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We begin with the functions of the striate cortex (area V1 of the visual cortex) and end with a review of the effects of damage to striate cortex or its inputs; namely, homonymous hemifield defects. Clinical and anatomical studies accrued over the past 25 years have modified our understanding of the role of V1 in vision. We discuss the evidence that V1 is not the sole recipient of visual signals; is not the earliest recipient of visual signals; and is not essential for conscious vision. In the second section, we give a brief history of how the visual field was found to be represented in striate cortex, then cover the work that has demonstrated the overrepresentation of the central region of vision in humans. The common patterns of visual field disturbance caused by damage to the retrochiasmal visual system are discussed, with some less common examples shown as brief case studies.

While there is a long history of rehabilitation for motor deficits following cerebral lesions, less is known about our ability to improve visual deficits. Vision therapy, prisms, occluders, and filters have been advocated for patients with mild traumatic brain injury, on the premise that some of their symptoms may reflect abnormal visual or ocular motor function, but the evidence for their efficacy is modest. For hemianopia, attempts to restore vision have had unimpressive results, though it appears possible to generate blindsight through training. Strategic approaches that train more efficient use of visual search in hemianopia have shown consistent benefit in visual function, while prism aids may help some patients. There are many varieties of alexia. Strategic adaptation of saccades can improve hemianopic alexia, but there has been less work and mixed results for pure alexia, neglect dyslexia, attentional dyslexia, and the central dyslexias. A number of approaches have been tried in prosopagnosia, with recent studies of small groups suggesting that face perception of prosopagnosic subjects can be enhanced through perceptual learning.

Motor conversion disorder (CD) entails genuine disturbances in the subjective experience of patients who maintain they are unable to perform a motor function, despite lack of apparent neurological damage. Abilities by which individuals assess their own capacities during performance in a task are called metacognitive, and distinctive impairment of such abilities is observed in several disorders of self-awareness such as blindsight and anosognosia. In CD, previous research has focused on the recruitment of motor and emotional brain systems, generally linking symptoms to altered limbic-motor interactions; however, metacognitive function has not been studied to our knowledge. Here we tested ten CD patients and ten age-gender matched controls during a visually-guided motor paradigm, previously employed in healthy controls (HC), allowing us to probe for motor awareness and metacognition. Participants had to draw straight trajectories towards a visual target while, unbeknownst to them, deviations were occasionally introduced in the reaching trajectory seen on the screen. Participants then reported both awareness of deviations and confidence in their response. Activity in premotor and cingulate cortex distinguished between conscious and unconscious movement corrections in controls better than patients. Critically, whereas controls engaged the left superior precuneus and middle temporal region during confidence judgments, CD patients recruited bilateral parahippocampal and amygdalo-hippocampal regions instead. These results reveal that distinct brain regions subserve metacognitive monitoring for HC and CD, pointing to different mechanisms and sources of information used to monitor and form confidence judgments of motor performance. While brain systems involved in sensory-motor integration and vision are more engaged in controls, CD patients may preferentially rely on memory and contextual associative processing, possibly accounting for how affect and memories can imbue current motor experience in these patients.

In this article we will present evidence that attention modulates awareness, but we have some awareness of unattended stimuli. Specifically, we will argue that attention is needed to solve the binding problem. Without attention, one can be aware of what object attributes are present in the scene, which allows for a surprising level of visual awareness, such as whether a given scene contains an animal or not. However, attention is needed to determine how the object attributes are related or “bound” together, so attention is needed to create coherent mental representations of the objects in the scene.

Studies of cortical blindness have suggested that some residual visual function may persist without perceptual awareness, a condition known as blindsight. To investigate electrophysiological evidence of unconscious processing of emotional stimuli, we examined the event-related oscillations (EROs) in a 62 year-old male patient (TN) with affective blindsight during random stimulation of three facial expressions (fearful, happy and neutral).Spectral power analysis in response to the different emotions revealed significant differences between fearful and happy faces over the right frontal regions at 7–8 Hz (low α), and between emotional and neutral faces over the left frontal sites at 12–13 Hz (low β) in a time period between 100–400 ms after visual stimulus onset.These results demonstrate that emotional face processing occurs very early in time in the absence of any functional striate cortex, and further reveals the existence of specific oscillatory frequencies that reflect unconscious processing of facial expressions in affective blindsight.Keywords: Affective blindsight, Brain oscillations, Time frequency analysis, Hemispheric asymmetry, Emotion

