Category Archives: Chronic Pain

Cannabis very effective as painkiller after a major sugery

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Fight For medical Marijuana

“The very existence of cannabis as a substance with possible medical use is a contentious topic, to say the least. Its status as an illicit substance is hotly debated, with proponents from both sides (for and against legalization) engaged in a decades-long battle.

The status of marijuana in the United States as a Schedule I Substance under the Controlled Substances Act means not only that it is highly illegal to possess, but it is classified along the likes of cocaine, heroine, and crystal meth.

Schedule I substances are those that a) have high potential to be abused; b) have no currently accepted medical use in treatment in the United States; and c) are lacking in accepted safety in use under medical supervision.

All of these qualifiers are potentially important in classifying drugs and substances, but many people argue that marijuana does not belong in Schedule I…

Pain after surgery remains a problem in the medical community, and traditional prescribed painkillers often have unpleasant side effects as well as diminishing benefits.

Cannabis extracts work due to the cannabinoid receptors in the human brain.

Cannabinoids from marijuana help to effectively strengthen the body’s ability to reduce pain sensation.”

http://www.royalqueenseeds.com/blog-cannabis-very-effective-as-painkiller-after-a-major-sugery–n55

Cannabis very effective as painkiller after a major sugery

Cannabis as painkiller

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ScienceDaily: Your source for the latest research news

“Cannabis-based medications have been demonstrated to relieve pain.

Cannabis medications can be used in patients whose symptoms are not adequately alleviated by conventional treatment.

The clinical effect of the various cannabis-based medications rests primarily on activation of endogenous cannabinoid receptors.

Consumption of therapeutic amounts by adults does not lead to irreversible cognitive impairment.”

http://www.sciencedaily.com/releases/2012/08/120807101232.htm

http://www.thctotalhealthcare.com/category/pain-2/

Role of ionotropic cannabinoid receptors in peripheral antinociception and antihyperalgesia

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Figure 1

“Although cannabinoids have been used for millennia for treating pain and other symptoms, their mechanisms of action remain obscure.

With the heralded identification of multiple G-protein-coupled receptors (GPCRs) mediating cannabinoid effects nearly two decades ago, the mystery of cannabinoid pharmacology was thought to be solved…

Despite the wealth of information on cannabinoid-induced peripheral antihyperalgesic and antinociceptive effects in many pain models, the molecular mechanism(s) for these actions remains unknown.

Although metabotropic cannabinoid receptors have important roles in many pharmacological actions of cannabinoids, recent studies have led to the recognition of a family of at least five ionotropic cannabinoid receptors (ICRs). The known ICRs are members of the family of transient receptor potential (TRP) channels and include TRPV1, TRPV2, TRPV4, TRPM8 and TRPA1.

Cannabinoid activation of ICRs can result in desensitization of the TRPA1 and TRPV1 channel activities, inhibition of nociceptors and antihyperalgesia and antinociception in certain pain models.

Thus, cannabinoids activate both metabotropic and ionotropic mechanisms to produce peripheral analgesic effects.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2863326/

[Tetrahydrocannabinol for treatment of chronic pain].

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“Even in the last century cannabis was used in the treatment of chronic pain. The main active component of cannabis Delta-9-Tetrahydrocannabinol (THC) has been increasingly used in the treatment of nausea, vomiting, loss of appetite and depression. It is also recommended in the treatment of chronic pain. We present our first experiences with THC in the treatment of patients with chronic pain.”

http://www.ncbi.nlm.nih.gov/pubmed/11810357

http://www.thctotalhealthcare.com/category/chronic-pain/

http://www.thctotalhealthcare.com/category/pain-2/

No more pain upon Gq -protein-coupled receptor activation: role of endocannabinoids.

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“Marijuana has been used to relieve pain for centuries. The analgesic mechanism of its constituents, the cannabinoids, was only revealed after the discovery of cannabinoid receptors (CB1 and CB2 ) two decades ago.

The subsequent identification of the endocannabinoids, anandamide and 2-arachidonoylglycerol (2-AG), and their biosynthetic and degradation enzymes discloses the therapeutic potential of compounds targeting the endocannabinoid system for pain control.

Inhibitors of the anandamide and 2-AG degradation enzymes, fatty acid amide hydrolase and monoacylglycerol lipase, respectively, may be superior to direct cannabinoid receptor ligands as endocannabinoids are synthesized on demand and rapidly degraded, focusing action at generating sites.

Recently, a promising strategy for pain relief was revealed in the periaqueductal gray (PAG). It is initiated by Gq -protein-coupled receptor (Gq PCR) activation of the phospholipase C-diacylglycerol lipase enzymatic cascade, generating 2-AG that produces inhibition of GABAergic transmission (disinhibition) in the PAG, thereby leading to analgesia.

