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Erschienen in: Neuroradiology 1/2012

01.01.2012 | Diagnostic Neuroradiology

Brain atrophy and lesion load are related to CSF lipid-specific IgM oligoclonal bands in clinically isolated syndromes

Erschienen in: Neuroradiology | Ausgabe 1/2012

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Abstract

Introduction

The objective of this work is to study the relationship between the presence of lipid-specific oligoclonal IgM bands (LS-OCMB) in CSF, with both T2 lesion volume (T2LV) accumulation and brain atrophy (percentage change of brain volume–PCBV–and brain parenchyma fraction–BPF) in patients with clinically isolated syndromes (CIS) suggestive of demyelination.

Methods

Twenty-four CIS patients were included in this prospective study. IgG oligoclonal bands (OCGB) and LS-OCMB were determined in paired serum and CSF samples within 3 months since clinical onset. Brain MRI studies were scheduled at baseline, 3 months, first and second years after CIS onset. Differences in T2LV, PCBV and BPF between CIS patients according to the type of OCB were studied.

Results

Nine patients had no OCB; 15 had only OCGB, and seven had OCGB + LS-OCMB present in the CSF. LS-OCMB were associated with greater T2LV in all scheduled MRI studies. At the end of follow-up (year 2), it was threefold higher in patients with these antibodies than in those without LS-OCMB (3.95 cm3 vs. 1.36 cm3, p = 0.001). At that point, brain atrophy was also higher in patients with LS-OCMB (BPF, 0.73 in LS-OCMB+ patients vs. 0.76 in negative ones, p = 0.03). The rate in brain atrophy was higher in the first group of patients as well. Considering only patients with OCGB, the presence of LS-OCMB was also related to greater T2LV, T2LV increase and a trend towards higher atrophy rate.

