Effects of Optic Neuritis, T2 Lesions, and Microstructural Diffusion Integrity in the Visual Pathway on Cortical Thickness in Pediatric-Onset Multiple Sclerosis.

Abstract

Pediatric-onset multiple sclerosis (POMS) is associated with focal inflammatory lesions and the loss of cortical and deep gray matter. Optic neuritis (ON) and white matter (WM) lesions in the visual pathway can directly contribute to visual cortical mantle thinning. We determine the relative contributions of MS insult on anterior and posterior visual pathway integrity. High- and low-contrast visual acuity, optical coherence tomography (OCT), and 3T MRI scans were obtained from 20 POMS patients (10 with remote ON) and 22 age- and sex-matched healthy controls. Cortical mantle thickness was measured using FreeSurfer. Fractional anisotropy (FA) and mean diffusivity were calculated for postchiasmal optic radiations (with and without WM lesions). Groups were compared using Student's t-test (adjusted for multiple comparisons), and simple linear regression was used to investigate interrelationships between measures. Mean cortical thickness of the whole brain was reduced in patients (2.49mm) versus controls (2.58mm,P = .0432) and in the visual cortex (2.07mm vs. 2.17mm,P = .0059), although the foveal confluence was spared. Mean FA of the optic radiations was reduced in POMS (.40) versus controls (.43,P = .0042) and correlated with visual cortical mantle thickness in POMS (P = .017). Visual acuity, OCT measures, and lesion volumes in the optic radiations were not associated with cortical mantle thickness. POMS negatively impacts the integrity of the anterior visual pathway, but it is the loss of WM integrity that drives anterograde loss of the cortical mantle. Preserved visual acuity and foveal sparing imply some degree of functional and structural resilience.