Junctional Scotoma and Patterns of Visual Field Defects Produced by Lesions Involving the Optic Chiasm

Original Contribution Section Editors: Clare Fraser, MD Susan Mollan, MD Junctional Scotoma and Patterns of Visual Field Defects Produced by Lesions Involving the Optic Chiasm Laura C. Donaldson, MD, PhD, Arshia Eshtiaghi, BSc, Simone Sacco, MD, Jonathan A. Micieli, MD, Edward A. Margolin, MD Background: Lesions of the optic chiasm (OC) typically produce bitemporal hemianopia (BTH) on visual field (VF) testing, whereas lesions located at the nasal optic nerve– chiasmal (ON-OC) junction have been proposed to produce junctional scotoma (JXS), a central defect in the ipsilateral eye with temporal field loss in the contralateral eye. In this study, we investigated whether the pattern of VF loss in patients with chiasmal compression predicted the appearance of the causative lesion on neuroimaging and described the clinical presentation of these patients with different types of VF defect. Methods: Retrospective chart review of patients seen in tertiary neuro-ophthalmology practice over 6 consecutive years with lesions abutting or displacing the OC was performed. Lesion size and location relative to the OC on neuroimaging was determined and correlated with VF defects as well as optical coherence tomography (OCT) of the peripapillary retinal nerve fiber layer and macular ganglion cell complex (GCC). Results: Fifty-three patients were enrolled. VFs demonstrated JXS (n = 18), BTH (n = 14), monocular VF defect (n = 4), and no VF defect (n = 17); 64.7% of cases with normal VFs had radiologic OC compression. Lesion volume was highest in the JXS group, and these patients also had the poorest presenting visual acuity. All patients with JXS showed involvement of the ON–OC junction; however, not all cases showed compression of the OC from the nasal direction (15 of 18), and 17 of 18 also showed compression of one or both prechiasmatic ONs. Compression of the ON–OC junction was also seen in 79% of BTH, 100% of monocular VF defect, and 59% of no VF defect cases. Fifty percent of patients with Department of Ophthalmology and Vision Sciences (LD, JM, EM), University of Toronto, Toronto, Canada; Faculty of Medicine (AE), University of Toronto, Toronto, Canada; Department of Medical Imaging (SS), University of Toronto, Toronto, Canada; and Department of Medicine (JM, EM), Division of Neurology, University of Toronto, Toronto, Canada. The authors report no conflicts of interest. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www. jneuro-ophthalmology.com). Address correspondence to Edward Margolin, MD, Department of Ophthalmology and Medicine (Neurology), University of Toronto, Faculty of Medicine, 801 Eglinton Avenue West Suite 301, Toronto ON M5N 1E3; E-mail: [e-mail] Donaldson et al: J Neuro-Ophthalmol 2022; 42: e203-e208 normal VFs already had thinning of the GCC on OCT. GCC thinning was most pronounced nasally in the BTH group, but diffuse bilateral thinning was found in 38% of cases compared with 60% of JXS. VFs improved in 6 of 6 patients with BTH but only in 5 of 8 JXS cases after treatment. Conclusions: JXS is more often seen with larger lesions and when there is compression of both the prechiasmatic ON and ON–OC junction. These patients have worse presenting visual acuity and poorer outcomes. Not all patients with radiologic compression had VF defects, although 50% of patients with normal VFs had evidence of compression on the macular GCC analysis, emphasizing the importance of macular OCT in the evaluation of patients with lesions involving the OC. Journal of Neuro-Ophthalmology 2022;42:e203–e208 doi: 10.1097/WNO.0000000000001394 © 2021 by North American Neuro-Ophthalmology Society R etinal ganglion cell axons travelling from the retina through the optic chiasm (OC) to the lateral geniculate nucleus maintain a precise, predictable organization. Classic teaching states that