The discovery by Walker1 that the administration of prostigmine and physostigmine to patients with myasthenia gravis is followed by definite improvement in muscular function was an important advance in the management of this condition. Both prostigmine and physostigmine depress the activity of the choline esterase and thereby decrease the rate of hydrolysis of acetylcholine, which, according to the studies of Dale and his colleagues,2 is liberated when cholinergic nerves are stimulated. The administration of prostigmine or physostigmine, therefore, produces effects similar to those seen after stimulation of cholinergic nerves. The chemical reactions involved in the liberation of acetylcholine when cholinergic nerves are stimulated and the effect of prostigmine and physostigmine on the destruction of acetylcholine are shown in figure 1.
The fact that prostigmine and, to a less extent, physostigmine often have a dramatic effect on the muscular symptoms has led some workers to believe that the defect