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      Unusual Presentations of Low-Tension Glaucoma

      case-report
      a , b , , a , b
      Case Reports in Ophthalmology
      S. Karger AG
      Glaucoma, Low-tension glaucoma, Visual field

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          Abstract

          Low-tension glaucoma can sometimes be difficult to diagnose, particularly if patients do not have a classic presentation. This case series shows the value of Humphrey visual field (HVF) 10-2 tests to identify deficits in central vision. Case 1 describes a female in her mid-60s who presented complaining of a “blind spot” in her right eye. While a HVF 24-2 suggested her test was “within normal limits,” an HVF 10-2 showed an unusually shaped scotoma in her right eye that matched her visual complaint. Case 2 describes a male in his mid-60s who was referred to the glaucoma service by a retina specialist. He complained of a “blind spot” in his left eye and was revealed to have a focal central scotoma on his HVF 10-2 test. Both patients presented with normal intraocular pressures, and both had been cleared by retina specialists and neuro-ophthalmologists. Both patients were then diagnosed with low-tension glaucoma, and treatment to date has been successful in slowing vision loss.

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          Most cited references3

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          Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressures. Collaborative Normal-Tension Glaucoma Study Group.

          (1998)
          To determine if intraocular pressure plays a part in the pathogenic process of normal-tension glaucoma. One eye of each eligible subject was randomized either to be untreated as a control or to have intraocular pressure lowered by 30% from baseline. Eyes were randomized if they met criteria for diagnosis of normal-tension glaucoma and showed documented progression or high-risk field defects that threatened fixation or the appearance of a new disk hemorrhage. The clinical course (visual field and optic disk) of the group with lowered intraocular pressure was compared with the clinical course when intraocular pressure remained at its spontaneous untreated level. One hundred-forty eyes of 140 patients were used in this study. Sixty-one were in the treatment group, and 79 were untreated controls. Twenty-eight (35%) of the control eyes and 7 (12%) of the treated eyes reached end points (specifically defined criteria of glaucomatous optic disk progression or visual field loss). An overall survival analysis showed a statistically significant difference between the two groups (P < .0001). The mean survival time +/-SD of the treated group was 2,688 +/- 123 days and for the control group, 1,695 +/- 143 days. Of 34 cataracts developed during the study, 11 (14%) occurred in the control group and 23 (38%) in the treated group (P = .0075), with the highest incidence in those whose treatment included filtration surgery. Intraocular pressure is part of the pathogenic process in normal-tension glaucoma. Therapy that is effective in lowering intraocular pressure and free of adverse effects would be expected to be beneficial in patients who are at risk of disease progression.
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            Risk factors for progression of visual field abnormalities in normal-tension glaucoma.

            To uncover risk factors for the highly variable individual rates of progression in cases of untreated normal-tension glaucoma. Visual field data were assembled from 160 subjects (160 eyes) enrolled in the collaborative normal-tension glaucoma study during intervals in which the eye under study was not receiving intraocular pressure-lowering treatment during prerandomization and postrandomization intervals. Analyses included multivariate analysis of time-dependent Cox proportional hazard, Kaplan-Meier analysis of "survival" without an increment of visual field worsening, and comparison of slopes of change in mean deviation global index over time. Most migraine occurred in women, but analysis demonstrated that gender and presence of migraine contribute separately to the overall risk. The risk ratio for migraine, adjusted for the other variables was 2.58 (P =.0058), for disk hemorrhage was 2.72 (P =.0036), and for female gender 1.85 (P =.0622). The average fall in the mean deviation index was faster in nonmigrainous women than in nonmigrainous men (P =.05). Suggesting genetic influence, Asians had a slower rate of progression (P =.005), and the few black patients enrolled had a tendency for faster progression. However, self-declared history of family with glaucoma or treated for glaucoma did not affect the rate of progression. Neither age nor the untreated level of intraocular pressure affected the rate of untreated disease progression, despite their known influence on prevalence. Whereas risk factors for prevalence help select populations within which to screen for glaucoma, the factors that affect the rate of progression help decide the expected prognosis of the individual's untreated disease and thereby the frequency of follow-up and aggressiveness of the therapy to be undertaken.
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              Normal tension glaucoma: review of current understanding and mechanisms of the pathogenesis

              Normal tension glaucoma (NTG) is an exception in the “glaucoma family” where the major risk factor, increased intraocular pressure, is missing. If not increased intraocular pressure, then what other causes can then lead to glaucomatous optic disc change and visual field loss in NTG? Several possibilities will be discussed. Among them a higher sensitivity to normal pressure, vascular dysregulation, an abnormally high translaminar pressure gradient and a neurodegenerative process due to impaired cerebrospinal fluid dynamics in the optic nerve sheath compartment. There are many excellent review papers published on normal tension glaucoma (NTG). The aim of this paper is therefore not to add another extensive review on NTG but rather to focus on and to discuss some possible mechanisms that are thought to be involved in the pathophysiology of NTG and to discuss the stronger and weaker aspects of each concept. The fact that several concepts exist suggests that NTG is still not very well understood and that no single mechanism on its own might adequately explain NTG.

                Author and article information

                Journal
                Case Rep Ophthalmol
                Case Rep Ophthalmol
                COP
                COP
                Case Reports in Ophthalmology
                S. Karger AG (Basel, Switzerland )
                1663-2699
                22 March 2023
                Jan-Dec 2023
                22 March 2023
                : 14
                : 1
                : 115-120
                Affiliations
                [a ]Department of Ophthalmology, David Geffen School of Medicine at UCLA, UCLA Stein Eye Institute, Los Angeles, CA, USA
                [b ]Doheny Eye Institute Doheny Image Reading Center, Los Angeles, CA, USA
                Author notes
                Correspondence to: Jody He, jodyzhe@ 123456gmail.com
                Article
                529666
                10.1159/000529666
                10035547
                36968809
                e8591bd7-945f-4e25-ac0d-73aa5704083c
                © 2023 The Author(s). Published by S. Karger AG, Basel

                This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC) ( http://www.karger.com/Services/OpenAccessLicense). Usage and distribution for commercial purposes requires written permission.

                History
                : 18 October 2022
                : 7 February 2023
                : 2023
                Page count
                Figures: 3, References: 3, Pages: 6
                Funding
                There was no funding of research relative to this study.
                Categories
                Case Report

                glaucoma,low-tension glaucoma,visual field
                glaucoma, low-tension glaucoma, visual field

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