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Abstract

We appreciate the clear and thoughtful comments presented by Killer et al.1Killer H.E. Jaggi G.P. Flammer J. et al.Cerebrospinal fluid dynamics between the intracranial and the subarachnoid space of the optic nerve Is it always bidirectional?.Brain. 2007; 130: 514-520Crossref PubMed Scopus (183) Google Scholar Although intracranial pressure (ICP) measured by lumbar puncture in the lateral decubitus position may not represent the exact pressure in the retrolaminar subarachnoid space (SAS), it is the best surrogate currently available. Killer et al rightly point out that the anatomy of the SAS is complex and the cerebrospinal fluid (CSF) dynamics are not well understood. To complicate matters further, humans spend considerable time in both vertical and horizontal positions. This would almost certainly lower the retrolaminar ICP while vertical, leading to an even higher translaminar pressure difference while standing or sitting. Although this seems to be the case, the intraocular pressure also changes with postural position, and the relationship between IOP and ICP in differing positions is not known. The work by Killer et al1Killer H.E. Jaggi G.P. Flammer J. et al.Cerebrospinal fluid dynamics between the intracranial and the subarachnoid space of the optic nerve Is it always bidirectional?.Brain. 2007; 130: 514-520Crossref PubMed Scopus (183) Google Scholar, 2Killer H.E. Jaggi G.P. Flammer J. et al.The optic nerve: a new window into cerebrospinal fluid composition.Brain. 2006; 129: 1027-1030Crossref PubMed Scopus (116) Google Scholar gives intriguing insight into the immediate surroundings of the retrolaminar optic nerve, suggesting that CSF does not flow freely into the blind-ending SAS enclosing the optic nerve. This stagnation may lead to alteration in the CSF composition and an inhospitable milieu for the optic nerve. If and how ICP changes CSF flow around the optic nerve merits study. Both our study and those of Killer et al suggest that the environment surrounding the extraocular optic nerve may have fundamental significance in the pathogenesis of glaucoma. Glaucoma and Cerebrospinal Fluid PressureOphthalmologyVol. 115Issue 12PreviewWe read with great interest the report by Berdahl et al1 on cerebrospinal fluid (CSF) pressure in patients with primary open-angle glaucoma (POAG). The authors rightly state that the precise mechanism causing optic nerve damage in POAG remains unknown. In their study, they found that the intracranial pressure (ICP) in patients with POAG was 33% lower than in the control group without POAG and concluded that their findings support the concept that a translaminar pressure difference may result not only from a high intraocular pressure (IOP) but also from reduced ICP, and that the level of ICP may play an important role in the development of glaucomatous optic neuropathy. Full-Text PDF Glaucoma and Cerebrospinal Fluid PressureOphthalmologyVol. 115Issue 12PreviewRegarding the paper by Berdahl et al, who used retrospective cerebrospinal fluid (CSF) pressure data to assess differences in CSF pressure between glaucoma patients and nonglaucoma control patients,1 we have a question regarding the control data and would like to comment on the use of different reference planes for pressure measurement. The mean CSF pressure in their glaucoma patients was 12.4 cm H2O versus 17.7 cm H2O for the controls. The only other study measuring CSF pressure in glaucoma patients found a higher CSF pressure range, from 11 to 17 cm H2O in 7 subjects, but did not report a mean or use a normal control group. Full-Text PDF