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In their study on cerebrospinal fluid exchange in the optic nerve in normal-tension glaucoma, Killer and colleagues performed a computerized tomographic cisternography of the brain and orbit in 18 patients with normal-pressure glaucoma and in four patients without glaucoma. After a lumbar puncture, ten ml of the contrast agent iopamidol was injected intrathecally. The patients were then turned to the prone position and the CT examination as carried out. The authors found that in the normal-pressure glaucoma group the density of contrast-loaded cerebrospinal fluid (CLCSF) in the orbital subarachnoidal space was significantly lower as compared with its density in the intracranial CSF spaces and as compared with its density in the orbital subarachnoidal space in the control group. The authors concluded that the difference in the concentration gradients between the CLCSF within the intracranial spaces and the SAS of the ONs in normal-pressure glaucoma supported the hypothesis of a disturbed CSF exchange between the CSF in the intracranial spaces and the CSF in the SAS surrounding the ONs. The disturbance of CSF dynamics in this specific CSF pathway can be explained by ON compartmentation. Despite the marked limitations of the study such as a small sample size and questions on the reproducibility of the measurements, the finding of a reduced density of CLCSF in the orbital subarachnoidal space may suggest an impediment of the flow of CSF from the brain into the orbit. If that is the case in the patients with normalpressure glaucoma, one may postulate a reduced CSF-pressure in the orbital subarachnoidal space, supporting the hypothesis that a reduced orbital CSF-pressure through an increased trans-lamina cribrosa pressure may lead to glaucomatous optic nerve damage in eyes with a normal intraocular pressure.