A 77-year-old woman was admitted to a local hospital with a 7-day history of vertigo and nausea, followed by gait disturbance. Magnetic resonance imaging showed extensive brain edema with a hemorrhagic component in the right cerebellum. The lesion was heterogeneously enhanced after administration of contrast medium. The presumptive diagnosis was malignant glioma based on these findings, as well as the presence of mass effect and abnormal enhancement. She was referred to our hospital. However, cerebral angiography did not reveal tumor stain or arterial occlusion, but confirmed corkscrew-like venous collaterals and absence of opacification of the superior petrosal vein (SPV) and superior petrosal sinus. Topography of the brain edema was consistent with the drainage territory of the SPV. These findings suggested that the lesion was vasogenic edema caused by thrombosis of the SPV. The patient was conservatively treated without anticoagulation therapy, and the neurological and imaging abnormalities resolved spontaneously. To avoid unnecessary biopsy, thrombosis of the SPV should be considered in the differential diagnosis of infratentorial lesion mimicking brain tumors. Knowledge of the posterior fossa venous anatomy is essential to achieve the correct diagnosis.

Glioblastoma (GBM) is a malignant tumor with a high recurrence rate and has very poor prognosis in humans. The median survival is still <2 years. Therefore, a new treatment strategy should be established. Recently, this cancer has been thought to be heterogeneous, consisting of cancer stem cells (CSCs) that are self-renewable, multipotent, and treatment resistant. So various strategies targeting glioma stem-like cells (GSCs) have been investigated. This study focused on strategies targeting GSCs through the induction of differentiation using bone morphogenetic protein 4 (BMP4). The expression of CD133, a cancer stem cell marker, under BMP4 treatment in GSCs was examined using flow cytometry, western blotting, and quantitative PCR. Immunofluorescent staining of GSCs was also performed to examine the type of cell division: asymmetric cell division (ACD) or symmetric cell division (SCD). We obtained the following results. The BMP4 treatment caused downregulation of CD133 expression. Moreover, it induced ACD in GSCs. While the ACD ratio was 23% without BMP4 treatment, it was 38% with BMP4 treatment (P=0.004). Furthermore, the tumor sphere assay demonstrated that BMP4 suppresses self-renewal ability. In conclusion, these findings may provide a new perspective on how BMP4 treatment reduces the tumorigenicity of GSCs.

OBJECTIVE Hypoxia induces angiogenesis and plays a major role in the progression of carotid plaques. During carotid intervention, plaques with high-intensity signals on time-of-flight (TOF) magnetic resonance angiography (MRA) often cause ischemic stroke and embolic complications. However, the role of intraplaque hypoxia before carotid endarterectomy (CEA) and carotid artery stenting is not presently understood. In this study the authors aimed to investigate the relationship between intraplaque hypoxia and MRA findings. METHODS Nineteen consecutive patients with 20 carotid artery stenoses who underwent CEA at Saga University Hospital between August 2008 and December 2014 were enrolled in the study. The expressions of hypoxia-inducible transcription factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) were analyzed by immunohistochemical analysis. In addition, the relationship between the findings on TOF MRA and pathology for the carotid plaques was analyzed. RESULTS High-intensity plaques on TOF MRA showed higher expression levels of HIF-1α (p = 0.015) and VEGF (p = 0.007) compared with isointensity plaques. The rate of intraplaque hemorrhage (IPH) on TOF MRA was also significantly higher in the high-intensity plaques than in the isointensity plaques (p = 0.024). Finally, the mean number of neovessels was significantly higher in those without plaque hemorrhage than in those with plaque hemorrhage (p = 0.010). CONCLUSIONS Plaques with high-intensity signals on TOF MRA were associated with IPH and evidence of intraplaque hypoxia. This fact may represent an opportunity to establish novel therapeutic agents targeting intraplaque hypoxia.

Subfrontal schwannomas arising from the olfactory groove are rare and their origin remains uncertain because olfactory bulbs do not possess Schwann cells. We present two cases of subfrontal schwannomas treated with surgical resection. In one case, the tumor was located between the endosteal and meningeal layers of the dura mater. This rare case suggests that subfrontal schwannomas may originate from the fi la olfactoria.

OBJECTIVE Intraplaque hemorrhage (IPH) is most often caused by the rupture of neovessels; however, the factors of intraplaque neovessel vulnerability remain unclear. In this study, the authors focused on pericytes and aimed to investigate the relationship between IPH and pericytes. METHODS The authors retrospectively analyzed the medical records of all patients with carotid artery stenoses who had undergone carotid endarterectomy at their hospitals between August 2008 and March 2016. Patients with carotid plaques that could be evaluated histopathologically were eligible for study inclusion. Intraplaque hemorrhage was analyzed using glycophorin A staining, and patients were divided into the following 2 groups based on the extent of granular staining: high IPH (positive staining area > 10%) and low IPH (positive staining area ≤ 10%). In addition, intraplaque neovessels were immunohistochemically evaluated using antibodies to CD34 as an endothelial cell marker or antibodies to NG2 and CD146 as pericyte markers. The relationship between IPH and pathology for intraplaque neovessels was investigated. RESULTS Seventy of 126 consecutive carotid stenoses were excluded due to the lack of a specimen for histopathological evaluation; therefore, 53 patients with 56 carotid artery stenoses were eligible for study inclusion. Among the 56 stenoses, 37 lesions had high IPH and 19 had low IPH. The number of CD34-positive neovessels was equivalent between the two groups. However, the densities of NG2- and CD146-positive neovessels were significantly lower in the high IPH group than in the low IPH group (5.7 ± 0.5 vs. 17.1 ± 2.4, p < 0.0001; 6.6 ± 0.8 vs. 18.4 ± 2.5, p < 0.0001, respectively). CONCLUSIONS Plaques with high IPH are associated with fewer pericytes in the intraplaque neovessels. This finding may help in the development of novel therapeutic strategies targeting pericytes.