T1 hypointense lesion load in secondary progressive multiple sclerosis: a comparison of pre versus post contrast loads and of manual versus semi automated threshold techniques for lesion segmentation
暂无分享,去创建一个
P. Tofts | L. Wang | J. O'riordan | D H Miller | J I O'Riordan | P Tofts | D. Compston | M Gawne Cain | A Coles | L Wang | D AS Compston | A. Coles | M. Cain | D. Miller
[1] J. Noseworthy,et al. Interrater variability with the Expanded Disability Status Scale (EDSS) and Functional Systems (FS) in a multiple sclerosis clinical trial , 1990, Neurology.
[2] A. Thompson,et al. Spinal cord MRI using multi‐array coils and fast spin echo , 1993, Neurology.
[3] G. Barker,et al. MRI dynamics of brain and spinal cord in progressive multiple sclerosis. , 1996, Journal of neurology, neurosurgery, and psychiatry.
[4] F. Barkhof,et al. Accumulation of hypointense lesions ("black holes") on T1 spin-echo MRI correlates with disease progression in multiple sclerosis , 1996, Neurology.
[5] A. S. Hall,et al. NUCLEAR MAGNETIC RESONANCE IMAGING OF THE BRAIN IN MULTIPLE SCLEROSIS , 1981, The Lancet.
[6] P. Matthews,et al. Use of proton magnetic resonance spectroscopy for monitoring disease progression in multiple sclerosis , 1994, Annals of neurology.
[7] D. Paty,et al. CORRELATION BETWEEN NMR SCAN AND BRAIN SLICE DATA IN MULTIPLE SCLEROSIS , 1984, The Lancet.
[8] J. Kurtzke. Rating neurologic impairment in multiple sclerosis , 1983, Neurology.
[9] S. Shapiro. ALLOPURINOL AND BONE-MARROW DEPRESSION , 1974 .
[10] J. Walker-Smith,et al. Cryptosporidiosis in England and Wales. , 1990, Communicable disease report. CDR weekly.
[11] R. Hohlfeld,et al. Human astrocytes are only partially competent antigen presenting cells. Possible implications for lesion development in multiple sclerosis. , 1994, Brain : a journal of neurology.
[12] H. Tobi,et al. Correlating MRI and clinical disease activity in multiple sclerosis , 1995, Neurology.
[13] A. Thompson,et al. Magnetisation transfer ratio measurement in the cervical spinal cord: a preliminary study in multiple sclerosis , 1997, Neuroradiology.
[14] A. Thompson,et al. Serial gadolinium‐enhanced MRI in relapsing/remitting multiple sclerosis of varying disease duration , 1992, Neurology.
[15] 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.
[16] G J Barker,et al. Serial proton magnetic resonance spectroscopy in acute multiple sclerosis lesions. , 1994, Brain : a journal of neurology.
[17] D. N. Landon,et al. The characterization of experimental gliosis by quantitative nuclear magnetic resonance imaging. , 1988, Brain : a journal of neurology.
[18] D. N. Landon,et al. Magnetic resonance imaging of experimental cerebral oedema. , 1986, Journal of neurology, neurosurgery, and psychiatry.
[19] G. Barker,et al. Quantification of MRI lesion load in multiple sclerosis: a comparison of three computer-assisted techniques. , 1996, Magnetic resonance imaging.
[20] C. Granger,et al. Intramuscular interferon beta‐1a for disease progression in relapsing multiple sclerosis , 1996, Annals of neurology.
[21] M Filippi,et al. A spinal cord MRI study of benign and secondary progressive multiple sclerosis , 1995, Journal of Neuroimmunology.
[22] D. Paty,et al. Interferon beta‐1b is effective in relapsing‐remitting multiple sclerosis , 1993, Neurology.
[23] G. Barker,et al. Correlation of magnetization transfer ration with clinical disability in multiple sclerosis , 1994, Annals of neurology.