Tag Archives: analgesic

Marijuana treatments for autoimmune disorders

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“Researchers from the University of South Carolina say that tetrahydrocannabinol, the principal constituent of marijuana, may have another medical use – treating those with autoimmune disorders.

Tetrahydrocannabinol (THC) is known to have analgesic effects so can be used to treat pain. It also aids relaxation and can reduce feelings of nausea and stimulate appetite…

Now, a new study, published in the Journal of Biological Chemistry, explores how analgesicmicroRNAs are influenced by THC.

MicroRNAs (miRNAs) are small, single-stranded, non-coding RNAs that play a vital role in regulating gene expression. And the authors claim that the ability to alter miRNA expression may be the key to successful treatment for many autoimmune diseases, including multiple sclerosis, arthritis and type 1 diabetes.”

More: http://www.medicalnewstoday.com/articles/269432.php

Cannabinoid CB2 Receptors Regulate Central Sensitization and Pain Responses Associated with Osteoarthritis of the Knee Joint.

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“Osteoarthritis (OA) of the joint is a prevalent disease accompanied by chronic, debilitating pain. Recent clinical evidence has demonstrated that central sensitization contributes to OA pain. An improved understanding of how OA joint pathology impacts upon the central processing of pain is crucial for the identification of novel analgesic targets/new therapeutic strategies.

Inhibitory cannabinoid 2 (CB2) receptors attenuate peripheral immune cell function and modulate central neuro-immune responses in models of neurodegeneration…

These findings suggest that targeting CB2 receptors may have therapeutic potential for treating OA pain.”

http://www.ncbi.nlm.nih.gov/pubmed/24282543

The endocannabinoid system, cannabinoids, and pain.

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“The endocannabinoid system is involved in a host of homeostatic and physiologic functions, including modulation of pain and inflammation… Exogenous plant-based cannabinoids (phytocannabinoids) and chemically related compounds, like the terpenes, commonly found in many foods, have been found to exert significant analgesic effects in various chronic pain conditions.

Currently, the use of Δ9-tetrahydrocannabinol is limited by its psychoactive effects and predominant delivery route (smoking), as well as regulatory or legal constraints.

 However, other phytocannabinoids in combination, especially cannabidiol and β-caryophyllene, delivered by the oral route appear to be promising candidates for the treatment of chronic pain due to their high safety and low adverse effects profiles.

This review will provide the reader with the foundational basic and clinical science linking the endocannabinoid system and the phytocannabinoids with their potentially therapeutic role in the management of chronic pain.”

http://www.ncbi.nlm.nih.gov/pubmed/24228165

Does the cannabinoid dronabinol reduce central pain in multiple sclerosis? Randomised double blind placebo controlled crossover trial.

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“Clinical reports indicate that cannabinoids may alleviate pain in different pain conditions, including multiple sclerosis related pain…

Randomised double blind placebo controlled crossover trial… To evaluate the effect of the oral synthetic delta-9-tetrahydrocannabinol dronabinol on central neuropathic pain in patients with multiple sclerosis…

CONCLUSIONS:

Dronabinol has a modest but clinically relevant analgesic effect on central pain in patients with multiple sclerosis. Adverse events, including dizziness, were more frequent with dronabinol than with placebo during the first week of treatment.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC498019/

The use of cannabinoids in chronic pain.

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“We present the case of a 56-year-old man who developed chronic pain following the excision of a facial cancer that was poorly controlled despite multiple analgesic medications. Following the starting of nabilone (a synthetic cannabinoid) his pain control was greatly improved and this had a huge impact on his quality of life.

We also managed to significantly reduce his doses of opioid analgesia and ketamine.

We review the current literature regarding the medicinal use of cannabinoids, with an emphasis on chronic pain, in an attempt to clarify their role and how to select patients who may benefit from this treatment.”

http://www.ncbi.nlm.nih.gov/pubmed/23893276

Marijuana for migraines – USAToday

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“Does marijuana have medicinal value for migraine headaches and other maladies?

“There is no question that cannabis is beneficial medicinally,” Bearman says. With migraines, “some people say it makes the pain go completely away or can prevent migraines from coming on. Others say it lessens the pain and allows them to focus on other things to get their work done.”

What cannabis does to alleviate migraines is complicated and not completely understood. “But it works on serotonin and dopamine receptors, and has anti-inflammatory activity,” says Russo, who is just finishing a paper for the Journal of Cannabis Therapeutics.

“Basically, it is a multi-modality agent that works on various aspects of migraine in a way that’s really unique. And it’s not just the THC — tetrahydrocannabinol, the psychoactive chemical — that does it. It appears now that it’s the result of the interaction of a combination of other cannabinoids and also the essential oils in the plant.”

