Pellkofer, Hannah Luise

[["dc.bibliographiccitation.firstpage","1213"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Otology & Neurotology"],["dc.bibliographiccitation.lastpage","1216"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Bertlich, Mattis"],["dc.contributor.author","Ihler, Friedrich"],["dc.contributor.author","Weiss, Bernhard G."],["dc.contributor.author","Freytag, Saskia"],["dc.contributor.author","Jakob, Mark"],["dc.contributor.author","Strupp, Michael"],["dc.contributor.author","Pellkofer, Hannah"],["dc.contributor.author","Canis, Martin"],["dc.date.accessioned","2020-12-10T18:19:57Z"],["dc.date.available","2020-12-10T18:19:57Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1097/MAO.0000000000001510"],["dc.identifier.issn","1531-7129"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75432"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Fingolimod (FTY-720) is Capable of Reversing Tumor Necrosis Factor Induced Decreases in Cochlear Blood Flow"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Pellkofer, Hannah"],["dc.contributor.author","Siebert, Nadja"],["dc.contributor.author","Korporal-Kuhnke, Mirjam"],["dc.contributor.author","Hümmert, Martin W."],["dc.contributor.author","Ringelstein, Marius"],["dc.contributor.author","Rommer, Paulus S."],["dc.contributor.author","Ayzenberg, Ilya"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Klotz, Luisa"],["dc.contributor.author","Asgari, Nasrin"],["dc.contributor.author","Zrzavy, Tobias"],["dc.contributor.author","Höftberger, Romana"],["dc.contributor.author","Tobia, Rafik"],["dc.contributor.author","Buttmann, Mathias"],["dc.contributor.author","Fechner, Kai"],["dc.contributor.author","Schanda, Kathrin"],["dc.contributor.author","Weber, Martin"],["dc.contributor.author","Asseyer, Susanna"],["dc.contributor.author","Haas, Jürgen"],["dc.contributor.author","Lechner, Christian"],["dc.contributor.author","Kleiter, Ingo"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.author","Rostasy, Kevin"],["dc.contributor.author","Reindl, Markus"],["dc.contributor.author","Kümpfel, Tania"],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Wildemann, Brigitte"],["dc.date.accessioned","2021-04-14T08:32:46Z"],["dc.date.available","2021-04-14T08:32:46Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s12974-020-01824-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17535"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84009"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1742-2094"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Cerebrospinal fluid findings in patients with myelin oligodendrocyte glycoprotein (MOG) antibodies. Part 1: Results from 163 lumbar punctures in 100 adult patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","38"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Current Neurology and Neuroscience Reports"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Kretzschmar, Benedikt"],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2018-11-07T10:16:31Z"],["dc.date.available","2018-11-07T10:16:31Z"],["dc.date.issued","2016"],["dc.description.abstract","Three oral disease-modifying drugs-fingolimod, teriflunomide, and dimethyl fumarate (DMF)-are available for treatment of relapsing forms of multiple sclerosis (MS). All three agents were approved in the last decade, primarily on the basis of a moderate to substantial reduction in the occurrence of MS relapses and central nervous system lesion formation detected by MRI. In the trials leading to approval, the first oral disease-modifying drug, fingolimod, reduced the annualized relapse rate (ARR) from 0.40 in placebo-treated patients to 0.18 (FREEDOMS) and from 0.33 in patients treated with interferon beta(1a) intramuscularly to 0.16 (TRANSFORMS). Teriflunomide, approved on the basis of the two placebo-controlled trials TEMSO and TOWER, demonstrated a reduction in the ARR from 0.54 to 0.37 and from 0.50 to 0.32 respectively. The latest oral MS medication, approved in 2014, is DMF, which had been used in a different formulation for treatment of psoriasis for decades. In the 2-year DEFINE study, the proportion of patients with a relapse was reduced to 27 %, compared with 46 % in placebo arm, whereas in the CONFIRM trial, the ARR was reduced from 0.40 (placebo) to 0.22 in the DMF-treated group of patients. In this review, we will elucidate the mechanisms of action of these three medications and compare their efficacy, safety, and