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Cerebral glucose metabolism in Fisher syndrome

Cited 18 time in Web of Science Cited 19 time in Scopus
Authors
Kim, Y K; Kim, J S; Jeong, S-H; Park, K-S; Kim, S E; Park, S-H
Issue Date
2008-12-11
Publisher
BMJ Publishing Group
Citation
J Neurol Neurosurg Psychiatry 2009;80(5):512-7
Keywords
Brain/radionuclide imagingBrain Chemistry/*physiologyFluorodeoxyglucose F18/diagnostic useGangliosides/immunologyGlucose/*metabolismGuillain-Barre Syndrome/geneticsImage Processing, Computer-AssistedMagnetic Resonance ImagingMiller Fisher Syndrome/*metabolism/*radionuclide imagingPositron-Emission TomographyRadiopharmaceuticals/diagnostic use
Abstract
BACKGROUND: Fisher syndrome (FS) is characterised by a triad of ophthalmoplegia, ataxia and areflexia. The lesion sites responsible for ataxia and ophthalmoplegia in FS require further exploration. The aim of this study was to determine the involvement of the central nervous system in FS using (18)F-fluorodeoxyglucose-positron emission tomography (FDG-PET). METHODS: Cerebral glucose metabolism in 10 patients with FS was compared with that of 60 age and sex matched normal controls using PET. For individual analyses, 15 age and sex matched controls were selected from the control group. Patients also underwent MRI of the brain and measurement of serum anti-GQ1b antibody. RESULTS: Group analyses revealed increased metabolism in the cerebellar vermis and hemispheres, pontine tegmentum, midbrain tectum, left thalamus and right inferior frontal cortex (p<0.001, uncorrected). In contrast, the visual association cortices (Brodmann areas 18 and 19) showed decreased metabolism bilaterally. Individual analyses disclosed hypermetabolism in the cerebellar vermis or hemispheres (n = 7), inferior frontal cortex (n = 5) and brainstem (n = 4, p<0.005, uncorrected). A negative correlation between the cerebellar hypermetabolism and the interval from symptom onset to PET (r = -0.745, p = 0.013) was also found. Hypermetabolism was normalised on follow-up PET with an improvement in ophthalmoplegia and ataxia in one patient. CONCLUSIONS: These findings indicate involvement of the central nervous system in FS, and the hypermetabolism in the cerebellum and brainstem suggests an antibody associated acute inflammatory process as a mechanism of this autoimmune disorder.
ISSN
1468-330X (Electronic)
Language
English
URI
https://hdl.handle.net/10371/62010
DOI
https://doi.org/10.1136/jnnp.2008.154765
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College of Medicine/School of Medicine (의과대학/대학원)Nuclear Medicine (핵의학전공)Journal Papers (저널논문_핵의학전공)
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