15 results on '"Frahm Jens"'
Search Results
2. Clinical proton MR spectroscopy in central nervous system disorders.
- Author
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Oz G, Alger JR, Barker PB, Bartha R, Bizzi A, Boesch C, Bolan PJ, Brindle KM, Cudalbu C, Dinçer A, Dydak U, Emir UE, Frahm J, González RG, Gruber S, Gruetter R, Gupta RK, Heerschap A, Henning A, Hetherington HP, Howe FA, Hüppi PS, Hurd RE, Kantarci K, Klomp DW, Kreis R, Kruiskamp MJ, Leach MO, Lin AP, Luijten PR, Marjańska M, Maudsley AA, Meyerhoff DJ, Mountford CE, Nelson SJ, Pamir MN, Pan JW, Peet AC, Poptani H, Posse S, Pouwels PJ, Ratai EM, Ross BD, Scheenen TW, Schuster C, Smith IC, Soher BJ, Tkáč I, Vigneron DB, and Kauppinen RA
- Subjects
- Central Nervous System Diseases metabolism, Central Nervous System Diseases pathology, Humans, Biomarkers metabolism, Central Nervous System Diseases diagnosis, Magnetic Resonance Spectroscopy methods
- Abstract
A large body of published work shows that proton (hydrogen 1 [(1)H]) magnetic resonance (MR) spectroscopy has evolved from a research tool into a clinical neuroimaging modality. Herein, the authors present a summary of brain disorders in which MR spectroscopy has an impact on patient management, together with a critical consideration of common data acquisition and processing procedures. The article documents the impact of (1)H MR spectroscopy in the clinical evaluation of disorders of the central nervous system. The clinical usefulness of (1)H MR spectroscopy has been established for brain neoplasms, neonatal and pediatric disorders (hypoxia-ischemia, inherited metabolic diseases, and traumatic brain injury), demyelinating disorders, and infectious brain lesions. The growing list of disorders for which (1)H MR spectroscopy may contribute to patient management extends to neurodegenerative diseases, epilepsy, and stroke. To facilitate expanded clinical acceptance and standardization of MR spectroscopy methodology, guidelines are provided for data acquisition and analysis, quality assessment, and interpretation. Finally, the authors offer recommendations to expedite the use of robust MR spectroscopy methodology in the clinical setting, including incorporation of technical advances on clinical units., (RSNA, 2014)
- Published
- 2014
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3. Untreated glioblastoma multiforme: increased myo-inositol and glutamine levels in the contralateral cerebral hemisphere at proton MR spectroscopy.
- Author
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Kallenberg K, Bock HC, Helms G, Jung K, Wrede A, Buhk JH, Giese A, Frahm J, Strik H, Dechent P, and Knauth M
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- Aged, Brain Neoplasms therapy, Case-Control Studies, Female, Glioblastoma therapy, Humans, Male, Middle Aged, Statistics, Nonparametric, Brain Neoplasms metabolism, Glioblastoma metabolism, Glutamine metabolism, Inositol metabolism, Magnetic Resonance Spectroscopy methods
- Abstract
Purpose: To use localized in vivo proton magnetic resonance (MR) spectroscopy of the contralateral hemisphere in patients with glioblastoma multiforme (GBM) to detect alterations in cerebral metabolites as potential markers of infiltrating GBM cells., Materials and Methods: The study was approved by the ethics committee, and written informed consent was obtained. Twenty-two patients with newly diagnosed and untreated GBM underwent in vivo single-voxel short echo time proton MR spectroscopy with a 3-T MR imaging system. Absolute metabolite concentrations in the hemisphere contralateral to the tumor were compared with data from five patients with low-grade gliomas (LGGs) and from a group of 14 age-matched control subjects by using analysis of variance and subsequent t tests or corresponding nonparametric tests., Results: In the contralateral hemisphere, MR spectroscopy revealed increased concentrations of myo-inositol and glutamine. Mean myo-inositol levels were significantly increased in patients with GBM (3.6 mmol/L +/- 0.8 [standard deviation]) relative to levels in control subjects (3.1 mmol/L +/- 0.6; P = .03) and tended to be higher relative to levels in patients with LGG (2.7 mmol/L +/- 0.8; P = .09). Mean glutamine concentrations in patients with GBM (3.4 mmol/L +/- 0.9) differed significantly from those in control subjects (2.7 mmol/L +/- 0.7; P = .01); mean concentrations in patients with GBM differed from those in patients with LGG (2.4 mmol/L +/- 0.5; P = .01). There were no significant differences between data in patients with LGG and in control subjects., Conclusion: Increased concentrations of myo-inositol and glutamine in the contralateral normal-appearing white matter of GBM patients are consistent with mild astrocytosis and suggest the detectability of early neoplastic infiltration by using proton MR spectroscopy in vivo.
