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Approach to the patient with anisocoria

Sachin Kedar, MD
Valérie Biousse, MD
Nancy J Newman, MD
Section Editor
Paul W Brazis, MD
Deputy Editor
Janet L Wilterdink, MD


Causes of anisocoria range in seriousness from a normal, physiologic condition to one that is immediately life threatening. When a patient presents with anisocoria, the fear of a serious condition, such as an intracranial aneurysm, often leads clinicians to obtain numerous tests, which are not always necessary. A logical clinical approach appreciating the mechanisms of anisocoria permits prompt recognition of true emergencies and often obviates the need for invasive and costly testing (algorithm 1) [1].


Pupillary size is governed by the balance of actions of two opposing muscle groups of the iris: the dilator and sphincter pupillae. Regulation of the pupillary size is predominantly achieved by reflex mechanisms in response to the amount of ambient light. Other factors influencing pupillary size include patient age, emotional state (adrenergic tone), state of arousal, and intraocular pressure [1,2].

Constriction — Pupillary constriction to light and near stimuli is mediated via parasympathetic (cholinergic) nerve fibers that travel along the third cranial nerve. The pupillary light reflex pathway is a four neuron pathway (figure 1) [1,2]:

Light information from retinal ganglion cells travels though the optic nerves, optic chiasm (where the nasal fibers decussate), and the optic tracts, before synapsing in the pretectal nuclei of the dorsal midbrain. Both pretectal nuclei receive input from both eyes.

Each pretectal nucleus sends axons to both Edinger-Westphal nuclei. This duality of pathways provides the anatomic basis for the consensual response to light (ie, the fact that both pupils constrict equally in response to a light stimulus in one eye).

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Literature review current through: Nov 2017. | This topic last updated: Jul 29, 2017.
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