摘要

Objective: The objective of our study was to evaluate the changes in quantitative diffusion tensor (DT) metrics and normalized T2-signal intensity (nT2-SI) values of normal-appearing cortical gray matter (CGM) and deep gray matter (DGM) in patients with multiple sclerosis (MS). Methods: Fifty patients with MS and 25 patients with no MS matched on sex/age were selected as controls. Conventional magnetic resonance imaging and DT imaging were performed. Fractional anisotropy (FA)/mean diffusivity (MD) and nT2-SI values of CGM and DGM were measured. Analyses of variance between the 2 groups were analyzed; Pearson correlations between DT metrics and nT2-SI values and brain parenchymal fraction (BPF) and T2 lesion volumes (LVs) were used. Results: Patients with MS showed larger MD/smaller FA values in the CGM region compared with controls (P < 0.05). However, MD/FA values were not statistically significant in the DGM between MS and healthy control group. In DGM of MS patients, a significant decrease of nT2-SI values were observed when compared with controls (P < 0.05), but nT2-SI values in the CGM of MS patients showed no significant decrease. In CGM, only MD values of frontal lobes in MS patients were significantly (negatively) correlated with BPF(right: P = 0.009, left: P = 0.036) or T2 LVs (right: P = 0.002, left: P = 0.047). Normalized T2-SI values in all DGM regions of MS patients were significantly correlated with BPF (r = 0.282-0.504, P < 0.05) except for the left thalamus and bilateral red nucleus. There was no correlation between nT2-SI in all DGM regions and T2 LVs of MS patients. Conclusion: In CGM, the change in quantitative DT metrics of MS patients and the association with BPF and T2 LVs suggest the existence of microstructural destruction corresponding to inflammation, demyelination, or wallerian degeneration, but the changes in CGM were independent of the concomitant changes in BPF and T2 lesion. In DGM, a decrease of nT2-SI in MS patients and the correlation of nT2-SI values with BPF (brain atrophy) suggest excessive iron deposition related to chronic destruction. Our investigation indicates the possibility of different mechanism of pathological change in CGM and DGM.