Myasthenia gravis, so named by Jolly1 in 1895, is clinically characterized by a syndrome which includes weakness, fatigue and in some cases actual wasting away of muscles without any pathologic changes microscopically demonstrable as specific to the disease.
There seems to be a predisposition for involvement of groups of muscles innervated by cranial nerves.
The causation is unknown, but it is believed that there is such an insufficiency of acetylcholine or some like substance at the myoneural junction that the neuromotor impulse is not transmitted across the junction. It has been postulated that this fault is caused either by underproduction of the choline-like substance at the motor end plates or by an accelerated disposal of it by an overabundance of acetylcholine esterase, a substance whose normal function is to destroy acetylcholine.2
This disease is no regarder of sex, approximately equal numbers of males and of females being affected.