Metz, Imke

[["dc.bibliographiccitation.firstpage","e1906"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","e1913"],["dc.bibliographiccitation.volume","97"],["dc.contributor.author","Tobin, W. Oliver"],["dc.contributor.author","Kalinowska-Lyszczarz, Alicja"],["dc.contributor.author","Weigand, Stephen D."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Tosakulwong, Nirubol"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2021-12-01T09:22:30Z"],["dc.date.available","2021-12-01T09:22:30Z"],["dc.date.issued","2021"],["dc.description.abstract","Background and Objectives The goal of this work was to compare clinical characteristics across immunopathologic subtypes of patients with multiple sclerosis. Methods Immunopathologic subtyping was performed on specimens from 547 patients with biopsy- or autopsy-confirmed CNS demyelination. Results The frequency of immunopathologic subtypes was 23% for pattern I, 56% for pattern II, and 22% for pattern III. Immunopatterns were similar in terms of age at autopsy/biopsy (median age 41 years, range 4–83 years, p = 0.16) and proportion female (54%, p = 0.71). Median follow-up after symptom onset was 2.3 years (range 0–38 years). In addition to being overrepresented among autopsy cases (45% vs 19% in biopsy cohort, p < 0.001), index attack-related disability was higher in pattern III vs II (median Expanded Disability Status Scale score 4 vs 3, p = 0.02). Monophasic clinical course was more common in patients with pattern III than pattern I or II (59% vs 33% vs 32%, p < 0.001). Similarly, patients with pattern III pathology were likely to have progressive disease compared to patients with patterns I or II when followed up for ≥5 years (24% overall, p = 0.49), with no differences in long-term survival, despite a more fulminant attack presentation. Conclusion All 3 immunopatterns can be detected in active lesions, although they are found less frequently later into the disease due to the lower number of active lesions. Pattern III is associated with a more fulminant initial attack than either pattern I or II. Biopsied patients appear to have similar long-term outcomes regardless of their immunopatterns. Progressive disease is less associated with the initial immunopattern and suggests convergence into a final common pathway related to the chronically denuded axon."],["dc.description.abstract","Background and Objectives The goal of this work was to compare clinical characteristics across immunopathologic subtypes of patients with multiple sclerosis. Methods Immunopathologic subtyping was performed on specimens from 547 patients with biopsy- or autopsy-confirmed CNS demyelination. Results The frequency of immunopathologic subtypes was 23% for pattern I, 56% for pattern II, and 22% for pattern III. Immunopatterns were similar in terms of age at autopsy/biopsy (median age 41 years, range 4–83 years, p = 0.16) and proportion female (54%, p = 0.71). Median follow-up after symptom onset was 2.3 years (range 0–38 years). In addition to being overrepresented among autopsy cases (45% vs 19% in biopsy cohort, p < 0.001), index attack-related disability was higher in pattern III vs II (median Expanded Disability Status Scale score 4 vs 3, p = 0.02). Monophasic clinical course was more common in patients with pattern III than pattern I or II (59% vs 33% vs 32%, p < 0.001). Similarly, patients with pattern III pathology were likely to have progressive disease compared to patients with patterns I or II when followed up for ≥5 years (24% overall, p = 0.49), with no differences in long-term survival, despite a more fulminant attack presentation. Conclusion All 3 immunopatterns can be detected in active lesions, although they are found less frequently later into the disease due to the lower number of active lesions. Pattern III is associated with a more fulminant initial attack than either pattern I or II. Biopsied patients appear to have similar long-term outcomes regardless of their immunopatterns. Progressive disease is less associated with the initial immunopattern and suggests convergence into a final common pathway related to the chronically denuded axon."],["dc.identifier.doi","10.1212/WNL.0000000000012782"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94416"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Clinical Correlation of Multiple Sclerosis Immunopathologic Subtypes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Openshaw, Harry"],["dc.contributor.author","Garcia-Merino, Antonio"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Freedman, Marc S."],["dc.contributor.author","Azzarelli, Biagio"],["dc.contributor.author","Kolar, Oldrich J."],["dc.contributor.author","Atkins, H. L."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T09:22:49Z"],["dc.date.available","2018-11-07T09:22:49Z"],["dc.date.issued","2006"],["dc.format.extent","S9"],["dc.identifier.isi","000241921400027"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29435"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","22nd Congress of the European-Committee-for-the-Treatment-and-Resarch-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Madrid, SPAIN"],["dc.relation.issn","1352-4585"],["dc.title","Multiple sclerosis pathology after autologous stem cell transplantation: ongoing demyelination and neurodegeneration despite suppressed inflammation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","728"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","738"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Weigand, Stephen D."],["dc.contributor.author","Popescu, Bogdan