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- 2009
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4. Serial proton MR spectroscopy and diffusion tensor imaging in infantile Balo's concentric sclerosis.
- Author
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Dreha-Kulaczewski SF, Helms G, Dechent P, Hofer S, Gärtner J, and Frahm J
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- Adolescent, Female, Humans, Protons, Tissue Distribution, Brain metabolism, Brain pathology, Diffuse Cerebral Sclerosis of Schilder metabolism, Diffuse Cerebral Sclerosis of Schilder pathology, Magnetic Resonance Imaging methods, Magnetic Resonance Spectroscopy methods
- Abstract
Introduction: Proton magnetic resonance spectroscopy (MRS) and diffusion tensor imaging (DTI) yield different parameters for characterizing the evolution of a demyelinating white matter disease. The purpose was to elucidate biochemical and microstructural changes in Balo's concentric sclerosis lesions and to correlate the findings with the clinical course., Methods: Localized short-echo time MRS and DTI were performed over 6 years in a left occipital lesion of a female patient (age at onset 13.8 years) with Balo's concentric sclerosis. A right homonym hemianopsia persisted., Results: Metabolite patterns were in line with initial active demyelination followed by gliosis and partial recovery of neuroaxonal metabolites. Fractional anisotropy and mean diffusivity of tissue water remained severely altered. Fiber tracking confirmed a disruption in the geniculo-calcarine tract as well as involvement of the corpus callosum., Conclusion: MRS and DTI depict complementary parameters, but DTI seems to correlate better with clinical symptoms.
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- 2009
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5. Quantitative proton MRS of cerebral metabolites in laminin alpha2 chain deficiency.
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Brockmann K, Dechent P, Bönnemann C, Schreiber G, Frahm J, and Hanefeld F
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- Adolescent, Aspartic Acid analogs & derivatives, Aspartic Acid metabolism, Child, Child, Preschool, Creatine metabolism, Dipeptides metabolism, Humans, Infant, Magnetic Resonance Imaging methods, Male, Muscular Dystrophies pathology, Muscular Dystrophies physiopathology, Phosphocreatine metabolism, Cerebral Cortex metabolism, Laminin deficiency, Magnetic Resonance Spectroscopy, Muscular Dystrophies diagnosis, Muscular Dystrophies metabolism, Protons
- Abstract
Congenital muscular dystrophy (CMD) due to merosin (laminin alpha2 chain) deficiency is an autosomal recessively inherited disorder characterized by severe muscular weakness and hypotonia from birth on. Brain involvement is the rule and characterized by variable T2 hyperintensities of white matter which appears swollen on cranial MRI. The pathophysiology of these white matter changes is not clear. In five patients with laminin alpha2 deficient CMD we performed short-echo time localized proton MRS with determination of absolute metabolite concentrations in grey and white matter. In affected white matter, a consistent pattern of metabolites was detected comprising reduced concentrations of N-acetylaspartate and N-acetylaspartylglutamate, creatine, and phosphocreatine, and to a milder degree of choline-containing compounds. In contrast, concentrations of myo-inositol were in the normal range. Spectra of cortical and subcortical grey matter were normal. The observed metabolite profile is consistent with white matter edema, that is reduced cellular density, and relative astrocytosis. This interpretation is in line with the hypothesis that laminin alpha2 deficiency results in leakage of fluids across the blood-brain barrier and a histopathological report of astrocytic proliferation in CMD.
