Myasthenia gravis (pronounced `my˖ĕs˖`thēēn˖ē˖ă `grăv˖ĭs), also known simply as MG, is a rare neuromuscular disorder. When the first case of MG was documented in 1672 by Thomas Willis, an Oxford physician, not much was known or understood about it. Today, we know there are multiple causes for MG as well as treatment options.
Myasthenia gravis (MG) is the most common primary disorder of neuromuscular transmission. The usual cause is an acquired immunological abnormality, but some cases result from genetic abnormalities at the neuromuscular junction. Much has been learned about the pathophysiology and immunopathology of myasthenia gravis during the past 20 years. What was once a relatively obscure condition of interest primarily to neurologists is now the best characterized and understood autoimmune disease. A wide range of potentially effective treatments are available, many of which have implications for the treatment of other autoimmune disorders.
What Happens in Your Body
The voluntary muscles of the entire body are controlled by nerve impulses that arise in the brain. These impulses travel down the nerves to the place where the nerves meet the muscle fibers. Nerve fibers do not actually connect with muscle fibers. There is a space between the nerve ending and muscle fiber, called the neuromuscular junction.
When the nerve impulse originating in the brain arrives at the nerve ending, it releases a chemical called acetylcholine. Acetylcholine travels across the space to the muscle fiber side of the neuromuscular junction where it attaches to many receptor sites. The muscle contracts when enough of the receptor sites have been activated by the acetylcholine.
For someone with MG, there can be as much as an 80% reduction in the number of these receptor sites. The reduction in the number of receptor sites is caused by an antibody that destroys or blocks the receptor site. Antibodies are proteins that play an important role in the immune system. They are normally directed at foreign proteins called antigens that attack the body. Such foreign proteins include bacteria and viruses. Antibodies help the body to protect itself from these foreign proteins.
While it is not still fully understood why, the immune system of the person with MG makes antibodies against the receptor sites of the neuromuscular junction. The antibodies destroy the receptor sites more rapidly than the body can replace them. Muscle weakness occurs when acetylcholine cannot activate enough receptor sites at the neuromuscular junction.
When it comes to diagnosing MG, abnormal antibodies can be measured in the blood of most people with MG, but not all.
To learn more about the Clinical Overview of MG, please SEE ADDITIONAL INFORMATION ABOUT MYASTHENIA ON OUR WEBSITE HERE.