Correct!
The bilateral centrocecal scotomas on the visual field examination are the chief clues to localization and pathogenesis! Such defects occur from selective
damage to the retinal ganglion cells located in the fovea and between the fovea and optic disc. Their axons are unmyelinated. Toxic, nutritional, and
hereditary optic neuropathies do that kind of damage, affecting mitochondria.
Optic neuritis does not usually cause such centrocecal scotomas. It causes vision loss more quickly and preferentially affects myelinated axons, which lie
mostly outside the maculopapillar bundles.
Compressive optic neuropathy would be expected to produce asymmetric damage to the optic nerves, and therefore an afferent pupil defect. It would not produce
such centrocecal defects.
This patient had had been treated with ethambutol for tuberculosis. Optic nerve toxicity is rare at daily ethambutol doses below 15mg/kg unless the patient
has reduced clearance from kidney disease. Scrupulous visual acuity and color vision monitoring is critical in patients treated with ethambutol because vision
loss may become irreversible—and especially disabling as it is binocular!