A three-year, multi-parametric MRI study in patients at presentation with CIS
Objectives To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify non-conventional magnetic resonance (MR) metrics predictive of evolution to definite MS. Methods Brain conventional and magnetization tra...
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| Published in: | Journal of neurology Vol. 255; no. 5; pp. 683 - 691 |
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| Main Authors: | , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Darmstadt
Steinkopff-Verlag
01.05.2008
Springer Springer Nature B.V |
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| ISSN: | 0340-5354, 1432-1459 |
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| Abstract | Objectives
To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify non-conventional magnetic resonance (MR) metrics predictive of evolution to definite MS.
Methods
Brain conventional and magnetization transfer (MT) MRI scans were obtained from 208 CIS patients and 55 matched healthy controls, recruited in four centres. Patients were assessed clinically at the time of MRI acquisition and after a median period of 3.1 years from disease onset. The following measures were derived: T2, T1 and gadolinium (Gd)- enhancing lesion volumes (LV), normalized brain volume (NBV), MTR histogram-derived quantities of the normal-appearing white matter (NAWM) and grey matter (GM).
Results
During the follow-up, 43 % of the patients converted to definite MS. At baseline, a significant inter-centre heterogeneity was detected for T2 LV (p = 0.003), T1 LV (p = 0.006), NBV (p < 0.001) and MTR histogram-derived metrics (p < 0.001). Pooled average MTR values differed between CIS patients and controls for NAWM (p = 0.003) and GM (p = 0.01). Gdactivity and positivity of International Panel (IP) criteria for disease dissemination in space (DIS), but not NAWM and GM MTR and NBV, were associated with evolution to definite MS. The final multivariable model retained only MRI IP criteria for DIS (p = 0.05; HR = 1.66, 95 % CI = 1.00–2.77) as an independent predictor of evolution to definite MS.
Conclusions
Although irreversible tissue injury is present from the earliest clinical stages of MS, macroscopic focal lesions but not "diffuse" brain damage measured by MTR are associated to an increased risk of subsequent development of definite MS in CIS patients. |
|---|---|
| AbstractList | Objectives
To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify non-conventional magnetic resonance (MR) metrics predictive of evolution to definite MS.
Methods
Brain conventional and magnetization transfer (MT) MRI scans were obtained from 208 CIS patients and 55 matched healthy controls, recruited in four centres. Patients were assessed clinically at the time of MRI acquisition and after a median period of 3.1 years from disease onset. The following measures were derived: T2, T1 and gadolinium (Gd)- enhancing lesion volumes (LV), normalized brain volume (NBV), MTR histogram-derived quantities of the normal-appearing white matter (NAWM) and grey matter (GM).
Results
During the follow-up, 43 % of the patients converted to definite MS. At baseline, a significant inter-centre heterogeneity was detected for T2 LV (p = 0.003), T1 LV (p = 0.006), NBV (p < 0.001) and MTR histogram-derived metrics (p < 0.001). Pooled average MTR values differed between CIS patients and controls for NAWM (p = 0.003) and GM (p = 0.01). Gdactivity and positivity of International Panel (IP) criteria for disease dissemination in space (DIS), but not NAWM and GM MTR and NBV, were associated with evolution to definite MS. The final multivariable model retained only MRI IP criteria for DIS (p = 0.05; HR = 1.66, 95 % CI = 1.00–2.77) as an independent predictor of evolution to definite MS.
