Phase images from eleven patients with glioma yielded statistically significant phase-shift values for calcification and hemorrhage compared with normal brain, whereas CT showed substantial overlap of Hounsfield units. Phase image analysis correctly differentiated between intratumoral calcification and hemorrhage in 86% of cases.
: Meniscal movement is most prominent in the anterior horn of the medial meniscus with the knee in the supine position in 90-degree flexion with external rotation. Meniscal protrusion is more frequently present in the medial meniscus and averaged less than 3 millimeters in normal volunteers in either the sagittal or coronal MR imaging plane.
Displaceable meniscal tears usually have longitudinal, radial, or complex configurations; such tears are associated with substantial ipsilateral collateral ligament lesions and pain.
Low-grade gliomas (LGGs) may harbor malignant foci, which are characterized by increased tumor cellularity and angiogenesis. We used diffusion-weighted MR imaging (apparent diffusion coefficient [ADC]) and PET with the amino acid O-(2-18 F-fluorethyl)-L-tyrosine ( 18 F-FET) to search for focal changes of diffusion (ADC) and amino acid uptake and to investigate whether focal changes in these parameters colocalize within LGGs. Methods: We retrospectively selected 18 patients with nonenhancing LGG. All patients had undergone 18 F-FET PET and MR imaging for preoperative evaluation or for therapy monitoring in recurrent or progressive LGG. Region-of-interest analysis was performed to compare 18 F-FET uptake and ADC values in areas with focal intratumoral maximum metabolic activity and diffusion restriction and between tumor and normal brain. 18 F-FET uptake was normalized to the mean cerebellar uptake (ratio). ADC values were also compared with the 18 F-FET uptake on a voxel-by-voxel basis across the whole tumor. Results: The mean focal maximum (mean ± SD, 1.69 ± 0.85) and global 18 F-FET uptake in tumors (1.14 ± 0.41) exceeded that of normal cortex (0.85 ± 0.09) and cerebrospinal fluid (0.82 ± 0.20). ADC values in the area with most restricted diffusion (1.07 ± 0.22 · 10 −3 mm 2 /s) and in the whole tumor (1.38 ± 0.27 · 10 −3 mm 2 /s) were in the range between normal cortex (0.73 ± 0.06 · 10 −3 mm 2 /s) and cerebrospinal fluid (2.84 ± 0.09 · 10 −3 mm 2 /s). 18 F-FET uptake did not correlate with corresponding (colocalizing) ADC values, either in the area with focal maximum metabolic activity or in the area with most restricted diffusion or in the whole tumor. Conclusion: There is no congruency between 18 F-FET uptake and diffusivity in nonenhancing LGG. Diffusion restriction in these tumors most likely represents changes in brain and tumor cell densities as well as alteration of water distribution and is probably not directly correlated with the density of tumor cells.
Hemorrhage is common in brain tumors. Due to characteristic magnetic field changes induced by hemosiderin it can be detected using susceptibility weighted MRI (SWI). Its relevance to clinical syndromes is unclear. Here we investigated the patterns of intra-tumoral SWI positivity (SWI(pos)) as a surrogate for hemosiderin with regard to the prevalence of epilepsy. We report on 105 patients with newly diagnosed supra-tentorial gliomas and brain metastasis. The following parameters were recorded from pre-operative MRI: (1) SWI(pos) defined as dot-like or fine linear signal changes; (2) allocation of SWI(pos) to tumor compartments (contrast enhancement, central hypointensity, non-enhancing area outside contrast-enhancement); (3) allocation of SWI(pos) to include the cortex, or SWI(pos) in subcortical tumor parts only; (4) tumor size on T2 weighted and gadolinium-enhanced T1 images. 80 tumors (76 %) showed SWI(pos) (4/14 diffuse astrocytoma WHO II, 5/9 anaplastic astrocytoma WHO III, 41/46 glioblastoma WHO IV, 30/36 metastasis). The presence of SWI(pos) depended on tumor size but not on patient's age, medication with antiplatelet drugs or anticoagulation. Seizures occurred in 60 % of patients. Cortical SWI(pos) significantly correlated with seizures in brain metastasis (p = 0.044), and as a trend in glioblastoma (p = 0.062). Cortical SWI(pos) may confer a risk for seizures in patients with newly diagnosed brain metastasis and glioblastoma. Whether development of cortical SWI(pos) induced by treatment or by the natural course of tumors also leads to the new onset of seizures has to be addressed in longitudinal studies in larger patient cohorts.
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