Magnetic resonance imaging and treatment effects of multiple sclerosis therapeutics

MRI is now an important component in the diagnosis and assessment of multiple sclerosis (MS). Evidence gleaned from imaging studies has changed our understanding of the pathophysiology and natural history of the disease and has enabled physicians to visualize the effects of immunomodulatory therapies. Serial MRI following the index CNS event has clarified the evolution of MS, demonstrating that a majority of patients with clinically isolated syndromes already have dissemination of lesions in space and, based on MRI characteristics, likely also in time. Imaging studies have also shown that axonal injury and brain atrophy occur early in the disease. MRI techniques, such as magnetic resonance spectroscopy and magnetization transfer imaging, that are generally not part of the imaging sequences obtained as part of regular care have provided additional insight into the degree and extent of the effect of the disease process on the CNS, tissue repair, and the neuroprotective effects of therapeutics. These data have contributed to improved clinical decision making and treatment outcomes.

[1]  P. Calabresi,et al.  Characterization of MRI response to treatment with interferon beta-1b: Contrast-enhancing MRI lesion frequency as a primary outcome measure , 1997, Neurology.

[2]  Marco Rovaris,et al.  Effect of early interferon treatment on conversion to definite multiple sclerosis: a randomised study , 2001, The Lancet.

[3]  Treatment with interferon beta-1b delays conversion to clinically definite and McDonald MS in patients with clinically isolated syndromes , 2007, Neurology.

[4]  A. Thompson,et al.  The prognostic value of brain MRI in clinically isolated syndromes of the CNS. A 10-year follow-up. , 1998, Brain : a journal of neurology.

[5]  P. Matthews.  Editorial commentary to Narayanan et al. Axonal metabolic recovery in multiple sclerosis patients treated with interferon beta-1b. , 2001, Journal of neurology.

[6]  Neal Jeffries,et al.  Evolution of T1 black holes in patients with multiple sclerosis imaged monthly for 4 years. , 2003, Brain : a journal of neurology.

[7]  M. Filippi,et al.  250 μg or 500 μg interferon beta-1b versus 20 mg glatiramer acetate in relapsing-remitting multiple sclerosis: a prospective, randomised, multicentre study , 2009, The Lancet Neurology.

[8]  R. Kinkel,et al.  A Wallerian degeneration pattern in patients at risk for MS , 2000, Neurology.

[9]  Xingchang Wei,et al.  A randomized blinded trial of combination therapy with cyclophosphamide in patients with active multiple sclerosis on interferon beta , 2005, Multiple sclerosis.

[10]  A. Compston,et al.  Recommended diagnostic criteria for multiple sclerosis: Guidelines from the international panel on the diagnosis of multiple sclerosis , 2001, Annals of neurology.

[11]  Michael Grüninger,et al.  Introduction , 2002, CACM.

[12]  R. Rudick,et al.  Use of the brain parenchymal fraction to measure whole brain atrophy in relapsing-remitting MS , 1999, Neurology.

[13]  M. Stangel.  Remyelinating and neuroprotective treatments in multiple sclerosis , 2004, Expert opinion on investigational drugs.

[14]  Zografos Caramanos,et al.  Axonal metabolic recovery in multiple sclerosis patients treated with interferon β–1b , 2001, Journal of Neurology.

[15]  P. Matthews,et al.  Beta-Interferon treatment does not always slow the progression of axonal injury in multiple sclerosis , 2003, Journal of Neurology.

[16]  C. Polman,et al.  Infratentorial lesions predict long-term disability in patients with initial findings suggestive of multiple sclerosis. , 2004, Archives of neurology.

[17]  N. Richert.  Glatiramer acetate reduces the proportion of new MS lesions evolving into "black holes". , 2002, Neurology.

[18]  F. Barkhof,et al.  Comparison of subcutaneous interferon beta-1a with glatiramer acetate in patients with relapsing multiple sclerosis (the REbif vs Glatiramer Acetate in Relapsing MS Disease [REGARD] study): a multicentre, randomised, parallel, open-label trial , 2008, The Lancet Neurology.

[19]  R. Tarducci,et al.  1H-MRS in patients with multiple sclerosis undergoing treatment with interferon β-1a: results of a preliminary study , 1998, Journal of neurology, neurosurgery, and psychiatry.