Conclusions
Although irreversible tissue injury is present from the earliest clinical stages of MS, macroscopic focal lesions but not "diffuse" brain damage measured by MTR are associated to an increased risk of subsequent development of definite MS in CIS patients. To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify non-conventional magnetic resonance (MR) metrics predictive of evolution to definite MS. Brain conventional and magnetization transfer (MT) MRI scans were obtained from 208 CIS patients and 55 matched healthy controls, recruited in four centres. Patients were assessed clinically at the time of MRI acquisition and after a median period of 3.1 years from disease onset. The following measures were derived: T2, T1 and gadolinium (Gd)- enhancing lesion volumes (LV), normalized brain volume (NBV), MTR histogram-derived quantities of the normal-appearing white matter (NAWM) and grey matter (GM). During the follow-up, 43 % of the patients converted to definite MS. At baseline, a significant inter-centre heterogeneity was detected for T2 LV (p = 0.003), T1 LV (p = 0.006), NBV (p < 0.001) and MTR histogram-derived metrics (p < 0.001). Pooled average MTR values differed between CIS patients and controls for NAWM (p = 0.003) and GM (p = 0.01). Gdactivity and positivity of International Panel (IP) criteria for disease dissemination in space (DIS), but not NAWM and GM MTR and NBV, were associated with evolution to definite MS. The final multivariable model retained only MRI IP criteria for DIS (p = 0.05; HR = 1.66, 95 % CI = 1.00-2.77) as an independent predictor of evolution to definite MS. Although irreversible tissue injury is present from the earliest clinical stages of MS, macroscopic focal lesions but not "diffuse" brain damage measured by MTR are associated to an increased risk of subsequent development of definite MS in CIS patients. [PUBLICATION ABSTRACT] To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify non-conventional magnetic resonance (MR) metrics predictive of evolution to definite MS.OBJECTIVESTo define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify non-conventional magnetic resonance (MR) metrics predictive of evolution to definite MS.Brain conventional and magnetization transfer (MT) MRI scans were obtained from 208 CIS patients and 55 matched healthy controls, recruited in four centres. Patients were assessed clinically at the time of MRI acquisition and after a median period of 3.1 years from disease onset. The following measures were derived: T2, T1 and gadolinium (Gd)- enhancing lesion volumes (LV), normalized brain volume (NBV), MTR histogram-derived quantities of the normal-appearing white matter (NAWM) and grey matter (GM).METHODSBrain conventional and magnetization transfer (MT) MRI scans were obtained from 208 CIS patients and 55 matched healthy controls, recruited in four centres. Patients were assessed clinically at the time of MRI acquisition and after a median period of 3.1 years from disease onset. The following measures were derived: T2, T1 and gadolinium (Gd)- enhancing lesion volumes (LV), normalized brain volume (NBV), MTR histogram-derived quantities of the normal-appearing white matter (NAWM) and grey matter (GM).During the follow-up, 43 % of the patients converted to definite MS. At baseline, a significant inter-centre heterogeneity was detected for T2 LV (p = 0.003), T1 LV (p = 0.006), NBV (p < 0.001) and MTR histogram-derived metrics (p < 0.001). Pooled average MTR values differed between CIS patients and controls for NAWM (p = 0.003) and GM (p = 0.01). Gdactivity and positivity of International Panel (IP) criteria for disease dissemination in space (DIS), but not NAWM and GM MTR and NBV, were associated with evolution to definite MS. The final multivariable model retained only MRI IP criteria for DIS (p = 0.05; HR = 1.66, 95 % CI = 1.00-2.77) as an independent predictor of evolution to definite MS.RESULTSDuring the follow-up, 43 % of the patients converted to definite MS. At baseline, a significant inter-centre heterogeneity was detected for T2 LV (p = 0.003), T1 LV (p = 0.006), NBV (p < 0.001) and MTR