F. G."],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T09:40:29Z"],["dc.date.available","2018-11-07T09:40:29Z"],["dc.date.issued","2014"],["dc.description.abstract","Objective: Multiple sclerosis (MS) lesions demonstrate immunopathological heterogeneity in patterns of demyelination. Previous cross-sectional studies reported immunopatterns of demyelination were identical among multiple active demyelinating lesions from the same individual, but differed between individuals, leading to the hypothesis of intraindividual pathological homogeneity and interindividual heterogeneity. Other groups suggested a time-dependent heterogeneity of lesions. The objective of our present study was to analyze tissue samples collected longitudinally to determine whether patterns of demyelination persist over time within a given patient. Methods: Archival tissue samples derived from patients with pathologically confirmed central nervous system inflammatory demyelinating disease who had undergone either diagnostic serial biopsy or biopsy followed by autopsy were analyzed immunohistochemically. The inclusion criteria consisted of the presence of early active demyelinating lesions-required for immunopattern classification-obtained from the same patient at 2 or more time points. Results: Among 1,321 surgical biopsies consistent with MS, 22 cases met the study inclusion criteria. Twenty-one patients (95%) showed a persistence of immunopathological patterns in tissue sampled from different time points. This persistence was demonstrated for all major patterns of demyelination. A single patient showed features suggestive of both pattern II and pattern III on biopsy, but only pattern II among all active lesions examined at autopsy. Interpretation: These findings continue to support the concept of patient-dependent immunopathological heterogeneity in early MS and suggest that the mechanisms and targets of tissue injury may differ among patient subgroups. These observations have potentially significant implications for individualized therapeutic approaches."],["dc.identifier.doi","10.1002/ana.24163"],["dc.identifier.isi","000337706100014"],["dc.identifier.pmid","24771535"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33519"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.title","Pathologic Heterogeneity Persists in Early Active Multiple Sclerosis Lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","45"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","64"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Popescu, Bogdan F. G."],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Webb, Samuel M."],["dc.contributor.author","Tham, Mylyne"],["dc.contributor.author","Adiele, Reginald C."],["dc.contributor.author","Robinson, Christopher A."],["dc.contributor.author","Fitz-Gibbon, Patrick D."],["dc.contributor.author","Weigand, Stephen D."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Nehzati, Susan"],["dc.contributor.author","George, Graham N."],["dc.contributor.author","Pickering, Ingrid J."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Hametner, Simon"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Yong, Guo"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T10:22:07Z"],["dc.date.available","2018-11-07T10:22:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) in which oligodendrocytes, the CNS cells that stain most robustly for iron and myelin are the targets of injury. Metals are essential for normal CNS functioning, and metal imbalances have been linked to demyelination and neuro-degeneration. Using a multidisciplinary approach involving synchrotron techniques, iron histochemistry and immunohistochemistry, we compared the distribution and quantification of iron and zinc in MS lesions to the surrounding normal appearing and periplaque white matter, and assessed the involvement of these metals in MS lesion pathogenesis. We found that the distribution of iron and zinc is heterogeneous in MS plaques, and with few remarkable exceptions they do not accumulate in chronic MS lesions. We show that brain iron tends to decrease with increasing age and disease duration of MS patients; reactive astrocytes organized in large astrogliotic areas in a subset of smoldering and inactive plaques accumulate iron and safely store it in ferritin; a subset of smoldering lesions do not contain a rim of iron-loaded macrophages/microglia; and the iron content of shadow plaques varies with the stage of remyelination. Zinc in MS lesions was generally decreased, paralleling myelin loss. Iron accumulates concentrically in a subset of chronic inactive lesions suggesting that not all iron rims around MS lesions equate with smoldering plaques. Upon degeneration of iron-loaded microglia/macrophages, astrocytes may form an additional protective barrier that may prevent iron-induced oxidative damage."],["dc.identifier.doi","10.1007/s00401-017-1696-8"],["dc.identifier.isi","000403235900004"],["dc.identifier.pmid","28332093"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14717"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42219"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Pathogenic implications of distinct patterns of iron and zinc in chronic MS lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e90"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Openshaw, Harry"],["dc.contributor.author","Garcia-Merino, Antonio"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Freedman, Marc S."],["dc.contributor.author","Azzarelli, Biagio"],["dc.contributor.author","Kolar, Oldrich J."],["dc.contributor.author","Atkins, H. L."