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Brain, Vol. 124, No. 7, 1396-1402, July 2001
© 2001 Oxford University Press

T1 hypointense lesions in secondary progressive multiple sclerosis: effect of interferon beta-1b treatment

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Frederik Barkhof1, Jan-Hein T. M. van Waesberghe1, Massimo Filippi2, Tarek Yousry3, David H. Miller4, Dietbert Hahn5, Alan J. Thompson4, Ludwig Kappos6, Peter Brex4, Carlo Pozzilli7, Chris H. Polman1 and for the European Study Group on Interferon beta-1b in Secondary Progressive Multiple Sclerosis,*

1 MR-MS centre, VU Medical Centre, Amsterdam, the Netherlands, 2 Neuroimaging Research Unit, Department of Neuroscience, Scientific Institute San Raffaele, University of Milan, 3 Department of Neurology, La Sapienza, Rome, Italy, 4 Department of Neuroradiology, Klinikum Grosshadern, Munich, 5 Institut for Röntgendiagnostik, Universität Würzburg, Germany, 6 NMR Research Group, Institute of Neurology, London, UK and 7 Department of Neurology, University Hospitals, Kantonsspittal, Basel, Switzerland

Correspondence to: Dr F. Barkhof, MS-MRI Centre and Department of Radiology, VU Medical Centre, PO Box 7057, 1007 MB Amsterdam, The Netherlands E-mail: f.barkhof{at}azvu.nl

Recently, the clinical efficacy of interferon ß-1b (IFNß-1b) was demonstrated for secondary progressive (SP) multiple sclerosis in a European multicentre study. We evaluated the effect of IFNß-1b treatment on the rate of development of hypointense T1 MRI lesions, a putative marker of axonal damage. Unenhanced T1-weighted images were obtained in a subgroup of 95 multiple sclerosis patients from five centres at 6-month intervals; this subgroup was similar to the total study population for all demographic, clinical and MRI parameters. An experienced observer blinded to the clinical data and treatment allocation measured volumes. The median baseline lesion load for hypointense T1 lesions was 5.1 cm3 for placebo-treated and 4.9 cm3 for IFNß-1b-treated patients (P = 0.56). Placebo-treated patients showed an increase in T1 lesion load by a median of 14% per year (P = 0.0002 compared with baseline); this was reduced to 7.7% per year in the IFNß-1b-treated patients (P = 0.003 versus placebo). In the IFNß-1b arm there was a statistically significant correlation between absolute change in Expanded Disability Status Scale scores and T1 lesion load by month 36 (r = 0.38, P = 0.0015). In patients with SP multiple sclerosis, IFNß-1b treatment reduces the development of hypointense T1 lesions, suggesting that reduced axonal damage in lesions may play a part in the beneficial effect that is observed clinically.


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