Macular Ganglion Cell Complex Reduction Preceding Visual Field Loss in a Patient With Chiasmal Compression With a 21-Month Follow-Up: Comment

Letters to the Editor software (Orion; Voxeleron LLC, Pleasanton, CA). These values were calculated in a circular fashion, according to the Early Treatment Diabetic Retinopathy Study, but rotated (45°) to provide quadrantic measurements respecting the vertical and horizontal meridians. After excluding the fovea, values were calculated for the inner and outer segments of each quadrant. A comparison of the first and last OCT measurements showed RGC-IPL reduction in the 4 nasal quadrantic measurements ranging from 11% to 34.5%, right eye, and from 12.2% to 25.3%, left eye. A small percentage thickness reduction was also found in the temporal inner segments bilaterally (Table 1). Several studies evaluating patients with VF defects from chiasmal compression have shown that peripapillary RNFL thickness and macular RGC layer thickness are significantly correlated with VF loss on SAP (4-8) and that patients with less structural damage experience greater visual improvement after chiasmal decompression (5-7). In many patients, VF improvement, despite persistent retinal structural damage, may be attributed to restoration of transmission of neuronal impulses in axons that remain viable (2). This had led to the concept that in compressive optic pathway lesions, functional VF loss precedes structural loss, a rationale challenged by the findings of Tieger et al (1). Our patient's preference for conservative management made it possible to compare VF and OCT data prospectively over an almost 2-year (21-month) follow-up period. There was mild deterioration of the VFs over this time period, yet OCT data (especially RGC-IPL thickness) displayed definite worsening in both eyes. Horton (2) suggested that the conventional size III target used in SAP may not be sensitive enough to detect subtle VF loss. The VF results in our patient support this, as the field loss was only well defined using size I (0.25 mm2), I/2e, and I/1e targets on careful GP in the right eye. Also, it is important to notice that even on GP, progressive visual loss was not clearly defined, despite definite reduction of the RGC layer in the left eye. Therefore, it is likely that in chronic compressive lesions, retinal structures are impaired before clinically detectable VF loss. Our findings suggest that structural retinal measurements in addition to VF testing are a useful aid in the diagnosis and follow-up of patients with compressive lesions of the anterior visual pathway. Macular Ganglion Cell Complex Reduction Preceding Visual Field Loss in a Patient With Chiasmal Compression With a 21-Month Follow-Up: Comment W e appreciate Dr. Montiero's comments sharing his experience with ganglion cell loss from compressive lesions. We did observe that patients can have normal visual fields and no symptoms, despite what seems to be rather severe ganglion cell complex (GCC) thinning on optical coherence tomography (OCT) both before Letters to the Editor: J Neuro-Ophthalmol 2018; 38: 122-133 Mário Luiz Ribeiro Monteiro, MD, PhD Division of Ophthalmology (MLRM), University of São Paulo Medical School, São Paulo, Brazil Supported by a grant from Conselho Nacional de Desenvolvimento Científico e Tecnológico (No. 307393/ 2014-3), Brasilia, Brazil. The author reports no conflicts of interest. REFERENCES 1. Tieger MG, Hedges TR, Ho J, Erlich-Malona NK, Vuong LN, Athappilly GK. Ganglion cell complex loss in chiasmal compression by brain tumors. J Neuroophthalmol. 2017;37:7-12. 2. Horton JC. Invited commentary: ganglion cell complex measurement in compressive optic neuropathy. J Neuroophthalmol. 2017;37:13-15. 3. Costello F. Invited commentary: form versus function: a state of disunion? J Neuroophthalmol. 2017;37:15-16. 4. Monteiro ML, Costa-Cunha LV, Cunha LP, Malta RF. Correlation between macular and retinal nerve fibre layer Fourier-domain OCT measurements and visual field loss in chiasmal compression. Eye (Lond). 2010;24:1382-1390. 5. Danesh-Meyer HV, Papchenko T, Savino PJ, Law A, Evans J, Gamble GD. In vivo retinal nerve fiber layer thickness measured by optical coherence tomography predicts visual recovery after surgery for parachiasmal tumors. Invest Ophthalmol Vis Sci. 2008;49:1879-1885. 6. Moon CH, Hwang SC, Ohn YH, Park TK. The time course of visual field recovery and changes of retinal ganglion cells after optic chiasmal decompression. Invest Ophthalmol Vis Sci. 2011;52:7966-7973. 7. Ohkubo S, Higashide T, Takeda H, Murotani E, Hayashi Y, Sugiyama K. Relationship between macular ganglion cell complex parameters and visual field parameters after tumor resection in chiasmal compression. Jpn J Ophthalmol. 2012;56:68-75. 