With no cure and few “successful” treatments for this disorder, it presents the medical community with a difficult therapeutic challenge. Even with the available drugs, surgery to remove the source of irritation or to damage the nerve’s ability to transmit pain and use of gamma radiation to damage the nerve and prevent pain transmission, some estimates say nearly 50 per cent of those affected are unable to obtain substantial relief in the long term (2). Some skilled surgeons and radiologists report 80-90 per cent “success rate” for the latter two treatments. Even so, after surgery and gamma knife treatments the pain can return for some within a few years. Such physiological interventions also come with their own risks such as paralysis of the face and not all patients are willing to face such risks without assurance of success (1).
In general, neuropathic pain conditions such as TN have proven resistant to conventional pain management methods such as treatment with opiates. One class of drug, however, stands out in the research as relatively effective in the management of pain related neuropathy, those which interact with the endocannabinoid system (3). This trend in the research lead Liang, Huang and Hsu, 2004, to propose the endocannabinoid system as a target for methods aimed at treating TN. Next they developed an animal model of TN using rats. In the animal model, neuronal injury is produced by artificial constriction chronically applied to part of the rat’s trigeminal nerve. Rats which underwent a sham surgery but received no constriction of the nerve behaved normally. Rats which received the full experimental procedure expressed signs of hyperresponsiveness, hyperalgesia (extreme reaction to painful stimuli), and allodynia (reaction of severe pain to non-painful stimuli) as do patients with TN. Liang, Huang and Hsu then tested how synthetic cannabinoids WIN 55,212-2 and HU 210 effected the expression of the TN-like behavior in the experimental rats. The doses of these cannabinoids used in this study did not significantly effect the ability of the rats to perform in a test of motor skills (degree of motor skill impairment is believed to be indicative of degree of intoxication). In 2007, Liang, Huang, Hsu published their results. Rats treated with either WIN (WIN 55,212-2) or HU 210 demonstrated significant dose-dependant reductions in hypersensitive behavior, and significant dose-dependant increases in tolerance to thermal or painful stimuli. Blocking the CB1 receptor antagonized the effect of the cannabinoid treatment. However, the effect was not altered by blockade of either the CB2 receptors or the vanilloid 1 receptors. Furthermore, the chronically constricted rat nerves were found to increase production the CB1 receptors over time following surgery. This lead Liang, Huang and Hsu to suggest therapies targeting CB1 receptor activation may prove to be a valuable tool in the treatment of TN (4).