Glatiramer acetate (Copaxone) treatment in relapsing–remitting MS

Objective: To evaluate the efficacy of glatiramer acetate (GA, Copaxone; Teva Pharmaceutical Industries, Ltd., Petah Tiqva, Israel) by MRI-based measures in patients with relapsing–remitting (RR) MS. Methods: Twenty-seven patients with clinically definite RR-MS were treated with either 20 mg of GA by daily subcutaneous self-injection (n = 14) or placebo (n = 13) for approximately 24 months. Axial dual-echo fast-spin-echo T2-weighted images and T1-weighted images before and after gadolinium (Gd) were acquired at 1.5 tesla and transferred into an image processing computer system. The main outcome measures were the number of Gd-enhanced T1 and T2 lesions and their volume as well as brain parenchyma volume. Results: The values of age, disease duration, Expanded Disability Status Scale (EDSS) score, the number of T1- and T2-weighted lesions, and their volume were similar between GA- and placebo-receiving groups at the entry of this study. There was a decrease in the number of T1-enhanced lesions (p = 0.03) and a significant percent annual decrease of their volume in GA recipients compared with those of placebo recipients. There were no significant differences between changes in the two groups in the number of T2 lesions and their volume. The loss of brain tissue was significantly smaller in the GA group compared with that of the placebo group. Conclusions: These results show that GA treatment may decrease both lesion inflammation and the rate of brain atrophy in RR-MS.

[1]  R I Grossman,et al.  Perspectives on multiple sclerosis. , 1998, AJNR. American journal of neuroradiology.

[2]  P. Gorelick,et al.  Calcific cerebral embolism in systemic calciphylaxis , 1998, Neurology.

[3]  J. Fricker.  The copolymer-1 story so far , 1998, The Lancet.

[4]  M. Sormani,et al.  Effect of copolymer-1 on serial gadolinium-enhanced MRI in relapsing remitting multiple sclerosis , 1998, Neurology.

[5]  J S Wolinsky,et al.  Extended use of glatiramer acetate (Copaxone) is well tolerated and maintains its clinical effect on multiple sclerosis relapse rate and degree of disability , 1998, Neurology.

[6]  Jeanelle Sheeder,et al.  Magnetic resonance studies of intramuscular interferon β–1a for relapsing multiple sclerosis , 1998 .

[7]  Supun Samarasekera,et al.  Multiple sclerosis lesion quantification using fuzzy-connectedness principles , 1997, IEEE Transactions on Medical Imaging.

[8]  J K Udupa,et al.  Computer-assisted quantitation of enhancing lesions in multiple sclerosis: correlation with clinical classification. , 1997, AJNR. American journal of neuroradiology.

[9]  J. Udupa,et al.  A new computer-assisted method for the quantification of enhancing lesions in multiple sclerosis. , 1997, Journal of computer assisted tomography.

[10]  A J Thompson,et al.  Progressive cerebral atrophy in multiple sclerosis. A serial MRI study. , 1996, Brain : a journal of neurology.

[11]  J A Frank,et al.  MRI studies of multiple sclerosis: Implications for the natural history of the disease and for monitoring effectiveness of experimental therapies , 1996, Multiple sclerosis.

[12]  A. Thompson,et al.  Spinal cord atrophy and disability in multiple sclerosis. A new reproducible and sensitive MRI method with potential to monitor disease progression. , 1996, Brain : a journal of neurology.

[13]  Supun Samarasekera,et al.  Fuzzy Connectedness and Object Definition: Theory, Algorithms, and Applications in Image Segmentation , 1996, CVGIP Graph. Model. Image Process..

[14]  Supun Samarasekera,et al.  Detection and quantification of MS lesions using fuzzy topological principles , 1996, Medical Imaging.

[15]  A Weindl,et al.  Deactivation of human visual cortex during involuntary ocular oscillations. A PET activation study. , 1996, Brain : a journal of neurology.

[16]  F. Barkhof,et al.  Guidelines for the use of magnetic resonance techniques in monitoring the treatment of multiple sclerosis , 1996, Annals of neurology.

[17]  A. Thompson,et al.  Persistent functional deficit in multiple sclerosis and autosomal dominant cerebellar ataxia is associated with axon loss. , 1995, Brain : a journal of neurology.

[18]  P. S. Albert,et al.  Changes in the amount of diseased white matter over time in patients with relapsing-remitting multiple sclerosis , 1995, Neurology.

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

[20]  J. W. Rose,et al.  Copolymer 1 reduces relapse rate and improves disability in relapsing‐remitting multiple sclerosis , 1995, Neurology.

[21]  H. McFarland,et al.  Outcomes assessment in multiple sclerosis clinical trials: a critical analysis , 1995, Multiple sclerosis.

[22]  D. Miller,et al.  Are magnetic resonance findings predictive of clinical outcome in therapeutic trials in multiple sclerosis? The dilemma of interferon‐β , 1994, Annals of neurology.

[23]  Dewey Odhner,et al.  3DVIEWNIX: an open, transportable, multidimensional, multimodality, multiparametric imaging software system , 1994, Medical Imaging.

[24]  W. I. McDonald,et al.  Quantitative brain MRI lesion load predicts the course of clinically isolated syndromes suggestive of multiple sclerosis , 1994, Neurology.

[25]  F. Barkhof,et al.  Gadolinium enhancement increases the sensitivity of MRI in detecting disease activity in multiple sclerosis. , 1993, Brain : a journal of neurology.

[26]  D. Paty,et al.  Interferon beta‐1b is effective in relapsing‐remitting multiple sclerosis , 1993, Neurology.

[27]  H. Weiner,et al.  T-cell recognition of an immuno-dominant myelin basic protein epitope in multiple sclerosis , 1990, Nature.

[28]  C. Pozzilli,et al.  Serial study of gadolinium‐DTPA MRI enhancement in multiple sclerosis , 1990, Neurology.

[29]  H I Goldberg,et al.  Multiple sclerosis: serial study of gadolinium-enhanced MR imaging. , 1988, Radiology.

[30]  H. Weiner.  Cop 1 therapy for multiple sclerosis. , 1987, The New England journal of medicine.

[31]  S. Wassertheil-Smoller,et al.  A pilot trial of Cop 1 in exacerbating-remitting multiple sclerosis. , 1987, The New England journal of medicine.

[32]  I. Schwartz,et al.  Calcification of the mitral annulus fibrosus with systemic embolization. A clinicopathologic study of 16 cases. , 1987, Archives of pathology & laboratory medicine.

[33]  J. Burns,et al.  Human cellular immune response to copolymer I and myelin basic protein , 1986, Neurology.

[34]  L. Rorke,et al.  Effect of treatment with copolymer 1 (Cop-1) on the in vivo and in vitro manifestations of experimental allergic encephalomyelitis (EAE) , 1983, Journal of the Neurological Sciences.

[35]  J. Kurtzke.  Rating neurologic impairment in multiple sclerosis , 1983, Neurology.

[36]  H. Powell,et al.  Pathology of multiple sclerosis. , 1983, Neurologic clinics.

[37]  O. Abramsky,et al.  Effect of a synthetic polypeptide (Cop 1) on patients with multiple sclerosis and with acute disseminated encephalomyelitis Preliminary report , 1977, Journal of the Neurological Sciences.

[38]  A. Meshorer,et al.  Suppression of experimental allergic encephalomyelitis by a synthetic polypeptide , 1971, European journal of immunology.

[39]  J. Dawson,et al.  XVIII.–The Histology of Disseminated Sclerosis , 1916, Transactions of the Royal Society of Edinburgh.