The Optic Canal Size Is Associated With the Severity of Papilledema and Poor Visual Function in Idiopathic Intracranial Hypertension

Vascular risk factors are increasing rapidly in the Middle East. Growing inactivity and obesity have contributed to an epidemic of Type 2 diabetes mellitus (DM) in the Arab population. Microvascular palsies of the third, fourth, and sixth cranial nerves, which occur in an isolated manner, are relatively common in patients with DM, hypertension, or other vascular risk factors.; ; In this retrospective analysis, patients with diabetes with microvascular palsies were assessed for the prevalence of diabetic retinopathy (DR). We compared these data with the prevalence of DR in the general population of diabetics in Saudi Arabia and to a similar published study done in an American population.; ; In total, 126 patients with diabetes were included in the study. The sixth nerve was most frequently involved in 67 patients (53%). Seventy-seven patients (61%) had DR, compared with 49 (39%) without DR. The prevalence of DR in the general population of Saudi patients with diabetes ranged from 30% to 36.1%.; ; Our study demonstrated a higher prevalence of DR in patients with microvascular palsies compared with the general population of patients with diabetes in the Arab population. This is in contrast to a previous study in an American population. Our results might be secondary to differences between the 2 populations, in particular, the continued increase in the prevalence of vascular risk factors (mainly diabetes) and poor control of these risk factors in the Middle East.

Original Contribution The Optic Canal Size Is Associated With the Severity of Papilledema and Poor Visual Function in Idiopathic Intracranial Hypertension Samuel Bidot, MD, Lindsay Clough, BA, Amit M. Saindane, MD, Nancy J. Newman, MD, Valérie Biousse, MD, Beau B. Bruce, MD, PhD Background: To determine whether the size of the bony optic canal is associated with the severity of papilledema and poor visual function in idiopathic intracranial hypertension (IIH). Methods: We performed a retrospective review of definite patients with IIH with requisite brain magnetic resonance imaging allowing for optic canal measurement. Clinical characteristics and automated (Humphrey) visual field results were reviewed; papilledema was graded according to the modified Frisén scale. Cross-sectional area of the optic canals was measured independently by 2 readers and averaged for each canal. Logistic regression modeling was applied. Results: Sixty-nine patients with IIH were included (mean age: 33; 91% women; 65% black). Controlling for age, sex, body mass index, race, and cerebrospinal fluid (CSF) opening pressure, each mm2 increase in canal size was associated with a 0.50 dB reduction in Humphrey visual field mean deviation (P = 0.006); this was likely mediated by the increased odds of Grade 4-5 papilledema or optic atrophy in patients with larger canals (odds ratio: 1.30 [95% CI: 1.10-1.55; P = 0.003] for Grade 4-5 papilledema or atrophy vs grade ,4 papilledema per mm2 increase in canal size). Departments of Ophthalmology (SB, LC, NJN, VB, BBB), Radiology and Imaging Science (AMS), Neurology (NJN, VB, BBB), and Neurological Surgery (NJN), Emory University School of Medicine, Atlanta, Georgia; and Department of Epidemiology (BBB), Rollins School of Public Health and Laney Graduate School, Emory University, Atlanta, Georgia. 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-EY006360 (Department of Ophthalmology). Dr. S. Bidot receives research support from Berthe Fouassier Foundation (Paris, France) and Philippe Foundation (New York, NY). Dr. B. B. Bruce receives research support from the NIH/NEI (K23-EY019341). Dr. N. J. Newman received the Research to Prevent Blindness Lew R. Wasserman Merit Award. The authors report no conflicts of interest. Address correspondence to Beau B. Bruce, MD, PhD, NeuroOphthalmology Unit, Emory Eye Center, The Emory Clinic, 1365-B Clifton Road NE, Atlanta, GA 30322; E-mail: [e-mail] 120 Conclusions: Poor visual function and severe papilledema or optic