The scientific study of the cerebral substrate of consciousness has been marked by significant recent achievements, resulting partially from an interaction between the exploration of cognition in both brain-damaged patients and healthy subjects. Several neuropsychological syndromes contain marked dissociations, which permit the identification of principles related to the neurophysiology of consciousness. The generality of these principles can then be evaluated in healthy subjects using a combination of experimental psychology paradigms, and functional brain-imaging tools. This chapter re-updates and extends a precedent review focusing on visual phenomenal consciousness, which is the aspect of consciousness most frequently investigated in neuroscience. Through the exploration of neuropsychological syndromes such as “blindsight,” visual form agnosia, optic ataxia, visual hallucinations, neglect but also Capgras delusion and split-brain cognition, I highlight several general principles and explain how their generality has been demonstrated in healthy subjects using conditions such as visual illusions or subliminal perception. Finally, I describe the bases of a scientific model of consciousness, based on the concept of a “global workspace,” which takes into account the data reviewed.

The visual system binds and segments the elements of an image into coherent objects and their surroundings. Recent findings demonstrate that primary visual cortex is involved in this process of figure-ground organization. In the primary visual cortex the late part of a neural response to a stimulus correlates with figure-ground segregation and perception. Such a late onset indicates an involvement of feedback projections from higher visual areas. To investigate the possible role of feedback in figure-ground perception we removed dorsal extra-striate areas of the monkey visual cortex. The findings show that figure-ground perception is reduced when the figure is presented in the lesioned hemifield and perception is normal when the figure appeared in the intact hemifield. In conclusion, our observations show the importance for recurrent processing in visual perception.

Although work in primates on higher-order visual areas has revealed how the individual and concerted activity of neurons correlates with behavioral reports of object recognition, very little is known about the underlying mechanisms for visual recognition memory. Low-level vision, even as early as primary visual cortex (V1) and even in subjects as unsophisticated as rodents, promises to fill this void. Although this latter approach sacrifices interrogation of many of the most astounding features of visual recognition, it does provide experimental constraint, proximity to sensory input, and a wide range of interventional approaches. The tractability of rodent visual cortex promises to reveal the molecular mechanisms and circuits that are essential for a fundamental form of memory., National Eye Institute (Grant RO1EY023037)

Controversy surrounds the question of whether the experience sometimes elicited by visual stimuli in blindsight (type-2 blindsight) is visual in nature or whether it is some sort of non-visual experience. The suggestion that the experience is visual seems, at face value, to make sense. I argue here, however, that the residual abilities found in type-1 blindsight (blindsight in which stimuli elicit no conscious experience) are not aspects of normal vision with consciousness deleted, but are based fragments of visual processes that, in themselves, would not be intelligible as visual experiences. If type-2 blindsight is a conscious manifestation of this residual function then it is not obvious that type-2 blindsight would be phenomenally like vision.

The primate orbitofrontal cortex receives inputs directly from the inferior temporal visual cortex. The orbitofrontal cortex contains visual neurons that learn in one trial which visual object is associated with a reward such as a taste and represent reward value; error neurons that respond if there is a mismatch between the reward expected based on the visual input, and the (taste) reward actually obtained; neurons that respond to the sight of faces encoding information about identity or about expression; and neurons that respond to novel visual stimuli. The human orbitofrontal cortex is activated by visual stimuli that show how much monetary reward has been obtained; and by mismatches in a visual discrimination reversal task between the face expression expected, and that obtained. Discrete lesions of the human orbitofrontal cortex impair visual discrimination reversal and face expression (but not face identity) discrimination. Thus the orbitofrontal cortex plays a fundamental role in visual processing related to emotion.

A brief overview of the most important cognitive alterations as a consequence of focal brain damage is presented. The discipline that studies the relationship between brain damage and higher cognitive functions is called neuropsychology and is mainly based on correlations between anatomy and function. Leaving aside the importance of the clinical impact that neuropsychology has on patients' treatment, its main experimental aim is to draw inferences from the pathological conditions to normal functions, on the assumption that if the lesion to a particular brain area or circuit has provoked a specific deficit, then that part of the brain is involved in or is necessary for sustaining the normal function. The main classical neuropsychological syndromes related to perceptual, spatial, linguistic, motor, and memory domain will be discussed, with a final part on syndromes in which conscious awareness is specifically altered.

Dysfunction of the lateral geniculate nucleus or its cerebral projections impairs vision. Hemianopia is the typical deficit associated with lesions in the primary geniculocalcarine visual pathway. It is characterized by impairment of visual perception to one side of midline. Details of the resulting visual field defect carry localizing and functional significance. Bilateral central visual pathway damage can produce profound generalized defects in perception. Common causes of persistent cerebral visual loss include stroke, hemorrhage, and tumors. Transient defects may result from migraine, focal seizure, or transient ischemic attack.

