Varges, Daniela

[["dc.bibliographiccitation.firstpage","2288"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2296"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Collie, Donald A."],["dc.contributor.author","Roeber, Sigrun"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:17:31Z"],["dc.date.available","2018-11-07T09:17:31Z"],["dc.date.issued","2006"],["dc.description.abstract","A typical clinical course and low sensitivity of established diagnostic tests are the main diagnostic problems in the MV2 subtype of sporadic Creutzfeldt-Jakob disease (sCJD). Clinical symptoms and signs, MRI, EEG and biochemical CSF markers were studied in 26 patients. Histological findings were semiquantitatively evaluated. Compared with typical sCJD, the disease duration was prolonged (median 12 months). Dementia, ataxia and psychiatric symptoms were present in all patients. Extrapyramidal signs were observed in 88%. T2-weighted MRI showed basal ganglia hyperintensities in 90%. Increased thalamic signal intensity was detected in 88% on diffusion-weighted MRI. Increased CSF tau-protein was found in 83%, and the 14-3-3 test was positive in 76%. The EEG revealed periodic sharp wave complexes in only two patients. Kuru plaques, severe thalamic and basal ganglia gliosis and spongiform changes, and neuronal loss in the pulvinar were the prominent histological features. At least one of the three diagnostic tests (MRI, tau- and 14-3-3 protein) supported the clinical diagnosis in all patients. MRI was the most sensitive of the diagnostic tests applied. Thalamic hyperintensities were observed unusually frequently. Prolonged disease duration, early and prominent psychiatric symptoms, absence of typical EEG, thalamic hyperintensities on MRI and relatively low 14-3-3 protein sensitivity may be suspicious for variant CJD. However, distinct sensory symptoms and young age at onset, which are often found in the latter, are not common in the MV2 subtype, and the pulvinar sign was observed in only one case."],["dc.identifier.doi","10.1093/brain/awl123"],["dc.identifier.isi","000240679700006"],["dc.identifier.pmid","16720682"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28191"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical findings and diagnostic tests in the MV2 subtype of sporadic CJD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1544"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1550"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Westner, I. M."],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Bosenberg, C."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:54:10Z"],["dc.date.available","2018-11-07T10:54:10Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: Recently, six molecular subtypes of sporadic CJD ( sCJD) have been identified showing differences regarding the disease course, neuropathologic lesion patterns, and sensitivity to diagnostic tools. Only isolated cases of the rare VV1 type have been reported so far. Objective: To describe the clinical characteristics and neuropathologic lesion profiles in nine cases. Methods: In the years 1993 until late 2003, 571 definite neuropathologically confirmed cases of sporadic CJD were identified in Germany. Of these, nine were homozygous for valine and displayed type 1 of the pathologic PrPSc in the brain ( VV1 type). Results: The authors describe eight men and one woman belonging to the VV1 type. All patients were relatively young at disease onset ( median 44 years vs 65 years in all sCJD) with prolonged disease duration ( median 21 months vs 6 months in all sCJD). During the initial stages, their main clinical signs were personality changes and slowly progressive dementia as well as focal neurologic deficits. None of the nine VV1 patients had periodic sharp- wave complexes ( PSWCs) in the EEG. Only two out of seven displayed the typical signal increase of the basal ganglia on MRI, whereas signal increase of the cortex was seen in all patients. The 14- 3- 3 protein levels were elevated in CSF in all cases tested. Conclusions: The clinical diagnosis of the VV1 type of sCJD can be best supported by the 14- 3- 3 test and cortical signal increase on MRI. Because of the young age at onset vCJD is sometimes suspected as a differential diagnosis. MRI plays an important role in differentiating these two disease types and should be performed early during the disease course."],["dc.identifier.doi","10.1212/01.wnl.0000184674.32924.c9"],["dc.identifier.isi","000233428100008"],["dc.identifier.pmid","16221949"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49508"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Sporadic Creutzfeldt-Jakob disease - Clinical and diagnostic characteristics of the rare VV1 type"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","654"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","659"],["dc.bibliographiccitation.volume","85"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Juan, P. Sanchez"],["dc.contributor.author","Ponto, Claudia"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T09:39:44Z"],["dc.date.available","2018-11-07T09:39:44Z"],["dc.date.issued","2014"],["dc.description.abstract","Background