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 Table of Contents  
Year : 2021  |  Volume : 59  |  Issue : 3  |  Page : 307-309

Overlapping visual fields – A “diagnostic” conundrum

Department of Glaucoma, Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirapalli, Tamil Nadu, India

Date of Submission21-Apr-2020
Date of Decision29-May-2020
Date of Acceptance22-Jun-2020
Date of Web Publication09-Sep-2021

Correspondence Address:
Dr. Sophia Louisraj
Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirapalli - 620 001, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/tjosr.tjosr_42_20

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A 55-year old male, a patient with established glaucoma, presented with worsening of visual complaints. Field analysis revealed an apparent progression of the pre-existing field changes. A possible overlap of a neurological field defect was however suspected. Computerised tomogram (CT) revealed an acute vascular event in the territory of the middle cerebral artery. Mistaking the new field defect as a sign of glaucoma progression, would have resulted in missing the cerebrovascular accident, with a possible ominous outcome. Careful interpretation of visual fields (especially in those with pre-existing field defects), is therefore, a must in every given clinical scenario.

Keywords: Field defect, glaucoma, neurological event

How to cite this article:
Louisraj S, Nelson Jesudasan C A. Overlapping visual fields – A “diagnostic” conundrum. TNOA J Ophthalmic Sci Res 2021;59:307-9

How to cite this URL:
Louisraj S, Nelson Jesudasan C A. Overlapping visual fields – A “diagnostic” conundrum. TNOA J Ophthalmic Sci Res [serial online] 2021 [cited 2022 Nov 27];59:307-9. Available from: https://www.tnoajosr.com/text.asp?2021/59/3/307/325735

  Introduction Top

Glaucoma causes a wide range of visual field defects, ranging from small paracentral scotomas to advanced defects involving central fixation. Un-controlled disease causes a rapid worsening of field defects. Advancing glaucomatous damage, however, may not be the sole cause of a worsening of a field defect, as we aim to show in this case report.

  Case Report Top

A 53-year-old male, a known case of glaucoma receiving anti-glaucoma medications, presented to us for the first time, with defective vision in the left eye. His visual acuity on presentation was 20/40 in both eyes (OU) and intraocular pressure was 17 and 16 mm Hg, respectively. Fundus examination revealed a cup-disc ratio of 0.8:1, with inferior thinning of the neuroretinal rims [Figure 1], OU. Humphrey field analysis showed a superior arcuate scotoma with a dense defect in the left inferior hemifield [Figure 2] and [Figure 3] (OU). The previous visual fields were however not available for comparison. Since a neurological event was suspected, imaging was advised. A computerized tomogram revealed a hypodense lesion in the right parietal-occipital region, suggesting an infarct in the middle cerebral artery (MCA) territory [Figure 4]. Anticoagulants were started per the advice of a neurologist. At review 6 months later, his vision remained stable at 20/40 (OU). The visual field defect remained stationary with no new field defect.
Figure 1: Fundus picture both eyes; 0.8:1 cupping and inferior thinning of neuroretinal rims noted

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Figure 2: Humphrey field analysis of the right eye; a superior arcuate scotoma with left inferior quadrantanopia noted

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Figure 3: Humphrey field analysis of the left eye; a superior arcuate scotoma with left inferior quadrantanopia noted

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Figure 4: Computerized tomography of brain; an infarct in the right middle cerebral artery territory (circled in red)

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  Discussion Top

Seeing involves not only our eyes but the brain as well, since our eyes send visual information to the different parts of the brain that are involved in sight.[1] Visual impairment after a cerebrovascular accident (CVA) impacts quality of life and leads to loss of independence and depression.[2] Vascular occlusion along the afferent or efferent visual pathways can produce myriad effects, including transient monocular vision loss, visual field deficits, or ocular dysmotility.[3]

The MCA is, by far, the largest cerebral artery and is the vessel most commonly affected by a CVA. The MCA supplies most of the outer convex brain surface, nearly all the basal ganglia, and the posterior and anterior internal capsules. Infarcts that occur within the vast distribution of this vessel lead to diverse neurologic sequelae such as hemiparesis or hemiplegia, sensory loss of the contralateral face, arm and leg, ataxia of contralateral extremities, speech impairments, aphasia, perceptual deficits, hemispatial neglect, anosognosia, apraxia, and spatial disorganization. Visual disorders commonly accompanying such infarcts include a gaze preference toward the side of the lesion and a contralateral homonymous hemianopia.[4] A neurological field defect, respects the vertical meridian and occurs around fixation, in contrast to glaucomatous defects that respect the horizontal meridian and occur around the blind spot.

Detecting such a field defect, that is, superimposed on a preexisting advanced glaucomatous field defect may pose a significant challenge.

Visual problems are often under-reported as a sign of stroke, and not as widely recognized, as are motor or speech deficits.[5] Often, the ocular signs are subtle, and symptoms may not be reported.[6] In some patients, however, visual symptoms (defective vision, field loss, and diplopia) may be the only complaint. In patients with preexisting eye conditions, such as cataract or glaucoma, the occurrence of new visual symptoms following a stroke, may be presumed, erroneously, to be due to worsening of eye disease and not due to a neurological event. Thus, such patients may initially present to the ophthalmologist. Our patient had preexisting glaucoma which was apparently well controlled, but had an acute deterioration in vision. This was thought to be due to disease progression. The neurological event could have been present earlier, but remained undiagnosed. The conundrum was in the diagnosis of the CVA based on the visual field defect alone, in the absence of significant neurological symptoms. A high degree of suspicion by the ophthalmologist is essential in such cases, especially when neurological signs and symptoms are subtle. A careful and meticulous elicitation of the case history, and corroboration of clinical findings with test results, may help identify an underlying, nonophthalmological problem, and permitting prompt initiation of specific remedial measures.

  Conclusion Top

The occurrence of new field changes, in a patient with preexisting glaucoma, is often considered as a sign of disease progression. However, other conditions (ocular and nonocular) can simulate a worsening field defect, causing a diagnostic dilemma. A sudden deterioration of the visual fields in a patient with glaucoma may arise due to other causes, such as the acute neurological event, seen in our patient, and not just due to worsening or progression of the glaucoma.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.


G. Dominic Rodriguez, MD, DNB; B. Dhipak Arthur, MS; M. Ramesh B. Opt.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Available from: https://www.rnib.org.uk/eye-health-eye-conditions.eye./stroke-related-eye-condition-. [Last accessed on 2018 Aug 20].  Back to cited text no. 1
Rowe FJ, Wright D, Brand D, Jackson C, Harrison S, Maan T, et al. A prospective profile of visual field loss following stroke: Prevalence, type, rehabilitation, and outcome. Biomed Res Int 2013;2013:719096.  Back to cited text no. 2
Pambakian A, Currie J, Kennard C. Rehabilitation strategies for patients with homonymous visual field defects. J Neuroophthalmol 2005;25:777-42.  Back to cited text no. 3
The Internet Stroke Center. Stroke Syndromes: Middle Cerebral Artery – Superior Division; 1999. Available from: http://www.strokecenter.org/prof/syndromes/syndromePage5.htm. [Last accessed on 2011 May 13].  Back to cited text no. 4
Pula JH, Yuen CA. Eyes and stroke: The visual aspects of cerebrovascular disease. Stroke Vasc Neurol 2017;2:210-20.  Back to cited text no. 5
Available from: https://www.bioj- online.com/articles/56/galley/55/download/. [Last accessed on 2018 Aug 21].  Back to cited text no. 6


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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