[20]  Jiani Hu,et al.  Axonal metabolic recovery and potential neuroprotective effect of glatiramer acetate in relapsing-remitting multiple sclerosis , 2005, Multiple sclerosis.

[21]  F. Barkhof,et al.  The effect of IFNβ-1b on the evolution of enhancing lesions in secondary progressive MS , 2001, Neurology.

[22]  Robert Zivadinov,et al.  Clinical–Magnetic Resonance Imaging Correlations in Multiple Sclerosis , 2005, Journal of neuroimaging : official journal of the American Society of Neuroimaging.

[23]  J H Simon,et al.  Eight-year follow-up study of brain atrophy in patients with MS , 2002, Neurology.

[24]  H. Tobi,et al.  Correlating MRI and clinical disease activity in multiple sclerosis , 1995, Neurology.

[25]  H. McFarland,et al.  Immunopathogenesis of the multiple sclerosis lesion , 2001, Current neurology and neuroscience reports.

[26]  A. Thompson,et al.  Disability and T2 MRI lesions: a 20-year follow-up of patients with relapse onset of multiple sclerosis. , 2008, Brain : a journal of neurology.

[27]  J. De Keyser,et al.  Treatment with interferon beta-1b delays conversion to clinically definite and McDonald MS in patients with clinically isolated syndromes , 2006, Neurology.

[28]  Marco Rovaris,et al.  MRI criteria for multiple sclerosis in patients presenting with clinically isolated syndromes: a multicentre retrospective study , 2007, The Lancet Neurology.

[29]  F. Barkhof,et al.  Axonal loss in multiple sclerosis lesions: Magnetic resonance imaging insights into substrates of disability , 1999, Annals of neurology.

[30]  F. Barkhof,et al.  Accumulation of hypointense lesions ("black holes") on T1 spin-echo MRI correlates with disease progression in multiple sclerosis , 1996, Neurology.

[31]  H P Hartung,et al.  Treatment with interferon beta-1b delays conversion to clinically definite and McDonald MS in patients with clinically isolated syndromes , 2006, Neurology.

[32]  A. Thompson,et al.  Serial gadolinium‐enhanced MRI in relapsing/remitting multiple sclerosis of varying disease duration , 1992, Neurology.

[33]  J H Simon,et al.  Intramuscular interferon beta-1a therapy initiated during a first demyelinating event in multiple sclerosis. CHAMPS Study Group. , 2000, The New England journal of medicine.

[34]  Hompson,et al.  A LONGITUDINAL STUDY OF ABNORMALITIES ON MRI AND DISABILITY FROM MULTIPLE SCLEROSIS , 2002 .

[35]  Interferon beta-1b in the treatment of multiple sclerosis: final outcome of the randomized controlled trial. The IFNB Multiple Sclerosis Study Group and The University of British Columbia MS/MRI Analysis Group. , 1995, Neurology.

[36]  Luca Roccatagliata,et al.  Magnetic resonance imaging as a potential surrogate for relapses in multiple sclerosis: A meta‐analytic approach , 2009, Annals of neurology.

[37]  P M Matthews,et al.  Proton magnetic resonance spectroscopy for metabolic characterization of plaques in multiple sclerosis , 1991, Neurology.

[38]  E. Haacke,et al.  Susceptibility-Weighted Imaging: Technical Aspects and Clinical Applications, Part 1 , 2008, American Journal of Neuroradiology.

[39]  David H. Miller,et al.  Application of the new McDonald criteria to patients with clinically isolated syndromes suggestive of multiple sclerosis , 2002, Annals of neurology.

[40]  O. Khan,et al.  Long‐Term Study of Brain 1H‐MRS Study in Multiple Sclerosis: Effect of Glatiramer Acetate Therapy on Axonal Metabolic Function and Feasibility of Long‐Term 1H‐MRS Monitoring in Multiple Sclerosis , 2008, Journal of neuroimaging : official journal of the American Society of Neuroimaging.

[41]  J. Olesen,et al.  Localized in vivo proton spectroscopy in the brain of patients with multiple sclerosis , 1991, Magnetic resonance in medicine.

[42]  M. Mintun,et al.  Brain volume decline in aging: evidence for a relation between socioeconomic status, preclinical Alzheimer disease, and reserve. , 2008, Archives of neurology.

[43]  R. Zivadinov.  Can imaging techniques measure neuroprotection and remyelination in multiple sclerosis? , 2007, Neurology.