In absence of a positive family history, the diagnosis of fatal familial insomnia (FFI) might be difficult because of atypical clinical features and low sensitivity of diagnostic tests. FFI patients usually do not fulfil the established classification criteria for Creutzfeldt-Jakob disease (CJD); therefore, a prion disease is not always suspected. Objective To propose an update of diagnostic pathway for the identification of patients for the analysis of D178-M129 mutation. Design and methods Data on 41 German FFI patients were analysed. Clinical symptoms and signs, MRI, PET, SPECT, polysomnography, EEG and cerebrospinal fluid biomarkers were studied. Results An algorithm was developed which correctly identified at least 81% of patients with the FFI diagnosis during early disease stages. It is based on the detection of organic sleep disturbances, either verified clinically or by a polysomnography, and a combination of vegetative and focal neurological signs and symptoms. Specificity of the approach was tested on three cohorts of patients (MM1 sporadic CJD patients, non-selected sporadic CJD and other neurodegenerative diseases). Conclusions The proposed scheme may help to improve the clinical diagnosis of FFI. As the sensitivity of all diagnostic tests investigated but polysomnography is low in FFI, detailed clinical investigation is of special importance."],["dc.identifier.doi","10.1136/jnnp-2013-305978"],["dc.identifier.isi","000336124400015"],["dc.identifier.pmid","24249784"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10971"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33354"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","1468-330X"],["dc.relation.issn","0022-3050"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","A proposal of new diagnostic pathway for fatal familial insomnia"],["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","762"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Journal of Neurology"],["dc.bibliographiccitation.lastpage","771"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Collie, Donald A."],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Summers, D. M."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Talbot, T."],["dc.contributor.author","Will, Robert G."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T11:12:23Z"],["dc.date.available","2018-11-07T11:12:23Z"],["dc.date.issued","2008"],["dc.description.abstract","Background and purpose: To establish radiological features in the atypical MV2 subtype of sCJD compared with the classical MM1 subtype, as well as region- and sequence-dependent inter-observer correlation. Methods: MRI hyperintensity of basal ganglia (BG), cortex and thalamus was evaluated in 31 MM1 and 32 MV2 patients. Each MR scan was analyzed independently by two neuroradiologists blinded to PRNP genotype/prion protein type. Results: Cumulative T2-sensitivity for BG hyperintensity was higher in the MV2 subtype (84% for both observers versus 61% in observer 1/42% in observer 2 in MM1 patients). Significant inter-observer agreement was found for BG and thalamus on T2, FLAIR, PD and DWI, but for cortex only on DWI. Thalamic changes were significantly more frequent in MV2 than in MM1 patients (cumulative sensitivity 86% vs. 12.5% on DWI). Discussion: The high frequency of thalamic hyperintensity in the MV2 subtype allowed differentiation from MM1 patients. Good inter-observer agreement was found for BG and thalamus in all sequences. DWI showed the highest inter-observer correlation independent of the investigated brain region and was therefore not only highly sensitive but also relatively independent of investigator bias. Since inter-observer correlation for cortical hyperintensity in T2, FLAIR and PD is relatively low, the cortical changes should not be over-interpreted with these sequences."],["dc.description.sponsorship","Department of Health"],["dc.identifier.doi","10.1111/j.1468-1331.2008.02209.x"],["dc.identifier.isi","000257715400013"],["dc.identifier.pmid","18684308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53654"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1468-1331"],["dc.relation.issn","1351-5101"],["dc.title","MRI in the classical MM1 and the atypical MV2 subtypes of sporadic CJD: an inter-observer agreement study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","533"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","543"],["dc.bibliographiccitation.volume","58"],["dc.contributor.author","Boesenberg, C."