The following information is presented for educational purposes only. Medical Marijuana Inc. provides this information to provide an understanding of the potential applications of cannabidiol. Links to third party websites do not constitute an endorsement of these organizations by Medical Marijuana Inc. and none should be inferred.
Neuropathy is the damage to the sensory, motor or automatic nerves that occurs from an underlying cause. Studies have shown cannabis is effective at significantly reducing neuropathic pain.
Overview of Neuropathy
Peripheral neuropathy, which is often simply referred to as neuropathy, is a condition where nerves are damaged, causing weakness, numbness and pain. Among the most common causes of neuropathy is diabetes mellitus, but the condition can also be caused by infections, alcoholism, traumatic injuries, autoimmune diseases, medications, infections, tumors, and inherited disorders.
The symptoms associated with neuropathy depend on what types of nerves are damaged. Damage to sensory nerves, which receive sensation and damage, can cause tingling and stabbing or burning pain. Damage to motor nerves, which control how the muscles move, can cause muscle weakness and a lack of coordination. If damage occurs in autonomic nerves, which control functions like blood pressure, heart rate, digestion, and bladder processes, an individual can experience heat intolerance, bowel and bladder problems, digestive issues and changes in blood pressure. Neuropathy can also increase the risk of infection and burns and other skin traumas because one may not realize they’re injured or feel temperature changes and pain.
Neuropathy treatment focuses on managing the underlying condition that is causing neuropathy and relieving symptoms. Medications are often used to manage pain. Transcutaneous electrical nerve stimulation (TENS), plasma exchange and intravenous immune globulin, and physical therapy can also help ease symptoms.
Findings: Effects of Cannabis on Neuropathy
Cannabis has been shown to be highly effective at relieving neuropathic pain (McDonough, McKenna, McCreary & Downer, 2014). Cannabinoids found in cannabis interact with the two main cannabinoid receptors (CB1 and CB2) of the endocannabinoid system within the body. These receptors regulate the release of neurotransmitter and central nervous system immune cells to manage pain levels (Woodhams, Sagar, Burston & Chapman, 2015).
Because of cannabis’ effectiveness at reducing pain, its use is prevalent among the chronic pain population. Luckily, studies indicate that long-term cannabis use for managing pain is safe. After a year of regular use, patients with chronic pain were found to be at no greater risk of serious adverse effects than non-cannabis users (Ware, et al., 2015).
Evidence also indicates that cannabinoids can support the health of neurons. Cannabinoid receptors have been shown to be involved in neuroprotection, indicating that cannabinoids can help protect from damage that leads to neuropathy and encourage neural cell survival (Blazquez, et al., 2015) (Castelli, et al., 2014), (Fernandez-Ruiz, et al., 2007)
States That Have Approved Medical Marijuana for Neuropathy
Currently, Arkansas, Montana, New Mexico, New York, Pennsylvania, and West Virginia have approved medical marijuana for the treatment of neuropathy. In Washington D.C., any condition can be approved for medical marijuana as long as a DC-licensed physician recommends the treatment. In addition, a number of other states will consider allowing medical marijuana to be used for the treatment of neuropathy with the recommendation from a physician. These states include: California (any debilitating illness where the medical use of marijuana has been recommended by a physician), Connecticut (other medical conditions may be approved by the Department of Consumer Protection), Massachusetts (other conditions as determined in writing by a qualifying patient’s physician), Nevada (other conditions subject to approval), Oregon (other conditions subject to approval), Rhode Island (other conditions subject to approval), and Washington (any “terminal or debilitating condition”).
Several states have approved medical marijuana specifically to treat “chronic pain,” a symptom commonly associated with neuropathy. These states include: Alaska, Arizona, California, Colorado, Delaware, Hawaii, Maine, Maryland, Michigan, Montana, New Mexico, Ohio, Oregon, Pennsylvania, Rhode Island, Vermont, and West Virginia. The states of Nevada, New Hampshire, North Dakota, Montana, Ohio and Vermont allow medical marijuana to treat “severe pain.” The states of Arkansas, Minnesota, Ohio, Pennsylvania, Washington, and West Virginia have approved cannabis for the treatment of “intractable pain.”
Recent Studies on Cannabis’ Effect on Neuropathy
- Blázquez, C., Chiarlone, A., Bellocchio, L., Resel, E., Pruunsild, P., García-Rincón, D., Sendtner, M., Timmusk, T., Lutz, B., Galve-Roperh, I., and Guzmán, M. (2015). The CB1 cannabinoid receptor signals striatal neuroprotection via a PI3K/Akt/mTORC1/BDNF pathway. Cell Death and Differentiation, 22(10), 1618–1629. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4563779/.
- Castelli, M.P., Madeddu, C., Casti, A., Casu, A., Casti, P., Scherma, M., Fattore, L., Fadda, P., and Ennas, M.G. (2014). Δ9-Tetrahydrocannabinol Prevents Methamphetamine-Induced Neurotoxicity. PLoS ONE, 9(5), e98079. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4028295/.
- Fernández-Ruiz, J., Romero, J., Velasco, G., Tolon, R.M., Ramos, J.A., and Guzman, M. (2007, January). Cannabinoid CB2 receptor: a new target for controlling neural cell survival. Trends in Pharmaceutical Sciences, 28(1), 39-45. Retrieved from http://www.cell.com/trends/pharmacological-sciences/fulltext/S0165-6147(06)00267-7.
