Abstract
Multiple sclerosis (MS) is an autoimmune disorder affecting the central nervous system, with varying clinical manifestations such as optic neuritis, sensory disturbances, and brainstem syndromes. Disease progression is monitored through methods like MRI scans, disability scales, and optical coherence tomography (OCT), which can detect retinal thinning, even in the absence of optic neuritis. MS progression involves neurodegeneration, particularly trans-synaptic degeneration, which extends beyond the initial injury site. This review focuses on the impact of different MS treatments on retinal thickness as assessed by OCT. Injectable drugs, such as interferon beta and glatiramer acetate (GA), have a relatively modest impact on retinal atrophy. Oral medications like Fingolimod, Teriflunomide, and Dimethyl fumarate also have different impacts on retinal thickness. Fingolimod has been shown to protect against retinal thinning but may lead to macular edema. DMF-treated patients had less ganglion cell-inner plexiform layer thinning than GA-treated patients but more thinning compared to natalizumab-treated patients and healthy controls. Teriflunomide's impact on retinal layers remains unexplored in human studies. Monoclonal antibodies, including Alemtuzumab, Rituximab, Ocrelizumab, and Natalizumab, had protective effects on retinal layer atrophy. Alemtuzumab-treated patients showed significantly less atrophy compared to interferon- and GA-treated patients. Rituximab initially increased atrophy rates in the first months but subsequently demonstrated potential neuroprotective effects. Ocrelizumab slowed the rate of inner nuclear layer thinning in progressive forms of the disease. Natalizumab is considered the most effective in reducing retinal layer atrophy, particularly the peripapillary retinal nerve fiber layer. It's important to note that the effectiveness of these treatments may vary depending on MS subtype and individual factors. Future research should explore the long-term effects of these treatments on retinal layers and their correlations with overall disease progression and disability in MS patients.
Published Version
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