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:55:04Z"],["dc.date.available","2018-11-07T10:55:04Z"],["dc.date.issued","2005"],["dc.description.abstract","Sporadic Creutzfeldt-jakob disease (sCJD) is a rare neurodegenerative disease with the greatest incidence occurring in patients between 60 and 70 years old. Younger patients may also be affected. In this study, we used all case material available from 52 patients with sCJD aged 50 years of younger at disease onset, who were identified between 1993 and 2003 in Germany. The objective of this study was to describe the psychiatric and neurological features of these young patients with emphasis on the different codon 129 genotypes and PrP types, and to compare them with elder patients with sCJD and patients with variant CJD. We also gave particular attention to electroencephalogram, magnetic resonance imaging, and 14-3-3 results, as well as to the neuropathological lesion profile. The clinical syndrome in young patients differs from elder patients with CJD with respect to clinical signs, disease duration, technical investigations, and neuropathological lesion profile. The psychiatric symptoms in young patients with sCJD are similar to the psychiatric symptoms expressed by patients with variant CJD; however, in contrast with the variant cases, young patients with sCJD experience development of prominent dementia early in the disease course."],["dc.identifier.doi","10.1002/ana.20568"],["dc.identifier.isi","000232309900006"],["dc.identifier.pmid","16037975"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49703"],["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 course in young patients with sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Prion"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T08:42:01Z"],["dc.date.available","2018-11-07T08:42:01Z"],["dc.date.issued","2010"],["dc.format.extent","223"],["dc.identifier.isi","000285872300279"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19601"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.publisher.place","Austin"],["dc.relation.issn","1933-6896"],["dc.title","Spongiform Encephalopathy in Siblings with No Evidence of Protease-Resistant Prion Protein or a Mutation in the Prion Protein Gene"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1871"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1879"],["dc.bibliographiccitation.volume","260"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Wemheuer, Wiebke M."],["dc.contributor.author","Damman, Insa"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Cramm, Maria"],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Shirneshan, Katayoon"],["dc.contributor.author","Elkenani, Manar"],["dc.contributor.author","Markwort, Susanne"],["dc.contributor.author","Faist, Michael"],["dc.contributor.author","Kohlhase, Juergen"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:23:06Z"],["dc.date.available","2018-11-07T09:23:06Z"],["dc.date.issued","2013"],["dc.description.abstract","We discuss relevant aspects in two siblings with a neurodegenerative process of unclear aetiology who developed progressive dementia with global aphasia and hyperoral behaviour at the ages of 39 and 46 years and who died 6 and 5 years after disease onset. The cases were reported to the National Reference Center for TSE Surveillance in Gottingen, Germany. Detailed clinical examinations, CSF, blood samples, and copies of the important diagnostic tests (magnetic resonance imaging, electroencephalogram, laboratory tests) were obtained. Further neuropathological and genetic analyses were performed. Cerebral magnetic resonance imaging of both siblings showed prominent changes in signal intensity, especially in the left medial temporal cortex, but also the hippocampal formation. Neuropathological examination revealed spongiform changes, neuronal loss, and astrocytic gliosis, which are typical in Creutzfeldt-Jakob disease. However, no prion protein deposits were detectable by immunohistochemical analysis, Western blot, or PET blot, though abundant tau protein deposits were observed. A mutation in the coding region of the prion protein genes of both siblings was excluded. A detailed search of the literature revealed no other cases with a similar clinical and neuropathological appearance. While the disease aetiology remains unclear, the findings point to a neurodegenerative process and most likely a genetic disease."],["dc.identifier.doi","10.1007/s00415-013-6897-z"],["dc.identifier.isi","000321610500025"],["dc.identifier.pmid","23546304"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29501"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.title","Spongiform encephalopathy in siblings with no evidence of protease-resistant prion protein or a mutation in the prion protein gene"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","119"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.lastpage","125"],["dc.bibliographiccitation.volume","88"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Manthey, Henrike"],["dc.contributor.author","Heinemann, Uta"],["dc.contributor.author","Ponto, Claudia"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Breithaupt, Maren"],["dc.contributor.author","Fincke, Fabian"],["dc.contributor.author","Kramer, Katharina"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T10:28:06Z"],["dc.date.available","2018-11-07T10:28:06Z"],["dc.date.issued","2017"],["dc.description.abstract","Objectives The main objective of the present study is to study the therapeutic efficiency of doxycycline in a double-blinded randomised phase II study in a cohort of patients with sporadic Creutzfeldt-Jakob disease (sCJD). Methods From the National Reference Center of TSE Surveillance in Germany, patients with probable or definite sCJD were recruited