Metz, Imke

[["dc.bibliographiccitation.firstpage","148"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","84"],["dc.contributor.author","Popescu, Bogdan F. G."],["dc.contributor.author","Guo, Yong"],["dc.contributor.author","Jentoft, Mark E."],["dc.contributor.author","Parisi, Joseph E."],["dc.contributor.author","Lennon, Vanda A."],["dc.contributor.author","Pittock, Sean J."],["dc.contributor.author","Weinshenker, Brian G."],["dc.contributor.author","Wingerchuk, Dean M."],["dc.contributor.author","Giannini, Caterina"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Shuster, Elizabeth A."],["dc.contributor.author","Carter, Jonathan"],["dc.contributor.author","Boyd, Clara D."],["dc.contributor.author","Clardy, Stacey Lynn"],["dc.contributor.author","Cohen, Bruce A."],["dc.contributor.author","Lucchinetti, Claudia F."],["dc.date.accessioned","2018-11-07T10:02:13Z"],["dc.date.available","2018-11-07T10:02:13Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: To assess, in a surgical biopsy cohort of active demyelinating lesions, the diagnostic utility of aquaporin-4 (AQP4) immunohistochemistry in identifying neuromyelitis optica (NMO) or NMO spectrum disorder (NMOSD) and describe pathologic features that should prompt AQP4 immunohistochemical analysis and AQP4-immunoglobulin G (IgG) serologic testing. Methods: This was a neuropathologic cohort study of 20 surgical biopsies (19 patients; 11 cord/9 brain), performed because of diagnostic uncertainty, interpreted as active demyelinating disease and containing 2 or more of the following additional features: tissue vacuolation, granulocytic infiltrates, or astrocyte injury. Results: AQP4 immunoreactivity was lost in 18 biopsies and increased in 2. Immunopathologic features of the AQP4 loss cohort were myelin vacuolation (18), dystrophic astrocytes and granulocytes (17), vascular hyalinization (16), macrophages containing glial fibrillary acid protein (GFAP)-positive debris (14), and Creutzfeldt-Peters cells (0). All 14 cases with available serum tested positive for AQP4-IgG after biopsy. Diagnosis at last follow-up was NMO/NMOSD (15) and longitudinally extensive transverse myelitis (1 each relapsing and single). Immunopathologic features of the AQP4 increased cohort were macrophages containing GFAP-positive debris and granulocytes (2), myelin vacuolation (1), dystrophic astrocytes (1), Creutzfeldt-Peters cells (1), and vascular hyalinization (1). Diagnosis at last follow-up was multiple sclerosis (MS) and both tested AQP4-IgG seronegative after biopsy. Conclusions: AQP4 immunohistochemistry with subsequent AQP4-IgG testing has diagnostic utility in identifying cases of NMO/NMOSD. This study highlights the importance of considering NMOSD in the differential diagnosis of tumefactive brain or spinal cord lesions. AQP4-IgG testing may avert biopsy and avoid ineffective therapies if these patients are erroneously treated for MS."],["dc.identifier.isi","000347996400012"],["dc.identifier.pmid","25503621"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38185"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Diagnostic utility of aquaporin-4 in the analysis of active demyelinating lesions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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 Journal"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Stork, Lidia"],["dc.contributor.author","Ellenberger, David"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Lucchinetti, C."],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Metz, Imke"],["dc.date.accessioned","2018-11-07T10:08:49Z"],["dc.date.available","2018-11-07T10:08:49Z"],["dc.date.issued","2016"],["dc.description.sponsorship","Teva Pharma; Biogen; Novartis; Genzyme"],["dc.format.extent","367"],["dc.identifier.isi","000383267201480"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39540"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","London, ENGLAND"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Apheresis therapy in multiple sclerosis patients with histopathologically classified immunopathological patterns"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Brain"],["dc.contributor.author","Baldassari, Laura E"],["dc.contributor.author","Wattjes, Mike P"],["dc.contributor.author","Cortese, Irene C M"],["dc.contributor.author","Gass, Achim"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Yousry, Tarek"],["dc.contributor.author","Reich, Daniel S"],["dc.contributor.author","Richert, Nancy"],["dc.date.accessioned","2022-04-01T10:00:37Z"],["dc.date.available","2022-04-01T10:00:37Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Progressive multifocal leukoencephalopathy (PML) is an opportunistic infection of the CNS caused by the JC virus, which infects white and grey matter cells and leads to irreversible demyelination and neuroaxonal damage. Brain MRI, in addition to the clinical presentation and demonstration of JC virus DNA either in the CSF or by histopathology, is an important tool in the detection of PML. In clinical practice, standard MRI pulse sequences are utilized for screening, diagnosis and monitoring of PML, but validated imaging-based outcome measures for use in prospective, interventional clinical trials for PML have yet to be established. We review the existing literature regarding the use of MRI and PET in PML and discuss the implications of PML histopathology for neuroradiology. MRI not only demonstrates the localization and extent of PML lesions, but also mirrors the tissue destruction, ongoing viral spread, and resulting inflammation. Finally, we explore the potential for imaging measures to serve as an outcome in PML clinical trials and provide recommendations for current and future imaging outcome measure development in this area."],["dc.identifier.doi","10.1093/brain/awab419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105471"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","The neuroradiology of progressive multifocal leukoencephalopathy: a clinical trial