Asymmetric Papilledema in Idiopathic Intracranial Hypertension: Comment

Letters to the Editor We are in complete agreement with Lertakyamanee et al that clinicians need to be aware that glomus jugulare tumors must not be overlooked as a potential cause of pseudotumor cerebri syndrome with papilledema and potential vision loss. Virna M. Shah, DO Vishma Prabhu, DNB Department of Neuro-Ophthalmology, Aravind Eye Hospital & Postgraduate Institute of Ophthalmology, Coimbatore, India Asymmetric Papilledema in Idiopathic Intracranial Hypertension: Comment W e found the article by Bidot et al (1) and Dr Killer's response letter (2) regarding astronauts very interesting and supportive of the concept that some forms of compartmentation may be involved in the etiology of asymmetric optic disc edema. Bidot et al propose that the narrower optic canal is associated with less disc edema because restricted cerebrospinal fluid (CSF) flow from the brain to the optic nerve (ON) sheath results in lower intraorbital CSF sheath pressure. In this scenario, compartmentation is believed to offer a protective effect. For this theory to hold true, there would have to be a sufficient narrowing and restriction through the optic canal so that the CSF flow into the ON sheath is severely restricted but return flow to the brain is not. This is in contrast to the larger optic canal side where the full force of increased CSF pressure from the brain would presumably be transmitted through the normal sized canal. This theory assumes that the CSF pressure within the orbital ON sheath on the "normal" side is equal to that of the brain CSF. Asymmetry of the optic canal certainly is a possible etiology for our astronauts' findings. Four of 7 long-duration astronauts with optic disc edema have displayed optic disc edema asymmetry. However, astronaut disc edema seems to have some unique findings (3). First, in those astronauts with optic disc edema asymmetry after long-duration space flight, the higher degree of disc edema has always been documented in the right eye. Of 4 astronauts with asymmetric disc edema after long-duration flights, 3 had Frisen Grade 1 right disc edema with a normal left disc as documented by retinal photography. One had highly asymmetric disc edema with Frisen Grade 3, right eye, and Grade 1, left eye. In contrast, Bidot et al found the higher grade disc edema on the right side in only 9 of 20 patients (45%). For the Bidot protective theory to hold true in astronauts, the optic canal would have to be consistently narrower on the left in each of these astronauts. Such a consistent anatomical finding in 4 astronauts would be unlikely. Second, in one previous astronaut case Letters to the Editor: J Neuro-Ophthalmol 2016; 36: 110-114 The authors report no conflicts of interest. REFERENCES 1. Lertakyamanee P, Srinivasan A, DeLott LB, Trobe JD. Papilledema and vision loss caused by jugular paragangliomas. J Neuroophthalmol. [published online ahead of print June 12, 2015]. doi: 10.1097/WNO.0000000000000281. 2. O'Leary MJ, Shelton C, Giddings NA, Kwartler J, Brackmann DE. Glomus tympanicum tumors: a clinical perspective. Laryngoscope. 1991;101:1038-1043. 3. Fayad JN, Keles B, Brackmann DE. Jugular foramen tumors: clinical characteristics and treatment outcomes. Otol Neurotol. 2010;31:299-305. report, a normal opening pressure on lumbar puncture was documented after a mission in the presence of asymmetric disc edema (4). In this same astronaut, we documented unilateral loss of spontaneous venous pulsations in the same eye during space flight that continued to be absent 21 months after return to Earth (5). We also documented, with optical coherence tomography and retinal photography, an astronaut with persistent asymmetric disc edema (right . left) 6 months following his mission in the presence of lumbar puncture opening pressures of 22 cm and 16 cm H2O, performed at one week and one year post mission, respectively (personal communication A.G.L.). These reports suggest that perhaps a unilateral ON sheath compartmentation existed on return to Earth in the presence of intracranial CSF pressures that had returned to normal after the mission. Although optic canal asymmetry could create ON sheath pressure differences in conjunction with elevated CSF pressure, it would not account for continued disc edema asymmetry in the presence of normal postmission opening pressure measurements. We are in agreement with Dr Killer than an examination of optic canal size in astronauts would be very informative and may shed light on the etiology of optic disc edema asymmetry in astronauts. Because of a paucity of objective information, this is currently a very hypothetical area of study. It might be appropriate to measure optic canal size in astronauts who have displayed well-documented disc asymmetry on previous long-duration missions. We suspect that computed tomography scan may be the best technique to measure optic canal size. A comparison of each of these astronaut's canal sizes with their degree of disc edema may provide very useful information. Thomas H. Mader, MD COL(R) US Army, Moab, Utah C. Robert Gibson, OD Coastal Eye Associates, Webster, Texas Stephen F. Hart, MD Life Sciences Division, NASA, Houston, Texas 111 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. 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.