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Show Literature Commentary NORDIC Idiopathic Intracranial Hypertension Study Group Writing Committee, Wall M, McDermott MP, Kieburtz KD, Corbett JJ, Feldon SE, Friedman DI, Katz DM, Keltner JL, Schron EB, Kupersmith MJ. Effect of acetazolamide on visual function in patients with idiopathic intracranial hypertension and mild visual loss: the idiopathic intracranial hypertension treatment trial. JAMA. 2014;311:1641-1651. Importance: Acetazolamide is commonly used to treat idiopathic intracranial hypertension (IIH), but there is insuffi-cient information to establish an evidence base for its use. Objective: To determine whether acetazolamide is benefi-cial in improving vision when added to a low-sodium weight-reduction diet in patients with IIH and mild visual loss. Design, Setting, and Participants: A multicenter, random-ized, double-masked, placebo-controlled study of acetazol-amide in 165 participants with IIH and mild visual loss who received a low-sodium weight-reduction diet. Participants were enrolled at 38 academic and private practice sites in North America from March 2010 to November 2012 and followed up for 6 months (last visit in June 2013). All participants met the modified Dandy criteria for IIH and had a perimetric mean deviation (PMD) between 22 and 27 dB. The mean age was 29 years, and all but 4 participants were women. Interventions: Low-sodium weight-reduction diet plus the maximally tolerated dosage of acetazolamide (up to 4 g/d) or matching placebo for 6 months. Main Outcomes and Measures: The planned primary out-come variable was the change in PMD from baseline to Month 6 in the most affected eye, as measured using a Humphrey field analyzer. PMD is a measure of global visual field loss (mean deviation from age-corrected normal values), with a range of 2 to 232 dB; larger negative values indicate greater vision loss. Secondary outcome variables included changes in papilledema grade, quality of life (Visual Function Questionnaire 25 [VFQ-25] and 36-Item Short Form Health Survey), headache disability, and weight at Month 6. Results: The mean improvement in PMD was greater with acetazolamide (1.43 dB, from 23.53 at baseline to 22.10 dB at Month 6; n = 86) than with placebo (0.71 dB, from 23.53 to 22.82 dB; n = 79); the difference was 0.71 dB (95% confidence interval [CI]: 0-1.43 dB; P = 0.050). Mean im-provements in papilledema grade (acetazolamide: 21.31, from 2.76 to 1.45; placebo: 20.61, from 2.76 to 2.15; treat-ment effect: 20.70; 95% CI: 20.99 to 20.41; P , 0.001) and vision-related quality of life as measured by the National Eye Institute VFQ-25 (acetazolamide: 8.33, from 82.97 to 91.30; placebo: 1.98, from 82.97 to 84.95; treatment effect: 6.35; 95% CI: 2.22-10.47; P = 0.003) and its 10-item neuro-ophthalmic supplement (acetazolamide: 9.82, from 75.45 to 85.27; placebo: 1.59, from 75.45 to 77.04; treatment effect: 8.23; 95% CI: 3.89-12.56; P , 0.001) were also observed with acetazolamide. Participants as-signed to acetazolamide also experienced a reduction in weight (acetazolamide: 27.50 kg, from 107.72 to 100.22 kg; placebo: 23.45 kg, from 107.72 to 104.27 kg; treatment effect: 24.05 kg; 95% CI: 26.27 to 21.83 kg; P , 0.001). Conclusions and Relevance: In patients with IIH and mild visual loss, the use of acetazolamide with a low-sodium weight-reduction diet compared with a diet alone resulted in modest improvement in visual field function. The clinical importance of this improvement remains to be determined. Acetazolamide has been the "standard of care" for treatment of mild visual loss in patients with idiopathic intracranial hypertension (IIH) for years. However, we now have evi-dence from this multicenter, double-masked, randomized, controlled clinical trial that acetazolamide provides modest improvement in visual function as measured by perimetric mean deviation. There was also an improvement in the grade of papilledema and quality of life measures. There are numerous limitations to this study, some nicely outlined in the accompanying editorial by Horton (1). First, those enrolled most often had only mild visual loss, limiting the ability to show benefit. This was necessary because those with more severe visual loss who are more likely to benefit would not be eligible for a placebo arm of the study. Indeed, those with more severe papilledema had more benefit than those with milder papilledema. Addition-ally, a weight-loss program was included, and those on acetazolamide lost more weight than those on placebo. The NORDIC IIHTT is likely the most important multicenter clinical trial in neuro-ophthalmology since