This patient has a right Adie’s pupil. Adie’s pupil is caused by ipsilateral damage to the ciliary ganglion or its axons.

 

Pupil constriction to both light and near accommodation shares a similar pathway. The efferent pathway consists of cholinergic parasympathetic fibers from cell bodies in the Edinger-Westphal nucleus, which then travel along CN III and synapse in the ciliary ganglion, and then proceed along the short ciliary nerves. The neurotransmitter Acetylcholine activates muscarinic receptors on the ciliary body (lens accommodation) and pupillary sphincter (pupil constriction). One difference in the light response and accommodation pathways is that there appear to be different cell bodies within the ciliary ganglion dedicated to each, and interestingly >95% of these parasympathetic fibers contribute to the near reflex, whereas only <5% to the light reflex. This may explain why damage to the ciliary ganglia will, in turn, cause a tonic pupil that does not respond at all to light, yet will respond (albeit slowly and sluggishly) to the near response. This damage in Adie’s tonic pupil will result in cholinergic hypersensitivity over time, and this is the reason a highly diluted cholinergic (pilocarpine 0.125%) will cause constriction. Diluted pilocarpine would not constrict normal pupils.

 

Adie’s pupil is usually idiopathic, but sometimes linked to various viral infections and/or general inflammation in the area of a ciliary ganglion or its axons. Autoimmune inflammation may also cause this. There has been a suggested association between Adie’s pupil and Sjogren’s syndrome and migraine.