Bilateral Visual Loss With Normal Pupillary Light Reaction
Bilateral Visual Loss With Normal Pupillary Light Reaction
A 77-year-old man awoke with blurred vision in each eye. His vision had been normal the night before. He had no headaches, jaw claudication, or other symptoms of giant cell arteritis. He denied any other focal neurologic deficits.
His past ocular history was notable for cataract extraction in both eyes. Routine examination 10 months prior had showed his vision to be 20/25 in the right eye and 20/40 in the left eye. He was taking aspirin and digoxin for a prior medical history of myocardial infarction and hypertension, and he had a 50 pack-year smoking history.
At presentation, best-corrected visual acuity was 20/400 OD and counting fingers at 6 inches OS. He was unable to identify any of the Ishihara pseudoisochromatic color plates with either eye. His pupils reacted briskly to light, and there was no relative afferent pupillary defect. With the exception of well-centered posterior chamber intraocular lenses in each eye, slit lamp examination and dilated funduscopy were unremarkable. He underwent kinetic perimetry (Figures 1A and 1B), which revealed a dense left homonymous hemianopia to the size V stimulus.
(Enlarge Image)
Homonymous hemianopia.
(Enlarge Image)
Homonymous hemianopia.
The search for lesion(s), which produces bilateral loss of acuity with normal pupillary light reaction, should be targeted to the following area:
View the correct answer.
<p>Visual pathways posterior to the lateral geniculate nuclei (LGN)</p>
A 77-year-old man awoke with blurred vision in each eye. His vision had been normal the night before. He had no headaches, jaw claudication, or other symptoms of giant cell arteritis. He denied any other focal neurologic deficits.
His past ocular history was notable for cataract extraction in both eyes. Routine examination 10 months prior had showed his vision to be 20/25 in the right eye and 20/40 in the left eye. He was taking aspirin and digoxin for a prior medical history of myocardial infarction and hypertension, and he had a 50 pack-year smoking history.
At presentation, best-corrected visual acuity was 20/400 OD and counting fingers at 6 inches OS. He was unable to identify any of the Ishihara pseudoisochromatic color plates with either eye. His pupils reacted briskly to light, and there was no relative afferent pupillary defect. With the exception of well-centered posterior chamber intraocular lenses in each eye, slit lamp examination and dilated funduscopy were unremarkable. He underwent kinetic perimetry (Figures 1A and 1B), which revealed a dense left homonymous hemianopia to the size V stimulus.
(Enlarge Image)
Homonymous hemianopia.
(Enlarge Image)
Homonymous hemianopia.
The search for lesion(s), which produces bilateral loss of acuity with normal pupillary light reaction, should be targeted to the following area:
Visual pathways posterior to the lateral geniculate nuclei (LGN)
Optic nerve
The optic chiasm
None of the above -- factitious vision loss is the only scenario that can produce these findings
View the correct answer.
<p>Visual pathways posterior to the lateral geniculate nuclei (LGN)</p>
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