tolerability as a practical guideline for their use. We will further discuss effects other than relapse reduction these small molecules may exert, including potential activities within the central nervous system, and briefly summarize emerging data on new oral MS drugs in clinical development."],["dc.identifier.doi","10.1007/s11910-016-0639-4"],["dc.identifier.isi","000372534500001"],["dc.identifier.pmid","26944956"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41053"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1534-6293"],["dc.relation.issn","1528-4042"],["dc.title","The Use of Oral Disease-Modifying Therapies in Multiple Sclerosis"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Traub, Jan W."],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Grondey, Katja"],["dc.contributor.author","Seeger, Ira"],["dc.contributor.author","Rowold, Christoph"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Husseini, Leila"],["dc.contributor.author","Häusser-Kinzel, Silke"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2021-06-01T10:48:04Z"],["dc.date.available","2021-06-01T10:48:04Z"],["dc.date.issued","2019"],["dc.description.abstract","Abstract Background In the past, multiple sclerosis (MS) medications have been primarily designed to modulate T cell properties. Based on the emerging concept that B cells are equally important for the propagation of MS, we compared the effect of four commonly used, primarily T cell-targeting MS medications on B cells. Methods Using flow cytometry, we analyzed peripheral blood mononuclear cells (PBMC) of untreated ( n  = 19) and dimethyl fumarate (DMF; n  = 21)-, fingolimod (FTY; n  = 17)-, glatiramer acetate (GA; n  = 18)-, and natalizumab (NAT; n  = 20)-treated MS patients, focusing on B cell maturation, differentiation, and cytokine production. Results While GA exerted minor effects on the investigated B cell properties, DMF and FTY robustly inhibited pro-inflammatory B cell function. In contrast, NAT treatment enhanced B cell differentiation, activation, and pro-inflammatory cytokine production when compared to both intraindividual samples collected before NAT treatment initiation as well as untreated MS controls. Our mechanistic in vitro studies confirm this observation. Conclusion Our data indicate that common MS medications have differential, in part opposing effects on B cells. The observed activation of peripheral B cells upon NAT treatment may be instructive to interpret its unfavorable effect in certain B cell-mediated inflammatory conditions and to elucidate the immunological basis of MS relapses after NAT withdrawal. Trial registration Protocols were approved by the ethical review committee of the University Medical Center Göttingen (#3/4/14)."],["dc.identifier.doi","10.1186/s12974-019-1593-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16681"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85818"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1742-2094"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Natalizumab promotes activation and pro-inflammatory differentiation of peripheral B cells in multiple sclerosis patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.journal","Cortex"],["dc.bibliographiccitation.lastpage","40"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Albrecht, Franziska"],["dc.contributor.author","Mueller, Karsten"],["dc.contributor.author","Ballarini, Tommaso"],["dc.contributor.author","Lampe, Leonie"],["dc.contributor.author","Diehl-Schmid, Janine"],["dc.contributor.author","Fassbender, Klaus"],["dc.contributor.author","Fliessbach, Klaus"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Jech, Robert"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Landwehrmeyer, Bernhard"],["dc.contributor.author","Lauer, Martin"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Lyros, Epameinondas"],["dc.contributor.author","Prudlo, Johannes"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Synofzik, Matthis"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Danek, Adrian"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Schroeter, Matthias