histogram-derived metrics (p < 0.001). Pooled average MTR values differed between CIS patients and controls for NAWM (p = 0.003) and GM (p = 0.01). Gdactivity and positivity of International Panel (IP) criteria for disease dissemination in space (DIS), but not NAWM and GM MTR and NBV, were associated with evolution to definite MS. The final multivariable model retained only MRI IP criteria for DIS (p = 0.05; HR = 1.66, 95 % CI = 1.00-2.77) as an independent predictor of evolution to definite MS.Although irreversible tissue injury is present from the earliest clinical stages of MS, macroscopic focal lesions but not "diffuse" brain damage measured by MTR are associated to an increased risk of subsequent development of definite MS in CIS patients.CONCLUSIONSAlthough irreversible tissue injury is present from the earliest clinical stages of MS, macroscopic focal lesions but not "diffuse" brain damage measured by MTR are associated to an increased risk of subsequent development of definite MS in CIS patients. Objectives: To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify non-conventional magnetic resonance (MR) metrics predictive of evolution to definite MS. Methods: Brain conventional and magnetization transfer (MT) MRI scans were obtained from 208 CIS patients and 55 matched healthy controls, recruited in four centres. Patients were assessed clinically at the time of MRI acquisition and after a median period of 3.1 years from disease onset. The following measures were derived: T2, T1 and gadolinium (Gd)- enhancing lesion volumes (LV), normalized brain volume (NBV), MTR histogram-derived quantities of the normal-appearing white matter (NAWM) and grey matter (GM). Results: During the follow-up, 43 % of the patients converted to definite MS. At baseline, a significant inter-centre heterogeneity was detected for T2 LV (p = 0.003), T1 LV (p = 0.006), NBV (p < 0.001) and MTR histogram-derived metrics (p < 0.001). Pooled average MTR values differed between CIS patients and controls for NAWM (p = 0.003) and GM (p = 0.01). Gdactivity and positivity of International Panel (IP) criteria for disease dissemination in space (DIS), but not NAWM and GM MTR and NBV, were associated with evolution to definite MS. The final multivariable model retained only MRI IP criteria for DIS (p = 0.05; HR = 1.66, 95 % CI = 1.00-2.77) as an independent predictor of evolution to definite MS. Conclusions: Although irreversible tissue injury is present from the earliest clinical stages of MS, macroscopic focal lesions but not "diffuse" brain damage measured by MTR are associated to an increased risk of subsequent development of definite MS in CIS patients. To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify non-conventional magnetic resonance (MR) metrics predictive of evolution to definite MS. Brain conventional and magnetization transfer (MT) MRI scans were obtained from 208 CIS patients and 55 matched healthy controls, recruited in four centres. Patients were assessed clinically at the time of MRI acquisition and after a median period of 3.1 years from disease onset. The following measures were derived: T2, T1 and gadolinium (Gd)- enhancing lesion volumes (LV), normalized brain volume (NBV), MTR histogram-derived quantities of the normal-appearing white matter (NAWM) and grey matter (GM). During the follow-up, 43 % of the patients converted to definite MS. At baseline, a significant inter-centre heterogeneity was detected for T2 LV (p = 0.003), T1 LV (p = 0.006), NBV (p < 0.001) and MTR histogram-derived metrics (p < 0.001). Pooled average MTR values differed between CIS patients and controls for NAWM (p = 0.003) and GM (p = 0.01). Gdactivity and positivity of International Panel (IP) criteria for disease dissemination in space (DIS), but not NAWM and GM MTR and NBV, were associated with evolution to definite MS. The final multivariable model retained only MRI IP criteria for DIS (p = 0.05; HR = 1.66, 95 % CI = 1.00-2.77) as an independent predictor of evolution to definite MS. Although irreversible tissue injury is present from the earliest clinical stages of MS, macroscopic focal lesions but not "diffuse" brain damage measured by MTR are associated to an increased risk of subsequent development of definite MS in CIS patients. |
