Transaqueous diffusion of acetylcholine to denervated iris sphincter muscle: a mechanism for the tonic pupil syndrome (Adie syndrome).

The accepted hypothesis for the pathophysiology of tonic pupil syndrome (Adie syndrome) was reexamined in light of recent developments concerning denervation supersensitivity of cholinergically innervated smooth muscle. Kinetic analysis suggests that enzymatic hydrolysis is unimportant relative to convective diffusion in the turnover of acetylcholine in the aqueous humor. We postulate that the greater response to near stimuli than to light stimuli and the delay in iris sphincter contraction and relaxation can be explained by release of acetylcholine from the neuromuscular junction of the ciliary muscle followed by transaqueous diffusion to receptor sites on denervated, supersensitive iris sphincter muscle.