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.
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 GravisAssociation of CTLA-4 polymorphisms with increased risks of myasthenia gravis. - Published by PubMed
Upper Eyelid Blepharoplasty: A Novel Method to Predict and Improve Outcomes. - Published by PubMed
Therapeutic Plasma Exchange Outcomes in Cairo University Hospitals: 6 Years Experience. - Published by PubMed
Pathogenic Mechanisms and Clinical Correlations in Autoimmune Myasthenic Syndromes. - Published by PubMed
New Pathways and Therapeutic Targets in Autoimmune Myasthenia Gravis. - Published by PubMed