Contributions
Abstract: P1866
Type: Poster
Abstract Category: Late breaking news
Background and goals: Recently reported changes in iron deposition at the lesion edge reignited interest in lesion expansion caused by slow burning inflammation as a potential mechanism of disease progression. In the current study we report preliminary result of longitudinal study aimed at investigating progressive tissue damage in and around chronic MS lesions in patients with RRMS.
Method: Pre- and post-gadolinium T1, T2 and DTI images were acquired from 55 consecutive RRMS patients at baseline and 42.3±9.7 months later. Chronic stable T2 lesions with lesion-free surrounding white matter were identified in 38 patients (total of 101 lesions). Progressive mean diffusivity (MD) change was analysed in the lesion “core” (lesional mask eroded by 1 voxel), lesion “rim” (eroded part of the lesion) and 2 gradually expanding external “shells”, each 1 voxel thick.
Result: The highest longitudinal increase in MD was observed in the lesion “core” (0.045±0.04µm2/ms, P< 0.001, paired t-test) with a progressively smaller longitudinal change in MD from the “rim” (0.03±0.04µm2/ms, P< 0.001), to perilesional white matter (0.011±0.03µm2/ms and 0.007±0.02µm2/ms for inner and outer shells respectively, P=0.01 for both). The observed increase of water diffusion in the lesion “core” was associated with progressive brain atrophy and demonstrated a male gender preponderance. However, while change of MD in the “core” and outermost external shell was not related to the degree of baseline lesional damage (as determined by T1 hypointensity), there was a significant negative correlation between the latter and progressive diffusivity increase in area around the lesion edge, i.e. in the lesional “rim” and innermost outer “shell” (r=0.27, P=0.01 and r=0.25, P=0.02 respectively).
Conclusion: This study demonstrated centrifugal pattern of progressive water diffusion increase in chronic MS lesions. The result of the study also suggests that different mechanisms may be responsible for the progressive tissue damage in the “core” and the edge of the chronic MS lesions. Thus, while change in the lesional “core” most likely reflects further enlargement of the extra-cellular space caused by ongoing tissue loss, rise of MD at the lesion edge may be related to increased water content caused by ongoing low-grade inflammation, which is more likely to be associated with severely damaged lesions.
Disclosure: Authors have nothing to disclose
Abstract: P1866
Type: Poster
Abstract Category: Late breaking news
Background and goals: Recently reported changes in iron deposition at the lesion edge reignited interest in lesion expansion caused by slow burning inflammation as a potential mechanism of disease progression. In the current study we report preliminary result of longitudinal study aimed at investigating progressive tissue damage in and around chronic MS lesions in patients with RRMS.
Method: Pre- and post-gadolinium T1, T2 and DTI images were acquired from 55 consecutive RRMS patients at baseline and 42.3±9.7 months later. Chronic stable T2 lesions with lesion-free surrounding white matter were identified in 38 patients (total of 101 lesions). Progressive mean diffusivity (MD) change was analysed in the lesion “core” (lesional mask eroded by 1 voxel), lesion “rim” (eroded part of the lesion) and 2 gradually expanding external “shells”, each 1 voxel thick.
Result: The highest longitudinal increase in MD was observed in the lesion “core” (0.045±0.04µm2/ms, P< 0.001, paired t-test) with a progressively smaller longitudinal change in MD from the “rim” (0.03±0.04µm2/ms, P< 0.001), to perilesional white matter (0.011±0.03µm2/ms and 0.007±0.02µm2/ms for inner and outer shells respectively, P=0.01 for both). The observed increase of water diffusion in the lesion “core” was associated with progressive brain atrophy and demonstrated a male gender preponderance. However, while change of MD in the “core” and outermost external shell was not related to the degree of baseline lesional damage (as determined by T1 hypointensity), there was a significant negative correlation between the latter and progressive diffusivity increase in area around the lesion edge, i.e. in the lesional “rim” and innermost outer “shell” (r=0.27, P=0.01 and r=0.25, P=0.02 respectively).
Conclusion: This study demonstrated centrifugal pattern of progressive water diffusion increase in chronic MS lesions. The result of the study also suggests that different mechanisms may be responsible for the progressive tissue damage in the “core” and the edge of the chronic MS lesions. Thus, while change in the lesional “core” most likely reflects further enlargement of the extra-cellular space caused by ongoing tissue loss, rise of MD at the lesion edge may be related to increased water content caused by ongoing low-grade inflammation, which is more likely to be associated with severely damaged lesions.
Disclosure: Authors have nothing to disclose