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Wostyn et al. published a thought-stimulating contribution to the pathophysiology of normal-tension glaucoma (NTG) and make an interesting link to as Alzheimer's disease.1 Based on anatomical considerations, it seems a logical consequence to look at the brain and the optic nerve ‐ a white matter of the brain ‐ in the same context. The traditional view on glaucoma is very much intraocular pressuredominated. The recent literature on glaucoma introduced a new concept, translaminar pressure which is based on the difference between the intraocular pressure and the intracranial pressure. A couple of studies demonstrated a low intracranial pressure in patients with normal-tension glaucoma. The problem with these studies, however, is that they measure the lumbar pressure as an indicator for the intracranial pressure. There are, however, serious doubts whether or not this extrapolation from lumbar pressure to the intracranial pressure and the pressure in the subarachnoid space of the optic nerve is legitimate. There is, however, good evidence for a decreased all-over turnover of cerebrospinal fluid (CSF) in patients with Alzheimer's disease as well as in normal-tension glaucoma patients. Investigation of cerebrospinal fluid dynamics performed with cisternography in patients with normal-tension glaucoma demonstrated a highly reduced CSF inflow from the chiasma cistern into the subarachnoid spaces of the optic nerve indicating a reduced local CSF turnover.2
An experimental animal model rendered evidence for a possible toxic effect of stagnant cerebrospinal fluid on the optic nerve.3 Given the evidence for a toxic effect of reduced cerebrospinal fluid circulation surrounding the 'white matter' tract optic nerve, senescence changes in CSF circulation might be an interesting candidate to explain intracranial white matter dysfunction (Alzheimer's disease) as well as normal-tension glaucoma which also represents a white matter disease of the optic nerve.