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Higher Cortical Visual Deficits Review Article Address correspondence to Dr Jason J. S. Barton, Beth Israel Deaconess Medical Higher Cortical Visual Center, 4807 Collingwood Street, Vancouver, BC V6S 2B5, [email protected]. Deficits Relationship Disclosure: Dr Barton receives personal Jason J. S. Barton, MD, PhD, FRCPC compensation for serving on the advisory board of Vycor Medical, Inc, and for speaking at the LAUNCH review course ABSTRACT for residents provided by EMD Serono, Inc. Dr Barton Purpose of Review: This article reviews the various types of visual dysfunction that has also provided expert can result from lesions of the cerebral regions beyond the striate cortex. review for several law firms Recent Findings: Patients with dyschromatopsia can exhibit problems with color and receives book royalties from Springer and UpToDate. constancy. The apperceptive form of prosopagnosia is associated with damage to Dr Barton’s laboratory is posterior occipital and fusiform gyri, and an associative/amnestic form is linked to supported by grants from the damage to more anterior temporal regions. Pure alexia can be accompanied by a Canadian Institutes of Health Research and Natural Sciences surface dysgraphia. New word-length effect criteria distinguish pure alexia from and Engineering Research hemianopic dyslexia. Subtler problems with perception of numbers and faces can Council of Canada. be seen in patients with pure alexia as well. Also, a developmental form of Unlabeled Use of topographic disorientation, which is due to problems with forming cognitive maps Products/Investigational Use Disclosure: of the environment, has been discovered. In Balint syndrome, added features of Dr Barton reports no disclosure. decreased flexibility of attention in simultanagnosia include local and global * 2014, American Academy capture. Balint syndrome can affect not just localization in space, but also in time, of Neurology. as manifest in sequence agnosia. Summary: Lesions at intermediate levels of a processing hierarchy can cause difficulty with color perception or motion perception. At a higher level, ventral lesions of the occipitotemporal lobes can lead to a variety of problems with object recognition. Dorsal lesions of the occipitoparietal lobes can cause difficulty with spatial localization and guidance. Continuum (Minneap Minn) 2014;20(4):922–941. Most lesions of the visual system from the ventral occipitotemporal cortex the retina to the striate cortex charac- affect what has been colloquially teristically cause scotomata, regions of called a ‘‘what’’ stream, involved ulti- the visual field where vision is lost mately in object identification. The surrounded by regions where it is ‘‘intermediate’’ level of this stream is preserved. Lesions of extrastriate cor- involved particularly in color process- tex lead to very different types of ing, and a lesion of this will lead deficits, however. Rather than a gen- to achromatopsia. Higher-level recog- eral loss of vision constrained to a nition deficits can lead to diverse specific location in the visual field, types of general visual agnosia or a they cause a loss of a specific type of number of selective agnosias, includ- visual function that often is neither ing prosopagnosia, pure alexia, and localized nor limited to one part of the topographagnosia. In contrast, lesions field. of the dorsal occipitoparietal cortex Diverse types of visual functions are cause problems with spatial process- affected by extrastriate lesions, which ing, in what some view as a ‘‘where’’ are grouped into two broad families stream1 and others view as a focus on according to anatomic location and preparation for visually guided action.2 functional relationships.1,2 Lesions of The intermediate deficit here is 922 www.ContinuumJournal.com August 2014 Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. KEY POINT akinetopsia, impaired motion process- find this unpleasant, as if things look dirty. h Cortical visual ing. High-level deficits are the compo- A partial defect is called dyschromatopsia. syndromes can be nents of Balint syndrome, including With dyschromatopsia, some color per- grouped into problems simultanagnosia, optic ataxia, and oc- ception remains, but the ability to with various types of ular motor apraxia, as well as distinguish one color from another is object recognition with astereognosis. reduced. For some patients, the world ventral occipitotemporal The lesions that cause the various takes on a specific tint. Rarely, patients lesions, and problems types of cortical syndromes discussed may report illusory spread of colors, in with spatial analysis and in this article are the usual suspects which an object’s color seeps out of its attention with dorsal for