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Editors Selection IGR 16-4

Basic Research: CSF and glaucoma

Comment by James Morgan on:

25137 Cerebrospinal Fluid Pressure in Glaucoma A Prospective Study, Ren R; Jonas JB; Tian G et al., Ophthalmology, 2010; 117: 259-266

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The article by Ren et al. (50) tests the hypothesis that the level of CSF pressure can influence the degree of cupping in patients with normaltension glaucoma. The key measure is the hydrostatic pressure difference across the optic nerve/lamina cribrosa estimated by subtraction of the CSF pressure as determined by lumbar puncture from the intraocular pressure. The hypothesis is reasonable and based on retrospective studies of glaucoma patients who have had incidental measurements of CSF pressure which suggest that a low CSF pressure is associated with progressive glaucoma. Work in animal models also supports the idea that the CSF pressure can influence the development of glaucomatous optic neuropathy. The rational for the study requires some qualification. In the introduction, the absence of cupping in a range of retina/optic nerve ischemic conditions is used to argue against a role for vascular factors in the generation of optic nerve head damage. It is important to note that this argument excludes arteritic optic neuropathies in which cupping does occur. While we do not have evidence that vascular factors on their own can cause glaucomatous damage, their contributory role in an optic nerve predisposed to damage cannot be excluded. The study is also little unusual in that many of the control patients were under investigation for AION ‐ it is unclear why, with this diagnosis, LPs were offered. While the test indicates that the gender break down of the various groups did not differ there are differences in that the LTG are 50% female whereas the high IOP group has a greater proportion of males. Given the effects of confounding variables, the use of a multivariate analysis to determine the relationship between field defect and translaminar pressure difference is reassuring. The inclusion of other variables in this analysis ‐ for example gender and corneal thickness ‐ might also have been informative.

The contributory role of vascular factors in an optic nerve predisposed to glaucomatous damage cannot be excluded

While the correlation between the translaminar pressure and clinical phenotype is reported as significant, inspection of the data plots suggests that the degree of scatter is considerable. I was unable to discern a clear relationship between the translaminar pressure and the degree of visual field loss. It would be interesting to know if the relationship was stronger for particular types of discs ‐ for example with larger discs where the effects of CSF pressure might be expected to have a greater effect. The plot of the translaminar pressure difference in the high and low IOP patients is, of course, explained in part by the higher IOP in both glaucoma groups; the difference between the glaucomatous and the control group although reported as statistically significant does not appear to be marked.

In eyes with low IOPs, further reduction of the IOP by use of carbonic anhydrase inhibitors may not necessarily be beneficial

The authors consider carefully the limitations of the study, drawing attention to the inclusion of neurology patients under investigation as the control group. Even so, this challenging study contributes to the debate over glaucomatous optic neuropathy. The absolute differences in translaminar pressures are small between the various groups, but the argument is made that this effect could be significant given data from other studies (e.g., AGIS) which have shown the detrimental effects of small differences in IOP. Even so, it would be unwise at this stage to attribute a principal effect of the translaminar pressure gradient to the development of glaucoma. Other important factors ‐ for example the extent to which this measure fluctuates ‐ need to be considered. The paper ends on a useful practical inference. In eyes with low IOPs, further reduction of the IOP by use of carbonic anhydrase inhibitors may not necessarily be beneficial since these could have a detrimental effect on the level of CSF pressure and exacerbate the translaminar pressure difference.

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