Conclusion

The presence of LS-OCMB in the first event suggestive of demyelination is related to an early increase in lesion load and brain atrophy. These data are in line with prospective studies showing the clinical prognostic value of LS-OCMB.
Literatur
1.
Zurück zum Zitat Miller D, Barkhof F, Montalbán X et al (2005) Clinically isolated syndromes suggestive of multiple sclerosis, part I: natural history, pathogenesis, diagnosis, and prognosis. Lancet Neurol 4:281–288PubMedCrossRef Miller D, Barkhof F, Montalbán X et al (2005) Clinically isolated syndromes suggestive of multiple sclerosis, part I: natural history, pathogenesis, diagnosis, and prognosis. Lancet Neurol 4:281–288PubMedCrossRef
2.
Zurück zum Zitat Miller D, Barkhof F, Montalbán X et al (2005) Clinically isolated syndromes suggestive of multiple sclerosis, part 2: non-conventional MRI, recovery processes, and management. Lancet Neurol 4:341–348PubMedCrossRef Miller D, Barkhof F, Montalbán X et al (2005) Clinically isolated syndromes suggestive of multiple sclerosis, part 2: non-conventional MRI, recovery processes, and management. Lancet Neurol 4:341–348PubMedCrossRef
3.
Zurück zum Zitat Confavreux C, Vukusic S (2006) Natural history of multiple sclerosis: a unifying concept. Brain 129:606–616PubMedCrossRef Confavreux C, Vukusic S (2006) Natural history of multiple sclerosis: a unifying concept. Brain 129:606–616PubMedCrossRef
4.
Zurück zum Zitat Poser CM, Paty DW, Scheinberg L et al (1983) New diagnostic criteria for multiple sclerosis: guidelines for research protocols. Ann Neurol 13:227–231PubMedCrossRef Poser CM, Paty DW, Scheinberg L et al (1983) New diagnostic criteria for multiple sclerosis: guidelines for research protocols. Ann Neurol 13:227–231PubMedCrossRef
5.
Zurück zum Zitat Polman CH, Reingold SC, Edan G et al (2005) Diagnostic criteria for multiple sclerosis: 2005 revisions to the “McDonald Criteria”. Ann Neurol 58:840–846PubMedCrossRef Polman CH, Reingold SC, Edan G et al (2005) Diagnostic criteria for multiple sclerosis: 2005 revisions to the “McDonald Criteria”. Ann Neurol 58:840–846PubMedCrossRef
6.
Zurück zum Zitat Barkhof F, Filippi M, Miller DH et al (1997) Comparison of MRI criteria at first presentation to predict conversion to clinically definite multiple sclerosis. Brain 120:2059–2069PubMedCrossRef Barkhof F, Filippi M, Miller DH et al (1997) Comparison of MRI criteria at first presentation to predict conversion to clinically definite multiple sclerosis. Brain 120:2059–2069PubMedCrossRef
7.
Zurück zum Zitat Brex PA, Ciccarelli O, O'Riordan JI et al (2002) A longitudinal study of abnormalities on MRI and disability from multiple sclerosis. N Engl J Med 346:158–164PubMedCrossRef Brex PA, Ciccarelli O, O'Riordan JI et al (2002) A longitudinal study of abnormalities on MRI and disability from multiple sclerosis. N Engl J Med 346:158–164PubMedCrossRef
8.
Zurück zum Zitat Fisniku LK, Brex PA, Altmann DR et al (2008) Disability and T2 MRI lesions: a 20-year follow-up of patients with relapse onset of multiple sclerosis. Brain 131:808–817PubMedCrossRef Fisniku LK, Brex PA, Altmann DR et al (2008) Disability and T2 MRI lesions: a 20-year follow-up of patients with relapse onset of multiple sclerosis. Brain 131:808–817PubMedCrossRef
9.
Zurück zum Zitat Tintoré M, Rovira A, Rio J et al (2006) Baseline MRI predicts future attacks and disability in clinically isolated syndrome. Neurology 67:968–972PubMedCrossRef Tintoré M, Rovira A, Rio J et al (2006) Baseline MRI predicts future attacks and disability in clinically isolated syndrome. Neurology 67:968–972PubMedCrossRef
10.
Zurück zum Zitat Sailer M, O'Riordan JI, Thompson AJ et al (1999) Quantitative MRI in patients with clinically isolated syndromes suggestive of demyelination. Neurology 52:599–606PubMed Sailer M, O'Riordan JI, Thompson AJ et al (1999) Quantitative MRI in patients with clinically isolated syndromes suggestive of demyelination. Neurology 52:599–606PubMed
