The earlier a firm diagnosiscan be made, the better the prognosis will befor the patient. The systemicmanifestations associated with thiscondition carry life impactingconsequences. The detection of thispupillary anomaly is significant and requiresimmediate referral for neurological, physicaland laboratory evaluations. Patients who present with miotic pupilsshould be further assessed for ArgyllRobertson pupil. The irisatrophies with a loss of its radial folds, and crypts have been reported. The abnormalityin pupillary function begins with a sluggishresponse to light and eventually progressesto a complete loss of the light reflex. The pupillary findings consistent withArgyll Robertson pupils develop over thecourse of months to years. Furthermore, oncethe Adie’s pupil reacts to accommodation, the pupiltends to remain tonically constricted and dilates veryslowly. In Adie’s pupil, which is caused by ciliary ganglion destruction, the reaction to light is absentor greatly diminished when tested in the routine examination however, Adie’s pupil does react slowly withprolonged maximal stimulation. 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.Īrgyll Robertson pupil should not be confused withAdie’s pupil, which may yield a similar result on cursory examination. Research has implicated the rostral midbrain in the vicinity of the sylvian aqueduct of the third ventricle as the most likely region of damage. Studies have failed to demonstrate a focal localizing lesion. The pathophysiologic mechanism which produces an Argyll Robertson pupil is unclear. However, lesions in this region have not been reliably demonstrated in syphilis. Because the Argyll Robertson pupils lack these features, it has been attributed to a dorsal midbrain lesion that interrupts the pupillary light reflex pathway but spares the more ventral pupillary near reflex pathway. Such features are considered typical of the light-near dissociation of Adie syndrome and of neuropathic tonic pupils, where damage to the ciliary ganglion or ciliary nerves is believed to be the mechanism.

Most descriptions of the Argyll Robertson pupils do not mention segmental iris sphincter constriction, or slow, sustained constriction with a near vision effort. It wasn’t until 30 years later that physicians realized the etiology of this pupillary anomaly was a manifestation of tertiary syphilis. In 1869, Douglas Argyll Robertson was the first to describe several patients whose pupils reacted poorly to light with a normal near response. The lesion spares the more ventrally located fibers that subserve the pupil reaction to near stimuli. In an Argyll Robertson pupil, the pupil’s better response to accommodation than to light stimuli occurs because the lesion involves the more dorsally located fibers that subserve the pupil’s response to light. The test requires no special equipment, holds great diagnostic yield, and takes less time to elicit than is needed to pronounce the eponym.

This pupillary reaction (Sidebar) is a simple way to confirm the integrity of the optic pathways and is a marker of such neurological disorders as neurosyphilis, neurosarcoidosis, and multiple sclerosis. The Argyll Robertson pupil, a miotic pupil that responds to an accommodation effort but fails to react to direct light, has been described in medical literature for more than a century. Argyll Robertson pupils: Description, Causes and Risk Factors:Ī form of reflex iridoplegia characterized by miosis, irregular shape, and a loss of the direct and consensual pupillary reflex to light, with normal pupillary constriction to a near vision effort (light-near dissociation) often present in tabetic neurosyphilis.

Argyll robertson pupil