Optic atrophy refers to death of the retinal ganglion cell axons that comprise the optic nerve with the resulting picture of a pale optic nerve on funduscopy. Optic atrophy is an end stage that arises from myriad causes of optic nerve damage anywhere from the retina to the geniculate. Since the optic nerve transmits retinal information to the brain, optic atrophy is associated with vision loss.
Anything that can compromise ganglion cell function can cause (over time) optic atrophy (and more broadly optic neuropathy).
Risk factors run the gamut from increased intraocular pressure (glaucoma), ischemia, compression (tumors), inflammation, infection, etc. See differential diagnosis.
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Optic atrophy is the end stage of a process causing damage to the optic nerve. Current medical practice is currently unable to return function (regrow axons) to an atrophic optic nerve and at best is able to stabilize whatever function remains. Primary prevention is the goal to prevent loss of axons and optic atrophy (neuropathy).
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History is critical in the diagnosis of optic atrophy since the physician wants to know how the eye arrived at this juncture. If this is not known then a careful history with attention to past medical history including all medications, time course of vision loss, associated symptoms etc. can be helpful.
A complete eye exam including visual field, assessing color and contrast vision, intraocular pressures, looking for afferent pupil defect, and funduscopy should be done.
Optic atrophy is a sign and typically is noted as optic nerve pallor which may be sectoral. This is the end stage of a process resulting in optic nerve damage.
The main symptom of optic atrophy is loss of vision. Any other symptoms are attributable to the underlying process that caused the atrophy (such as pain with angle closure glaucoma.
Optic atrophy is usually not difficult to diagnose but the cause for the optic atrophy may be very difficult to ascertain. Sometimes the cause of vision loss may be difficult to differentiate between subtle optic neuropathy and disease of the retina (or both). Electrophysiology can be helpful (ERG, mERG) in that case.Presented with unexplained optic atrophy the following work up should be considered:
Visual fields 30-2
MRI of brain and orbit with contrast
CT with contrast (check bony disease, sinuses)
Blood pressure and check of cardiovascular health (carotids, etc.)
Glucose, B12, VDRL, ANA, homocysteine, ACE, Antiphospholipid antibodies,
Optic atrophy is not usually difficult to diagnose but might be confused with optic nerve hypoplaia, myelinated nerve fibers, myopic or scleral crescent, or tilted disc.
The causes for optic atrophy include:
Compressive – secondary to papilledema, tumor, bony growth, disc drusen, increased intraocular pressure (glaucoma)
Vascular – arteritic and non-arteritic ischemic optic neuropathy, diabetes,
Inflammatory – sarcoid, systemic lupus, Behcet’s, demyelination (MS),
Infectious – viral, bacterial, fungal infections
Toxic – many medications such as ethambutol, methanol, etc.
Metabolic – diabetes, vitamin deficiency,
Neoplastic – lymphoma, leukemia, tumor,
Genetic – Kjer’s (OPA1), Leber’s optic atrophy, Behr
Radiation optic neuropathy
Traumatic optic neuropathy
The primary management is to intervene before optic atophy is noted or to save remaining function. This will depend on the underlying cause for the optic nerve damage. For instance, intraocular pressure control in glaucoma, control of inflammation in sarcoid, etc.
Medical follow up
Surgical follow up
Studies in glaucoma have shown that the optic nerve has some reserve before vision loss is noted but after that reserve is depleted small changes in nerve fiber loss lead to significant changes in vision loss. Early detection is key since we have not way to replace dead axons.
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