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NEUROLOGY 2009;72:1693-1701
© 2009 American Academy of Neurology


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MRI features of benign multiple sclerosis

Toward a new definition of this disease phenotype

M. Rovaris, MD, F. Barkhof, MD, M. Calabrese, MD, N. De Stefano, MD, F. Fazekas, MD, D. H. Miller, MD, X. Montalban, MD, C. Polman, MD, M. A. Rocca, MD, A. J. Thompson, MD, T. A. Yousry, MD and M. Filippi, MD

From the Multiple Sclerosis Centre (M.R.), Scientific Institute Santa Maria Nascente, Fondazione Don Gnocchi, Milan, Italy; Departments of Radiology (F.B.) and Neurology (C.P.), VU Medical Centre, Amsterdam, The Netherlands; The Multiple Sclerosis Centre of Veneto Region–First Neurology Clinic (M.C.), Department of Neurosciences, University Hospital of Padua, Italy; Department of Neurological and Behavioural Sciences (N.D.), University of Siena, Italy; Department of Neurology (F.F.), Medical University of Graz, Austria; Departments of Neuroinflammation (D.H.M.), Brain Repair/Rehabilitation (A.J.T.), and Radiology (T.A.Y.), UCL Institute of Neurology, London, UK; Unitat de Neuroimmunologia Clinica (X.M.), Hospitals Vall d’Hebron, Barcelona, Spain; and Neuroimaging Research Unit (M.A.R., M.F.), Department of Neurology, Scientific Institute and University Ospedale San Raffaele, Milan, Italy.

Address correspondence and reprint requests to Dr. Massimo Filippi, Neuroimaging Research Unit, Department of Neurology, Scientific Institute and University Ospedale San Raffaele, via Olgettina 60, 20132 Milan, Italy filippi.massimo{at}hsr.it

It is well known that the current classification of patients with benign multiple sclerosis (BMS), i.e., those with absent or minimal locomotor disability several years after disease onset, suffers from not having any prognostic value for the subsequent evolution of multiple sclerosis (MS). The identification of markers predictive of the longer-term course of MS will help define BMS more reliably and would allow better counseling of patients, particularly when advising on the initiation of a disease-modifying treatment. MRI-based evidence suggests that there are three potential, but not mutually exclusive, explanations for the scarce clinical impact of BMS: 1) the paucity of tissue damage within and outside MS lesions; 2) the relative sparing of clinically eloquent regions; and 3) the presence of effective compensatory mechanisms. In addition, the results of correlative MRI/neuropsychology studies underpin the need for a new definition of BMS, which should consider the maintenance of a normal cognitive profile as an additional criterion.

Abbreviations: BMS = benign multiple sclerosis; CIS = clinically isolated syndromes; EDSS = Expanded Disability Status Scale; fMRI = functional MRI; Gd = gadolinium; GM = gray matter; ICL = intracortical lesions; MR = magnetic resonance; MS = multiple sclerosis; MT = magnetization transfer; MTR = magnetization transfer ratio; NAA = N-acetylaspartate; NAWM = normal-appearing white matter; RR = relapsing-remitting; RT = relaxation time; SP = secondary progressive; TD = triple-dose.


The design and preparation of this review were done under the auspices of the European Community–funded Network for Magnetic Resonance Research in MS (MAGNIMS). The Amsterdam MS Centre is supported by the Dutch MS Research Foundation (grant # 06-538c). The MS NMR Research Unit at the Institute of Neurology, London, is supported by the MS Society of Great Britain and Northern Ireland. The Siena MS Centre was supported by the Fondazione Italiana Sclerosi Multipla (grant # 2005/R/9).

Disclosure: The authors report no disclosures.

Received December 18, 2008. Accepted in final form February 9, 2009.




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