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.
Highlights
The retinal ganglion cells (RGC) are of unrivaled interest in the investigation of the ophthalmological conditions, and in many inflammatory and neurodegenerative diseases of the central nervous system (CNS)
Wicki et al reviewing the optical coherence tomography (OCT) utility in multiple sclerosis (MS) [7] reported that the ganglion cell inner plexiform layer (GCIPL) and the inner nuclear layer (INL) are the most widely studied in MS with potential biomarker properties
They indicate that OCT might provide hallmarks of the posterior visual pathway in MS, where peripapillary retinal nerve fiber layer (pRNFL) thinning in NON might be induced by trans-synaptic retrograde degeneration
Summary
The retinal ganglion cells (RGC) are of unrivaled interest in the investigation of the ophthalmological conditions, and in many inflammatory and neurodegenerative diseases of the central nervous system (CNS). Wicki et al reviewing the OCT utility in MS [7] reported that the ganglion cell inner plexiform layer (GCIPL) and the inner nuclear layer (INL) are the most widely studied in MS with potential biomarker properties They indicate that OCT might provide hallmarks of the posterior visual pathway in MS, where pRNFL thinning in NON might be induced by trans-synaptic retrograde degeneration (via the lateral geniculate nucleus). One study employing multifocal visual evoked potentials (mfVEP) reported reduced amplitudes and delayed peak time for both HON and NON associated with structural changes at the GCIPL and pRNFL [19]. Wilkins et al [21] used full field electroretinography (ffERGs) to demonstrate that subclinical rod and cone dysfunction were associated with structural deficits of the RGC in NON, which suggests an abnormality of both outer and inner retinal layers.
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