the ONTT, helping to move our field forward from one of the describing phenomenology on individual experiences to an evidence-based subspecialty. Although it helps put us "on the map," we need more studies to overcome headlines like this from the May 9, 2014 issue of ASCRS EyeWorld Weekly Update as it reported on the IIHTT: "Glaucoma drug improves vision in women with IIH." Someday we hope to see "Neuro-Ophthalmology drug improves vision in patients with glaucoma." -Mark L. Moster, MD Six subjects on acetazolamide were hospitalized for kidney stones, elevated liver function, pancreatitis, and diverticulitis. There was 1 subject with an allergic reaction and 1 with hypokalemia. We are not told what dose of acetazolamide they 306 Moster and Lee: J Neuro-Ophthalmol 2014; 34: 306-310 Literature Commentary Section Editors: Mark L. Moster, MD Michael S. Lee, MD Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. were on. The treatment paradigm for the IIHTT called for increasing the Diamox as tolerated up to 4 g/d. I do not know that I can fully recommend that strategy. However, in this study, the mean maximal dose was 2.5 g/d, and the IIHTT suggests that this dose is relatively safe, so there may be a significant "wiggle room" to move up from the standard 1 g/d that many folks use. I have seen less than 1% of my patients develop kidney stones on an average of 1 g/d and none have developed pancreatitis or elevated liver function tests. This may be a dose-related issue. -Michael S. Lee, MD REFERENCE 1. Horton JC. Acetazolamide for pseudotumor cerebri. Evidence from the NORDIC trial. JAMA. 2014;311:1618-1619. Shams PN, Ma R, Pickles T, Rootman J, Dolman PJ. Reduced risk of compressive optic neuropathy using orbital radiotherapy in patients with active thyroid eye disease. Am J Ophthalmol. 2014;157:1299-1305. Purpose: To compare the risk of developing compressive optic neuropathy in patients with active thyroid eye disease (TED) treated with corticosteroids with or without orbital radiotherapy. Design: A retrospective single-center case-control study. Methods: The clinical charts of 351 patients with active TED who received corticosteroids with or without orbital radiother-apy between 1999 and 2010 were reviewed. Patients with compressive optic neuropathy at the time of presentation were excluded. Group 1 received corticosteroids only and Group 2 received corticosteroids and orbital radiotherapy. The primary outcome measure was the development of compressive optic neuropathy. Secondary outcome meas-ures were changes in other parameters indicating the activity or severity of TED including soft tissue inflammation, diplopia, ocular motility restriction, and appearance. Results: There were 144 cases in Group 1 and 105 in Group 2. Both groups were matched for age, gender, and stability of thyroid function. The 2 groups differed only in the modality of treatment for active TED. The main indication for treatment in both groups was soft tissue inflammation. Corticosteroids were initiated at an average of 2.6 months in Group 1 and 2.5 months in Group 2 after symptom onset. Group 2 received orbital radiotherapy on an average of 4.2 months after the initiation of corticosteroid therapy, and 8% of the cases were intolerant to corticosteroids. At an average of 3.2-year follow-up, compressive optic neuropa-thy had developed in 17% (n = 25) of Group 1 and 0% of Group 2 (P , 0.0001), on average 5.5 months after the initiation of corticosteroid therapy. Although both groups experienced a significant reduction in periocular inflamma-tion, the radiotherapy-treated group demonstrated a signifi-cantly greater improvement in ocular motility. Conclusions: The rate of compressive optic neuropathy was significantly lower and improvement in ocular motility greater in patients receiving orbital radiotherapy in addition to cortico-steroids. Patients with active TED seem to have an effective and sustained response to orbital radiotherapy combined with corticosteroids, which is protective against disease progres-sion and the development of compressive optic neuropathy. In this retrospective study, patients with active thyroid eye disease (TED), defined as a score of .4 on the VISA clas-sification, were offered 50 mg of oral prednisone. If the response was positive, then the patient was given 250- 500 mg IV Solu-Medrol weekly and tapered slowly. Inves-tigators offered fractionated, orbital external beam radiation therapy (XRT) to patients with any of the following char-acteristics: 1) double vision, 2) ophthalmoplegia, or 3) poorly responsive to, intolerant of, or dependent on cortico-steroids. Both groups began steroids