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Individuals are able to discriminate visual stimuli they report not consciously seeing. This phenomenon is known as "subliminal perception." Such capacity is often assumed to be relatively automatic in nature and rely on stimulus-driven activity in low-level cortical areas. Instead, here we asked to what extent neural activity before stimulus presentation influences subliminal perception. We asked participants to discriminate the location of a briefly presented low-contrast visual stimulus and then rate how well they saw the stimulus. Consistent with previous studies, participants correctly discriminated with slightly above chance-level accuracy the location of a stimulus they reported not seeing. Signal detection analyses indicated that while subjects categorized their percepts as "unconscious," their capacity to discriminate these stimuli lay on the same continuum as conscious vision. We show that the accuracy of discriminating the location of a subliminal stimulus could be predicted with relatively high accuracy (AUC = 0.70) based on lateralized electroencephalographic (EEG) activity before the stimulus, the hemifield where the stimulus was presented, and the accuracy of previous trial's discrimination response. Altogether, our results suggest that rather than being a separate unconscious capacity, subliminal perception is based on similar processes as conscious vision., (© 2021 The Authors. European Journal of Neuroscience published by Federation of European Neuroscience Societies and John Wiley & Sons Ltd.)

After damage to the primary visual cortex (V1), conscious vision is impaired. However, some patients can respond to visual stimuli presented in their lesion-affected visual field using residual visual pathways bypassing V1. This phenomenon is called "blindsight." Many studies have tried to identify the brain regions responsible for blindsight, and the pulvinar and/or lateral geniculate nucleus (LGN) are suggested to play key roles as the thalamic relay of visual signals. However, there are critical problems regarding these preceding studies in that subjects with different sized lesions and periods of time after lesioning were investigated; furthermore, the ability of blindsight was assessed with different measures. In this study, we used double dissociation to clarify the roles of the pulvinar and LGN by pharmacological inactivation of each region and investigated the effects in a simple task with visually guided saccades (VGSs) using monkeys with a unilateral V1 lesion, by which nearly all of the contralesional visual field was affected. Inactivating either the ipsilesional pulvinar or LGN impaired VGS toward a visual stimulus in the affected field. In contrast, inactivation of the contralesional pulvinar had no clear effect, but inactivation of the contralesional LGN impaired VGS to the intact visual field. These results suggest that the pulvinar and LGN play key roles in performing the simple VGS task after V1 lesioning, and that the visuomotor functions of blindsight monkeys were supported by plastic changes in the visual pathway involving the pulvinar, which emerged after V1 lesioning. SIGNIFICANCE STATEMENT Many studies have been devoted to understanding the mechanism of mysterious symptom called "blindsight," in which patients with damage to the primary visual cortex (V1) can respond to visual stimuli despite loss of visual awareness. However, there is still a debate on the thalamic relay of visual signals. In this study, to pin down the issue, we tried double dissociation in the same subjects (hemi-blindsight macaque monkeys) and clarified that the lateral geniculate nucleus (LGN) plays a major role in simple visually guided saccades in the intact state, while both pulvinar and LGN critically contribute after the V1 lesioning, suggesting that plasticity in the visual pathway involving the pulvinar underlies the blindsight., (Copyright © 2021 the authors.)

We recently published the results of a study on the occurrence of blindsight among eight, post-stroke homonymous hemianopic (HH) patients (Garric et al., 2019), in whom we measured blindsight through forced-choice tasks and assessed perceptual experiences by a new awareness scale, the Sensation Awareness Scale (SAS). Within the cohort, we found different profiles of dissociation between objective and subjective performance. Importantly, we were able to describe several cases of a dissociation phenomenon that we named blindsense, whereby patients exhibited marked subjective sensitivity in their blind hemifield despite being unable to discriminate the different stimuli. Following publication of our article (Garric et al., 2019), Prof. Ian Phillips (Phillips, 2019) wrote a Commentary in which he questioned the methodology we used to measure and analyze objective and subjective perception in our HH patients. As opposed to our original interpretation of our results to describe the new profile of blindsense, based on a non-visual experience hypothesis (Kentridge, 2015), Prof. Phillips re-evaluated the different blindsight profiles that we identified in our study through the lens of a degraded conscious vision hypothesis (Overgaard, Fehl, Mouridsen, Bergholt, & Cleeremans, 2008). In the present response, we explain that, although we agree that dichotomous visual scales lead to highly conservative responses and mask conscious perceptual experience of patients, we still support the notion that nuanced report protocols can enable more-sensitive measurements of perceptual experiences in the hemianopic, so-called blind visual field. Furthermore, we affirm that the additional awareness-scale phenomenal levels that such protocols enable are more consistent with patients' experiences and lead patients to provide more liberal responses when describing their subjective perceptions., Competing Interests: Declaration of Competing Interest None., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Recent visual masking studies that have measured visual awareness with graded subjective scales have often failed the show any evidence for unconscious visual processing in normal observers in a paradigm similar to that used in studies on blindsight patients. Without any reported awareness of the target, normal observers typically cannot discriminate target's features better than chance. The present study examined processing of color and orientation by measuring graded awareness and forced-choice discriminations for both features in each trial. When no awareness for either feature was reported, discrimination of each feature succeed better than expected by chance, even when the other feature was incorrectly discriminated in the same trial. However, the characteristics of the mask determined whether or not masked blindsight was observed. We conclude that when the processing channels are free from intra-channel interference, unbound or weakly bound features can guide behaviour without any reported awareness in normal observers., (Copyright © 2020 Elsevier Inc. All rights reserved.)