- Published
- 2007
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6. Cerebral metabolic and structural alterations in hereditary spastic paraplegia with thin corpus callosum assessed by MRS and DTI.
- Author
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Dreha-Kulaczewski S, Dechent P, Helms G, Frahm J, Gärtner J, and Brockmann K
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- Adult, Age of Onset, Case-Control Studies, Female, Humans, Spastic Paraplegia, Hereditary genetics, Corpus Callosum metabolism, Corpus Callosum pathology, Diffusion Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy, Spastic Paraplegia, Hereditary metabolism, Spastic Paraplegia, Hereditary pathology
- 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.
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- 2006
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7. Low-field vs. high-field proton MRS of mouse brain in vivo.
- Author
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Michaelis T and Frahm J
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- Analysis of Variance, Animals, Image Processing, Computer-Assisted methods, Mice, Mice, Inbred C57BL, Models, Animal, Protons, Reproducibility of Results, Sensitivity and Specificity, Species Specificity, Brain Chemistry, Glucose metabolism, Lactic Acid metabolism, Magnetic Resonance Spectroscopy methods, Taurine metabolism
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- 2005
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8. Use of phased array coils for a determination of absolute metabolite concentrations.
- Author
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Natt O, Bezkorovaynyy V, Michaelis T, and Frahm J
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- Adult, Brain Chemistry, Female, Humans, Magnetic Resonance Spectroscopy instrumentation, Male, Phantoms, Imaging, Brain metabolism, Magnetic Resonance Spectroscopy methods
- Abstract
This work describes the use of phased array coils for a quantification of absolute metabolite concentrations. The method is demonstrated for single-voxel localized proton MRS of human brain with an eight-element receive-only head coil. It is based on the transmitter reference amplitude of the body coil used for RF transmission. A relative sensitivity of every element of the phased array coil is derived from a combination of two reference scans without water suppression that correspond to either the body coil in transmit-receive mode or the phased array coil in conjunction with body coil excitation. Experimental results were obtained at 2.9 T for both phantoms and 12 human subjects in different locations of gray and white matter. The data demonstrate that the procedure is technically robust and without a penalty in measuring time. Moreover, it takes full advantage of the signal-to-noise gain for quantitative proton MRS and may be extended to other phased array coils without the need for a recalibration., (Copyright 2004 Wiley-Liss, Inc.)
- Published
- 2005
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9. Safety aspects of chronic low-frequency transcranial magnetic stimulation based on localized proton magnetic resonance spectroscopy and histology of the rat brain.
- Author
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Liebetanz D, Fauser S, Michaelis T, Czéh B, Watanabe T, Paulus W, Frahm J, and Fuchs E
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- Animals, Basigin, Brain cytology, Cell Count, Ectodysplasins, Electric Stimulation adverse effects, Glial Fibrillary Acidic Protein metabolism, Hippocampus metabolism, Immunohistochemistry, Lumbosacral Region, Male, Membrane Glycoproteins metabolism, Membrane Proteins metabolism, Rats, Rats, Wistar, Spinal Cord metabolism, Time Factors, Antigens, CD, Antigens, Neoplasm, Antigens, Surface, Astrocytes metabolism, Avian Proteins, Blood Proteins, Brain metabolism, Electromagnetic Fields adverse effects, Magnetic Resonance Spectroscopy, Microglia metabolism
- Abstract
Because repetitive transcranial magnetic stimulation (rTMS) is capable of inducing lasting alterations of cortical excitability, it represents a promising therapeutic tool in several neuropsychiatric disorders. However, rTMS, especially when applied chronically, may cause harmful effects in the stimulated tissue. To study the safety of chronic rTMS we used a novel small stimulation coil, which was specially designed to treat rats, and investigated brain tissue using in vivo localized proton magnetic resonance spectroscopy (MRS) and post mortem histological analysis. Histology was based on a modified stereology method in combination with immunohistochemistry applying antibodies against OX-6, OX-42, ED, and GFAP to detect any microglial and/or astrocytic activation 48 h after the last TMS session. Conscious rats were treated with a daily suprathreshold rTMS regimen of 1000 stimuli applied on 5 consecutive days at a frequency of 1 Hz. In comparison with control animals receiving magnetic stimulation over the lumbar spine, quantitative evaluations of cerebral metabolite concentrations by proton MRS revealed no significant alterations of N-acetyl-aspartate, creatine and phosphocreatine, choline-containing compounds, myo-inositol, glucose and lactate after chronic rTMS. Similarly to the in vivo results, post mortem histology revealed no changes in microglial and astrocytic activation after rTMS. In conclusion, these data provide support for the safety of chronic rTMS. However, they do not exclude acute changes on neurotransmitters systems or other physiologic responses during or directly after the rTMS treatment.
