Optic neuritis: new therapeutic strategies

ARANDA, MARCOS L.; DEVOUASSOUX, JULIÁN D.; KELLER SARMIENTO, MARÍA I.; ROSENSTEIN, RUTH E; GONZÁLEZ FLEITAS, MARÍA F.; ALTSCHULER, FLORENCIA; SANDE, PABLO H.; DIEGUEZ, HERNÁN H.; CHIANELLI MÓNICA S; DORFMAN, DAMIÁN

The Optic Nerve: Structure, Functions and Clinical Aspects

Nova Science Publishers

Lugar: New York; Año: 2019; p. 67 - 102

Optic neuritis, the most common optic neuropathyaffecting young adults, is a condition involving primary inflammation,demyelination, and axonal injury in the optic nerve which leads to retinalganglion cell death and visual dysfunction. Clinical features of optic neuritisinclude peri- or retro-ocular pain accentuated by eye movement, abnormal visualacuity and field, distorted color vision, afferent pupillary defect, andabnormal visual evoked potentials. Optic neuritis manifests as acute and severedecreased vision for 1 - 2 weeks, then self-recovers over 1 - 3 months in mostof the patients; however, varying degree of permanent visual dysfunction canoccur in ~ 50% of patients. Even if visual acuity improves, most patients havesome residual visual function deficits. Moreover, repeated episodes of opticneuritis can result in optic nerve atrophy and vision loss, which correlateswith retinal ganglion cell loss.Optic neuritis has many causes; it may be associatedto a broad range of autoimmune or infectious diseases, and it is closelyassociated with multiple sclerosis. On the other hand, acute optic neuritisoften occurs as an isolated clinical event, without contributory systemicabnormalities, and it is retrospectively diagnosed as idiopathic (or primary)optic neuritis.Corticosteroids are the current mainstays of therapy for thetreatment of ON.However, though steroids can be used to speed visual recovery,the overall visual improvement is unaffected by treatment (Beck and Gal, 2008).In fact, corticosteroids do not prevent axonallossor improve visual outcome(Gal et al., 2015; Hickman et al., 2003). Therefore, a key area of therapeuticresearch is to identify neuroprotective drugs that can prevent axon and RCGloss, and hopefully lead to better visual outcomes. In this chapter, we willdiscuss evidence supporting the neuroprotective effect of two differentstrategies: i) the exposure to enriched environment, and 2) a treatment withmelatonin, a very safe compound (even at high doses) for human use. Bothstrategies prevent and slow down the progression of retinal ganglion cell andoptic nerve damage induced by primary optic neuritis in rodents, and as such,they could be considered as new therapeutic resources for the management ofoptic neuritis.