The most common visual defect to follow a lesion of the retrochiasmal pathways is homonymous hemianopia (HH), whereby patients are blind to the contralesional visual field of each eye. Homonymous hemianopia has been studied in terms of its deleterious consequences on perceptual, cognitive and motor tasks as well as because it represents an interesting model of vision loss after a unilateral lesion of the occipital lobe. From a behavioral perspective, in addition to exhibiting a severe deficit in their contralesional visual field, HH patients can also exhibit dissociations between perception and awareness. Firstly, HH patients suffering from anosognosia may be unaware of their visual field defect. Secondly, HH patients can present with unconscious visual abilities in the blind hemifield, a phenomenon referred to as blindsight. Thirdly, recent reports demonstrate that HH patients can suffer from a subtle deficit in their ipsilesional visual field that they are unaware of, a condition called sightblindness (i.e. the reverse case of 'blindsight'). Finally, HH patients may also exhibit visual hallucinations in their blind field; however, such patients are not systematically aware that their perceptions are unreal. In this review, we provide an overview of the visual-field losses in HH patients after a left or right unilateral occipital lesion. Furthermore, we explore the implications of these four phenomena for models of visual processing and rehabilitation of visual field defects in HH patients. Finally, in contrast to the traditional view that HH is solely a visual-field defect, we discuss why this deficit is an interesting model for studying the dissociation between perception and awareness.

After a post-chiasmatic lesion, some patients may retain unconscious visual function, known as blindsight, in their contralesional visual field. Despite the importance of blindsight in the study of consciousness, little is known about the nature of patients' experience in their hemianopic field. To address this knowledge gap, we measured blindsight, and assessed the perceptual experience in the contralesional visual field, of seventeen homonymous hemianopic (HH) patients. To ensure that the stimuli were shown in a "blind" sector of the visual field, we selected a subgroup of eight complete-HH patients, as determined by automatic perimetry. Firstly, we measured blindsight through a forced-choice task in which the patients had to identify letters displayed on a screen. Secondly, we compared the patients' binary responses ("Something was presented" vs "Nothing was presented") to responses on a new, five-level scale, the Sensation Awareness Scale (SAS), which we designed to include visual as well as non-visual answers (e.g., "I felt something"). Interestingly, only one of the eight complete-HH patients met the criteria for blindsight. More importantly, our SAS enabled us to identify a previously unreported dissociation, which we have named blindsense, in four of the eight complete-HH patients. Specifically, these four patients exhibited better-than-chance sensitivity to the presence of a stimulus on the subjective scale, despite being unable to identify the stimulus during the forced-choice task. Our findings highlight the importance of awareness-assessment methods to investigate perceptual experiences in the contralesional visual field and suggest a low incidence of blindsight in post-stroke HH patients., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Prism adaptation is a time-honored tool for studying how the motor system adapts to sensory perturbations. Past research on the neural substrates of prism adaptation has implicated the posterior parietal cortex (PPC) and the cerebellum, under the assumption that these structures gain their visual input from the dominant retinogeniculate pathway to V1. Here we question whether this pathway is even required for visuomotor adaptation to occur. To investigate this, we examined prism adaptation in 'MC', someone who is blind to static stimuli following bilateral lesions that encompass much of her occipital cortex and the caudal-most areas of ventrotemporal cortex. Remarkably, MC shows evidence of prism adaptation that is similar to healthy control participants. First, when pointing with either the left or the right hand, MC shows spatial realignment; the classical after-effect exhibited by most people when adapting to displacing prisms. Second, MC demonstrates strategic recalibration - a reduction in her pointing error over time - that is similar in magnitude to healthy controls. These findings suggest that the geniculostriate pathway is not necessary for visuomotor adaptation to take place. Alternatively, we suggest that an extrageniculostriate pathway which provides visual inputs to the cerebellum from area MT and the PPC via the dorsolateral pons plays a significant and appreciable role in the guidance of unconscious automatic visuomotor adaptation., (Crown Copyright © 2019. Published by Elsevier Ltd. All rights reserved.)

Lesions of primary visual cortex (V1) lead to loss of conscious visual perception with significant impact on human patients. Understanding the neural consequences of such damage may aid the development of rehabilitation methods. In this rare case of a Rhesus macaque (monkey S), likely born without V1, the animal's in-group behaviour was unremarkable, but visual task training was impaired. With multi-modal magnetic resonance imaging, visual structures outside of the lesion appeared normal. Visual stimulation under anaesthesia with checkerboards activated lateral geniculate nucleus of monkey S, while full-field moving dots activated pulvinar. Visual cortical activation was sparse but included face patches. Consistently across lesion and control monkeys, functional connectivity analysis revealed an intact network of bilateral dorsal visual areas temporally correlated with V5/MT activation, even without V1. Despite robust subcortical responses to visual stimulation, we found little evidence for strengthened subcortical input to V5/MT supporting residual visual function or blindsight-like phenomena., Competing Interests: HB, AB, MA, JS, EP, BA, AM, US, MB, BT, KM, RM, AP, KK No competing interests declared, (© 2019, Bridge et al.)

Blindsight has been central to theories of phenomenal awareness; that a lesion to primary visual cortex (V1) abolishes all phenomenal awareness while unconscious visual functions can remain has led to the view that this region plays a crucial role in generating visual consciousness. However, since the early 20th century, there have been reports, many of which controversial, of phenomenal awareness in patients with V1 lesions. These reports include selective sparing of motion awareness, hemianopic completion and visual aftereffects. More recently, there have been successful attempts of inducing visual qualia with noninvasive brain stimulation. Here we critically review this evidence and discuss their implications to theoretical understanding of phenomenal awareness., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