Vision is central to human experience. The neural substrate of vision is a network of cortical and subcortical brain areas, organized in partially segregated but interacting processing streams. Collectively, neurons across this network analyze the various components of the visual scene, which are then assembled into a coherent visual percept. Dysfunctions of the visual system range from scotomas, in which vision in part of the visual field is diminished or absent, to impairments of high-order visual functions that result in perplexing neurological symptoms such as deficiency in face recognition or an inability to distinguish between self- and externally generated motion. Advances in imaging and neural-stimulation techniques are paving the way to novel treatments of visual abnormalities and provide invaluable research tools to elucidate the neural basis of vision.

A significant proportion of human cortex is involved in visual processing. Cerebral regions beyond striate cortex show specialization for specific stimulus properties: damage to these regions leads to syndromes that also reflect this specialization. These syndromes can be grouped into two broad categories. In the ventral group, there is damage to medial occipitotemporal structures that participate in object identification and recognition. This can result in a variety of syndromes, including achromatopsia, general visual object agnosia, or more selective object recognition deficits such as prosopagnosia, alexia, and certain forms of topographagnosia, such as landmark agnosia. In the second, dorsal group, there is damage to lateral occipitoparietal structures that participate in visuospatial processing and localization. Patients with such damage may have akinetopsia (impaired motion processing), various components of Balint syndrome, or astereopsis. Finally, it is also possible to find patients in whom residual visual processing is evident despite damage to the geniculostriate pathway; this blindsight may reflect residual function of either subcortical structures, such as the superior colliculus, or alternate afferent routes to surviving extrastriate cortex.

Patient RP suffers a unilateral right homonymous quadrant anopia but demonstrates better than chance discrimination for stimuli presented in the blind field at temporal frequencies between 33 and 47 Hz (all significant at p

Publisher Summary This chapter provides an overview of vision that may be the most important of the five senses for getting around in everyday life and getting things done. Primary visual cortex seems to be important for the ability to perceive any visual feature at all, while higher brain areas may be important for perceiving particular visual features or objects. The chapter outlines the functional properties of neurons, as visual signals travel up from the retina to the primary visual cortex and onward to higher areas in the dorsal and ventral visual pathways. Progressing up the visual pathway, receptive fields gradually become larger and respond to more complex stimuli, following the hierarchical organization of the visual system. V1 is selective for many visual features, including orientation, motion, and binocular disparity. Damage to V1 can severely impair or eliminate conscious vision, although remaining activity in extrastriate areas may support the ability to detect visual events even without being visually conscious, the condition called blindsight.

Conscious awareness can be assessed by a number of behavioral and brain-based measures, each presupposing different theories of the nature of consciousness. Such measures can be used to indicate the effects of stimuli people are not conscious of; the effects of mental states people are not conscious of (in the domains of both perception and learning); and the overall level of consciousness of an individual. Finally, the different theories imply different possible functions of consciousness.

The primate orbitofrontal cortex receives inputs directly from the inferior temporal visual cortex. The orbitofrontal cortex contains different types of neurons: visual neurons that learn in one trial which visual object is associated with a reward such as a taste; error neurons that respond if there is a mismatch between the reward expected, based on the visual input, and the (taste) reward actually obtained; neurons that respond to the sight of faces, encoding information about identity or about expression; and neurons that respond to novel visual stimuli. The human orbitofrontal cortex is activated by visual stimuli that show how much monetary reward has been obtained and by mismatches in a visual discrimination reversal task between the face expression expected and that obtained. Discrete lesions of the human orbitofrontal cortex impair visual discrimination reversal and face expression (but not face identity) discrimination. Thus the orbitofrontal cortex plays a fundamental role in visual processing related to emotion.

The scientific study of the cerebral substrate of consciousness has been marked by significant recent achievements, resulting partially from an interaction between the exploration of cognition in both brain-damaged patients and healthy subjects. Several neuropsychological syndromes contain marked dissociations, which permit the identification of principles related to the neurophysiology of consciousness. The generality of these principles can then be evaluated in healthy subjects using a combination of experimental psychology paradigms, and functional brain-imaging tools. This chapter re-updates and extends a precedent review focusing on visual phenomenal consciousness, which is the aspect of consciousness most frequently investigated in neuroscience. Through the exploration of neuropsychological syndromes such as “blindsight,” visual form agnosia, optic ataxia, visual hallucinations, neglect but also Capgras delusion and split-brain cognition, I highlight several general principles and explain how their generality has been demonstrated in healthy subjects using conditions such as visual illusions or subliminal perception. Finally, I describe the bases of a scientific model of consciousness, based on the concept of a “global workspace,” which takes into account the data reviewed.

An understanding of the neural basis of perceptual awareness requires solving two problems. First, the brain mechanisms that regulate access to conscious perceptual experience need to be identified. Second, the brain regions encoding the contents of consciousness have to be localized. This article deals with the neural mechanisms of perceptual experience in the visual modality. A number of different experimental approaches will be presented and their implications for mechanisms of awareness will be discussed. This reveals that the contents of perceptual experiences are encoded in distributed subregions of modality-specific cortex. In addition, a multitude of brain regions including prefrontal cortex control the access to consciousness.

This article discusses the influence of selective attention on consciousness. It is argued that attention is necessary, although not sufficient, for the awareness of the relationship or conjunction of different aspects of a scene or object. It is suggested that a primary function of attention is to permit the binding of features into recognizable objects. When attention is occupied elsewhere, there is a degree of awareness of the presence of visual features, though not of their relationships, and this may allow one to perform certain simple tasks such as determining whether an image includes either an animal or a vehicle.

Blind people must adjust by using their remaining senses to interact with their environment. Adjustments occur even in adults with late-onset blindness and transiently in visually deprived sighted individuals. Section 6.18.1 discusses reading braille as an example adjustment that depends on information transmitted from specific mechanoreceptors in the fingertips. When blind people learn to discriminate subtle patterns of raised dots and to translate these into linguistic information, they extensively practice motor and perceptual skills. Additionally, blind people must utilize nonvisual information in all aspects of daily existence. As a consequence, blind individuals exhibit performance advantages in attending to touch. They also excel at several auditory tasks, but these skills will not be considered here. Section 6.18.2 argues that heightened acuity occurs in tasks that require practice in processing tactile information. Furthermore, prior visual experience influences, especially, spatial perception, and this impacts the artistic and spatial cognitive skills of blind people. Section 6.18.3 reviews the evidence that an expanded somatosensory cortex representation for the braille reading finger(s) in blind people is an example alteration that possibly underlies enhanced tactile acuity. However, findings in blind people do not consistently indicate somatosensory cortex reorganization, nor do they reveal an underlying Hebbian mechanism of enhanced synaptic efficacy. Section 6.18.4 explores evidence of more dramatic plasticity – cross-modal tactile and auditory inputs activating visually deprived occipital cortex. Visual deprivation, whether permanent in blind people or transient through blindfolding sighted persons, apparently does not silence visual cortex, which adjusts by processing nonvisual modalities. A significant question is whether altered visual cortex activity provides for relevant adjustments to blindness. Evidence is reviewed regarding which perceptual and cognitive processes activate visual cortex in early- and late-onset blind people. An important issue is whether reorganized visual cortex follows functional subdivisions that resemble those identified in sighted people. Section 6.18.5 examines whether inherent capabilities, unmasked by visual deprivation, contribute to visual cortex plasticity and whether cross-modal responses reflect new or physiologically altered connections. Possible anatomical and physiological sources of cross-modal inputs to visual cortex are described. However, limited evidence links these to explicit visual cortex reorganization in blindness. A mostly hypothetical discussion considers whether visual cortex reorganizes through changes in effective intracortical connectivity from multisensory areas.

It is usually taken as given that consciousness involves superior or more elaborate forms of information processing. Contemporary models equate consciousness with global processing, system complexity, or depth or stability of computation. This is in stark contrast with the powerful philosophical intuition that being conscious is more than just having the ability to compute. I argue that it is also incompatible with current empirical findings. I present a model that is free from the strong assumption that consciousness predicts superior performance. The model is based on Bayesian decision theory, of which signal detection theory is a special case. It reflects the fact that the capacity for perceptual decisions is fundamentally limited by the presence and amount of noise in the system. To optimize performance, one therefore needs to set decision criteria that are based on the behaviour, i.e. the probability distributions, of the internal signals. One important realization is that the knowledge of how our internal signals behave statistically has to be learned over time. Essentially, we are doing statistics on our own brain. This 'higher-order' learning, however, may err, and this impairs our ability to set and maintain optimal criteria for perceptual decisions, which I argue is central to perception consciousness. I outline three possibilities of how conscious perception might be affected by failures of 'higher-order' representation. These all imply that one can have a dissociation between consciousness and performance. This model readily explains blindsight and hallucinations in formal terms, and is beginning to receive direct empirical support. I end by discussing some philosophical implications of the model.