compression of the OC impacts decussating nasal retinal axons producing a bitemporal hemianopia (BTH) (1). In fact, visual field (VF) defects resulting from chiasmal lesions are highly variable, and complete BTH is uncommon (2,3). One large series of patients with chiasmal lesions found BTH in 11% and anterior junction syndrome in 13% (4). Anterior chiasmal syndrome, also known as junctional scotoma (JXS), refers to a specific pattern of VF loss: central defect in one eye with temporal defect, usually superiorly, in the fellow eye. This has been postulated to occur as a result of compression of the optic nerve (ON)–OC junction where crossing nasal axons were proposed to make a short anterolateral detour into the ON of the contralateral eye forming a structure, which was termed Wilbrand knee (5). JXS has been reported to occur in patients with pituitary macroadenoma as well as other parasellar compressive lesions and inflammatory optic neuropathies (6–9). e203 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution A number of previous studies have asked whether the presence or absence of a VF defect may be predicted by the radiologic appearance of a chiasmal lesion. In general, larger masses with more displacement of the OC are more likely to affect the VF (10,11). The specific pattern of VF defect produced by lesions compressing the OC from different directions and whether there is agreement with theoretical predictions based on anatomical organization is not well known. This study examined the patterns of VF defects seen in a group of patients with lesions affecting the OC. We asked whether there is a correlation between the type of VF defect and the imaging characteristics of a parasellar lesion. METHODS A retrospective chart review of patients presenting to a tertiary neuro-ophthalmology clinic between January 2014 and November 2020 was performed. The research protocol was approved by the University of Toronto Research Ethics Board. Patients with parasellar lesions abutting the OC who underwent automated VF testing were included in the study. VF defects at the first presentation to clinic were assessed using Humphrey 24-2 SITA-Fast automated perimetry and classified into 1 of the 4 categories: JXS, BTH, monocular defect, and normal by a neuro-ophthalmologist (J.M. or E.M.) and a neuro-ophthalmology fellow (L.D.). All patients had at least one reliable VF available for analysis; thus, none were excluded for this reason. Patients who were monocular due to another cause (not compressive optic neuropathy) were excluded. Single VFs were excluded if there were more than one-third fixation losses or false-negatives or more than 20% false-positives. Only patients with no previous treatment (surgery, radiation, or medical) were included. Charts were reviewed to determine demographic information and visual acuity. Where available, optical coherence tomography (OCT) data of the peripapillary retinal nerve fiber layer and macular ganglion cell complex (GCC, including ganglion cell layer and inner plexiform layer, Zeiss Cirrus 600, Oberkochen, Germany) were included. OCT data of the GCC were manually reviewed to ensure appropriate segmentation, and thinning was defined by manufacturer’s cutoff of ,5% of the normative database. Follow-up appointments were included if the patient was seen at least 30 days after the initial visit. Neuroimaging was reviewed by a single neuroradiologist (S.S.) who was blinded to the category of VF defect present. Fifty-two patients had a 1.5 or 3 Tesla MRI and 1 patient had a CT scan only. Lesion volume was calculated by measuring the maximum width, height, and depth then multiplying these values. OC displacement was measured by drawing a line connecting the most inferolateral aspect of the OC and measuring the perpendicular distance between this line and the inferior border of the OC at the area of maximum compression. Position of the OC was