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.
Myasthenia gravis is a neuromuscular disease that causes weakness and rapid
fatigue and is more common in women younger than 40 and men older than 60.
Studies have shown cannabis provides therapeutic effects by limiting
acetylcholine degradation and thus improving nerve and muscle communication.
Overview of Myasthenia Gravis
Myasthenia gravis is a chronic autoimmune neuromuscular disease
characterized by a breakdown in communication between nerves and muscles,
resulting in weakness and rapid fatigue. The muscle weakness associated with
myasthenia gravis increases when one is active, but then improves after
periods of rest. The degree of muscle weakness varies greatly between
Myasthenia gravis causes the immune system to produce antibodies that either
block or destroy muscles’ receptor sites for the neurotransmitter
acetylcholine. With some receptors blocked, the muscles receive fewer
signals and subsequently prevent muscles from contracting, resulting in
weakness. Production of the antibodies that block acetylcholine is likely
triggered by the thymus, which is found to be abnormally large in people
with myasthenia gravis. Sometimes the antibodies, rather than block receptor
sites, block the function of a protein called muscle-specific receptor
tyrosine kinase, which is involved in creating the nerve-muscular junction.
Due to muscular weakness and fatigue, myasthenia gravis also commonly causes
eyelids to droop and can make it difficult to speak, swallow, chew, and make
facial expressions. The neck and breathing muscles can also be affected in
There is no cure for myasthenia gravis. However, anticholinesterase
medications are effective at inhibit the enzyme acetylcholinesterase, which
is responsible for catalyzes the breakdown of acetylcholine. By inhibiting
acetylcholinesterase, the amount of acetylcholine at the neuromuscular
junction increases and eventually overcomes the blocked receptors.
Findings: Effects of Cannabis on Myasthenia Gravis
Research suggests that cannabis, like anticholinesterase agents, has the
capability of inhibiting acetylcholinesterase, the enzyme responsible for
the degradation of acetylcholine. By inhibiting acetylcholinesterase,
acetylcholine has more time to interact with its receptor before its
breakdown, or turnover, and can therefore overcome the blocked receptor and
cause muscle contractions.
Multiple cannabinoids have demonstrated effective at increasing
acetylcholine levels and slowing acetylcholine turnover. One study found
that tetrahydrocannabinol (THC), a major cannabinoid found in cannabis,
completely inhibited acetylcholinesterase, thereby raising the levels of the
neurotransmitter (Eubanks, et al., 2006). Another study showed that three
cannabinoids, including THC, cannabidiol (CBD), and cannabinol (CBN), each
caused a significant elevation of acetylcholine in the brain and THC and CBN
caused a decrease in acetylcholine turnover (Tripathi, Vocci, Brase & Dewey,
1987). Additional studies have demonstrated THC and CBD’s effectiveness at
decreasing acetylcholine turnover rate (Revuelta, Moroni, Cheney & Costa,
1978) (Revuelta, et al., 1980).
Cannabinoids’ long understood pharmacological effects are caused by their
activation of cannabinoid receptors. However, the cannabinoid’s effects on
enzymes and neurotransmitter transporters appear to be due to a mechanism
other than their activation of cannabinoid receptors, but the exact method
is yet to be fully understood (Oz, et al., 2014).
States That Have Approved Medical Marijuana for Myasthenia Gravis
Currently, only the state of Illinois has
approved medical marijuana specifically for the treatment of myasthenia
gravis. However, in Washington
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
myasthenia gravis 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
conditions subject to approval), and Washington (any
“terminal or debilitating condition”).
Recent Studies on Cannabis’ Effect on Myasthenia Gravis
THC shown to completely inhibit acetylcholinesterase, the enzyme
responsible for the degradation of acetylcholine.
A Molecular Link Between the Active Component of Marijuana and
Alzheimer’s Disease Pathology.
Animal trials show THC, CBN and CBD significantly increases
acetylcholine in the brain and THC and CBD decreased acetylcholine
Effects of cannabinoids on levels of acetylcholine and choline and on
turnover rate of acetylcholine in various regions of the mouse brain.
Eubanks, L. M., Rogers, C. J., Beuscher, A. E., Koob, G. F., Olson, A. J.,
Dickerson, T. J., & Janda, K. D. (2006). A Molecular Link Between the Active
Component of Marijuana and Alzheimer’s Disease Pathology. Molecular
Myasthenia gravis. (2013, April 23). Mayo
Retrieved from http://www.mayoclinic.org/diseases-conditions/myasthenia-gravis/basics/definition/con-20027124.
Myasthenia Gravis Fact Sheet. (2015, July 27). National
Institute of Neurological Disorders and Stroke.
Retrieved from http://www.ninds.nih.gov/disorders/myasthenia_gravis/detail_myasthenia_gravis.htm.
Oz, M., Al Kury, L., Keun-Hang, S.Y., Mahgoub, M., and Galadari, S. (2014,
May 15). Cellular approaches to the interaction between cannabinoid receptor
ligands and nicotinic acetylcholine receptors. European
Journal of Pharmacology,
Revuelta, A.V., Cheney, D.L., Costa, E., Lander, N., and Mechoulam, R.
(1980, August 18). Reduction of hippocampal acetylcholine turnover in rats
treated with (-)-delta 8-tetrahydrocannabinol and its 1′,2′-dimethyl-heptyl
Revuelta, A.V., Moroni, F., Cheney, D.L., and Costa, E. (1978, September).
Effect of cannabinoids on the turnover rate of acetylcholine in rat
hippocampus, striatum and cortex. Naunyn-Schmiedeberg’s
Achives of Pharmacology,
Tripathi, H.L., Vocci, F.J., Brase, D.A., and Dewey, W.L. (1987). Effects of
cannabinoids on levels of acetylcholine and choline and on turnover rate of
acetylcholine in various regions of the mouse brain. Alcohol
and Drug Research,
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