atrophy were associated with a larger optic canal. Potential mechanisms include alteration of local CSF flow or bony remodeling at the optic canals. Journal of Neuro-Ophthalmology 2016;36:120-125 doi: 10.1097/WNO.0000000000000318 © 2015 by North American Neuro-Ophthalmology Society H igh-grade papilledema is a risk factor for irreversible visual loss in IIH (1), but factors contributing to the severity of papilledema remain unclear. Atrophy is a wellknown mechanism that prevents the optic disc from swelling (1,2), but it does not fully explain the variability of the optic disc response to raised CSF pressure. Other factors, such as the magnitude of the CSF pressure elevation (3-5), the intraocular pressure (6), and structural changes in the lamina cribrosa (7) or the optic nerve sheath (8), have been inconsistently associated with the degree of papilledema, suggesting that additional factors may interfere with the development of papilledema. We recently found using magnetic resonance imaging (MRI) that the largest optic canal was always on the side of the worst papilledema in a series of 8 patients with idiopathic intracranial hypertension (IIH) and very asymmetric papilledema (9). We hypothesized that bony optic canal size might be one of the factors associated with papilledema grade. We acknowledge that computerized tomography (CT) would have been more appropriate for bony optic canal measurement, but CT is not routinely performed in our patients with IIH. To decide whether our observation in patients with IIH and very asymmetric papilledema was worth further pursuit in a prospective study using CT to generalize our results on a larger sample of patients with a more typical presentation of IIH, we conducted this retrospective pilot investigation using MRI. Bidot et al: J Neuro-Ophthalmol 2016; 36: 120-125 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution METHODS Clinical Evaluation Our study was approved by our Institutional Review Board and fulfilled the tenets of the Declaration of Helsinki. Using our patient database, we identified all adult patients ($18 years) with definite IIH according to the modified Dandy criteria (10) evaluated initially at our institution since 2009 when volumetric MRI allowing multiplanar reconstruction was implemented for routine evaluation of patients with presumed intracranial hypertension. Of those, we included patients with brain MRI performed at our institution with the appropriate protocol allowing for optic canal measurement (additional details below). All patients were evaluated in a standardized fashion, including fundus photographs at presentation. All fundus photographs were graded independently using the modified Frisén scale (11) by 1 neuroophthalmologist (SB) and 1 premedical student (LC), who were masked to the patients' demographics and clinical data. A grade of "optic disc atrophy" was added to capture resolving papilledema secondary to optic atrophy. In the case of disagreement, a second neuro-ophthalmologist (BBB) was asked to grade the papilledema. Demographic data, including age, sex, body mass index (BMI), and race, were collected. Symptoms (subjective visual loss, transient visual obscurations, diplopia, tinnitus, headaches), Snellen visual acuity, intraocular pressure, mean deviation (MD) on automated perimetry (Humphrey Field Analyzer II using the SITA-standard 24-2 protocol [Humphrey visual field (HVF)], Carl Zeiss Meditec, Dublin, CA), and cerebrospinal fluid opening pressure (CSF-OP) were recorded at initial presentation. Neuroimaging Evaluation MRI was performed at either 3.0-T (Siemens Trio, Erlangen, Germany) or 1.5-T (Siemens Avanto, Erlangen, Germany or GE Signa, Milwaukee, WI) using a standard head coil. All patients underwent a standardized protocol including 1-mm isotropic volumetric precontrast or postcontrast T1-weighted images. Postcontrast images were preceded by intravenous gadolinium contrast material injection at a standard dose (0.1 mmol/kg Multihance; Bracco Diagnostics Inc., Monroe Township, NJ). After half-day protocol training with an experienced neuroradiologist (AS), all MRIs were reviewed by a neuroophthalmologist (SB) and a premedical student (LC) masked to the neuro-ophthalmic examination. The smallest cross-sectional areas of both right and left optic canals were manually determined and measured by reformatting into a coronal oblique plane orthogonal to the axis of each optic canal using Osirix Imaging Software 5.9 and Osirix Imaging Software MD 3.0 (Pixmeo SARL, Bernex, Switzerland) (Fig. 1). Because the optic canal caliber is generally not Bidot et al: J Neuro-Ophthalmol 2016; 36: 120-125 always regular along its course, each canal was measured independently by each reader on 3 separate occasions and averaged to provide a single measurement. For each patient, the eye with the worst papilledema or, in the case of symmetric papilledema, either the right or the left optic canal was included randomly based on a computer-generated pseudo-random number sequence. Statistical Analyses All statistical analyses were performed with R: A language and environment for statistical computing (R Foundation for Statistical Computing, http://www.R-project.org). Visual acuity was converted to logMAR for analysis. Bland-Altman plot was used to evaluate systematic differences in rater measurement of the optic canal. Intraclass correlation was used to determine interrater agreement. Significance was set at 5%. Linear regression was used to examine the relationship between HVF MD and optic canal size controlling for age, sex, BMI, race, MRI field strength, and CSF-OP as these variables either have or may have associations with HVF MD, optic canal size, or both. In addition, as some of our patients had Goldmann visual fields (GVF) because of poor vision, we conducted an additional sensitivity analysis by imputing a theoretical MD value of 233 dB for patients with GVF. Mediation by papilledema was assessed by including the papilledema grade as dummy variables. Logistic regression was used to examine the relationship between papilledema (Grade 4 or 5 or optic atrophy vs grade ,4) and optic canal size controlling for the same variables as in the linear model. RESULTS Of the 250 adult patients with definite IIH seen over 5 years, 69 had the requisite brain MRI for optic canal measurement. Six were included in our previous report on asymmetric papilledema in IIH, but new measurements, using different software, were performed (the other 2 patients from that series were excluded since they were seen before 2009) (9). There were 63 (91%) women; 64 (93%) were overweight or obese (BMI $ 25) with a median (interquartile range) BMI of 35 (30-41) kg/m2. The most frequent symptom was headache (n = 37, 54%), and 9 (13%) patients were asymptomatic. Although all our patients had definite IIH with documented elevated CSFOP, details regarding the specific CSF-OP values were unavailable in 3 (4%) patients. The lumbar puncture (LP) was performed the same day or after the fundus photographs in the 46 (70%) patients in whom the date of the LP was available (n = 66, 96%). Regarding the ophthalmologic findings, 64 (94%) had active papilledema, and 2 (3%) had optic nerve atrophy in the included eye (Table 1). Brain imaging was performed at 1.5-T in 46 (67%) patients with the remainder performed at 3.0-T; 64 (93%) patients received contrast. The intergrader agreement for 121 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution FIG. 1. Example of cross-sectional area measurement of the right optic canal on magnetic resonance imaging after reconstruction along its sagittal (A), axial (B), and coronal (C) axis. Figure (D) shows the delineation of the optic canal content allowing measurement of the canal (21.0 mm2 in this patient). interocular difference in optic canal measurement was fair to moderate (intraclass correlation: 0.50 [95% CI: 0.30- 0.66]). There was a positive association between optic canal size and HVF MD, and also between optic canal size and the severity of papilledema (Fig. 2). Controlling for age, sex, BMI, race, MRI field strength, and CSF-OP, each mm2 increase in canal size was associated with a 0.50 dB reduction in HVF MD (P = 0.006). When