L."],["dc.contributor.author","Anderl-Straub, Sarah"],["dc.contributor.author","Brüggen, Katharina"],["dc.contributor.author","Fischer, Marie"],["dc.contributor.author","Förstl, Hans"],["dc.contributor.author","Hammer, Anke"],["dc.contributor.author","Homola, György"],["dc.contributor.author","Just, Walter"],["dc.contributor.author","Levin, Johannes"],["dc.contributor.author","Marroquin, Nicolai"],["dc.contributor.author","Marschhauser, Anke"],["dc.contributor.author","Nagl, Magdalena"],["dc.contributor.author","Oberstein, Timo"],["dc.contributor.author","Polyakova, Maryna"],["dc.contributor.author","Pellkofer, Hannah"],["dc.contributor.author","Richter-Schmidinger, Tanja"],["dc.contributor.author","Rossmeier, Carola"],["dc.contributor.author","Schuemberg, Katharina"],["dc.contributor.author","Semler, Elisa"],["dc.contributor.author","Spottke, Annika"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Thöne-Otto, Angelika"],["dc.contributor.author","Uttner, Ingo"],["dc.contributor.author","Zech, Heike"],["dc.date.accessioned","2020-12-10T14:23:17Z"],["dc.date.available","2020-12-10T14:23:17Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.cortex.2019.02.015"],["dc.identifier.issn","0010-9452"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16567"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71890"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Unraveling corticobasal syndrome and alien limb syndrome with structural brain imaging"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","995"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Headache The Journal of Head and Face Pain"],["dc.bibliographiccitation.lastpage","1003"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Schankin, Christoph J."],["dc.contributor.author","Kaestele, Fabian"],["dc.contributor.author","Gerdes, Lisa Ann"],["dc.contributor.author","Winkler, Tobias"],["dc.contributor.author","Csanadi, Endy"],["dc.contributor.author","Hoegen, Tobias"],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Straube, Andreas"],["dc.date.accessioned","2018-11-07T10:13:15Z"],["dc.date.available","2018-11-07T10:13:15Z"],["dc.date.issued","2016"],["dc.description.abstract","ObjectiveWe tested the hypotheses (i) that autoimmune encephalitis is associated with new-onset headache, and (ii) that the occurrence of headache is associated with the presence of anti-N-methyl-D-aspartate (NMDA)-receptor antibodies. BackgroundAutoimmune encephalitis presents with cognitive dysfunction as well as neuro-psychiatric symptoms. Its pathophysiology might involve antibody-mediated dysfunction of the glutamatergic system as indicated by the presence of anti-NMDA-receptor antibodies in some patients. MethodsIn this cross-sectional study, patients with autoimmune encephalitis were assessed with a standardized interview for previous headache and headache associated with autoimmune encephalitis. Headache was classified according to the International Classification of Headache Disorders, second edition. Clinical and paraclinical findings were correlated with the occurrence of headache. ResultsOf 40 patients with autoimmune encephalitis, 19 did not have a history of headache. Of those, nine suffered from encephalitis-associated headache. Seven of these nine had anti-NMDA-receptor antibodies in contrast to only two among the remaining 10 patients without new-onset headache (P=.023, odds ratio: 14, 95% confidence interval: 1.5; 127). In most patients headache occurred in attacks on more than 15 days/month, was severe, and of short duration (less than 4 hours). International Headache Society criteria for migraine were met in three patients. ConclusionsNew-onset headache is a relevant symptom in patients with autoimmune encephalitis who have no history of previous headache, especially in the subgroup with anti-NMDA-receptor antibodies. This indicates a thorough investigation for secondary headaches including anti-NMDA-R antibodies for patients with new-onset headache and neuropsychiatric findings. Glutamatergic dysfunction might be important for the generation of head pain but may only occasionally be sufficient to trigger migraine-like attacks in nonmigraineurs."],["dc.description.sponsorship","German Migraine and Headache Society; Friedrich Baur Foundation [58/14]"],["dc.identifier.doi","10.1111/head.12853"],["dc.identifier.isi","000379154300008"],["dc.identifier.pmid","27241874"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40392"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1526-4610"],["dc.relation.issn","0017-8748"],["dc.title","New-Onset Headache in Patients With Autoimmune Encephalitis Is Associated With anti-NMDA-Receptor Antibodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e407"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","e418"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Ringelstein, Marius"],["dc.contributor.author","Harmel, Jens"],["dc.contributor.author","Zimmermann, Hanna"],["dc.contributor.author","Brandt, Alexander U."],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Haarmann, Axel"],["dc.contributor.author","Buttmann, Mathias"],["dc.contributor.author","Hümmert, Martin W."],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.author","Schroeder, Christoph"],["dc.contributor.author","Ayzenberg, Ilya"],["dc.contributor.author","Kleiter, Ingo"],["dc.contributor.author","Hellwig, Kerstin"],["dc.contributor.author","Havla, Joachim"],["dc.contributor.author","Kümpfel, Tania"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Rommer, Paulus"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Pellkofer, Hannah"],["dc.contributor.author","Röpke, Luise"],["dc.contributor.author","Geis, Christian"],["dc.contributor.author","Retzlaff, Nele"],["dc.contributor.author","Zettl, Uwe"],["dc.contributor.author","Deppe, Michael"],["dc.contributor.author","Klotz, Luisa"],["dc.contributor.author","Young, Kim"],["dc.contributor.author","Stellmann, Jan-Patrick"],["dc.contributor.author","Kaste, Matthias"],["dc.contributor.author","Kermer, Pawel"],["dc.contributor.author","Marouf, Wael"],["dc.contributor.author","Lauda, Florian"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Graf, Jonas"],["dc.contributor.author","Klistorner, Alexander"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Albrecht, Philipp"],["dc.date.accessioned","2020-12-10T18:41:46Z"],["dc.date.available","2020-12-10T18:41:46Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1212/WNL.0000000000008684"],["dc.identifier.eissn","1526-632X"],["dc.identifier.issn","0028-3878"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77670"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Longitudinal optic neuritis-unrelated visual evoked potential changes in NMO spectrum disorders"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e71500"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Havla, Joachim"],["dc.contributor.author","Hauer, Daniela"],["dc.contributor.author","Schelling, Gustav"],["dc.contributor.author","Azad, Shahnaz C."],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Magerl, Walter"],["dc.contributor.author","Huge, Volker"],["dc.date.accessioned","2018-11-07T09:21:20Z"],["dc.date.available","2018-11-07T09:21:20Z"],["dc.date.issued","2013"],["dc.description.abstract","Recurrent myelitis is one of the predominant characteristics in patients with neuromyelitis optica (NMO). While paresis, visual loss, sensory deficits, and bladder dysfunction are well known symptoms in NMO patients, pain has been recognized only recently as another key symptom of the disease. Although spinal cord inflammation is a defining aspect of neuromyelitis, there is an almost complete lack of data on altered somatosensory function, including pain. Therefore, eleven consecutive patients with NMO were investigated regarding the presence and clinical characteristics of pain. All patients were examined clinically as well as by Quantitative Sensory Testing (QST) following the protocol of the German Research Network on Neuropathic Pain (DFNS). Additionally, plasma endocannabinoid levels and signs of chronic stress and depression were determined. Almost all patients (10/11) suffered from NMO-associated neuropathic pain for the last three months, and 8 out of 11 patients indicated relevant pain at the time of examination. Symptoms of neuropathic pain were reported in the vast majority of patients with NMO. Psychological testing revealed signs of marked depression. Compared to age and gender-matched healthy controls, QST revealed pronounced mechanical and thermal sensory loss, strongly correlated to ongoing pain suggesting the presence of deafferentation-induced neuropathic pain. Thermal hyperalgesia correlated to MRI-verified signs of spinal cord lesion. Heat hyperalgesia was highly correlated to the time since last relapse of NMO. Patients with NMO exhibited significant mechanical and thermal dysesthesia, namely dynamic mechanical allodynia and paradoxical heat sensation. Moreover, they presented frequently with either abnormal mechanical hypoalgesia or hyperalgesia, which depended significantly on plasma levels of the endogenous cannabinoid 2-arachidonoylglycerole (2-AG). These data emphasize the high prevalence of neuropathic pain and hyperalgesia in patients