for a double-blinded randomised study with oral doxycycline (EudraCT 2006-003934-14). In addition, we analysed the data from patients with CJD who received compassionate treatment with doxycycline in a separate group. Potential factors which influence survival such as age at onset, gender, codon 129 polymorphism and cognitive functions were evaluated. The primary outcome measure was survival. Results Group 1: in the double-blinded randomised phase II study, 7 patients in the treatment group were compared with 5 controls. Group 2: 55 patients with sCJD treated with oral doxycycline were analysed and compared with 33 controls by a stratified propensity score applied to a Cox proportional hazard analysis. The results of both studies were combined by means of a random-effects meta-analysis. A slight increase in survival time in the doxycycline treatment group was observed (p=0.049, HR=0.63 (95% CI 0.402 to 0.999)). Conclusions On the basis of our studies, a larger trial of doxycycline should be performed in persons in the earliest stages of CJD."],["dc.identifier.doi","10.1136/jnnp-2016-313541"],["dc.identifier.isi","000393903700007"],["dc.identifier.pmid","27807198"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43348"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Bmj Publishing Group"],["dc.relation.issn","1468-330X"],["dc.relation.issn","0022-3050"],["dc.title","Doxycycline in early CJD: a double-blinded randomised phase II and observational study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","876"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","ARCHIVES OF NEUROLOGY"],["dc.bibliographiccitation.lastpage","880"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Krasnianski, Anna"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Kallenberg, Kai"],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T09:43:02Z"],["dc.date.available","2018-11-07T09:43:02Z"],["dc.date.issued","2006"],["dc.description.abstract","Objective: To describe clinical features and diagnostic tests of the MM2 cortical subtype in sporadic Creutzfeldt-Jakob disease. Methods: Clinical symptoms, magnetic resonance imaging studies, electroencephalograms, and cerebrospinal fluid markers were studied in 12 patients with genetically and neuropathologically verified sporadic Creutzfeldt-Jakob disease. Histological findings were semiquantitatively evaluated. Results: Compared with classical sporadic Creutzfeldt-Jakob disease, the disease duration was prolonged ( median, 14 months). All patients had dementia and early and prominent neuropsychological signs such as spatial disorientation, aphasia, or apraxia. Alzheimer disease was the most frequent initial diagnosis (33%). Increased S100B protein in the cerebrospinal fluid was found in 100%; the 14-3-3 protein test was positive in 91%. Electroencephalograms revealed periodic sharp wave complexes in 42%. T2-weighted magnetic resonance imaging showed basal ganglia hyperintensities in only 1 patient, and cortical hyperintensities were not necessarily present. Severe cortical damage was the most prominent histological feature. Conclusions: The S100B (100%) and 14-3-3 (91%) protein investigations were the most sensitive diagnostic tests. Prolonged disease duration, dementia as the only typical Creutzfeldt-Jakob disease symptom for a longer time, and low sensitivity of magnetic resonance imaging studies and electroencephalograms make the diagnosis in the MM2 cortical subtype difficult. Therefore, detailed clinical investigation is especially important in this sporadic Creutzfeldt-Jakob disease subtype. We suggest that rapidly progressive dementia with early and prominent neuropsychological deficits in older patients should lead to suspicion of the MM2 cortical subtype even if other neurological deficits are absent. At least some cases of MM2 cortical sporadic Creutzfeldt-Jakob disease may be misdiagnosed as rapidly progressive Alzheimer disease."],["dc.identifier.doi","10.1001/archneur.63.6.876"],["dc.identifier.isi","000238197600013"],["dc.identifier.pmid","16769870"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34091"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Medical Assoc"],["dc.relation.issn","0003-9942"],["dc.title","Clinical features and diagnosis of the MM2 cortical subtype of sporadic Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","Heinemann, U."],["dc.contributor.author","Hengst, S."],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Varges, Daniel. A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Schulz-Schaffer, W."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:48:35Z"],["dc.date.available","2018-11-07T10:48:35Z"],["dc.date.issued","2004"],["dc.format.extent","72"],["dc.identifier.isi","000222500400264"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48232"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.publisher.place","Darmstadt"],["dc.relation.conference","14th Meeting of the European-Neurological-Society"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","0340-5354"],["dc.title","Biopsy as a diagnostic tool in Creutzfeldt-Jakob disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]