Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential
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I didn't review papers from smaller labs in other countries doing some remarkable research, and I was too dismissive of the loud chorus of legitimate patients whose symptoms improved on cannabis. I mistakenly believed the Drug Enforcement Agency listed marijuana as a Schedule 1 substance because of sound scientific proof. It doesn't have a high potential for abuse, and there are very legitimate medical applications. In fact, sometimes marijuana is the only thing that works. We have been terribly and systematically misled for nearly 70 years in the United States, and I apologize for my own role in that.
The Epilepsy Foundation has asked the DEA to relax its marijuana restrictions to allow for medical research to proceed, and in April , the American Academy of Neurology published a consensus statement on the use of medical marijuana in neurologic disorders. In that consensus, they concluded that certain forms of medical marijuana, cannabinoids, and synthetic formulations can effectively treat some symptoms of MS, including spasticity, painful spasms, central pain, and overactive bladder, although efficacy was uncertain for the other neurologic conditions evaluated.
They recommended that cannabinoids should be studied as other drugs are in order to continue seeking answers as to the potential benefits of marijuana use in patients who have neurologic illness, and if found to be effective, it should be prescribed. In , California was the first state to pass the Compassionate Use Act, which allowed the legal use of marijuana for medicinal purposes. The bill proposes to exclude industrial hemp and CBD from the definition of marijuana in the Controlled Substances Act, so that patients can have legal access to CBD oil and therapeutic hemp.
A breakthrough in the understanding of how cannabis works in the brain occurred with the discovery of the endogenous cannabinoids and receptors, 40 - 44 which comprise the endocannabinoid system. This is in contrast to CB2 receptors, which are concentrated primarily in the peripheral tissues and immune cells where they influence the release of cytokines and cell migration, although are also present to a lesser degree in the nervous system. The presence of CB1 receptors in this wide array throughout the central and peripheral nervous system provides the substrate for a multitude of potential therapeutic neurologic targets.
The CB1 receptors are widely expressed throughout the rest of the body and organ systems, but this is beyond the scope of this review. The CB2 receptors are primarily concentrated in the peripheral tissues, especially cells of the immune system, but can be found in lower concentrations in some brain regions including the PAG and some neuronal subpopulations astrocytes, microglia, and oligodendrocytes.
The plant genus Cannabis is within the plant family Cannabaceae.
Cannabis and Cannabinoids : Pharmacology, Toxicology, and Therapeutic Potential
Three cannabis species are described: C. The leaves and flowering tops of cannabis plants contain at least distinct compounds among 18 different chemical classes, and contain at least different phytocannabinoid compounds identified thus far, potentially holding therapeutic benefit individually, or in variable combinations. Its actions at the CB1 receptor account for the psychoactive effects of cannabis, thought to be mediated to some extent by suppression of both glutamate and GABA release. Little is known about the potential therapeutic role of the extensive number of other compounds that cannabis contains, including flavonoids, terpenes, phenols, amino acids, vitamins, proteins, steroids, nitrogenous compounds, enzymes, glycoproteins, simple alcohols, hydrocarbons, ketones, aldehydes, fatty acids, simple esters and lactones, and pigments.
Variable routes of administration add to this complexity. Ultimately, studying each isolated constituent is mandatory to determine each compound's individual therapeutic benefits. These interactions also raise the question of a theoretical role in helping patients to wean down or off of opiates. Components of the endocannabinoid system are found throughout the nervous system in supraspinal, spinal, and peripheral pain pathways.
Given the pharmacology and reported therapeutic benefits of cannabis in pain medicine, it is only logical that this benefit may extend to the arena of headache medicine, including migraine. There is supporting literature for this, although it is primarily anecdotal and case based.
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Cannabinoids are active through CB1 receptors in areas of the brain and brainstem involved with migraine pathophysiology including the PAG which may be a migraine generator area , rostral medulla, area postrema of the medulla, nucleus trigeminal caudalis, 49 , - and trigeminal ganglia. The endogenous endocannabinoid AEA modulates pain signaling in the central nervous system in various ways. Modulation of serotonergic pain transmission is well established in migraine treatment, particularly with the mechanism of action of the triptans.
Endocannabinoids interact with serotonergic neurons in the brainstem dorsal raphe to modulate pain mechanisms, , and AEA potentiates 5HT 1A and inhibits 5HT 2A receptors. Triptans are suspected to inhibit GABAergic and glutamatergic signaling in the PAG by preventing neurotransmitter release from nerve terminals as part of their mechanism of action.
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This is suspected to be due to decreased glutamatergic transmission via inhibitory NMDA modulation, although modulation of NO, CGRP, or lipoxygenase and cyclooxygenase pathways are also possible contributors to the suppressive effect of cannabinoids on CSD. Endocannabinoid deficiency has been theorized as a possible cause for migraine and other chronic pain disorders, including chronic migraine and medication overuse headache. Unfortunately, there have been no controlled clinical trials evaluating smoked or oral formulations of medicinal cannabis or prescription cannabinoids for either acute or prophylactic therapy in migraine or other headache disorders.
A small case series of cannabis use for patients with pain included 3 subjects with chronic headaches that were relieved by smoking cannabis, with results similar or superior to ergotamine and aspirin. A case of a migraineur who had failed standard medical therapy, and ultimately received relief with small doses of smoked marijuana was reported.
One study suggested that cannabinoid compounds may provide benefit in migraine treatment due to platelet stabilization and inhibition of serotonin release. Medicinal cannabis may have a role in headache disorders other than migraine as well. A case study reported a woman with pseudotumor cerebri would smoke a marijuana cigarette about once per week when her headache was more severe.
She would have complete resolution of her headache within 5 minutes, and it would not recur that day.
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In phase II trials in Israeli hospitals, it lowered intracranial pressure with a trend toward faster and better neurologic outcome. Cannabis has been reported to treat cluster headache. Notably, CB1 receptors have a dense concentration in the hypothalamus, 56 of which the posterior inferior ipsilateral hypothalamus has been suspected to be a site of activation in cluster headache. Thus, in almost three quarters, the cluster headache subjects did not report efficacy.
The authors noted the need for controlled trials with synthetic selective cannabinoids to show a more convincing therapeutic benefit. Cannabis can be used by smoked, vaporized, oral, oral mucosal, topical, or rectal routes of administration.
The majority of cannabinoid metabolism occurs in the liver, with variable levels of different metabolites, dependent on the route of administration. Smoking cannabis by vaporization is a more recent technique of smoking cannabis, developed due to the fact that inhalation of a combustion product is an undesirable delivery system. It is typically used once to twice daily, and dose ranges vary from 2. Each spray delivers a total dose of 2. Topical transdermal formulations of cannabinoids exist in ointments, creams, and lotions, although there are no clinical studies evaluating these.
However, some research has been done evaluating a dermal patch for delivery of synthetic cannabinoids with good permeation results, suggesting the utility for development of a transdermal therapeutic system. There are a multitude of variables that may influence the presence or severity of adverse effects with cannabis use, as well as benefits. The majority of information regarding adverse effects reported with cannabis use come from studies and case reports primarily evaluating recreational users, rather than from controlled therapeutic clinical studies.
It is important to remember that none of the studies or reported adverse effects of cannabis specifically compare and take into account many potential variables. These include route of administration, patient age, concurrent medications being taken, patient comorbidities, standardized dosing, type of cannabis strain, ratio of the phytocannabinoids in the cannabis strain particularly the CBD:THC ratio , sterility of cannabis growing conditions, cannabis analyzation for commonly encountered issues of toxins, pesticides, and fungal and bacterial microbial contaminants, among others.
This is synonymous to evaluating adverse reactions in a random combination of the widely variable antidepressant medications, and then lumping all reported adverse effects into the same adverse effect profile for antidepressants as a general class. However, in reality, it is understood that different antidepressants have different pharmacologic properties and adverse reactions. Cannabis use as a medication should be thought of no differently.
Therefore, these reported adverse side effects should not be assumed to be universal cannabis side effects, but need to be more appropriately correlated with specific phytocannabinoids, phytocannabinoid ratios, and the aforementioned variables as medical research moves forward. This is critical for evaluating adverse side effects, as well as therapeutic benefits.
Unfortunately, cannabinoid science and associated medical research is in its infancy, and these many variables and factors have yet to be evaluated and incorporated into research for more specific data regarding both benefits and adverse side effects. Regarding cannabis dependency, the problem may be less significant compared with other substances. The question of cannabis overuse headache and withdrawal headache remains unstudied. To date, there has been no documented evidence of death exclusively attributed to cannabis overdose or use.
Results showed that alcohol was the deadliest substance, followed by heroin, cocaine, tobacco, ecstasy, methamphetamine, and lastly, cannabis. These results suggested that cannabis was approximately times less lethal than alcohol, and reinforced similar results in comparative toxicology studies and drug safety rankings developed decades prior under different methodologies. There are no studies evaluating the therapeutic benefits correlating to varying cannabis strains or CBD:THC ratios, despite the wide spectrum of diseases and symptoms that the medical literature suggests cannabis is beneficial for.
This is clearly a wide open area containing many potential therapeutic medical treatments for which research is desperately needed. Determining which cannabis strains and CBD:THC ratios are the most effective for specific diseases and symptoms, including acute and chronic pain should be a primary research focus. There are an extensive number of variables that make it difficult for establishing standardized dosing schedules.
The historical use of cannabis for medicinal purposes is described for numerous diseases.
There is an abundance of support for its many medicinal uses as well as potential benefit in some forms of headache disorders, including migraine and cluster. Cannabis contains an extensive number of pharmacological and biochemical compounds, of which only a small fraction are understood, so many therapeutic uses likely remain undiscovered. Cannabinoids appear to modulate and interact at many pathways inherent to migraine, triptan mechanisms of action, and opiate pathways, suggesting a potential synergistic or related benefit.