Myasthenia gravis, which occurs in about 1 in every 20,000 persons, causes muscle paralysis because of inability of the neuromuscular junctions to transmit enough signals from the nerve fibers to the muscle fibers. Pathologically, antibodies that attack the acetyl-choline-gated sodium ion transport proteins have been demonstrated in the blood of most patients with myasthenia gravis. Therefore, it is believed that myas-thenia gravis is an autoimmune disease in which the patients have developed immunity against their own acetylcholine-activated ion channels.
Regardless of the cause, the end plate potentials that occur in the muscle fibers are mostly too weak to stimu-late the muscle fibers. If the disease is intense enough, the patient dies of paralysis—in particular, paralysis of the respiratory muscles. The disease usually can be ame-liorated for several hours by administering neostigmine or some other anticholinesterase drug, which allows larger than normal amounts of acetylcholine to accu-mulate in the synaptic space. Within minutes, some of these paralyzed people can begin to function almost normally, until a new dose of neostigmine is required a few hours later.