Patient has a right Adie’s pupil; occurs due to ipsilateral damage to the ciliary ganglion or its axonsÂ
– usually idiopathic, but sometimes linked to various viral infections and/or general inflammation in the area of the ciliary ganglion or its axons. Autoimmune inflammation may also cause thisÂ
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Pupil constriction to light and near accomodation shares a similar pathwayÂ
The efferent pathway consists of cholinergic parasympathetic fibers from cell bodies in the Edinger-Westphal nucleus, which then travels along CN III and synapse in the ciliary ganglion, and then proceed along the short ciliary nerves.Â
– Ach activates muscarinic receptors on the ciliary body (lens accommodation) and pupillary sphincter (pupil constriction).Â
One different in the light response and accommodation pathways is that there appears 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.Â
– this may explain why damage to the ciliary ganglion 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 responseÂ
This damage in Aldie’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.Â
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