From time to time the Argyll Robertson pupil has been attributed to a lesion outside the central nervous system, as in the oculomotor nerve, the ciliary ganglion or the ciliary nerves. The most recent proponents of this theory are Nathan and Turner.1 On the basis of 2 cases of their own and of 8 cases collected from the literature, they concluded that the Argyll Robertson pupil may be caused by damage to the peripheral efferent pathway to the iris. They also argued that there must be two efferent routes for pupillary constriction. "Parasympathetic pupilloconstrictor fibers relay not only in the... cells of the ciliary ganglion but also in the more peripherally situated episcleral ganglia." All their evidence, however, was casuistic, and their observations were not complete.
Although they constantly dealt with the problem, they neglected to mention the common diagnostic signs of the Argyll Robertson pupil, which are miosis,
BENDER MB. SYNKINETIC PUPILLARY PHENOMENA AND THE ARGYLL ROBERTSON PUPIL. Arch NeurPsych. 1945;53(6):418–422. doi:10.1001/archneurpsyc.1945.02300060021003
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