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The visuomotor symptoms (optic ataxia) can be accounted for by both visual and proprioceptive mislocalizations in an oculocentric reference frame, leading to field and hand effects, respectively. This new pathophysiological account is presented along with a model of posterior parietal cortex organization in which the superior part is devoted to covert attention, while the right inferior part is involved in visual remapping. When the right inferior parietal cortex is damaged, additional representational mislocalizations across saccades worsen the clinical picture of peripheral mislocalizations due to an impairment of covert attention.Alexia refers to a reading disorder caused by some form of acquired brain pathology, most commonly a stroke or tumor, in a previously literate subject. In neuropsychology, a distinction is made between central alexia (commonly seen in aphasia) and peripheral alexia (a perceptual or attentional deficit). The prototypical peripheral alexia is alexia without agraphia (pure alexia), where patients can write but are impaired in reading words and letters. selleck compound Pure alexia is associated with damage to the left ventral occipitotemporal cortex (vOT) or its connections. Hemianopic alexia is associated with less extensive occipital damage and is caused by a visual field defect, which creates problems reading longer words and passages of text. Reading impairment can also arise due to attentional deficits, most commonly following right hemisphere or bilateral lesions. Studying patients with alexia, along with functional imaging studies of normal readers, has improved our understanding of the neurobiological processes involved in reading. A key question is whether an area in the left ventral occipitotemporal cortex is specialized for or selectively involved in word processing, or whether reading relies on tuning of more general purpose perceptual areas. Reading deficits may also be observed in dementia and traumatic brain injury, but often with less consistent deficit patterns than in patients with focal lesions.We generate mental representations of space to facilitate our ability to remember things and navigate our environment. Many studies implicitly assume that these representations simply reflect the environments that they represent without considering other factors that influence the extent to which this is the case. Here, we bring together findings from cognitive psychology, environmental psychology, geography, urban planning, and neuroscience to discuss how internalizing the environment involves a complex interplay between bottom-up and top-down mental processes and depends on key characteristics of the physical environment itself. We describe how mental space is structured, the ways in which mental and physical space converge and diverge, and the disparate but complementary techniques used to assess these relationships. Finally, we contextualize this knowledge in the clinical populations affected by acquired and developmental topographical disorientation, exploring mechanisms that cause these patients to get lost in familiar surroundings.Face recognition is a form of expert visual processing. Acquired prosopagnosia is the loss of familiarity for facial identity and has several functional variants, namely apperceptive, amnestic, and associative forms. Acquired forms are usually caused by either occipitotemporal or anterior temporal lesions, right or bilateral in most cases. In addition, there is a developmental form, whose functional and structural origins are still being elucidated. Despite their difficulties with recognizing faces, some of these subjects still show signs of covert recognition, which may have a number of explanations. Other aspects of face perception can be spared in prosopagnosic subjects. Patients with other types of face processing difficulties have been described, including impaired expression processing, impaired lip-reading, false familiarity for faces, and a people-specific amnesia. Recent rehabilitative studies have shown some modest ability to improve face perception in prosopagnosic subjects through perceptual training protocols.The term visual agnosia is used to refer to recognition disorders that are confined to the visual modality, that are not due to an impairment in sensory functions, and that cannot be explained by other cognitive deficits or by general reduction in intellectual ability. Here, we describe the different types of visual agnosia that have been reported (form agnosia, integrative agnosia, associative agnosia, transformational and orientation agnosia as well as category-specific impairments such as pure alexia and prosopagnosia) and how they relate to the current understanding of visual object recognition. Together with related disorders such as simultanagnosia, texture agnosia, aphantasia, and optic aphasia, these visual perceptual impairments can have severe consequences for those affected. We suggest how in-depth assessment can be carried out to determine the type and the extent of these impairments. In the context of clinical assessment, a step-by-step approach reflecting a posterior to anterior gradient in visual object recognition, from more perceptual to more memory-related processes, is suggested. Individually tailored interventions targeting the identified impairments can be initiated based on the results of the assessment.Color is a fundamental aspect of normal visual experience. This chapter provides an overview of the role of color in human behavior, a survey of current knowledge regarding the genetic, retinal, and neural mechanisms that enable color vision, and a review of inherited and acquired defects of color vision including a discussion of diagnostic tests.Amblyopia is a neurodevelopmental abnormality that results in physiological alterations in the visual pathways and impaired vision in one eye, less commonly in both. It reflects a broad range of neural, perceptual, oculomotor, and clinical abnormalities that can occur when normal visual development is disrupted early in life. Aside from refractive error, amblyopia is the most common cause of vision loss in infants and young children. It causes a constellation of perceptual deficits in the vision of the amblyopic eye, including a loss of visual acuity, position acuity, and contrast sensitivity, particularly at high spatial frequencies, as well as increased internal noise and prolonged manual and saccadic reaction times. There are also perceptual deficits in the strong eye, such as certain types of motion perception, reflecting altered neural responses and functional connectivity in visual cortex (Ho et al., 2005). Treatment in young children consists of correction of any refractive error and patching of the strong eye.