Myasthenia Gravis

Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction. Pathogenic antibodies—most often against the acetylcholine receptor (AChR), but also against MuSK or LRP4—reduce the effectiveness of signal transmission from motor nerve to skeletal muscle. The nerve can still release acetylcholine, but the muscle has fewer reliable postsynaptic “receiving sites.” Its safety margin for contraction becomes small. Repeated use then exposes the problem: muscle strength fades during sustained activity and partially returns after rest. This is fatigable weakness, not ordinary tiredness. The pattern often begins with the extraocular muscles, causing fluctuating ptosis or diplopia. It may progress to facial, jaw, tongue, pharyngeal, neck, limb, and respiratory muscles. Ocular symptoms may be worse late in the day; bulbar or limb weakness may appear after prolonged speaking, chewing, walking, or other repeated activity. Sensation is usually intact, and the pupils are generally spared because MG primarily affects voluntary skeletal-muscle transmission rather than sensory pathways or autonomic pupillary function. “Generalized MG” means weakness extends beyond the eyes, especially when bulbar, neck, limb, or respiratory muscles are involved. A patient who shifts from...