perspective"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1618"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.lastpage","1632"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Stork, Lidia"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","von Gottberg, Phillip"],["dc.contributor.author","Pulkowski, Ulrich"],["dc.contributor.author","Kirsten, Florian"],["dc.contributor.author","Glatzel, Markus"],["dc.contributor.author","Rauer, Sebastian"],["dc.contributor.author","Scheibe, Franziska"],["dc.contributor.author","Radbruch, Helena"],["dc.contributor.author","Hammer, Eckhard"],["dc.contributor.author","Stürner, Klarissa H"],["dc.contributor.author","Kaulen, Barbara"],["dc.contributor.author","Heesen, Christoph"],["dc.contributor.author","Hoffmann, Frank"],["dc.contributor.author","Brock, Sebastian"],["dc.contributor.author","Pawlitzki, Marc"],["dc.contributor.author","Bopp, Tobias"],["dc.contributor.author","Metz, Imke"],["dc.date.accessioned","2020-12-10T18:38:31Z"],["dc.date.available","2020-12-10T18:38:31Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1177/1352458518819098"],["dc.identifier.eissn","1477-0970"],["dc.identifier.issn","1352-4585"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77350"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Severe meningo-/encephalitis after daclizumab therapy for multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S131"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","S132"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Zeis, Thomas"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Schaeren-Wiemers, Nicole"],["dc.date.accessioned","2018-11-07T11:23:42Z"],["dc.date.available","2018-11-07T11:23:42Z"],["dc.date.issued","2009"],["dc.identifier.isi","000270075500546"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56245"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.publisher.place","Hoboken"],["dc.relation.conference","9th European Meeting on Glial Cells in Health and Disease"],["dc.relation.eventlocation","Paris, FRANCE"],["dc.relation.issn","0894-1491"],["dc.title","GENE EXPRESSION ANALYSIS OF PARAFFIN EMBEDDED BIOPSIES FROM EARLY MS CASES"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.lastpage","91"],["dc.bibliographiccitation.volume","286"],["dc.contributor.author","Kuhlmann, T."],["dc.contributor.author","Goldschmidt, Thomas"],["dc.contributor.author","Antel, Jack P."],["dc.contributor.author","Wegner, C."],["dc.contributor.author","Koenig, Fatima Barbara"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Brueck, Wolfgang"],["dc.date.accessioned","2018-11-07T11:22:05Z"],["dc.date.available","2018-11-07T11:22:05Z"],["dc.date.issued","2009"],["dc.description.abstract","Multiple sclerosis (MS) lesions are histopathologically characterized by inflammation, demyelination/remyelination, axonal damage and gliosis. Animal experimental and in vitro studies suggest that sex hormones influence the immune system and contribute to the increased likelihood in women of developing MS. However, a variety of studies have also shown that remyelination is more marked in female rodents or that female sex hormones are beneficial for myelin repair. To determine whether gender influences the histopathology of MS lesions, we compared the extent of inflammation, axonal damage and remyelination in MS lesions of female and male MS patients. We observed no differences in the composition of inflammatory infiltrates, axonal damage or cortical pathology. Similar numbers of oligodendroglial progenitor cells and mature oligodendrocytes were present in MS lesions. Remyelination is slightly, but not significantly, more extensive in women than men in early MS lesions. The absence of significant differences in lesion pathology between female and male MS patients might be explained by a lack of a gender influence, but also might be due to the limited number of tissue samples available for histopathological analysis. (C) 2009 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jns.2009.07.014"],["dc.identifier.isi","000271621800020"],["dc.identifier.pmid","19674757"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55923"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","14th European-Charcot-Foundation Symposium"],["dc.relation.eventlocation","Taormina, ITALY"],["dc.relation.issn","0022-510X"],["dc.title","Gender differences in the histopathology of MS?"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Singh, S."],["dc.contributor.author","van Horssen, Jack"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","van der Pol, Susanne"],["dc.contributor.author","Gerritsen, Wouter"],["dc.contributor.author","Kooi, E.-J."],["dc.contributor.author","Witte, Maarten E."],["dc.contributor.author","de Vries, Helga E."],["dc.contributor.author","van der Valk, Paul"],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Amor, Sandra"],["dc.date.accessioned","2018-11-07T08:51:30Z"],["dc.date.available","2018-11-07T08:51:30Z"],["dc.date.issued","2011"],["dc.format.extent","S323"],["dc.identifier.isi","000209137301094"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21946"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.issn","1477-0970"],["dc.relation.issn","1352-4585"],["dc.title","Preactive multiple sclerosis lesions reveal innate immune activation and immune-regulation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","467"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","468"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Stork, Lidia"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Bar-Or, Amit"],["dc.contributor.author","Metz, Imke"],["dc.date.accessioned","2018-11-07T10:00:35Z"],["dc.date.available","2018-11-07T10:00:35Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1007/s00401-015-1391-6"],["dc.identifier.isi","000350203000012"],["dc.identifier.pmid","25604548"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37837"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","High CCR5 expression in natalizumab-associated progressive multifocal leukoencephalopathy immune reconstitution inflammatory syndrome supports treatment with the CCR5 inhibitor maraviroc"],["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.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"]]