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Bitemporal haemianopsia is the classic visual field defect of disorders that involve the optic chiasm, caused by the involvement of the crossing nasal–retinal fibres of each optic nerve. Chiasmal visual field defects are usually categorised as extrinsic because of mechanical compression from adjacent structures, although lesions involving the substance of the chiasm itself also exist.1
We describe a unique case of chiasmal neuritis, a woman with serologically proven neuromyelitis optica (NMO).2 Our study addresses the cortical consequences of this acquired bitemporal haemianopsia. Functional MRI (fMRI) was used to evaluate the cortical activation patterns and its correspondence with visual field representation during the attack and subsequent recovery.
A 36-year-old woman presented with acute bilateral visual loss progressing during several days before her admission. Her history included serologically positive myasthenia gravis at the age of 10 years, which required immunosuppressive treatment that led to clinical remission and cessation of all drug treatment at age 13 years. She was asymptomatic until age 26 years, when she presented with an episode of transverse myelitis. Since then, she has had another three severe myelitic episodes, without optic nerve involvement and was, therefore, under maintained treatment of prednisone and cyclophosphamide. Six months before her current admission, she was tested positive for NMO–immunoglobulin.2 To note is that her daily cyclophosphamide dosage was reduced just before her current admission. Her clinical examination revealed a parapyramidal syndrome with sensory level at T5 and mild left optic disc temporal pallor. No relative afferent pupillary defect was detected. Snellen visual acuity measurements were 6/60 …
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