Overview
- Editors:
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Karl Einhäupl
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Klinikum Grosshadern, Ludwig-Maximilians-University, Munich, Germany
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Oliver Kempski
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Institute for Neurosurgical Pathophysiology, Johannes Gutenberg-University, Mainz, Germany
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Alexander Baethmann
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Klinikum Grosshadern, Ludwig-Maximilians-University, Munich, Germany
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Table of contents (21 chapters)
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Front Matter
Pages i-viii
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Structural and Functional Basis
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- J. Cervos-Navarro, S. Kannuki
Pages 15-25
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- M. Deckert, K. Frerichs, P. Mehraein, O. Kempski, A. Baethmann, K. Einhäupl
Pages 39-42
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- S. Kannuki, J. Cervos-Navarro, K. Matsumoto, Y. Nakagawa
Pages 43-52
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- K. Frerichs, M. Deckert, O. Kempski, K. Einhäupl, A. Baethmann
Pages 53-58
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Mechanisms of Brain Tissue Damage
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- P. Schmiedek, K. Einhäupl, E. Moser, U. Büll, G. Leinsinger, T. Kreisig
Pages 75-83
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- O. Kempski, F. Staub, G.-H. Schneider, M. Zimmer, A. Baethmann
Pages 93-104
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Clinical Aspects of Sinus Vein Thrombosis
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Front Matter
Pages 141-141
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- K. M. Einhäupl, A. Villringer, R. L. Haberl, W. Pfister, M. Deckert, H. Steinhoff et al.
Pages 149-155
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- A. Hartmann, J. Wappenschmidt, L. Solymosi, F. Brassel
Pages 171-186
About this book
Contrary to the neurological manifestations of arterial cerebral blood flow disturbances, respective conditions resulting fram obstruction of the cerebro-venous system are far less well understood. Hence, cerebral sinus vein thrombosis (CSVT) ranks prominently among the group of neglected diseases of the brain. This might be attributable (a) to the diagnostic difficulties of the disorder and (b) to the fact that CSVT is associated with a host of heterogeneous neurological symptoms which often are not specific for the underlying venous flow disorder. Another complicating aspect is that CSVT is a consequence of other diseases as disparate as focal infection, trauma, neoplasia, or a thrombosis disposition caused by oral contraceptive use. Although progress has been made in establishing the correct diagnosis of the syndrome, many problems remain as the discussions contained within this volume vividly demonstrate. The same is true for the present understanding of the pathophysiological basis of the disease, eg, concerning the cerebro-venous circulation, the hemodynamic and neuropathological consequences in particular. Part of these deficits may be attributed to a scarcity of solid experimental data due to the limited availability of animal models. However, relevant experimental models are required for an in-depth analysis of the pathophysiological mechanisms, eg, causing brain tissue damage in relationship with the topographical distribution of the venous flow obstruction and, most importantly, for the testing of specific methods of treatment.