As with some patients with primary visual cortex (V1) damage, transcranial magnetic stimulation (TMS) over V1 reliably induces blindsight, whereby observers can correctly discriminate the attributes of visual stimuli despite being unable to detect them. This TMS-induced blindsight has been demonstrated to reflect a form of unconscious vision that relies upon different neural pathways than with conscious vision. However, the timing of the neural processes mediating TMS-induced blindsight has been unclear, especially when considering suggestions that TMS interferes with feedback processes to V1 that mediate conscious visual perception. To better elucidate the neural mechanisms that give rise to blindsight, we tested TMS-induced blindsight for the orientation of visual stimuli across a range of stimulus onset asynchronies (SOAs) to assess how different latencies of visual cortex disruption, relative to a visual stimulus, affect detection rates and forced-choice discrimination accuracy. At all TMS latencies, including at SOAs with substantial visual suppression from TMS, discrimination performance was significantly above-chance, demonstrating the consistency of TMS-induced blindsight. Crucially, we observed two windows of maximum visual suppression from TMS at SOAs between 65 and 105 ms, but consistent above-chance discrimination performance accuracy across these windows. However, at longer SOAs, detection and discrimination covaried, suggesting a dependency of discrimination performance on detection only when detection rates exceed threshold levels of normal vision. Taken together, these results indicate that unconscious discrimination occurs independently of detection, including at TMS intervals that optimally interfere with conscious visual perception. They further suggest that forced-choice discrimination is less dependent on feedback processes to V1 than visual awareness and that TMS-induced blindsight is not the same as near-threshold vision., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Damage to the primary visual cortex (V1) leads to a visual field loss (scotoma) in the retinotopically corresponding part of the visual field. Nonetheless, a small amount of residual visual sensitivity persists within the blind field. This residual capacity has been linked to activity observed in the middle temporal area complex (V5/MT+). However, it remains unknown whether the organization of hV5/MT+ changes following early visual cortical lesions. We studied the organization of area hV5/MT+ of five patients with dense homonymous defects in a quadrant of the visual field as a result of partial V1+ or optic radiation lesions. To do so, we developed a new method, which models the boundaries of population receptive fields directly from the BOLD signal of each voxel in the visual cortex. We found responses in hV5/MT+ arising inside the scotoma for all patients and identified two possible sources of activation: 1) responses might originate from partially lesioned parts of area V1 corresponding to the scotoma, and 2) responses can also originate independent of area V1 input suggesting the existence of functional V1-bypassing pathways. Apparently, visually driven activity observed in hV5/MT+ is not sufficient to mediate conscious vision. More surprisingly, visually driven activity in corresponding regions of V1 and early extrastriate areas including hV5/MT+ did not guarantee visual perception in the group of patients with post-geniculate lesions that we examined. This suggests that the fine coordination of visual activity patterns across visual areas may be an important determinant of whether visual perception persists following visual cortical lesions., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The division of labour between the dorsal and ventral visual pathways is well established. The ventral stream supports object identification, while the dorsal stream supports online processing of visual information in the service of visually guided actions. Here, we report a case of an individual with a right inferior quadrantanopia who exhibited accurate spontaneous rotation of his wrist when grasping a target object in his blind visual field. His accurate wrist orientation was observed despite the fact that he exhibited no sensitivity to the orientation of the handle in a perceptual matching task. These findings indicate that non-geniculostriate visual pathways process basic volumetric information relevant to grasping, and reinforce the observation that phenomenal awareness is not necessary for an object's volumetric properties to influence visuomotor performance.

Lesions of striate cortex (V1) trigger massive retrograde degeneration of neurons in the LGN. In primates, these lesions also lead to scotomas, within which conscious vision is abolished. Mediation of residual visual capacity within these regions (blindsight) has been traditionally attributed to an indirect visual pathway to the extrastriate cortex, which involves the superior colliculus and pulvinar complex. However, recent studies have suggested that preservation of the LGN is critical for behavioral evidence of blindsight, raising the question of what type of visual information is channeled by remaining neurons in this structure. A possible contribution of LGN neurons to blindsight is predicated on two conditions: that the neurons that survive degeneration remain visually responsive, and that their receptive fields continue to represent the region of the visual field inside the scotoma. We tested these conditions in male and female marmoset monkeys ( Callithrix jacchus ) with partial V1 lesions at three developmental stages (early postnatal life, young adulthood, old age), followed by long recovery periods. In all cases, recordings from the degenerated LGN revealed neurons with well-formed receptive fields throughout the scotoma. The responses were consistent and robust, and followed the expected eye dominance and retinotopy observed in the normal LGN. The responses had short latencies and preceded those of neurons recorded in the extrastriate middle temporal area. These findings suggest that the pathway that links LGN neurons to the extrastriate cortex is physiologically viable and can support residual vision in animals with V1 lesions incurred at various ages. SIGNIFICANCE STATEMENT Patients with a lesion of the primary visual cortex (V1) can retain certain visually mediated behaviors, particularly if the lesion occurs early in life. This phenomenon ("blindsight") not only sheds light on the nature of consciousness, but also has implications for studies of brain circuitry, development, and plasticity. However, the pathways that mediate blindsight have been the subject of debate. Recent studies suggest that projections from the LGN might be critical, but this finding is puzzling given that the lesions causes severe cell death in the LGN. Here we demonstrate in monkeys that the surviving LGN neurons retain a remarkable level of visual function and could therefore be the source of the visual information that supports blindsight., (Copyright © 2018 the authors 0270-6474/18/383955-16$15.00/0.)

Unilateral damage to the primary visual cortex (V1) leads to clinical blindness in the opposite visual hemifield, yet nonconscious ability to transform unseen visual input into motor output can be retained, a condition known as "blindsight." Here we combined psychophysics, functional magnetic resonance imaging, and tractography to investigate the functional and structural properties that enable the developing brain to partly overcome the effects of early V1 lesion in one blindsight patient. Visual stimuli appeared in either the intact or blind hemifield and simple responses were given with either the left or right hand, thereby creating conditions where visual input and motor output involve the same or opposite hemisphere. When the V1-damaged hemisphere was challenged by incoming visual stimuli, or controlled manual responses to these unseen stimuli, the corpus callosum (CC) dynamically recruited areas in the visual dorsal stream and premotor cortex of the intact hemisphere to compensate for altered visuomotor functions. These compensatory changes in functional brain activity were paralleled by increased connections in posterior regions of the CC, where fibers connecting homologous areas of the parietal cortex course., Competing Interests: The authors declare no conflict of interest., (Copyright © 2017 the Author(s). Published by PNAS.)

In this review, we outline the history of our current understanding of the organization of the pulvinar complex of mammals. We include more recent evidence from our own studies of both New and Old World monkeys, prosimian galagos, and close relatives of primates, including tree shrews and rodents. Based on cumulative evidence, we provide insights into the possible evolution of the visual pulvinar complex, as well as the possible co-evolution of the inferior pulvinar nuclei and temporal cortical visual areas within the MT complex., (© 2017 Wiley Periodicals, Inc.)

