Myasthenia Gravis Basics

Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction, where a motor nerve communicates with a skeletal muscle. With each nerve impulse, acetylcholine is released into the junction and binds to receptors on the muscle membrane. In MG, antibodies most often target acetylcholine receptors (AChR); less commonly, they target muscle-specific kinase (MuSK) or other proteins involved in receptor function and organisation. The result is an inadequate “safety margin” for muscle activation. A single impulse may produce an adequate contraction, but repeated use exposes the weakness because neuromuscular transmission becomes less reliable. This explains the characteristic pattern: ptosis or limb weakness may worsen during the day or after sustained activity, then improve after rest. The problem is not loss of sensation or consciousness. It is failure to maintain skeletal-muscle contraction. The muscles most likely to reveal this failure are the extraocular, facial, bulbar, neck, limb, and respiratory muscles. Weakness may remain ocular for a time or progress to generalised disease. Respiratory muscle involvement is the dangerous pivot because a patient can become unable to ventilate effectively even while appearing...