Bilateral Occipital Lobe Strokes Presenting With Bilateral Sectoranopia Pattern Visual Field Loss

Clinical Correspondence Section Editors: Robert Avery, DO Karl C. Golnik, MD Caroline Froment, MD, PhD An-Guor Wang, MD Bilateral Occipital Lobe Strokes Presenting With Bilateral Sectoranopia Pattern Visual Field Loss Conrad Goerz, MD, Esseddeeg Ghrooda, MBBCh, FRCPC, Janine L. Johnston, MD, FRCPC A 65-year-old hypertensive man presented with blurred vision and peripheral visual loss. Examination showed visual acuities of 20/30 + 2 right eye and 20/25 2 2 left eye. Automated perimetry showed homonymous wedge-shaped defects in the left hemifields consistent with horizontal homonymous sectoranopia (Fig. 1A); in the right hemifields, superior and inferior segments of the visual fields were lost with sparing of the inner wedge, consistent with quadruple homonymous sectoranopia (Fig. 1C). The appearance of his visual fields did not change over the subsequent 10 months. The remainder of his neuroophthalmological examination was normal. MRI (Fig. 2) showed acute ischemia involving left cerebellum and right occipital lobe and encephalomalacia of left occipital lobe consistent with remote ischemia. CT angiography demonstrated extracranial dissection involving the V1 segment of the left vertebral artery; the right vertebral artery was normal. Whereas ischemic lesions of the occipital cortex in the distribution of the posterior cerebral artery (PCA) cause homonymous hemianopia/quadrantanopsia, with or without macular sparing (1), sectoranopias are typically due to partial lesions of the lateral geniculate nucleus. Two types of sectoranopias occur: the first is a homonymous horizontal wedge defect associated with posterior lateral choroidal artery stroke (2). The second is an “inversion” of the first with loss of superior and inferior segments of homonymous hemifields, sparing the horizontal wedge (quadruple sectoranopia), and typically associated with anterior choroidal artery stroke (3). Literature review reveals only 6 cases of sectoranopias due to damage of primary visual cortex and 12 cases due to visual radiation lesions. In all but 2 reports, the sectoranopia was unilateral and followed the pattern of posterior lateral choroidal artery infarct. Our patient’s left hemifield defect mimicked right posterior lateral choroidal artery infarct but occurred with acute ischemia of the right calcarine cortex Section of Neurology, Department of Medicine (CG, EG, JLJ) and Department of Ophthalmology (JLJ), University of Manitoba, Winnipeg, Canada. The authors report no conflicts of interest. Address correspondence to Janine L. Johnston, MD, FRCPC, 1835 Corydon Avenue, Winnipeg, MB R3N0K6, Canada; E-mail: novl@ shaw.ca e174 subsequent to vertebral artery dissection. Ischemia from arterial dissection is the result of thromboembolism, hypoperfusion or both, distal to the dissection. Horton and Adams (1) have demonstrated that the arterial supply of the primary visual cortex is provided by the calcarine artery and its superior and inferior branches. The superior calcarine artery territory includes the upper border of the primary visual cortex representing the lower vertical meridian, and the inferior calcarine artery supplies the lower border representing the upper vertical meridian. Visual fields at the horizontal meridian are represented deep within the calcarine fissure (4). Based on this anatomy, Horton and Adams (1) postulated a series of striate cortex lesions and visual field defects that should and should not occur in the context of occlusion of a calcarine artery by a single embolus. Specifically, single embolus occlusion of the calcarine artery or one of its branches should cause loss of visual field along the vertical meridians, not sparing, as seen in our patient. One possibility to account for the left homonymous sectoranopia could be if the right striate cortex was supplied almost exclusively by the superior calcarine artery. Sparing of the inferior calcarine artery would result in preservation of the visual field adjacent to the superior vertical meridian (Fig. 1B), but would not account for sparing of the visual field next to the inferior vertical meridian beyond the macular representation. A second possibility would be collateral flow from the arteriolar surface reticulum that preserved vision along both upper and lower striate borders. A third possibility could be that cortex deep within the calcarine fissure is more vulnerable to embolic stroke than more superficial areas so that a shower of emboli could lead to discrete ischemia in the deep calcarine fissure, sparing the upper and lower borders of the calcarine cortex. Similarly, if there is transient