Blindsight patients with damage to the visual cortex can discriminate objects but report no conscious visual experience. This provides an intriguing opportunity to allow the study of subjective awareness in isolation from objective performance capacity. However, blindsight is rare, so one promising way to induce the effect in neurologically intact observers is to apply transcranial magnetic stimulation (TMS) to the visual cortex. Here, we used a recently-developed criterion-free method to conclusively rule out an important alternative interpretation of TMS-induced performance without awareness: that TMS-induced blindsight may be just due to conservative reporting biases for conscious perception. Critically, using this criterion-free paradigm we have previously shown that introspective judgments were optimal even under visual masking. However, here under TMS, observers were suboptimal, as if they were metacognitively blind to the visual disturbances caused by TMS. We argue that metacognitive judgments depend on observers' internal statistical models of their own perceptual systems, and introspective suboptimality arises when external perturbations abruptly make those models invalid - a phenomenon that may also be happening in actual blindsight., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Responses of midbrain dopamine (DA) neurons reflecting expected reward from sensory cues are critical for reward-based associative learning. However, critical pathways by which reward-related visual information is relayed to DA neurons remain unclear. To address this question, we investigated Pavlovian conditioning in macaque monkeys with unilateral primary visual cortex (V1) lesions (an animal model of 'blindsight'). Anticipatory licking responses to obtain juice drops were elicited in response to visual conditioned stimuli (CS) in the affected visual field. Subsequent pharmacological inactivation of the superior colliculus (SC) suppressed the anticipatory licking. Concurrent single unit recordings indicated that DA responses reflecting the reward expectation could be recorded in the absence of V1, and that these responses were also suppressed by SC inactivation. These results indicate that the subcortical visual circuit can relay reward-predicting visual information to DA neurons and integrity of the SC is necessary for visually-elicited classically conditioned responses after V1 lesion.

Objective: We investigated neuronal correlates of faces versus non-faces processing in a cortically blind patient (TN) and a group of healthy age-matched controls in order to test electrophysiological correlates of the processing of pertinent stimuli in this patient., Methods: An EEG paradigm was used, in which intact and scrambled faces were displayed on a screen. First, time-frequency transforms were conducted on the patients' data alone. These oscillations were then compared to the frontal activity of six control participants., Results: Post stimulus oscillatory modulations (synchronisation in theta and alpha frequency bands) of both intact and scrambled faces at frontal scalp sites were observed in TN. These modulations were different for correct and incorrect responses. A more important increase in the theta band for incorrect responses was observed. The oscillatory rhythms highlighted in blindsight and in frontal regions differ from the ones observed in control participants., Conclusion: Despite the destruction of the visual cortex, oscillatory rhythms are not cancelled out but are shifted to anterior regions, revealing the activity of an alternate pathway for residual visual function., Significance: The results provide evidence for a top-down cognitive control process in blindsight., (Copyright © 2017 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.)

Recent experiments demonstrate that invisible stimulus features can induce binocular rivalry, indicating the phenomenon may be caused by differences in perceptual signal strength rather than conscious selection processes. Here, we clarify binocular rivalry's role in consciousness research by highlighting a critical difference between two distinct types of visual awareness., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Patients with cortical blindness following a lesion to the primary visual cortex (V1) may retain nonconscious visual abilities (blindsight). One intriguing, though largely unexplored question, is whether nonconscious vision in the blind hemifield of hemianopic patients can be sensitive to higher-order perceptual organization, and which V1-independent structure underlies such effect. To answer this question, we tested two rare hemianopic patients who had undergone hemispherectomy, and in whom the only post-chiasmatic visual structure left intact in the same side of the otherwise damaged hemisphere was the superior colliculus (SC). By using a variant of the redundant target effect (RTE), we presented single dots, patterns composed by the same dots organized in quadruple gestalt-like configurations, or patterns of four dots arranged in random configurations, either singly to the intact visual hemifield or bilaterally to both hemifields. As reported in a number of prior studies on blindsight patients, we found that bilateral stimulation yielded faster reaction times (RTs) than single stimulation of the intact field for all conditions (i.e., there was an implicit RTE). In addition to this effect, both patients showed a further speeding up of RTs when the gestalt-like, but not the random shape, quadruple patterns were projected to their blind hemifield during bilateral stimulation. Because other retino-recipient subcortical and cortical structures in the damaged hemisphere are absent, the SC on the lesioned side seems solely responsible for such an effect. The present results provide initial support to the notion that nonconscious vision might be sensitive to perceptual organization and stimulus configuration through the pivotal contribution of the SC, which can enhance the processing of gestalt-like or structured stimuli over meaningless or randomly assembled ones and translate them into facilitatory motor outputs., (Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The neuropsychological phenomenon of blindsight has been taken to suggest that the primary visual cortex (V1) plays a unique role in visual awareness, and that extrastriate activation needs to be fed back to V1 in order for the content of that activation to be consciously perceived. The aim of this review is to evaluate this theoretical framework and to revisit its key tenets. Firstly, is blindsight truly a dissociation of awareness and visual detection? Secondly, is there sufficient evidence to rule out the possibility that the loss of awareness resulting from a V1 lesion simply reflects reduced extrastriate responsiveness, rather than a unique role of V1 in conscious experience? Evaluation of these arguments and the empirical evidence leads to the conclusion that the loss of phenomenal awareness in blindsight may not be due to feedback activity in V1 being the hallmark awareness. On the basis of existing literature, an alternative explanation of blindsight is proposed. In this view, visual awareness is a "global" cognitive function as its hallmark is the availability of information to a large number of perceptual and cognitive systems; this requires inter-areal long-range synchronous oscillatory activity. For these oscillations to arise, a specific temporal profile of neuronal activity is required, which is established through recurrent feedback activity involving V1 and the extrastriate cortex. When V1 is lesioned, the loss of recurrent activity prevents inter-areal networks on the basis of oscillatory activity. However, as limited amount of input can reach extrastriate cortex and some extrastriate neuronal selectivity is preserved, computations involving comparison of neural firing rates within a cortical area remain possible. This enables "local" read-out from specific brain regions, allowing for the detection and discrimination of basic visual attributes. Thus blindsight is blind due to lack of "global" long-range synchrony, and it functions via "local" neural readout from extrastriate areas., (Copyright © 2014 The Author. Published by Elsevier Inc. All rights reserved.)

