Overview of Myoclonus

Myoclonus is a symptom characterized by a sudden, involuntary muscle jerk. Myoclonic twitches can involve a single muscle or a group of muscles and can feature a single twitch or contractions that happen a sequence and repeat at various speeds. In some cases, myoclonus can cause a person to experience persistent, shock-like contractions in a group of muscles. Severe cases can severely limit the ability to eat, talk or walk.

The types of myoclonus can be classified as physiological, essential, epileptic, or symptomatic (secondary). The most common form of myoclonus is symptomatic, which occurs as a result of some underlying condition, such as a neurological disorder, a reaction to a medication, prolonged oxygen deprivation, kidney or liver failure, infection, head or spinal cord injury, or a metabolic condition. It’s not uncommon for multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, or epileptic patients to develop myoclonus. Healthy individuals experience physiological myoclonus, such as hiccups or jerking suddenly just before falling asleep, and do not need to be treated. Essential myoclonus occurs on its own, unrelated to an underlying illness and typically without other symptoms. Epileptic myoclonus occurs in association with an epileptic disorder.

According to the National Institute of Neurological Disorders and Stroke, most myoclonus is caused by a disturbance of the central nervous system. Scientists think that over-excitability of the motor pathways that control movement is responsible for symptoms. Abnormalities or deficiencies in the receptors of certain neurotransmitters may also be involved.

Treatment of myoclonus varies depending on its type and whether there is a treatable underlying condition. In the cases where the underlying condition can be fixed, such as changing the medication that causes jerking, myoclonus symptoms can be eliminated. However, most underlying causes cannot be cured or eliminated, so treatment efforts focus on easing myoclonus symptoms with anticonvulsant or tranquilizer medications. Botox injections can be helpful in treating myoclonus when it occurs in a single area. Surgery may be necessary when myoclonus is caused by a tumor or lesion on the brain or spinal cord.

Findings: Effects of Cannabis on Myoclonus

Research looking into cannabis’ direct effect on myoclonus is lacking. However, cannabis has been shown to have anticonvulsant and antiseizure effects. Multiple scientific reviews conclude that a major cannabinoid found in cannabis, cannabidiol (CBD), has demonstrated the ability to reduce or even eliminate seizures (Blair, Deshpande & DeLorenzo, 2015) (Rosenberg, Tsien, Whalley & Devinsky, 2015) (Szaflarski & Bebin, 2014) (Devinsky, et al., 2014). In preclinical trials, the administration of CBD and other cannabis cannabinoids have shown to provide significant anticonvulsant effects in mice and rats (Turkansis, et al., 1979) (Hill, et al., 2013). Most of the traditional medications used to treat myoclonus are also used to treat epilepsy, which suggests that cannabis, already demonstrating effective for epilepsy, may also prove beneficial for myoclonus.

CBD’s ability to decrease or eliminate seizures is due to its effects on the endocannabinoid system. CBD activates cannabinoid receptor 1 (CB1); The CB1 receptor then dampens neurotransmission and produces an overall reduction in neuronal excitability (Wallace, Wiley, Martin & DeLorenzo, 2001) (Hoffman & Frazier, 2013). This finding suggests that CBD may be able to combat myoclonus caused by over excitability.

Cannabinoids have also proven beneficial for curtailing tics and tremors in movement disorders like Parkinson’s disease and Huntington’s disease (Kluger, Triolo, Jones & Jankovic, 2015) (Fernandez-Ruiz, 2009) (Fernandez-Ruiz & Gonzales, 2005). Researchers suggest that cannabinoids may help alleviate involuntary motor symptoms because both CB1 and CB2 receptors, which cannabinoids act upon, have been found to be located in the basal ganglia and cerebellum. These are areas of the brain that control movement (Fernandez-Ruiz & Gonzales, 2005).

References

  1. Blair, R.E., Deshpande, L.S., and  DeLorenzo, R.J. (2015, September). Cannabinoids: is there a potential treatment role in epilepsy? Expert Opinion on Pharmacology, 16(13), 1911-4. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4845642/.

  2. Devinsky, O., Cilio, M.R., Cross, H., Fernandez-Ruiz, J., French, J., Hill, C., Katz, R., Di Marzo, V., Jutras-Aswad, D., Notcutt, W.G., Martinez-Orgado, J., Robson, P.J., Rohrback, B.G., Thiele, E., Whalley, B., and Friedman, D. (2014, June). Cannabidiol: pharmacology and potential therapeutic role in epilepsy and other neuropsychiatric disorders. Epilepsia, 55(6), 791-802. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4707667/.

  3. Fernandez-Ruiz, J. (2009, April). The endocannabinoid system as a target for the treatment of motor dysfunction. British Journal of Pharmacology, 156(7), 1029-40. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2697699/.

  4. Fernandez-Ruiz, J., and Gonzales, S. (2005). Cannabinoid control of motor function at the basal ganglia. Handbook of Experimental Pharmacology, 168, 479-507. Retrieved from http://link.springer.com/chapter/10.1007%2F3-540-26573-2_16.

  5. Hill, T.D., Cascio, M.G., Romano, B., Duncan, M., Pertwee, R.G., Williams, C.M., Whalley, B.J., and Hill, A.J. (2013, October). Cannabidivarin-rich cannabis extracts are anticonvulsant in mouse and rat via a CB1 receptor-independent mechanism. British Journal of Pharmacology, 170(3), 679-92. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792005/.

  6. Hoffman, M.E., and Frazier, C.J. (2013, June). Marijuana, endocannabinoids, and epilepsy: potential and challenges for improved therapeutic intervention. Experimental Neurology, 244, 43-50. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3332149/.

  7. Myoclonus. (2012, December 20). Mayo Clinic. Retrieved from http://www.mayoclinic.org/diseases-conditions/myoclonus/basics/definition/con-20027364.

  8. Myoclonus Fact Sheet. (2015, February 23). National Institute of Neurological Disorders and Stroke. Retrieved from http://www.ninds.nih.gov/disorders/myoclonus/detail_myoclonus.htm.

  9. Rosenberg, E.C., Tsien, R.W., Whalley, B.J., and Devinsky, O. (2015, August 18). Cannabinoids and Epilepsy. Neurotherapeutics, Epub ahead of print. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/26282273.

  10. Szaflarski, J.P. and Bebin, E.M. (2014, December). Cannabis, cannabidiol, and epilepsy–from receptors to clinical response. Epilepsy & Behavior, 41, 277-82. Retrieved from http://www.epilepsybehavior.com/article/S1525-5050(14)00413-2/fulltext.

  11. Turkanis, S.A., Smiley, K.A., Borys, H.K., Olsen, D.M., and Karler, R. (1979, August). An electrophysiological analysis of the anticonvulsant action of cannabidiol on limbic seizures in conscious rats. Epilepsia, 20(4), 351-63. Retrieved from http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1157.1979.tb04815.x/pdf.

  12. Wallace, M.J., Wiley, J.L., Martin, B.R., and DeLorenzo, R.J. (2001, September 28). Assessment of the role of CB1 receptors in cannabinoid anticonvulsant effects. European Journal of Pharmacology, 428(1), 51-7. Retrieved from http://www.sciencedirect.com/science/article/pii/S0014299901012432.

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