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. 2022 Oct;25(Suppl 2):S106-S112.
doi: 10.4103/aian.aian_136_22. Epub 2022 Oct 19.

Cerebral Visual Loss

Affiliations

Cerebral Visual Loss

Jason J S Barton. Ann Indian Acad Neurol. 2022 Oct.

Abstract

Cerebral visual disorders include a range of common and rare deficits. They can be divided into effects on low-, intermediate-, and high-level forms of visual processing. Low-level deficits are various forms of homonymous hemifield scotomata, which affect all types of vision within their borders. Intermediate-level deficits refer to impairments of colour or motion perception, which affect either one hemifield or the entire field when lesions are bilateral. High-level deficits are divided into those of the ventral (occipitotemporal) or dorsal (occipitoparietal) stream. Occipitotemporal lesions affect various aspects of object recognition, ranging from general visual agnosia to selective agnosias, such as prosopagnosia or topographagnosia from right or bilateral lesions, and pure alexia from left-sided lesions. Occipitoparietal lesions cause the various components of Bálint syndrome, namely, simultanagnosia, optic ataxia, and ocular motor apraxia. They can also cause other impairments of visuospatial or visuotemporal processing, such as astereopsis and sequence-agnosia. Because of anatomic proximity, certain deficits cluster together to form a number of cerebral visual syndromes. Treatment of these disorders remains challenging, with frequent reliance on strategic substitutions rather than restorative approaches.

Keywords: Agnosia; balint; hemianopia.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Figure 1
Figure 1
A framework for thinking about cerebral visual disorders. These can be divided into low-, intermediate-, and high-level problems. The latter two can be separated into distinct dorsal and ventral streams
Figure 2
Figure 2
Hemifield defects from lesions of striate cortex. Defects are highly retinotopic, in that the part of the visual field affected correlates with the location of the lesion, indicated by colour coding. Damage that spares the occipital pole causes a hemianopia with macula-sparing, whereas sparing of striate cortex just behind the parieto-occipital fissure will cause a hemianopia with sparing of the monocular temporal crescent, the most peripheral part of the field. A lesion of the mid-portion of striate cortex will cause a homonymous peripheral scotoma. The right figure illustrates that damage to the superior calcarine bank will cause an inferior quadrantanopia, whereas damage to the inferior bank will be associated with a superior quadrantanopia
Figure 3
Figure 3
A homonymous central hemifield scotoma in a patient with a left occipital pole hemorrhage
Figure 4
Figure 4
Results of Farnsworth-Munsell 100-hue testing. The ring shows the different colour chips, and the error score for each chip is plotted as a thick black line. A perfect score would be indicated by a black line on the inner circle. The further the black line is away from this central circle, the greater the error in sorting for that colour. a) Normal performance. b) Performance of a patient with achromatopsia
Figure 5
Figure 5
General visual agnosia. Axial FLAIR magnetic resonance images of a patient with posterior cortical atrophy. The occipital sulci and posterior horns of the lateral ventricles are enlarged, indicating localized atrophy
Figure 6
Figure 6
Overlapping line figures. Three objects are depicted superimposed. The subject must determine which line segments group together to identify the three objects, which is difficult for subjects with general visual agnosia to do
Figure 7
Figure 7
Prosopagnosia. Coronal T1-weighted magnetic resonance images showing bilateral inferior occipitotemporal infarcts
Figure 8
Figure 8
Pure alexia. Axial FLAIR magnetic resonance images of a patient with a posterior cerebral arterial infarct affecting the left medial occipitotemporal cortex, extending anteriorly to involve the visual word form area in the fusiform gyrus
Figure 9
Figure 9
Navon figures. These show large 'global' letters (H, T), made up of small 'local' letters (B, S). Subjects with simultanagnosia have trouble seeing both, and often report just the local letters, which is called 'local capture'. If the global letter is made stronger by increasing the density of the local elements, as on the right, the probability that they will report the global letter increases
Figure 10
Figure 10
Cerebral visual syndromes. Certain deficits cluster together because of the anatomy, to form dorsal and ventral visual syndromes

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References

    1. McFadzean R, Brosnahan D, Hadley D, Mutlukan E. Representation of the visual field in the occipital striate cortex. Brit J Ophthalmol. 1994;78:185–90. - PMC - PubMed
    1. Shahinfar S, Johnson LN, Madsen RW. Confrontation visual field loss as a function of decibel sensitivity loss on automated static perimetry. Implications on the accuracy of confrontation visual field testing. Ophthalmology. 1995;102:872–7. - PubMed
    1. Zeki SM. A century of cerebral achromatopsia. Brain. 1990;113:1721–77. - PubMed
    1. Bouvier SE, Engel SA. Behavioral deficits and cortical damage loci in cerebral achromatopsia. Cereb Cortex. 2006;16:183–91. - PubMed
    1. Moroz D, Corrow SL, Corrow JC, Barton AR, Duchaine B, Barton JJ. Localization and patterns of cerebral dyschromatopsia: A study of subjects with prospagnosia. Neuropsychologia. 2016;89:153–60. - PMC - PubMed