approximately 2.5 months after presentation, and the XRT group received radiation at an average of 6.7 months after presentation. Interestingly, compressive optic neuropathy did not develop in the XRT group but occurred in 17% of the steroid-only group at an average of 8.1 months after presentation. This study continues to add to the debate on the efficacy of orbital XRT in active TED. There were reasonable number of patients in each group, and both groups had similar doses of corticosteroids making XRT the main difference in treatment. The biggest limitation here is the selection bias-not all patients were given the option of orbital XRT. However, I like that patients received orbital XRT relatively early into the course of their disease. Overall, I have not been a big fan of orbital XRT for TED. I use it, but not that often. This article raises my interest level in considering it. -Michael S. Lee, MD Michael, I agree that the main limitation may be the selection bias you have noted. Another confounding issue is that 48% of those with compressive optic neuropathy were on disease-modulating agents besides corticosteroids. The patients who received these agents were those with aggressive disease who for various reasons were not given XRT, including systemic vascular disease. It is possible that they are at a higher risk of developing compressive optic neuropathy. XRT did show benefit on subjective diplopia and objective ocular motility measurements in these patients. With the above limitations noted, it is likely that XRT also may protect some from developing compressive optic neuropathy. -Mark L. Moster, MD Lyrer PA, Brandt T, Metso TM, Metso AJ, Kloss M, Debette S, Leys D, Caso V, Pezzini A, Bonati LH, Thijs V, Bersano A, Touzé E, Gensicke H, Martin JJ, Lichy C, Tatlisumak T, Engelter ST, Grond-Ginsbach C; Cervical Artery Dissection and Ischemic Stroke Patients (CADISP) Study Group. Clinical import of Horner syndrome in internal carotid and vertebral artery dissection. Neurology. 2014;82:1653-1659. Moster and Lee: J Neuro-Ophthalmol 2014; 34: 306-310 307 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Objective: To study the prognostic importance of Horner syndrome (HS) in patients with internal carotid artery dissection (ICAD) or vertebral artery dissection (VAD). Methods: In this observational study, characteristics and outcome of patients with ICAD or VAD from the CADISP (Cervical Artery Dissection and Ischemic Stroke Patients) database were analyzed. The presence of HS was system-atically assessed using a standardized questionnaire. Patients with HS (HS+) were compared with HS2 patients. Crude odds ratios (ORs) with 95% confidence intervals and ORs adjusted for age, sex, center, arterial occlusion, bilat-eral dissection, stroke severity, and type of antithrombotic treatment were calculated. Results: We analyzed 765 patients (n = 496 with ICAD, n = 269 with VAD, n = 303 prospective, n = 462 retrospective). HS was present in 191 (38.5%) of the patients with ICAD and 36 (13.4%) of the patients with VAD (P , 0.001). HS+ ICAD patients presented less often with stroke or TIA (P , 0.001), less often had bilateral (P = 0.019) or occlusive (P = 0.001) dissections, and had fewer severe strokes (P = 0.041) than HS2 ICAD patients. HS+ ICAD patients had a better functional 3-month outcome than those without HS (ORcrude = 4.0 [2.4-6.7]) and also after adjustment for outcome-relevant covariates (ORadjusted = 2.0 [1.1- 4.0]). HS+ ICAD patients were less likely to have new strokes than HS2 ICAD patients (P = 0.039). HS+ VAD patients more often had vessel occlusion (P = 0.014) than HS2 patients but did not differ in any of the other afore-mentioned variables. Conclusions: In patients with ICAD, HS is an easily assess-able marker that might indicate a more benign clinical course. HS had no prognostic meaning in patients with VAD. In clinical practice, we often see isolated Horner syndrome (HS) as the presentation of an internal carotid artery dissection (ICAD). In the past, almost all of these patients were treated with anticoagulation, but there has been a move toward antiplatelet agents in the stroke community even in acute cases and, with either treatment, patients have done relatively well. This study looked at the prognosis of the presence or absence of HS (not necessarily isolated), and the main finding was that there were fewer strokes and less severe strokes if HS was present. The authors postulate that an HS presentation may represent a more benign tear in the outer wall of the internal carotid artery, compared with those that are closer to the inner wall that spare the sympathetic