8. Monteiro ML, Hokazono K, Fernandes DB, Costa-Cunha LV, Sousa RM, Raza AS, Wang DL, Hood DC. Evaluation of inner retinal layers in eyes with temporal hemianopic visual loss from chiasmal compression using optical coherence tomography. Invest Ophthalmol Vis Sci. 2014;55:3328-3336. and after decompression of the chiasm (1). However, patients can have visual field loss and symptoms before structural changes are observed from axonal compression or, more specifically, because of reversible distortion of the nodes of Ranvier (2). Therefore, visual field testing in patients with compressive lesions remains very important. Because OCT is an easier test for patients and is objective, we believe that OCT should also be used in the detection of compressive lesions and during followup of affected individuals, especially because we and Dr. Montiero have shown that GCC loss can precede visual field loss. 127 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Letters to the Editor In Dr. Horton's comments about our article, he stated that conventional visual field testing may not be sensitive enough to detect functional changes associated with ganglion cell damage (3). We agree, but we also have been impressed with the possibility that, despite what seems to be significant GCC loss, there are enough ganglion cells remaining, especially in the macula, for patients to retain excellent visual function. In other words, the GCC loss may not have reached a "tipping point" as suggested by Dr. Costello, who also commented on our study (4). This seems to occur in other conditions, including Leber hereditary optic neuropathy in which, despite what seems to be almost complete loss of macular ganglion cells, some patients, over time, may regain excellent visual acuity and visual fields. Marisa Gobuty, MD Thomas R. Hedges, III, MD Joseph Ho, MD Natalie Erlich-Malona, MD Laurel N. Vuong, MD Geetha K. Athappilly, MD New England Eye Center, Tufts University School of Medicine, Weighing the Risks and Benefits of Antidepressants in Idiopathic Intracranial Hypertension W e read with interest the recent State of the Art Review on "Obesity and weight loss in idiopathic intracranial hypertension" by Subramaniam and Fletcher (1) and would like to share our thoughts on a related topic. Obesity, especially in young women, can provoke a negative body image and increase the risk of depression (2). As patients with idiopathic intracranial hypertension (IIH) not only have to tackle their weight but also the debilitating effects of chronic headaches and the fear of potential vision loss, it is not surprising that mood disorders and functional overlay often coexist (3). As a result, many patients with IIH are prescribed antidepressants. Increased antidepressant exposure has been identified as a contributory factor to the obesity pandemic (4). In fact, multiple studies have shown that the tricyclics such as amitriptyline (Elavil, Vanatrip), nortriptyline (Aventyl, Pamelor), and imipramine (Tofranil) and the noradrenergic and specific serotonergic antidepressant mirtazapine (Remeron) are associated with weight gain (5-7). Mirtazapine, in particular, has been shown to induce carbohydrate craving and often leads to significant weight gain in a short period of time (8,9). This is especially relevant in the context of patients with comorbid IIH, intractable headache, and low mood, where tricyclics and mirtazapine, at least in the United Kingdom, are commonly prescribed (10,11). In addition, 128 Tufts Medical Center, Boston, MA Carlos E. Mendoza-Santiesteban, MD New England Eye Center, Tufts University School of Medicine, Tufts Medical Center, Boston, MA Bascom Palmer Eye Institute, Miami, FL The authors report no conflict of interest. REFERENCES 1. Tieger MG, Hedges TR, 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. 2. Ochoa J, Danta G, Fowler T, Gilliati R. Nature of nerve lesion caused by pneumatic tourniquet. Nature. 1971;233:265-266. 3. Horton JC. Ganglion cell complex measurement in compressive optic neuropathy. J Neuroophthalmol. 2017;37:13-14. 4. Costello F. Form versus function: a state of disunion? J Neuroophthalmol. 2017;37:15-16. use of selective serotonin reuptake inhibitors, with the exception of fluoxetine (Prozac), also has been associated with weight gain of 7% or more in 40% of patients (12). Indeed, most psychotropic medications are associated with weight gain, with the notable exception of topiramate (Topamax), an anticonvulsant and mood stabilizer, also used in the treatment of IIH (13). There is no doubt that acetazolamide (Diamox), cerebrospinal fluid diversion procedures such as lumboperitoneal shunting, and optic nerve sheath fenestration are invaluable in the management of IIH (14). However, it must be emphasized that although they alter physiology, they do not address the underlying pathophysiology of the disease. In other words, these interventions can only provide symptomatic relief, rather than a cure. In addition, all medical and surgical treatment options have the potential for adverse effects. Although the exact mechanism remains unclear, the only cure for IIH is weight loss (15). Intentional weight loss in any setting can be difficult, which is why bariatric surgery has become increasingly popular as one of the treatment strategies in IIH (16). Bariatric surgery is by no means without risks and may be complicated by various long-term health problems such as malabsorption and nutrient deficiencies (17). Therefore, except in fulminant cases, natural weight loss remains the best treatment strategy for IIH. Furthermore, although reversal of papilledema and prevention of visual loss should always be the main treatment goal in IIH, the importance of weight loss to improve our patients' general health should not be underestimated. Antidepressants are an important group of medications, several of which have multiple applications other than treating Letters to the Editor: J Neuro-Ophthalmol 2018; 38: 122-133 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.