| Author | Polman, C. Barkhof, F. Agosta, F. Korteweg, T. Filippi, M. Rocca, M. A. Sormani, M. P. Tintorè, M. Montalban, X. Fernando, K. Tortorella, P. Miller, D. H. Thompson, A. Rovira, A. |
| Author_xml | – sequence: 1 givenname: M. A. surname: Rocca fullname: Rocca, M. A. organization: Neuroimaging Research Unit, Dept. of Neurology, Scientific Institute and University Ospedale, San Raffaele – sequence: 2 givenname: F. surname: Agosta fullname: Agosta, F. organization: Neuroimaging Research Unit, Dept. of Neurology, Scientific Institute and University Ospedale, San Raffaele – sequence: 3 givenname: M. P. surname: Sormani fullname: Sormani, M. P. organization: Neuroimaging Research Unit, Dept. of Neurology, Scientific Institute and University Ospedale, San Raffaele, Biostatistics Unit, Dept. of Health Sciences, University of Genoa – sequence: 4 givenname: K. surname: Fernando fullname: Fernando, K. organization: Dept. of Neuroinflammation and Headache, Institute of Neurology, University College London – sequence: 5 givenname: M. surname: Tintorè fullname: Tintorè, M. organization: Dept. of Neuroimmunology, Hospital Vall d'Hebron – sequence: 6 givenname: T. surname: Korteweg fullname: Korteweg, T. organization: Dept. of Neuroradiology, VU University Medical Centre – sequence: 7 givenname: P. surname: Tortorella fullname: Tortorella, P. organization: Neuroimaging Research Unit, Dept. of Neurology, Scientific Institute and University Ospedale, San Raffaele – sequence: 8 givenname: D. H. surname: Miller fullname: Miller, D. H. organization: Dept. of Neuroinflammation and Headache, Institute of Neurology, University College London – sequence: 9 givenname: A. surname: Thompson fullname: Thompson, A. organization: Brain Injury and Neurorehabilitation, Institute of Neurology, University College London – sequence: 10 givenname: A. surname: Rovira fullname: Rovira, A. organization: Dept. of Radiology, Hospital Vall d'Hebron – sequence: 11 givenname: X. surname: Montalban fullname: Montalban, X. organization: Dept. of Neuroimmunology, Hospital Vall d'Hebron – sequence: 12 givenname: C. surname: Polman fullname: Polman, C. organization: Dept. of Neurology, VU University Medical Centre – sequence: 13 givenname: F. surname: Barkhof fullname: Barkhof, F. organization: Dept. of Neuroradiology, VU University Medical Centre – sequence: 14 givenname: M. surname: Filippi fullname: Filippi, M. email: m.filippi@hsr.it organization: Neuroimaging Research Unit, Dept. of Neurology, Scientific Institute and University Ospedale, San Raffaele |
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| Keywords | predictors magnetization transfer disease evolution MRI clinically isolated syndrome multiple sclerosis Human Nervous system diseases Multiple sclerosis Magnetization Nuclear magnetic resonance imaging Inflammatory disease Central nervous system disease Evolution |
| Language | English |
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| PublicationSubtitle | Official Journal of the European Neurological Society |
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| References | TintoreAJNR Am J Neuroradiol200021702107827811:STN:280:DC%2BD3c3kt1yktw%3D%3D BarkhofAnn Neurol2003537181278341710.1002/ana.10551 TintoreNeurology2006679681700096210.1212/01.wnl.0000237354.10144.ec1:STN:280:DC%2BD28rnt1SitQ%3D%3D BjartmarNeurology2001571248115918441:STN:280:DC%2BD3MrksVyhtw%3D%3D PetersonAnn Neurol2001503891155879610.1002/ana.11231:STN:280:DC%2BD3MrhtFCnug%3D%3D PolmanAnn Neurol2005588401628361510.1002/ana.20703 DaltonBrain200412711011499891410.1093/brain/awh126 BrexN Engl J Med20023461581179684910.1056/NEJMoa011341 KortewegLancet Neurol200652211648837710.1016/S1474-4422(06)70353-2 IannucciAJNR Am J Neuroradiol2000211034108710091:STN:280:DC%2BD3cvosVyqsg%3D%3D DaltonJ Neurol Neurosurg Psychiatry2002731411212217010.1136/jnnp.73.2.1411:STN:280:DC%2BD38zns1Gkug%3D%3D CHAMPSNeurology200259998 FilippiBrain20031264331253840910.1093/brain/awg0381:STN:280:DC%2BD3s%2FmvFCjsg%3D%3D