Correlation of Macular Sparing and Homonymous Paracentral Scotomas With MRI Lesions in Posterior Cerebral Artery Infarction. Issue 3 (14th September 2022)

• Record Type: Journal Article
• Authors: Cho, Juno; Liao, Eric; Trobe, Jonathan D.
• Editors: Fraser, Clare; Mollan, Susan; Fraser, Clare; Mollan, Susan
• Is Part Of: Journal of neuro-ophthalmology. Volume 42:Issue 3(2022)
• Page Start: 367
• Page End: 371
• Publication Date: 2022-09-14
• Subjects: Neuroophthalmology -- Periodicals; 617.7
• DOI: 10.1097/WNO.0000000000001603
• Languages: English
• ISSNs: 1070-8022

Abstract

Abstract : Background: The concepts of the representation of visual field in primary visual cortex are based on studies of war wounds and correlations with brain imaging in small cohorts. Because of the difficulty of judging brain lesion extent and the small number of studied patients, there is lingering controversy as to whether the central 15° of visual field are mapped onto the posterior 25% of primary visual cortex or onto a larger area. To improve the delineation of MRI lesion extent, we have studied only patients with posterior cerebral artery (PCA) ischemic strokes. Methods: We accrued a cohort of 92 patients with PCA strokes from an electronic medical records search between 2009 and 2020 at a single tertiary care academic institution. Patients had reliable static perimetry demonstrating homonymous hemianopias and high-definition reviewable brain imaging. We divided the primary visual cortex on the MRI T1 sagittal sequence into 8 equal segments in right and left cerebral hemispheres and located lesions according to the segments they occupied. We correlated lesion locations with 3 visual field defects (VFDs): macular-sparing homonymous quadrantanopias, macular-splitting homonymous quadrantanopias, and homonymous paracentral scotomas. Results: Among 25 cases with macular sparing, 13 had lesion-sparing confined to the posterior 25% of visual cortex. Among 6 cases with homonymous paracentral scotomas, 2 had lesions confined to the posterior 25% of visual cortex. Macular-splitting quadrantanopia did not occur in any patients with lesions confined to the posterior 25% of visual cortex, but did occur in 3 patients with lesions confined to the posterior 50% of visual cortex. These phenomena would not be expected if the central 15° of visual field were mapped onto a region extending beyond the posterior 25% of visual cortex. In patients with PCA strokes that involved the retrogeniculate visual pathway proximal to visual cortex, the visual cortex lesions were often less extensive than predicted by the VFDs, perhaps because of widespread damage to axons before they reached their destination in visual cortex. Conclusions: These results support the concept that the central 15° of the visual field are represented in the posterior 25% of visual cortex. Although this study contributes a larger cohort of patients with better-defined lesion borders than in past reports, its conclusions must be tempered by the variability of patient attention during visual field testing, the subjectivity in the interpretation of the defect patterns, and the difficulty in judging MRI lesion extent even on diffusion-weighted and precontrast T1 sagittal sequences.