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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. And, to make matters more confusing, these conditions are usually labeled as optic neuropathies! The unmyelinated axons of those 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 of these conditions (all labeled as optic neuropathies when most of the damage is to retinal ganglion cells): ethambutol toxicity, thiamine (B1) and hydroxycobalamin (B12) deficiencies, alcoholism, starvation diets, non-adherence to vitamin supplementation after bariatric surgery, hereditary dominant (OPA 1) and Leber 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.

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