Characteristic Visual Field Defect From Lateral Geniculate Body Stroke

A 58-year-old man presented with a complaint of subjective visual field loss on the right side and hypertensive emergency. Examination revealed a right homonymous hemianopia. Computed tomography imaging revealed an acute stroke of the left lateral geniculate body. A few months later, automated perimetry revealed characteristic visual field changes associated with this lesion. In this report, the anatomy, pathophysiology, clinical findings, and previously reported etiologies of lateral geniculate body lesions are reviewed

Photo and Video Essay Section Editors: Melissa W. Ko, MD Dean M. Cestari, MD Peter Quiros, MD Characteristic Visual Field Defect From Lateral Geniculate Body Stroke Mina M. Naguib, MD, Matthew B. Woodland, BS, Rod Foroozan, MD FIG. 1. Noncontrast CT of head with hyperdensity in the left lateral geniculate nucleus (A). Automated perimetry with a right homonymous inferior wedge-shaped defect (B). Abstract: A 58-year-old man presented with a complaint of subjective visual field loss on the right side and hypertensive emergency. Examination revealed a right homonymous hemianopia. Computed tomography imaging revealed an acute stroke of the left lateral geniculate body. A few months later, automated perimetry revealed characteristic visual field changes associated with this lesion. In this report, the anatomy, pathophysiology, clinical findings, and previously reported etiologies of lateral geniculate body lesions are reviewed. Journal of Neuro-Ophthalmology 2021;41:e756–e758 doi: 10.1097/WNO.0000000000001226 © 2021 by North American Neuro-Ophthalmology Society A 58-year-old man with a history of hypertension presented to the emergency room complaining of vision Department of Ophthalmology, Baylor College of Medicine, Houston, Texas. The authors report no conflicts of interest. Address correspondence to Rod Foroozan, MD, Department of Ophthalmology, Baylor College of Medicine, 1977 Butler Boulevard, Houston, TX 77030; E-mail: [e-mail] e756 loss on the right side of the right eye for 3 days. Onset was sudden, painless, nonprogressive, and not associated with headache, flashes, floaters, numbness, or weakness. The patient denied any ocular history or surgery. Visual acuity was 20/20 in both eyes without relative afferent pupillary defect. Extraocular motility was full, and intraocular pressure was normal. Confrontation visual fields revealed an incomplete right homonymous hemianopia, and funduscopy was normal in each eye. Blood pressure was 250/140 mm Hg, and noncontrast computed tomography (CT) of the head showed a 0.9 · 1.1 · 0.8 cm hyperdensity in the left lateral geniculate nucleus (Fig. 1A). He was admitted to the intensive care unit for blood pressure management. Two months later, automated perimetry revealed a right homonymous wedge-shaped inferior defect (Fig. 1B) consistent with the left lateral geniculate nucleus lesion noted on the prior CT. The lateral geniculate body (LGB), also referred to as the lateral geniculate nucleus, receives visual input from both retinas. The nucleus is arranged in a pattern with 6 distinct layers. Layers 1, 4, and 6 receive input from the contralateral nasal retina, whereas Layers 2, 3, and 5 receive their input from the ipsilateral temporal retina (1). This complex Naguib et al: J Neuro-Ophthalmol 2021; 41: e756-e758 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo and Video Essay FIG. 2. Schematic of expected visual field defect with left lateral choroidal artery ischemia (A). Schematic of expected visual field defect with left anterior choroidal artery ischemia (B). arrangement, combined with a dual blood supply, provide the anatomical basis for the 2 main patterns of visual deficits observed during vascular damage to the LGB. Isolated lesions of the LGB are relatively uncommon and produce characteristic visual field defects correlating to the specific blood supply affected (Fig. 2). Ischemia affecting the lateral choroidal artery, as suspected in the present case, produces wedge-shaped defects that are congruent and extend superiorly and/or inferiorly from the horizontal midline. Lesions involving the anterior choroidal artery produce superior and inferior quadrantic defects that spare a wedgeshaped area just above and below the horizontal midline. Therefore, lesions of the anterior choroidal artery spare the area of the defect seen in lateral choroidal artery lesions. However, the literature is conflicting regarding the expected congruency of the resulting visual field defects as the characteristic findings are often incomplete (1–4). A possible explanation for incongruency is an anastomotic connection between the anterior and lateral choroidal arteries allowing partial recovery of sight if the nucleus can be perfused. In addition, there is variability in the exact territories supplied by the 2 arteries of interest (5), although some authors believe that the anterior and lateral choroidal arteries do not anastomose within the LGB (4,6,7). Other causes of LGB lesions include astrocytoma (3), bilateral geniculitis associated with diarrhea (8), syphilitic arteritis (9), myelinolysis (2,10,11), influenza virus infection (12,13), and arteriovenous malformation (1). In one report of a patient with central pontine myelinolysis and damage to both LGBs, automated perimetry revealed an Naguib et al: J Neuro-Ophthalmol 2021; 41: e756-e758 hourglass-shaped field defect in each eye, consistent with what would be expected in bilateral anterior choroidal artery infarction (2). As automated perimetry is widely used in clinical practice, it is important for clinicians to be familiar with the appearance of a visual field defect from a lesion of the LGB. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: M. M. Naguib, M. B. Woodland, and R. Foroozan; b. Acquisition of data Mina: M. Naguib, MD, M. B. Woodland, and R. Foroozan; c. Analysis and interpretation of data: M. M. Naguib, M. B. Woodland, and R. Foroozan. Category 2: a. Drafting the manuscript: M. M. Naguib, M. B. Woodland, and R. Foroozan; b. Revising it for intellectual content: M. M. Naguib, M. B. Woodland, and R. Foroozan. Category 3: a. Final approval of the completed manuscript: M. M. Naguib, M. B. Woodland, and R. Foroozan. REFERENCES 1. Luco C, Hoppe A, Schweitzer M, Vicuña X, Fantin A. Visual field defects in vascular lesions of the lateral geniculate body. J Neurol Neurosurg Psychiatry. 1992;55:12–15. 2. Donahue SP, Kardon RH, Thompson HS. Hourglass-shaped visual fields as a sign of bilateral lateral geniculate myelinolysis. Am J Ophthalmol. 1995;119:378–380. 3. Gunderson CH, Hoyt WF. Geniculate hemianopia: incongruous homonymous field defects in two patients with partial lesions of the lateral geniculate nucleus. J Neurol Neurosurg Psychiatry. 1971;34:1–6. 4. Shacklett DE, O’Connor PS, Dorwart RH, Linn D, Carter JE. Congruous and incongruous sectoral visual field defects with e757 Copyright © North American Neuro-Ophthalmology Society. 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Vision loss caused by retinal and lateral geniculate nucleus infarction in H1N1 influenza. J Neuroophthalmology. 2015;35:265–269. Naguib et al: J Neuro-Ophthalmol 2021; 41: e756-e758 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited.