Blindsight is a kind of residual vision found in people with lesions to V1. Subjects with blindsight typically report no visual awareness, but they are nonetheless able to make above-chance guesses about the shape, location, color and movement of visual stimuli presented to them in their blind field. A different kind of blindsight, sometimes called type 2 blindsight, is a kind of residual vision found in patients with V1 lesions in the presence of some residual awareness. Type 2 blindsight differs (...) from ordinary visual experience in lacking the particularity, transparency and fine-grainedness often taken to be essential to visual experience, at least in veridical cases. I argue that the case of type 2 blindsight provides a counterexample to the view that these characteristics are essential to veridical visual experience and that this gives us reason to resist the view that visual experience is essentially a perceptual relation to external objects. In the second part of the paper I argue that the case of type 2 blindsight yields important insights into the effects of attentional modulation on perceptual content and that cases of attentional modulation of appearance are not at odds with the view that the phenomenology of visual experience flows from its content. (shrink)

This review considers a number of recent theories on the neural basis of consciousness, with particular attention to the theories of Bogen, Crick, Llinás, Newman, and Changeux. These theories allot different roles to various key brain areas, in particular the reticular and intralaminar nuclei of the thalamus and the cortex. Crick's hypothesis is that awareness is a function of reverberating corticothalamic loops and that the spotlight ofintramodalattention is controlled by the reticular nucleus of the thalamus. He also proposed different mechanisms (...) for attention and intention . The current review presents a new hypothesis, based on elements from these hypotheses, includingintermodalattention and olfaction and pain, which may pose problems for Crick's original theory. This work reviews the possible role in awareness and intermodal attention and intention of the cholinergic system in the basal forebrain and the tegmentum; the reticular, the intralaminar, and the dorsomedial thalamic nuclei; the raphe and locus coeruleus; the reticular formation; the ventral striatum and extended amygdala; insula cortex, and other selected cortical areas. Both clinical and basic research data are covered. The conclusion is reached that the brain may work by largely nonlinear parallel processing and much intramodal shifts of attention may be effected by intracortical, or multiple corticothalamic mechanisms . But this is constrained by the functional anatomy of the circuits concerned and waking “awareness” is modulated by the many “nonspecific” systems . But the principal agents for intermodal attention shifts, the “searchlight,” may be two key nuclei of the cholinergic system in the mesencephalon. Clinical loss of consciousness results from damage to these nuclei but not from damage to the cholinergic nucleus basalis of the basal forebrain. (shrink)

Traditionally, philosophers have appealed to the phenomenological similarity between visual experience and visual imagery to support the hypothesis that there is significant overlap between the perceptual and imaginative domains. The current evidence, however, is inconclusive: while evidence from transcranial brain stimulation seems to support this conclusion, neurophysiological evidence from brain lesion studies (e.g., from patients with brain lesions resulting in a loss of mental imagery but not a corresponding loss of perception and vice versa) indicates that there are functional and (...) anatomical dissociations between mental imagery and perception. Assuming that the mental imagery and perception do not overlap, at least, to the extent traditionally assumed, then the question arises as to what exactly mental imagery is and whether it parallels perception by proceeding via several functionally distinct mechanisms. In this review, we argue that even though there may not be a shared mechanism underlying vision for perception and conscious imagery, there is an overlap between the mechanisms underlying vision for action and unconscious visual imagery. On the basis of these findings, we propose a modification of Kosslyn’s model of imagery that accommodates unconscious imagination and explore possible explanations of the quasi-pictorial phenomenology of conscious visual imagery in light of the fact that its underlying neural substrates and mechanisms typically are distinct from those of visual experience. (shrink)

GY, an extensively studied human hemianope, is aware of salient visual events in his cortically blind field but does not call this ''vision.'' To learn whether he has low-level conscious visual sensations or whether instead he has gained conscious knowledge about, or access to, visual information that does not produce a conscious phenomenal sensation, we attempted to image process a stimulus s presented to the impaired field so that when the transformed stimulus T(s) was presented to the normal hemifield it (...) would cause a sensation similar to that caused by s in the impaired field. While degradation of contrast, spatio-temporal filtering, contrast reversal, and addition of smear and random blobs all failed to match the response to a flashed bar sf, moving textures of low contrast were accepted to match the response to a moving contrast-defined bar, sm. Orientation and motion direction discrimination of the perceptually matched stimuli [sm and T(sm)] was closely similar. We suggest that the existence of a satisfactory match indicates that GY has phenomenal vision. (shrink)