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:18:29Z"],["dc.date.available","2018-11-07T11:18:29Z"],["dc.date.issued","2008"],["dc.identifier.doi","10.1093/brain/awm181"],["dc.identifier.isi","000252903900002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55045"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Autologous hematopoietic stem cell transplantation: the glass seems to be half full for aggressive, early forms of MS and half empty for advanced MS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","20"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Weigand, S."],["dc.contributor.author","Popescu, Bogdan F. G."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Parisi, J."],["dc.contributor.author","Guo, Y."],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lucchinetti, C."],["dc.date.accessioned","2018-11-07T09:18:50Z"],["dc.date.available","2018-11-07T09:18:50Z"],["dc.date.issued","2013"],["dc.identifier.isi","000328751400023"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28489"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","Copenhagen, DENMARK"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Immunopathologic heterogeneity persists in early active multiple sclerosis lesions"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1254"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1262"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Openshaw, Harry"],["dc.contributor.author","Garcia-Merino, Antonio"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Freedman, Marc S."],["dc.contributor.author","Atkins, H. L."],["dc.contributor.author","Azzarelli, Biagio"],["dc.contributor.author","Kolar, Oldrich J."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:02:36Z"],["dc.date.available","2018-11-07T11:02:36Z"],["dc.date.issued","2007"],["dc.description.abstract","The present study analyses autopsy material from five multiple sclerosis patients who received autologous stem cell transplantation. A total of 53 white matter lesions were investigated using routine and immunohistochemical stainings to characterize the demyelinating activity, inflammatory infiltrates, acutely damaged axons and macrophages/microglial cells. We found evidence for ongoing active demyelination in all of the five patients. The inflammatory infiltrate within the lesions showed only very few T cells and CD8+ cytotoxic T cells dominated the T cell population. B cells and plasma cells were completely absent from the lesions. High numbers of acutely damaged axons were found in active lesion areas. Tissue injury was associated with activated macrophages/microglial cells. The present results indicate that ongoing demyelination and axonal degeneration exist despite pronounced immunosuppression. Our data parallel results from some of the clinical phase I/II studies showing continued clinical disease progression in multiple sclerosis patients with high expanded disability system scores despite autologous stem cell transplantation."],["dc.identifier.doi","10.1093/brain/awl370"],["dc.identifier.isi","000246293400010"],["dc.identifier.pmid","17293360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51422"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Autologous haematopoietic stem cell transplantation fails to stop demyelination and neurodegeneration in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","710"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","721"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Frischer, Josa M."],["dc.contributor.author","Weigand, Stephen D."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Kale, Nilufer"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Pirko, Istvan"],["dc.contributor.author","Mandrekar, Jay"],["dc.contributor.author","Bramow, Stephan"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T09:49:40Z"],["dc.date.available","2018-11-07T09:49:40Z"],["dc.date.issued","2015"],["dc.description.abstract","ObjectiveAn extensive analysis of white matter plaques in a large sample of multiple sclerosis (MS) autopsies provides insights into the dynamic nature of MS pathology. MethodsOne hundred twenty MS cases (1,220 tissue blocks) were included. Plaque types were classified according to demyelinating activity based on stringent criteria. Early active, late active, smoldering, inactive, and shadow plaques were distinguished. A total of 2,476 MS white matter plaques were identified. Plaque type distribution was analyzed in relation to clinical data. ResultsActive plaques were most often found in early disease, whereas at later stages, smoldering, inactive, and shadow plaques predominated. The presence of early active plaques rapidly declined with disease duration. Plaque type distribution differed significantly by clinical course. The majority of plaques in acute monophasic and relapsing-remitting MS (RRMS) were active. Among secondary progressive MS (SPMS) cases with attacks, all plaque types could be distinguished including active plaques, in contrast to SPMS without attacks, in which inactive plaques predominated. Smoldering plaques were frequently and almost exclusively found in progressive MS. At 47 years of age, an equilibrium was observed between active and inactive plaques, whereas smoldering plaques began to peak. Men displayed a higher proportion of smoldering plaques. InterpretationDisease duration, clinical course, age, and gender contribute to the dynamic nature of white matter MS pathology. Active MS plaques predominate in acute and early RRMS and are the likely substrate of clinical attacks. Progressive MS transitions to an accumulation of smoldering plaques characterized by microglial activation and slow expansion of pre-existing plaques. Whether current MS therapeutics impact this pathological driver of disease progression