What Do We Really Know About Translaminar Pressure?

Letters to the Editor Andrew G. Lee, MD Department of Ophthalmology, The Methodist Hospital, Houston, Texas The authors have no conflict of interest to disclose. REFERENCES 1. Bidot S, Bruce BB, Saindane AM, Newman NJ, Biousse V. Asymmetric papilledema in idiopathic intracranial hypertension. J Neuroophthalmol. 2015;35:31-36. What Do We Really Know About Translaminar Pressure? W e read with great interest the article by McCulley on cerebrospinal fluid (CSF) pressure and glaucoma, especially the part about translaminar pressure (TLP) (1). Although the topic of TLP has gained wide interest, there are-at least to my understanding-some weaknesses in the concept that were not addressed adequately. One concern is that the intracranial pressure (ICP) (which, in fact, is the CSF pressure during lumbar puncture) is mostly based on retrospective studies in nonhomogenous populations with neurological diseases (2). Such patients cannot really be considered to be a control group of normals. Another cohort was taken from a purely non-white population (3). Next to these considerations, there are, however, more serious problems that violate the physical law of pressure. Pressure (p = F/A) is defined as a force over an area. In the published articles on TLP, neither the local force is known nor the area of involved pressure. The force that is used is the pressure measured during lumbar puncture, a site more than 100 cm away from the lamina cribrosa. The claim is that lumbar pressure equals ICP. This is true if the CSF pathways would be a Bernoulli tube, and the CSF was a Newton fluid. The CSF pathway, however, is not necessarily patent, as in an elderly population, the CSF pathway is deformed and compromised by disc herniations. But even if the CSF pressure measured during lumbar pressure represents the ICP, it is purely speculative if the pressure in the subarachnoid space surrounding the optic nerve is of the same value. The only studies that render data of the local CSF pressure in the subrarachnoid space (SAS) of the optic nerve were performed in cadavers and in dogs by Morgan et al (4). Evidence for compartmentation of CSF spaces has been described in the brain (5) and even more so in the subarachnoid space of the optic nerve (6-9). There is histological evidence that the SAS is permeated by trabeculae and septae up to 112 2. Killer HE. Asymmetric papilledema in idiopathic intracranial hypertension- comment. J Neuroophthalmol. 2015;35:330-331. 3. Mader TH, Gibson CR, Pass AF, Kramer LA, Lee AG, Fogarty J, Tarver WJ, Dervay JP, Hamilton DR, Sargsyan A, Phillips JL, Duc Tran, Lipsky W, Choi J, Stern C, Kuyumfian R, Polk JD. Optic disc edema, globe flattening, choroidal folds, and hyperopic shifts observed in astronauts after long-duration space flight. Ophthalmology. 2011;118:2058-2069. 4. Mader TH, Gibson CR, Pass AF, Lee AG, Killer HE, Hansen HC, Dervay JP, Barratt MR, Tarver WJ, Sargsyan AE, Kramer LA, Riascos R, Bedi DG, Pettit DR. Optic disc edema in an astronaut after repeat long-duration space flight. J Neuroophthalmal. 2013;33:249-255. 5. Mader TH, Gibson CR, Lee AG, Patel NB, Hart SF, Pettit DR. Unilateral loss of spontaneous venous pulsations in an astronaut. J Neuroophthalmol. 2015;35:226-227. the lamina cribrosa that subdivides the SAS into a multitude of compartments. Furthermore, the area (A) of CSF filled SAS is not a simple annulus, a circle but a complex multidivided structure of singe elements (10). Intraocular pressure (IOP) and CSF pressure fluctuate in a quasi sinusoidal fashion. These two waves are, however, not synchronized, and we therefore have no correlation between the two amplitudes. Unless one measures the ICP (local behind the lamina cribrosa) and the IOP at the same time and integrating the fragments of SAS spaces into a combined area (A), the data on TLP are more that vague. If the concept of TLP as a possible mechanical insult to the optic nerve in glaucoma will be further developed, more sophisticated methods need to be developed to fulfill the physical requirements for this concept. As Einstein said, everything should be explained as simply as possible, but not any simpler. Ophthalmologists should take care not to violate simple principles of physics to create new concepts. Hanspeter E. Killer, MD Achmed Pircher, MD Department of Ophthalmology Kantonssital Aarau Aarau, Switzerand The authors report no conflicts of interest. REFERENCES 1. McCulley TJ, Chang JR, Piluek WJ. Intracranial pressure and glaucoma. J Neuroophthalmol. 2015;35(suppl 1):38-44. 2. Berdahl JP, Fautsch MP, Stinnett SS, Allingham RR. Intracranial pressure in primary open angle glaucoma, normal tension glaucoma, and ocular hypertension: a case-control study. Invest Ophthalmol Vis Sci. 2008;49:5412-5418. 3. Ren R, Jonas JB, Tian G, Zhen Y, Ma K, Li S, Wang H, Li B, Zhang X, Wang N. Cerebrospinal fluid pressure in glaucoma: a prospective study. Ophthalmology. 2010;117:259-266. 