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High-Resolution Contrast-Enhanced, Susceptibility-Weighted MR Imaging at 3T in Patients with Brain Tumors: Correlation with Positron-Emission Tomography and Histopathologic Findings

K. Pinkera, I.M. Noebauer-Huhmanna, I. Stavroub, R. Hoeftbergerc, P. Szomolanyia, G. Karanikasd, M. Webera, A. Stadlbauere, E. Knospb, K. Friedricha and S. Trattniga

a MR Centre of Excellence, Department of Radiology, Medical University Vienna, Vienna, Austria
b Department of Neurosurgery, Medical University Vienna, Vienna, Austria
c Institute of Neurology, Medical University Vienna, Vienna, Austria
d Department of Nuclear Medicine, Medical University Vienna, Vienna, Austria
e Department of Neurosurgery, University Erlangen-Nuremberg, Erlangen, Germany


Figure 1
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Fig 1. A 36-year-old male patient with right temporomesial glioblastoma WHO IV.

A, Axial 3T HR-CE-SW-MR images demonstrated a brain lesion with high frequency of SusE.

B, Axial 3T HR-CE-SW-MR images demonstrated a brain lesion with marked CE in HR-SW sequence.

C, Axial 3T HR-CE-SW-MR images demonstrated a brain lesion with marked CE in T1-weighted SE sequence.

D, FDG/MET-PET showed hypermetabolism temporal right (yellow arrow).

E and F, The lesion was determined by histopathology (H&E staining, x200) as a glioblastoma WHO IV.

A and B, Intralesional SusE (yellow arrow) could be correlated to conglomerates of vessel proliferations (black arrows in D and E).


Figure 2
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Fig 2. A 40-year-old male patient with an oligoastrocytoma WHO II frontotemporal left.

A and B, Axial 3T HR-CE-SW-MR images depicted no SusE (A), as well as no significant contrast enhancement of the lesion in T1-weighted SusE and HR-SW images (B).

C, FDG/MET-PET showed a hypometabolism frontotemporal right (yellow arrow).

D, Histopathology (H&E staining, x200) demonstrated no formations of SusE conglomerates.


Figure 3
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Fig 3. A 65-year-old male patient with glioblastoma multiforme (WHO IV).

A and B, Axial 3T HR-CE-SW-MR imaging demonstrated medium frequency of intralesional SusE refined to the medial part of the lesion and formation of SusE conglomerates (A) and marked peripheral contrast enhancement (B).