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In primates including humans, most retinal ganglion cells send signals to the lateral geniculate nucleus (LGN) of the thalamus. The anatomical and functional properties of the two major pathways through the LGN, the parvocellular (P) and magnocellular (M) pathways, are now well understood. Neurones in these pathways appear to convey a filtered version of the retinal image to primary visual cortex for further analysis. The properties of the P-pathway suggest it is important for high spatial acuity and red-green color vision, while those of the M-pathway suggest it is important for achromatic visual sensitivity and motion vision. Recent work has sharpened our understanding of how these properties are built in the retina, and described subtle but important nonlinearities that shape the signals that cortex receives. In addition to the P- and M-pathways, other retinal ganglion cells also project to the LGN. These ganglion cells are larger than those in the P- and M-pathways, have different retinal connectivity, and project to distinct regions of the LGN, together forming heterogenous koniocellular (K) pathways. Recent work has started to reveal the properties of these K-pathways, in the retina and in the LGN. The functional properties of K-pathways are more complex than those in the P- and M-pathways, and the K-pathways are likely to have a distinct contribution to vision. Nanvuranlat They provide a complementary pathway to the primary visual cortex, but can also send signals directly to extrastriate visual cortex. At the level of the LGN, many neurones in the K-pathways seem to integrate retinal with non-retinal inputs, and some may provide an early site of binocular convergence.For over a century, research has demonstrated that damage to primary visual cortex does not eliminate all capacity for visual processing in the brain. From Riddoch's (1917) early demonstration of intact motion processing for blind field stimuli, to the iconic work of Weiskrantz et al. (1974) showing reliable spatial localization, it is clear that secondary visual pathways that bypass V1 carry information to the visual brain that in turn influences behavior. In this chapter, we briefly outline the history and phenomena associated with blindsight, before discussing the nature of the secondary visual pathways that support residual visual processing in the absence of V1. We finish with some speculation as to the functional characteristics of these secondary pathways.Visual imagery allows us to revisit the appearance of things in their absence and to test out virtual combinations of sensory experience. Visual imagery has been linked to many cognitive processes, such as autobiographical and visual working memory. Imagery also plays symptomatic and mechanistic roles in neurologic and mental disorders and is utilized in treatment. A large network of brain activity spanning frontal, parietal, temporal, and visual cortex is involved in generating and maintain images in mind. The ability to visualize has extreme variations, ranging from completely absent (aphantasia) to photo-like (hyperphantasia). The anatomy and functionality of visual cortex, including primary visual cortex, have been associated with individual differences in visual imagery ability, pointing to a potential correlate for both aphantasia and hyperphantasia. Preliminary evidence suggests that lifelong aphantasia is associated with prosopagnosia and reduction in autobiographical memory; hyperphantasia is associated with synesthesia. Aphantasic individuals can also be highly imaginative and are able to complete many tasks that were previously thought to rely on visual imagery, demonstrating that visualization is only one of many ways of representing things in their absence. The study of extreme imagination reminds us how easily invisible differences can escape detection.As we live in a dynamic world, motion is a fundamental aspect of our visual experience. The advent of computerized stimuli has allowed controlled study of a wide array of motion phenomena, including global integration and segmentation, speed and direction discrimination, motion aftereffects, the optic flow that accompanies self-motion, perception of object form derived from motion cues, and point-light biological motion. Animal studies first revealed the existence of a motion-selective region, the middle temporal (MT) area, also known as V5, located in the lateral occipitotemporal cortex, followed by areas such as V5A (also known as MST, the middle superior temporal area), V6/V6A, the ventral intraparietal area, and others. In humans there are rare cases of bilateral lesions of the V5/V5A complex causing cerebral akinetopsia, a severe impairment of motion perception. Unilateral V5/V5A lesions are more common but cause milder asymptomatic deficits, often limited to the contralateral hemifield, while parietal lesions can impair perception of point-light biological motion or high-level motion tasks that are attentionally demanding. Impairments of motion perception have also been described in optic neuropathy, particularly glaucoma, as well as Alzheimer's disease, Parkinson's disease with dementia, and dementia with Lewy body disease. Prematurity with or without periventricular leukomalacia and developmental syndromes such as Williams' syndrome, autism, and dyslexia have also been associated with impaired motion perception, suggesting a developmental vulnerability of the dorsal pathway.This chapter starts by reviewing the various interpretations of Bálint syndrome over time. We then develop a novel integrative view in which we propose that the various symptoms, historically reported and labeled by various authors, result from a core mislocalization deficit. This idea is in accordance with our previous proposal that the core deficit of Bálint syndrome is attentional (Pisella et al., 2009, 2013, 2017) since covert attention improves spatial resolution in visual periphery (Yeshurun and Carrasco, 1998); a deficit of covert attention would thus increase spatial uncertainty and thereby impair both visual object identification and visuomotor accuracy. In peripheral vision, we perceive the intrinsic characteristics of the perceptual elements surrounding us, but not their precise localization (Rosenholtz et al., 2012a,b), such that without covert attention we cannot organize them to their respective and recognizable objects; this explains why perceptual symptoms (simultanagnosia, neglect) could result from visual mislocalization.