Brockmann, Knut

[["dc.bibliographiccitation.firstpage","893"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Neuroradiology"],["dc.bibliographiccitation.lastpage","898"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Dreha-Kulaczewski, Steffi F."],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Helms, Gunther"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Brockmann, Knut"],["dc.date.accessioned","2017-09-07T11:49:54Z"],["dc.date.available","2017-09-07T11:49:54Z"],["dc.date.issued","2006"],["dc.description.abstract","Introduction Hereditary spastic paraplegia with thin corpus callosum (HSP-TCC) is a complicated form of autosomal-recessive hereditary spastic paraplegia. Characteristic clinical features comprise progressive spastic gait, cognitive impairment, and ataxia. Diagnostic MRI findings include thinning of the corpus callosum and non-progressive white matter (WM) alterations. Methods To study the extent of axonal involvement, we performed localized proton magnetic resonance spectroscopy (MRS) of the cerebral WM and cortical grey matter (GM) in a patient with HSP-TCC at 20 and 25 years of age. The second investigation included diffusion tensor imaging (DTI). Results While MRS of the GM was normal, affected WM was characterized by major metabolic alterations such as reduced concentrations of N-acetylaspartate and N-acetylaspartyl-glutamate, creatine and phosphocreatine, and choline-containing compounds as well as elevated levels of myo-inositol. These abnormalities showed progression over a period of 5 years. DTI revealed increased mean diffusivity as well as reduced fractional anisotropy in periventricular WM. The metabolic and structural findings are consistent with progressive neuroaxonal loss in the WM accompanied by astrocytic proliferation-histopathological changes known to occur in HSP-TCC. Conclusion Our results are in agreement with the hypothesis that the primary pathological process in HSP-TCC affects the axon, possibly due to impaired axonal trafficking."],["dc.identifier.doi","10.1007/s00234-006-0148-2"],["dc.identifier.gro","3143582"],["dc.identifier.isi","000242365500005"],["dc.identifier.pmid","17013586"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1111"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","0028-3940"],["dc.title","Cerebral metabolic and structural alterations in hereditary spastic paraplegia with thin corpus callosum assessed by MRS and DTI"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","869"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Inherited Metabolic Disease"],["dc.bibliographiccitation.lastpage","876"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Rosewich, Hendrik"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Krause, Cindy"],["dc.contributor.author","Ohlenbusch, Andreas"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Gärtner, Jutta"],["dc.date.accessioned","2017-09-07T11:44:32Z"],["dc.date.available","2017-09-07T11:44:32Z"],["dc.date.issued","2016"],["dc.description.abstract","Defects in the biogenesis of peroxisomes cause a clinically and genetically heterogeneous group of neurometabolic disorders, the Zellweger syndrome spectrum (ZSS). Diagnosis predominantly is based on characteristic clinical symptoms, a typical biochemical profile, as well as on identification of the molecular defect in any of the 12 known human PEX genes. The diagnostic workup can be hindered if the typical clinical symptoms are missing and predicting the clinical course of a given patient is almost unfeasible. As a safe and noninvasive method to analyze specific chemical compounds in localized brain regions, in vivo proton magnetic resonance spectroscopy (MRS) can provide an indication in this diagnostic process and may help predict the clinical course. However, to date, there are very few reports on this topic. In this study, we performed localized in vivo proton MRS without confounding contributions from T1- and T2-relaxation effects at 2 Tesla in a comparably large group of seven ZSS patients. Patients' absolute metabolite concentrations in cortical gray matter, white matter, and basal ganglia were assessed and compared with age-matched control values. Our results confirm and extend knowledge about in vivo MRS findings in ZSS patients. Besides affirmation of nonspecific reduction of N-acetylaspartate + N-acetylaspartylglutamate (tNAA) in combination with lipid accumulation as a diagnostic hint for this disease group, the amount of tNAA loss seems to reflect disease burden and may prove to be of prognostic value regarding the clinical course of an already diagnosed patient."],["dc.identifier.doi","10.1007/s10545-016-9965-6"],["dc.identifier.gro","3141599"],["dc.identifier.isi","000386383500011"],["dc.identifier.pmid","27488561"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/10"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.eissn","1573-2665"],["dc.relation.issn","0141-8955"],["dc.title","Diagnostic and prognostic value of in vivo proton MR spectroscopy for Zellweger syndrome spectrum patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","701"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","706"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Hanefeld, Folker"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Pouwels, Petra J. W."],["dc.contributor.author","Wilken, Barbara"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Dechent, Peter"],["dc.date.accessioned","2018-11-07T10:55:47Z"],["dc.date.available","2018-11-07T10:55:47Z"],["dc.date.issued","2005"],["dc.description.abstract","Background: Pelizaeus-Merzbacher disease (PMD) is a rare X-linked recessive neurologic disorder caused by a mutation in the proteolipid protein (PLP) gene on chromosome Xq22. The associated depletion of PLP and severe reduction of other major myelin proteins results in dysmyelination. MRI reveals loss of T1 contrast between gray and affected white matter and T2 hyperintensities of white matter due to elevated water content. Methods: In vivo proton magnetic resonance spectroscopy (MRS) was used to determine cerebral metabolite patterns in five patients with genetically proven PMD. Absolute metabolite concentrations were obtained in cortical gray matter, affected white matter, and basal ganglia and compared to age-matched control values. Results: In comparison to age-matched controls, MRS of affected white matter resembled the metabolite pattern of cortical gray matter, as indicated by increased concentrations of N-acetylaspartate and N-acetylaspartylglutamate (tNAA), glutamine (Gln), myo-inositol ( Ins), and creatine and phosphocreatine. Most remarkably, the concentration of choline-containing compounds was reduced. Parietal gray matter and basal ganglia appeared normal but showed a tendency for elevated tNAA, Gln, and Ins. Conclusions: Magnetic resonance spectroscopy (MRS)-detected alterations are consistent with enhanced neuroaxonal density, astrogliosis, and reduction of oligodendroglia. These disturbances in cellular composition are in close agreement with the histopathologic features characteristic of dys- and hypomyelination. The proton MRS profile of Pelizaeus-Merzbacher disease (PMD) differs from the pattern commonly observed in demyelinating disorders and allows PMD to be distinguished from other leukodystrophies."],["dc.identifier.doi","10.1212/01.wnl.0000174642.32187.20"],["dc.identifier.isi","000231821300009"],["dc.identifier.pmid","16157902"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49865"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Quantitative proton MRS of Pelizaeus-Merzbacher disease - Evidence of dys- and hypomyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","234"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuropediatrics"],["dc.bibliographiccitation.lastpage","238"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Groeschel, Sonja"],["dc.contributor.author","Dreha-Kulaczewski, Steffi F."],["dc.contributor.author","Reinhardt, Konstanze"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Dechent, Peter"],["dc.date.accessioned","2017-09-07T11:46:49Z"],["dc.date.available","2017-09-07T11:46:49Z"],["dc.date.issued","2009"],["dc.description.abstract","Observations of extreme unilateral widening of Virchow-Robin spaces (VRS) are rare and hitherto confined to adult, mainly old-aged patients. Magnetic resonance imaging (MRI) was performed in two unrelated boys aged 3 years with developmental coordination disorders. In one of these patients, follow-up MRI and diffusion tensor imaging (DTI) were carried out 5 years later. In both boys, MRI incidentally revealed numerous intracerebral cysts strictly confined to one hemisphere. Localization, size, shape, and signal isointensity to cerebrospinal fluid indicated unilateral marked widening of VRS. In one patient, follow-up investigation after 5 years showed unchanged dilation of VRS on MRI, but mild facial hemihypertrophy, ipsilateral to the widened VRS. DTI indicated displacement rather than disruption of fiber tracks adjacent to the dilated VRS. Unilateral widening of VRS may be detected fortuitously on neuroimaging already in early childhood."],["dc.identifier.doi","10.1055/s-0029-1246158"],["dc.identifier.gro","3143051"],["dc.identifier.isi","000275698300006"],["dc.identifier.pmid","20221960"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/522"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","0174-304X"],["dc.title","Unilateral Dilation of Virchow-Robin Spaces in Early Childhood"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","444"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Pediatric Research"],["dc.bibliographiccitation.lastpage","449"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Dreha-Kulaczewski, Steffi F."],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Finsterbusch, Jurgen"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Hanefeld, Folker A."],["dc.date.accessioned","2017-09-07T11:48:46Z"],["dc.date.available","2017-09-07T11:48:46Z"],["dc.date.issued","2008"],["dc.description.abstract","The neuropathology of vanishing white matter (VWM) disease is characterized by a loss of white matter (WM). Although recent histopathological studies suggest a primary glial dysfunction, the purpose of this work was to assess the extent of axonal involvement in VWM using long-term follow-up proton MR spectroscopy. White and gray matter of nine children with genetically proven VWM and late infancy/early childhood onset were investigated with short-echo time, single-voxel proton MR spectroscopy over up to 8 years starting as early as less than 2 years after the onset of symptoms (5 patients). Total N-acetyl-aspartate (-51% from normal control), creatine and phosphocreatine (-47%), and myo-inositol (-49%) were reduced in WM at early disease stages. Choline-containing compounds were less severely decreased (-31%). Follow-up investigations revealed progressive reduction of all metabolites in WM. In gray matter, no distinct changes were detected at early stages. Later total N-acetyl-aspartate decreased slightly (-22%). Assuming the metabolite alterations to primarily reflect changes in cellular composition, the observed pattern indicates early axonal involvement or loss as well as relatively enhanced turnover of myelin. These early stages are followed by a complete cellular loss in cerebral WM."],["dc.identifier.doi","10.1203/01.pdr.0000304934.90198.25"],["dc.identifier.gro","3143328"],["dc.identifier.isi","000254374300021"],["dc.identifier.pmid","18356755"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/830"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0031-3998"],["dc.title","Early reduction of total N-acetyl-aspartate-compounds in patients with classical vanishing white matter disease. A long-term follow-up MRS study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","91"],["dc.bibliographiccitation.journal","JIMD reports"],["dc.bibliographiccitation.lastpage","99"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Dreha-Kulaczewski, S."],["dc.contributor.author","Kalscheuer, V."],["dc.contributor.author","Tzschach, A."],["dc.contributor.author","Hu, H."],["dc.contributor.author","Helms, G."],["dc.contributor.author","Brockmann, K."],["dc.contributor.author","Weddige, A."],["dc.contributor.author","Dechent, P."],["dc.contributor.author","Schlüter, G."],["dc.contributor.author","Krätzner, R."],["dc.contributor.author","Ropers, H. H."],["dc.contributor.author","Gärtner, J."],["dc.contributor.author","Zirn, B."],["dc.date.accessioned","2018-02-15T10:23:08Z"],["dc.date.available","2018-02-15T10:23:08Z"],["dc.date.issued","2013"],["dc.description.abstract","X-linked creatine transport (CRTR) deficiency, caused by mutations in the SLC6A8 gene, leads to intellectual disability, speech delay, epilepsy, and autistic behavior in hemizygous males. Additional diagnostic features are depleted brain creatine levels and increased creatine/creatinine ratio (cr/crn) in urine. In heterozygous females the phenotype is highly variable and diagnostic hallmarks might be inconclusive. This survey aims to explore the intrafamilial variability of clinical and brain proton Magnetic Resonance Spectroscopy (MRS) findings in males and females with CRTR deficiency. X-chromosome exome sequencing identified a novel missense mutation in the SLC6A8 gene (p.G351R) in a large family with X-linked intellectual disability. Detailed clinical investigations including neuropsychological assessment, measurement of in vivo brain creatine concentrations using quantitative MRS, and analyses of creatine metabolites in urine were performed in five clinically affected family members including three heterozygous females and one hemizygous male confirming the diagnosis of CRTR deficiency. The severe phenotype of the hemizygous male was accompanied by most distinct aberrations of brain creatine concentrations (-83% in gray and -79% in white matter of age-matched normal controls) and urinary creatine/creatinine ratio. In contrast, the heterozygous females showed varying albeit generally milder phenotypes with less severe brain creatine (-50% to -33% in gray and -45% to none in white matter) and biochemical urine abnormalities. An intrafamilial correlation between female phenotype, brain creatine depletion, and urinary creatine abnormalities was observed. The combination of powerful new technologies like exome-next-generation sequencing with thorough systematic evaluation of patients will further expand the clinical spectrum of neurometabolic diseases."],["dc.identifier.doi","10.1007/8904_2013_261"],["dc.identifier.pmid","24190795"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12255"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.isbn","978-3-642-54148-3"],["dc.relation.isbn","978-3-642-54149-0"],["dc.title","A Novel SLC6A8 Mutation in a Large Family with X-Linked Intellectual Disability: Clinical and Proton Magnetic Resonance Spectroscopy Data of Both Hemizygous Males and Heterozygous Females"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1049"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1058"],["dc.bibliographiccitation.volume","255"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Dreha-Kulaczewski, Steffi F."],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Boennemann, Carsten"],["dc.contributor.author","Helms, Gunther"],["dc.contributor.author","Kyllerman, Marten"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Huehne, Kathrin"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Rautenstrauss, Bernd"],["dc.date.accessioned","2017-09-07T11:48:16Z"],["dc.date.available","2017-09-07T11:48:16Z"],["dc.date.issued","2008"],["dc.description.abstract","Mutations in the mitofusin 2 (MFN2) gene are a major cause of primary axonal Charcot-Marie-Tooth (CMT) neuropathy. This study aims at further characterization of cerebral white matter alterations observed in patients with MFN2 mutations. Molecular genetic, magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), and diffusion tensor imaging (DTI) investigations were performed in four unrelated patients aged 7 to 38 years with early onset axonal CMT neuropathy. Three distinct and so far undescribed MFN2 mutations were detected. Two patients had secondary macrocephaly and mild diffuse predominantly periventricular white matter alterations on MRI. In addition, one boy had symmetrical T2-hyperintensities in both thalami. Two patients had optic atrophy, one of them with normal MRI. In three patients proton MRS revealed elevated concentrations of total N-acetyl compounds (neuronal marker), total creatine (found in all