Chronic pain & cannabinoids: what your drugstore is hiding you
Neuropathic and inflammatory pain
Nociception (pain perception) is a critical mechanism of the body self-defence, inducing to discontinue a stimuli potentially deteriorating.
When pain is experienced chronically, often as a consequence of a neural or metabolic dysfunction, as in the case of neuropathic pain (NP), it is fundamental to find agents able to target the pathways producing allodynia (sensation of pain evoked by a stimulus which would not, normally, produce it) and ultimately to eradicate them. 
It has been estimated that 7-8% of the entire population of Western Countries develops neuropathic pain, which is often caused by other pathologies (cancer, diabetes, MS, HIV or stroke, just to mention a few).
Despite the aetiology of the disease is multifarious, it causes the nervous system to be hypersensitised due to prolonged impulses.
Neuropathic pain alone is a chronic debilitating disease that affects up to 4 million people just in Europe; given the poor outcome of the medicines currently in use for the management of symptoms, (gabapentin, opioids and tricyclic antidepressant mainly) many studies are focused on this field of study. 
Why using cannabinoids for chronic pain?
Phytocannabinoids have been extensively used throughout history for various therapeutic purposes, particularly analgesic. However, the cannabinoid circuitry is relatively young, with only 20 years since its first characterization by the pioneering studies of Raphael Mechoulam, whose discoveries conveyed these chemicals from traditional home remedies to pharmacological investigation. 
Since the discovery of Cannabinoid receptors, pain regulation became one of the main area of study.
Compelling evidence has shown that cannabinoids decrease allodynia both thermal and mechanical, proving their role for treating neuropathic pain. 
Cannabinoids vs opioids
The benefit of targeting directly CB1 receptors is endorsed by their anatomical distribution in core pain centers of the brain (Periaqueductal grey-substantia gelatinosa-medulla oblongata-dorsal horn). 
CB1 agonists (all the drugs that activate CB1 receptors, such as THC) prevent “wind-up” phenomenon in the dorsal horn (an exaggerated sensitization to pain leading to allodynia and hyperalgesia and hallmark of neuropathic pain). (Hyperalgesia =increased sensation to pain, usually due to damaged pain receptors and nerve terminals)
It is hence crucial to pinpoint that manipulating cannabinoid circuitry is more advantageous than targeting directly opioids for the treatment of neuropathic pain. [6, 7] (Check out morphine for cancer and post-operative pain here)
Moreover, the medicines that activate CB1 receptors maintain their efficacy, at the opposite of morphine, which is less potent over time (so that more doses are needed, and with it, an increase in side effects).
Importantly, the spontaneous discharge (which lead to pain sensation) has been located mainly in primary afferent myelinated A-fibres, which are rich in cannabinoid receptors rather than opioids. 
The current medications for treating pain are still mainly opioids, but only approximately 50% of the sufferers finds relief with the available cures, thus highlighting how the clinic would greatly benefit from drugs oriented on cannabinoids modulation. 
On the ring today…
Opioids are prescribed worldwide to deal with pain.
Here are some facts, all the side effects for both medications.
Remember that researching cannabinoids medications does not necessarily mean using THC-based medications and lots of research is going through in this direction, making cannabinoid-based drugs even safer and non-psychoactive.
Notice that some of the effects reported for cannabis, are not “unwanted effects” by patients, such as bronchodilation, aid sleep, easing cramps, anti-inflammatory properties or antispasmodic, we report them for comparing them to Morphine.
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List of references
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- Mao, J., Price, D.D., Lu, J., Keniston, L., Mayer, D.J. (2000) Two distinctive antinociceptive systems in rats with pathological pain. Neurosci. Lett., 280, 13-16.
- Selph, S Carson, S Fu, R et al. (2011). Drug Class Review Neuropathic Pain. Available:http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0016164/pdf/TOC.pdf. Last accessed 4/3/13.
- British Medical Association (1997) Therapeutic Uses of Cannabis. London, Harwood Academic Publishers
- Fox, A., Kesingland, A., Gentrym C., McNair, K., Patel, S., Urban, L., James, I. (2001) The role of central and peripheral Cannabinoid 1 receptors in the antihyperalgesic activity of cannabinoids in a model of neuropathic pain. Pain, 92, 91-100.
- Martin, B.R., Lichtman, A.H. (1998) Cannabinoid transmission and pain perception. Neurobiol.Dis., 5, 447-461.
- Lichtman, A.H., Martin, B.R. (1991) Spinal and supraspinal components of cannabinoid-induced antinociception. J.Pharmacol. Exp. Ther., 258, 517-523.