Retinal changes

[frodo]

Barriers in Healthcare to the Use of Optical Coherence Tomography Angiography in Multiple Sclerosis

https://link.springer.com/article/10.10 ... 24-00670-1

Retinal Vascular Changes in MS

MS causes not only neuroinflammatory and neurodegenerative changes but also changes in the retinal vascularity: reductions in parafoveal VD in the SVP and in peripapillary VD in MS are described in several studies ([35,36,37]). In contrast, a reduction in the DVP is rarely seen [35, 38] or not observed at all [39].

With regard to the subtypes of MS, to our knowledge there are currently no published data on OCT-A in people with CIS and PPMS. One study suggested a sectoral significant reduction in VD in RRMS [40]. A comparative analysis of RRMS and SPMS showed a decrease in VD and perfusion density in SPMS compared to RRMS, with the greatest reduction observed in SPMS with ON [41].

The history of ON appears to be an important contributing factor to the development of retinal vascular changes in general. A systematic review, which mainly included data from patients with RRMS but also data from patients with other subtypes of MS as well as NMOSD, showed a significant difference in peripapillary VD and VD of the SVC between the ON group (4.96%/4.30%) and the non-ON group (2.28%/2.27%), with a higher decrease in ON eyes [39]. Further, no vessel loss was observed in the fellow eyes or in eyes of patients experiencing non-ON relapses (RRMS or CIS), but ON eyes showed a reduction in the VD of the SVC that reached a plateau between 90 and 180 days, within a first significant vessel loss occurred early after acute ON [42].

The results suggest that the atrophy of neuronal and axonal structures and the reduced VD are closely pathophysiologically linked. Three potential explanations for this currently exist, all of which might contribute to the effect. Firstly, neurodegeneration might lead to reduced metabolic activity and a lower oxygen demand within the RNFL and GCIPL. This could then lead to reduced local blood perfusion as detected by OCT-A and subsequent to the regression of blood vessels. This would also explain why the SVP is more affected than the DVP, as the SVP supplies the RNFL and GCIPL. Secondly, microvascular abnormalities could be part of the primary pathology inducing neurodegeneration. However, neurodegeneration would then be expected to occur after retinal microvascular change, which has not been observed so far. Thirdly, the neurodegeneration and the rarefication of the microvasculature could both be caused by the inflammatory process.

With regard to vision-related QoL, there are currently no published data on the retinal vasculature. However, there is evidence indicating that reduced VD in the SVP is associated with disease duration, visual acuity (high and low contrast visual acuity) [37] and disability (measured by Expanded Disability Status Scale) in MS [37, 43].

Some studies report conflicting results about retinal vascular changes in MS, including an unaffected flow index (MS with and without ON) [44] or even increased VD (MS without ON) [38, 45] in parafoveal SVP. Yet, differences in cohort characteristics (such as sex, ethnicity, small sample size), and heterogenous pre- and postprocessing methodologies are still a challenge to comparability.