Marcus Gunn pupil?

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bgibney

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Sorry to bother you all with what is probably an easy question but...why does the pupil dilate with a Marcus Gunn pupil? I understand that it usually indicates some form of optic neuritis, and therefore understand why it does not constrict, but not quite sure why it dilates. Is there some form of up-regulating sympathetics or down-regulation in parasympathetics? Any help is most appreciated.

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Originally posted by bgibney
Sorry to bother you all with what is probably an easy question but...why does the pupil dilate with a Marcus Gunn pupil? I understand that it usually indicates some form of optic neuritis, and therefore understand why it does not constrict, but not quite sure why it dilates. Is there some form of up-regulating sympathetics or down-regulation in parasympathetics? Any help is most appreciated.

Hi there,

The Marcus Gunn pupil is the same thing as a Relative Afferent Pupillary Defect (RAPD). To understand why a RAPD occurs, you must first know your visual afferent and pupil efferent pathways.

Light hits the retina and a signal travels down the optic nerve. After the optic chiasm and before the optic tract reaches the lateral geniculate nucleus, the pupil afferent fibers break off and go to the Edinger-Westphal nuclei (EWN- pupil control center). The EWN sends efferent fibers to BOTH eyes to control pupil responses to light.

Now, imagine the retina as a light sensor for the pupils. In the RAPD test, a light is swung from one eye to the second eye, and then repeated. If 100 units of light hit the right eye, then BOTH pupils constrict to 100 units of light b/c of equal innervation by the EWN. When the light is swung to the left eye, this eye also detects 100 units of light, and BOTH pupils constrict to 100 units of light. In the normal patient, there's no difference in pupil size with the swinging flashlight test.

In a RAPD, there's a defect in one eye that prevents detection of light relative to the other eye. This relative defect will only exist if there is a lesion that occurs BEFORE the chiasm (althout a chiasmal lesion may produce a RAPD b/c there's unequal crossing of optic nerve fibers, ~52%-48%). These lesions include pre-chiasmal tumors, unilateral trauma, unilateral optic nerve disease (e.g., congenital, sarcoid, optic neuritis, etc...), or unilateral retinal diseases.

Let's assume the left eye has a defect. When 100 units of light are shown in the right eye, BOTH pupils constrict to 100 units of light. When 100 units of light are shown in the defective left eye, the left eye may only detect 50% of the light; thus, BOTH pupils will constrict to 50 units of light, which causes dilation of the pupils when the light is swung from the right to left eye. Notice that BOTH pupils will dilate when the light hits the left eye, but both pupils will constrict when light hits the right eye.
 
Well stated by Dr. Doan. The only additional advice I'd give is that the key to learning Neuro-ophth is learning the pathways. Once you can visualize the pathways, things like RAPD will come easy.
 
Thank you very much Dr. Doan, I appreciate it
 
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