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Update on intracranial hypertension and hypotension

Hoffmann, Jana; Goadsby, Peter J.b

Current Opinion in Neurology: June 2013 - Volume 26 - Issue 3 - p 240–247
doi: 10.1097/WCO.0b013e328360eccc
HEADACHE: Edited by Peter J. Goadsby
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Purpose of review The aim of this article is to review recent findings on the pathophysiology of idiopathic changes in intracranial pressure. The review will focus on idiopathic intracranial hypertension (IIH) and spontaneous intracranial hypotension (SIH).

Recent findings Substantial evidence indicates that IIH is associated with delayed absorption of cerebrospinal fluid (CSF). Stenoses of the transverse sinus are common in IIH, but their clinical significance has not been entirely clarified. Despite the observed efficacy of endovascular treatment in some IIH patients, a correlation between the extent of observed stenoses and the clinical course of the disease could not be demonstrated. The underlying cause of SIH is a spontaneous CSF leakage into the epidural space. Conservative treatment and the epidural blood patch remain the treatment of choice for this rare syndrome.

Summary Recent clinical evidence indicates that IIH is probably a result of CSF outflow abnormality rather than of CSF production. Further research is needed to elucidate the causes of elevated intracranial pressure and the mechanism leading to visual loss. Prospective randomized clinical trials are needed to clarify a possible therapeutic potential of endovascular treatment. Research efforts on SIH should focus further on associated connective tissue disorders predisposing to CSF leaks.

aDepartment of Neurology, Charité - Universitätsmedizin Berlin, Berlin, Germany

bDepartment of Neurology, Headache Group, University of California San Francisco, San Francisco, California

Correspondence to Dr med Jan Hoffmann, Department of Neurology, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany. Tel: +49 30 450 560 276; fax: +49 30 450 560 912; e-mail: jan.hoffmann@charite.de

© 2013 Lippincott Williams & Wilkins, Inc.