4. Morgan WH, Yu DY, Alder VA, Cringle SJ, Cooper RL, House PH, Constable IJ. The correlation between cerebrospinal fluid pressure and retrolaminar tissue pressure. Invest Ophthalmol Vis Sci. 1998;39:1419-1428. Letters to the Editor: J Neuro-Ophthalmol 2016; 36: 110-114 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Letters to the Editor 5. Mindermann T. Pressure gradients within the central nervous system. J Clin Neurosci. 1999;6:464-466. 6. Killer HE, Mironow A, Flammer J. Optic neuritis with marked distension of the optic nerve sheath due to fluid congestion. Br J Ophthamol. 2003;87:249. 7. Killer HE, Flammer J. Unilateral papilledema in a patient with a fronto-parieto-occipital arachnoid cyst. Am J Ophthalmol. 2001;132:589-591. 8. Killer HE, Jaggi GP, Flammer J, Miller NR, Huber AR, Mironov A. Cerebrospinal fluid dynamics between the intracranial -and the subarachnoid space of the optic nerve. Is it always bidirectional? Brain. 2007;129:1027-1030. 9. Killer HE, Miller NR, Flammer J, Meyer P, Weinreb RN, Remonda L, Jaggi GP. Cerebrospinal fluid dynamics in normal-tension glaucoma. Br J Ophthalmol. 2012;96: 544-548. 10. Killer HE, Laeng HR, Flammer J, Groscurth P. The arachnoid trabeculae and septae in the subarachnoid space of the human optic nerve: Anatomy and clinical considerations. Br J Ophthalmol. 2003;87:777-781. What Do We Really Know About Translaminar Pressure?: Response nized and we, therefore, have no correlation between the two amplitudes" at lumbar and optic nerve regions. It is unlikely that such a resonant fluid pressure anticorrelation would develop based on fluid dynamics. So left to the static relationship between pressures throughout the cavity, it seems reasonable that there would be some correlations. Put another way, in an organ pipe, there are surely anticorrelated pressure fluctuations at the two ends of the pipe. However, if you force 1,000 psi of air into that pipe, both ends will have relatively high pressure: no need to quote Einstein! In conclusion, our understanding of the relationship between intraocular pressure, ICP, and glaucoma is in its infancy. Existing data are far from conclusive but are suggestive that there is validity to the seemingly reasonable hypothesis that ICP as a component of the translaminar pressure gradient impacts the development of glaucoma. Further investigation is needed. W e appreciate the interest in our recent review article and that despite recent efforts, there is much surrounding the relationship between intracranial pressure (ICP) and glaucoma that existing data fail to elucidate (1). It is a valid criticism that some investigations retrospectively used patients who underwent lumbar puncture for a variety of causes. However, one must recognize ethical issues surrounding prospectively performing lumbar punctures on healthy patients in whom such procedures are not otherwise indicated. We should also like to point out that not all published studies were retrospective (2). With regard to the lesson in physics from Killer and Piecher, we agree with the assertion that the pressure in these two widely separated regions (the lumbar spinal column and the optic nerve sheath) is not expected to be identical. This point is worthy of further consideration. A "Newtonian fluid" is basically one in which the pressure forces conduct freely through the system, like in a balloon. In the spinal fluid cavity, there are undoubtedly pressure differences owing to 1) the constrictions in the cavity (where surface effects could play a larger role), 2) the specific properties of spinal fluid, and 3) nonuniform motion of the spinal fluid. Regarding 1) and 2), it would seem that even accounting for these nonlinearities in the fluid or the cavity, there would be some correlations between these pressures. Regarding 3), this is much more complicated. There are indeed cases where there is an anticorrelation in the pressure variations in a Newtonian fluid. For example, in a closed organ pipe (the air supplied from an open end and the other end of the pipe closed), the pressure on one side is high (closed end), whereas the open end is low. But, this is a so-called resonant condition, and it requires a special relationship between the speed of sound and the length and shape of the pipe cavity. Calculating the volume of the cavity from lumbar to optic nerve would be very complicated, and there are probably certain fluid velocity distributions that would give rise to an anticorrelation. But, as Killer points out, the pressure waves of spinal fluid ". . . are not synchro- Letters to the Editor: J Neuro-Ophthalmol 2016; 36: 110-114 Timothy J. McCulley, MD Jessica R. Chang, MD The Wilmer Eye Institute, Johns Hopkins School of Medicine, Baltimore, MD Christopher R. Monroe, PhD Department of Physics, University of Maryland, College Park, MD The authors report no conflicts of interest. REFERENCES 1. McCulley TJ, Chang JR, Piluek WJ. Intracranial pressure and glaucoma. J Neuroophthalmol. 2015;35(suppl 1):S38- S44. 2. Ren R, Jonas JB, Tian G, Zhen Y, Ma K, Li S, Wang H, Li B, Zhang X, Wang N. Cerebrospinal fluid pressure in glaucoma: a prospective study. Ophthalmology. 2010;117:259-266. 113 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.