In neuroinflammatory diseases of the central nervous system (CNS) such as multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD) and anti-MOG antibody-associated disorders (MOGAD), neuronal degeneration is the consequence of inflammatory and demyelinating lesions in the brain, optic nerve and spinal cord. Both white and grey matter are systematically affected. Lesions of the perivascular spaces containing cerebrospinal fluid (CSF) and meningeal inflammation seem to play an important role in the pathophysiology of these neuroinflammatory diseases. Currently, the interrelation of all these aspects is not clearly established in the pathophysiology of these diseases. In order to better understand the mechanisms that lead to and underlie the clinical disability of patients with these diseases, we need in vivo study models that allow the in-depth study of the neurodegenerative process and the identification of its causes. In this perspective, we make the hypothesis that the visual pathways model is very relevant to measure neuro-axonal loss and to explore the different mechanisms involved in neurodegeneration during MS and other CNS demyelinating diseases. Researchers have at their disposal many tools that allow them to analyse and quantify the neurodegenerative process in a reproducible and very precise manner from a structural and functional point of view, while taking into account possible vascular involvement (MRI, optical coherence tomography - angiography, etc…).
Study Type
OBSERVATIONAL
Enrollment
100
MRI sequences for research, pupillometry, OCT-angiography, evaluation of visual cognition
Hop Fontan Chu
Lille, France
RECRUITINGPresence of enhancement of the optic nerve sheath on the axial T1 dixon MRI sequence post gadolinium at the acute phase of optic neuritis.
Time frame: at inclusion
Low contrast monocular visual acuity (2.5%, LogMAR unit) at distance from acute optic neuritis
Time frame: at 12 months
Presence of enhancement of the optic nerve sheath on the axial T1 dixon MRI sequence post gadolinium. Macular GCIPL atrophy will be assessed by the variation of mGCIPL volume between inclusion and the maximal follow-up.
Time frame: at inclusion and at 12 months follow-up
Optic nerve lesion length on 3D-DIR sequence. Alteration of retinal microvascularisation between inclusion and the maximal follow-up.
Time frame: at inclusion and at 12 months follow-up
Acute alteration of retinal microvascularisation is assessed by the difference of retinal vascular density between inclusion (V0) and one month later (V1).
Time frame: at inclusion and at 1 months follow-up
Low contrast monocular visual acuity (2.5%, LogMAR unit) measured at 12 months (V5)
Time frame: at inclusion and at 12 months follow-up
Amplitude of the melanopsin-mediated sustained constriction phase in the blue light-induced pupillary response is assessed at 12 months (V5).
Time frame: at inclusion and at 12 months follow-up
Optic nerve lesion length assessed at inclusion (V0)
Time frame: at inclusion
mGCIPL atrophy/retinal vascular alteration are assessed by mGCIPL volume/retinal vessel density difference between inclusion (V0) and at 12 months (V5).
Time frame: at inclusion and at 12 months follow-up
Presence of leptomeningeal cerebral enhancement
Time frame: at inclusion, at 6 months and at 12 months follow-up
T2 lesions brain and spinal cord volumes
Time frame: at inclusion, at 6 months and at 12 months follow-up
Brain grey matter volumes and brain perfusion (3D-ASL)
Time frame: at inclusion, at 6 months and at 12 months follow-up
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