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Reversible variable binocular visual field defects with normal colour vision in systemic methotrexate therapy

Poster Details

First Author: S.Srinivas UK

Co Author(s):    R. Haslett              

Abstract Details


The purpose of this poster is to present a unique case of variable binocular visual field defects with decreased vision and preservation of normal colour vision in systemic Methotrexate therapy at a dosage of 25mg per week. The visual field defects of different types, resolved with improved vision on the cessation of Methotrexate therapy.


A 57 year old female nurse presented with worsening decreased vision in both eyes of 10-12 weeks duration in April 2011 in HM Stanley Eye unit, Abergele, North Wales, UK. Her past ophthalmic history was significant with relatively poor vision in left eye from childhood due to strabismic amblyopia. She was treated for esotropia by surgery in childhood but resulted in large angle consecutive exotropia with amblyopia subsequently. She suffered with three attacks of anterior uveitis during previous nine months which were successfully treated with topical Prednisolone and Cyclopentolate eye drops. She also suffered with seven episodes of episcleritis during previous five years which were resolved with Fluorometholone eye drops. She was moderate hyperope of 6 diopters in both eyes. She suffered from psoriatic arthritis and hypertension. She was on systemic medication of Prednisolone 30mg and Methotrexate 12.5 mg per week for her psoriatic arthritis along with 10 mg of Folic acid, Vitamin D3 supplementation and Ramipril for hypertension. She was HLA B27 negative, positive for p-ANCA( Perinuclear anti-neutrophil cytoplasmic antibodies) antibodies, negative for Rheumatoid factor, ANA (Antinuclear antibodies) and ds-DNA (Double stranded DNA) antibodies with elevated ESR (Erythrocyte Sedimentation Rate) and CRP ( C-Reactive Protein) levels from previous investigations.


Examination revealed 0.10 in right eye(RE) and 0.50 vision in left eye(LE) on log Mar chart, with normal anterior and posterior segments in both eyes. Colour vision was normal. Nasal visual defects were detected in both eyes. Optical Coherence Tomography(OCT) revealed normal maculae. Fluctuating decreased vision was noted over next 8 months with variable nasal, central and peripheral constriction field defects at different times. The brain and orbits were normal on MRI. Patient presented again 21 months later with decreased vision of 0.70 in RE and 0.70 in LE of 4 days duration with peripheral constricted visual fields when Methotrexate dosage was increased to 25mg per week and oral Prednisolone was stopped for her worsened arthritis. Vision deteriorated to 1.00 in both eyes over next few weeks. Clinical examination was normal with normal colour vision. Her vision was decreased severely enough to register her as partially sighted. Patient underwent routine blood tests, B12, red cell folate, iron and Ferritin along with Electro diagnostic(EDT) tests. 4 weeks follow up visit revealed improved vision of 0.24 in RE and 0.50 in LE when medication of Methotrexate stopped by patient herself as she noticed that her vision deteriorated following the increase in dosage.


Investigations showed normal maculae on OCT. Blood investigations including full blood count(FBC), serum B12, red cell folate, iron and Ferritin levels were normal. However, ESR and CRP levels were elevated. Electro diagnostic tests(EDTs) including ERG(Electroretinogram) and VEP(Visually Evoked Potentials) were unremarkable with no abnormal patterns. Vision improved to previous acuities of 0.10 in right eye and better than previous visual acuity of 0.32 in left eye following the cessation of Methotrexate therapy by patient herself . Visual field examinations revealed normal visual fields in right eye and a very few missed spots in the left amblyopic eye. Left eye vision was at its best in many years and patient requested to be deregistered as partially sighted as she needed to drive for her work.


Worsened vision with visual defects on increasing the dosage of Methotrexate to 25 mg per week strongly suggested its association with symptoms. Patient was on supplementation therapy of Folic acid 10 mg to counter the side effects of Methotrexate. Dramatic improved vision with resolved visual fields defects on cessation of Methotrexate therapy by patient herself when she noticed that her vision deteriorated with increased dosage of Methotrexate over a few days suggests the strong association of visual symptoms with Methotrexate. Her vision improved to better then previous visual acuity also suggests and confirms by association that her previous visual disturbances and visual field defects are due to Methotrexate toxicity. Methotrexate related possible posterior toxic optic neuropathy appears to cause visual disturbances with fluctuating vision and visual field defects of various types including central, peripheral & nasal defects. Colour vision does not appear to be affected by Methotrexate toxicity. Methotrexate related toxic optic neuropathy appears to occur despite the supplementation therapy of Folic acid. Visual field defects and visual disturbances due to Methotrexate reported in the literature in the past. FINANCIAL INTEREST: NONE

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