remains uncertain. Ann Neurol 2015;78:Ann Neurol 2015;78:679-696"],["dc.identifier.doi","10.1002/ana.24497"],["dc.identifier.isi","000363727900006"],["dc.identifier.pmid","26239536"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35550"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1531-8249"],["dc.relation.issn","0364-5134"],["dc.title","Clinical and pathological insights into the dynamic nature of the white matter multiple sclerosis plaque"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e335"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology - Neuroimmunology Neuroinflammation"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Körtvélyessy, Peter"],["dc.contributor.author","Breu, Markus"],["dc.contributor.author","Pawlitzki, Marc"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Heinze, Hans-Jochen"],["dc.contributor.author","Matzke, Mike"],["dc.contributor.author","Mawrin, Christian"],["dc.contributor.author","Rommer, Paulus"],["dc.contributor.author","Kovacs, Gabor G."],["dc.contributor.author","Mitter, Christian"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Höftberger, Romana"],["dc.contributor.author","Leypoldt, Frank"],["dc.date.accessioned","2020-12-10T18:41:41Z"],["dc.date.available","2020-12-10T18:41:41Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1212/NXI.0000000000000335"],["dc.identifier.eissn","2332-7812"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77650"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","ADEM-like presentation, anti-MOG antibodies, and MS pathology: TWO case reports"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1759"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1775"],["dc.bibliographiccitation.volume","131"],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.contributor.author","Gavrilova, R. H."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Scheithauer, Bernd W."],["dc.contributor.author","Weigand, S."],["dc.contributor.author","Thomsen, K."],["dc.contributor.author","Mandrekar, Jay"],["dc.contributor.author","Altintas, A."],["dc.contributor.author","Erickson, Bradley J."],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Giannini, Caterina"],["dc.contributor.author","Lassmann, Hans"],["dc.contributor.author","Linbo, L."],["dc.contributor.author","Pittock, Sean J."],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:13:15Z"],["dc.date.available","2018-11-07T11:13:15Z"],["dc.date.issued","2008"],["dc.description.abstract","Atypical imaging features of multiple sclerosis lesions include size > 2 cm, mass effect, oedema and/or ring enhancement. This constellation is often referred to as 'tumefactive multiple sclerosis'. Previous series emphasize their unifocal and clinically isolated nature, however, evolution of these lesions is not well defined. Biopsy may be required for diagnosis. We describe clinical and radiographic features in 168 patients with biopsy confirmed CNS inflammatory demyelinating disease (IDD). Lesions were analysed on pre- and post-biopsy magnetic resonance imaging (MRI) for location, size, mass effect/oedema, enhancement, multifocality and fulfilment of Barkhof criteria. Clinical data were correlated to MRI. Female to male ratio was 1.2 : 1, median age at onset, 37 years, duration between symptom onset and biopsy, 7.1 weeks and total disease duration, 3.9 years. Clinical course prior to biopsy was a first neurological event in 61%, relapsing-remitting in 29% and progressive in 4%. Presentations were typically polysymptomatic, with motor, cognitive and sensory symptoms predominating. Aphasia, agnosia, seizures and visual field defects were observed. At follow-up, 70% developed definite multiple sclerosis, and 14% had an isolated demyelinating syndrome. Median time to second attack was 4.8 years, and median EDSS at follow-up was 3.0. Multiple lesions were present in 70% on pre- biopsy MRI, and in 83% by last MRI, with Barkhof criteria fulfilled in 46% prior to biopsy and 55% by follow-up. Only 17% of cases remained unifocal. Median largest lesion size on T2-weighted images was 4 cm ( range 0.5-12), with a discernible size of 2.1cm( range 0.5-7.5). Biopsied lesions demonstrated mass effect in 45% and oedema in 77%. A strong association was found between lesion size, and presence of mass effect and/or oedema (P < 0.001). Ring enhancement was frequent. Most tumefactive features did not correlate with gender, course or diagnosis. Although lesion size > 5 cm was associated with a slightly higher EDSS at last follow-up, long-term prognosis in patients with disease duration > 10 years was better ( EDSS 1.5) compared with a population-based multiple sclerosis cohort matched for disease duration ( EDSS 3.5; P < 0.001). Given the retrospective nature of the study, the precise reason for biopsy could not always be determined. This study underscores the diagnostically challenging nature of CNS IDDs that present with atypical clinical or radiographic features. Most have multifocal disease at onset, and develop RRMS by follow-up. Although increased awareness of this broad spectrum may obviate need for biopsy in many circumstances, an important role for diagnostic brain biopsy may be required in some cases."],["dc.description.sponsorship","NCRR NIH HHS [UL 1 RR24150-01]; NINDS NIH HHS [R01 NS049577, NS049577]"],["dc.identifier.doi","10.1093/brain/awn098"],["dc.identifier.isi","000257397100010"],["dc.identifier.pmid","18535080"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53846"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical and radiographic spectrum of pathologically confirmed tumefactive multiple sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]