Presumed optic neuritis of non-infectious origin in dogs treated with immunosuppressive medication: 28 dogs (2000-2015).

L Bedos,A Shea,V Crespo,R Tetas

doi:10.1111/jsap.13233

Abstract

To describe the clinical findings, magnetic resonance imaging features, management and outcome of canine cases with presumed optic neuritis of non-infectious origin that were presented to a UK referral centre from January 2000 to December 2015. The clinical database was searched for optic neuritis. Dogs with acute-onset vision impairment, systemic immunosuppressive treatment and follow-up of ≥6months were included. Information collected included: age; gender; breed; clinical signs and duration; physical, ophthalmic and neurological examination findings; concurrent systemic disease; and results of electroretinogram, magnetic resonance imaging, cerebrospinal fluid analysis, polymerase chain reaction and serology testing for Toxoplasma gondii, Neospora caninum and canine distemper virus, haematology and serum biochemistry profiles, abdominal ultrasound, thoracic radiography, treatment and outcome. Twenty-eight dogs were included, with a total of 48 affected optic nerves. Age at presentation ranged from 6 months to 10.5 years. Fundoscopic evidence of optic nerve disease was present in 34 of 48 (71%) optic nerves. Magnetic resonance imaging revealed enlargement of 32 of 48 (67%) nerves and contrast enhancement of 28 of 48 (58%) nerves. Cerebrospinal fluid analysis performed in 25 of 28 (89%) dogs revealed pleocytosis (>5 nucleated cells/uL) in 11 of 25 (44%) and increased protein (>0.35 g/L) in 11 of 25 (44%). Immunosuppressive prednisolone was administered to all dogs. Prednisolone was used alone in 9 of 28 (32%) dogs; the remaining 19 dogs received a combination of prednisolone with cytosine arabinoside, cyclosporine and/or azathioprine. Vision was recovered in 24 eyes (50%) of 18 affected dogs. A positive response to treatment was observed in 64% of dogs with presumptively diagnosed optic neuritis treated with immunosuppressive medication.

Highlights

The optic nerve (CN II) is formed by the axons of the retinal ganglion cells, whose soma are found in the innermost part of the retina (Glass & DeLahunta 2009)
Clinical significance: A positive response to treatment was observed in 64% of dogs with presumptively diagnosed optic neuritis treated with immunosuppressive medication
Inclusion criteria included all canine cases with presumptive diagnoses of optic neuritis (ON) that underwent complete physical examination, ophthalmic examination, neurological examination, full haematology and comprehensive serum biochemistry pro- files, serological titres or polymerase chain reaction testing [per- formed on blood or cerebrospinal fluid (CSF)] for infectious diseases (Toxoplasma gondii, Neospora caninum, Canine distemper virus); 1.5T MRI scanner (Signa Echospeed, General Electric, Milwaukee, WI) of the head; and a minimum of 6 months’ follow-up during which there was no evidence of progression that would be incompatible with, or call into question, a diagnosis of a primary inflammatory condition

Summary

Introduction

The optic nerve (CN II) is formed by the axons of the retinal ganglion cells, whose soma are found in the innermost part of the retina (Glass & DeLahunta 2009). Differential diagnoses for acute onset of blindness in dogs include sudden acquired retinal degeneration syndrome (SARDS) (Montgomery et al 2008), retinal detachment, glaucoma (Grozdanic et al 2007), retrobulbar disease (Mason et al 2001), optic neuritis (ON) and tumours affecting the visual pathways (Davidson et al 1991, Seruca et al 2010). Less commonly, conditions such as cerebrovascular ischaemic infarction, head trauma The use of MRI in conjunction with full physical, neurologic and ophthalmic examination, cerebrospinal fluid (CSF) analysis and serological testing are paramount to detection and characterisation of ON in dogs (Armour et al 2011)

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