scholarly journals The Relationship between Gray Matter Quantitative MRI and Disability in Secondary Progressive Multiple Sclerosis

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0161036 ◽  
Author(s):  
René-Maxime Gracien ◽  
Alina Jurcoane ◽  
Marlies Wagner ◽  
Sarah C. Reitz ◽  
Christoph Mayer ◽  
...  
2009 ◽  
Vol 15 (6) ◽  
pp. 687-694 ◽  
Author(s):  
J Furby ◽  
T Hayton ◽  
D Altmann ◽  
R Brenner ◽  
J Chataway ◽  
...  

Background Although MRI measures of grey matter abnormality correlate with clinical disability in multiple sclerosis, it is uncertain whether grey matter abnormality measured on MRI is entirely due to a primary grey matter process or whether it is partly related to disease in the white matter. Methods To explore potential mechanisms of grey matter damage we assessed the relationship of white matter T2 lesion volume, T1 lesion volume, and mean lesion magnetisation transfer ratio (MTR), with MRI measures of tissue atrophy and MTR in the grey matter in 117 subjects with secondary progressive multiple sclerosis. Results Grey matter fraction and mean grey matter MTR were strongly associated with lesion volumes and lesion MTR mean ( r = ±0.63–0.72). In contrast, only weak to moderate correlations existed between white matter and lesion measures. In a stepwise regression model, T1 lesion volume was the only independent lesion correlate of grey matter fraction and accounted for 52% of the variance. Lesion MTR mean and T2 lesion volume were independent correlates of mean grey matter MTR, accounting for 57% of the variance. Conclusions Axonal transection within lesions with secondary degeneration into the grey matter may explain the relationship between T1 lesions and grey matter fraction. A parallel accumulation of demyelinating lesions in white and grey matter may contribute to the association of T2 lesion volume and lesion MTR with grey matter MTR.


1994 ◽  
Vol 241 (4) ◽  
pp. 246-251 ◽  
Author(s):  
M. Filippi ◽  
G. J. Barker ◽  
M. A. Horsfield ◽  
P. R. Sacares ◽  
D. G. MacManus ◽  
...  

2019 ◽  
Vol 61 (1) ◽  
pp. 85-92
Author(s):  
Ramona Woitek ◽  
Fritz Leutmezer ◽  
Assunta Dal-Bianco ◽  
Julia Furtner ◽  
Gregor Kasprian ◽  
...  

Background Despite strongly overlapping patterns of clinical and histopathologic findings in primary and secondary progressive multiple sclerosis, differences concerning motor symptoms, central nervous system inflammation, atrophy, and demyelination that cannot be accounted for by lesion load alone remain to be elucidated. Purpose To evaluate the normal-appearing deep gray matter in patients with primary and secondary progressive multiple sclerosis, diffusion tensor imaging was used in this study. Material and Methods In 14 multiple sclerosis patients with primary and secondary progressive multiple sclerosis, axial echo-planar single-shot diffusion tensor imaging sequences with 32 diffusion-encoding directions and axial FLAIR sequences were acquired on a 3T system using an eight-channel SENSE head coil. FLAIR hyperintense multiple sclerosis lesions were outlined semi-automatically and normal-appearing deep gray matter was outlined manually (caudate nucleus, globus pallidus, putamen, thalamus, substantia nigra, and red nucleus). Fractional anisotropy and mean diffusivity values within the normal-appearing deep gray matter for the two groups were compared. Results Interhemispheric differences in mean diffusivity values (but not in fractional anisotropy), were significantly higher in primary progressive multiple sclerosis than in secondary progressive multiple sclerosis for the substantia nigra ( P = 0.04) and the putamen ( P = 0.021). Volumes, mean diffusivity, or fractional anisotropy of the remaining normal-appearing deep gray matter did not differ significantly. Conclusion This study showed a higher interhemispheric difference in the mean diffusivity in the substantia nigra and putamen in patients with primary progressive multiple sclerosis than in those with secondary progressive multiple sclerosis. These changes may represent edema, as well as axonal and myelin loss that can affect the normal-appearing deep gray matter of the two hemispheres differently and may point to differences in the laterality of motor symptoms.


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