Sydney University

Author Of 1 Presentation

Imaging Poster Presentation

P0574 - Expansion of chronic lesions associated with disease progression in RRMS patients. (ID 1062)

Speakers
Presentation Number
P0574
Presentation Topic
Imaging

Abstract

Background

It was suggested that slow-burning inflammation isassociated with lesion expansion and leads to progressive loss of axons and disability worsening. However, in vivo evidence linking lesion expansion with biomarkers of disease progression, particularly during relapsing-remitting stage of the disease, is lacking.

Objectives

To examine the incidence and extent of chronic white matter lesion expansion in relapsing-remitting MS (RRMS) patients followed for 5 yearsand to evaluate its relationship with clinical and imaging biomarkers of disease progression.

Methods

Pre- and post-gadolinium T1, FLAIR and diffusion tensor images were acquired from 33 patients. Lesion expansion was analysed between baseline and 48 months using custom-designed software written in Phyton. Percentage brain volume change (PBVC) was calculated using SIENA/FSL. Progression of clinical disability was assessed by EDSS. Progressive tissue damage inside chronic lesions was measured as an increase of Mean Diffusivity (MD).

Results

There were 569 lesions identified as chronic at baseline, of which 261 (46%) were expanding (total volume change:31320 mm3), 236 (42%) were stable (total volume change:1380 mm3) and 72 (12%) were shrinking (total volume change: -2664 mm3). In addition, 139 new free-standing and confluent lesions were detected (total volume:13867).

No association was found between change of volume in chronic lesions and the volume of new lesions (p=0.4). There was a significant increase in total brain lesion volume during the follow-up period (6680+/-5509 vs 7951+/-6315 mm3), the bulk of which was accounted for by an increase of chronic lesions group volume (67.3% or 855+/-1066 mm3), while only 32.7% (or 420+/-633 mm3) was attributable to new lesions.

There was significant negative correlation of chronic lesion volume change with the rate of brain atrophy (r=-0.57, p=0.001) and change of EDSS during the follow-up period (r=0.38, p=0.03). A strong positive correlation was also observed between the rate of chronic lesion volume change and an increase of MD inside the lesions during the follow-up period (r=0.75, p<0.001).

Conclusions

In RRMS patients the expansion of chronic white matter lesions dominates the process of total lesion load accumulation and is a significant contributing factor to the disease progression. Furthermore, our results suggest that low-grade inflammation at the lesion rim associated with significant degree of axonal loss both inside chronic lesions (MD increase) and in NAWM (brain atrophy). In addition, lack of correlation between an expansion of chronic lesion and volume of newly appearing lesions supports the notion that different mechanisms underpin the development of the new lesions and progressive changes in chronic pre-existing lesions.

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