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- 2003
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10. Localized proton MRS of cerebral metabolite profiles in different mouse strains.
- Author
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Schwarcz A, Natt O, Watanabe T, Boretius S, Frahm J, and Michaelis T
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- Animals, Aspartic Acid metabolism, Choline metabolism, Creatine metabolism, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Protons, Aspartic Acid analogs & derivatives, Brain metabolism, Brain Ischemia metabolism, Magnetic Resonance Spectroscopy methods
- Abstract
Localized proton MR spectroscopy (MRS) was used to quantify cerebral metabolite concentrations in NMRI (n = 8), BALB/c (n = 7), and C57BL/6 (n = 8) mice in vivo and 1 hr after global irreversible ischemia (2.35 T, STEAM, TR/TE/TM = 6000/20/10 ms, 4 x 3 x 4 mm(3) volume, corrections for cerebrospinal fluid). Anatomical MRI and proton MRS revealed significant differences of the C57BL/6 strain in comparison with both BALB/c and NMRI mice. While MRI volumetry yielded larger ventricular spaces of the C57BL/6 strain, proton MRS resulted in elevated concentrations of N-acetylaspartate (tNAA), creatine and phosphocreatine (tCr), choline-containing compounds (Cho), glucose (Glc), and lactate (Lac) relative to BALB/c mice and elevated Glc relative to NMRI mice. Apart from the expected decrease of Glc and increase of Lac 1 hr post mortem, C57BL/6 mice presented with significant reductions of tNAA, tCr, and Cho, whereas these metabolites remained unchanged in BALB/c and NMRI mice. The results support the hypothesis that the more pronounced vulnerability of C57BL/6 mice to brain ischemia is linked to strain-dependent differences of the cerebral energy metabolism., (Copyright 2003 Wiley-Liss, Inc.)
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- 2003
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11. Cerebral proton magnetic resonance spectroscopy in infantile Alexander disease.
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Brockmann K, Dechent P, Meins M, Haupt M, Sperner J, Stephani U, Frahm J, and Hanefeld F
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- Alexander Disease diagnostic imaging, Aspartic Acid analysis, Brain diagnostic imaging, Child, Child, Preschool, Demyelinating Diseases pathology, Disease Progression, Female, Gliosis pathology, Humans, Infant, Inositol analysis, Lactic Acid analysis, Magnetic Resonance Imaging, Male, Nerve Degeneration pathology, Radiography, Alexander Disease metabolism, Alexander Disease pathology, Aspartic Acid analogs & derivatives, Brain metabolism, Brain pathology, Magnetic Resonance Spectroscopy
- Abstract
Alexander disease (AD) is a rare genetic disorder of the central nervous system due to a dysfunction of astrocytes. The most common infantile form presents as a progressive leukodystrophy with macrocephalus. Recently, heterozygous de novo mutations in the gene encoding glial fibrillary acidic protein (GFAP) have been demonstrated to be associated with AD. We used localized proton magnetic resonance spectroscopy (MRS) to assess metabolic abnormalities in grey and white matter, basal ganglia, and cerebellum of 4 patients with infantile AD and GFAP mutations. Strongly elevated concentrations of myo-inositol in conjunction with normal or increased choline-containing compounds in all regions investigated point to astrocytosis and demyelination. Neuroaxonal degeneration, as reflected by a reduction of N-acetylaspartate, was most pronounced in cerebral and cerebellar white matter. The accumulation of lactate in affected white matter is in line with infiltrating macrophages. Metabolic alterations demonstrated by in vivo proton MRS are in excellent agreement with known neuropathological features of AD.