Here, we introduce the antinociceptive properties of exogenous cannabinoids and endocannabinoids, involving their biosynthesis and degradation processes, particularly in the PAG. We also review recent studies disclosing the Gq PCR-phospholipase C-diacylglycerol lipase-2-AG retrograde disinhibition mechanism in the PAG, induced by activating several Gq PCRs, including metabotropic glutamatergic (type 5 metabotropic glutamate receptor), muscarinic acetylcholine (M1/M3), and orexin 1 receptors.

Disinhibition mediated by type 5 metabotropic glutamate receptor can be initiated by glutamate transporter inhibitors or indirectly by substance P, neurotensin, cholecystokinin and capsaicin. Finally, the putative role of 2-AG generated after activating the above neurotransmitter receptors in stress-induced analgesia is discussed.”

http://www.ncbi.nlm.nih.gov/pubmed/24494686

Anandamide in primary sensory neurons: too much of a good thing?

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“The quest for possible targets for the development of novel analgesics has identified the activation of the cannabinoid type 1 (CB1) receptor outside the CNS as a potential means of providing relief from persistent pain, which currently constitutes an unmet medical need.

Increasing tissue levels of the CB1 receptor endogenous ligand N-arachidonoylethanolamine (anandamide), by inhibiting anandamide degradation through blocking the anandamide-hydrolysing enzyme fatty acid amide hydrolase, has been suggested to be used to activate the CB1 receptor.

However, recent clinical trials revealed that this approach does not deliver the expected relief from pain. Here, we discuss one of the possible reasons, the activation of the transient receptor potential vanilloid type 1 ion channel (TRPV1) on nociceptive primary sensory neurons (PSNs) by anandamide, which may compromise the beneficial effects of increased tissue levels of anandamide.

We conclude that better design such as concomitant blocking of anandamide hydrolysis and anandamide uptake into PSNs, to inhibit TRPV1 activation, could overcome these problems.”

http://www.ncbi.nlm.nih.gov/pubmed/24494681

Endocannabinoids and neuropathic pain: focus on neuron-glia and endocannabinoid-neurotrophin interactions.

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“Although originally described as a signalling system encompassing the cannabinoid CB1 and CB2 receptors, their endogenous agonists (the endocannabinoids), and metabolic enzymes regulating the levels of such agonists, the endocannabinoid system is now viewed as being more complex, and including metabolically related endocannabinoid-like mediators and their molecular targets as well.

The function and dysfunction of this complex signalling system in the molecular and cellular mechanisms of pain transduction and control has been widely studied over the last two decades.

In this review article, we describe some of the latest advances in our knowledge on the role of the endocannabinoid system, in its most recent and wider conception, in pain pathways, by focusing on: (1) neuron-glia interactions; and (2) emerging data on endocannabinoid cross-talk with neurotrophins, such as nerve growth factor and brain-derived neurotrophic factor.”

http://www.ncbi.nlm.nih.gov/pubmed/24494680

Endocannabinoids: a unique opportunity to develop multitarget analgesics.

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“After 4 millennia of more or less documented history of cannabis use, the identification of cannabinoids, and of Δ(9)-tetrahydrocannabinol in particular, occurred only during the early 1960s, and the cloning of cannabinoid CB1 and CB2 receptors, as well as the discovery of endocannabinoids and their metabolic enzymes, in the 1990s.

Despite this initial relatively slow progress of cannabinoid research, the turn of the century marked an incredible acceleration in discoveries on the “endocannabinoid signaling system,” its role in physiological and pathological conditions, and pain in particular, its pharmacological targeting with selective agonists, antagonists, and inhibitors of metabolism, and its previously unsuspected complexity.

The way researchers look at this system has thus rapidly evolved towards the idea of the “endocannabinoidome,” that is, a complex system including also several endocannabinoid-like mediators and their often redundant metabolic enzymes and “promiscuous” molecular targets.

These peculiar complications of endocannabinoid signaling have not discouraged efforts aiming at its pharmacological manipulation, which, nevertheless, now seems to require the development of multitarget drugs, or the re-visitation of naturally occurring compounds with more than one mechanism of action.

In fact, these molecules, as compared to “magic bullets,” seem to offer the advantage of modulating the “endocannabinoidome” in a safer and more therapeutically efficacious way.

This approach has provided so far promising preclinical results potentially useful for the future efficacious and safe treatment of chronic pain and inflammation.”

http://www.ncbi.nlm.nih.gov/pubmed/23623250

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