imputing a value of 233 dB for GVFs (n = 5), the magnitude of the association was stronger (20.62 dB/mm2, P = 0.01). In addition, there was an increased odds of Grade 4 or 5 papilledema or optic atrophy in patients with larger canals (odds ratio: 1.30 [95% CI: 1.10-1.55; P = 0.003] vs. grade ,4 papilledema per mm2 increase in canal size). Controlling for Frisén grade, the association between HVF MD and optic canal size became smaller (20.14 dB/mm2, P = 0.37; when imputing GVFs: 20.24 dB/mm2, P = 0.35), whereas Frisén grade was significantly associated with HVF MD (F = 8, df = 6, P , 0.001), suggesting substantial mediation of the effect of canal size on visual loss by the degree of papilledema. When excluding the 6 patients with asymmetric papilledema from our previous report (9), the odds ratio for Grade 4 or 5 papilledema or optic atrophy in patients with larger canals 122 was 1.45 (95% CI: 1.14-1.84; P = 0.003), and the association between optic canal size and visual field remained strong (20.74 dB/mm2, P = 0.0004; when imputing GVFs: 20.89 dB/mm2, P = 0.002). Age, race, duration of symptoms before diagnosis, MRI field strength, and CSF-OP were not significantly associated with optic canal size. DISCUSSION Our results agree with our previous study in patients with IIH and very asymmetric papilledema (9) and show that larger optic canals are associated with more severe papilledema and poor visual function. Vision loss is the main complication leading to permanent disability in IIH, occurring in at least 1 eye in up to 10% of cases (12). Several demographic and clinical factors associated with poor visual prognosis have been identified or suggested (1,13-17), and although the diagnosis of IIH requires the absence of structural changes causing raised intracranial pressure on appropriate brain imaging (10), several common neuroimaging findings have been identified in IIH (18,19). To our knowledge, only 4 studies have systematically addressed the association between visual Bidot et al: J Neuro-Ophthalmol 2016; 36: 120-125 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 1. Characteristics of the 69 patients with IIH included in our study n (%) or median (IQR) Demographics Age, y 33 (27 to 38) Gender, men 6 (9%) Race Black 45 (65%) White 24 (35%) 35 (30 to 41) BMI, kg/m2 Initial symptoms Duration, days (n = 53) 50 (13 to 152) Headache 37 (54%) TVOs 12 (17%) Subjective visual loss 10 (14%) Diplopia 4 (6%) Tinnitus 5 (7%) None 9 (13%) LP (n = 66) CSF-OP, cm H2O 36 (30 to 44) Time after photographs, days 1 (23 to 26) Ophthalmic findings (included eye) Frisén grade 3 (0 to 5) VA, logMAR (n = 68) 0.0 (0.0 to 0.1) IOP, mm Hg (n = 62) 15 (12 to 17) HVF, mean deviation (dB) 23.60 (25.47 to 22.24) (n = 64) Frisén grade 0 3 (4%) 1 12 (17%) 2 21 (30%) 3 20 (29%) 4 8 (13%) 5 3 (4%) Atrophy 2 (3%) BMI, body mass index; CSF-OP, cerebrospinal fluid opening pressure; HVF, Humphrey visual field; IIH, idiopathic intracranial hypertension; IOP, intraocular pressure; IQR, interquartile range; LP, lumbar puncture; TVO, transient visual obscurations; VA, visual acuity. function and these radiologic findings (17,19-21), but none of the findings have consistently emerged as prognostic factors. The potential role of the optic canals in the pathophysiology of IIH recently has emerged (9,22). Only one previous study has considered optic canals (17) as a potential visual risk factor, but it failed to demonstrate any association between their size and visual function. However, the optic canal measurement was only one of 9 factors considered, and only a single diameter was measured. Because the optic canals are not generally perfectly circular, we believed that the cross-sectional area rather than the diameter would be more informative. We found a significant, albeit moderate, association between large optic canals and poor visual prognosis. In addition, we found that consistent measurement required the averaging of multiple independent measurements. Bidot et al: J Neuro-Ophthalmol 2016; 36: 120-125 It is unclear why larger optic canals and the severity of papilledema are