The neural basis of binocular rivalry has beenthe subject of vigorous debate. Do discrepantmonocular patterns rival for awareness becauseof neural competition among patternrepresentations or monocular channels? In thisarticle, I briefly review psychophysical andneurophysiological evidence pertaining to boththeories and discuss important new neuroimagingdata which reveal that rivalry is fullyresolved in monocular visual cortex. These newfindings strongly suggest that interocularcompetition mediates binocular rivalry and thatV1 plays an important role in the selection ofconscious visual information. They furthersuggest that rivalry is not a unitaryphenomenon. (...) Interocular competition may fullyaccount for binocular rivalry whereas aseparate mechanism involving patterncompetition likely accounts for monocular andstimulus rivalry. (shrink)

Metaethics has recently been confronted by evidence from cognitive neuroscience that tacit emotional processes play an essential causal role in moral judgement. Most neuroscientists, and some metaethicists, take this evidence to vindicate a version of metaethical sentimentalism. In this paper we argue that the ‘dual process’ model of cognition that frames the discussion within and without philosophy does not do justice to an important constraint on any theory of deliberation and judgement. Namely, decision-making is the exercise of a capacity for (...) agency. Agency, in turn, requires a capacity to conceive of oneself as temporally extended: to inhabit, in both memory and imagination, an autobiographical past and future. To plan, to commit to plans, and to act in accordance with previous plans requires a diachronic self, able to transcend the present moment. While this fact about agency is central to much of moral philosophy (e.g. in discussions of autonomy and moral responsibility) it is opaque to the dual process framework and those meta-ethical accounts which situate themselves within this model of cognition. We show how this is the case and argue for an empirically adequate account of moral judgement which gives sufficient role to memory and imagination as cognitive prerequisites of agency. We reconsider the empirical evidence, provide an alternative, agentive, interpretation of key findings, and evaluate the consequences for metaethics. (shrink)

The visual brain consists of several parallel, functionally specialized processing systems, each having several stages (nodes) which terminate their tasks at different times; consequently, simultaneously presented attributes are perceived at the same time if processed at the same node and at different times if processed by different nodes. Clinical evidence shows that these processing systems can act fairly autonomously. Damage restricted to one system compromises specifically the perception of the attribute that that system is specialized for; damage to a given (...) node of a processing system that leaves earlier nodes intact results in a degraded perceptual capacity for the relevant attribute, which is directly related to the physiological capacities of the cells left intact by the damage. By contrast, a system that is spared when all others are damaged can function more or less normally. Moreover, internally created visual percepts-illusions, afterimages, imagery, and hallucinations-activate specifically the nodes specialized for the attribute perceived. Finally, anatomical evidence shows that there is no final integrator station in the brain, one which receives input from all visual areas; instead, each node has multiple outputs and no node is recipient only. Taken together, the above evidence leads us to propose that each node of a processing-perceptual system creates its own microconsciousness. We propose that, if any binding occurs to give us our integrated image of the visual world, it must be a binding between microconsciousnesses generated at different nodes. Since any two microconsciousnesses generated at any two nodes can be bound together, perceptual integration is not hierarchical, but parallel and postconscious. By contrast, the neural machinery conferring properties on those cells whose activity has a conscious correlate is hierarchical, and we refer to it as generative binding, to distinguish it from the binding that might occur between the microconsciousnesses. (shrink)

Cortical color blindness, or cerebral achromatopsia, has been likened by some authors to ''blindsight'' for color or an instance of ''covert'' processing of color. Recently, it has been shown that, although such patients are unable to identify or discriminate hue differences, they nevertheless show a striking ability to process wavelength differences, which can result in preserved sensitivity to chromatic contrast and motion in equiluminant displays. Moreover, visually evoked cortical potentials can still be elicited in response to chromatic stimuli. We suggest (...) that these demonstrations reveal intact residual processes rather than the operation of covert processes, where proficient performance is accompanied by a denial of phenomenal awareness. We sought evidence for such covert processes by conducting appropriate tests on achromatopsic subject M.S. An ''indirect'' test entailing measurement of reaction times for letter identification failed to reveal covert color processes. In contrast, in a forced choice oddity task for color, M.S. was unable to verbally indicate the position of the different color, but was surprisingly adept at making an appropriate eye movement to its location. This ''direct'' test thus revealed the possible covert use of chromatic differences. (shrink)

Block () highlights two experimental studies of neglect patients which, he contends, provide ‘dramatic evidence’ for unconscious seeing. In Block's hands this is the highly non-trivial thesis that seeing of the same fundamental kind as ordinary conscious seeing can occur outside of phenomenal consciousness. Block's case for it provides an excellent opportunity to consider a large body of research on clinical syndromes widely held to evidence unconscious perception. I begin by considering in detail the two studies of neglect to which (...) Block appeals. I show why their interpretation as evidence of unconscious seeing faces a series of local difficulties. I then explain how, even bracketing these issues, a long-standing but overlooked problem concerning our criterion for consciousness problematizes the appeal to both studies. I explain why this problem is especially pressing for Block given his view that phenomenal consciousness overflows access consciousness. I further show that it is epidemic—not only affecting all report-based studies of unconscious seeing in neglect, but also analogous studies of the condition most often alleged to show unconscious seeing, namely blindsight. (shrink)

