NR AUSR
AU Meissner,B.; Kallenberg,K.; Krasnianski,A.; Bartl,M.; Heinemann,U.; Krebs,B.; Kretzschmar,H.A.; Knauth,M.; Schulz-Schaeffer,W.J.; Zerr,I.
TI MRI lesion patterns in sporadic Creutzfeldt-Jakob disease
QU TSE-Forum, 6. Kongress - Nationale TSE-Forschungsplattform, Greifswald 26.6.-28.6.2006, Poster: Diagnostik DIA-07
PT Konferenz-Poster
AB
Objective
Hyperintense basal ganglia on T2w (T2 weighted images) and FLAIR (fluid attenuated inversion recovery) - corresponding to restricted diffusivity on DWI (diffusion-weighted images) - have been reported as the classical finding in CJD. Signal increase in further brain regions has been additionally described. Until the present study, however, no large study has directly compared the sensitivities of these three MRI techniques applied to hyperintense cortical and subcortical structures.
Methods
The T2w, FLAIR and diffusion-weighted MR scans (from one examination) of 55 CJD patients were assessed for signal increase (T2w, FLAIR) or restricted diffusion (DWI) of the single cortical areas, basal ganglia, thalamus and cerebellum.
Results
Signal increase of the basal ganglia was found in 60% (DWI) and 47% (each on FLAIR and T2). Cortical signal increase was found in 91% (DWI), 76% (FLAIR) and 38% (T2). The frontal and temporal lobes were most frequently affected (82% and 75% on DWI). Considering MRI lesion patterns, a combined affection of basal ganglia and cortex (58% on DWI) occurred most frequently, followed by isolated cortical signal increase (33% on DWI). FLAIR could improve the high sensitivity of DWI with respect to basal ganglia, cerebellar and hippocampal signal increase.
Conclusions
FLAIR and DWI should be used in combination. Isolated cortical signal increase - in the appropriate clinical context - should also arouse suspicion of CJD.
AD Bettina Meissner, Anna Krasnianski, Mario Bartl, Daniela Varges, Uta Heinemann, Inga Zerr, National Reference Center for transmissible spongiform encephalopathies, Department of Neurology, Georg-August University Göttingen, Germany; Kai Kallenberg, Bjarne Krebs, Hans A. Kretzschmar, Center for Neuropathology and Prion Research, Ludwig-Maximilians-University, Feodor-Lynen-Str. 23, 81377 Munich, Germany; Henriette J. Tschampa (Henriette.Tschampa@ukb.uni-bonn.de), Department of Radiology, University of Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany; Michael Knauth, Department of Neuroradiology, Georg-August-Universität Göttingen, Germany; W.J.Schulz-Schaeffer, Department of Neuropathology, Georg-August University Göttingen, Germany; Corresponding author: Bettina Meissner, Department of Neurology, University of Göttingen, Robert-Koch-Str. 40, D-37075 Göttingen, Germany, Phone: +49 551 39-6636, Fax: +49 551 39-7020, E-mail: betti.meissner@med.uni-goettingen.de
SP englisch
PO Deutschland
EA Photo des Posters, welches nach Auskunft von Frau Meissner aktueller als der Text im Tagungsband ist und bewußt die im Tagungsband genannten Coautoren H.J.Tschampa und D.Varges nicht mehr nennt, Details 1, Details 2
OR Tagungsband