Subependymomas are rare, representing only 0.51% of all central nervous system tumors operated on during an 8-year period at the University of Utah. Clinical symptoms were associated with tumor location: intracranial masses caused headaches, seizures, and neurological complaints, and spinal cord locations resulted in neurological deficit. The authors review the clinical presentation, management, and contemporary radiographic appearance of this rare tumor.

VEGF and HIF-1alpha are elevated in malignant gliomas. HIF-1alpha inhibition results in VEGF secretion inhibition. HIF-1alpha expression affects glioma tumor growth, suggesting clinical applications for malignant glioma treatment.

Cerebrospinal fluid (CSF) leaks are one of the common complications after traumatic brain injuries (TBI). The risks of CSF leaks can be detrimental to the outcomes of the patients. Early diagnosis and proper management is imperative for it is strongly associated with a better long-term prognosis of the patients. Diagnostic tools for CSF leaks are still under debate. Nevertheless, many reports of successful treatments for CSF leaks have been published with introduction of various repair techniques for leakage sites even though it is surgically challenging. Hereby, we review about the pathophysiology, manifestations as well as the update of the clinical diagnosis and current management of CSF leaks.

Purpose: Higher-grade gliomas are distinguished by increased vascular endothelial cell proliferation and peritumoral edema. These are thought to be instigated by vascular endothelial growth factor, which, in turn, is regulated by cellular oxygen tension. Hypoxia inducible factor-1a (HIF-1a) is a main responder to intracellular hypoxia and is overexpressed in many human cancers, including gliomas. Experimental Design: We investigated the role of HIF-1a in glioma growth in vivo using RNA interference (RNAi) in U251, U87, and U373 glioma cells. Results: We found that RNAi can be used to significantly attenuate glioma growth by reducing HIF-1alevels constitutively using short hairpin RNAs and transiently using small interfering RNAs (siRNA). HIF-1a levels on average were reduced 55% in normoxia and 71% in hypoxia. Vascular endothelial growth factor and GLUT-1levels were reduced 81% and 71%, respectively, in the stable HIF-1a^reduced clones. These clones showed significant growth attenuation (up to 73%) compared with negative controls when grown in vivo in mouse flanks. Cellular proliferation was also reduced significantly, as determined by MIB-1staining.Treating gliomas grown in mouse flank transiently with siRNA against HIF-1a by intratumoral injection resulted in a significant reduction of HIF-1a activity. This activity was followed using a hypoxia-responsive luciferase construct that enabled hypoxia imaging in vivo. Tumor volume in these siRNA injection experiments was reduced by 50% over the negative controls. Conclusions: These results indicate that transient RNAi directed against HIF-1a can effectively curb glioma growth in vivo.Among the features that distinguish higher-grade gliomas such as glioblastoma multiforme (GBM) from low-grade gliomas are vascular endothelial cell proliferation and peritumoral edema (1). Vascular endothelial growth factor (VEGF) is thought to be the major mediator of these properties and has been implicated in glioma growth and angiogenesis (2, 3). VEGF expression is regulated by cellular hypoxia mediated by hypoxia-inducible factor-1a (HIF-1a) under normal physiologic conditions (4) and possibly under pathologic situations such as tumorigenesis. Overexpression of HIF-1a has been described in common human cancers and their metastases, among them a limited number of human brain tumors, including gliomas (5, 6). The role of HIF-1 in solid tumor growth is still not entirely clear, but previous work suggests that this transcription factor is necessary for growth and angiogenesis of these tumors (7,8). Although very little is known of the role of HIF-1a in glioma growth and angiogenesis, it is logical that similar processes take place in these tumors. A direct correlation between tumor grade and HIF-1 expression in GBMs has been shown (9). We support the proposition that HIF-1a expression represents an ''angiogenic switch'' that facilitates the progression of a lowgrade astrocytoma to a GBM and promotes cell survival in hypoxic conditions by elevating glycolysis and angiogenesis ...

ObjectiveAlthough the detection of crossed cerebellar diaschisis (CCD) by means of different imaging modalities is well described, little is known about its diagnosis by computed tomography perfusion (CTP) imaging. We investigated the detection rate of CCD by CTP imaging and the factors related to CCD on CTP images in patients with acute ischemic stroke.Materials and MethodsCT perfusion maps of cerebral blood volume (CBV), cerebral blood flow (CBF), mean transit time (MTT), and time-to-peak (TTP) obtained from 81 consecutive patients affected by an acute ischemic stroke were retrospectively reviewed. Whole-brain perfusion maps were obtained with a multichannel CT scanner using the toggling-table technique. The criteria for CCD was a unilateral supratentorial ischemic lesion and an accompanying decrease in perfusion of the contralateral cerebellar hemisphere on the basis of CTP maps by visual inspection without a set threshold. Maps were quantitatively analyzed in CCD positive cases.ResultsThe criteria for CCD were fulfilled in 25 of the 81 cases (31%). Detection rates per CTP map were as follows: MTT (31%) > TTP (21%) > CBF (9%) > CBV (6%). Supratentorial ischemic volume, degree of perfusion reduction, and infratentorial asymmetry index correlated strongly (R, 0.555-0.870) and significantly (p < 0.05) with each other in CCD-positive cases.ConclusionIt is possible to detect CCD on all four of the CTP-based maps. Of these maps, MTT is most sensitive in detecting CCD. Our data indicate that CTP imaging is a valid tool for the diagnosis of CCD in patients affected by an acute hemispheric stroke.

This was the first study to investigate the accuracy of PCT with the toggling table technique in detection of infratentorial stroke lesions. Clinically, PCT is highly reliable and accurate in detecting infratentorial stroke lesions.

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We investigated effects of Neuregulin 1 (NRG1) on the expression of nicotinic acetylcholine receptor (nAChR) in major pelvic ganglion (MPG) from adult rat. MPG neurons were found to express transcripts for type I and III NRG1s as well as α and β-type epidermal growth factor (EGF)-like domains. Of the four ErbB receptor isoforms, ErbB1, ErbB2, and ErbB3 were expressed in MPG neurons. Treating MPG with NRG1β significantly increased the transcript and protein level of the nAChR α3 and β4 subunits. Consistent with these molecular data, nicotinic currents (I(ACh) ) were significantly up-regulated in NRG1β-treated sympathetic and parasympathetic MPG neurons. In contrast, the type III NRG1 and the α form of the NRG1 failed to alter the I(ACh) . Inhibition of the ErbB2 tyrosine kinase completely abolished the effects of NRG1β on the I(ACh) . Stimulation of the ErbB receptors by NRG1β activated the phosphatidylinositol-3-kinase (PI3K) and mitogen-activated protein kinase (MAPK). Immunoblot analysis revealed that PI3K-mediated activation of Akt preceded Erk1/2 activation in NRG1β-treated MPG neurons. Furthermore, specific PI3K inhibitors abrogated the phosphorylation of Erk1/2, while inhibition of MEK did not prevent the phosphorylation of Akt. Taken together, these findings suggest that NRG1 up-regulates nAChR expression via the ErbB2/ErbB3-PI3K-MAPK signaling cascade and may be involved in maintaining the ACh-mediated synaptic transmission in adult autonomic ganglia.