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Microcystic Macular Changes in Primary Open-Angle Glaucoma

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Microcystic Macular Changes in Primary Open-Angle Glaucoma ORIGINAL STUDY Microcystic Macular Changes in Primary Open-angle Glaucoma Joanne C. Wen, MD, Sharon F. Freedman, MD, Mays A. El-Dairi, MD, and Sanjay Asrani, MD thinning, and a disproportionately preserved macular reti- Purpose: To describe microcystic macular changes in patients with nal thickness, which could confound the diagnosis of moderate to advanced primary open-angle glaucoma. glaucoma using OCT. Patients and Methods: Eleven eyes of 6 unrelated patients were retrospectively identified based on a disproportionately preserved METHODS macular thickness on optical coherence tomography (OCT) despite This study was approved by the institutional review severe peripapillary retinal nerve fiber layer thinning. Patient demographic, history, and examination findings were reviewed. board of Duke University. We retrospectively identified 6 patients from our OCT database of adult glaucoma patients Results: All identified patients were African American, relatively with severe peripapillary RNFL thinning (n = 160 total young (mean age, 43.8 y) and 5 of the 6 patients were males. patients from 2010 to 2012) who had a normal macular Examination of individual macular OCT sections through areas of thickness and normal macular topography in the absence of disproportionately preserved macular thickness invariably dem- other ocular pathologies. Each patient had a comprehensive onstrated numerous small cystic cavities within the inner nuclear layer. These microcystic changes were seen in areas of the macula ocular examination, including best-corrected visual acuity, that corresponded with areas of glaucoma-related ganglion cell anterior segment examination, dilated biomicroscopic loss, therefore mimicking the normal appearance of retinal thick- examination of the macula, and optic nerve. Patients also ness in the macular region. No other retinal pathologies were had spectral domain optical coherence tomography (SD- identified on the macular OCT to account for these changes. OCT; Spectralis, Heidelberg Engineering, CA) imaging of the optic nerve and macula. Two patients underwent fluo- Conclusions: This study describes microcystic macular changes in mostly young, African American males with moderate to advanced rescein angiography. primary open-angle glaucoma. Vitreous adherence to the internal limiting membrane preventing retinal collapse is a proposed RESULTS mechanism. The disproportionately preserved macular volume may The demographic and clinical findings of the 6 identified confound the diagnosis of glaucoma in these patients. patients are shown in the Table 1. A total of 11 eyes were Key Words: microcysts, primary open-angle glaucoma, inner identified with microcystic changes within the inner nuclear nuclear layer cysts or pseudocysts layer (INL). All of the patients were African American and 5 of the 6 patients were male. The ages of the patients ranged (J Glaucoma 2016;25:258–262) from 33 to 51 years (mean, 43.8 y) at the time of diagnosis of the microcysts. All of the patients had minimal systemic ill- nesses and none were diabetic. All 6 of the patients were laucomatous damage is characterized by a progressive diagnosed with primary open-angle glaucoma (POAG) and Gloss of retinal ganglion cells and their axons.1 Optical had elevated intraocular pressures on presentation. The age at coherence tomography (OCT) allows for an objective and the time of glaucoma diagnosis ranged from 30 to 45 years quantitative assessment of this degeneration in the retina (mean, 38 y). Four of the 6 patients had never undergone and optic nerve. A number of studies have demonstrated ocular surgery. Patient 3 had undergone trabeculectomy sur- that changes detected by OCT of the peripapillary retinal gery in both the eyes and patient 6 had undergone trabecu- nerve fiber layer (RNFL) and the macula correlate well lectomy surgery in the right eye. The best-corrected visual with changes detected on functional tests such as standard acuity ranged from 20/20 to hand motion and optic nerve automated perimetry.2–6 In patients with advanced glau- cupping ranged from a cup-to-disc ratio of 0.7 up to 1.0 at the coma, severe peripapillary RNFL thinning is evident on time of diagnosis. None of the patients had any other macular OCT and is typically associated with diffuse thinning on pathology identified on dilated funduscopic examination. OCT macular retinal thickness maps (Fig. 1). We identified a scansrevealedanattachedhyaloidfaceinalleyes. group of unrelated patients in the setting of moderate to In all cases, corresponding areas associated with sig- advanced glaucoma with severe peripapillary RNFL nificant peripapillary RNFL thinning were associated with a disproportionately