|Year : 2021 | Volume
| Issue : 3 | Page : 307-309
Overlapping visual fields – A “diagnostic” conundrum
Sophia Louisraj, CA Nelson Jesudasan
Department of Glaucoma, Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirapalli, Tamil Nadu, India
|Date of Submission||21-Apr-2020|
|Date of Decision||29-May-2020|
|Date of Acceptance||22-Jun-2020|
|Date of Web Publication||09-Sep-2021|
Dr. Sophia Louisraj
Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirapalli - 620 001, Tamil Nadu
Source of Support: None, Conflict of Interest: None
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
| Introduction|| |
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|| |
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|
Click here to view
|Figure 2: Humphrey field analysis of the right eye; a superior arcuate scotoma with left inferior quadrantanopia noted|
Click here to view
|Figure 3: Humphrey field analysis of the left eye; a superior arcuate scotoma with left inferior quadrantanopia noted|
Click here to view
|Figure 4: Computerized tomography of brain; an infarct in the right middle cerebral artery territory (circled in red)|
Click here to view
| Discussion|| |
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. Visual impairment after a cerebrovascular accident (CVA) impacts quality of life and leads to loss of independence and depression. Vascular occlusion along the afferent or efferent visual pathways can produce myriad effects, including transient monocular vision loss, visual field deficits, or ocular dysmotility.
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. 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. Often, the ocular signs are subtle, and symptoms may not be reported. 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|| |
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|| |
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.
Pambakian A, Currie J, Kennard C. Rehabilitation strategies for patients with homonymous visual field defects. J Neuroophthalmol 2005;25:777-42.
Pula JH, Yuen CA. Eyes and stroke: The visual aspects of cerebrovascular disease. Stroke Vasc Neurol 2017;2:210-20.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]