What is the role the primary visual cortex (V1) in vision? Is it necessary for conscious sight, as indicated by the cortical blindness that results from V1 destruction? Is it even necessary for blindsight, the nonreflexive visual functions that can be evoked with stimuli presented to cortically blind fields? In the context of this controversial issue, I present evidence indicating that not only is blindsight possible, but that conscious vision may, to a varying degree, return to formerly blind fields with time and practice even in cases where functional neuroimaging reveals no V1 activation.

Publisher Summary This chapter illustrates that because vision is the primary sense, it is not surprising that a large part of the human brain is devoted to processing the image of the visual world to generate visual percept. Visual brain provides with a percept that is true to the external visual world. Visual percept, obtained from the information it receives from the two eyes, may sometimes be distorted as a result of physiological interactions among neurons in the visual brain because of the pattern of their connections. The visual brain also has to restrict what one sees as processing all the visual information received by the eyes would require a visual brain much larger than ours.

Many theories of emotion propose that emotional input is processed preferentially due to its relevance for the organism. Further, because consciousness has limited capacity, these considerations imply that emotional input ought to be processed even if participants are perceptually unaware of the input (subliminal perception). Although brain imaging has studied effects of unattended, suppressed (in binocular rivalry), and visually masked emotional pictures, conclusions regarding subliminal perception have been mixed. The reason is that subliminal perception demands a concept of an awareness threshold or limen, but there is no agreement on how to define and measure this threshold. Although different threshold concepts can be identified in psychophysics (signal detection theory), none maps directly onto perceptual awareness. Whereas it may be tempting to equate unawareness with the complete absence of objective discrimination ability (d′=0), this approach is incompatible with lessons from blindsight and denies the subjective nature of consciousness. This review argues that perceptual awareness is better viewed as a continuum of sensory states than a binary state. When levels of awareness are characterized carefully in terms of objective discrimination and subjective experience, findings can be informative regarding the relative independence of effects from awareness and the potentially moderating role of awareness in processing emotional input. Thus, because the issue of a threshold concept may never be resolved completely, the emphasis is to not prove subliminal perception but to compare effects at various levels of awareness.

Publisher Summary Disorders of color vision can occur from retinal and cortical disorders. The most frequent abnormality in color perception (dyschromatopsia) is seen in color blindness because of photoreceptor genetic disorders. This chapter discusses the abnormalities in color perception because of the central nervous system lesions (acquired central achromatopsia or dyschromatopsia). Acquired central dyschromatopsia has been reported in disorders of the optic nerve and chiasma or in cerebral lesions (acquired cerebral achromatopsia). Cerebral achromatopsia has been reported limited to one hemifield (hemiachromatopsia) or involving all spared visual fields. The most frequent acquired central dyschromatopsia (ACD) is because of the optic neuritis, with desaturation in color appearance, abnormalities in the Ishihara plate test and other discrimination tests. In a prospective study on optic neuritis, Celesia et al. found that during the acute phase of the disease, all patients had abnormalities on color vision as tested with L’Anthony new color test. Recovery of vision varied for different visual functions. This differential recovery may reflect the patchy recovery of the optic nerve fibers and the persistence of isolated nerve fiber pathology, and is consistent with the concept of independent channels within the visual pathways. Other pathology affecting the optic nerve or the chiasma may produce ACD..

Publisher Summary This chapter discusses perception disorders, including the most severe acquired disorder of perception: cortical blindness. The cortically blind patient may be unable to perceive any visual stimulus or only have preserved rudimentary vision of light and shadows. Yet, some of these patients will deny their blindness and claim to be able to see (Anton's syndrome or visual anosognosia). Anosognosia of the visual deficit is also seen in hemianopic subjects (hemianopic anosognosia). In the current scheme of visual processing, cortical blindness is predicted when both primary visual cortices are disabled either because they are destroyed or because they are disconnected from the extrastriate visual areas. These issues are complex and relate to the difficult problem of brain and mind. To quote Zeki, “The study of the visual system is a profoundly philosophical enterprise; it entails an inquiry into how the brain acquires knowledge of the external word, which is no simple matter.”

The scientific study of the cerebral substrate of consciousness has been marked by significant recent achievements, resulting partially from an interaction between the exploration of cognition in both brain-damaged patients and healthy subjects. Several neuropsychological syndromes contain marked dissociations that permit the identification of principles related to the neurophysiology of consciousness. The generality of these principles can then be evaluated in healthy subjects using a combination of experimental psychology paradigms, and functional brain-imaging tools. In this chapter, I review some of the recent results relevant to visual phenomenal consciousness, which is an aspect of consciousness most frequently investigated in neuroscience. Through the exploration of neuropsychological syndromes such as “blindsight,” visual form agnosia, optic ataxia, visual hallucinations, and neglect, I highlight four general principles and explain how their generality has been demonstrated in healthy subjects using conditions such as visual illusions or subliminal perception. Finally, I describe the bases of a scientific model of consciousness on the basis of the concept of a “global workspace,” which takes into account the data reviewed.