11.
Zurück zum Zitat Di Filippo M, Anderson VM, Altmann DR et al (2008) Brain atrophy and lesion load measures over 1 year relate to clinical status after 6 years in patients with clinically isolated syndromes. J Neurol Neurosurg Psychiatry 81:204–208CrossRef Di Filippo M, Anderson VM, Altmann DR et al (2008) Brain atrophy and lesion load measures over 1 year relate to clinical status after 6 years in patients with clinically isolated syndromes. J Neurol Neurosurg Psychiatry 81:204–208CrossRef
12.
Zurück zum Zitat van den Elskamp IJ, Boden B, Dattola V et al (2010) Cerebral atrophy as outcome measure in short-term phase 2 clinical trials in multiple sclerosis. Neuroradiology 52:875–881PubMedCrossRef van den Elskamp IJ, Boden B, Dattola V et al (2010) Cerebral atrophy as outcome measure in short-term phase 2 clinical trials in multiple sclerosis. Neuroradiology 52:875–881PubMedCrossRef
13.
Zurück zum Zitat Martola J, Bergström J, Fredrikson S et al (2010) A longitudinal observational study of brain atrophy rate reflecting four decades of multiple sclerosis: a comparison of serial 1D, 2D, and volumetric measurements from MRI images. Neuroradiology 52:109–17PubMedCrossRef Martola J, Bergström J, Fredrikson S et al (2010) A longitudinal observational study of brain atrophy rate reflecting four decades of multiple sclerosis: a comparison of serial 1D, 2D, and volumetric measurements from MRI images. Neuroradiology 52:109–17PubMedCrossRef
14.
Zurück zum Zitat Anderson VM, Fernando KT, Davies GR et al (2007) Cerebral atrophy measurement in clinically isolated syndromes and relapsing remitting multiple sclerosis: a comparison of registration-based methods. J Neuroimaging 17:61–68PubMedCrossRef Anderson VM, Fernando KT, Davies GR et al (2007) Cerebral atrophy measurement in clinically isolated syndromes and relapsing remitting multiple sclerosis: a comparison of registration-based methods. J Neuroimaging 17:61–68PubMedCrossRef
15.
Zurück zum Zitat Dalton CM, Brex PA, Jenkins R et al (2002) Progressive ventricular enlargement in patients with clinically isolated syndromes is associated with the early development of multiple sclerosis. J Neurol Neurosurg Psychiatry 73:141–147PubMedCrossRef Dalton CM, Brex PA, Jenkins R et al (2002) Progressive ventricular enlargement in patients with clinically isolated syndromes is associated with the early development of multiple sclerosis. J Neurol Neurosurg Psychiatry 73:141–147PubMedCrossRef
16.
Zurück zum Zitat Villar LM, Masjuan J, González-Porqué P et al (2002) Intrathecal IgM synthesis predicts the onset of new relapses and a worse disease course in MS. Neurology 59:555–559PubMed Villar LM, Masjuan J, González-Porqué P et al (2002) Intrathecal IgM synthesis predicts the onset of new relapses and a worse disease course in MS. Neurology 59:555–559PubMed
17.
Zurück zum Zitat Villar LM, Masjuan J, González-Porqué P et al (2003) Intrathecal IgM synthesis is a prognostic factor in multiple sclerosis. Ann Neurol 53:222–226PubMedCrossRef Villar LM, Masjuan J, González-Porqué P et al (2003) Intrathecal IgM synthesis is a prognostic factor in multiple sclerosis. Ann Neurol 53:222–226PubMedCrossRef
18.
Zurück zum Zitat Perini P, Ranzato F, Calabrese M et al (2006) Intrathecal IgM production at clinical onset correlates with a more severe disease course in multiple sclerosis. J Neurol Neurosurg Psychiatry 77:953–955PubMedCrossRef Perini P, Ranzato F, Calabrese M et al (2006) Intrathecal IgM production at clinical onset correlates with a more severe disease course in multiple sclerosis. J Neurol Neurosurg Psychiatry 77:953–955PubMedCrossRef
19.
