The term optic neuritis describes an inflammatory process of a part or whole of the optic nerve. The lesion may involve exclusively the intraocular part of the nerve, defined the papilla or optic disc (thereby causing papillitis), involve both the intraocular part of the nerve and the retrobulbar component, or affect only the retrobulbar part of the nerve. The inflammation may be unilateral or involve both optic nerves. Optic neuritis may be present together with other generalised lesions of the retina or may be limited exclusively to the optic nerve.
AETIOLOGY
From an aetiological point of view, optic neuritis can be divided into primary and secondary forms. The primary forms include idiopathic, inflammatory, neoplastic, granulomatous (granulomatous meningoencephalitis), toxic, deficiency-related (vitamin A deficiency), traumatic (following bulbar proptosis or fracture of the orbit), immune-mediated and infectious forms. Inflammatory diseases originating from the sclera, uvea, retina, central nervous system, orbit (cellulitis or abscesses) and the paranasal sinuses can cause secondary optic neuritis through local spread. Infectious causes of optic neuritis in the dog include distemper virus, fungi (blastomycosis, cryptococcosis, histoplasmosis), ehrlichiosis and toxoplasmosis. In cats, feline infectious peritonitis virus and cryptococcosis are recognized infectious causes of optic neuritis.
In the dog, the primary neoplastic forms of optic neuritis that have been reported include teratoid medulloepithelioma, ganglioma and meningioma. Lymphomas, orbital tumours and neoplasms originating in the nasal cavities or derived from the central nervous system (meningioma) may, on the other hand, lead to secondary involvement of the optic nerve.
CLINICAL SIGNS
Clinically the acute form of optic neuritis has a sudden onset, causing severe visual defects which may lead to irreversible loss of vision. If both optic nerves are involved, the pupils appear mydriatic and do not react to light. In the case that only one optic nerve is affected, the ipsilateral pupil is mydriatic and lacks both the direct and consensual reflexes, while the contralateral pupil reacts normally and the indirect papillary reflex is also present. At ophthalmoscopic examination of an animal with papillitis, the optic disc often has an indistinct border, the surface details are not discernible and the disc is swollen and oedematous with vessels that can appear congested and raised (Fig. 1). The physiological optic cup may no longer be evident and there may be haemorrhages above or at the periphery of the papilla. These signs are often associated with peripapillary retinal involvement with inflammatory oedema with or without retinal detachment. Opacities and exudate may appear in the adjacent vitreous humour. If only the retrobulbar component of the optic nerve is involved there are often no obvious ophthalmoscopic clinical signs, the fundus may appear perfectly normal and the only findings, which depend on whether one or both nerves are involved, are unilateral or bilateral blindness with mydriasis.
In chronic forms of optic neuritis, the optic disc atrophies and appears pale, greyish-coloured and slightly sunken (Fig. 2) with possible attenuation of the retinal vessels. Retinal degeneration with areas of peripapillary hyperreflection may be present.
DIAGNOSIS
In cases of optic neuritis with papillary involvement, the diagnosis is primarily made on clinical grounds. As previously mentioned, localisation of the neuritis to the retrobulbar part of the optic nerve may be ophthalmologically silent and for this reason diagnostic imaging may be useful (ultrasonography, magnetic resonance imaging and computed axial tomography). If central nervous system involvement is suspected, analysis of the cerebrospinal fluid, in association with a specialist neurological examination, may be important. Unless there is an important concomitant involvement of the neuroretina, an electroretinogram of an animal with optic neuritis appears normal, while visual evoked potentials are reduced.
Given the possible infectious aetiology, a full blood count, blood-chemistry profile, protein electrophoresis and chest X-rays should be performed and a causal agent should be searched for using various methods.
In the case of optic neuritis localised to the papilla, the differential diagnoses of papilloedema and pseudopapilloedema must be considered.
TREATMENT
Optic neuritis is very often idiopathic. The use of systemically administered prednisone is suggested in cases of suspected immune-mediated aetiology or granulomatous meningoencephalitis. The dose is 2-4 mg/kg as initial therapy followed by tapered doses over a certain period depending on the signs. This treatment can be combined with other immunosuppressive drugs. In the case that the inflammation has an infectious cause, aetiologically-targeted treatment must be used against the microbe responsible.
Papilloedema
Papilloedema is characterized clinically by swelling of the optic disc which appears enlarged and slightly raised, with twisted retinal vessels on its surface. Unlike papillitis, papilloedema is not strictly related to a reduction in or loss of vision, except in advanced or terminal forms or as a result of the primary lesion that caused it. Papilloedema may be unilateral although more frequently it is bilateral. From a pathogenic point of view, the most probable cause of papilloedema is thought to be stasis of axoplasmic flow at the cribriform plate of the optic nerve as a result of increased intracranial pressure, while obstruction and venous dilatation are considered secondary factors. From an aetiological point of view any space-occupying mass in the central nervous system which increases the pressure of the cerebrospinal fluid can produce papilloedema, even though the most common causes are cerebral tumours such as astrocytomas, microgliomas, meningiomas, oligodendrogliomas and spindle cell sarcomas. Papilloedema may also be secondary to lesions in the orbit, such as neoplasms, haemorrhages, infections or inflammation. Other reported causes include hydrocephalus, polycythaemia and gammopathies which cause hyperviscosity syndrome and systemic hypertension.
Pseudopapilledema
In dogs and cats the layer of retinal fibres is not myelinated. In the dog, myelinisation begins at the level of the cribriform plate of the sclera, causing the characteristic ophthalmoscopic picture of the optic disc (Fig. 3).
There are variations between subjects and between breeds. As a general rule, animals from large breeds may show an excess of myelin or precocious myelinisation which is defined pseudopapilloedema. This has been reported frequently in Retrievers, Toy Poodles, English SpringerSpaniels, German Shepherd dogs, Boxers and Rottweilers. This completely physiological phenomenon, which causes no clinical symptoms, is characterized by a slightly raised optic disc and in some cases the myelinisation can also run along some retinal vessels contributing to giving the optic disc an irregular outline (Fig. 4). This anatomical feature must be differentiated from clinically similar situations such as papillitis and papilloedema.
Suggested readings
- Adamo F, O'Brien R. Use of cyclosporine to treat granulomatous meningoencephalitis in three dogs". 2004 J Am Vet Med Assoc 225 (8): 1211–6
- Gelatt, Kirk N. (2007). Veterinary Ophthalmology (4 rd ed.). Blackwell Publishing
- Garmer NL, Naeser P, Bergman AJ. Reticulosis of the eyes and the central nervous system in a dog. J Small Anim Pract.1981 Jan;22(1):39-45.
- Fischer CA, Jones GT. Optic neuritis in dogs. J Am Vet Med Assoc. 1972 Jan 1;160(1):68-79.
- Palmer AC, Malinowski W, Barnett KC. Clinical signs including papilloedema associated with brain tumours in twenty-one dogs. J Small Anim Pract. 1974 Jun;15(6):359-86.