Myasthenia Gravis (prounced My-as-theen-ee-a grav-us) comes from the Greek and Latin workds meaning "grave muscular weakness." The most common form of MG is a chronic autoimmune neuromuscular disorder thatis characterized by fluctuating weakness of the voluntary muscle groups.
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.