The near response in tonic pupils is slow and prolonged The two different types of near response are caused by different underlying disease processes.
Adie's pupil is caused by damage to peripheral pathways to the pupil (parasympathetic neurons in the ciliary ganglion that cause pupillary constriction to bright light and with near vision).
Argyll Robertson pupils (AR pupils or, colloquially, "prostitute's pupils") are bilateral small pupils that reduce in size on a near object (i.e., they accommodate), but do not constrict when exposed to bright light (i.e., they do not react to light).
They are a highly specific sign of neurosyphilis; however, Argyll Robertson pupils may also be a sign of diabetic neuropathy.
Research has implicated the rostral midbrain in the vicinity of the cerebral aqueduct of the third ventricle as the most likely region of damage.
A lesion in this area would involve efferent pupillary fibres on the dorsal aspect of the Edinger-Westphal nucleus (associated with the response to light) while sparing the fibres associated with the response to near, which lie slightly more ventrally.
The exact relationship between syphilis and the two types of pupils (AR pupils and tonic pupils) is not known at the present time.
In the early 20th century, William John Adie described a second type of pupil that could “accommodate but not react.” Adie’s tonic pupil is usually associated with a benign peripheral neuropathy (Adie syndrome), not with syphilis.
When penicillin became widely available in the 1940s, the prevalence of AR pupils (which develop only after decades of untreated infection) decreased dramatically. A patient whose pupil “accommodates but does not react” almost always has a tonic pupil, not an AR pupil.
In the 1950s, Loewenfeld distinguished between the two types of pupils by carefully observing the exact way in which the pupils constrict with near vision.
The near response in AR pupils is brisk and immediate.
The pathophysiologic mechanism which produces an Argyll Robertson pupil is unclear, but is believed to be the result of bilateral damage to the pretectal nuclei in the midbrain.Studies have failed to demonstrate a focal localising lesion.