Myasthenia Gravis

Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction. IgG autoantibodies interfere with signalling at the postsynaptic membrane, where acetylcholine released from the motor nerve normally binds and triggers a muscle action potential. With anti-acetylcholine receptor (AChR) antibodies, three processes reduce transmission: complement activation forms a membrane attack complex that damages the postsynaptic membrane; cross-linking accelerates internalisation of AChRs; and some antibodies directly block acetylcholine from binding. The result is not a shortage of acetylcholine. The problem is that too few functional receptors can receive its signal. The clinical signature is fatigable weakness. A patient may have clear speech and a normal eyelid position early in an assessment, then develop nasal or slurred speech, ptosis, or difficulty holding the head upright after sustained activity. Rest temporarily improves transmission. Ocular symptoms may remain limited to ptosis and diplopia, while generalized disease adds facial, bulbar, neck, limb, and respiratory weakness. Sensation, cognition, and pupillary responses are usually preserved. This pattern helps separate MG from disorders that affect sensory pathways, consciousness, or autonomic function. Lambert–Eaton myasthenic syndrome more often produces proximal...