Unlike most headache medications, cannabis is unique in that it works as both a preventive agent and an analgesic. “At any point in the migraine, they could use cannabis by smoking, vaporizer, etc., and about 80% of these people get significant or total relief,” he says. “And, if someone has a chronic migraine, daily use in whatever form will often lead to a complete remission.””

http://usatoday30.usatoday.com/life/health/doctor/lhdoc227.htm

Therapeutic Utility of Cannabinoid Receptor Type 2 (CB2) Selective Agonists.

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“The cannabinoid receptor type 2 (CB2), is a class A GPCR that was cloned in 1993 while looking for an alternate receptor that could explain the pharmacological properties of 9- tetrahydrocannabinol. CB2 was identified among cDNAs based on its similarity in amino-acid sequence to the CB1 receptor and helped provide an explanation for the established effects of cannabinoids on the immune system.

In addition to the immune system, CB2 has widespread tissue expression and has been found in brain, PNS and GI tract. Several “mixed” cannabinoid agonists are currently in clinical use primarily for controlling pain and it is believed that selective CB2 agonism may afford a superior analgesic agent devoid of the centrally mediated CB1 effects.

Thus, selective CB2 receptor agonists represent high value putative therapeutics for treating pain and other disease states. In this perspective, we seek to provide a concise update of progress in the field.”

http://www.ncbi.nlm.nih.gov/pubmed/23865723

1′,1′-Dimethylheptyl-delta-8-tetrahydrocannabinol-11-oic acid: a novel, orally effective cannabinoid with analgesic and anti-inflammatory properties.

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“Chemical structures of Δ-9-THC (dronabinol), nabilone, and CT-3”

Figure 1

“1′,1′-Dimethylheptyl-Delta-8-tetrahydrocannabinol-11-oic acid (CT-3) is a novel cannabinoid that is under development by Atlantic Pharmaceuticals as an anti-inflammatory and analgesic drug.

The objective of the study was to investigate the effects of CT-3 on overt symptom complex (Irwin’s test), nociception, gastrointestinal (GI) ulceration, and pharmacological availability after intragastric (i.g.) and intraperitoneal (i.p.) administration.

  The evidence indicates that CT-3 exhibits a large dissociation between its anti-inflammatory/analgesic effects and its ulcerogenic actions. CT-3 warrants clinical development as a novel anti-inflammatory and analgesic drug.”

Full text: http://jpet.aspetjournals.org/content/291/1/31.long

Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial.

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“To determine the effect of smoked cannabis on the neuropathic pain of HIV-associated sensory neuropathy and an experimental pain model…  randomized placebo-controlled trial… involving adults with painful HIV-associated sensory neuropathy.

Patients were randomly assigned to smoke either cannabis (3.56% tetrahydrocannabinol) or identical placebo cigarettes with the cannabinoids extracted three times daily for 5 days. Primary outcome measures included ratings of chronic pain and the percentage achieving >30% reduction in pain intensity.

Acute analgesic and anti-hyperalgesic effects of smoked cannabis were assessed using a cutaneous heat stimulation procedure and the heat/capsaicin sensitization model.

RESULTS:

Fifty patients completed the entire trial. Smoked cannabis reduced daily pain by 34% (median reduction; IQR = -71, -16) vs 17% (IQR = -29, 8) with placebo (p = 0.03). Greater than 30% reduction in pain was reported by 52% in the cannabis group and by 24% in the placebo group (p = 0.04).

The first cannabis cigarette reduced chronic pain by a median of 72% vs 15% with placebo (p < 0.001).

Cannabis reduced experimentally induced hyperalgesia to both brush and von Frey hair stimuli (p < or = 0.05) but appeared to have little effect on the painfulness of noxious heat stimulation.

No serious adverse events were reported.

CONCLUSION:

Smoked cannabis was well tolerated and effectively relieved chronic neuropathic pain from HIV-associated sensory neuropathy. The findings are comparable to oral drugs used for chronic neuropathic pain.”

http://www.ncbi.nlm.nih.gov/pubmed/17296917

[From cannabis to selective CB2R agonists: molecules with numerous therapeutical virtues].

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“Originally used in Asia for the treatment of pain, spasms, nausea and insomnia, marijuana is the most consumed psychotropic drug worldwide. The interest of medical cannabis has been reconsidered recently, leading to many scientific researches and commercialization of these drugs.

Natural and synthetic cannabinoids display beneficial antiemetic, anti-inflammatory and analgesic effects in numerous diseases, however accompanied with undesirable effects due to the CB1 receptor. Present researches focus on the design of therapeutical molecules targeting the CB2 receptors, and thus avoiding central side effects and therefore psychotropic effects caused by the CB1 receptor.”

http://www.ncbi.nlm.nih.gov/pubmed/23732102