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Relative afferent pupillary defect

From Wikipedia, the free encyclopedia
(Redirected fromMarcus Gunn pupil)
When one eye's exposure to light creates a muted pupil response in both eyes
For the jaw-winking syndrome, seeMarcus Gunn phenomenon.
Medical condition
Relative afferent pupillary defect
Other namesMarcus Gunn pupil
The leftoptic nerve and theoptic tracts. A Marcus Gunn pupil indicates anafferent defect, usually at the level of theretina oroptic nerve. Moving a bright light from the unaffected eye to the affected eye would causeboth eyes to dilate, because the ability to perceive the bright light is diminished.
SpecialtyOphthalmology,Optometry

Arelative afferent pupillary defect (RAPD), also known as aMarcus Gunn pupil (afterRobert Marcus Gunn), is amedical sign observed during theswinging-flashlight test[1] whereupon the patient'spupils excessivelydilate when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced.

Depending on severity, different symptoms may appear during the swinging flash light test:[citation needed]

Mild RAPD initially presents as a weak pupil constriction, after which dilation occurs.[citation needed]

When RAPD is moderate, pupil size initially remains same, after which it dilates.[citation needed]

When RAPD is severe, the pupil dilates quickly.[citation needed]

Presentation

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Cause

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Normally, the optic nerve is responsible for sensing light while the oculomotor nerve is responsible for contracting the pupil in response to this light.

The most common cause of Marcus Gunn pupil is alesion of theoptic nerve (between the retina and theoptic chiasm) due toglaucoma, a severeretinal disease, or due tomultiple sclerosis. It is named afterScottishophthalmologistRobert Marcus Gunn.[2]A second common cause of Marcus Gunn pupil is a contralateraloptic tract lesion, due to the different contributions of the intact nasal and temporal hemifields.[3]

Diagnosis

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The Marcus Gunn pupil is a relative afferent pupillary defect indicating a decreased pupillary response to light in the affected eye.[3]

In theswinging flashlight test, a light is alternately shone into the left and right eyes. A normal response would be equal constriction of both pupils, regardless of which eye the light is directed at. This indicates an intact direct and consensualpupillary light reflex. When the test is performed in an eye with an afferent pupillary defect, light directed in the affected eye will cause only mild constriction of both pupils (due to decreased response to light from the afferent defect), while light in the unaffected eye will cause a normal constriction of both pupils (due to an intact efferent path, and an intact consensual pupillary reflex). Thus, light shone in the affected eye will produce less pupillary constriction than light shone in the unaffected eye.[citation needed]

Anisocoria is absent. A Marcus Gunn pupil is seen, among other conditions, in unilateraloptic neuritis.[4] It is also common in retrobulbar optic neuritis due tomultiple sclerosis but unreliable in bilateral optic neuritis.[4][5]

A totaloptic nerve (CN II) lesion, in which the affected eye perceivesno light, is very similar to a Marcus Gunn pupil; to distinguish them, in a complete optic nerve lesion shining the light in the affected eye produces zero dilation nor constriction.[citation needed]

See also

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References

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  1. ^"Pupillary Responses".Stanford University School of Medicine. Retrieved2015-11-04.
  2. ^doctor/2687 atWhonamedit?
  3. ^abPearce J (November 1996)."The Marcus Gunn pupil".J. Neurol. Neurosurg. Psychiatry.61 (5): 520.doi:10.1136/jnnp.61.5.520.PMC 1074053.PMID 8937350.
  4. ^abPetzold, Axel; Fraser, Clare L; Abegg, Mathias; Alroughani, Raed; Alshowaeir, Daniah; Alvarenga, Regina; Andris, Cécile; Asgari, Nasrin; Barnett, Yael; Battistella, Roberto; Behbehani, Raed; Berger, Thomas; Bikbov, Mukharram M; Biotti, Damien; Biousse, Valerie (2022)."Diagnosis and classification of optic neuritis"(PDF).The Lancet Neurology.21 (12):1120–1134.doi:10.1016/s1474-4422(22)00200-9.hdl:2078.1/276419.ISSN 1474-4422.PMID 36179757.S2CID 252564095.[permanent dead link]
  5. ^Mumenthaler Neurology 4ed, Thieme 2004, page 486 Demyelinating diseases

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