For the most part, pain is caused by the after affects of an illness or injury. However, in regards to neuropathic pain, no injury or accident causes the pain directly. Instead, the brain receives signals of pain without reason or warning. This type of pain can be ongoing, or randomly occur.
A person experiencing neuropathic pain may encounter certain symptoms such as; burning/stabbing pain, tingling or numbness, evoked pain or issues with sleeping. People that have missing limbs may also experience a pain called ‘phantom limb syndrome’. When a person has had a limb amputated, their brain may at times send faulty pain signals to that certain area.
This paper describes the analgesic effect a selective synthetic cannabinoid has on chronic neuropathic nerve pain.
Here is the full scientific article if you wish to download it.
A randomized, placebo-mediated, double-blind crossover trial took place in Germany from May-September 2002. Twenty-one patients (8 women and 13 men) aged 29 to 65 years (mean, 51 years) who had a clinical evaluation and reviewed consistent with chronic neuropathic pain (for at least 6 months) with hyperalgesia (n = 21) and allodynia (n = 7).
People were randomized to two 7-day treatment orders in a crossover structured experiment. The results from this experiment suggested that the selective synthetic cannabinoids CT-3 was efficient in treating chronic pain in humans.
1′,1′Dimethylheptyl-Δ8-tetrahydrocannabinol-11-oic acid (CT-3) possibly held the effectiveness to treat neuropathic pain and muscle stiffness without the psychotropic faults of cannabis. CT-3 is a synthetic analog of tetrahydrocannabinol (THC)-11-oic acid, one of the endogenous transformation offspring of THC, in which a dimethylheptyl side chain is switched for the pentyl side chain. In other words, CT-3 was discovered to be a strong anti-inflammatory, therapeutic, and antiallodynic agent without psychoactive abilities in healing nerve fibers.
Although the exact neurobiological method is not transparent, some truths lie within that apart from the famous cannabinoid receptors (CB1 and CB2), 1 or more unfounded cannabinoid receptors are cahoots with the regulation of the therapeutic and anti-inflammatory impacts of CT-3. More so, additional research indicates potential postreceptor mechanisms, including inducing of eicosanoid synthesis and down-regulation of cyclooxygenase 2.
Recent results suggest that the peroxisome proliferator–activated receptor γ (PPARγ) may act as an intracellular receptor for CT-3.The triggering of PPARγ is directly linked to common causes of anti-inflammatory and antitumor functions.