Central scotoma
Specialty: Ophthalmology.
Why it occurs
- Retrobulbar or anterior optic neuritis
- Age-related macular degeneration (AMD) in the geographic atrophy phase
- Maculopathy due to drug toxicity (especially associated with hydroxychloroquine or chloroquine in long-term treatments)
- Non-arteritic anterior ischemic optic neuropathy (NAION-NA)
- Leber hereditary optic neuropathy
- Stargardt macular dystrophy
Initial workup
Computerized visual campimetry (10-2 or 24-2 central threshold strategy to accurately map scotoma size and density); Optical Coherence Tomography (OCT) of the retinal nerve fiber layer (RNFL) and the macula; Magnetic Resonance (MRI) of the brain and orbits with gadolinium contrast to assess demyelination or compression of the optic nerve; Visual Evoked Potentials (VEP) to analyze the latency of nerve conduction.
red flags
Sudden or subacute loss of the unilateral central visual field associated with intense pain when performing eye movements, loss of color perception and presence of relative afferent pupillary defect (RAD), indicating an optic neuritis of possible demyelinating etiology.
Standard management
- Methylprednisolone — 1 g intravenous daily divided into single doses for 3 to 5 days for the treatment of acute demyelinating optic neuritis, with the aim of accelerating visual recovery
- Prednisone — orally, progressive decrease regimen after intravenous therapy, usually starting with 1 mg/kg/day to avoid early relapses
- Complex of group B vitamins (vitamin B1, B6 and B12, indicated orally as nutritional support in optic neuropathies of toxic-deficiency origin, although with variable clinical response).
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Ophthalmology
- Listed causes
- 6
- Treatment options
- 3