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Brain Advance Access published online on November 17, 2006
Brain, doi:10.1093/brain/awl324
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received September 8, 2006
Revised October 10, 2006
Accepted October 17, 2006

Article

Cerebrospinal fluid dynamics between the intracranial and the subarachnoid space of the optic nerve. Is it always bidirectional?

H. E. Killer 1 *, G. P. Jaggi 2, J. Flammer 3, N. R. Miller 4, A. R. Huber 5, and A. Mironov 6

1 Eye Institute, University of Basel, Kantonsspital Aarau, Switzerland; Department of Ophthalmology, Kantonsspital Aarau, Switzerland
2 Department of Ophthalmology, Kantonsspital Aarau, Switzerland
3 Eye Institute, University of Basel, Kantonsspital Aarau, Switzerland
4 Wilmer Ophthalmological Institute, Johns Hopkins Hospital, Baltimore, MD, USA
5 Department of Laboratory Medicine, Kantonsspital Aarau, Switzerland
6 Institute of Neuroradiology, Kantonsspital Aarau, Switzerland

* To whom correspondence should be addressed.
H. E. Killer, E-mail: Killer{at}ksa.ch


  Abstract

CSF is thought to flow continuously from the site of production in the ventricles into interconnected spaces; i.e. cisterns and subarachnoid spaces (SASs). Since the SAS of the optic nerve is defined by a cul-de-sac anatomy, it is not evident how local CSF might recycle from that region to the general SAS. The concept of free communication of CSF has recently been challenged by the description of a concentration gradient of beta-trace protein, a lipocalin-like prostaglandin D-synthase (L-PGDS), between the spinal CSF and that in the SAS of the optic nerve, indicating diminished local clearance or local overproduction of L-PGDS here. In fact, computed cisternography with a contrast agent in three patients with idiopathic intracranial hypertension and asymmetric papilloedema demonstrate a lack of contrast-loaded CSF in the SAS of the optic nerve despite it being present in the intracranial SAS, thus suggesting compartmentation of the SAS of the optic nerve. The concept of an optic nerve compartment syndrome is further supported by a concentration gradient of brain-derived L-PGDS between the spinal CSF and the CSF from the optic nerve SAS in the same patients.

Keywords: beta-trace protein; cerebrospinal fluid dynamics; computed cisternography; idiopathic intracranial hypertension; optic nerve subarachnoid space.
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