Positron emission tomography and histopathology in Creutzfeldt‐Jakob disease

Goldman, Serge; Liard, A; Flament-Durand, J; Luxen, André; Bidaut, Luc; Stanus, Etienne; Hildebrand, Jerzy; Przedborski, Serge

doi:10.1212/wnl.43.9.1828

Cited by 35 publications

(17 citation statements)

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“…Asymmetry in the distribution of the hypometabolic regions has been found, and frontal, parietal and temporal reduction in glucose uptake has been described [24,25,26]. However, in order to perform the PET examinations, anaesthesia was necessary in these severely demented patients, which raised the question of the effects of propofol administration on rCMR glu and DED binding.…”

Section: The Effect Of Anaesthesiamentioning

confidence: 99%

Multitracer study with positron emission tomography in Creutzfeldt-Jakob disease

Engler

Lundberg

Ekbom

et al. 2003

European Journal of Nuclear Medicine and Molecular Imaging

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During the period February 1997 to April 2000, 15 patients with clinical symptoms of Creutzfeldt-Jakob disease (CJD) were referred to Uppsala University PET Centre. Positron emission tomography (PET) was performed to detect characteristic signs of the disease, e.g. neuronal death and/or astrocytosis in the brain. The examinations were performed in one session starting with oxygen-15 labelled water scan to measure regional cerebral blood flow, followed by imaging with the monoamine oxidase B inhibitor N-[(11)C-methyl]- L-deuterodeprenyl (DED) to assess astrocytosis in the brain and finally imaging with fluor-18 2-fluorodeoxyglucose (FDG) to assess regional cerebral glucose metabolism (rCMR(glu)) [corrected]. Nine of the patients fulfilled the clinical criteria of probable CJD. In eight of them, FDG and DED imaging revealed, in comparison with normal controls, a typical pattern characterized by a pronounced regional decrease (<2SD) in glucose brain metabolism, indicative of neuronal dysfunction; this was accompanied by a similar increase (>2SD) in DED binding, indicating astrocytosis. These changes were most pronounced in the cerebellum and the frontal, occipital and parietal cortices, whereas the pons, the thalamus and the putamen were less affected and the temporal cortex appeared unaffected. The cerebral blood flow showed a pattern similar to that observed with FDG. In the ninth patient, analysis with DED was not possible. The diagnosis of definite CJD according to international consensus criteria was confirmed in six of these patients. In one patient with probable CJD, protease-resistant prion protein (PrPres) could not be demonstrated. In two patients with probable CJD, autopsy was not allowed. Computed tomography and magnetic resonance imaging, performed in four and seven of these nine patients respectively, showed unspecific, mainly atrophic changes. In six other patients, the PET examinations gave a different pattern. In three of them, high rCMR(glu) was noticed in parts of the brain, particularly in the temporal lobes and basal ganglia, which could suggest encephalitis. One of the patients had Sjögren's syndrome, one had paraneoplastic limbic encephalitis and the third recovered spontaneously. In the other three patients, the DED binding was normal despite a hypometabolic glucose pattern. In conclusion, the PET findings obtained using DED and FDG paralleled neuropathological findings indicating neuronal dysfunction and astrocytosis, changes that are found in CJD.

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Section: The Effect Of Anaesthesiamentioning

confidence: 99%

Multitracer study with positron emission tomography in Creutzfeldt-Jakob disease

Engler

Lundberg

Ekbom

et al. 2003

European Journal of Nuclear Medicine and Molecular Imaging

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“…In CJD disseminated areas of hypometabolism (PET) [12,16,18,23,45] or hypoperfusion (SPECT) [1,8,11,18,21,26,27,32,36,44,47] of cortical and subcortical structures in CJD were described in single case reports or few cases. The aim of this study was to explore whether typical sites or even patterns of regional metabolic changes could be found in a larger sample of CJDcases and to evaluate possible correlations between PET findings, MRI and the clinical symptomatology.…”

Section: Introductionmentioning

confidence: 99%

Positron emission tomography with [ 18 F]FDG in the diagnosis of Creutzfeldt-Jakob disease (CJD)

Henkel

Zerr

Hertel

et al. 2002

Journal of Neurology

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The aim of this study was to explore the sites of metabolic changes with [(18)F]2-fluoro-2-desoxy-D-glucose (FDG) and positron emission tomography (PET) in patients with Creutzfeldt-Jakob disease and to correlate the findings with clinical symptoms. Static [(18)F]FDG-PET studies of eight patients with the diagnosis of confirmed or probable CJD were retrospectively analysed by two physicians from departments of nuclear medicine independently with a strong interrater agreement (kappa=0,98). The clinical data of the patients, based on a standardized evaluation by physicians from the German Creutzfeldt-Jakob disease surveillance study, was correlated with the PET findings. [(18)F]FDG-PET shows widespread hypometabolism in CJD. All patients had a reduction of cerebral glucose metabolism in at least one temporal or parietal region. Additionally in 7 of our own 8 cases and 3 of 4 cases from the literature the occipital lobe, the cerebellum or the basal ganglia were involved. These findings differ from typical patterns of hypometabolism in Alzheimer's disease and other neurodegenerative disorders. In two thirds of the cases the distribution was markedly asymmetric. Myoclonus was present in five out of our eight own cases. Our data suggest that myoclonus might correlate with metabolic impairment of contralateral parietal and temporal lobes. In three of four patients with visual symptoms FDG uptake was reduced in the visual cortex bilaterally. Typical hyperintensities on MRI were only found in two of the eight cases at the time of PET-studies. Our results demonstrate that [(18)F]FDG-PET appears to be a sensitive investigation in CJD and could be useful to differentiate CJD from other neurodegenerative disorders.

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“…Disruption of the CPC tract may have contributed to cerebellar-like ataxia in our patient. Previous studies of CJD patients have reported that MRI or FDG PET, neuropathological, and clinical findings closely correlate [9][10][11][12]. Disruption of cerebro-cerebellar loops, resulting in crossed cerebellar diaschisis, is a novel finding that may provide a clue to the mechanism underlying ataxic hemiparesis in CJD.…”

mentioning

confidence: 85%

Crossed cerebellar diaschisis: a clue to the mechanism of ataxic hemiparesis in Creutzfeldt-Jakob disease?

et al. 2001

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Positron emission tomography and histopathology in Creutzfeldt‐Jakob disease

Cited by 35 publications

References 0 publications

Multitracer study with positron emission tomography in Creutzfeldt-Jakob disease

Multitracer study with positron emission tomography in Creutzfeldt-Jakob disease

Positron emission tomography with [ 18 F]FDG in the diagnosis of Creutzfeldt-Jakob disease (CJD)

Crossed cerebellar diaschisis: a clue to the mechanism of ataxic hemiparesis in Creutzfeldt-Jakob disease?

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