Multiple Sclerosis (MS) is an autoimmune disease that effectively disrupts cell communication in the nervous system. Nerve cells communicate with each other via electrical signals that pass though the neuron and are protected and conducted by myelin, a fatty substance surrounding the axon. During MS attacks the body’s immune system attacks the myelin, slowing action potentials, causing pain, inflammation and motor difficulty. While these attacks do not last indefinitely, the remyelination process that occurs afterward does not fully heal the cells, leading to the lasting cell communication problems associated with MS. An estimated 23,000 Australians suffer from MS and currently there is no cure.
The antioxidant and anti-inflammatory properties of cannabinoids are thought to improve remyelination by protecting repair cells and reducing the inflammatory response. Symptoms such as spasticity, pain and poor sleep have been reported to improve with cannabinoid therapy.
This image is a simplification for website aesthetics only. For more information please refer to the clinical studies referenced below.
Additionally, while studies examining the effect of CB receptor activation on the recurrence and severity of MS attacks are few in number, there is evidence to suggest that the anti-inflammatory, anti-excitotoxicity and remyelination benefits of cannabinoids can be helpful for decreasing the severity and frequency of attacks as well as increasing post-attack recovery.
MS and the Endocannabinoid System
Endocannabinoid activation has been shown to exhibit remyelinating properties in viral-induced models of demyelination, in close association with attenuation of the inflammatory response. Thus cannabiniods have promising neuro-protective qualities for retaining efficient cell communication.
Various clinical studies show that activation of CB1 and CB2 receptors has a significant effect on alleviating certain signs and symptoms of MS:
Cannabinoids, especially cannabidiol (CBD), are potent anti-inflammatories. The retrograde signalling helps to control glutamate release, through activation of CB1, suggesting the crucial role of this receptor for excitotoxicity control in neuroinflammation.
Cannabinoids have been shown to reduce the destruction of myelin sheaths in viral-induced models of demyelination; which is believed to be closely associated with its attenuation of the inflammatory response. Furthermore, they enhance the remyelination of damaged sheaths by increasing the survival of oligodendrocyte progenitors, glial cells, whose promary job is remyelination.
CBD has been shown to help with neuropathic pain as well as headaches, joint and muscle pain. Activation of the endocannabinoid system has been shown to reduce pain signals in both the peripheral and central nervous system; specifically via excitation of the descending antinociceptive pathway as well as inhibition of painful inflammatory mediators.
Both anecdotal evidence and clinical studies have shown that cannabinoids produce a significant increase in quality of sleep and reduction of pain related disturbance in patients with multiple sclerosis as well as other conditions effecting sleep . While the exact mechanism of action is unknown, at certain doses CBD has been shown to be calming and can increase slow-wave (deep) sleep.
While studies in this area warrant more exploration, there is evidence to suggest relief of muscle stiffness and reduction of spasms. This was judged on the mean spasticity Numeric Rating Scale (NRS), in a number of small human studies.
Few studies have been dedicated to whether incontinence can be helped by activation of CB1 and CB2; however studies geared towards other symptoms of MS show the possibility of a reduction in this symptom.
Fernández-Ruiz, J., Pazos, M. R., García-Arencibia, M., Sagredo, O., & Ramos, J. A. (2008). Role of CB 2 receptors in neuroprotective effects of cannabinoids.Molecular and cellular endocrinology, 286(1), S91-S96.
Grundy, R. I., Rabuffetti, M., & Beltramo, M. (2001). Cannabinoids and neuroprotection. Molecular neurobiology, 24(1-3), 29-51.
Pertwee, R. G. (2002). Cannabinoids and multiple sclerosis. Pharmacology & therapeutics, 95(2), 165-174.
Rog, D. J., Nurmikko, T. J., & Young, C. A. (2007). Oromucosal Δ 9-tetrahydrocannabinol/cannabidiol for neuropathic pain associated with multiple sclerosis: an uncontrolled, open-label, 2-year extension trial. Clinical therapeutics, 29(9), 2068-2079.
Zajicek, J. P., & Apostu, V. I. (2011). Role of cannabinoids in multiple sclerosis.CNS drugs, 25(3), 187-201.