Glaucoma and the Role of Cerebrospinal Fluid Dynamics

The authors thank Wostyn and colleagues¹ for their letter and their interest in our study.² Wostyn and colleagues mentioned studies on normal-tension glaucoma (NTG) patients who showed a reduction in cerebrospinal fluid pressure (CSFP),^3–6 and proposed that the lower CSFP reported in NTG patients could be an indicator of CSF circulatory failure, which could ultimately result in reduced clearance of toxic substances in the subarachnoid space surrounding the optic nerve and lead to glaucomatous damage.¹ 

According to our study, short-term lowering of CSFP is associated with an impediment in both the orthograde axoplasmic flow and the retrograde axonal transport in the retinal ganglion cell axons,^2,7 which partially supports this hypothesis. In addition, Jaggi and colleagues⁸ demonstrated in a previous study the CSF circulatory failure in the optic nerve by blocking the subarachnoid space could lead to severe nerve damage. This CSF circulatory dysfunction has also been found in subjects with NTG through computed tomography cisternography of the brain and orbits.⁹ 

However, the results of our study showed that the retinal layers, including the retinal ganglion cell layer, appeared grossly intact in the low-CSFP study group.^2,7 Wostyn and colleagues¹ further speculated that CSF aspiration during the study period could reduce the CSF outflow resistance and may improve CSF turnover, which could provide a protective effect against glaucomatous damage due to enhanced removal of potentially neurotoxic waste products that would accumulate in the optic nerve. This hypothesis could potentially explain the absence of retinal ganglion cell loss in the low-CSFP rat model. The authors fully agree with their notion, and it may imply that both the hydrostatic pressure and the dynamics of CSF may be of potentially high importance for the physiological stability of the optic nerve.