After decades of research, blindsight is still a mysterious and controversial topic in consciousness research. Currently, many researchers tend to think of it as an ideal phenomenon to investigate neural correlates of consciousness, whereas others believe that blindsight is in fact a kind of degraded vision rather than "truly blind". This article considers both perspectives and finds that both have difficulties understanding all existing evidence about blindsight. In order to reconcile the perspectives, we suggest two specific criteria for a good model of blindsight, able to encompass all evidence. We propose that the REF-CON model (Overgaard & Mogensen, 2014) may work as such a model., (Copyright © 2014 Elsevier Inc. All rights reserved.)

The concept of relative blindsight, referring to a difference in conscious awareness between conditions otherwise matched for performance, was introduced by Lau and Passingham (2006) as a way of identifying the neural correlates of consciousness (NCC) in fMRI experiments. By analogy, absolute blindsight refers to a difference between performance and awareness regardless of whether it is possible to match performance across conditions. Here, we address the question of whether relative and absolute blindsight in normal observers can be accounted for by response bias. In our replication of Lau and Passingham's experiment, the relative blindsight effect was abolished when performance was assessed by means of a bias-free 2AFC task or when the criterion for awareness was varied. Furthermore, there was no evidence of either relative or absolute blindsight when both performance and awareness were assessed with bias-free measures derived from confidence ratings using signal detection theory. This suggests that both relative and absolute blindsight in normal observers amount to no more than variations in response bias in the assessment of performance and awareness. Consideration of the properties of psychometric functions reveals a number of ways in which relative and absolute blindsight could arise trivially and elucidates a basis for the distinction between Type 1 and Type 2 blindsight., (Copyright © 2015. Published by Elsevier Inc.)

Three patients with visual field defects were stimulated with a square matrix pattern, either static, or flickering at frequencies that had been found to either promote or not promote blindsight performance. Comparison between pre- and post-stimulation perimetric maps revealed an increase in the size of the intact visual field but only for flicker frequencies previously found to promote blindsight. These changes were temporary but dramatic - in two instances the intact field was increased by an area of ∼30 deg(2) of visual angle. These results indicate that not only does specific high-frequency stimulus flicker promote blindsight, but that intact visual field size may be increased by stimulation at the same frequencies. Our findings inform speculation on both the brain mechanisms and the potency of temporal modulation for altering the functional visual field., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Type-2 blindsight is often characterised as involving a non-visual form of awareness that blindsight subjects experience under certain presentation conditions. This paper evaluates the claim that type-2 awareness is non-visual and the proposal that it is a cognitive form of awareness. It is argued that, contrary to the standard account, type-2 awareness is best characterised as visual both because it satisfies certain criteria for being visual and because it can accommodate facts about the phenomenon that the cognitive account cannot. The conclusion is made that type-2 blindsight is best characterised as involving a form of abnormal, degraded visual awareness., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Large amount of data concerning the neural mechanisms that mediate unconscious vision come from cortically blind patients who can process stimuli presented in their blind visual field. How well the findings generalize to neurologically healthy humans remains open., Objective: Using transcranial magnetic stimulation (TMS), we studied whether chromatic processing depends on the early visual cortex in healthy participants., Method: We employed a phenomenon called the redundant target effect (RTE): simple reaction times to two stimuli are faster than to one stimulus, even when one of the stimuli is presented outside consciousness., Results: The RTE produced by chromatically defined stimuli disappeared when the contralateral stimulus of two bilateral stimuli was suppressed from consciousness., Conclusions: In contrast to studies on blindsight patients, the results imply that the early visual cortex is necessary for the processing of chromatic information in neurologically healthy humans., (Copyright © 2014 Elsevier Inc. All rights reserved.)

In social interactions, the location of relevant stimuli is often indicated by the orientation of gaze. It has been proposed that the direction of gaze might produce an automatic cueing of attention, similar to what is observed with exogenous cues. However, several reports have challenged this claim by demonstrating that the behavioral gain that arises with gaze cueing could be explained by shifts of attention, which are intentional and not automatic. We reasoned that if cueing by gaze was truly automatic, it should occur without awareness and should be sustained by subcortical circuits, including the amygdalae, independently of the main geniculo-striate visual pathway. We presented a cross-modal version of the Posner cueing paradigm to a patient (TN) with bilateral lesions of occipital cortex (Burra et al., 2013; Pegna, Khateb, Lazeyras, & Seghier, 2005). TN was asked to localize a sound using a key press. The location of the sound was congruent or incongruent with the direction of gaze of a face-cue. In groups of healthy young and age-matched participants, we observed significantly longer response times for incongruent than congruent sounds, suggesting that gaze direction interfered with processing of localized sounds. By contrast, TN׳s performance was not affected by sound-gaze congruence. The results suggest that the processing of gaze orientation cannot occur in the absence of geniculo-striate processing, suggesting that it is not automatic., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

This article proposes a new model to interpret seemingly conflicting evidence concerning the correlation of consciousness and neural processes. Based on an analysis of research of blindsight and subliminal perception, the reorganization of elementary functions and consciousness framework suggests that mental representations consist of functions at several different levels of analysis, including truly localized perceptual elementary functions and perceptual algorithmic modules, which are interconnections of the elementary functions. We suggest that conscious content relates to the 'top level' of analysis in a 'situational algorithmic strategy' that reflects the general state of an individual. We argue that conscious experience is intrinsically related to representations that are available to guide behaviour. From this perspective, we find that blindsight and subliminal perception can be explained partly by too coarse-grained methodology, and partly by top-down enhancing of representations that normally would not be relevant to action.