defined in the mid sagittal plane as prefixed (overlying the tuberculum sellae), e204 normal (overlying the diaphragm sellae), and postfixed (overlying the dorsum sellae) (12). Chiasmal lesions were compared between patients with JXS, BTH, monocular VF defects, and no VF defects using analysis of variance testing when comparing continuous outcomes and Fisher exact test when comparing categorical outcomes. In comparisons between the better and worse eye of patients, the left eye was taken to be the worse eye when central visual acuities were equal between both eyes. Patients with missing data on any clinical variable were excluded for analysis for that given variable. RESULTS Fifty-three patients with previously untreated chiasmal lesions were included in the study. Twenty-nine were women, and the mean age was 47.8 ± 18.0 years. Fiftyone percent presented with subjective decrease in vision in one or both eyes and 17% with headache; 25% were asymptomatic. Pituitary adenoma was the most common lesion (Table 1), accounting for 51% of cases. VF defect patterns observed at presentation were JXS (n = 18), BTH (n = 14), monocular VF defect (n = 4), and no VF defect (n = 17). Complete BTH was seen in 43% (6 of 14). In patients presenting with JXS, the scotoma contralateral to the central vision loss was superotemporal in 17% of cases (3 of 18), inferotemporal in 11% (2 of 18), and a complete temporal defect in 72% (13 of 18). Most VF defects in the BTH group respected the vertical midline (93%, 13 of 14), while this was less often seen in the JXS eyes with the primarily temporal VF defect (67%, 12 of 18). Patients with JXS had worse presenting visual acuity, VF mean deviation, and retinal nerve fiber layer thickness in the central scotoma (worse) eye when compared with the other groups (Table 1). Lesion volume was also highest in patients with JXS (Table 2). Compression of the ON–OC junction was seen in 100% of JXS cases but was also seen in 79% of BTH group, 100% of monocular VF defects, and 59% of the no VF defect cases. The direction of compression of the ON–OC junction in JXS was nasal in 78%, temporal in 17%, and combined in 6%. The amount of vertical displacement of prechiasmatic ON, OC, and postchiasmatic OT was highest in the JXS group (Table 2). Within each group, the amount of chiasm displacement was highly variable. Within the group with normal VF, the maximum amount of OC compression was 7 mm, and 2 mm for patients who also had normal GCC. The OC was also more often in a pre- or postfixed position in JXS and BTH groups relative to the normal VF group, whereas in monocular VF defect cases, the OC was either in the normal (2/4) or postfixed (2/4) position (see Supplemental Digital Content, Table E1, http://links.lww.com/ WNO/A507). In addition to the OC, compression of the prechiasmatic ON was found in 94% of JXS cases with both prechiasmatic ONs involved in 72%. The BTH group had prechiasmatic ON compression in 71%. Donaldson et al: J Neuro-Ophthalmol 2022; 42: e203-e208 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 1. Baseline clinical characteristics in patients with different patterns of visual field defect JXS (n = 18) BTH (n = 14) Monocular (n = 4) Normal (n = 17) Age, yr Gender (% female) Presenting symptom 45.2 ± 19.8 44.4 55.4 ± 16.7 50.0 44.5 ± 8.9 75.0 Headache (4) Unilateral vision (9)* Bilateral vision (6) Asymptomatic (0)* Other/NS (3) Headache (2) Unilateral vision (4) Bilateral vision (3) Asymptomatic (4) Other/NS (2) Lesion type Pituitary adenoma (7) Rathke cyst (1) Craniopharyngioma (4) Meningioma (3) Other (3): germ cell tumor, epidermoid cyst, granuloma Pituitary adenoma (7) Rathke cyst (1) Craniopharyngioma (1) Meningioma (1) Other (4): 2 unspecified tumors, arachnoid cyst, vascular tumor 0.049 ± 0.082 Headache (0) Headache (3) Unilateral VA Unilateral vision (0) Bilateral vision (1) (4)* Bilateral visionAsymptomatic (9) Other/NS (5) (0) Asymptomatic (0) Other/NS (1) Pituitary Pituitary adenoma adenoma (13) (2) Craniopharyngioma Meningioma (1) (2) Rathke cyst (2) Other (1): arachnoid cyst 0.024 ±0.042 0.028 ±0.052 0.38 ± 0.32 0.73 ± 0.87 0.11 ± 0.12 26.94 ± 4.70* 28.26 ± 4.42 VA better eye 0.22 ± 0.31* (logMAR) VA worse eye 1.35 ± 0.90* (logMAR) VF MD better eye213.67 ± 6.18* VF MD worse eye221.06 ± 9.17* Mean RNFL better eye (mm) Mean RNFL worse eye (mm) 45.2 ± 16.9 64.7 78.6 ± 14.0 77.5 ± 13.9 21.76 ± 0.52 21.89 ± 0.92 210.54 ± 22.62 ± 1.28 8.41 101.0 ± 13.2 89.4 ± 12.9 70.5 ± 15.3* 77.1 ± 12.9 79.5 ± 11.3 88.3 ± 11.6 *Adjusted P value of ,0.05 when comparing the outcomes of patients in each VF defect category to the patients with no VF defects. BTH, bitemporal hemianopia; JXS, junctional scotoma; logMAR, logarithm of the minimum angle of resolution; MD, mean deviation; NS, not specified; RNFL, retinal nerve fibre later; VA, visual acuity; VF, visual field. Macular GCC analysis revealed significant thinning in both eyes in the JXS group (Table 3). The BTH group showed specific loss of the nasal ganglion cells, corresponding to the temporal VF defects; this pattern was more apparent in the GCC than the RNFL (see Supplemental Digital Content, Table E2, http://links.lww.com/WNO/A508). Overall, thinning of the GCC in the JXS group was more severe than was reflected in the VF defect, with diffuse bilateral thinning in 60% of cases. In the BTH group, 25% showed the expected pattern of binasal thinning; however, 37.5% had diffuse bilateral thinning (Table 4) and 50% of patients with no VF defect already had GCC thinning. Thirty-two patients completed follow-up, with a median duration of 497 days from the first to the last appointment. Of the patients undergoing treatment, 63% (5 of 8) in the JXS group had improvement in the VF compared with 100% (6 of 6) of patients in the BTH group. VF mean Donaldson et al: J Neuro-Ophthalmol 2022; 42: e203-e208 deviation in the worse seeing eye in the BTH group improved with treatment (better eye: 4.4 ± 3.7 dB; worse eye: +6.1 ± 3.4 dB), while treatment did not affect mean deviation in either eye within the JXS group (better eye +2.6 ± 5.0 dB; worse eye 4.1 ± 13.4 dB). There was also a trend toward improvement in visual acuity in the worse eye in the BTH group, although this was not significant. DISCUSSION The precise anatomical organization of retinal ganglion cell axons traversing the anterior visual pathway into the OC theoretically allows for the VF defect to predict the location of the causative lesion. We found that the type of VF defect was only closely linked to lesion size, with larger lesions more likely to produce JXS. The second major finding of the present study is that radiologic compression does not always e205 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 2. Lesion size and compression of the optic nerve, chiasm, and tract on neuroimaging Lesion volume (mm3) OC compression Prechiasmatic ON compression ON-OC junction compression Postchiasmatic OT compression Displacement prechiasmatic ON (mm) Displacement OC (mm) Displacement postchiasmatic OT (mm) JXS (n = 18) BTH (n = 14) Monocular (n = 4) Normal (n = 17) 28,817 ± 36,949* 100 (18/18)* 94.4 (17/18)* 100 (18/18)* 72.2 (13/18)* 8.8 ± 9.6* 12.7 ± 10.4* 7.7 ± 6.4* 7,743 ± 6,535 85.7 (12/14) 71.4 (10/14) 78.6 (11/14) 64.3 (9/14)* 6.5 ± 4.2* 10.0 ± 5.1* 1.9 ± 3.2 10,359 ± 7,035 100 (4/4) 100 (4/4) 100 (4/4) 50.0 (2/4) 3.6 ± 4.2 3.3 ± 4.1 1.0 ± 1.7 3,360 ± 5,738 64.7 (11/17) 35.3 (6/17) 58.8 (10/17) 11.8 (2/17) 0.8 ± 1.6 1.9 ± 2.6 0.2 ± 1.0 *Adjusted P value of ,0.05 when comparing the outcomes of patients in each VF defect category to the patients with no VF defects. BTH, bitemporal hemianopia; JXS, junctional scotoma; OC, optic chiasm; ON, optic nerve; OT, optic tract; VF, visual field. lead to a VF defect because 65% of individuals with normal VFs had radiologic evidence of OC compression. All patients