cerebral pathology, eg, stroke, boundaries. occipitoparietal lesions. tumors, and encephalitis. In most Color vision is processed by a cases, the temporal pattern of the network in the occipitotemporal cor- problem is the key to diagnosing the tex. Cerebral dyschromatopsia is asso- cause. For syndromes that are more ciated with bilateral lesions of the likely to emerge after bilateral lesions, lingual gyri5 (Figure 7-3); its severity such as achromatopsia or Balint syn- reflects how much of the cortical color drome, etiologies that can have bilat- network is lost.6 Unilateral lesions may eral effects should be considered. not cause a symptomatic deficit, but Thus, among the different kinds of when tested carefully, patients with stroke, postoperative watershed in- such lesions are shown to have farctions, embolic showers, and vascu- hemiachromatopsia, impaired discrim- litis would be suspects. Other causes ination of colors in the contralateral of bilateral lesions include posterior hemifield. reversible encephalopathy syndrome, An impairment of color perception multiple cerebral metastases, and her- is often associated with superior field pes simplex encephalitis. Patients with defects and other higher-order prob- a slower, progressive course of visual lems of recognition, such as proso- dysfunction may have posterior corti- pagnosia and topographagnosia. cal atrophy or the Heidenhain variant Not all color function is lost in of Creutzfeldt-Jakob disease. At the patients with achromatopsia; special other end of the spectrum from tests can show evidence of retained neurodegeneration, increased recog- red/green and blue/yellow color nition exists that some people are opponency that is based on processing born with a selective visual agnosia, by retinal ganglion cells. This residual as has been described, for example, in ability is likely responsible for the fact congenital prosopagnosia3 and devel- that such patients can perceive bound- opmental topographic disorientation.4 aries between areas of different colors, In some cases the deficit appears to but cannot identify what the respective run in families, suggesting an inherited colors are.7 Clinically, this can lead to genetic defect. the phenomenon in which they cannot read the Ishihara plates up close (at a SYNDROMES OF THE VENTRAL distance where they can see the dots, STREAM and, hence, the visible boundaries are Achromatopsia those between each dot and the white Acquired brain lesions can impair background), but can read the plates if color vision.5 Complete impairment they are far enough away that the dots is called achromatopsia, and patients merge, so that the only visible bound- with this condition see the world in aries are those between red and green grayscale (Case 7-1). Some patients regions. Continuum (Minneap Minn) 2014;20(4):922–941 www.ContinuumJournal.com 923 Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited. Higher Cortical Visual Deficits Case 7-1 A 41-year-old man awoke one day with a sense of distortion between the right and left halves of his vision, along with nausea and imbalance. A CT scan showed a left occipital infarction and a right vertebral arterial dissection. The next day in the hospital the patient had a right occipital infarction and noted many visual problems, which slowly improved over time. He had trouble recognizing faces, seeing their shapes, and identifying ethnicity and age of faces. Everyone appeared good-looking. He recognized people by their voices, clothing, physical posture, facial moles, or hairstyles. He could not visualize the faces of well-known actors when he heard their names. Initially the world appeared black and white, but later he saw some color tints, although he had trouble distinguishing colors that were similar to each other, such as blue and green. Although the patient was a sports car enthusiast, all cars looked the same to him. He could not recognize different buildings, which all looked like a ‘‘bunch of squares.’’ He had trouble navigating his neighborhood and got lost following a short but twisting route to the supermarket across the street. His memory for daily events was poor, causing problems. On examination, the patient’s visual acuity was normal, but he had bilateral superior altitudinal defects (Figure 7-1). The Farnsworth-Munsell color test showed severe difficulties with color discrimination (Figure 7-2). He recognized 47 of 50 words on the Warrington Recognition Memory Test but only 28 of 50 faces. Only 60% of celebrity faces were familiar, even though he recognized 100% of their names. He also performed poorly on a test of his ability to visualize the shapes and features of famous faces. MRI showed bilateral occipitotemporal ischemic lesions involving
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