This study used TMS to examine the role played by striate cortex (V1) in processing the emotional content of visual stimuli. Participants learned to discriminate two sets of body posture images. For half of each set, the posture's emotional significance (threat versus pleasant) provided a redundant cue for the discrimination; the other half were emotionally neutral. An image was briefly presented at a lateral location in the visual field where a TMS pulse produced a phosphene, or at a control location in the opposite hemifield. A TMS pulse 70-140 ms after stimulus presentation at the phosphene location impaired discrimination of neutral stimuli with little effect on discrimination of emotional stimuli; the two classes of stimuli were equally discriminable when presented at the control location. The results are consistent with the proposal that emotionally salient patterns, such as social threat, can be discriminated independently of the geniculo-striate pathway., (© 2013 Elsevier Ltd. All rights reserved.)

A central implication of the two-visual-systems hypothesis (TVSH) is that the dorsal visuomotor system (vision-for-action) can make use of invisible information, whereas the ventral system (vision-for-perception) cannot (Milner & Goodale, 1995). Therefore, actions such as grasping movements should be influenced by invisible information while conscious reports remain unaffected. To test this assumption, we used a dichoptic stimulation technique--continuous flash suppression (CFS)--which has the potency to render stimuli invisible for up to seconds (Tsuchiya & Koch, 2005). In two experiments using CFS, participants were asked to grasp for invisible bars of different sizes (Experiment 1) or orientations (Experiment 2), or to report both measures verbally. Target visibility was measured trial-by-trial using the perceptual awareness scale (PAS). We found no evidence for the use of invisible information by the visuomotor system despite extensive training (600 trials) and the availability of haptic feedback. Participants neither learned to scale their maximum grip aperture to the size of the invisible stimulus, nor to align their hand to its orientation. Careful control of stimulus visibility across training sessions, however, revealed a robust tendency towards decreasing perceptual thresholds under CFS. We discuss our results within the framework of the TVSH and with respect to alternative models which emphasize the close functional interaction between the dorsal and ventral visual systems., (© 2013 Elsevier Ltd. All rights reserved.)

Legally blind participants (uncorrected vision of 20/200+) were able to identify a visual stimulus attribute (clock hand position) in the absence of consciously identifying its presence. Specifically, participants--with their corrective lenses removed--correctly guessed the hour-hand position above chance (8%) on a clockface shown on a computer screen. This occurred both when presented in a 1-clockface display (28%), as well as when shown a display containing 4 clockfaces (21%), in which only 1 face contained a hand. Even more striking, hand identification accuracy in the 4-clockface condition was comparable whether the clockface containing the hand was (21%) or was not (20%) correctly identified. That legally blind individuals are capable of identifying stimulus attributes without conscious awareness provides an additional vehicle for exploring implicit perception. Consistent with previous research, the visual system can apparently cope with degraded visual input through information available through a(n unconscious) secondary pathway via the superior colliculi., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Purpose: We investigated systematically the effect of repeated exposure on detection and reported awareness of visual stimuli presented deep within the field defect of 5 hemianopic patients., Methods: An objective measure of sensitivity (detection in a temporal two-alternative forced-choice paradigm) and subjective reports of awareness were recorded on trial by trial bases. Visual stimulus to be detected was a temporally modulated (10 Hz) circular patch (6° diameter) of vertical grating (1 c/°). Hemianopic patients took part in the study 8 to 15 months after injury, so that the findings could not be attributed to spontaneous recovery., Results: Initially, high contrast (90%) target stimuli were detected at or near chance level with little reported awareness. In 4 of 5 cases, repeated stimulation led to improved sensitivity, indicated by increased detection scores and higher incidence of awareness. In a fifth case, there was no change in sensitivity despite extensive exposure (>22,000 trials)., Conclusions: At retinal locations deep within the field defect, repeated stimulation can lead to blindsight performance (type I detection without awareness), followed by detection with reported awareness (type II blindsight), and eventual reported visual experiences. The findings indicate that conscious awareness of stimuli lies on a continuous spectrum and repeated systematic training can lead to improved visual sensitivity.

Visual learning has been intensively studied in higher mammals, both during development and in adulthood. What is less clear is the extent and properties such plasticity may acquire following permanent damage to the adult visual system. Answering this question is important. Aside from improving our understanding of visual processing in the absence of an intact visual circuitry, such knowledge is essential for the development of effective therapies to rehabilitate the increasing number of people who suffer the functional consequences of damage at different levels of their visual cortical hierarchy. This review summarizes the known characteristics of visual learning after adult visual cortex damage and begins to dissect some of the neural correlates of this process., (Copyright © 2009 Cognitive Science Society, Inc.)

Key message: The Riddoch syndrome is thought to be caused by damage to the primary visual cortex (V1), usually following a vascular event. This study shows that damage to the anatomical input to V1, i.e., the optic radiations, can result in selective visual deficits that mimic the Riddoch syndrome. The results also highlight the differential susceptibility of the magnocellular and parvocellular visual systems to injury. Overall, this study offers new insights that will improve our understanding of the impact of brain injury and neurosurgery on the visual pathways. The Riddoch syndrome, characterised by the ability to perceive, consciously, moving visual stimuli but not static ones, has been associated with lesions of primary visual cortex (V1). We present here the case of patient YL who, after a tumour resection surgery that spared his V1, nevertheless showed symptoms of the Riddoch syndrome. Based on our testing, we postulated that the magnocellular (M) and parvocellular (P) inputs to his V1 may be differentially affected. In a first experiment, YL was presented with static and moving checkerboards in his blind field while undergoing multimodal magnetic resonance imaging (MRI), including structural, functional, and diffusion, acquired at 3 T. In a second experiment, we assessed YL's neural responses to M and P visual stimuli using psychophysics and high-resolution fMRI acquired at 7 T. YL's optic radiations were partially damaged but not severed. We found extensive activity in his visual cortex for moving, but not static, visual stimuli, while our psychophysical tests revealed that only low-spatial frequency moving checkerboards were perceived. High-resolution fMRI revealed strong responses in YL's V1 to M stimuli and very weak ones to P stimuli, indicating a functional P lesion affecting V1. In addition, YL frequently reported seeing moving stimuli and discriminating their direction of motion in the absence of visual stimulation, suggesting that he was experiencing visual hallucinations. Overall, this study highlights the possibility of a selective loss of P inputs to V1 resulting in the Riddoch syndrome and in hallucinations of visual motion. [ABSTRACT FROM AUTHOR]

