Gray Matter Pathology in MS: A 3-Year Longitudinal Study in a Pediatric Population

Gray matter lesions are common in adult patients with MS. These authors assessed 92 children within 12 months of onset and every 3 years thereafter for this type of lesion. They found that cortical lesions and diffuse gray matter atrophy were associated with the biologic onset of MS and preceded linearly and independently of white matter lesions. The findings support the concept that MS should be considered as a “2-component“ disease in which gray matter damage occurs separately from white matter damage. BACKGROUND AND PURPOSE: GM pathology is considered a major determinant of disability in MS, but the comprehension of its origin and progression rate is limited by the uncertainty of dating the biologic disease onset. Thus, we planned a longitudinal study aimed at analyzing and comparing cortical pathology in pediatric and adult MS patients at clinical onset. MATERIALS AND METHODS: Within 12 months from clinical onset, 35 patients with cMS and 57 with aMS were included in a longitudinal study. At T0, GMf and CL number and volume were analyzed. Percentages of Δ-GMf and number of new CLs were assessed every year for 3 years (T1-T3). Twenty-eight age- and sex-matched NCs constituted the reference population. RESULTS: At T0, GMf did not differ between cMS and NC (P = .18), while it was lower in patients with aMS compared with both NCs (P < .001) and patients with cMS (P < .001). The number of patients with CLs, as well as CL number and volume, were higher in patients with aMS than in those with cMS (P < .001). At T3, Δ-GMf was higher in both patients with cMS (1.6% ± 0.5%; range 0.7%–3.4%; P < .001) and aMS (1.6% ± 0.6%; range 0.6%–3.4%; P < .001) compared with NCs (0.7% ± 0.2%; range 0.4%–1.1%), whereas no difference was observed between patients with cMS and aMS (P = .93). Δ-GMf significantly correlated with increased CL volume (cMS: r = 0.46; aMS: r = 0.48) and with the appearance of new CLs (cMS: r = 0.51; aMS: r = 0.49). CONCLUSIONS: Our findings suggest that focal (CLs) and diffuse (atrophy) GM damage are strictly associated with the biologic onset of MS, and proceed linearly and partly independently of WM pathology.