associated. It is well known that chronically elevated CSF pressure in IIH has been associated with bony remodeling of the sella turcica, the foramen ovale, and several thin bones at the base of the skull (23-25). We previously found that patients with IIH and very asymmetric papilledema were older compared to those with symmetric papilledema. One might hypothesize that larger optic canals might be an acquired process, by bony remodeling under high CSF pressure (9). However, because CSF normally flows through the optic canals (unlike the foramen ovale or the skull base), it is unclear whether the same hydrodynamic forces that lead to remodeling in other areas of the skull can be extrapolated to the optic canals. We note that spontaneous cephaloceles and CSF leak from the optic canal into the sphenoid sinus has never been reported despite the thinness of the medial wall of the optic canal (26) (0.3 mm), in distinction to the cephaloceles and CSF leaks that arise in other locations where bony remodeling occurs (27). Another hypothesis for the association between larger optic canal and severity of papilledema involves the concept of compartmentation of the perioptic subarachnoid space developed by Killer and Subramanian (22). These authors hypothesize that the perioptic subarachnoid spaces are partially separated from the suprasellar cistern at the level of the optic canal, interfering with the CSF flow exchange between these 2 spaces, thereby reducing CSF turnover around the optic nerves. They suggest that this partial perioptic sequestration of the CSF might result in CSF changes in composition and local prolonged pressures that would contribute to visual loss progression in some patients with IIH despite satisfactory intracranial pressure control. Our study provides data to suggest an alternate mechanism stemming from compartmentation. Pascal's principle states that at a given elevation, in the absence of flow, an enclosed fluid has the same pressure throughout. In fluid dynamics, in the absence of a flow-restricting stenosis, larger tubes lead to lower pressure and, therefore, one might have expected higher perioptic CSF pressure exerting on the wall of smaller optic canals. However, when axial CSF flow is present along the optic nerve, the situation is more complex. For example, a smaller canal could represent a "choke point" resulting in a larger pressure drop than would occur if the canal was larger, which would lead to lower perioptic CSF pressures with smaller canals. Because it is generally assumed that worse papilledema arises from higher perioptic CSF pressure, our data could suggest that smaller optic canals may limit flow into the perioptic CSF compartment, whereas a larger canal facilitates the transmission of the CSF pressure to the lamina cribrosa resulting in worse papilledema. Our results challenge the rationale behind the use of optic canal decompression with preservation of the optic nerve sheath (i.e., without opening the optic nerve sheath when removing the medial wall of the optic canals) recently reported in 123 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution FIG. 2. Box-and-whisker plots depicting the relationship between the grade of papilledema (x axis) and the optic canal size (y axis). The optic canal size is smaller when the optic disc is normal, and increases in case of Grade 5 papilledema or optic disc atrophy. a, atrophy. 10 patients with IIH (28). These authors concluded that this technique was effective, but the results must be interpreted cautiously, as the study was uncontrolled and no formal neuro-ophthalmic examination was completed, with clinical improvement in many patients occurring often months after the procedure. Our study has several limitations, including the relatively small number of patients with high-grade papilledema or optic atrophy, the use of the Frisén scale instead of modern optic nerve head imaging, and more importantly, the use of MRI to assess the optic canal size. We acknowledge that optic nerve head imaging would have provided quantitative data that would have been more objective than the