- Fishbein, M., Gov, S., Assaf, F., Gafni, M., Keren, O., and Sarne, Y. (2012, September). Long-term behavioral and biochemical effects of an ultra-low dose of Δ9-tetrahydrocannabinol (THC): neuroprotection and ERK signaling. Experimental Brain Research, 221(4), 437-48. Retrieved from http://link.springer.com/article/10.1007%2Fs00221-012-3186-5.
- Jiang, W., Zhang, Y., Xiao, L., Van Cleemput, J., Ji, S.P., Bai, G., and Zhang, X. (2005). Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects. Journal of Clinical Investigation, 115(11), 3104–3116. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1253627/.
- Kim, S.H., Won, S.J., Mao, X.O., Jin, K., and Greenberg, D.A. (2006, March). Molecular mechanisms of cannabinoid protection from neuronal excitotoxicity. Molecular Pharmacology, 69(30), 691-6. Retrieved from http://molpharm.aspetjournals.org/content/69/3/691.long.
- López Rodríguez, A.B., Siopi, E., Finn, D.P., Marchand-Leroux, C., Garcia-Segura, L.M., Jafarian-Tehrani, M.H., and Viveros, M.P. (2013). CB1 and CB2 cannabinoid receptor antagonists prevent minocycline-induced neuroprotection following traumatic brain injury in mice. Cerebral Cortex. Retrieved from http://cercor.oxfordjournals.org/content/early/2013/08/19/cercor.bht202.abstract.
- Marsicano, G., Goodenough, S., Monory, K., Hermann, H., Eder, M., Cannich, A., Azad, S.C., Cascio, M.G., Gutiérrez, S.O., van der Stelt, M., López-Rodriguez, M.L., Casanova, E., Schütz, G., Zieglgänsberger, W., Di Marzo, V., Behl, C., and Lutz, B. (2003, October 3). CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity. Science, 302(5642), 84-8. Retrieved from http://science.sciencemag.org/content/302/5642/84.
- McDonough, P., McKenna, J.P., McCreary, C., and Downer, E.J. (2014, October). Neuropathic orofacial pain: cannabinoids as a therapeutic avenue. The International Journal of Biochemistry & Cell Biology, 55, 72-8. Retrieved from http://www.sciencedirect.com/science/article/pii/S1357272514002581.
- Panikashvili, D., Simeonidou, C., Ben-Shabat, S., Hanus, L., Breuer, A., Mechoulam, R., Shohami, E. (2001, October). An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature, 413(6855), 527-31. Retrieved from http://www.nature.com/nature/journal/v413/n6855/full/413527a0.html.
- Peripheral neuropathy. (2014, December 2). Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/peripheral-neuropathy/basics/definition/con-20019948.
- Pryce, G., Ahmed, Z., Hankey, D.J., Jackson, S.J., Croxford, J.L. Pocock, J.M., Ledent, C., Petzold, A., Thompson, A.J., Giovannoni, G., Cuzner, M.L., and Baker, D. (2003, October). Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. Brain, 126(Pt 10), 2191-202. Retrieved from https://academic.oup.com/brain/article/126/10/2191/314489/Cannabinoids-inhibit-neurodegeneration-in-models.
- Sagredo, O., Garcia-Arencibia, M., de Lago, E., Finetti, S., Decio, A., and Fernandez-Ruiz, J. (2007, August). Cannabinoids and Neuroprotection in Basal Ganglia Disorders. Molecular Neurobiology, 36(1), 82-91. Retrieved from http://link.springer.com/article/10.1007%2Fs12035-007-0004-3.
- van der Stelt, M., Veldhuis, W.B., Bar, P.R., Veldink, G.A., Vliegenthart, J.F., and Nicolay, K. (2001, September 1). Neuroprotection by Δ9-Tetrahydrocannabinol, the Main Active Compound in Marijuana, against Ouabain-Induced In Vivo Excitotoxicity. The Journal of Neuroscience, 21(17), 6475-9. Retrieved from http://www.jneurosci.org/content/21/17/6475.long.
- Ware, M.A., Wang, T., Shapiro, S., and Collet, J.P. (2015, September 15). Cannabis for the Management of Pain: Assessment of Safety Study (COMPASS). The Journal of Pain. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/26385201.
- Witting, A., Chen, L., Cudaback, E., Straiker, A., Walter, L., Rickman, B., Moller, T., Brosnan, C., and Stella, N. (2006, April 18). Experimental autoimmune encephalomyelitis disrupts endocannabinoid-mediated neuroprotection. PNAS, 103(16), 6362-7. Retrieved from http://www.pnas.org/content/103/16/6362.full.
- Woodhams, S.G., Sagar, D.R., Burston, J.J., and Chapman, V. (2015). The role of the endocannabinoid system in pain. Handbook of Experimental Pharmacology, 227, 119-43. Retrieved from http://link.springer.com/chapter/10.1007%2F978-3-662-46450-2_7.
- Xapelli, S., Agasse, F., Sardà-Arroyo, L., Bernardino, L., Santos, T., Ribeiro, F.F., Valero, J., Braganca, J., Schitine, C., de Melo Reis, R.A., Sebastiao, A.M., and Malva, J.O. (2013). Activation of Type 1 Cannabinoid Receptor (CB1R) Promotes Neurogenesis in Murine Subventricular Zone Cell Cultures. PLoS ONE, 8(5), e63529. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3660454/.
- Zogopoulos, P., Vasileiou, I., Patsouris, E., and Theocharis, S. (2013, April). The neuroprotective role of endocannabinoids against chemical-induced injury and other adverse effects. Journal of Applied Toxicology, 33(4), 246-64. Retrieved from http://onlinelibrary.wiley.com/wol1/doi/10.1002/jat.2828/full.