History
Mrs. Lau was a 50-year-old lady. She was a non-smoker and non-drinker. She had a past medical history of diabetes, hyperlipidemia, and gastrointestinal stromal tumor with resection performed.
She presented with a 3-month history of gradual, simultaneous onset, asymmetrical, progressive bilateral blurring of vision. Her vision worsened until she could only perceive light.
There was no fever or headache.
Physical examination
Physical examination was pertinent for a right relative afferent pupillary defect, bilateral partial visual field defect (central scotoma, constricted vision), and failed Ishihara tests.
There was no disc swelling.
Investigations
A contrast MRI brain and orbit demonstrated abnormal thickening of both optic nerve sheaths with T2 hyperintensities and contrast enhancement.
CSF biochemistry was not suggestive of meningeal inflammation. Oligoclonal bands were absent.
Myelin oligodendrocyte glycoprotein antibody was weakly positive.
Thought process
The pathology was likely localized to the optic nerves.
Given the compatible clinical syndrome and positive antibody, the etiology was likely MOG associated disease.
Next steps
Mrs. Lau was treated with pulse steroids. There was an exquisite clinical response.
The pulse steroids were followed by rapid oral taper. This was temporally related to a recurrence of her visual symptoms.
It has been postulated that a slow oral glucocorticoid taper over a few months may reduce the risk of early relapse. She was therefore resumed on high dose oral steroids before reattempting a slow taper.