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Show cessation of the visual disturbances. The symptoms experi-enced by our patients expand the spectrum of visual complaints experienced by patients taking topiramate. Vincenzo Belcastro, MD, PhD Neurology Unit, Department of Medicine, S. Anna Hospital, Como, Italy Umberto Aguglia Department of Medical and Surgical Sciences, Magna Graecia University of Catanzaro, Catanzaro, Italy Regional Epilepsy Center, Bianchi-Melacrino-Morelli Hospital, Reggio Calabria, Italy Laura R. Pisani, MD IRCCS, Centro Neurolesi "Bonino-Pulejo," Messina, Italy Edoardo Ferlazzo Department of Medical and Surgical Sciences, Magna Graecia University of Catanzaro, Catanzaro, Italy Regional Epilepsy Center, Bianchi-Melacrino-Morelli Hospital, Reggio Calabria, Italy The authors report no conflicts of interest. REFERENCES 1. Yun SH, Lavin PJ, Schatz MP, Lesser RL. Topiramate-induced palinopsia: a case series and review of the literature. J Neuroophthalmol. 2015;35:148-151. 2. Belcastro V, Cupini LM, Corbelli I, Pieroni A, D'Amore C, Caproni S, Gorgone G, Ferlazzo E, Di Palma F, Sarchielli P, Calabresi P. Palinopsia in patients with migraine: a case-control study. Cephalalgia. 2011;31:999-1004. 3. Crespel A, Gelisse P, Reed RC, Ferlazzo E, Jerney J, Schmitz B, Genton P. Management of juvenile myoclonic epilepsy. Epilepsy Behav. 2013;28(suppl 1):S81-S86. Asymmetric Papilledema in Idiopathic Intracranial Hypertension: Comment We would like to congratulate Bidot et al (1) for their article on asymmetric papilledema. Their study is the first to demonstrate a morphological difference in the diameter of the optic canals in patients with asymmetric papilledema. The optic canal consists of 2 components: bone and meningothelial cells (2). Although bone is rigid, the meningothelial cells of the pia-arachnoid react to a variety of biological and mechanical stimuli (3,4). For example, increased intracranial pressure (ICP) causes proliferation of the number of meningothelial cells as well as an in-crease in their size (4). This, in turn, can result in thick-ening of the meningothelial cell layer, leading to narrowing of the subarachnoid space (SAS) surrounding the optic nerve and, eventually, to optic nerve compart-mentation, perhaps protecting the optic nerve from the effects of increased ICP. This process has been demon-strated in an animal model (5) as well as in patients with papilledema who have undergone computed tomographic cisternography before and after intrathecal (spinal) injec-tion of iodinated contrast material (6,7). In these patients, there is a decreased gradient of contrast between the lum-bar SAS and the SAS surrounding the optic nerve (7). It would be interesting to see whether the Frisén grade of papilledema correlates with the contrast gradient. A fur-ther interesting aspect of the work by Bidot et al is that the visual field in the eye with the larger optic canal was more affected, although visual acuity was the same in both eyes. This finding also suggests that compartmentation might offer at least a temporary protective effect on the optic nerve; however, the effect of chronic compartmentation on cerebro-spinal fluid circulation needs to be studied further. In addition to patients with increased ICP and papil-ledema, it might be worthwhile assessing the diameters of the optic canals in astronauts in whom optic disc swelling has developed during prolonged spaceflight (8) and com-paring them with the optic canals of astronauts who never developed optic disc swelling. If the size of the optic canal is a major determinant of whether or not an individual devel-ops optic disc swelling from increased ICP or another cause, one would expect that astronauts in whom disc swelling has been observed should have larger canals than those in whom optic disc swelling has not developed. In the meantime, we agree with Bidot et al that asymmetry of the diameter of the bony optic canal may produce a compartmentation phenomenon that protects the optic nerve from the effects of increased ICP and would add that it is possible that an increase in the thickness of meningothelial cell layer caused by a reaction to increased ICP may play a role as well, both in this setting and possibly in other optic nerve disorders (9). Hanspeter E. Killer, MD Kantonsspital Aarau, Aarau, Switzerland The author reports no conflicts of interest. 