Publisher Summary People who are partially blind due to brain damage or surgery that has compromised their visual system can occasionally respond to stimuli placed within their region of clinically defined blindness. This phenomenon has come to be called “blindsight” because the patients show “sight” where they are clinically “blind.” Blindsight, by its very nature, continues to be controversial. Their sight is not normal, in that, patients are often unaware of seeing anything presented within their blind field; however, they are often able to respond to stimuli presented within their blind field. This phenomenon—blindsight—has been operationally defined as “residual visual abilities within a field defect in the absence of acknowledged awareness.” This chapter discusses the history of blindsight, outlines the three prominent hypotheses regarding the neurobiological underpinnings of blindsight and describes research key to analyzing these hypotheses, and concludes with clinical implications concerning residual vision, blindsight and visual restitution.

After lesions of striate cortex in primates, there is still the capacity to detect and localize visual stimuli. In this chapter we review three aspects of our study of this phenomenon in macaques. First, we found that macaques that received their striate lesions as infants had considerably greater ability to detect and localize stimuli than those that received similar lesions as adults. Second, we suggest that the visual functions that survive striate lesions in macaques made in adulthood resemble those in human ‘blindsight’. Third, we report that monkeys with striate lesions made in infancy are able to discriminate direction of visual motion.

The aim of this chapter is to discuss evidence bearing on two related issues, namely, first, whether the neural pathways of subliminal perception are the same as those subserving suprathreshold perception. Second, whether the pathways for subliminal perception in normals are similar to those subserving blindsight in brain-damaged patients. As to the former question, the overall balance is in favor of the different-pathway hypothesis while a tentative answer to the second question might be that blindsight is basically similar to subliminal perception in normals. The differences undoubtedly existing between the two conditions depend mainly on the differences in the stimuli used to reveal them.

Background perturbation techniques using both static and dynamic luminance contrast and chromatic contrast noise have been employed to investigate the interaction between luminance and chromatic contrast signals. A number of experiments involving contrast detection thresholds for static stimuli, simple reaction times, and pupil color responses yield evidence for independent processing of luminance and color signals. One exception is the perception of color-defined coherent motion of randomly distributed checks when dynamic, luminance-defined, motion signals can disrupt completely the perception of coherent motion. When the moving stimulus contains color-defined, recognizable features that are spatially distinct from background noise, the perception of coherent motion is restored and becomes completely independent of dynamic luminance contrast noise. Feature-tracking mechanisms must therefore play a major part in the detection of color-defined motion. Other findings reveal the existence of a motion channel that receives exclusively achromatic inputs and a separate channel that extracts and combines luminance contrast and color-defined motion signals. Further studies carried out to investigate the interaction between luminance and chromatic signals show that color-defined, position-change thresholds are mediated by motion detection mechanisms and are, therefore, also disrupted by dynamic luminance contrast noise. In spite of the perceived uncertainty of spatial location, other experiments show that accurate, color-defined position information is preserved and available for use in other tasks. For example, accurate position information can be used to detect the vertical misalignment of color-defined checks, independently of luminance contrast noise, even when position-change thresholds are severely impaired. The analogy with 'blindsight' is obvious and irresistible. 'Blindsight' describes the ability to make accurate use of visual information in the absence of conscious visual perception. The findings that have emerged from this investigation reveal the ability of normal subjects to discard misleading, consciously perceived visual signals. The ability to override perception and to make good use of accurate visual information, in spite of misleading percepts, can best be described as 'Double-blindsight'.

The anatomical connections between visual areas can be organized in ‘feedforward’, ‘feedback’ or ‘horizontal’ laminar patterns. We report here four experiments that test the function of some of the feedback projections in visual cortex. Projections from V5 to V1 have been suggested to be important in visual awareness, and in the first experiment we show this to be the case in the blindsight patient GY. This demonstration is replicated, in principle, in the second experiment and we also show the timing of the V5–V1 interaction to correspond to findings from single unit physiology. In the third experiment we show that V1 is important for stimulus detection in visual search arrays and that the timing of V1 interference with TMS is late (up to 240 ms after the onset of the visual array). Finally we report an experiment showing that the parietal cortex is not involved in visual motion priming, whereas V5 is, suggesting that the parietal cortex does not modulate V5 in this task. We interpret the data in terms of Bullier's recent physiological recordings and Ahissar and Hochstein's reverse hierarchy theory of vision.