with NMO. The degree of mechanical hyperalgesia reflecting central sensitization of nociceptive pathways seems to be controlled by the major brain endocannabinoid 2-AG."],["dc.identifier.doi","10.1371/journal.pone.0071500"],["dc.identifier.isi","000326473200051"],["dc.identifier.pmid","23951176"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9229"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29084"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","The Major Brain Endocannabinoid 2-AG Controls Neuropathic Pain and Mechanical Hyperalgesia in Patients with Neuromyelitis Optica"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","14"],["dc.bibliographiccitation.journal","Journal of Neuroinflammation"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Ruprecht, Klemens"],["dc.contributor.author","Wildemann, Brigitte"],["dc.contributor.author","Kuempfel, Tania"],["dc.contributor.author","Ringelstein, Marius"],["dc.contributor.author","Geis, Christian"],["dc.contributor.author","Kleiter, Ingo"],["dc.contributor.author","Kleinschnitz, Christoph"],["dc.contributor.author","Berthele, Achim"],["dc.contributor.author","Brettschneider, Johannes"],["dc.contributor.author","Hellwig, Kerstin"],["dc.contributor.author","Hemmer, Bernhard"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Lauda, Florian"],["dc.contributor.author","Mayer, Christoph A."],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Melms, Arthur"],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.author","Stangel, Martin"],["dc.contributor.author","Marziniak, Martin"],["dc.contributor.author","Hoffmann, Frank"],["dc.contributor.author","Schippling, Sven"],["dc.contributor.author","Faiss, Juergen H."],["dc.contributor.author","Neuhaus, Oliver"],["dc.contributor.author","Ettrich, Barbara"],["dc.contributor.author","Zentner, Christian"],["dc.contributor.author","Guthke, Kersten"],["dc.contributor.author","Hofstadt-van Oy, Ulrich"],["dc.contributor.author","Reuss, Reinhard"],["dc.contributor.author","Pellkofer, Hannah L."],["dc.contributor.author","Ziemann, Ulf"],["dc.contributor.author","Kern, Peter"],["dc.contributor.author","Wandinger, Klaus-Peter"],["dc.contributor.author","Bergh, Florian Then"],["dc.contributor.author","Boettcher, Tobias"],["dc.contributor.author","Langel, Stefan"],["dc.contributor.author","Liebetrau, Martin"],["dc.contributor.author","Rommer, Paulus S."],["dc.contributor.author","Niehaus, Sabine"],["dc.contributor.author","Muench, Christoph"],["dc.contributor.author","Winkelmann, Alexander"],["dc.contributor.author","Zettl U, Uwe K."],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Veauthier, Christian"],["dc.contributor.author","Sieb, Joern P."],["dc.contributor.author","Wilke, Christian"],["dc.contributor.author","Hartung, Hans-Peter"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Paul, Friedemann"],["dc.date.accessioned","2018-11-07T09:14:18Z"],["dc.date.available","2018-11-07T09:14:18Z"],["dc.date.issued","2012"],["dc.description.abstract","Background: The diagnostic and pathophysiological relevance of antibodies to aquaporin-4 (AQP4-Ab) in patients with neuromyelitis optica spectrum disorders (NMOSD) has been intensively studied. However, little is known so far about the clinical impact of AQP4-Ab seropositivity. Objective: To analyse systematically the clinical and paraclinical features associated with NMO spectrum disorders in Caucasians in a stratified fashion according to the patients' AQP4-Ab serostatus. Methods: Retrospective study of 175 Caucasian patients (AQP4-Ab positive in 78.3%). Results: Seropositive patients were found to be predominantly female (p < 0.0003), to more often have signs of co-existing autoimmunity (p < 0.00001), and to experience more severe clinical attacks. A visual acuity of <= 0.1 during acute optic neuritis (ON) attacks was more frequent among seropositives (p < 0.002). Similarly, motor symptoms were more common in seropositive patients, the median Medical Research Council scale (MRC) grade worse, and MRC grades <= 2 more frequent, in particular if patients met the 2006 revised criteria (p < 0.005, p < 0.006 and p < 0.01, respectively), the total spinal cord lesion load was higher (p < 0.006), and lesions >= 6 vertebral segments as well as entire spinal cord involvement more frequent (p < 0.003 and p < 0.043). By contrast, bilateral ON at onset was more common in seronegatives (p < 0.007), as was simultaneous ON and myelitis (p < 