The Influence of Translaminar Pressure Gradient and Intracranial Pressure in Glaucoma

To the Editor: We thank Price et al1 for their interesting review article “The Influence of Translaminar Pressure Gradient and Intracranial Pressure in Glaucoma: A review” and for citing some of our work. The optic canal might indeed play a crucial role in cerebrospinal fluid (CSF) dynamics between the suprachiasmatic cistern and the subarachnoid space (SAS) of the optic nerve. The SAS measures the smallest diameter within the optic canal, and it is confined by bone. Contingent on this given anatomical condition, there is no possibility for the SAS to extend as response to CSF pressure in this location, which indeed can work as a bottle neck for CSF dynamics. In a cohort of normal-tension glaucoma (NTG) patients, our group demonstrated impaired contrast-loaded CSF filling within the optic nerve SAS applying computer tomography–assisted cisternography, a condition we called optic nerve sheath compartmentation.2 Such a compartmentation of the SAS influences both CSF flow and pressure within the SAS and the composition of CSF as well. In our study on translaminar pressure3 in our cohort of NTG patients, CSF pressure was within a normal range, while other studies4 reported lower CSF pressures. In our study,3 all measurements were performed by the same experienced neuroradiologist. It is a well-known fact that the pressure readings during lumbar puncture are dependendent on the position of the patient and on the time the needle is in place. These parameters might have influenced other studies, especially those4 based on data from charts, in which such critical information is not known. We further should not forget that the pressure measured during lumbar puncture does not necessarily reflect the pressure in the SAS behind the lamina cribrosa. Considering this fact, the term translaminar pressure gradient is somehow a misnomer. Interestingly, our NTG patients demonstrated enlarged optic nerve sheath diameters in the retrolaminar region,5 a feature that is typically seen in patients with papilledema as a consequence of elevated intracranial pressure. As the lumbar CSF pressure was normal in our cohort of NTG patients, the distension of the ON sheath might have been caused by a higher local CSF pressure or a change in the compliance of the dura sheath. The lumbar CSF pressure might, therefore, very likely not match the retrolaminar CSF pressure we are looking for in the calculation for the translaminar pressure gradient. We totally agree with the authors that future research should focus on a reliable device for a noninvasive measurement method of the retrolaminar CSF pressure. Besides CSF pressure, CSF velocity is another parameter for flow dynamics. Both terms are linked in the Bernoulli equations. When we are talking about CSF pressure, we should, therefore, also consider CSF velocity. A functional CSF flow velocity along the optic nerve might not only be crucial for the transport of nutrients but also for the removal of potentially toxic waste products. Pathologic CSF pressure gradients might, therefore, also be associated with changes in the biochemical composition of the CSF surrounding the optic nerve, which might play a crucial role for the integrity of axons and function of the optic nerve. We would like to encourage further studies in this field.


To the Editor:
We thank Price et al 1 for their interesting review article "The Influence of Translaminar Pressure Gradient and Intracranial Pressure in Glaucoma: A review" and for citing some of our work.
The optic canal might indeed play a crucial role in cerebrospinal fluid (CSF) dynamics between the suprachiasmatic cistern and the subarachnoid space (SAS) of the optic nerve. The SAS measures the smallest diameter within the optic canal, and it is confined by bone. Contingent on this given anatomical condition, there is no possibility for the SAS to extend as response to CSF pressure in this location, which indeed can work as a bottle neck for CSF dynamics.
In a cohort of normal-tension glaucoma (NTG) patients, our group demonstrated impaired contrast-loaded CSF filling within the optic nerve SAS applying computer tomography-assisted cisternography, a condition we called optic nerve sheath compartmentation. 2 Such a compartmentation of the SAS influences both CSF flow and pressure within the SAS and the composition of CSF as well.
In our study on translaminar pressure 3 in our cohort of NTG patients, CSF pressure was within a normal range, while other studies 4 reported lower CSF pressures. In our study, 3 all measurements were performed by the same experienced neuroradiologist. It is a well-known fact that the pressure readings during lumbar puncture are dependendent on the position of the patient and on the time the needle is in place. These parameters might have influenced other studies, especially those 4 based on data from charts, in which such critical information is not known. We further should not forget that the pressure measured during lumbar puncture does not necessarily reflect the pressure in the SAS behind the lamina cribrosa. Considering this fact, the term translaminar pressure gradient is somehow a misnomer.
Interestingly, our NTG patients demonstrated enlarged optic nerve sheath diameters in the retrolaminar region, 5 a feature that is typically seen in patients with papilledema as a consequence of elevated intracranial pressure. As the lumbar CSF pressure was normal in our cohort of NTG patients, the distension of the ON sheath might have been caused by a higher local CSF pressure or a change in the compliance of the dura sheath. The lumbar CSF pressure might, therefore, very likely not match the retrolaminar CSF pressure we are looking for in the calculation for the translaminar pressure gradient. We totally agree with the authors that future research should focus on a reliable device for a noninvasive measurement method of the retrolaminar CSF pressure.
Besides CSF pressure, CSF velocity is another parameter for flow dynamics. Both terms are linked in the Bernoulli equations. When we are talking about CSF pressure, we should, therefore, also consider CSF velocity. A functional CSF flow velocity along the optic nerve might not only be crucial for the transport of nutrients but also for the removal of potentially toxic waste products. Pathologic CSF pressure gradients might, therefore, also be associated with changes in the biochemical composition of the CSF surrounding the optic nerve, which might play a crucial role for the integrity of axons and function of the optic nerve. We would like to encourage further studies in this field. In Reply: We appreciate the commentary, discussion, and attention to detail brought to our manuscript "The influence of translaminar pressure gradient and intracranial pressure in glaucoma: a review" by Pircher and Killer. The authors correctly point out the dynamic variability and potential difficulties of obtaining accurate and reproducible measurements of cerebrospinal fluid and translaminar pressures and their variants. Similarity can be seen in factors including corneal thickness and curvature influencing 1 intraocular pressure and estimations of translatability to the retina and optic nerve. We thank the authors for further expanding upon their findings in DOI