A 34-year-old, recently diagnosed HIV-positive male presented to us with complaints of sudden painless decrease in vision in both eyes, 1 week before. On ocular examination, patient denied perception of light with indirect ophthalmoscope in dark room. Pupils were equal in size, and direct and consensual reflexes were normal. Ocular movements were full. Anterior segment slit lamp biomicroscopy and fundus examination with indirect ophthalmoscope were clinically within the normal limits. Systemic evaluation revealed no definite focal neurological deficits.
A clinical diagnosis of cortical blindness was made. The patient underwent visual evoked potential (VEP) and magnetic resonance imaging (MRI). VEP showed non-recordable response (Figure 1). Axial T2-Flair MRI of the brain and orbit (Figure 2a) showed hyperintense signal intensity lesions bilaterally in the parieto-occipital white matter. Axial T2-Flair diffuse-weighted image (Figure 2b) showed hyperintense lesions bilaterally in the parieto-occipital white matter. MR spectroscopy showed elevated lactate and choline peak and reduction in the N-acetyl aspartate (NAA). These features were suggestive of demyelination. Optic nerve course, caliber, and signals were within the normal limits. Patient was evaluated systemically by the AIDS care physician and neurologist. Clinically, no cognitive or neurological deficits or other manifestations related to parieto-occipital and frontal disease were found. Patient CD4 count was 104 cells/mm3. Blood and CSF analyses to rule out other neurological illness commonly seen in patients with HIV such as cerebral tuberculosis, toxoplasmosis, Cryptococcus infection, or lymphoma were negative. The patient was initiated on highly active antiretroviral therapy (HAART) but refused inpatient treatment. Patient was brought to us few weeks later in an unresponsive state with terminal neurological illness and died within few hours.