Lesional activity during 4 years of follow-up was analysed using custom-build software, which segmented expanding part of the chronic lesions, new confluent lesions and new free-standing lesions. 
custom-build software
Mechanisms of central brain atrophy in multiple sclerosis.BACKGROUND
 Change in ventricular volume has been suggested as surrogate measure of central brain atrophy (CBA) applicable to the everyday management of multiple sclerosis (MS) patients.


 OBJECTIVES
 We investigated the contribution of inflammatory activity (including the severity of lesional tissue damage) to CBA.


 Fifty patients with relapsing-remitting multiple sclerosis (RRMS) were enrolled.  Lesional activity during 4 years of follow-up was analysed using custom-build software, which segmented expanding part of the chronic lesions, new confluent lesions and new free-standing lesions.  The degree of lesional tissue damage was assessed by change in mean diffusivity (MD).  Volumetric change of lateral ventricles was used to measure CBA.


 During follow-up, ventricles expanded on average by 12.6% ± 13.7% (mean ± <i>SD</i>).  There was a significant increase of total lesion volume, 69.3% of which was due to expansion of chronic lesions.  Correlation between volume of combined lesional activity and CBA (<i>r</i><sup>2</sup> = 0.67) increased when lesion volume was adjusted by the degree of tissue damage severity (<i>r</i><sup>2</sup> = 0.81).  Regression analysis explained 90% of CBA variability, revealing that chronic lesion expansion was by far the largest contributor to ventricular enlargement.


 DISCUSSION
 CBA is almost entirely explained by the combination of the volume and severity of lesional activity.  The expansion of chronic lesions plays a central role in this process.
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