Frisén scale. However, in the setting of optic disc edema, these technologies cannot differentiate loss of fiber from resolving papilledema (4), and their accuracy to measure the retinal nerve fiber layer thickness declines with the severity of papilledema (11). The optical coherence tomography measurement of the macular ganglion cell layer may have helped with this dilemma but was not in widespread clinical use during the period of study. Regarding the use of MRI to assess the optic canal size, systematic measurement of the optic canals has been seldom reported in the literature, and usually only to provide anatomic landmarks on CT to assist with craniofacial surgery (29-31). We acknowledge that high-resolution CT likely would have provided more accurate and reproducible data, but all patients in our retrospective study had MRIs as first-line brain imaging consistent with the criteria for the diagnosis of IIH (10). Given that the cortical bone appears dark on T1-weighted and T2weighted images, we did not directly measure the optic canal; rather, we estimated its size by outlining its contents. We showed a good interreader agreement on MRI, which shows that it provides consistent relative measurements, but 124 its absolute accuracy compared to the CT deserves further investigation. In conclusion, poor visual field function in IIH is associated with a larger optic canal, likely mediated by increased odds of severe papilledema and optic atrophy. The association between larger optic canal and severe papilledema remains unclear. Whether a larger optic canal is only related to bony remodeling or a factor facilitating transmission of CSF pressure to the optic disc, leading to more severe papilledema, will require additional studies. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: S. Bidot, A. M. Saindane, N. J. Newman, V. Biousse, and B. B. Bruce; b. acquisition of data: S. Bidot, L. Clough, A. M. Saindane, N. J. Newman, V. Biousse, and B. B. Bruce; c. analysis and interpretation of data: S. Bidot, L. Clough, A. M. Saindane, N. J. Newman, V. Biousse, and B. B. Bruce. Category 2: a. Drafting the manuscript: S. Bidot, L. Clough, A. M. Saindane, N. J. Newman, V. Biousse, and B. B. Bruce; b. revising it for intellectual content: S. Bidot, L. Clough, A. M. Saindane, N. J. Newman, V. Biousse, and B. B. Bruce. Category 3: a. Final approval of the completed manuscript: S. Bidot, L. Clough, A. M. Saindane, N. J. Newman, V. Biousse, and B. B. Bruce. ACKNOWLEDGMENTS The authors acknowledge Dr. Ross Ethier (Georgia Institute of Technology, Atlanta, GA) with permission for his assistance with the discussion of fluid dynamics. REFERENCES 1. Wall M, White WN. Asymmetric papilledema in idiopathic intracranial hypertension: prospective interocular comparison of sensory visual function. Invest Ophthalmol Vis Sci. 1998;39:134-142. Bidot et al: J Neuro-Ophthalmol 2016; 36: 120-125 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution 2. Hayreh SS. Pathogenesis of oedema of the optic disc (papilloedema). A preliminary report. Br J Ophthalmol. 1964;48:522-543. 3. Pollak L, Zohar E, Glovinsky Y, Huna-Baron R. Reevaluation of presentation and course of idiopathic intracranial hypertension -a large cohort comprehensive study. Acta Neurol Scand. 2013;127:406-412. 4. Rebolleda G, Munoz-Negrete FJ. Follow-up of mild papilledema in idiopathic intracranial hypertension with optical coherence tomography. Invest Ophthalmol Vis Sci. 2009;50:5197-5200. 5. Heckmann JG, Weber M, Jünemann AG, Neundörfer B, Mardin CY. Laser scanning tomography of the optic nerve vs CSF opening pressure in idiopathic intracranial hypertension. Neurology. 2004;62:1221-1223. 6. Brosh K, Strassman I. Unilateral papilledema in pseudotumor cerebri. Semin Ophthalmol. 2013;28:242-243. 7. Lepore FE. Unilateral and highly asymmetric papilledema in pseudotumor cerebri. Neurology. 1992;42:676-678. 8. Moster ML, Slavin M, Wall M. Unilateral disk edema in a young woman. Surv Ophthalmol. 1995;39:409-416. 9. Bidot S, Bruce BB, Saindane AM, Newman NJ, Biousse V. Asymmetric papilledema in idiopathic intracranial hypertension. J Neuroophthalmol. 