fibers. The findings are consistent with prior reports of a less-frequent stroke risk with HS than other presentations. Nonetheless, the stroke risk is still high, and it is hard to predict who is at risk and we still have to figure out the optimal treatment. Not surprisingly, in vertebral artery dissection, the presence of a HS made little difference because in those cases the Horner syndrome is a manifestation of the brain stem infarct, rather than related to any fibers in the vertebral artery. -Mark L. Moster, MD About 85% of the ICAD without HS and 37% of the ICAD with HS had a stroke or transient ischemic attack (TIA) at baseline. We know that patients with stroke or TIA are more likely to experience another stroke. In this study, after adjusting for age, gender, medical facility, vessel occlusion, bilateral ICAD, and anticoagulation, HS2 patients were more likely to have a stroke in the following 3 months. However, they did not adjust for stroke/TIA at baseline. I wonder if they had performed this, whether it would have changed the "pro-tective effect" of HS. Did the greater likelihood of stroke among those who did not have HS occur because they had more strokes at baseline rather than the HS itself? -Michael S. Lee, MD Yang D, Fu J, Hou R, Liu K, Jonas JB, Wang H, Chen WW, Li Z, Sang J, Zhang Z, Liu S, Cao Y, Xie X, Ren R, Lu Q, Weinreb RN, Wang N. Optic neuropathy induced by experimentally reduced cerebrospinal fluid pressure in monkeys. Invest Ophthalmol Vis Sci. 2014;55:3067-3073. Purpose: To examine the influence of experimentally reduced cerebrospinal fluid pressure on retinal nerve fiber layer (RNFL) thickness and neuroretinal rim area of the optic nerve head. Methods: The experimental study included 9 monkeys that underwent an implantation of a lumbar-peritoneal cerebrospi-nal fluid (CSF) shunt. In the study group (n = 4 monkeys), the shunt was opened to achieve a CSF of approximately 40 mm H2O, whereas the shunt remained closed in the control group (n = 5 monkeys). At baseline and in monthly intervals thereaf-ter, optical coherence tomographic and photographic images of the optic nerve head and RNFL were taken of all monkeys. Results: Two of the 4 monkeys of the study group showed bilaterally a progressive reduction in RNFL thickness between 12% and 30%, reduction in neuroretinal rim area and volume, and an increase in cup/disc area ratios. A third monkey developed a splinter-like disc hemorrhage in 1 eye. The fourth monkey of the study group did not develop morphologic changes during follow-up, nor did any monkey of the control group. Conclusions: Experimental and chronic reduction in CSF in monkeys was associated with the development of an optic neuropathy in some monkeys. In this experimental animal study, the investigators im-planted a programmable lumboperitoneal shunt into 9 rhesus monkeys. The valve was not opened in 5 control monkeys, and the valve was set to achieve a cerebrospinal fluid pressure (CSFP) of 4 cm H2O in 4 monkeys. The CSFP, measured intraoperatively and postoperatively, declined in the study animals from 7.4 mm Hg (10 cm H2O) at baseline to less than 2 mm Hg (2.7 cm H2O) for the study. The CSFP did not change significantly in the control animals. The following parameters were assessed at baseline and monthly for 1 year: retinal nerve fiber layer (RNFL) thickness, optic nerve head area, neuroretinal rim area, and cup-to-disc ratio. At 1-year follow-up, 2 monkeys showed progressive thinning of the mean RNFL of 20-30 mm. 308 Moster and Lee: J Neuro-Ophthalmol 2014; 34: 306-310 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. The area of the neuroretinal rim significantly decreased and the cup-to-disc ratio significantly increased. The other 2 study animals and the control animals had no appreciable changes in the study parameters, but 1 low-pressure monkey had a disc hemorrhage. The intraocular pressure did not change over the study period in either group, and no morphologic changes of the lamina cribrosa were observed. This has implications for patients with glaucoma or with low CSFP. Ren et al (1) found a significantly lower CSFP among patients with low-tension glaucoma compared with controls. There have been 2 reports of optic neuropathy associated with spontaneous intracranial hypotension (2,3). I have observed patients with idiopathic intracranial hypertension progressively lose vision after receiving a shunt. I have thought of the visual loss occurring despite maxi-mally lowering the CSFP, but perhaps a component may be because the CSFP was maximally lowered. -Michael S. Lee, MD There is a small growing literature supporting the importance of trans-lamina cribrosa pressure (intraocular pressure 2 intracranial pressure [ICP]) in the pathogenesis and prognosis of glaucoma. However, the studies in humans are limited by the measurement of ICP at 1 point in time, during a lumbar puncture. Animal studies like this one will help clarify the true importance of translaminar pressure differences in patients with both glaucoma and papilledema. -Mark L. Moster, MD REFERENCES 1. 