The past decade has provided a wealth of data for theorists of visual awareness. Two empirical approaches, both seeking to dissociate conscious from unconscious neural processes, have been particularly fruitful. The first has focused on the neural correlates of changes in experience occurring in the absence of change in external stimuli, for example during binocular rivalry; the second has investigated the neural correlates of unconscious processes such as blindsight. Several of the theories based on these data propose that visual consciousness arises from interactions between thalamo-cortical modules whose independent operation is unconscious; popular candidate 'modules' include visual regions in the 'ventral' visual pathway and parieto-frontal regions associated with action planning. These theories can be tested against recent findings from patients in the vegetative state, a state of 'wakefulness without awareness', which can follow major insults to the brain. The findings indicate that stimulus-evoked cortical activity occurs in the vegetative state, but tends to be limited in extent, is often restricted to primary sensory areas, and is poorly integrated with activity elsewhere in the cerebrum. The theories of visual awareness reviewed previously predict that such activity should not give rise to visual experience. This prediction is reassuring, but can we be sure that it is correct? Reflection on the indirect nature of the evidence available to theorists of visual awareness makes it doubtful that we can confidently specify the minimum conditions for awareness, unless we are prepared to modify our everyday concept of consciousness. O'Regan and Noe have recently proposed a sophisticated redefinition of visual awareness along these lines. Progress at this frontier of visual neuroscience requires that scientists and philosophers join forces to clarify the concepts of experience and consciousness.

Publisher Summary This chapter presents a study on disorders of higher visual function. The term "higher visual disorders" denotes visual deficits following injury to cortical brain structures. It is now generally accepted that the posterior brain is a patchwork of more than 30 functionally specialized visual areas, arranged in a modular form and with flexible networks to subserve complex visual abilities, for example, visual spatial orientation and visual recognition. Despite this functional segregation, isolated visual disorders are only rarely observed, as focal brain injury is seldom limited to one single visual cortical area. Under the aspects of diagnostics, the higher visual disorders caused by brain injury can be classified into two main groups—disorders of basic visual functions, for example, visual field and visual acuity, and disorders of complex visual abilities, for example, visual cognition. Not every procedure that shows positive results represents a clinically valid and useful method of treatment, which also fulfills the criteria of ecological validity and cost effectiveness. . The chapter discusses cerebral blindness, spatial contrast sensitivity, visual adaptation and color vision, visual illusions and hallucinations, and others.

Higher-order visual impairments are those that cannot be accounted for by deficits in visual acuity, visual fields, or gaze mechanisms. Most higher-order visual impairments are caused by lesions in visual association cortex (Brodmann's areas 18 and 19) or by the outflow from those regions to multimodal association cortex in the temporal lobe (particularly area 37) and hippocampus or in parietal lobes (particularly areas 7, 39, and 40). The clinical approach to these impairments is facilitated by the fact that the higher-order deficits are readily divided along three separate dimensions. The first dimension is lesion laterality. Damage to the left hemisphere causes deficits in processing visual stimuli for language content or associations. Deficits in processing visual material for some spatial relations, for some perceptual properties, and for some aspects of emotional content usually are caused by right hemisphere lesions. The second dimension is dorsal-ventral. Damage to the ventral (inferior) visual association cortex and pathways impairs discrimination and identification of stimuli: the "what" system. Damage to the dorsal (superior) visual association cortex and pathways impairs attentional, spatial, and kinesthetic analyses: the "where" system ( Table 141-1 ). The third dimension is the scale of visual attention. Attention can be paid to large components of a visual array, such as overall configuration, sometimes called global attention or a "floodlight." Attention can also be paid to small items within a visual array, such as specific letters or faces, sometimes called local attention or a "spotlight." In normal subjects under normal conditions, visual attention may be a composite of the two or switch between them, either unconsciously or consciously, as when searching for a face in a crowd. Damage to the left visual association cortex, particularly dorsal, reduces sensitivity to high spatial frequency (local or detailed) properties of stimuli. Damage to the right reduces sensitivity to low spatial frequency (global or configurational) aspects of stimuli. These differences in scale of attention underlie some of the characteristic findings of lateralized lesions: the markedly different error patterns in drawing and other spatial manipulations of visual stimuli and the very asymmetrical clinical manifestations of hemifield spatial neglect after right or left brain lesions.