FernandoBrain200512829111621967310.1093/brain/awh6541:STN:280:DC%2BD2MnivV2muw%3D%3D BeckArch Ophthalmol199311177385124771:STN:280:DyaK3s3ptVGntw%3D%3D KapposNeurology20066712421691469310.1212/01.wnl.0000237641.33768.8d1:CAS:528:DC%2BD28XhtFyqtLfL MillerAnn Neurol198926635281783810.1002/ana.4102605081:STN:280:DyaK3c%2FlsFSksQ%3D%3D van WaesbergheAnn Neurol1999467471055399210.1002/1531-8249(199911)46:5<747::AID-ANA10>3.0.CO;2-41:STN:280:DC%2BD3c%2FhvFChsg%3D%3D PoserAnn Neurol198313227684713410.1002/ana.4101303021:STN:280:DyaL3s3gt1OgtQ%3D%3D JacobsN Engl J Med20003438981100636510.1056/NEJM2000092834313011:CAS:528:DC%2BD3cXntFOkt7k%3D FilippiNeurology19944463581648161:STN:280:DyaK2c3hslyrug%3D%3D McDonaldAnn Neurol2001501211145630210.1002/ana.10321:STN:280:DC%2BD38%2FitFOhug%3D%3D AgostaBrain200612926201695140910.1093/brain/awl208 SmithNeuroImage2002174791248210010.1006/nimg.2002.1040 MillerJ Neurol Neurosurg Psychiatry198851156932212241:STN:280:DyaL1M7isV2gtQ%3D%3D SchmiererAnn Neurol2004564071534986810.1002/ana.20202 BrexJ Neurol Neurosurg Psychiatry2001703901118186510.1136/jnnp.70.3.3901:STN:280:DC%2BD3M3gsFWkuw%3D%3D CharilLancet Neurol200658411698773110.1016/S1474-4422(06)70572-5 RovarisNeurology20056515261630147710.1212/01.wnl.0000184471.83948.e01:STN:280:DC%2BD2MnitVGjsQ%3D%3D FernandoBrain200412713611512861510.1093/brain/awh1531:STN:280:DC%2BD2c3mslKisg%3D%3D CaramiaMagn Reson Imaging2002203831220686210.1016/S0730-725X(02)00519-2 MorrisseyBrain1993116135845345410.1093/brain/116.1.135 TraboulseeNeurology200259126121053211:STN:280:DC%2BD38zmtVOguw%3D%3D KurtzkeNeurology198333144466852371:STN:280:DyaL2c%2FktValsQ%3D%3D AllenJ Neurol Sci1979418143884510.1016/0022-510X(79)90142-41:STN:280:DyaE1M7nsVOitQ%3D%3D FilippiLancet200436414891550089310.1016/S0140-6736(04)17271-11:CAS:528:DC%2BD2cXovVKrtrw%3D GalloArch Neurol2005628031588326910.1001/archneur.62.5.803 RovarisJ Neurol1997244266911259710.1007/s0041500500831:STN:280:DyaK2s3ms1ykug%3D%3D MillerLancet Neurol200543411590773810.1016/S1474-4422(05)70095-81:CAS:528:DC%2BD2MXls1eis7g%3D ComiLancet200135715761137764510.1016/S0140-6736(00)04725-51:CAS:528:DC%2BD3MXjslSit78%3D KaiserAJNR Am J Neuroradiol2000211043108710111:STN:280:DC%2BD3cvosVyqsA%3D%3D EvangelouAnn Neurol2000473911071626410.1002/1531-8249(200003)47:3<391::AID-ANA20>3.0.CO;2-J1:STN:280:DC%2BD3c7nvFSjug%3D%3D O'RiordanBrain1998121495954952510.1093/brain/121.3.495 BrexNeurology2000541689107625181:STN:280:DC%2BD3c3islyrsA%3D%3D MillerJ Neurol Neurosurg Psychiatry19915468319409381:STN:280:DyaK38%2FksVGksw%3D%3D10.1136/jnnp.54.8.683 TintoreAnn Neurol2005572101566896510.1002/ana.20363 AndersonJ Neuroimaging200717611723887110.1111/j.1552-6569.2006.00081.x MillerLancet Neurol200542811584784110.1016/S1474-4422(05)70071-5 BarkhofBrain19971202059939702110.1093/brain/120.11.2059 CHAMPS (776_CR12) 2002; 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To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to... To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to identify... Objectives: To define the extent of overall brain damage in patients with clinically isolated syndromes (CIS) suggestive of multiple sclerosis (MS) and to... |
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| SubjectTerms | Adult Atrophy - diagnosis Atrophy - physiopathology Biological and medical sciences Brain - pathology Brain - physiopathology Brain damage Disability Evaluation Disease Progression Female Humans Image Processing, Computer-Assisted Longitudinal Studies Magnetic Resonance Imaging - methods Male Mass Screening Medical sciences Medicine Medicine & Public Health Multiple sclerosis Multiple Sclerosis - diagnosis Multiple Sclerosis - physiopathology Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Neurology Neuroradiology Neurosciences Original Communication Predictive Value of Tests Prognosis Retrospective Studies Risk Factors Severity of Illness Index Spinal cord Syndrome |
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| Title | A three-year, multi-parametric MRI study in patients at presentation with CIS |
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