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Reply: Because venous sinus stenoses in idiopathic intracranial hypertension (IIH) can be reversed by lowering the intracranial pressure, I believe that these stenoses are caused primarily by elevated intracranial pressure. I think there might, furthermore, be a feedback mechanism in IIH such that an increase in intracranial pressure (due to impaired absorption of CSF?) leads to stenoses of the transverse sinuses and that these stenoses lead to an increase in intravenous pressure proximal to the stenoses (which can be measured directly by a catheter). This again could hamper absorption of CSF, leading to a further increase in pressure. (In theory, pressure would then rise infinitely, but in reality it does not. Therefore, the mechanisms must be somewhat more complex.) We saw cases of secondary intracranial hypertension demonstrating narrowing of large segments of the intracranial sinuses, whereas in IIH, there seems to be a predilection for the development of the stenoses in the lateral parts of the transverse sinuses. Therefore, patients with IIH probably have some pathoanatomic change in this region of the sinus ("vulnerable segments" may be secondary to hormonal changes). I agree with Bateman that patients might profit from stent angioplasty, which interrupts the feedback mechanism. However, the http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Neuroradiology American Journal of Neuroradiology

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Publisher
American Journal of Neuroradiology
Copyright
Copyright © 2010 by the American Society of Neuroradiology.
ISSN
0195-6108
eISSN
1936-959X
DOI
10.3174/ajnr.A0941
Publisher site
See Article on Publisher Site

Abstract

Because venous sinus stenoses in idiopathic intracranial hypertension (IIH) can be reversed by lowering the intracranial pressure, I believe that these stenoses are caused primarily by elevated intracranial pressure. I think there might, furthermore, be a feedback mechanism in IIH such that an increase in intracranial pressure (due to impaired absorption of CSF?) leads to stenoses of the transverse sinuses and that these stenoses lead to an increase in intravenous pressure proximal to the stenoses (which can be measured directly by a catheter). This again could hamper absorption of CSF, leading to a further increase in pressure. (In theory, pressure would then rise infinitely, but in reality it does not. Therefore, the mechanisms must be somewhat more complex.) We saw cases of secondary intracranial hypertension demonstrating narrowing of large segments of the intracranial sinuses, whereas in IIH, there seems to be a predilection for the development of the stenoses in the lateral parts of the transverse sinuses. Therefore, patients with IIH probably have some pathoanatomic change in this region of the sinus ("vulnerable segments" may be secondary to hormonal changes). I agree with Bateman that patients might profit from stent angioplasty, which interrupts the feedback mechanism. However, the

Journal

American Journal of NeuroradiologyAmerican Journal of Neuroradiology

Published: Feb 1, 2008

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