For a study, researchers sought to examine whether there was a correlation between the levels of sNfL in individuals with relapsing-remitting multiple sclerosis over 2 years and the clinical disability and gray matter (GM) atrophy after 10 years. In the 10-year follow-up visit were 85 patients who had initially signed up to participate in a multicenter, randomized trial of ω-3 fatty acids. The levels of sNfL were measured by Simoa once every 4 weeks up until month 12 and then once every month after that. The appearance of new gadolinium-enhancing (Gd+) lesions was evaluated every month between the baseline and month 9 and then at months 12 and 24. Measurements of the patient’s brain atrophy were taken with FreeSurfer during the 10-year follow-up appointment. Higher mean sNfL levels during early periods of active inflammation (Gd+ lesions present or recently present) were predictive of lower total (β=−0.399, P=0.040) and deep (β=−0.556, P=0.010) GM volume, as well as lower mean cortical thickness (β=−0.581, P=0.010) and higher T2 lesion count (β=−0.498, P=0.018). Higher inflammatory sNfL was associated with greater impairment as determined by the dominant hand Nine-Hole Peg Test (β=0.593, P=0.004). This was one of the clinical outcomes. The mean values of sNfL during periods of remission (no Gd+ lesions present or recently present) could not accurately predict the course of GM atrophy or impairment. However, a greater GM atrophy and certain characteristics of clinical impairment 10 years later were predicted by higher sNfL levels observed during periods of active inflammation. The findings pointed to neuroaxonal deterioration within new lesions as the primary cause of eventual long-term GM atrophy.
Source – jnnp.bmj.com/content/93/8/849