cells) and myo-inositol (astrocytic marker) in cerebral white and gray matter though with regional variation. These alterations were most pronounced in the two patients with abnormal MRI. DTI of these patients revealed mild reductions of fractional anisotropy and mild increase of mean diffusivity in white matter. The present findings indicate an enhanced cellular density in cerebral white matter of MFN2 neuropathy which is primarily due to a reactive gliosis without axonal damage and possibly accompanied by mild demyelination."],["dc.identifier.doi","10.1007/s00415-008-0847-1"],["dc.identifier.gro","3143273"],["dc.identifier.isi","000258025000016"],["dc.identifier.pmid","18425620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/769"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0340-5354"],["dc.title","Cerebral involvement in axonal Charcot-Marie-Tooth neuropathy caused by mitofusin2 mutations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","38"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","46"],["dc.bibliographiccitation.volume","52"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Bjornstad, A."],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Korenke, C. G."],["dc.contributor.author","Smeitink, J."],["dc.contributor.author","Trijbels, JMF"],["dc.contributor.author","Athanassopoulos, S."],["dc.contributor.author","Villagran, R."],["dc.contributor.author","Skjeldal, O. H."],["dc.contributor.author","Wilichowski, E."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2018-11-07T10:19:26Z"],["dc.date.available","2018-11-07T10:19:26Z"],["dc.date.issued","2002"],["dc.description.abstract","A deficiency of succinate dehydrogenase is a rare cause of mitochondrial encephalomyopathy. Three patients, 2 sisters and I boy from an unrelated family, presented with symptoms and magnetic resonance imaging signs of leukoencephalopathy. Localized proton magnetic resonance spectroscopy indicated a prominent singlet at 2.40ppm in cerebral and cerebellar white matter not present in gray matter or basal ganglia. The signal was also elevated in cerebrospinal fluid and could be identified as originating from the two equivalent methylene groups of succinate. Subsequently, an isolated deficiency of complex II (succinate:ubiquinone oxidoreductase) was demonstrated in 2 patients in muscle and fibroblasts. One of the sisters died at the age of 18 months. Postmortem examination showed the neuropathological characteristics of Leigh syndrome. Her younger sister, now 12 months old, is also severely affected; the boy, now 6 years old, follows a Milder, fluctuating clinical course. Magnetic resonance spectroscopy provides a characteristic pattern in succinate dehydrogenase deficiency."],["dc.identifier.doi","10.1002/ana.10232"],["dc.identifier.isi","000176451800007"],["dc.identifier.pmid","12112045"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41656"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0364-5134"],["dc.title","Succinate in dystrophic white matter: A proton magnetic resonance spectroscopy finding characteristic for complex II deficiency"],["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","Brain and Development"],["dc.bibliographiccitation.lastpage","50"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Brockmann, Knut"],["dc.contributor.author","Pouwels, Petra J.W."],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Flanigan, Kevin M."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Hanefeld, Folker"],["dc.date.accessioned","2021-06-01T10:50:17Z"],["dc.date.available","2021-06-01T10:50:17Z"],["dc.date.issued","2003"],["dc.description.abstract","Magnetic resonance imaging of a girl with giant axonal neuropathy revealed a progressive white matter disease. In close agreement with histopathological features reported previously, localized proton magnetic resonance spectroscopy at 9 and 12 years of age indicated a specific damage or loss of axons (reduced N-acetylaspartate and N-acetylaspartylglutamate) accompanied by acute demyelination (elevated choline-containing compounds, myo-inositol, and lactate) in white matter as well as a generalized proliferation of glial cells (elevated choline-containing compounds and myo-inositol) in both gray and white matter. (C) 2002 Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/s0387-7604(02)00154-7"],["dc.identifier.isi","000180767900008"],["dc.identifier.pmid","12536033"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86597"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0387-7604"],["dc.title","Cerebral proton magnetic resonance spectroscopy of a patient with giant axonal neuropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","39"],["dc.bibliographiccitation.journal","European Journal of Paediatric Neurology"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Dreha-Kulaczewski, S."],["dc.contributor.author","Dechent, P."],["dc.contributor.author","Helms, G."],["dc.contributor.author","Frahm, J."],["dc.contributor.author","Gaertner, J."],["dc.contributor.author","Brockmann, K."],["dc.date.accessioned","2018-04-23T11:47:36Z"],["dc.date.available","2018-04-23T11:47:36Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1016/s1090-3798(08)70391-x"],["dc.identifier.gro","3142236"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13360"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","1090-3798"],["dc.title","DO06 Complete recovery of NAA reduction in white matter disorders demonstrated by serial proton MRS"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]