AI Article Synopsis

  • The study investigates damage to retinal ganglion cells (RGC) in patients with multiple sclerosis, focusing on those with a history of optic neuritis (HON) and those without (NON).
  • Both groups showed reduced foveal amplitude in multifocal pattern electroretinography (mfPERG) compared to healthy controls, indicating potential axonal dysfunction in RGCs.
  • Optical coherence tomography (OCT) findings revealed significant reductions in ganglion cell layer thickness in HON patients and similar, though less pronounced, changes in NON patients.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8037992PMC
http://dx.doi.org/10.3390/ijms22073419DOI Listing

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