Marcus Gunn pupil
Summary
Marcus Gunn pupil is a relative afferent pupillary defect (RAPD): when a light is swung from the normal eye to the affected eye, both pupils paradoxically dilate instead of constricting. It indicates unilateral or asymmetric optic nerve or severe retinal disease, such as optic neuritis in multiple sclerosis.
Detail
DEFINITION: Marcus Gunn pupil, also called a relative afferent pupillary defect (RAPD), is an asymmetry in the afferent limb of the pupillary light reflex. It is found with the swinging flashlight test.
PATHOPHYSIOLOGY (pupillary light reflex pathway): - Afferent limb: retinal ganglion cells -> optic nerve (CN II) -> optic chiasm -> optic tract -> pretectal nucleus (midbrain). Pretectal neurons then project bilaterally to both Edinger-Westphal nuclei. - Efferent limb: Edinger-Westphal nucleus -> CN III (parasympathetic) -> ciliary ganglion -> short ciliary nerves -> pupillary sphincter muscle -> miosis. - Because of the bilateral projection from the pretectal nuclei, light in one eye causes both pupils to constrict (direct and consensual reflexes). - With a damaged afferent limb in one eye, less signal reaches the midbrain when that eye is lit. Both pupils constrict less (or dilate relative to the response when the healthy eye is lit).
SWINGING FLASHLIGHT TEST: - Light the normal eye: both pupils constrict. - Swing quickly to the affected eye: both pupils dilate, or show paradoxical dilation, because the input is weaker. - Swing back to the normal eye: both pupils constrict again. - Anisocoria is NOT present in a pure RAPD. The efferent pathway is intact, so pupil sizes are equal at rest.
CAUSES (unilateral or asymmetric disease of the optic nerve or severe retina): - Optic neuritis (classic; associated with multiple sclerosis; pain with eye movement, central scotoma, color desaturation) - Ischemic optic neuropathy (e.g., giant cell arteritis, nonarteritic AION) - Glaucoma (asymmetric advanced) - Optic nerve compression or trauma (e.g., tumor, orbital mass) - Extensive retinal detachment - Central retinal artery or vein occlusion - Severe macular degeneration (less common)
KEY POINTS: - Cataract, vitreous hemorrhage, and corneal opacities do NOT cause an RAPD, unless they are extremely dense. Mild media opacity may even produce a slight opposite-side effect from light scatter. - Lesions of the optic tract can cause a mild contralateral RAPD, because of the asymmetry between nasal and temporal retinal fibers (the contralateral eye has more crossed fibers). - Lesions behind the pretectal nuclei (e.g., occipital cortex) do not cause an RAPD, because the pupillary pathway branches off before the lateral geniculate nucleus. Cortical blindness therefore leaves pupillary reflexes intact. - Bilateral symmetric optic nerve disease may not produce an RAPD, since there is no difference between the eyes. - Efferent defects (CN III palsy) cause anisocoria with a poorly reactive pupil. Unlike an RAPD, the affected pupil is abnormal in size. - Compare: Argyll Robertson pupil (accommodates but does not react; neurosyphilis) and Horner syndrome (miosis, ptosis, anhidrosis; sympathetic lesion).
CLINICAL PEARL: The finding is named after Robert Marcus Gunn, a Scottish ophthalmologist. On Step questions, "swinging flashlight causes paradoxical dilation" + "pain with eye movement in a young woman" = optic neuritis -> MRI of brain for MS lesions. Treatment of acute optic neuritis is IV high-dose methylprednisolone.
Sources
- First Aid for the USMLE Step 1 (Neurology and Ophthalmology sections)
- Kaplan USMLE Step 1 Lecture Notes: Neuroscience
- Bates' Guide to Physical Examination and History Taking (cranial nerve and eye exam)
- Kanski's Clinical Ophthalmology
- AAO Basic and Clinical Science Course: Neuro-Ophthalmology
- Pathoma/Boards and Beyond: Neuroanatomy of the pupillary light reflex
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