occlusion of the main calcarine artery, the relative hypotension might affect this same region first. Supportive evidence for this possibility comes from a functional MRI study, where the deep calcarine sulcus showed earlier BOLD response (a marker of hemodynamic response) compared with other regions of the calcarine cortex (5). Therefore, emboli in the inferior or superior calcarine artery may travel toward the sulcus because regional blood flow is directed to that area. As a consequence, deep areas subserving the horizontal meridian would be preferentially damaged. This data suggest a Goerz et al: J Neuro-Ophthalmol 2024; 44: e174-e175 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Clinical Correspondence FIG. 1. Visual fields and corresponding cortical representation: left homonymous horizontal sectoranopia (A) by automated perimetry and schematic representation of theoretical lesion involving the right calcarine cortex (B) and (C) right homonymous quadruple sectoranopia with schematic representation of theoretical lesion involving the left calcarine cortex (D). relative dichotomy between function and structure. Whereas the anatomy of the calcarine arteries suggests only specific visual deficits are possible, functionally, this may not be the case. Teleologically, this makes sense because most human viewing is central and along the horizontal meridian. Temporal prioritization of blood supply to the horizontal meridian, deep within the calcarine sulcus would be important. The contralateral (right) quadruple sectoranopia in our case mimics damage to the lateral geniculate in the distribution of the anterior choroidal artery; it has a less definitive anatomical explanation. The MRI demonstrates encephalomalacia at the left occipital pole, with possible extension rostral into the calcarine cortex. The cause of this damage is unknown, but if it is presumed due to vertebral artery dissection, then the mechanism of damage may be hypoperfusion as opposed to thromboembolism. The lesion must spare the cortex deep within the calcarine sulcus, responsible for vision at the horizontal meridian while damaging the upper and lower borders of the striate cortex responsible for the vertical meridians beyond 10° superiorly and 15° inferiorly (Fig. 1C, D). As discussed above, there is no vascular supply to this region that would differentially affect deep and superficial calcarine cortex. However, although primary blood flow to the calcarine cortex comes from the PCA, there may be collateral supply from the middle cerebral artery (MCA) to the occipital pole. The appearance of right homonymous quadrantic sectoranopia may represent sparing of macular fibers by the MCA. In addition, there has likely been damage to adjacent white matter pathways subserving more peripheral visual fields superiorly and inferiorly, perhaps in a watershed region between MCA and PCA, leaving intact white matter tracts lateral to the striate cortex, which subserve the horizontal meridian. Goerz et al: J Neuro-Ophthalmol 2024; 44: e174-e175 FIG. 2. MRI at time of presentation: MRI diffusion-weighted imaging demonstrates acute ischemia in the right occipital lobe (A–C), and MRI FLAIR imaging demonstrates encephalomalacia of the left occipital lobe (D–F). This is the first reported case of both horizontal and quadruple homonymous sectoranopia due to occipital strokes, demonstrating that even classical patterns of visual field loss may not be strictly localizing nor may they follow the conventional pattern of visual field loss from embolic damage to the striate cortex. STATEMENT OF AUTHORSHIP Conception and design: C. Goerz, J. Johnston. Acquisition of data: C. Goerz, E. Ghrooda, J. Johnston. Analysis and interpretation of data: C. Goerz, E. Ghrooda, J. Johnston. Drafting the manuscript: C. Goerz, J. Johnston. Revising the manuscript for intellectual content: C. Goerz, E. Ghrooda, J. Johnston. Final approval of the completed manuscript: C. Goerz, E. Ghrooda, J. Johnston. ACKNOWLEDGMENT Special thanks to Dr. Sam Kim for reformatting and preparation of MRI images. REFERENCES 1. Horton JC, Adams DL. Patterns of cortical visual field defects from embolic stroke explained by the anastomotic organization of vascular microlobules. J Neuroophthalmol. 2018;38:538– 550. 2. Frisén L, Holmegaard L, Rosencrantz M. Sectoral optic atrophy and homonymous horizontal sectoranopia: a lateral choroidal artery syndrome? J Neurol Neurosurg Psychiatry. 1978;41:374– 380. 3. Frisén L. Quadruple sectoranopia and sectorial optic atrophy: a syndrome of the distal anterior choroidal artery. J Neurol Neurosurg Psychiatry. 1979;42:590–594. 4. Galetta SL, Grossman RI. 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