with a parasellar lesion should be evaluated with a macular OCT of the GCC because this provides a more sensitive measure of chiasmal compression than VF defects, with 50% of patients in the normal VF group showing GCC thinning. JXS on VFs has been previously proposed to specifically predict compression of Wilbrand knee at the prechiasmatic ON near the ON–OC junction (5). While all JXS patients did have ON–OC junction compression, compression of the OC itself was also present in all cases. In addition, many patients with BTH and monocular VF defects also showed prechiasmatic ON and ON–OC junction compression on neuroimaging. All of this is in keeping with the recent data that refuted the existence of Wilbrand knee in normal individuals (13). Wilbrand knee was originally described in 2 patients with monocular blindness (5); however, attempts to replicate this finding in others have been unsuccessful. One study appeared to verify its presence in human autopsy specimens (14); more recent analysis strongly suggested that this to be an artifact of image processing (13). JXS can alternately be explained by the lesion compressing the prechiasmatic ON on one side creating a diffuse or central VF defect, extending to compress the nearby OC and thus producing bitemporal field loss, which is discernible in the fellow eye where central vision is spared. This theory is supported by our data showing that all patients with JXS had OC compression, and 17 of 18 patients had compression of one or both prechiasmatic ONs. JXS was associated with a larger lesion size, and a larger parasellar lesion is simply more likely to extend from the OC to involve the prechiasmatic ONs. Compression of the prechiasmatic ON in JXS likely also accounts for the worse presenting visual acuity in these patients. Central acuity is not usually diminished in hemianopic defects, and in BTH, decreased vision has been linked to defects extending past the midline into the nasal hemifield (15). It has been proposed that chiasmal lesions predominantly produce temporal VF defects as nasal axons may be selectively damaged either due to their anatomical location in the center of the OC or because of greater stretching force transmitted to axons that are crossing one another as opposed to running parallel (16). This “crossing theory” predicts that nasal axons will be preferentially damaged regardless of the direction of OC compression. The findings in our current cohort support this notion. First, 93% (13 of 14) of BTH field defects respected the vertical midline, and the temporal axons remained spared with even large volume lesions and variable compression patterns on imaging. The single case of BTH that crossed the vertical midline had compression of the OC and bilateral prechiasmatic ONs, which likely caused more diffuse axonal loss. Second, the cases of JXS where TABLE 3. Mean ganglion cell complex (GCC) thickness (in micrometers) Better seeing eye Average GCC Nasal Temporal Worse seeing eye Average GCC Nasal Temporal JXS (n = 17) BTH (n = 10) Monocular (n = 3) Normal (n = 10) 64.9 ± 8.9* 59.1 ± 11.1* 71.9 ± 9.7 69.3 ± 9.9 65.6 ± 10.4* 74.5 ± 10.2 80.7 ± 5.7 80.8 ± 7.8 80.7 ± 5.0 79.1 ± 6.9 77.9 ± 7.5 80.2 ± 8.0 55.3 ± 16.3* 54.6 ± 14.6* 56.0 ± 18.3* 63.4 ± 14.5 61.6 ± 11.0* 66.2 ± 17.5 63.3 ± 16.3 62.2 ± 19.7 64.3 ± 15.1 78.0 ± 7.1 77.9 ± 8.3 78.1 ± 7.5 *Adjusted P value of ,0.05 when comparing the outcomes of patients in each VF defect category to the patients with no VF defects. BTH. bitemporal hemianopia; JXS, junctional scotoma; VF, visual field. e206 Donaldson et al: J Neuro-Ophthalmol 2022; 42: e203-e208 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 4. Pattern of ganglion cell complex thinning in different visual field patterns Thinning present Unilateral Bilateral diffuse Bilateral nasal Nasal + contralateral diffuse Other pattern bilateral JXS (n = 16) BTH (n = 10) Monocular (n = 3) Normal (n = 10) 93.8% (15/16) 6.7% (1/15) 60.0% (9/15)* 0 33.3% (5/15) 0 80.0% (8/10) 12.5% (1/8) 37.5% (3/8) 25.0% (2/8) 25.0% (2/8) 0 66.7% (2/3) 50.0% (1/2) 50.0% (1/2) 0 0 0 50% (5/10) 0 0 20% (1/5) 20% (1/5) 60% (3/5) Other bilateral patterns were homonymous (1), bilateral temporal (1) and temporal + contralateral diffuse. *Adjusted P value of ,0.05 when comparing the outcomes of patients in each VF defect category to the patients with no VF defects. BTH, bitemporal hemianopia; JXS, junctional scotoma; VF, visual field. ON–OC junction compression occurred from the temporal direction is better explained by the crossing theory because this theory does not require involvement of the OC from any specific direction as the Wilbrands knee theory does. Binasal thinning of the GCC has been reported to precede bitemporal VF defects in patients with chiasmal lesions (17–19). The nasal GCC is normally thicker than the temporal side in healthy subjects, and loss of this asymmetry is also indicative of chiasm compression (18). We found that 50% of cases in our series with normal VFs already showed thinning of GCC. In addition, abnormalities in GCC were often more widespread than VF changes within the other groups, with bilateral diffuse thinning seen in 64% of JXS cases and 38% of BTH cases. Macular GCC analysis is also useful when patients are unreliable VF test takers and can provide supportive evidence that a VF defect respects the vertical midline and requires investigation with neuroimaging (20). Presence of GCC thinning has prognostic value for VF outcomes postoperatively (17), and the results of our study support the assertion that GCC analysis is a critical component of the neuro-ophthalmological examination of patients with lesions of the OC and abnormalities should be interpreted as evidence of compression, which must factor in to decisions on intervention. There were a few patients in our study with VF defects with no thinning of the macular GCC. This scenario is less common but has been previously reported in patients with OC lesions (18,21). Structural changes may lag behind VF changes if chiasm compression is of new onset, and macular ganglion cells may be anatomically intact but poorly functional. This is a reminder that despite the utility of OCT, it should not be performed or interpreted in isolation. Limitations of the current study include its retrospective nature. Not all patients had GCC data available from their initial visit (39/53 or 74%). No follow-up data were available for 36% of cases (19 of 53), so we were unable to correlate initial VF and OCT parameters with outcomes. While previous studies have often included only patients with pituitary adenomas, we included patients with a variety of lesion types, thus the nature and the duration of OC compression was more heterogeneous in our study. Donaldson et al: J Neuro-Ophthalmol 2022; 42: e203-e208 CONCLUSIONS Larger lesions are more likely to produce JXS, and these patients have worse presenting vision, VFs, and more thinning on OCT and poorer outcomes after treatment. Radiologic compression does not lead to VF defects in many cases, and all patients with parasellar lesions should undergo neuro-ophthalmologic examination, including OCT of the macular GCC to detect early chiasmal compression. Neuroimaging in all JXS cases shows involvement of the OC, not only in the prechiasmatic ON or OC– OC junction, which argues against the existence of Wilbrand knee. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: E. Margolin and L. Donaldson; b. Acquisition of data: S. Sacco, L. Donaldson, and A. Eshtiaghi; c. Analysis and interpretation of data: L. Donaldson and A. Eshtiaghi. Category 2: a. Drafting the manuscript: L. Donaldson and A. Eshtiaghi; b. Revising it for intellectual content: E. Margolin, L. Donaldson, A. Eshtiaghi, J. Micieli, and S. Sacco. Category 3: a. Final approval of the completed manuscript: E. Margolin, L. Donaldson, A. Eshtiaghi, J. Micieli, and S. Sacco. REFERENCES 1. O’Connell JE. The anatomy of the optic chiasma and heteronymous hemianopia. J Neurol Neurosurg Psychiatry. 