Optic Coherence Tomography Angiography in Multiple Sclerosis: A Tool for Evaluation of Neuroinflammation

Abstract

Purpose: This study aims to evaluate changes in retinal microvasculature in patients with multiple sclerosis (MS) by means of optic coherence tomography angiography (OCTA). Material and Methods: A total of 60 patients with MS (18 clinically isolated syndrome [CIS], 27 relapsing remitting MS [RRMS], 15 secondary progressive MS [SPMS]) and 56 healthy controls participated in the study. Demographic and clinical data, including optic neuritis history, ophthalmic examination findings, and OCTA parameters, were recorded. OCTA parameters included the following vascular structures: vascular density (VD) in the retinal superficial capillary plexus, deep capillary plexus, and radial peripapillary capillaries. Retinal nerve fiber layer as a structural spectral domain optic coherence tomography parameter was also evaluated. Results: Superficial and peripapillary vascular plexus densities and retinal nerve fiber layer thickness values were significantly reduced in patients with MS (p=0.0001). Deep capillary plexus densities showed no difference between groups (p=0.279). Patients with a previous history of optic neuritis (ON+) showed significant reduction in VD, compared to patients without a previous history of optic neuritis (ON-), and control groups (p=0.0001). The SPMS group had lower perifoveal values than patients with RRMS and CIS, and patients with RRMS had lower levels than the CIS group (p=0.012; p=0.03; p=0.035). Expanded disability status scores and VD values inversely correlated (r=-0.264; p=0.003). No significant difference between MS and control groups in the foveal avascular zone was found (p=0.296). Conclusion: OCTA findings showed reduced peripapillary and superficial vascular plexus densities in patients with MS. While this reduction was more prominent in patients with SPMS and history of optic neuritis, patients with CIS and without history of optic neuritis still showed significant reduction compared to healthy controls. These results indicate vascular regression caused by reduced metabolic demand, and microvascular damage caused by chronic inflammation.