The topic of pain and pain control is a very complex one with many different areas of concern and consideration. I will try to outline this complex topic as it applies to the endocannabinoid system. In my last article I briefly outlined this system and described it as an internal “buffer” the main function of which is to create homeostasis within our body. When considering the topic of pain, a buffering process would be one that minimizes this pain perception.
“Pain is only pain, the physical suffering or discomfort, when it is perceived by the nervous system and reaches the brain”. Various internal and external forces help to minimize this perception. External forces would be entities such as pain medications, topical preparations, and physical therapy. Internal forces would be entities like biofeedback and our endocannabinoid system (ECS). As mentioned earlier this system consists of CB1 and CB2 receptors in different sites throughout the body. Evidence clearly shows that activation of both receptors in the nervous system will help reduce the nerve transmission of the painful stimuli and minimize an individual’s perception of pain.
Pain usually is divided into two distinct types or categories neuropathic and nociceptive. Nociceptive pain is that pain resulting from a noxious stimulus such as a cut, a burn, a kidney stone, or arthritic joint pain. On the other hand, neuropathic pain is not a result of such stimuli but a result of changes or damages to nerves. Diabetic peripheral neuropathy or pain associated with multiple sclerosis (MS) would be examples of the latter. Unfortunately, pain conditions are complex, and in many situations, a painful condition cannot be simply classified as one of the above but rather a combination of both.
As far as this discussion, our endocannabinoid system buffers our perception of the pain regardless of cause by altering the nerve conduction of this painful stimuli at various points within our nervous system.
For a painful stimulus to reach the brain a series of transmissions through our nervous system must occur. Pain sensation will travel up a peripheral nerve to the spinal cord. Transmission up the spinal cord results in a stimulation of the midbrain and finally this transmission ends in our cerebral cortex when the sensation of pain is appreciated, and behavior is then triggered as a result of that pain. The connection from one nerve to another is called a synapse and at each of these synapses CB1 and or CB2 receptors can be activated to inhibit the nerve conduction thereby decreasing our perception of the pain. Perception is the process by which pain is recognized and interpreted by the brain. Suffering is subjective and individual.
Narcotic pain killers (e.g., opioids) work by buffering the brain's perception of and response to painful stimuli. These medications work very effectively at specific opioid sites but unfortunately with significant short and long-term side effects. Opioids can cause significant sedation acutely and we are now all aware of the addictive nature of this family of medications.
Since opioids do not work within the endocannabinoid system and since this system provides a buffering of painful stimuli then it would make sense that adding a medication that would activate the CB1 and CB2 receptors could make the opioid more effective, and this has been shown in clinical trials. Using this principle, it has also been shown that adding a cannabinoid to a pain treatment plan can provide effective pain relief using a much lower and therefore less dangerous dose of any narcotic medication.
It would stand to reason that given the above facts that using targeted medication specifically designed to work on the CB1 and CB2 pain receptors could provide analgesia (pain relief) without using any narcotic products. Recent research has confirmed this and offers an exciting opportunity to provide safe and effective first line pain relief for acute, chronic, and inflammatory based pain.
Check our website for upcoming articles where I examine the ECS further.
Dr. John Maynard, B.Sc., M.D.