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J Neurol Neurosurg Psychiatry doi:10.1136/jnnp.2006.106690

Progression of non-age related callosal brain atrophy in multiple sclerosis. A nine years longitudinal MRI study representing four decades of disease development

  1. Juha Martola (juha.martola{at}karolinska.se)
  1. Karolinska Institutet, Sweden
    1. Leszek Stawiarz (leszek.stawiarz{at}ki.se)
    1. Karolinska Institutet, Sweden
      1. Sten Fredrikson (sten.fredrikson{at}ki.se)
      1. Karolinska Institutet, Sweden
        1. Jan Hillert (jan.hillert{at}ki.se)
        1. Karolinska Institutet
          1. Jakob Bergström (jakob.bergstrom{at}ki.se)
          1. Karolinska Institutet, Sweden
            1. Olof Flodmark (olof.flodmark{at}karolinska.se)
            1. Karolinska Institutet, Sweden
              1. Maria Kristoffersen-Wiberg (maria.kristoffersen.wiberg{at}ki.se)
              1. Karolinska Institutet, Sweden
                • Published Online First 21 November 2006

                Abstract

                Background: In multiple sclerosis (MS) multiple periventricular lesions are commonly the first findings in magnetic resonance imaging (MRI). However, most of these MS lesions are clinically silent. The brain atrophy rate has shown better correlation to physical disability, but it is not clear how atrophy develops over decades.

                Objectives: Corpus callosum (CC) forms the roof of the third and lateral ventricles. The size of CC measured as area (CCA) in a midsagittal image is age independent in normal adult population up to 7th decade, therefore can be used as a marker for non-age related, pathological, brain atrophy. We investigated whether and how CCA decreases in size over time in MS patients.

                Methods: In a clinical observational study we followed 37 MS patients with a wide range of disease duration at baseline (1-33 years). Three different MS-courses were represented. The mean of individual MRI follow-up was 9 years. We also applied multiple sclerosis severity score (MSSS) in evaluation of disability at baseline and at 9 years follow-up.

                Results: We found a significant decrease of CCA over nine years (P<0.0001) and a persisting association between CCA and the disability status. The atrophy rate was similar during four decades of MS for all MS-courses. The mean annual CCA decrease was 9.25 mm2 (1.8%). Surprisingly, atrophy rate correlated neither to gender, disease duration, age at MS-onset nor to MS-course.

                Conclusions: Serial evaluations of CCA might be a robust method in monitoring a non-age related decrease of CCA, reflecting progression of irreversible destructive changes in MS.

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