0.001); accordingly, the time to diagnosis of NMO was shorter in the seronegative group (p < 0.029). The course of disease was more often monophasic in seronegatives (p < 0.008). Seropositives and seronegatives did not differ significantly with regard to age at onset, time to relapse, annualized relapse rates, outcome from relapse (complete, partial, no recovery), annualized EDSS increase, mortality rate, supratentorial brain lesions, brainstem lesions, history of carcinoma, frequency of preceding infections, oligoclonal bands, or CSF pleocytosis. Both the time to relapse and the time to diagnosis was longer if the disease started with ON (p < 0.002 and p < 0.013). Motor symptoms or tetraparesis at first myelitis and > 1 myelitis attacks in the first year were identified as possible predictors of a worse outcome."],["dc.identifier.doi","10.1186/1742-2094-9-14"],["dc.identifier.isi","000300949700001"],["dc.identifier.pmid","22260418"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7222"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27377"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1742-2094"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: A multicentre study of 175 patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e1184"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","e1196"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Hümmert, Martin W."],["dc.contributor.author","Schöppe, Louisa M."],["dc.contributor.author","Bellmann-Strobl, Judith"],["dc.contributor.author","Siebert, Nadja"],["dc.contributor.author","Paul, Friedemann"],["dc.contributor.author","Duchow, Ankelien"],["dc.contributor.author","Pellkofer, Hannah"],["dc.contributor.author","Kümpfel, Tania"],["dc.contributor.author","Havla, Joachim"],["dc.contributor.author","Jarius, Sven"],["dc.contributor.author","Trebst, Corinna"],["dc.contributor.authorgroup","on behalf of the Neuromyelitis Optica Study Group (NEMOS)"],["dc.date.accessioned","2022-04-01T10:02:06Z"],["dc.date.available","2022-04-01T10:02:06Z"],["dc.date.issued","2022"],["dc.description.abstract","Background and Objectives To evaluate costs and health-related quality of life (HRQoL) of neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD). Methods In this multicenter cross-sectional study, data on consumption of medical and nonmedical resources and work ability were assessed via patient questionnaires. Costs were analyzed in Euros for 2018 from the societal perspective. HRQoL was captured by the EuroQoL Group 5 Dimension 5 Level Scale (EQ-5D-5L) questionnaire. Clinical data were retrieved from the Neuromyelitis Optica Study Group (NEMOS) database. Results Two hundred twelve patients (80% women, median age 50 [19–83] years, median disease duration 7 [0–43] years, median Expanded Disability Status Scale [EDSS] score 3.5 [0–8.5], 66% aquaporin-4 immunoglobulin G [IgG] positive, 22% MOG IgG positive, 12% double seronegative) were analyzed. The mean total annual per capita cost of illness accounted for €59,574 (95% CI 51,225–68,293 or US dollars [USD] 70,297, 95% CI 60,445–80,586), and the mean index value of the EQ-5D-5L was 0.693 (95% CI 0.65–0.73). The most important cost drivers were informal care costs (28% of total costs), indirect costs (23%), and drugs (16%), especially immunotherapeutics. Costs showed a positive correlation with disease severity (ρ = 0.56, 95% CI 0.45–0.65); in the EDSS score 6.5 to 8.5 subgroup, the mean annual costs were €129,687 (95% CI 101,946–160,336 or USD 153,031, 95% CI 120,296–189,196). The HRQoL revealed a negative correlation to disease severity (ρ = −0.69, 95% CI −0.76 to −0.61); in the EDSS score 6.5 to 8.5 subgroup, the EQ-5D-5L mean index value was 0.195 (95% CI 0.13–0.28). Neither antibody status nor disease duration influenced the total annual costs or HRQoL. Discussion These German data from the era without approved preventive immunotherapies show enormous effects of the diseases on costs and quality of life. An early and cost-effective therapy should be provided to prevent long-term disability and to preserve quality of life."],["dc.identifier.doi","10.1212/WNL.0000000000200052"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105822"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Costs and Health-Related Quality of Life in Patients With NMO Spectrum Disorders and MOG-Antibody–Associated Disease"],["dc.title.alternative","CHANCE\n NMO\n Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]