OBJECTIVE: To investigate the medium-term evolution of grey matter (GM) damage in patients at presentation with clinically isolated syndrome suggestive of multiple sclerosis (MS), and to assess whether it is associated with clinical disease activity during the initial stage of MS. METHODS: In 30 patients enrolled within three months from the onset of a clinically isolated syndrome, conventional and diffusion tensor MRI scans of the brain were acquired at baseline and after 3 years. Percentage brain volume change between baseline and follow-up scans was computed. Histograms of mean diffusivity and fractional anisotropy for the normal-appearing white matter and histograms of mean diffusivity for the GM were produced. RESULTS: Mean percentage brain volume change was -1.04 % (p < 0.001 vs. null change). GM mean diffusivity showed an increase at follow-up (p = 0.004), whose magnitude was greater, but not significantly, in patients who relapsed than in those who did not. There was no correlation between on-study relapse rate and GM mean diffusivity changes over time. CONCLUSIONS: In patients with clinically isolated syndrome suggestive of MS, GM damage begins to accumulate during the initial stage of the disease, possibly as a consequence of GM lesion accumulation. The magnitude of such a damage does not seem to be associated with the concomitant clinical activity.
OBJECTIVE: To investigate the medium-term evolution of grey matter (GM) damage in patients at presentation with clinically isolated syndrome suggestive of multiple sclerosis (MS), and to assess whether it is associated with clinical disease activity during the initial stage of MS. METHODS: In 30 patients enrolled within three months from the onset of a clinically isolated syndrome, conventional and diffusion tensor MRI scans of the brain were acquired at baseline and after 3 years. Percentage brain volume change between baseline and follow-up scans was computed. Histograms of mean diffusivity and fractional anisotropy for the normal-appearing white matter and histograms of mean diffusivity for the GM were produced. RESULTS: Mean percentage brain volume change was -1.04 % (p < 0.001 vs. null change). GM mean diffusivity showed an increase at follow-up (p = 0.004), whose magnitude was greater, but not significantly, in patients who relapsed than in those who did not. There was no correlation between on-study relapse rate and GM mean diffusivity changes over time. CONCLUSIONS: In patients with clinically isolated syndrome suggestive of MS, GM damage begins to accumulate during the initial stage of the disease, possibly as a consequence of GM lesion accumulation. The magnitude of such a damage does not seem to be associated with the concomitant clinical activity.
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