Publisher Summary This chapter discusses insight and its conceptualization and assessment. Insight refers to the various cognitive functions and mental phenomena. Insight is an understanding of the motivations behind an individual's thoughts or behaviors. It is the recognition of the sources of an individual's emotional or mental problems. Terms— such as insight, judgment, knowledge, and metacognition are often used interchangeably in academic and clinical settings. The phenomena of blindsight and the phantom limb highlight the differences when these concepts operate relatively independently. Blind sighted individuals learn over time to orient toward light, identify the presence and absence of stimuli, discriminate shapes and edges, and can avoid obstacles while walking or running. It appears that blindsight, or unconscious vision, is made possible as the brain recruits intact pathways of the primitive subcortical mammalian visual pathway that are not normally used in humans and monkeys. Insight remains a somewhat vague and certainly complex construct that appears multi-determined and, likewise, influenced by many more internal and external factors.

In this paper, we present work that started as an interest in visual consciousness with the study of the blindsight phenomena and color processing. This led us to develop an intraocular reflection and absorption model of the human eye that is sufficient to account for luminance and color detection in blindsight subjects. Luminance and color thresholds were obtained in the good and blind field of hemidecorticated patients under controlled conditions. To determine the role of internal scatter and absorption properties of the human eye we tested the model predictions in three ways. By psychophysical means, by measuring absorption and scatter properties of the human eye, and by building an electromechanical sensor apparatus mimicking Lambertian reflection in the eye. The results of the simulations and measurements support the notion that the sensitivity functions obtained with the hemidecorticated patients can be explained by reflection and absorption properties of the human eye that have not been fully accounted for in the blindsight literature. In the light of such findings, future blindsight experiments must necessarily account for intraocular absorption and reflective properties of the human eye of the type described.

Blindsight, residual visual function in the absence of conscious awareness, can sometimes be found within the scotomas of patients with lesions to primary visual cortex. However, cases in which blindsight is distributed across large regions of a scotoma are extremely rare. In contrast, blindsight is relatively frequent within small islands of residual visual function. We review the evidence for the existence of these islands. We argue that blindsight is likely to depend on vestiges of geniculostriate function, and that in humans the secondary retinotectal pathway has little functional utility in the absence of geniculostriate support. To account for the frequency of blindsight within residual islands of function, we speculate that patients may be unaware of such islands precisely because they are islands, which are isolated from the integrated network of neural activity that represents visual space. The relationship of blindsight to the hemispatial neglect is considered in this context.

Perception without awareness denotes the fact that a stimulus exerts causal influence on mental processes or behavior without being phenomenally experienced. The main challenge has been to demonstrate that perception without awareness exists. The article reports several routes aimed at demonstrating perception without awareness, for example, presentation of stimuli below threshold or examining patients who suffer from blindsight. More recently, qualitative dissociations between perception with and without awareness have been found. Future research may aim at establishing the durability of unconscious perceptual effects and at finding neural pathways related to perception without awareness.

Destruction of the striate cortex has traditionally been thought to lead to permanent blindness in the contralateral visual field and to the dogma that this region is indispensable for vision in primates. For over 25 years now, evidence has been accumulating that hemianopic human subjects and monkeys possess wide-ranging residual visual capacities or 'blindsight' in the blind part of their visual field. For some researchers, isolated islands of the striate cortex have been associated with patches of degraded vision and made responsible for blindisight. Artefacts such as light scatter, criterion effects, macular sparing, eccentric fixation and minute eye movements have also been linked with the residual vision. For others, the fact that certain aspects of the visual information can be processed without the geniculostriate pathway suggests mediation by the visual subsystems such as extrastriate visual cortical areas which receive visual information via subcortical pathways, that escaped the cortical damage. Subjects who have had a whole cerebral hemisphere removed or disconnected (for the treatment of uncontrollable epilepsy) and who show residual vision in their blind field offer a remarkable opportunity to help clear the controversy regarding the neural substrate of blindsight. Because it is certain that no functional striate or extrastriate cortex remains on the ablated side, these subjects have contributed significantly to identifying the critical pathways involved in blindsight.

This chapter focuses on the visual awareness. Visual self-awareness is only useful for primates in a social setting. Self-awareness helps human to quantitate certain characteristics of others such as tallness, thinness, beauty, and so on. Patients with two unusual brain conditions have symptoms that support the notion that a visual awareness center exists. The first condition, known as “denial of blindness” or Anton's syndrome, is usually caused by a tumor or injury of the brain or a cerebral vascular stroke that affects both sides of the visual cortex. The visual awareness center is probably working in these patients. However, they are responding to imagined images instead of the real ones and they do not seem to appreciate the difference. There is a second neurologic syndrome that adds further support to the argument that there exists a center of visual awareness. It is a condition known as blind sight. These patients have also suffered severe damage to their visual cortex. Using conventional visual field testing, they too are either totally blind or blind in a sizable part of their visual field.