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. 2. Horton JC, Fishman RA. Neurovisual findings in the syndrome of spontaneous intracranial hypotension from dural cerebrospinal fluid leak. Ophthalmology. 1994;101:244-251. 3. Goksel BK, Yildirim T, Sizmaz S, Reyhan M, Karatas M. Optic neuropathy associated with spontaneous intracranial hypotension. Acta Neurol Belg. 2012;112:361-365. Strapazzon G, Brugger H, Dal Cappello T, Procter E, Hofer G, Lochner P. Factors associated with optic nerve sheath diameter during exposure to hypobaric hypoxia. Neurology. 2014;82:1-5. Objective: To monitor the changes in optic nerve sheath diameter (ONSD) induced by acute exposure to hypobaric hypoxia and to investigate the factors associated with these changes, including the development of acute mountain sickness (AMS). Methods: In this cohort study, neurologic signs and symptoms, cardiovascular parameters, and ultrasonography of ONSD were prospectively assessed in 19 healthy low-landers at baseline and after ascent to 3,830 m (3 hr, 9 hr, 24 hr, 48 hr, 72 hr, and 8 d) by blinded investigators. Potential confounding factors (e.g., altitude variations and physical effort) were minimized. A multivariate analysis of factors associated with ONSD was performed by means of generalized estimating equations. Results: ONSD increased with exposure to altitude in all participants (P , 0.001). The increase between 9 and 24 hours was larger in patients who developed AMS (P = 0.001). There was no influence of sex, oxygen saturation, or acclimatization on ONSD. Conclusions: Both physiologic and pathologic responses to hypobaric hypoxia were independently associated with changes in ONSD. Studies on a larger cohort, at a range of altitudes, and with baseline neuroimaging techniques are necessary to further understand the clinical significance of increased ONSD during exposure to hypobaric hypoxia. This small study demonstrated an increase in optic nerve sheath diameter (ONSD) within 3 hours of reaching 3,830-m altitude by helicopter with further increase at 24 hours and a parabolic pattern, decreasing a little at 72 hours and then stable until 8 days. The 3 patients who developed acute mountain sickness (AMS) had a greater increase in ONSD between 9 and 24 hours than those without AMS. If these findings hold up in larger studies, then orbital ultrasound may be used clinically to predict AMS presymptomatically with possible earlier intervention. This article is another example where examination of the eye provides insights into neurologic disease. -Mark L. Moster, MD Obviously, the change in ONSD is the greatest concern here, but the differences in technique and results of the ultrasound are worth noting. In this study, the authors describe placing the probe on the temporal part of the closed upper eyelid. The mean baseline ONSD was 5.45 mm when measured 3 mm behind the globe. Others have reported that the upper limit of normal is 3 mm and that patients with papilledema are more apt to have ONSD greater than 3.3 mm (1). This likely has to do with probe placement and angle of imaging. -Michael S. Lee, MD REFERENCE 1. Neudorfer M, Ben-Haim MS, Leibovitch I, Kesler A. The efficacy of optic nerve ultrasonography for differentiating papilloedema from pseudopapilloedema in eyes with swollen optic discs. Acta Ophthalmol. 2013;91:376-380. Moss HE, Gao W, Balcer LJ, Joslin CE. Association of race/ethnicity with visual outcomes following acute optic neuritis: an analysis of the optic neuritis treatment trial. JAMA Ophthalmol. 