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- 2003
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12. Succinate in dystrophic white matter: a proton magnetic resonance spectroscopy finding characteristic for complex II deficiency.
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Brockmann K, Bjornstad A, Dechent P, Korenke CG, Smeitink J, Trijbels JM, Athanassopoulos S, Villagran R, Skjeldal OH, Wilichowski E, Frahm J, and Hanefeld F
- Subjects
- Brain enzymology, Brain pathology, Child, Dementia, Vascular genetics, Electron Transport Complex II, Female, Humans, Infant, Male, Multienzyme Complexes genetics, Oxidoreductases genetics, Pedigree, Protons, Succinate Dehydrogenase genetics, Dementia, Vascular diagnosis, Dementia, Vascular enzymology, Magnetic Resonance Spectroscopy, Multienzyme Complexes deficiency, Oxidoreductases deficiency, Succinate Dehydrogenase deficiency
- Abstract
A deficiency of succinate dehydrogenase is a rare cause of mitochondrial encephalomyopathy. Three patients, 2 sisters and 1 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.
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- 2002
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13. Cerebral involvement in axonal Charcot-Marie-Tooth neuropathy caused by mitofusin2 mutations
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Brockmann, Knut, Dreha-Kulaczewski, Steffi, Dechent, Peter, Bönnemann, Carsten, Helms, Gunther, Kyllerman, Marten, Brück, Wolfgang, Frahm, Jens, Huehne, Kathrin, Gärtner, Jutta, and Rautenstrauss, Bernd
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- 2008
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14. Cystic megalencephalic leukoencephalopathy - clinical, MRI/MRS and EEG findings
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Mejaški-Bošnjak, Vlatka, Hanefeld, Folker, Frahm, Jens, Brockmann, Knut, Čačić, Melita, Marušić-Della Marina Branka, and Veličković Perat, Milivoj
- Subjects
Megalencephalic leukoencephalopathy ,Magnetic Resonance Imaging ,Magnetic Resonance Spectroscopy - Abstract
Van der Knaap et al. (1995) described recently a new entity of heredodegenerative white matter disease, based on clinical and morphological criteria as visualized by MRI. We report od 5 further cases of this entity. Three out of 5 patients have pregressive neuromotor disorders and suffer from epilepsy, demonstrating distinctive EEG findings with slow high-voltage background activity combined with spikes and spike-wave complexes, as well as marked photoparoxysmal response of generalized discharges of spikes, polispikes and waves. These three children have extensive lesions to the cerebral white matter on MRI, particulary the huge subcortical cysts frontally and temporally. Localized proton MRS in these patients revealed complete loss of all brain metabolities within altered white matter and cysts. In contrast, the other two children follow the milder clinical course and morphology, showing MR spectra with only decrease of creatine.
- Published
- 1998
15. Cerebral proton magnetic resonance spectroscopy of a patient with giant axonal neuropathy
- Author
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Brockmann, Knut, Pouwels, Petra J.W., Dechent, Peter, Flanigan, Kevin M., Frahm, Jens, and Hanefeld, Folker
- Subjects
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SPECTRUM analysis , *PEOPLE with neurosis - 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. [Copyright &y& Elsevier]
- Published
- 2003
- Full Text
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