Visual evoked potentials in multiple sclerosis: P100 latency and visual pathway damage including the lateral geniculate nucleus

• Published in: Clinical neurophysiology Vol. 161; pp. 122 - 132
• Main Authors: Papadopoulou, Athina, Pfister, Armanda, Tsagkas, Charidimos, Gaetano, Laura, Sellathurai, Shaumiya, D'Souza, Marcus, Cerdá-Fuertes, Nuria, Gugleta, Konstantin, Descoteaux, Maxime, Chakravarty, Mallar M., Fuhr, Peter, Kappos, Ludwig, Granziera, Cristina, Magon, Stefano, Sprenger, Till, Hardmeier, Martin
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.05.2024
• Subjects: Adult; Advanced magnetic resonance imaging; Evoked Potentials, Visual - physiology; Female; Geniculate Bodies - diagnostic imaging; Geniculate Bodies - physiopathology; Humans; LGN; Magnetic Resonance Imaging; Male; Middle Aged; Multiple Sclerosis - diagnostic imaging; Multiple Sclerosis - physiopathology; Neurology; Optic Neuritis - diagnostic imaging; Optic Neuritis - physiopathology; Optic radiations; Optical coherence tomography; Tomography, Optical Coherence - methods; VEP; Visual Pathways - diagnostic imaging; Visual Pathways - physiopathology; VEP; ON-eyes; RRMS; OCT; NAOR-FA; Optical coherence tomography; P100; MRI; Optic radiations; V1; EDSS; ON; GCIPL; pRNFL; OR; OR-WML; Advanced magnetic resonance imaging; MS; NON-eyes; LMM; LGN; WML; DTI; FA; HC; FE; fellow eye (non affected eye of a subject with positive history of optic neuritis on the other eye); magnetic resonance imaging; eyes with no history of optic neuritis on either eye; optical coherence tomography; eyes with a positive history of optic neuritis; (thickness of the) peripapillary retinal nerve fiber layer; expanded disability status scale; diffusion weighted tractography imaging; visual evoked potentials; healthy controls; main component of the VEP; fractional anisotropy of the normal-appearing optic radiations; optic radiations; (thickness of the) primary visual cortex; multiple sclerosis; (volume of) lateral geniculate nucleus; white matter lesion volume in optic radiations; advanced magnetic resonance imaging; (volume of) ganglion cell and inner plexiform layers; optic neuritis; relapsing-remitting multiple sclerosis; fractional anisotropy; white matter lesions; linear mixed model
• ISSN: 1388-2457; 1872-8952; 1872-8952
• DOI: 10.1016/j.clinph.2024.02.020

•P100-latency delay is mainly driven by pre-chiasmatic lesions but independently influenced by postchiasmatic damage.•After optic neuritis, P100-latency is associated with lateral geniculate nucleus atrophy, possibly indicating synaptopathy.•Better understanding of the contributors to the VEP signal may strengthen its interpretability as a biomarker. To explore associations of the main component (P100) of visual evoked potentials (VEP) to pre- and postchiasmatic damage in multiple sclerosis (MS). 31 patients (median EDSS: 2.5), 13 with previous optic neuritis (ON), and 31 healthy controls had VEP, optical coherence tomography and magnetic resonance imaging. We tested associations of P100-latency to the peripapillary retinal nerve fiber layer (pRNFL), ganglion cell/inner plexiform layers (GCIPL), lateral geniculate nucleus volume (LGN), white matter lesions of the optic radiations (OR-WML), fractional anisotropy of non-lesional optic radiations (NAOR-FA), and to the mean thickness of primary visual cortex (V1). Effect sizes are given as marginal R2 (mR2). P100-latency, pRNFL, GCIPL and LGN in patients differed from controls. Within patients, P100-latency was significantly associated with GCIPL (mR2 = 0.26), and less strongly with OR-WML (mR2 = 0.17), NAOR-FA (mR2 = 0.13) and pRNFL (mR2 = 0.08). In multivariate analysis, GCIPL and NAOR-FA remained significantly associated with P100-latency (mR2 = 0.41). In ON-patients, P100-latency was significantly associated with LGN volume (mR2 = −0.56). P100-latency is affected by anterior and posterior visual pathway damage. In ON-patients, damage at the synapse-level (LGN) may additionally contribute to latency delay. Our findings corroborate post-chiasmatic contributions to the VEP-signal, which may relate to distinct pathophysiological mechanisms in MS.