Structure-Function Relationship of Retinal Ganglion Cells in Multiple Sclerosis.

The retinal ganglion cells (RGC) may be considered an easily accessible pathophysiological site of degenerative processes in neurological diseases, such as the RGC damage detectable in multiple sclerosis (MS) patients with (HON) and without a history of optic neuritis (NON). We aimed to assess and interrelate RGC functional and structural damage in different retinal layers and retinal sites. We included 12 NON patients, 11 HON patients and 14 healthy controls for cross-sectional multifocal pattern electroretinography (mfPERG) and optical coherence tomography (OCT) measurements. Amplitude and peak times of the mfPERG were assessed. Macula and disc OCT scans were acquired to determine macular retinal layer and peripapillary retinal nerve fiber layer (pRNFL) thickness. In both HON and NON patients the foveal N2 amplitude of the mfPERG was reduced compared to controls. The parafoveal P1 peak time was significantly reduced in HON only. For OCT, parafoveal (pfGCL) and perifoveal (pGCL) ganglion cell layer thicknesses were decreased in HON vs. controls, while pRNFL in the papillomacular bundle sector (PMB) showed reductions in both NON and HON. As the mfPERG derived N2 originates from RGC axons, these findings suggest foveal axonal dysfunction not only in HON, but also in NON patients.

MS optic neuritis-induced long-term structural changes within the visual pathway.

BACKGROUND: The visual pathway is commonly involved in multiple sclerosis (MS), even in its early stages, including clinical episodes of optic neuritis (ON). The long-term structural damage within the visual compartment in patients with ON, however, is yet to be elucidated. OBJECTIVE: Our aim was to characterize visual system structure abnormalities using MRI along with optical coherence tomography (OCT) and pattern-reversal visual evoked potentials (VEPs) depending on a single history of ON. METHODS: Twenty-eight patients with clinically definitive MS, either with a history of a single ON (HON) or without such history and normal VEP findings (NON), were included. OCT measures comprised OCT-derived peripapillary retinal nerve fiber layer (RNFL) and macular ganglion cell/inner plexiform layer (GCIPL) thickness. Cortical and global gray and white matter, thalamic, and T2 lesion volumes were assessed using structural MRI. Diffusion-weighted MRI-derived measures included fractional anisotropy (FA), mean (MD), radial (RD), and axial (AD) diffusivity within the optic radiation (OR). RESULTS: Mean (SD) duration after ON was 8.3 (3.7) years. Compared with the NON group, HON patients showed significant RNFL (p = 0.01) and GCIPL thinning (p = 0.002). OR FA (p = 0.014), MD (p = 0.005), RD (p = 0.007), and AD (p = 0.004) were altered compared with NON. Global gray and white as well as other regional gray matter structures did not differ between the 2 groups. CONCLUSION: A single history of ON induces long-term structural damage within the retina and OR suggestive of both retrograde and anterograde neuroaxonal degeneration.