Updated: Mar 29, 2021
  • Author: Eric R Eggenberger, DO, MS, FAAN; Chief Editor: Edsel B Ing, MD, PhD, MBA, MEd, MPH, MA, FRCSC  more...
  • Print


Anisocoria, or unequal pupil sizes, is a common condition. The varied causes have implications ranging from benign to life-threatening, and a clinically guided history and examination is the first step in establishing a diagnosis.



The causes of anisocoria are varied, and relate to alterations of the autonomic nervous system and/or the iris muscle.

From the autonomic nerve standpoint, the parasympathetic system constricts the iris, whereas the anatomically distinct sympathetic channels dilate the iris. The sympathetic system begins in the hypothalamus, descends through the brain stem (including the lateral medulla) and into the cervical cord to synapse in the ciliospinal center of Budge-Waller at the C8-T1 level. The second-order neuron then exits the C8-T1 nerve root, travels over the lung apex, and ascends to the superior cervical ganglia with the carotid artery. The third-order neuron leaves the superior cervical ganglia to ascend as a plexus around the internal carotid artery through the cavernous sinus, where fibers destined for the pupil dilator and the Mueller muscle of the eyelid travel with the trigeminal nerve through the superior orbital fissure to their orbital targets. Fibers destined to modulate sweating of the face travel with the external carotid artery.

The parasympathetic fibers begin in the Edinger-Westphal subnucleus of cranial nerve III in the midbrain. Parasympathetic fibers travel with the oculomotor (cranial nerve III) nerve, traverse the cavernous sinus, and enter the orbit via the superior orbital fissure to synapse in the ciliary ganglia. The short ciliary nerves then innervate the iris sphincter and muscles of accommodation.




United States

Anisocoria is common, although no overall prevalence statistics are available. The incidence and prevalence data for anisocoria vary by the specific pathophysiology and population. The presence of physiologic anisocoria has been estimated at 20% of the normal population, so some degree of pupil difference may be expected in at least 1 in 5 clinic patients.


Mortality and morbidity rates associated with anisocoria depend entirely upon the specific pathophysiology.

Several causes of anisocoria are life threatening, including Horner syndrome due to carotid dissection or third nerve palsy due to an aneurysm or uncal herniation.  Anisocoria may also be caused by sight-threatening origins, such as angle closure glaucoma.  Yet other causes of anisocoria are completely benign (eg, simple or physiologic anisocoria), although the unnecessary evaluation of these disorders may produce morbidity inadvertently.