330 Letters to the Editor: J Neuro-Ophthalmol 2015; 35: 329-332 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. REFERENCES 1. Bidot S, Bruce BB, Saindane AM, Newman NJ, Biousse V. Asymmetric papilledema in idiopathic intracranial hypertension. J Neuroophthalmol. 2015;35:31-36. 2. Killer HE, Laeng HR, Flammer P, 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. 3. Fan B, Bordigari G, Flammer J, Killer HE, Meyer P, Neutzner A. Meningothelial cells participate in immunological processes in the cerebrospinal fluid. J Neuroimmunol. 2012;244:45-50. 4. Xin X, Fan B, Flammer J, Miller NR, Jaggi GP, Killer HE, Meyer P, Neutzner A. Meningothelial cells react to elevated pressure and oxidative stress. PLoS One. 2011;6:e20142. 5. Jaggi G, Harlev M, Zeigler U, Dothan S, Miller NR, Killer HE. Cerebrospinal fluid segregation optic neuropathy: an experimental animal model. Br J Ophthalmol. 2010;94:1088-1093. 6. 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. 7. Killer HE, Jaggi GP, Miller NR, Huber AR, Londolt H, Mironov A, Meyer P, Remonda L. Cerebrospinal fluid dynamics between the basal cisterns and the subarachnoid space of the optic nerve in patients with papilloedema. Br J Ophthalmol. 2010;95:822-827. 8. Mader TH, Gibson CR, Pass AF, Lee AG, Killer HE, Hansen HC, Devray 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 Neuroophthalmol. 2013;33:249-255. 9. Killer HE, Miller NR, Flammer J, Meyer P, Weinreb RN, Remonder A, Jaggi BP. Cerebrospinal fluid exchange in normal-tension glaucoma. Br J Ophthalmol. 2012;96:544-548. Asymmetric Papilledema in Idiopathic Intracranial Hypertension: Response We thank Killer et al for their comments on our article (1) and for sharing their expertise on the emerging concept of compartmentation of the perioptic subarachnoid spaces (2). We believe that compartmen-tation of the perioptic subarachnoid spaces probably plays an important role in the development of papillede-ma by interfering with the transmission of the cerebro-spinal fluid (CSF) pressure between the intracranial subarachnoid spaces and the lamina cribrosa. Our results may provide a new insight into the underlying mechanisms and the potential consequences of the compartmentation in idio-pathic intracranial hypertension (IIH), by protecting the optic disc from increased CSF pressure. This is likely not specific to IIH, and we agree with Killer et al that the optic canals might also play a role in other ocular conditions in which a disorder of the CSF pressure has been suggested, such as optic disc edema after prolonged spaceflight (3), or in glaucoma. Samuel Bidot, MD Department of Ophthalmology, Emory University School of Medicine, Atlanta, GA Beau B. Bruce, MD, PhD Departments of Ophthalmology and Neurology, Emory University School of Medicine, Atlanta, GA Department of Epidemiology, Rollins School of Public Health and Laney Graduate School, Atlanta, GA Amit M. Saindane, MD Department of Radiology and Imaging Science, Emory University School of Medicine, Atlanta, GA Nancy J. Newman, MD Departments of Ophthalmology, Neurology, and Neurological Surgery, Emory University School of Medicine, Atlanta, GA Valérie Biousse, MD Departments of Ophthalmology and Neurology, Emory University School of Medicine, Atlanta, GA Supported in part by an unrestricted departmental grant (Department of Ophthalmology) from Research to Prevent Blindness, Inc, New York, and by NIH/NEI core grant P30- EY06360 (Department of Ophthalmology). S. Bidot receives research support from Berthe Fouassier Foundation (Paris, France) and the Philippe Foundation (New York, New York). B. B. Bruce receives research support from the NIH/ NEI (K23-EY019341). N. J. Newman received the Research to Prevent Blindness Lew R. Wasserman Merit Award. The authors report no conflicts of interest. REFERENCES 1. Bidot S, Bruce BB, Saindane AM, Newman NJ, Biousse V. Asymmetric papilledema in idiopathic intracranial hypertension. J Neuroophthalmol. 2015;35:31-36. 2. Killer HE, Subramanian PS. Compartmentalized cerebrospinal fluid. Intl Ophthalmol Clin. 2014;54:95-102. 3. Mader TH, Gibson CR, Pass AF, Lee AG, Killer HE, Hansen HC, Devray 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 Neuroophthalmol. 2013;33:249-255. Letters to the Editor: J Neuro-Ophthalmol 2015; 35: 329-332 331 Letters to the Editor Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |