Corpus callosum atrophy in MS is halted by autologous haematopoietic stem cell transplantation
ECTRIMS Online Library. Tolf A. 10/27/17; 199908; P1888
Andreas Tolf
Andreas Tolf

Abstract: P1888

Type: Poster

Abstract Category: Late breaking news

Background: In Sweden, autologous haemotopoietic stem cell transplantation (HSCT) has been used as a treatment for highly aggressive relapsing-remitting multiple sclerosis (RRMS) since 2004. In December 2016, HSCT was approved by the Swedish National Board of Health and Welfare as second-line treatment for RRMS or first-line treatment for highly aggressive multiple sclerosis (MS). Brain atrophy is a well-known consequence of MS, but the rate can be altered with effective treatment. Previous reports suggest that the atrophy rate approaches normal age dependent atrophy 2.5 years after HSCT. Measurement of the midsagittal corpus callosum area (CCA) with magnetic resonance tomography (MR) is a robust method for evaluating brain atrophy in MS but has previously not been used in this patient group.
Objective: To estimate long-term brain atrophy after HSCT for MS.
Methods: All patients treated with HSCT for RRMS between 2004 and 2007 at Uppsala University Hospital were enrolled in the study (n=10). All available MR investigations were reviewed. For each patient, a series of comparable sequences was selected for further assessments, in total 81 (range 4 to 13 per patient).
The MR images were anonymized and then randomized. The midsagittal corpus callosum area (CCA) was obtained by manually outlining the margins of the corpus callosum. The CCA was normalized (nCCA) to the total intracranial volume (midline internal skull surface area, MISS) to ensure comparability over time. In each image the CCA and MISS was measured five times by one single investigator. The mean values were used thereafter. Statistical analysis was performed using a linear effects mixed model with random intercept.
Results: Median MR follow-up time was 10 years (range 9.8 to 12). The pooled coefficient of variation for the CCA measurements obtained from each separate image was 1.9% and for the MISS measurements 0.26%. The estimated change of nCCA before HSCT was -10%/year (95% CI -13 to -7.2); in the time period from HSCT to 2.5 years after HSCT, the change was -8.0%/year (95% CI -10 to -5.6); and from 2.5 years after HSCT to the last MR scan (range 7.5 to 11 years after HSCT, median 10 years) +0.51%/year (95% CI -0.40 to +1.4).
Conclusion: Brain atrophy is prominent in patients with aggressive MS. The atrophy rate is still high in the first years after HSCT, but thereafter subsides. 2.5 years post-HSCT no further atrophy development could be demonstrated on a group level.
Disclosure: Anne-Marie Landtblom: Disclosures concern honoraria for lectures, projects, travel expenses from Biogen, TEVA, Sanofi, Genzyme, Serono, Bayer, Roche.

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