1973;36:710–723. 2. Lee JP, Park IW, Chung YS. The volume of tumor mass and visual field defect in patients with pituitary macroadenoma. Korean J Ophthalmol. 2011;25:37–41. 3. Lee IH, Miller NR, Zan E, Tavares F, Blitz AM, Sung H, Yousem DM, Boland MV. Visual defects in patients with pituitary adenomas: the myth of bitemporal hemianopsia. AJR Am J Roentgenol. 2015;205:W512–W518. 4. Schiefer U, Isbert M, Mikolaschek E, Mildenberger I, Krapp E, Schiller J, Thanos S, Hart W. Distribution of scotoma pattern related to chiasmal lesions with special reference to anterior junction syndrome. Graefes Arch Clin Exp Ophthalmol. 2004;242:468–477. 5. Wilbrand H, Saenger A. Die Neurologie des Auges 3(1). Wiesbaden, Germany: J. Bergmann, 1904:98–120. 6. Jin HD, O’Brien JC, Siatkowski RM. Suprasellar arachnoid cyst causing reversible junctional scotoma. Am J Ophthalmol Case Rep. 2020;18:100720. e207 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution 7. Alvarez-Fernandez D, Rodriguez-Balsera C, Shehadeh-Mahmalat S, Señaris-Gonzalez A, Alvarez-Coronado M. Junctional scotoma. Arch Soc Esp Oftalmol. 2019;94:445–448. 8. Lavaque AJ, Yilmaz T, Cordero-Coma M. Localized bi-nasal macular edema in optic chiasmal syndrome. Indian J Ophthalmol. 2013;61:351–353. 9. Achiron L, Strominger M, Witkin N, Primo S. Sarcoid optic neuropathy: a case report. J Am Optom Assoc. 1995;66:646–651. 10. Frisén L, Jensen C. How robust is the optic chiasm? Perimetric and neuro-imaging correlations. Acta Neurol Scand. 2008;117:198–204. 11. Ryu WHA, Starreveld Y, Burton JM, Liu J, Costello F; PITNET Study Group. The utility of magnetic resonance imaging in assessing patients with pituitary tumors compressing the anterior visual pathway. J Neuroophthalmol. 2017;37:230–238. 12. Long H, Qi ST, Song Y, Pan J, Zhang XA, Yang KJ. Topographic variations of the optic chiasm and the pituitary stalk: a morphometric study based on midsagittal T2-weighted MR images. Surg Radiol Anat. 2014;36:775–781. 13. Horton JC. Wilbrand’s knee: to be or not to be a knee? J Neuroophthalmol. 2020;40(suppl 1):S7–S14. 14. Shin RK, Qureshi RA, Harris NR, Bakar D, Li TP, Jafri MS, Tang CM. Wilbrand knee. Neurology. 2014;82:459–460. 15. Manor RS, Dickerman Z. Relationship between visual acuity and nasal field thresholds in patients with temporal hemianopia. J Clin Neuroophthalmol. 1991;11:66–69. e208 16. Kane EJ, Ashton DE, Mews PJ, Reid K, Neely A, Lueck CJ. Correlation of MRI findings with patterns of visual field loss in patients with pituitary tumors. J Neuroophthalmol. 2019;39:333–338. 17. Tieger MG, Hedges TR III, Ho J, Erlich-Malona NK, Vuong LN, Athappilly GK, Mendoza-Santiesteban CE. Ganglion cell complex loss in chiasmal compression by brain tumors. J Neuroophthalmol. 2017;37:7–12. 18. Jørstad ØK, Wigers AR, Marthinsen PB, Moe MC, Evang JA. Loss of horizontal macular ganglion cell complex asymmetry: an optical coherence tomography indicator of chiasmal compression. BMJ Open Ophthalmol. 2018;3:e000195. 19. Suh H, Choi H, Jeon H. The radiologic characteristics and retinal thickness are correlated with visual field defect in patients with a pituitary mass. J Neuroophthalmol. 2020 (epub ahead of print). 20. Shin HY, Park HY, Choi JA, Park CK. Macular ganglion cell-inner plexiform layer thinning in patients with visual field defect that respects the vertical meridian. Graefes Arch Clin Exp Ophthalmol. 2014;252:1501–1507. 21. Lukewich MK, Micieli JA. Chronic chiasmal compression and persistent visual field defect without detectable changes in optical coherence tomography of the macular ganglion cell complex. Am J Ophthalmol Case Rep. 2019;16:100533. Donaldson et al: J Neuro-Ophthalmol 2022; 42: e203-e208 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.