Causes of Myasthenia Gravis
Voluntary muscles of our body are controlled by nerve impulses fired from the brain. There is a space between the nerve fibres supplying muscles and the muscle fibres, the neuromuscular junction. A chemical called Acetylcholine gets released into this space from the nerve ending at the arrival of a nerve impulse. This acetylcholine traverses the space, attaches to the receptors; activates them and then the muscle contracts.
In Myasthenia gravis, the number of receptor sites reduces (up to 80% reduction may occur). Hence due to the lack of the number of activated receptors muscle contraction doesn’t happen. This reduction is due to the attack of receptors (or their blockage) by antibodies. Antibodies are proteins that our immune system produces to fight foreign bodies. But, in some individuals (with autoimmune diseases) the immune system loses its capacity to recognise ‘self from non-self’. As a result antibodies attack the body’s own tissues.
The exact mechanism why such an autoimmune mechanism initiates is not yet known. Some evidences suggest an association with thymus, a ductless gland at the base of the neck that normally takes part in immunity but atrophies with age.
Association with other autoimmune diseases, esp. Thyroid diseases is also suggested. The antibodies may get transferred from an affected mother to the newborn resulting in transient features (neonatal myasthenia).
Latest Publications and Research on Myasthenia GravisMyasthenia Gravis and Pregnancy. - Published by PubMed
Thoracoscopic thymectomy: technical pearls to a 21st century approach. - Published by PubMed
Antibodies to active zone protein ERC1 in Lambert-Eaton myasthenic syndrome. - Published by PubMed
Nephrotic syndrome after thymectomy for myasthenia gravis. - Published by PubMed
Complications in patients treated with plasmapheresis in the intensive care unit. - Published by PubMed