Abstract
The main causes of optic neuritis (ON) are multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody disease, also known as MOGAD. When all screening is negative, we can speak of idiopathic ON, although this diagnosis should be provisional. ON can be diagnosed clinically and paraclinical tests are not routinely required to confirm it. However, tests such as magnetic resonance imaging (MRI), visual evoked potentials (VEP) and optical coherence tomography (OCT) can lend support to the diagnosis if the clinical presentation is atypical. The use of new MRI sequences, OCT, multifocal VEPs and the determination of neurofilaments has allowed ON to be used as a model for remyelination and neuroprotection, leading to phase II clinical trials. Some of these drugs, such as opicinumab, clemastine, phenytoin or simvastatin, have shown positive results; however, their clinical effect remains to be defined. It is accepted that corticosteroids do not improve the long-term prognosis of ON, although some retrospective studies suggest that there is a therapeutic window from the onset of symptoms. Plasmapheresis has also been shown to be effective in patients with ON. In this review we will address basic aspects of the management of ON, in the fundamental context of MS, NMOSD and MOGAD, with emphasis on etiopathogenic, diagnostic, prognostic and therapeutic developments.