Pupillary Disorders

Abstract

Pupillary abnormalities range from benign isolated findings to harbingers of significant, even life‐threatening, conditions. A complete understanding of the neuroanatomy underlying the innervations to the antagonistic pupillary sphincter and dilator muscles is essential to detecting, and discerning the importance of, a particular pupillary abnormality. The sphincter muscle receives neuronal input from the parasympathetic division of the autonomic nervous system, whereas the dilator muscle receives input from the sympathetic division. Afferent input carrying light information to the brain is transmitted by retinal ganglion cell axons via the optic nerves, chiasm, and tracts. The parasympathetic innervation to the pupil originates in the Edinger‐Westphal nucleus in the midbrain. The sympathetic innervation to the pupil consists of a three‐neuron pathway originating in the hypothalamus. Important pupillary disorders include physiologic anisocoria, relative afferent pupillary defect, amaurotic pupil, Argyll Robertson pupils, cranial nerve III palsy, pharmacologic mydriasis, tonic pupil, and Horner syndrome. Key Concepts: Examination of the pupil is an important part of the physician's neurological and ophthalmological evaluation of a patient. The size of the pupil is controlled by the actions of antagonistic muscles located within the iris: the pupillary sphincter and dilator. Constriction of the pupils is mediated by the parasympathetic nervous system, whereas dilation of the pupils is mediated by the sympathetic nervous system. Pupillary constriction to light occurs via an involuntary reflex arc. Retinal ganglion cell axons involved in carrying light information for the pupillary light reflex exit the optic tract (proximal to the lateral geniculate nucleus) to synapse in the midbrain pretectal nucleus. The parasympathetic output controlling pupillary constriction originates in the Edinger‐Westphal nucleus in the midbrain and terminates at the pupil sphincter muscle. Pupillary dilation involves a ‘three‐neuron’ sympathetic pathway, which originates in the posterolateral hypothalamus and terminates at the pupil dilator muscle. A relative afferent pupillary defect is caused by a decreased amount of light information from the affected eye reaching the pretectal nuclei in the midbrain and is most commonly a sign of ipsilateral optic nerve pathology. Damage to cranial nerve III can result in injury to the parasympathetic fibres travelling to the pupillary sphincter muscle, thus disrupting the efferent arc of the pupillary light reflex, resulting in deficient pupillary constriction on the involved side. Horner syndrome, characterised by miosis, ptosis, and facial anhidrosis, results from disruption of the oculosympathetic pathway.