New radiation modalities have made it possible to prolong the survival of individuals with malignant brain tumors, but symptomatic radiation necrosis becomes a serious problem that can negatively affect a patient's quality of life through severe and lifelong effects. Here we review the relevant literature and introduce our original concept of the pathophysiology of brain radiation necrosis following the treatment of brain, head, and neck tumors. Regarding the pathophysiology of radiation necrosis, we introduce two major hypotheses: glial cell damage or vascular damage. For the differential diagnosis of radiation necrosis and tumor recurrence, we focus on the role of positron emission tomography. Finally, in accord with our hypothesis regarding the pathophysiology, we describe the promising effects of the anti-vascular endothelial growth factor antibody bevacizumab on symptomatic radiation necrosis in the brain.

In U-HRCT scans, a large matrix size maintained the spatial resolution and improved the image quality and assessment of lung diseases, despite an increase in image noise, when compared to a 512 matrix size.

ObjectivesTo compare the image quality of the lungs between ultra-high-resolution CT (U-HRCT) and conventional area detector CT (AD-CT) images.MethodsImage data of slit phantoms (0.35, 0.30, and 0.15 mm) and 11 cadaveric human lungs were acquired by both U-HRCT and AD-CT devices. U-HRCT images were obtained with three acquisition modes: normal mode (U-HRCTN: 896 channels, 0.5 mm × 80 rows; 512 matrix), super-high-resolution mode (U-HRCTSHR: 1792 channels, 0.25 mm × 160 rows; 1024 matrix), and volume mode (U-HRCTSHR-VOL: non-helical acquisition with U-HRCTSHR). AD-CT images were obtained with the same conditions as U-HRCTN. Three independent observers scored normal anatomical structures (vessels and bronchi), abnormal CT findings (faint nodules, solid nodules, ground-glass opacity, consolidation, emphysema, interlobular septal thickening, intralobular reticular opacities, bronchovascular bundle thickening, bronchiectasis, and honeycombing), noise, artifacts, and overall image quality on a 3-point scale (1 = worst, 2 = equal, 3 = best) compared with U-HRCTN. Noise values were calculated quantitatively.ResultsU-HRCT could depict a 0.15-mm slit. Both U-HRCTSHR and U-HRCTSHR-VOL significantly improved visualization of normal anatomical structures and abnormal CT findings, except for intralobular reticular opacities and reduced artifacts, compared with AD-CT (p < 0.014). Visually, U-HRCTSHR-VOL has less noise than U-HRCTSHR and AD-CT (p < 0.00001). Quantitative noise values were significantly higher in the following order: U-HRCTSHR (mean, 30.41), U-HRCTSHR-VOL (26.84), AD-CT (16.03), and U-HRCTN (15.14) (p < 0.0001). U-HRCTSHR and U-HRCTSHR-VOL resulted in significantly higher overall image quality than AD-CT and were almost equal to U-HRCTN (p < 0.0001).ConclusionsBoth U-HRCTSHR and U-HRCTSHR-VOL can provide higher image quality than AD-CT, while U-HRCTSHR-VOL was less noisy than U-HRCTSHR.Key Points • Ultra-high-resolution CT (U-HRCT) can improve spatial resolution. • U-HRCT can reduce streak and dark band artifacts. • U-HRCT can provide higher image quality than conventional area detector CT. • In U-HRCT, the volume mode is less noisy than the super-high-resolution mode. • U-HRCT may provide more detailed information about the lung anatomy and pathology. Electronic supplementary materialThe online version of this article (10.1007/s00330-018-5491-2) contains supplementary material, which is available to authorized users.

Radiation necrosis (RN) after intensive radiation therapy is a serious problem. Using human RN specimens, we recently proved that leaky angiogenesis is a major cause of brain edema in RN. In the present study, we investigated the same specimens to speculate on inflammation's effect on the pathophysiology of RN. Surgical specimens of symptomatic RN in the brain were retrospectively reviewed by histological and immunohistochemical analyses using hematoxylin and eosin (H&E) staining as well as immunohistochemical staining for VEGF, HIF-1α, CXCL12, CXCR4, GFAP, CD68, hGLUT5, CD45, IL-1α, IL-6 TNF-α and NF-kB. H&E staining demonstrated marked angiogenesis and cell infiltration in the perinecrotic area. The most prominent vasculature was identified as thin-walled leaky angiogenesis, i.e. telangiectasis surrounded by prominent interstitial edema. Two major cell phenotypes infiltrated the perinecrotic area: GFAP-positive reactive astrocytes and CD68/hGLUT5-positive cells (mainly microglias). Immunohistochemistry revealed that CD68/hGLUT5-positive cells and GFAP-positive cells expressed HIF-1α and VEGF, respectively. GFAP-positive cells expressed chemokine CXCL12, and CD68/hGLUT5-positive cells expressed receptor CXCR4. The CD68/hGLUT5-positive cells expressed pro-inflammatory cytokines IL-1α, IL-6 and TNF-α in the perinecrotic area. VEGF caused leaky angiogenesis followed by perilesional edema in RN. GFAP-positive cells expressing CXCL12 might attract CXCR4-expressing CD68/hGLUT5-positive cells into the perinecrotic area. These accumulated CD68/hGLUT5-positive cells expressing pro-inflammatory cytokines seemed to aggravate the RN edema. Both angiogenesis and inflammation might be caused by the regulation of HIF-1α, which is well known as a transactivator of VEGF and of the CXCL12/CXCR4 chemokine axis.

No abstract