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THE TRUTH about Cannabis vs Morphine: Cannabinoids and chronic pain. What your drugstore does not want you to know.
By Admins (from 11/09/2014 @ 05:09:18, in en - Science and Society, read 1027 times)

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. [1]
 
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, Multiple Sclerosis, HIV or stroke, just to mention a few).[2]
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 focussed on this field of study. [3]


 
Why using cannabinoids?
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. [4]
 
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. [5]
 
Cannabinoids vs opioids
The main mediator of the antinociceptive effect is thought to
be the cannabinoid CB1 receptor. 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). [6]
 
 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]
 
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. [8]
 
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. [2]

On the ring today...

Opioids are prescribed worldwide to deal with pain.
Only recently Sativex has been approved for treatment of pain in 2 Countries only! If you want to know more click here.
Here are some facts, all the side effects, both very common and rare for both medications.
Remember that researching cannabinoids medications does not necessarly mean using THC-based medications and lots of research is going through in this direction, making cannabinoid-based drugs even safer and non-psychoactive.

 
Side effects Cannabis Morphine
    blood pressure chages
    constriction of the pupil of the eye
    irregular heart rate
  increased heart rate erectile dysfunction
Cardiovascular redness of the eyes eye or eyesight problems
  vasodilatation/facial flush facialflushing
    irregular heart rate
    oedema of the extremities
    palpitations
     
  aids sleeping difficult sleeping
Circadian somnolence sleepiness
     
  aids gastrointestinal functions (diarrhea is rare) biliary problems
Gastrointestinal anti-emetic, can cause nausea when overdosed constipation
  eases cramps gastrointestinal problems
  abdominal pain can occur (rare) indigestion
    nausea
    vomiting
    stomachpain
     
    amenorrhoea
Hormonal   decreased libido
     
    allergic reactions
    anaphylactic reactions
Immunologic anti-inflamatory itching
    skin rash or rashes
    worsening of pancreatitis
    urticaria
     
Muscolar muscle relaxant abnormal muscle movement
  unsteadiness muscle twitching
     
    confusion
    drowsiness
    headaches
    loss of appetite
    thinking problems
    weakness
  confusion convulsions
  drowsiness dysphoria- euphoria
  increased appetite fainting
  weakness feeling agitated
Neurologic euphoria general feeling of being unwell
  sense of well-being hallucinations
  depersonalization mood changes
  hallucination physical dependence
  paranoid reaction psychological dependence
    vertigo
    withdrawal symptoms
     
    bronchospasm
Respiratory bronchodilator pulmonary oedema
    respiratory depression
     
    severe dry mouth
    sweating
Salivation dry mouth renal spasms
    urinary retention


List of references:

1. Scadding, J. (2003). Neuropathic Pain.ACNR. 3 (2), 8-14.
2. 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.
3. Selph, S Carson, S Fu, R et al. (2011). Drug Class Review Neuropathic Pain. Available: ncbi.nlm.nih.gov . Last accessed 4/3/13 .
4. British Medical Association (1997) Therapeutic Uses of Cannabis. London, Harwood Academic Publishers
5. 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.
6. Martin, B.R., Lichtman, A.H. (1998) Cannabinoid transmission and pain perception. Neurobiol.Dis., 5, 447-461.
7. Lichtman, A.H., Martin, B.R. (1991) Spinal and supraspinal components of cannabinoid-induced antinociception. J.Pharmacol. Exp. Ther., 258, 517-523.

Author: Viola Brugnatelli, BSc Neuroscience - Source: Casey McClain at naturegoingsmart.com/

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