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Leonardo Rangel-Castilla, Jonathan J. Russin, Eduardo Martinez-del-Campo, Hector Soriano-Baron, Robert F. Spetzler and Peter Nakaji

% after this period. Mortality is reported at 10% after hemorrhage, and residual major disability occurs in 20%–30% of patients. 7 , 9 , 10 , 14 , 15 , 18–20 , 29 , 36 , 40 , 44 , 55 , 57 Feeding artery pressures, compartmentalization, venous drainage, flow phenomena, and vascular steal all contribute to the complex physiology of cerebral AVMs. Intranidal vessels are exposed to abnormally high blood flow and shear forces that activate molecular pathways in smooth muscle cells and brain endothelial cells (BECs), leading to proliferation and vascular remodeling. 32 , 33

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Daniel M. Sciubba, Rafael De la Garza Ramos, C. Rory Goodwin, Nancy Abu-Bonsrah, Ali Bydon, Timothy F. Witham, Chetan Bettegowda, Ziya L. Gokaslan and Jean-Paul Wolinsky

report and the present one are inclusion of more patients for analysis, stratification of patients based on Enneking classification (the previous investigation did not take into account surgical margins—only en bloc vs intralesional resection), and analysis of molecular prognostic factors. For the present study, data such as patient age, sex, history of previous tumor surgery, previous radiation, previous chemotherapy, metastatic status, tumor histological data, Enneking classification, number of vertebral levels spanned by the tumor, and biomarker positivity or

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Nicholas F. Marko and Robert J. Weil

, these 5 tumors represent molecularly and clinically unique entities, and, for this reason, collectivization of these tumors (along with WHO Grade I gliomas) under the heading of “low-grade gliomas” is rapidly falling out of favor. Nonetheless, Grade II tumors differ considerably from WHO Grade I, III, and IV gliomas, and so the 5 Grade II gliomas are often discussed together. Managing and predicting the course of these tumors has historically proven challenging, so basic and translational research in Grade II gliomas continues in the hopes of identifying novel

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Henry H. Schmidek

development of cell fusion and gene transfer. As a result, several developmentally important genes and their activities have recently been elucidated, and areas of knowledge that had previously been considered relatively discrete are now seen to be interrelated. To appreciate these developments requires some familiarity with concepts in developmental biology, molecular genetics, cellular transformation, and growth factors, as well as with a number of techniques that have allowed the exploration and manipulation of the mammalian genome. This review focuses on those areas

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Diane J. Aum, David H. Kim, Thomas L. Beaumont, Eric C. Leuthardt, Gavin P. Dunn and Albert H. Kim

G lioblastoma is the most common primary malignant brain tumor in adults and continues to portend poor prognosis despite decades of research. Even with aggressive resection followed by concomitant chemotherapy and radiation, there is a high recurrence rate with median survival of less than 15 months. 58 Indeed, fewer than 5% of patients survive 5 years. 45 Extensive investigation of the cellular and molecular biology of glioblastoma over the last decade has identified several histopathological and chromosomal hallmarks that have enhanced diagnosis and

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Spontaneous spinal hematomas and low-molecular-weight heparin

Report of four cases and review of the literature

Peter A. Heppner, Stephen J. Monteith and Andrew J. J. Law

L ow -molecular-weight heparin is increasingly used to provide simple anticoagulation in preventative and therapeutic settings. Spontaneous spinal hematomas (that is, those not related to trauma, surgery, or lumbar puncture) are a rare clinical entity first described by Shiller and colleagues 24 more than 50 years ago. Several causes have been identified, including acquired and congenital clotting abnormalities and underlying vascular lesions. Among the acquired coagulopathies, aspirin, warfarin, tissue plasminogen activator, and heparin have all be implicated

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Jennifer Kosty and Timothy W. Vogel

I n 1993, Jabs et al. 11 were the first to identify a genetic cause for craniosynostosis with the MSX2 gene mutation resulting in “Boston-type” craniosynostosis. Shortly thereafter, the role of fibroblast growth factor receptor (FGFR) in Crouzon syndrome was identified, 35 and transforming growth factor b (TGFb) was recognized as a powerful modulator of suture fusion. 33 From these early investigations, our understanding of the molecular pathways contributing to craniosynostosis has greatly expanded, and additional molecular and genetic pathways

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John Richard Apps and Juan Pedro Martinez-Barbera

presentation, tumors may be variably solid to cystic and variably invasive and destructive of neighboring structures. 39 Disease course can vary, with some tumors remaining indolent despite incomplete resection with or without radiotherapy, whereas others may rapidly recur despite apparent gross-total resections and radiotherapy. 39 A better understanding of the molecular pathology of these tumors will provide novel insights into the underlying mechanisms responsible for this heterogeneity in clinical course. In addition, such understanding will form the first steps toward

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Yoon-Hee Cha, John H. Chi and Nicholas M. Barbaro

puncture. Low-molecular-weight heparin therapy has become favored in the treatment of venous thromboembolisms and acute cardiac ischemia because of its predictable anticoagulant response, longer half-life, and its lack of blood monitoring requirements. 10 To date, there are no known cases of spinal spontaneous SDHs occurring in patients undergoing LMWH therapy when spinal instrumentation is not also being used. 9, 11 We present the case of a patient in whom an acute spinal spontaneous SDH developed while she was receiving LMWH and discuss possible contributing factors

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Athula Karunanyaka, Jian Tu, Amy Watling, Kingsley P. Storer, Apsara Windsor and Marcus A. Stoodley

Response C entral nervous system AVMs predominantly rupture in children and young adults with a 15–20% mortality rate and a 35–45% rate of neurological complications. 7 , 17 , 31 These lesions consist of a nidus of arterial-to-venous fistulous connections with feeding arteries and draining veins. Although the vessels in AVMs are morphologically recognizable as arteries and veins, they are thicker than normal vessels and also have molecular differences, particularly in endothelial cells. 28 Arteriovenous malformations are generally assumed to be