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Introduction to Myasthenia Gravis

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Introduction to Myasthenia Gravis

Myasthenia Gravis, also Known as “grave muscle weakness” is a chronic muscle disease that causes abnormally rapid fatigue of the skeletal muscle system, which are the voluntary muscles. The affected muscles tire quickly but regain strength after a period of rest. Myasthenia Gravis is termed an autoimmune disease. The immune system usually makes antibodies to attack bacteria, viruses and germs. With the autoimmune disease, the immune system makes antibodies against parts of one’s own body tissues.

In a person with normal immune system, muscles are stimulated to contract by the transmission of nerve impulses to the muscle fibers. The nerve impulses cause

neurotransmitter acetylcholine to be released into the synaptic cleft. There it is picked up by the acetylcholine receptors on the muscle fiber. In return this causes the myosin and the actin to slide past each other and link. This causes the muscle to contract. In myasthenia gravis, the numbers of acetylcholine receptors appear to be reduced. There is evidence to indicate that the receptor deficit is caused by an attack on the acetylcholine receptors by the body’s own immune system.

With the numbers of acetylcholine receptors reduced, it causes the nerve impulse to be prevented from reaching the muscles. The result is weakness and rapid fatigue only in the affected muscles. About 10-15 % patients have weakness in the eye muscles only, termed ocular myasthenia. The majority of other patients will go on to develop weakness in other muscle groups.

Other types of myasthenia gravis include congenital MG, which is an inherited condition caused by a genetic defect instead of an immune disorder. It develops in an infant shortly after being born to a mother with myasthenia gravis and usually has generalized symptoms. Transient neonatal MG is a temporary condition that develops in approximately 10-20% of infants born to a mother with myasthenia gravis. It is caused by the circulation of the mother’s antibodies through the placenta and lasts as long as the mother’s antibodies remain in the infant.

This disease can affect animals and humans of any age. Most commonly it affects twice as many women than men. Onset usually

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