2014;132:421-427. Importance: Retrospective studies have demonstrated disparate outcomes after acute optic neuritis in individuals of African descent compared with individuals of white race/ ethnicity. However, published analyses of the prospectively Moster and Lee: J Neuro-Ophthalmol 2014; 34: 306-310 309 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. collected Optic Neuritis Treatment Trial (ONTT) data identi-fied no association between worse visual outcomes and black race/ethnicity. Objectives: To investigate the associations of age, sex, and race/ethnicity with visual outcomes after acute optic neuritis through application of longitudinal data analysis techniques to the ONTT data set. Design: Secondary analysis of the ONTT (a prospective randomized controlled trial) data set. Our models included effects of treatment (placebo, oral prednisone, or intrave-nous methylprednisolone), time, and treatment · time interaction, as well as demographic covariates of age, sex, and race/ethnicity. Setting and Participants: The ONTT data were collected at multiple centers in the United States. Patients of black (n = 58) and white (n = 388) race/ethnicity with acute optic neuritis who enrolled in the ONTT within 8 days of symptom onset were included in the analyses. Main Outcomes and Measures: The contrast sensitivity (CS) and visual acuity (logMAR) in the affected eye were modeled using 2-stage mixed-effects regression techni-ques. All available follow-up data from baseline to 15 to 18 years were included. Results: The data identified no relationship of age, sex, or treatment with CS or visual acuity outcomes. Race/ethnicity was significantly related to CS (P , 0.001) and visual acu-ity (P , 0.001) for a 15-year period after acute optic neu-ritis, with black race/ethnicity being associated with worse scores for both. Conclusions and Relevance: Race/ethnicity seems to be associated with CS and visual acuity outcomes in affected eyes after acute optic neuritis. To our knowledge, this is the largest cohort of black race/ethnicity with acute optic neuritis to be studied and represents the first evidence from a prospectively collected data set to support a hypoth-esis of race-/ethnicity-dependent visual outcomes of acute optic neuritis. The authors downloaded the publically available data set from the Optic Neuritis Treatment Trial (ONTT) to assess visual outcomes based on race. The original ONTT publications compared cross-sectional visual outcomes at each follow-up visit and found no racial differences in outcomes. Moss et al used longitudinal data analyses, which better model changes in individual outcomes and differences between groups. These analyses also are less affected by missing data points. The authors found that black race/ ethnicity was significantly associated with poorer visual acuity and contrast sensitivity (CS) at baseline and all time points for the 15-year follow-up. These data comport with other studies that have shown worse outcomes for patients of black race/ethnicity. The reasons for these findings are unclear and may be biologic, socioeconomic, or due to other factors. I find it fascinating that newer statistical models can uncover significantly different observations from original publications, and it makes me wonder what other large studies could have different findings based on reanalysis of the data. It is great that these data are publically available. I went to the following Web site and downloaded the ONTT data for myself: http://lons.jaeb.org. It comes as a zip file with multiple data tables. I have not taken a look at the data yet, but who knows what one might find? -Michael S. Lee, MD This reevaluation of ONTT data found poorer visual acuity (VA) and CS at all times in the black patients. The authors claim "the magnitude of the effect is within the range of significant changes based on the variability of the Pelli- Robson test and is clinically significant because of correla-tions between CS and vision-associated quality of life." How-ever, if one looks at the graphs of the recovery in blacks and whites, the visual outcome is very similar for both, and the logMAR VA is very close to 0.0 even in the black population. An additional concern that was raised by the authors is that the ONTT data were analyzed before our current neuro-myelitis optica (NMO) diagnostic criteria. Indeed, NMO, with its much poorer recovery in even a few patients could shift the recovery curve to the degree reported in this study. The authors quote 2 other studies, showing poorer outcome in patients of African descent. These were also before our current understanding of NMO and one of the studies (1) is clearly describing a different population of pa-tients. This retrospective study of 10 patients in South Africa included 8 of the 10 cases with bilateral involvement, 8 of the 10 with optic disc edema (mild to severe), and none (of 6 patients who had a cerebrospinal fluid examination) with oligoclonal bands. These features contrast with the ONTT population and really represent atypical optic neuritis. -Mark L. Moster, MD REFERENCE 1. Pokroy R, Modi G, Saffer D. Optic neuritis in an urban black African community. Eye (Lond). 2001;15:469-473. 310 Moster and Lee: J Neuro-Ophthalmol 2014; 34: 306-310 Literature Commentary Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |
