as unsteadiness, dizziness, difficulty concentrating, drowsiness, dryness of the mouth, and/or headache, are related to depression of the central nervous system.
• Chronic cannabis use does not produce serious cognitive disorders, as occurs with other substances like alcohol, but it can aggravate pre-existing mental disease.
• one of the best documented therapeutic uses of cannabinoid derivatives, and the one most widely approved today, is as an antiemetic drug
• have proven to be extremely effective for relieving nausea and emesis due to gastrointestinal distress caused by acquired immunodeficiency syndrome (AIDS) medications or cancer chemotherapy.
• Postoperative pain interfere with functioning and healing, and it can grow to intolerable levels. However, there is no drug for this condition which produces adequate analgesia with no side effects. Some clinical trials, using cannabinoid derivatives in postoperative pain, have been undertaken or are in progress (Table ​(Table22).
• Chronic Pain
• Multiple Sclerosis
• Multiple sclerosis (MS) is a life-long chronic disease in which nerve cells are attacked by the immune system, originating painful muscle spasms and many other problems, including neuropathic pain
• Smoking cannabis not only has helped to stop spasms, but has halted the progression of multiple sclerosis.
• Medications prepared from whole plant cannabis extract, containing known amounts of THC and CBD as the principal components have been prepared to be administered by oral spray to relieve MS symptoms, as well as for the treatment of other disorders with severe neuropathic pain. This product has undergone phase III placebo-controlled trials
• Neuropathic Pain
• It is important to emphasise that cannabinoid receptor agonists are more effective than opioids in the management of neuropathic pain
• This means that cannabinoid receptor agonists have more capacity for suppressing pathophysiologic mechanisms like the wind-up phenomenon linked to this type of pain
• Cancer Pain
• Cannabinoids are among the compounds under development for the treatment of these patients, and they seem to have analgesic activity
• Fibromyalgia
• data that support their therapeutic potential thanks to their anti-inflammatory and sedative properties
• Migraine
• Historically, cannabis was prescribed for its management in the early 20^th century. At present, the antimigraine properties of cannabis have been recognised [137] and there are studies that affirm that the pain relief it produces is comparable, or better than, that achieved with ergotamine and aspirin
• CONCLUDING REMARKS
• Cannabinoids have antinociceptive mechanisms different from that of other drugs currently in use, which thus opens a new line of promising treatment to mitigate pain that fails to respond to the pharmacologic treatments available, especially for neuropathic and inflammatory pains.
• One of the drawbacks of investigating cannabinoids is their typification as substances of abuse. However, compounds blunting severe pain allow patients to perform daily activities more easily, so the potential benefits should be weighed against possible adverse effects.

  • YES YES !!!!!!!!!!!
• Clinical trials seem to indicate that either extracts of the Cannabis sativa plant containing known amounts of the active compounds (mainly THC and CBD) or diverse synthetic derivatives of THC are promising treatments for painful conditions that do not respond to available treatments, such as neuropathic, inflammatory and oncologic pain.
• Specifically, cannabis extracts have shown effectiveness to relief some symptoms of the patients with multiple sclerosis, mainly for pain and spasticity.
• CB2 receptor selective agonists with no central effects are other promising pain treatment under investigation.
• Fundacion Neurociencias y Envejecimiento

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• Spinal cord injury (SCI) has a number of severe and disabling consequences, including chronic pain, and around 40% of patients develop persistent neuropathic pain.
• Thus far, there is no cure for the pain and oral pharmaceutical intervention is often inadequate, commonly resulting in a reduction of only 20-30% in pain intensity.
• Gabapentin, pregabalin and amitriptyline showed a significant reduction in neuropathic pain following SCI. Cannabinoids have been found to relieve other types of central pain, and serotonin noradrenaline reuptake inhibitors as well as opioids relieve peripheral neuropathic pain and may be used to treat patients with SCI pain.

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