Lights Out

A 78 year-old man presented with a one-month history of progressive painless binocular vision loss. Hehad sustained head trauma without loss of consciousness three days prior to the onset of vision loss. Onthe morning of his presentation to us, he had awoken with complete binocular vision loss and had beenstarted on oral prednisone (70 mg daily) by his local eye care provider. He denied symptoms of giantcell arteritis. His past medical history was remarkable for hypertension, diabetes, and a distant history ofprostate cancer that was thought to be in remission. Neurologic review of systems was unremarkable.Examination revealed no light perception OU. The pupils were dilated and minimally reactive to light.There was no RAPD. Intraocular pressures were within normal limits OU. Extraocular movements werefull OU. Anterior segment examination revealed pseudophakia OU. Dilated funduscopic examinationrevealed diffuse optic atrophy OU. Neurologic examination was unremarkable.There were no choroidal filling defects or perfusion abnormalities on fundus fluorescein angiography.ESR, CRP, and PSA were all within normal limits. MRI brain revealed enlargement and heterogeneousenhancement of the optic chiasm. An enhancing lesion was seen adjacent to the anterior horn of the rightlateral ventricle. CSF examination revealed markedly elevated protein and glucose levels, with negativecultures, cytology, and flow cytometry. Bone scan was negative for bony metastases. In an attempt toimprove his vision, intravenous methylprednisolone was given for five days, followed by a taper of oralprednisone over seven days. The right frontal lesion decreased in size dramatically with the steroidtreatment, making biopsy difficult, but his vision did not improve. Repeat MRI brain obtained twoweeks after completion of the steroids revealed interval growth of the right frontal lesion, withsurrounding vasogenic edema, and growth of the chiasmal lesion. A diagnostic procedure wasperformed