To the Editor:
We thank Baneke et al. [1] for their stimulation contribution on the topic of intracranial pressure (ICP) and glaucoma and for quoting some of our work.
The optic nerve (ON) subarachnoid space is indeed divided by a complex system of trabeculae and septae that arranged between the arachnoid and the pia layer of the ON. Their surface is covered with meningothelial cells which are highly metabolically active in keeping a homeostasis for the ON. They also were shown to react with growth and proliferation to mechanical stress. Such structures are therefore not only involved in fluid dynamics, but also in biochemical processes.
Baneke et al. state that the “cerebrospinal fluid (CSF)” we investigated following ON sheath fenestration for an ON sheath compartment syndrome, “may have been composed of interstitial fluid originating in the ON itself”. If this is true for CSF from the subarachnoid space of the ON it is true for every CSF sampled from lumbar puncture as well. The authors hypothesized “the structure of the ON sheath prevents influx of contrast more significantly than it prevents influx of CSF”. If so, why is this is not the case in the controls in whom contrast medium reaches the lamina cribrosa? [2] The authors suggested that the ON sheath compartment in the patients in our study [3] would have confounded the results. As other NTG studies did not look for ON sheath compartmentation, they just might have missed it, even it was present. NTG might be partially due to a compartmentation of the ON sheath.
Concerning table 1, we missed our study [3] on 38 NTG patients which indeed represents the so far largest number of lumbar CSF pressure measurements in NTG patients. We further would recommend adding the well performed study from Linden et al. [4] to the list of “most reliable studies” in which the ICP and IOP simultaneously were measured in different body positions.
We question the role of the lamina cribrosa in the pathophysiology of glaucoma. Mice can develop glaucoma but do not have a lamina cribrosa [5].
References
Baneke AJ, Aubry J, Viswanathan AC, Plant GT. The role of intracranial pressure in glaucoma and therapeutic implications. Eye. 2020;34:178–91.
Pircher A, Montali M, Wostyn P, Pircher J, Berberat J, Remonda L, et al. Impaired cerebrospinal fluid dynamics along the entire optic nerve in normal-tension glaucoma. Acta Ophthalmol. 2018;96:e562–9.
Pircher A, Remonda L, Weinreb RN, Killer HE. Translaminar pressure in Caucasian normal tension glaucoma patients. Acta Ophthalmol. 2017;95:e524–31.
Linden C, Qvarlander S, Johannesson G, Johansson E, Östlund F, Malm J, et al. Normal-tension glaucoma has normal intracranial pressure: a prospective study of intracranial pressure and intraocular pressure in different body positions. Ophthalmology. 2018;125:361–8.
May CA, Lütjen-Drecoll E. Morphology of the murine optic nerve. Investig Ophthalmol Vis Sci. 2002;43:2206–12.
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Pircher, A., Killer, H.E. Comment on: The role of intracranial pressure in glaucoma. Eye 35, 1793 (2021). https://doi.org/10.1038/s41433-020-0975-0
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DOI: https://doi.org/10.1038/s41433-020-0975-0