Zurück zum Zitat Mandrioli J, Sola P, Bedin R et al (2008) A multifactorial prognostic index in multiple sclerosis. Cerebrospinal fluid IgM oligoclonal bands and clinical features to predict the evolution of the disease. J Neurol 255:1023–1031PubMedCrossRef Mandrioli J, Sola P, Bedin R et al (2008) A multifactorial prognostic index in multiple sclerosis. Cerebrospinal fluid IgM oligoclonal bands and clinical features to predict the evolution of the disease. J Neurol 255:1023–1031PubMedCrossRef
20.
Zurück zum Zitat Villar LM, Sádaba MC, Roldán E et al (2005) Intrathecal synthesis of oligoclonal IgM against myelin lipids predicts an aggressive disease course in MS. J Clin Invest 115:187–194PubMed Villar LM, Sádaba MC, Roldán E et al (2005) Intrathecal synthesis of oligoclonal IgM against myelin lipids predicts an aggressive disease course in MS. J Clin Invest 115:187–194PubMed
21.
Zurück zum Zitat Villar LM, García-Barragán N, Espiño M et al (2008) Influence of oligoclonal IgM specificity in multiple sclerosis disease course. Mult Scler 14:183–187PubMedCrossRef Villar LM, García-Barragán N, Espiño M et al (2008) Influence of oligoclonal IgM specificity in multiple sclerosis disease course. Mult Scler 14:183–187PubMedCrossRef
22.
Zurück zum Zitat Sádaba MC, González Porqué P, Masjuan J et al (2004) An ultrasensitive method for the detection of oligoclonal IgG bands. J Immunol Methods 284:141–145PubMedCrossRef Sádaba MC, González Porqué P, Masjuan J et al (2004) An ultrasensitive method for the detection of oligoclonal IgG bands. J Immunol Methods 284:141–145PubMedCrossRef
23.
Zurück zum Zitat Pascual AM, Martínez-Bisbal MC, Boscá I et al (2007) Axonal loss is progressive and partly dissociated from lesion load in early multiple sclerosis. Neurology 69:63–67PubMedCrossRef Pascual AM, Martínez-Bisbal MC, Boscá I et al (2007) Axonal loss is progressive and partly dissociated from lesion load in early multiple sclerosis. Neurology 69:63–67PubMedCrossRef
24.
Zurück zum Zitat Smith SM, De Stefano N, Jenkinson M et al (2001) Normalized accurate measurement of longitudinal brain change. J Comput Assist Tomogr 25:466–475PubMedCrossRef Smith SM, De Stefano N, Jenkinson M et al (2001) Normalized accurate measurement of longitudinal brain change. J Comput Assist Tomogr 25:466–475PubMedCrossRef
25.
Zurück zum Zitat Smith SM, Zhang Y, Jenkinson M et al (2002) Accurate, robust, and automated longitudinal and cross-sectional brain change analysis. Neuroimage 17:479–489PubMedCrossRef Smith SM, Zhang Y, Jenkinson M et al (2002) Accurate, robust, and automated longitudinal and cross-sectional brain change analysis. Neuroimage 17:479–489PubMedCrossRef
26.
Zurück zum Zitat Miller DH, Barkhof F, Frank JA et al (2002) Measurement of atrophy in multiple sclerosis: pathological basis, methodological aspects and clinical relevance. Brain 125:1676–1695PubMedCrossRef Miller DH, Barkhof F, Frank JA et al (2002) Measurement of atrophy in multiple sclerosis: pathological basis, methodological aspects and clinical relevance. Brain 125:1676–1695PubMedCrossRef
27.
Zurück zum Zitat Molyneux PD, Filippi M, Barkhof F et al (1998) Correlations between monthly enhanced MRI lesion rate and changes in T2 lesion volume in multiple sclerosis. Ann Neurol 43:332–339PubMedCrossRef Molyneux PD, Filippi M, Barkhof F et al (1998) Correlations between monthly enhanced MRI lesion rate and changes in T2 lesion volume in multiple sclerosis. Ann Neurol 43:332–339PubMedCrossRef
28.
Zurück zum Zitat Filippi M, Rovaris M, Inglese M et al (2004) Interferon beta-1a for brain tissue loss in patients at presentation with syndromes suggestive of multiple sclerosis: a randomised, double-blind, placebo-controlled trial. Lancet 364:1489–1496PubMedCrossRef Filippi M, Rovaris M, Inglese M et al (2004) Interferon beta-1a for brain tissue loss in patients at presentation with syndromes suggestive of multiple sclerosis: a randomised, double-blind, placebo-controlled trial. Lancet 364:1489–1496PubMedCrossRef
29.