Conscious visual motion information follows a cortical pathway from the retina to the lateral geniculate nucleus (LGN) and on to the primary visual cortex (V1) before arriving at the middle temporal visual area (MT/V5). Alternative subcortical pathways that bypass V1 are thought to convey unconscious visual information. One flows from the retina to the pulvinar (PUL) and on to medial temporal visual area (MT); while the other directly connects the LGN to MT. Evidence for these pathways comes from non‐human primates and modest‐sized studies in humans with brain lesions. Thus, the aim of the current study was to reconstruct these pathways in a large sample of neurotypical individuals and to determine the degree to which these pathways are myelinated, suggesting information flow is rapid. We used the publicly available 7T (N = 98; 'discovery') and 3T (N = 381; 'validation') diffusion magnetic resonance imaging datasets from the Human Connectome Project to reconstruct the PUL–MT (including all subcompartments of the PUL) and LGN–MT pathways. We found more fibre tracts with greater density in the left hemisphere. Although the left PUL–MT path was denser, the bilateral LGN–MT tracts were more heavily myelinated, suggesting faster signal transduction. We suggest that this apparent discrepancy may be due to 'adaptive myelination' caused by more frequent use of the LGN–MT pathway that leads to greater myelination and faster overall signal transmission. [ABSTRACT FROM AUTHOR]

The Riddoch syndrome is one in which patients blinded by lesions to their primary visual cortex can consciously perceive visual motion in their blind field, an ability that correlates with activity in motion area V5. Our assessment of the characteristics of this syndrome in patient ST, using multimodal MRI, showed that: 1. ST's V5 is intact, receives direct subcortical input, and decodable neural patterns emerge in it only during the conscious perception of visual motion; 2. moving stimuli activate medial visual areas but, unless associated with decodable V5 activity, they remain unperceived; 3. ST's high confidence ratings when discriminating motion at chance levels, is associated with inferior frontal gyrus activity. Finally, we report that ST's Riddoch Syndrome results in hallucinatory motion with hippocampal activity as a correlate. Our results shed new light on perceptual experiences associated with this syndrome and on the neural determinants of conscious visual experience. [ABSTRACT FROM AUTHOR]

Although subjective conscious experience and introspection have long been considered unscientific and banned from psychology, they are indispensable in scientific practice. These terms are used in scientific contexts today; however, their meaning remains vague, and earlier objections to the distinction between conscious experience and unconscious processing, remain valid. This also applies to the distinction between conscious visual perception and unconscious visual processing. Damage to the geniculo-striate pathway or the visual cortex results in a perimetrically blind visual hemifield contralateral to the damaged hemisphere. In some cases, cerebral blindness is not absolute. Patients may still be able to guess the presence, location, shape or direction of movement of a stimulus even though they report no conscious visual experience. This "unconscious" ability was termed "blindsight". The present paper demonstrates how the term conscious visual experience can be introduced in a logically precise and methodologically correct way and becomes amenable to scientific examination. The distinction between conscious experience and unconscious processing is demonstrated in the cases of conscious vision and blindsight. The literature on "blindsight" and its neurobiological basis is reviewed. It is shown that blindsight can be caused by residual functions of neural networks of the visual cortex that have survived cerebral damage, and may also be due to an extrastriate pathway via the midbrain to cortical areas such as areas V4 and MT/V5. [ABSTRACT FROM AUTHOR]

Blindsight patients with damage to the visual cortex can discriminate objects but report no conscious visual experience. This provides an intriguing opportunity to allow the study of subjective awareness in isolation from objective performance capacity. However, blindsight is rare, so one promising way to induce the effect in neurologically intact observers is to apply transcranial magnetic stimulation (TMS) to the visual cortex. Here, we used a recently-developed criterion-free method to conclusively rule out an important alternative interpretation of TMS-induced performance without awareness: that TMS-induced blindsight may be just due to conservative reporting biases for conscious perception. Critically, using this criterion-free paradigm we have previously shown that introspective judgments were optimal even under visual masking. However, here under TMS, observers were suboptimal, as if they were metacognitively blind to the visual disturbances caused by TMS. We argue that metacognitive judgments depend on observers internal statistical models of their own perceptual systems, and introspective suboptimality arises when external perturbations abruptly make those models invalid - a phenomenon that may also be happening in actual blindsight.

• Does blindsight generalize to neurologically healthy individuals? • Non-invasive brain stimulation (TMS) does not reveal unconscious blindsight. • TMS-studies demonstrate a weaker, not strictly unconscious blindsight-like capacity. • Differences between patients and healthy may indicate neural reorganization. • We propose that blindsight is preserved or partially recovered conscious vision. The visual pathways that bypass the primary visual cortex (V1) are often assumed to support visually guided behavior in humans in the absence of conscious vision. This conclusion is largely based on findings on patients: V1 lesions cause blindness but sometimes leave some visually guided behaviors intact—this is known as blindsight. With the aim of examining how well the findings on blindsight patients generalize to neurologically healthy individuals, we review studies which have tried to uncover transcranial magnetic stimulation (TMS) induced blindsight. In general, these studies have failed to demonstrate a completely unconscious blindsight-like capacity in neurologically healthy individuals. A possible exception to this is TMS-induced blindsight of stimulus presence or location. Because blindsight in patients is often associated with some form of introspective access to the visual stimulus, and blindsight may be associated with neural reorganization, we suggest that rather than revealing a dissociation between visually guided behavior and conscious seeing, blindsight may reflect preservation or partial recovery of conscious visual perception after the lesion. [ABSTRACT FROM AUTHOR]