preserved total (internal limiting membrane to retinal pigment epithelium) macular thickness Received for publication December 15, 2013; accepted August 21, 2014. From the Department of Ophthalmology, Duke University Eye Center, on OCT (Fig. 1). Examination of individual macular OCT Durham, NC. sections through these regions invariably demonstrated Disclosure: The authors declare no conflict of interest. numerous small cystic cavities within the INL (Fig. 2). Reprints: Sanjay Asrani, MD, Department of Ophthalmology, Duke These INL cavities were located in areas underlying mac- University Eye Center, 2351 Erwin Road DUMC 3802, Durham, NC 27710 (e-mail: [email protected]). ular ganglion cell loss (Fig. 2) and therefore artificially Copyright r 2014 Wolters Kluwer Health, Inc. All rights reserved. maintained the total macular thickness. No other patho- DOI: 10.1097/IJG.0000000000000129 logies were identified on the macular OCT such as outer 258 | www.glaucomajournal.com J Glaucoma Volume 25, Number 3, March 2016 Copyright r 2016 Wolters Kluwer Health, Inc. All rights reserved. J Glaucoma Volume 25, Number 3, March 2016 Microcystic Macular Changes in POAG FIGURE 1. A, Severe thinning of the peripapillary retinal nerve fiber layer (RNFL) is typically associated with (B) decreased macular thickness. C, Severe thinning of the peripapillary RNFL with a (D) disproportionately preserved macular thickness in patient 1. retinal changes or epiretinal membranes. Fluorescein epiretinal membranes, vitreomacular traction, age-related angiography performed in 2 patients did not reveal any dye macular degeneration, diabetic macular edema, posterior leakage in the macula (Fig. 3). uveitis or macular telangiectasias, or recent intraocular surgery. Furthermore, none of the patients had evidence of distortion of the macula on OCT imaging, which would DISCUSSION suggest vitreous traction. Other reports of macular micro- We report microcystic macular changes in 11 eyes of 6 cystic changes have hypothesized an underlying inflamma- unrelated patients with glaucoma, who were identified by a tory mechanism for the formation of these microcysts.7,8 discrepancy between the degree of peripapillary RNFL However, fluorescein angiography in our patients did not thinning and the amount of expected macular thinning. All reveal any dye leakage to support this mechanism. patients had a normal macular thickness and topography We hypothesize that the cystic cavities observed in our despite peripapillary RNFL thinning and had no other patients develop as a result of severe ganglion cell loss with ocular pathologies to account for these findings. A micro- trans-synaptic loss of structures within the INL in the cystic macular edema has been described in patients with presence of an intact hyaloid face and formed vitreous. multiple sclerosis and was associated with greater disease Gills and Wadsworth13 studied cadaveric eyes from patients severity.7,8 Recent reports describe other cases of micro- with ganglion cell loss due to optic nerve and chiasm lesions cystic macular edema or microcystic macular changes and found a decrease in INL cellularity on histopathologic associated with optic neuropathies of various etiologies examination, supporting a trans-synaptic degeneration including ischemic, compressive, hereditary, inflammatory, mechanism. Furthermore, 2 of the eyes in their series were or traumatic.9–12 To our knowledge, this is the first series to found to have INL cystic cavities much like what we have specifically describe the INL microcystic macular changes observed on OCT in our patients.13 in the context of glaucoma alone. We believe that the intact hyaloid face and vitreous All 6 of our patients were diagnosed with POAG based provides generalized support of the macula, which prevents on a history of elevated intraocular pressures, optic nerve collapse and thinning after the loss of INL structures and appearance, and visual field loss consistent with glaucoma. results in these cystic cavities. A similar mechanism has None of our patients had a history of multiple sclerosis or been proposed for the development of intraretinal cystoid other causes of optic neuropathy. Careful examination of spaces in myopic eyes with posterior staphylomas.14 The the fundus revealed no other abnormalities causing the rigidity of the internal limiting membrane is thought to microcystic changes. None of the patients had evidence of prevent the retinal surface from conforming to the contour Copyright r 2014 Wolters Kluwer Health, Inc. All rights reserved. www.glaucomajournal.com | 259 Copyright r 2016 Wolters Kluwer Health, Inc. All rights reserved. Wen et al J Glaucoma Volume 25, Number 3, March 2016 TABLE 1. Summary of Clinical Findings in Patients With Macular Microcystic Changes and POAG Age at Pre-tx Cup-to- Patient No./ POAG Dx IOP (mm Disc OCT PPA RNFL
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