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A 35 year old man reports slowly progressive vision loss in both eyes of many months’ duration. Visual acuity is 20/200 (6/60, 0.1) in both eyes. There is no afferent pupil defect. Optic discs show mild temporal pallor, but the examination is otherwise normal. These are the visual fields.
Where is the lesion?
Incorrect
Correct!
The visual field defects are “cecocentral scotomas” (also called “centrocecal scotomas”) because they affect the visual field that lies between fixation
and the physiologic blind spot. Whenever you encounter this pattern of visual field loss in both eyes, think mitochondria of retinal ganglion cells, even
though the optic disc pallor will make you think that this is an optic neuropathy. These conditions are confusingly labeled as optic neuropathies!
The unmyelinated axons of the damaged retinal ganglion cells lie in the temporal portion of the optic disc, which is why that portion of the optic disc eventually appears pale.
The pathology thins out the retinal nerve fiber layer around the fovea and between the fovea and the optic disc, which will be evident on optical
coherence tomography (OCT).
Toxic, metabolic (including nutritional deficiency), and hereditary conditions are behind this kind of damage. Here are some of the common causes: ethambutol toxicity, thiamine (B1) and hydroxycobalamin (B12) deficiencies, alcoholism, starvation diets, non-adherence to vitamin supplementation after bariatric surgery, dominant (OPA 1) and Leber hereditary optic neuropathies.
This patient admitted to severe alcoholism. Treatment consisted of heavy thiamine dosing and abstinence. Vision is more likely to recover if the patient is adherent to the treatment regimen, if the optic discs have not developed pallor, and if OCT does not show thinning. Hence the importance of early diagnosis, especially in patients taking ethambutol, where scrupulous monitoring of visual acuity and color vision is advisable, so that the medication can be discontinued at the first sign of optic nerve toxicity.
The unmyelinated axons of the damaged retinal ganglion cells lie in the temporal portion of the optic disc, which is why that portion of the optic disc eventually appears pale.
Toxic, metabolic (including nutritional deficiency), and hereditary conditions are behind this kind of damage. Here are some of the common causes: ethambutol toxicity, thiamine (B1) and hydroxycobalamin (B12) deficiencies, alcoholism, starvation diets, non-adherence to vitamin supplementation after bariatric surgery, dominant (OPA 1) and Leber hereditary optic neuropathies.
This patient admitted to severe alcoholism. Treatment consisted of heavy thiamine dosing and abstinence. Vision is more likely to recover if the patient is adherent to the treatment regimen, if the optic discs have not developed pallor, and if OCT does not show thinning. Hence the importance of early diagnosis, especially in patients taking ethambutol, where scrupulous monitoring of visual acuity and color vision is advisable, so that the medication can be discontinued at the first sign of optic nerve toxicity.
Incorrect
Incorrect