Zurück zum Zitat Sharief MK, Thompson EJ (1991) The predictive value of intrathecal immunoglobulin synthesis and magnetic resonance imaging in acute isolated syndromes for subsequent development of multiple sclerosis. Ann Neurol 29:147–151PubMedCrossRef Sharief MK, Thompson EJ (1991) The predictive value of intrathecal immunoglobulin synthesis and magnetic resonance imaging in acute isolated syndromes for subsequent development of multiple sclerosis. Ann Neurol 29:147–151PubMedCrossRef
30.
Zurück zum Zitat Jongen PJ, Lycklama a Nijeholt G, Lamers KJ et al (2007) Cerebrospinal fluid IgM index correlates with cranial MRI lesion load in patients with multiple sclerosis. Eur Neurol 58:90–95PubMed Jongen PJ, Lycklama a Nijeholt G, Lamers KJ et al (2007) Cerebrospinal fluid IgM index correlates with cranial MRI lesion load in patients with multiple sclerosis. Eur Neurol 58:90–95PubMed
31.
Zurück zum Zitat Zivadinov R, Locatelli L, Cookfair D et al (2007) Interferon beta-1a slows progression of brain atrophy in relapsing-remitting multiple sclerosis predominantly by reducing gray matter atrophy. Mult Scler 13:490–501PubMed Zivadinov R, Locatelli L, Cookfair D et al (2007) Interferon beta-1a slows progression of brain atrophy in relapsing-remitting multiple sclerosis predominantly by reducing gray matter atrophy. Mult Scler 13:490–501PubMed
32.
Zurück zum Zitat Jacobs LD, Cookfair DL, Rudick RA et al (1996) Intramuscular interferon beta-1a for disease progression in relapsing multiple sclerosis. The Multiple Sclerosis Collaborative Research Group (MSCRG). Ann Neurol 39:285–294PubMedCrossRef Jacobs LD, Cookfair DL, Rudick RA et al (1996) Intramuscular interferon beta-1a for disease progression in relapsing multiple sclerosis. The Multiple Sclerosis Collaborative Research Group (MSCRG). Ann Neurol 39:285–294PubMedCrossRef
33.
Zurück zum Zitat (1998) Randomised double-blind placebo-controlled study of interferon beta-1a in relapsing/remitting multiple sclerosis. PRISMS (Prevention of Relapses and Disability by Interferon beta-1a Subcutaneously in Multiple Sclerosis) Study Group. Lancet 352:1498–1504 (1998) Randomised double-blind placebo-controlled study of interferon beta-1a in relapsing/remitting multiple sclerosis. PRISMS (Prevention of Relapses and Disability by Interferon beta-1a Subcutaneously in Multiple Sclerosis) Study Group. Lancet 352:1498–1504
34.
Zurück zum Zitat Paty DW, Li DK, UBC MS/MRI Study Group, IFNB Multiple Sclerosis Study Group (1993) Interferon beta-1b is effective in relapsing-remitting multiple sclerosis. II. MRI analysis results of a multicenter, randomized, double-blind, placebo-controlled trial. Neurology 43:662–667PubMed Paty DW, Li DK, UBC MS/MRI Study Group, IFNB Multiple Sclerosis Study Group (1993) Interferon beta-1b is effective in relapsing-remitting multiple sclerosis. II. MRI analysis results of a multicenter, randomized, double-blind, placebo-controlled trial. Neurology 43:662–667PubMed
35.
Zurück zum Zitat Boscá I, Magraner MJ, Coret F et al (2010) The risk of relapse after a clinically isolated syndrome is related to the pattern of oligoclonal bands. J Neuroimmunol 226:143–146PubMedCrossRef Boscá I, Magraner MJ, Coret F et al (2010) The risk of relapse after a clinically isolated syndrome is related to the pattern of oligoclonal bands. J Neuroimmunol 226:143–146PubMedCrossRef
36.
Zurück zum Zitat Tintoré M, Rovira A, Rio J et al (2005) Is optic neuritis more benign than other first attacks in multiple sclerosis? Ann Neurol 57:210–215PubMedCrossRef Tintoré M, Rovira A, Rio J et al (2005) Is optic neuritis more benign than other first attacks in multiple sclerosis? Ann Neurol 57:210–215PubMedCrossRef
Metadaten
Titel
Brain atrophy and lesion load are related to CSF lipid-specific IgM oligoclonal bands in clinically isolated syndromes
Publikationsdatum
01.01.2012
Erschienen in
Neuroradiology / Ausgabe 1/2012
Print ISSN: 0028-3940
Elektronische ISSN: 1432-1920
DOI
https://doi.org/10.1007/s00234-011-0841-7

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