2015;35:31-36. 10. Friedman DI, Jacobson DM. Diagnostic criteria for idiopathic intracranial hypertension. Neurology. 2002;59:1492-1495. 11. Scott CJ, Kardon RH, Lee AG, Frisén L, Wall M. Diagnosis and grading of papilledema in patients with raised intracranial pressure using optical coherence tomography vs clinical expert assessment using a clinical staging scale. Arch Ophthalmol. 2010;128:705-711. 12. Ball AK, Clarke CE. Idiopathic intracranial hypertension. Lancet Neurol. 2006;5:433-442. 13. Bruce BB, Kedar S, Van Stavern GP, Monaghan D, Acierno MD, Braswell RA, Preechawat P, Corbett JJ, Newman NJ, Biousse V. Idiopathic intracranial hypertension in men. Neurology. 2009;72:304-309. 14. Bruce BB, Preechawat P, Newman NJ, Lynn MJ, Biousse V. Racial differences in idiopathic intracranial hypertension. Neurology. 2008;70:861-867. 15. Szewka AJ, Bruce BB, Newman NJ, Biousse V. Idiopathic intracranial hypertension: relation between obesity and visual outcomes. J Neuroophthalmol. 2013;33:4-8. 16. Wall M, George D. Idiopathic intracranial hypertension. A prospective study of 50 patients. Brain. 1991;114:155-180. 17. Saindane AM, Bruce BB, Riggeal BD, Newman NJ, Biousse V. Association of MRI findings and visual outcome in idiopathic intracranial hypertension. AJR Am J Roentgenol. 2013;201:412-418. 18. Degnan AJ, Levy LM. Pseudotumor cerebri: brief review of clinical syndrome and imaging findings. AJNR Am J Neuroradiol. 2011;32:1986-1993. Bidot et al: J Neuro-Ophthalmol 2016; 36: 120-125 19. Bialer OY, Rueda MP, Bruce BB, Newman NJ, Biousse V, Saindane AM. Meningoceles in idiopathic intracranial hypertension. AJR Am J Roentgenol. 2014;202:608-613. 20. Padhye LV, Van Stavern GP, Sharma A, Viets R, Huecker JB, Gordon MO. Association between visual parameters and neuroimaging features of idiopathic intracranial hypertension. J Neurol Sci. 2013;332:80-85. 21. Riggeal BD, Bruce BB, Saindane AM, Ridha MA, Kelly LP, Newman NJ, Biousse V. Clinical course of idiopathic intracranial hypertension with transverse sinus stenosis. Neurology. 2013;80:289-295. 22. Killer HE, Subramanian PS. Compartmentalized cerebrospinal fluid. Int Ophthalmol Clin. 2014;54:95-102. 23. Butros SR, Goncalves LF, Thompson D, Agarwal A, Lee HK. Imaging features of idiopathic intracranial hypertension, including a new finding: widening of the foramen ovale. Acta Radiol. 2012;53:682-688. 24. Ranganathan S, Lee SH, Checkver A, Sklar E, Lam BL, Danton GH, Alperin NJ. Magnetic resonance imaging finding of empty sella in obesity related idiopathic intracranial hypertension is associated with enlarged sella turcica. Neuroradiology. 2013;55:955-961. 25. Pérez MA, Bialer OY, Bruce BB, Newman NJ, Biousse V. Primary spontaneous cerebrospinal fluid leaks and idiopathic intracranial hypertension. J Neuroophthalmol. 2013;33:330- 337. 26. Chou PI, Sadun AA, Lee H. Vasculature and morphometry of the optic canal and intracanalicular optic nerve. J Neuroophthalmol. 1995;15:186-190. 27. Crovetto M, Whyte J, Rodriguez OM, Lecumberri I, Martinez C, Eléxpuru J. Anatomo-radiological study of the superior semicircular canal dehiscence radiological considerations of superior and posterior semicircular canals. Eur J Radiol. 2010;76:167-172. 28. Sencer A, Akcakaya MO, Basaran B, Yorukoglu AG, Aydoseli A, Aras Y, Sencan F, Satana B, Aslan I, Unal OF, Izgi N, Canbolat A. Unilateral endoscopic optic nerve decompression for idiopathic intracranial hypertension: a series of 10 patients. World Neurosurg. 2014;82:745-750. 29. Hart CK, Theodosopoulos PV, Zimmer LA. Anatomy of the optic canal: a computed tomography study of endoscopic nerve decompression. Ann Otol Rhinol Laryngol. 2009;118:839-844. 30. Liu S, Chen Y, Song J, Tian Y, Xia C, Li Y. Optic canal location by computed tomography. J Craniofac Surg. 2013;24:284-286. 31. Zhihai L, Qixue G, Baohong T, Jingyao L, Zhiyi C. Threedimensional reconstruction of the optic canal-based on multislice helical CT: a comparison analysis with skull dissection of 40 postmortem cases. Anat Rec. 2008;291:1662-1672. 125 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.