Empirical work is reviewed which correlates the presence or absence of various parts of the auditory evoked potential with the disappearance and reemergence of auditory sensation during induction of and recovery from anesthesia. As a result, the hypothesis is generated that the electrophysiological correlate of auditory sensation is whatever neural activity generates the middle latency waves of the auditory evoked potential. This activity occurs from 20 to 80 ms poststimulus in the primary and secondary areas of the auditory cortex. Evidence (...) is presented suggesting that earlier or later waves in the auditory evoked potential do not covary with auditory sensation (as opposed to auditory perception) and it is therefore suggested that they are possibly not the electrophysiological correlates of sensation. (shrink)

It has been shown that visual awareness in the blind hemifield of hemianopic cats that have undergone unilateral ablations of visual cortex can be restored by sectioning the commissure of the superior colliculus or by destroying a portion of the substantia nigra contralateral to the cortical lesion (the Sprague effect). We propose that the visual awareness that is recovered is due to synchronized oscillatory activities in the superior colliculus ipsilateral to the cortical lesion. These oscillatory activities are normally partially suppressed (...) by the inhibitory, GABAergic contralateral nigrotectal projection, and the destruction of the substantia nigra, or the sectioning of the collicular commissure, disinhibits the collicular neurons, causing an increase in the extent of oscillatory activity and/or synchronization between activities at different sites. This increase in the oscillatory and synchronized character is sufficient for the activities to give rise to visual awareness. We argue that in rodents and lower vertebrates, normal visual awareness is partly due to synchronized oscillatory activities in the optic tectum and partly due to similar activities in visual cortex. It is only in carnivores and primates that visual awareness is wholly due to cortical activities. Based on von Baerian recapitulation theory, we propose that, even in humans, there is a period in early infancy when visual awareness is partially due to activities in the superior colliculus, but that this awareness gradually disappears as the nigrotectal projection matures. (shrink)

Some patients with damaged striate cortex have blindsight-the ability to discriminate unseen stimuli in their clinically blind visual field defects when forced-choice procedures are used. Blindsight implies a sharp dissociation between visual performance and visual awareness, but signal detection theory indicates that it might be indistinguishable from the behavior of normal subjects near the lower limit of conscious vision, where the dissociations could arise trivially from using different response criteria during clinical and forced-choice tests. We tested the latter possibility with (...) a hemianopic subject during yes-no and forced-choice detection of static and moving targets. His response criterion differed significantly between yes-no and forced-choice responding, and the difference was sufficient to produce a blindsight-like dissociation with bias-sensitive measures of performance. When measured independently of bias, his sensitivity to static targets was greater in the forced-choice than in the yes-no task (unlike normal control subjects), but his sensitivity to moving targets did not differ. Differences in response criterion could therefore account for dissociations between yes-no and forced-choice detection of motion, but not of static pattern. The results explain why patients with blindsight are apparently more often ''aware'' of moving stimuli than of static stimuli. However, they also imply that blindsight is unlike normal vision near threshold, and that pattern- and motion-detection in blindsight may depend on different sets of neural mechanisms during yes-no and forced-choice tests. (shrink)

In three macaque monkeys with unilateral removal of primary visual cortex and in one unoperated monkey, we measured reaction times to a visual target that was presented at a lateral eccentricity of 20o in the normal, left, visual hemifield. When an additional stimulus was presented at the corresponding position in the right hemifield (hemianopic in three of the monkeys), it significantly slowed the reaction time to the left target if it preceded it by delays from 100-500 msec. The most effective (...) delay depended on the particular experimental paradigm and perhaps on the experience of the monkey with the task. The results show that reaction times to seen targets in the normal hemifield of monkeys are influenced by the presentation of ''unseen'' targets in the anopic hemifield, as in some patients with cortically blind visual field defects. (shrink)

It remains unclear what is being processed in blindsight in response to faces, colours, shapes, and patterns. This was investigated in two hemianopes with chromatic and achromatic stimuli with sharp or shallow luminance or chromatic contrast boundaries or temporal onsets. Performance was excellent only when stimuli had sharp spatial boundaries. When discrimination between isoluminant coloured Gaussians was good it declined to chance levels if stimulus onset was slow. The ability to discriminate between instantaneously presented colours in the hemianopic field depended (...) on their luminance, indicating that wavelength discrimination totally independent of other stimulus qualities is absent. When presented with narrow-band colours the hemianopes detected a stimulus maximally effective for S-cones but invisible to M- and L-cones, indicating that blindsight is mediated not just by the mid-brain, which receives no S-cone input, or that the rods contribute to blindsight. The results show that only simple stimulus features are processed in blindsight. (shrink)