Adibi Armin, Adibi Iman, Javidan Milad
Department of Neurology, Isfahan University of Medical Sciences, Isfahan, Iran.
Neuroscience Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
CNS Neurosci Ther. 2025 Jan;31(1):e70225. doi: 10.1111/cns.70225.
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.
多发性硬化症（MS）是一种影响中枢神经系统的自身免疫性疾病，具有多种临床表现，如视神经炎、感觉障碍和脑干综合征。通过MRI扫描、残疾量表和光学相干断层扫描（OCT）等方法监测疾病进展，这些方法即使在没有视神经炎的情况下也能检测到视网膜变薄。MS的进展涉及神经退行性变，特别是跨突触变性，其范围超出了初始损伤部位。本综述重点关注不同MS治疗方法对OCT评估的视网膜厚度的影响。
注射用药物，如干扰素β和醋酸格拉替雷（GA），对视网膜萎缩的影响相对较小。口服药物，如芬戈莫德、特立氟胺和富马酸二甲酯，对视网膜厚度也有不同影响。芬戈莫德已被证明可预防视网膜变薄，但可能导致黄斑水肿。与GA治疗的患者相比，接受DMF治疗的患者神经节细胞-内丛状层变薄较少，但与那他珠单抗治疗的患者和健康对照相比，变薄更多。在人体研究中，特立氟胺对视网膜层的影响尚未得到探索。单克隆抗体，包括阿仑单抗、利妥昔单抗、奥瑞珠单抗和那他珠单抗，对视网膜层萎缩有保护作用。与干扰素和GA治疗的患者相比，接受阿仑单抗治疗的患者萎缩明显较少。利妥昔单抗最初在最初几个月增加了萎缩率，但随后显示出潜在的神经保护作用。奥瑞珠单抗减缓了疾病进展形式的内核层变薄速度。那他珠单抗被认为在减少视网膜层萎缩方面最有效，特别是视乳头周围视网膜神经纤维层。
需要注意的是，这些治疗方法的有效性可能因MS亚型和个体因素而异。未来的研究应探索这些治疗方法对视网膜层的长期影响及其与MS患者整体疾病进展和残疾的相关性。
