Pupillary abnormalities

Deborah I Friedman MD MPH (

Dr. Friedman received honorariums from Alder BioPharmaceuticals, Allergan, Amgen/Novartis, Biohaven Pharmaceuticals, electroCore, Revance, Supernus, Teva, and Zosano  as an advisory board member and/or speaker; honorariums and grant support from Autonomic Technologies, Eli Lily, and Merck as clinical trial investigator; and honorariums from Promius as a consultant.

Jonathan D Trobe MD, editor. (Dr. Trobe of the University of Michigan has no relevant financial relationships to disclose.)
Originally released August 28, 1998; last updated August 5, 2014; expires August 5, 2017
Notice: This article has expired and is therefore not available for CME credit.


Does the patient have an aneurysm or physiologic anisocoria? The pupil exam is to the eye what the deep tendon reflexes are to the neurologic exam: objective, helpful, and difficult to fake. The author discusses causes of anisocoria and abnormal pupillary activity. Her “low tech” algorithm leads the clinician through the evaluation process to know whether the patient can be reassured or needs additional testing.

Key points


• The “no fail” pupil examination includes: measurement of the pupil size in the light and in the dark, assessment of the pupillary light reaction in each eye, and the swinging flashlight test to determine the presence of a relative afferent pupillary defect. If 1 or both pupils do not react well to light, check the near response.


• Parasympathetic pupils (Adie tonic pupil, oculomotor palsy pupil) look the same but may be distinguished by the company they keep. Consider diplopia, ptosis (oculomotor palsy), light-near dissociation, and vermiform movements of the iris sphincter (Adie pupil).


• Apraclonidine is useful for pharmacologic testing of a suspected Horner syndrome and, unlike cocaine drops, is commercially available.

Historical note and terminology

Around 200 AD, Galen likened the iris to an elastic circular ring that was passively inflated or deflated by vital spirits sent from the brain to enhance vision. It was not until the first half of the 18th century that it became widely accepted that iris movement and pupil size were due to active interaction of 2 iris muscles: a longitudinal radial dilator and a circular sphincter muscle.

Many contributions to our understanding of pupillary physiology and pathology were made in the 20th century, including the description of the swinging flashlight test for assessing a relative afferent pupillary defect (Thompson 2003).

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