After damage to the primary visual cortex (V1), conscious vision is impaired. However, some patients can respond to visual stimuli presented in their lesion-affected visual field using residual visual pathways bypassing V1. This phenomenon is called "blindsight." Many studies have tried to identify the brain regions responsible for blindsight, and the pulvinar and/or lateral geniculate nucleus (LGN) are suggested to play key roles as the thalamic relay of visual signals. However, there are critical problems regarding these preceding studies in that subjects with different sized lesions and periods of time after lesioning were investigated; furthermore, the ability of blindsight was assessed with different measures. In this study, we used double dissociation to clarify the roles of the pulvinar and LGN by pharmacological inactivation of each region and investigated the effects in a simple task with visually guided saccades (VGSs) using monkeys with a unilateral V1 lesion, by which nearly all of the contralesional visual field was affected. Inactivating either the ipsilesional pulvinar or LGN impaired VGS toward a visual stimulus in the affected field. In contrast, inactivation of the contralesional pulvinar had no clear effect, but inactivation of the contralesional LGN impaired VGS to the intact visual field. These results suggest that the pulvinar and LGN play key roles in performing the simple VGS task after V1 lesioning, and that the visuomotor functions of blindsight monkeys were supported by plastic changes in the visual pathway involving the pulvinar, which emerged after V1 lesioning. [ABSTRACT FROM AUTHOR]

When the primary visual cortex (V1) is damaged, cortical blindness results. However, visual information obtained from the superior colliculus (SC) or direct thalamic afferents to higher visual cortices produces unconscious visual functions called blindsight. Alarming visual stimuli suggesting the approach of a predator are known to trigger escape behaviors via visual information mediated by the SC and amygdala in small animals, and salient and dynamic visual stimuli also produce some conscious visual experience even in patients with blindsight. Fresh cortical blindness sometimes recovers spontaneously in patients with fresh cerebral damages, and recovery can be accelerated by early rehabilitation. However, the mechanisms underlying recovery are not well-known. We analyzed a patient with cortical blindness caused by an old cerebral infarction. After repeated presentation of alarming visual stimuli, the ability to detect visual stimuli in the impaired visual field showed behavioral short-term improvement (STI) within a few minutes. Repeated behavioral STI induction was followed by behavioral long-term improvement (LTI) lasting more than several days. After behavioral LTI, the patient partially recovered the ability to read letters presented in the impaired visual field. The behavioral STI experiment, which can be performed within 10 min, may serve as a clinical screening test for anticipating recovery from cortical blindness. [ABSTRACT FROM AUTHOR]

Brain imaging offers a valuable tool to observe functional brain plasticity by showing how sensory inputs reshape cortical activations after a visual impairment. Following a unilateral post-chiasmatic lesion affecting the visual cortex, patients may suffer a contralateral visual loss referred to homonymous hemianopia. Nevertheless, these patients preserve the ability to unconsciously detect, localize and discriminate visual stimuli presented in their impaired visual field. To investigate this paradox, known as blindsight , we conducted a study using functional magnetic resonance imaging (fMRI) to evaluate the structural and functional impact of such lesion in a 33-year old patient (ML), who suffers a complete right hemianopia without macular sparing and showing strong evidences of blindsight. We thus performed whole brain and sliced thalamic fMRI scan sequences during an event-related motion detection task. We provided evidence of the neuronal fingerprint of blindsight by acquiring and associating neural correlates, specific structures and functional networks of the midbrain during blindsight performances which may help to better understand this condition. Accurate performance demonstrated the presence of residual vision and the ability to unconsciously perceive motion presented in the blind hemifield, although her reaction time was significantly higher in her blind-field. When the normal hemifield was stimulated, we observed significant contralateral activations in primary and secondary visual areas as well as motion specific areas, such as the supramarginal gyrus and middle temporal area. We also demonstrated sub-thalamic activations within the superior colliculi (SC) and the pulvinar. These results suggest a role of secondary subcortical structures in normal spontaneous motion detection. In a similar way, when the lesioned hemifield was stimulated, we observed contralateral activity in extrastriate areas with no activation of the primary lesioned visual cortex. Moreover, we observed activations within the SC when the blind hemifield was stimulated. However, we observed unexpected ipsilateral activations within the same motion specific areas, as well as bilateral frontal activations. These results highlight the importance of abnormal secondary pathways bypassing the primary visual area (V1) in residual vision. This reorganization in the structure and function of the visual pathways correlates with behavioral changes, thus offering a plausible explanation for the blindsight phenomenon. Our results may potentially impact the development of rehabilitation strategies to target subcortical pathways. • Unconscious, yet accurate motion detection in a cortically blind individual. • Midbrain fMRI data acquisition during blindsight performances. • Cortical blindness alters BOLD activations of motion specific areas. • Blindsight elicits sub-thalamic BOLD activations within the superior colliculi and pulvinar. • Specific subcortical pathways process visual information in the blindfield. [ABSTRACT FROM AUTHOR]

Introduction: Visual consciousness is affected when the primary visual cortex is damaged. However, sighted behavior can persist within the areas of cortical blindness. This phenomenon is called blindsight, and it describes the ability to respond to visual stimuli in the absence of conscious awareness. With practice, visual awareness within a blind field can be trained through repeated visual stimulation. Case Report: A 70-year-old female with blindsight presented for a visual skills evaluation following a left-sided ischemic stroke. She perceived light in only very limited areas of her visual field, yet she was able accurately to identify colors, orientation, and the location of various visual targets presented in her blind field. Vision therapy was initiated to maximize the use of her residual vision, as well as to improve overall visual awareness. Within two months of starting therapy, her vision improved to 20/100 in the right eye and 20/125 in the left eye with near normal visual fields. Conclusions: With practice, responses to visual stimuli within the blind field can improve, perceptual learning can occur over time, and awareness can be trained. Rehabilitation of individuals with blindsight is highly recommended as it may present some therapeutic value as well as rehabilitative. [ABSTRACT FROM AUTHOR]