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Key Clinical Updates in Optic Neuritis
Newer therapies include monoclonal antibodies against immune cells and cell-based therapies to deplete or modulate T- and B-cell responses.
Derdelinckx J et al. Int J Mol Sci. [PMID: 34360690]
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ESSENTIALS OF DIAGNOSIS
Subacute, usually unilateral, visual loss.
Pain exacerbated by eye movements.
Optic disk is usually normal in acute stage but subsequently develops pallor.
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GENERAL CONSIDERATIONS
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Inflammatory optic neuropathy is strongly associated with demyelinating disease (typical optic neuritis), particularly multiple sclerosis, but it also occurs in acute disseminated encephalomyelitis; sarcoidosis; neuromyelitis optica spectrum disorder, which is characterized by serum antibodies to aquaporin-4; in association with serum antibodies to myelin oligodendrocyte glycoprotein; following viral infection (usually in children); in varicella zoster virus infection; in autoimmune disorders, particularly SLE and Sjögren syndrome; during treatment with biologics; and by spread of inflammation from the meninges, orbital tissues, or paranasal sinuses.
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Optic neuritis in demyelinating disease is characterized by unilateral loss of vision developing over a few days. Visual acuity ranges from 20/30 (6/9) to no perception of light, with more severe visual loss being associated with low serum vitamin D. In almost all cases there is pain behind the eye, exacerbated by eye movements, central visual field loss, color vision loss, and a relative afferent pupillary defect. In about two-thirds of cases, the optic nerve is normal during the acute stage (retrobulbar optic neuritis). In the remainder, the optic disk is swollen (papillitis) with occasional flame-shaped peripapillary hemorrhages. Visual acuity usually improves within 2–3 weeks and returns to 20/40 (6/12) or better in 95% of previously unaffected eyes. Optic atrophy subsequently develops if there has been extensive optic nerve fiber damage (eFigure 7–65). Any patient without a known diagnosis of multiple sclerosis in whom visual recovery does not occur, or if there is continuing deterioration of vision, or pain persisting after 2 weeks, should undergo MRI of the head and orbits to look for periventricular white matter demyelination or a lesion compressing the optic nerve.
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In acute demyelinating optic neuritis, intravenous methylprednisolone (1 g daily for 3 days followed by a tapering course of oral prednisolone) has been shown to accelerate visual recovery but not to improve final vision. However, in clinical practice, the oral taper is not often prescribed. Use in an individual patient is determined by the degree of visual loss, the state of the other eye, and the patient’s visual requirements. Newer therapies include monoclonal antibodies against immune cells and cell-based therapies to deplete or modulate T and B cell responses.
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Atypical optic neuritis due to sarcoidosis, neuromyelitis optica, herpes zoster, or SLE generally has a poorer prognosis, requires ...