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Comment by Jost Jonas on:

66320 Fast circulation of cerebrospinal fluid: an alternative perspective on the protective role of high intracranial pressure in ocular hypertension, Wostyn P; De Groot V; Van Dam D et al., Clinical and Experimental Optometry, 2016; 99: 213-218

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As an anatomical fact, the optic nerve as brain fascicle is surrounded by the optic nerve meninges and imbedded into the cerebrospinal fluid (CSF) with its pressure. Based on this fact, the pressure difference in the lamina cribrosa (as the most likely site of glaucomatous optic nerve fiber damage) is the difference of intraocular pressure minus the tissue pressure of the optic nerve and the orbital CSF pressure. It led to the hypothesis that patients with glaucoma and normal IOP may have a low orbital CSF pressure leading to an increased trans-lamina cribrosa pressure difference. Subsequent clinical and experimental studies suggested that an abnormally low CSF pressure may indeed be associated with glaucomatous optic nerve damage. As a corollary, studies suggested that increased CSF pressure may protect the optic nerve against the development of glaucomatous damage in eyes with ocular hypertension. As a different aspect of the role the CSF pressure may play for the development of glaucomatous optic nerve damage, Peter Wostyn, Hans-Peter Killer and their team proposed that the potentially protective effect of higher CSF pressure could be due to a faster cerebrospinal CSF production leading to increased fluid turnover with enhanced removal of potentially neurotoxic waste products, in particular in the optic nerve CSF space. It could lead to a faster removal of β-amyloid which accumulates in glaucoma as well as in Alzheimer's disease. This model also refers to the optic nerve compartment syndrome as described by Killer and colleagues, If confirmed, procedures to increase the CSF flow could be helpful against glaucomatous optic neuropathy.

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