Myasthenia Gravis (MG) is a rare chronic autoimmune disorder in which the antibodies destroy the communication between nerves and muscle, causing weakness of skeletal muscles.
Among the muscles MG impacts are voluntary, especially ones that control the eyes, mouth, throat, and limbs. MG impacts people of any gender, age, or race, but is mostly seen in young women aged 20 to 30 and men 50 and older. Those who experience a crisis will find it difficult to swallow or breathe.
On myastheniagravisnews.com, a report divides the disorder into five types – congenital myasthenia gravis, generalized myasthenia gravis, ocular myasthenia gravis, transient neonatal myasthenia gravis, and juvenile myasthenia gravis. The categories are divided based on the timing of the disease, the specific cause of the neuromuscular dysfunction, and the muscle groups affected.
The cause of MG is unknown and there is not a cure, but early detection and fast medical management can help people live longer and lead more functional lives, according to John’s Hopkins Medicine.
MG isn’t inherited (or contagious) and is a result of an abnormal immune reaction in which the body’s natural immune defenses (ie. Antibodies) inappropriately attack and gradually injure certain receptors in muscles that receive nerve impulses (antibody- mediated autoimmune response). These antibodies block a certain chemical-acetylcholine, which is needed to stimulate muscle contraction. Pregnant women who have the disorder may pass the antibodies to the fetus in a temporary form of MG. This generally resolves in two to three months.
Our body’s ability to move and control our voluntary muscles are stimulated by nerve impulses sent out from the brain. These nerve impulses travel to the point where the nerves meet muscle fibres in our muscles, however, nerve fibres do not actually connect with muscle fibres. There is a space between the nerve ending and muscle fibre – called the neuromuscular junction.
When the nerve impulse that originates from the brain arrives at the nerve ending, it releases a chemical called acetylcholine. Acetylcholine travels across the space to the muscle fibre 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. In MG, there is as much as an 80% reduction in the number of these receptor sites. The reduction is caused by an antibody that destroys or blocks the receptor site, making it difficult for acetylcholine to bind and cause the muscle to contract.
It’s not understood why MG patients make antibodies against the receptor sites of the neuromuscular junction or why MG develops but there are treatments available to manage the symptoms. Treatment plans are based on each patients’ specific needs and disease progression but the main goal, like all treatment plans, is to reduce MG related symptoms. Typical medications prescribed include anticholinesterase drugs (cholinesterase inhibitors) or ones that alter the disease course, such as immunosuppressive drugs or surgery (thymectomy).
Initial treatment commonly includes the use of cholinesterase inhibitors, which increase muscle strength by preventing the normal breakdown of the neurotransmitter acetylcholine. Pyridostigmine by mouth (orally) is primarily used.
Although treatments currently exist for MG, more research is needed into finding more suitable treatments and cures. Clinical research is crucial to find advancements in care and provide additional treatment options to patients.
For more information about research in your local area please contact the Medical Arts Health Research Group at email@example.com or visit our website at https://healthresearch.ca.