Through its processes, cannabis can be used to reduce migraine pain. Cannabinoid analgesia (numbing) occurs via the suppression of nociceptive neurons.
Endocannabinoids, the endogenous cannabinoid or eCB, have been shown to modulate pain by behaving as analgesics in both acute nociception and in clinical pain such as inflammation and painful neuropathy. Endocannabinoids have effects on short-term memory, neurogenesis, appetite stimulation, analgesia, inhibition of immune function, and reduction of the HPA axis during stress.
When a patient has inflammatory hyperalgesia, eCBs are able to mediate the pain because their receptors are found in neurons responsible for pain processing and in immune cells that regulate the neuro-immune interactions.
Peripheral CB2 receptors have been shown to mediate anti-nociceptive responses in neuropathic pain or inflammatory hyperalgesia by acting locally on immune cells in the periphery and microglia in the central nervous system. CB2 receptors were found on B-endorphin containing keratinocytes, which explains the potential interplay and cross communication with the μ-opioid systems, resulting in an indirect activation of opioid effects.
Endocannabinoid deficiency has been documented in patients with migraine headaches who demonstrated low levels of CSF and serum anandamide, and adding this could make a difference in treating migraine pain.
Barrie N, Manolios N. The endocannabinoid system in pain and inflammation: Its relevance to rheumatic disease. Eur J Rheumatol 2017; 4: 210-8.Rosaria Greco1*, Chiara Demartini 1, Anna M. Zanaboni 1,2, Daniele Piomelli 3 and Cristina Tassorelli 1,2Endocannabinoid System and Migraine Pain: An Update. Front. Neurosci., 19 March 2018