Abstract
Understanding of the role of focal inflammation, a treatable feature, on neuro-axonal injury, is paramount to optimize neuroprotective strategy in MS. To quantify the impact of focal inflammatory activity on the rate of neuro-axonal injury over the MS course. We quantified the annualized rates of change in peripapillary retinal nerve fiber layer, ganglion cell plus inner plexiform layer (GCIPL), whole-brain, gray matter and thalamic volumes in patients with and without focal inflammatory activity in 161 patients followed over 5 years. We used mixed models including focal inflammatory activity (the presence of at least one relapse or a new/enlarging T2-FLAIR or gadolinium- enhancing lesion), and its interaction with time adjusted by age, sex, use of disease-modifying therapies and steroids, and prior optic neuritis. The increased rate of neuro-axonal injury during the first five years after onset was more prominent among active patients, as reflected by the changes in GCIPL thickness (p = 0.02), whole brain (p = 0.002) and thalamic volumes (p < 0.001). Thereafter, rates of retinal and brain changes stabilized and were similar in active and stable patients. Focal inflammatory activity is associated with neurodegeneration early in MS which reinforces the use of an early intensive anti-inflammatory therapy to prevent neurodegeneration in MS.
Highlights
Understanding of the role of focal inflammation, a treatable feature, on neuro-axonal injury, is paramount to optimize neuroprotective strategy in Multiple sclerosis (MS)
Abbreviations 95% percentile confidence intervals (95% CI) 95% confidence interval Akaike Information Criterion (AIC) Akaike information criterion clinically isolated syndrome (CIS) Clinically isolated syndrome central nervous system (CNS) Central nervous system DMD Disease-modifying drug fluid-attenuated inversion recovery (FLAIR) Fluid-attenuated inversion recovery Gad+ Gadolinium enhancing lesions ganglion cell plus inner plexiform layer (GCIPL) Ganglion cell plus inner plexiform layer magnetisation prepared rapid acquisition gradient echo (MPRAGE) Magnetisation prepared rapid acquisition gradient echo magnetic resonance imaging (MRI) Magnetic resonance imaging
Out of the 171 patients included in the cohort, 13 and 15 patients were excluded from this study due to: a disease duration longer than 30 years (MRI = 1, optical coherence tomography (OCT) = 1), loss of follow-up at baseline (MRI = 5, OCT = 3), not reaching the first-year follow-up (MRI = 6, OCT = 6), recent corticosteroid administration or pregnancy (MRI = 2, OCT = 0), refusal to undergo more than 1 MRI (MRI = 1) or bilateral retinal problems (OCT = 3)
Summary
Understanding of the role of focal inflammation, a treatable feature, on neuro-axonal injury, is paramount to optimize neuroprotective strategy in MS. We quantified the annualized rates of change in peripapillary retinal nerve fiber layer, ganglion cell plus inner plexiform layer (GCIPL), wholebrain, gray matter and thalamic volumes in patients with and without focal inflammatory activity in 161 patients followed over 5 years. New algorithms to quantify brain volume and retinal thicknesses have been developed using magnetic resonance imaging (MRI)[3] and optical coherence tomography (OCT)[4], fostering more intense research into the dynamics of neuro-axonal injury. We set out to quantify the impact of focal inflammatory activity on the rate of retinal and brain neuro-axonal damage over the course of MS in the 161 out of the 171 patients of the ongoing MS-VisualPath prospective cohort who fulfilled eligibility criteria using all available visits up to the fifth year of follow-up
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