Although the study by Liang, Huang and Hsu (2007) was the first to speak so directly to the use of cannabinoids in the treatment of TN, there are several other studies of neuralgia as well as anecdotal evidence from sufferers of TN indicating they are on to something.
Neuropathic Pain and WIN 55,212-2
Neuralgia and neuropathic pain are synonyms and therefore interchangeable, however, trigeminal neuralgia is not necessarily synonymous with all neuropathic pain. That said, I have tried to present here some of the studies which are most relevant to the topic of trigeminal neuralgia. To start with, one might wonder how effective are cannabinoids at treating neuropathic allodynia, like that seen in TN, when compared to opiates? This question was addressed by Rahn, Makriyannis and Hohmann in 2007. They found in a rat model of vaccine-induced allodynia that not only was the synthetic cannabinoid WIN able to attenuate the expression of allodynia in vaccine-treated rats but that is was also able to do so at doses which were 75 to 80 per cent smaller than that required for morphine to produce the same level of attenuation. This suggests that WIN is 4 or 5 times more potent than morphine at treating this kind of pain (5). TN also produces hyperalgesia and another study found that WIN administered directly to the site of neural injury at a non-systemically active dose, dose-dependently suppressed hyperalgesia as evidenced by reduced hypersensitivity. This effect was found to be CB1 and CB2 dependant only for acute administration of WIN whereas chronic administration of WIN appeared to be antihyperalgesic via the CB1 receptor only (6).
Although the last study indicated that only local activation of the CB1 receptors in the periphery was required for WIN to decrease some neuropathic pain, another study suggests that the ability of WIN to reduce the sensation of neuralgia may have roots in the central nervous system (CNS) as well. In this case, WIN was found to effectively ameliorate both allodynia and hyperalgesia in rats with neuralgia inducing spinal injury. HU 210 and CP 55,940 were only tested on hyperalgesia but were both effective. WIN was further tested by administration either locally in the paw that was used for tests of hyperalgesia or to the CNS both with co-administration for a CB1 receptor antagonist and without. When administered alone WIN reduced hyperalgesia in both cases. The effect of WIN was blocked when the CB1 antagonist was administered to the same location as was the WIN. When the CB1 antagonist was administered to the CNS and WIN to the periphery, it was not able to block the effect of WIN to reduce hyperalgesia. This suggests that systemic administration of WIN produces antineuralgia via both CNS and peripheral mechanisms (7).