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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.

Some patients with damage to the primary visual cortex (V1) exhibit visuomotor ability, despite loss of visual awareness, a phenomenon termed “blindsight”. We review a series of studies conducted mainly in our laboratory on macaque monkeys with unilateral V1 lesioning to reveal the neural pathways underlying visuomotor transformation and the cognitive capabilities retained in blindsight. After lesioning, it takes several weeks for the recovery of visually guided saccades toward the lesion-affected visual field. In addition to the lateral geniculate nucleus, the pathway from the superior colliculus to the pulvinar participates in visuomotor processing in blindsight. At the cortical level, bilateral lateral intraparietal regions become critically involved in the saccade control. These results suggest that the visual circuits experience drastic changes while the monkey acquires blindsight. In these animals, analysis based on signal detection theory adapted to behavior in the “Yes–No” task indicates reduced sensitivity to visual targets, suggesting that visual awareness is impaired. Saccades become less accurate, decisions become less deliberate, and some forms of bottom-up attention are impaired. However, a variety of cognitive functions are retained such as saliency detection during free viewing, top–down attention, short-term spatial memory, and associative learning. These observations indicate that blindsight is not a low-level sensory-motor response, but the residual visual inputs can access these cognitive capabilities. Based on these results we suggest that the macaque model of blindsight replicates type II blindsight patients who experience some “feeling” of objects, which guides cognitive capabilities that we naïvely think are not possible without phenomenal consciousness.

The visual pathways that guide actions do not necessarily mediate conscious perception. Patients with primary visual cortex (V1) damage lose conscious perception but often retain unconscious abilities (e.g. blindsight). Here, we asked if saccade accuracy and post-saccadic following responses (PFRs) that automatically track target motion upon saccade landing are retained when conscious perception is lost. We contrasted these behaviors in the blind and intact-fields of 11 chronic V1-stroke patients, and in 8 visually-intact controls. Saccade accuracy was relatively normal in all cases. Stroke patients also had normal PFR in their intact-fields, but no PFR in their blind-fields. Thus, V1 damage did not spare the unconscious visual processing necessary for automatic, post-saccadic smooth eye movements. Importantly, visual training that recovered motion perception in the blind-field did not restore the PFR, suggesting a clear dissociation between pathways mediating perceptual restoration and automatic actions in the V1-damaged visual system.

Evidence for the influence of unaware signals on behaviour has been reported in both patient groups and healthy observers using the Redundant Signal Effect (RSE). The RSE refers to faster manual reaction times to the onset of multiple simultaneously presented target than those to a single stimulus. These findings are robust and apply to unimodal and multi-modal sensory inputs. A number of studies on neurologically impaired cases have demonstrated that RSE can be found even in the absence of conscious experience of the redundant signals. Here, we investigated behavioural changes associated with awareness in healthy observers by using Continuous Flash Suppression to render observers unaware of redundant targets. Across three experiments, we found an association between reaction times to the onset of a consciously perceived target and the reported level of visual awareness of the redundant target, with higher awareness being associated with faster reaction times. However, in the absence of any awareness of the redundant target, we found no evidence for speeded reaction times and even weak evidence for an inhibitory effect (slowing down of reaction times) on response to the seen target. These findings reveal marked differences between healthy observers and blindsight patients in how aware and unaware information from different locations is integrated in the RSE.

According to the textbooks, blindsight is a neuropsychological condition characterized by preserved capacities for voluntary visual discrimination unaccompanied by visual awareness. So construed, blindsight precipitated a revolution in theorizing consciousness. In Phillips (Psychological Review, 2021), I argued that the textbooks are wrong and the revolution ill-founded. Blindsight is exclusively a matter of conscious, albeit qualitatively degraded, vision which appears unconscious because of conservative response bias. Michel and Lau (Psychological Review, 2021) object: first, that residual awareness in blindsight cannot account for patients' impressive, feature-specific discriminatory abilities; and second, that performance matching makes response-bias explanations of unreported awareness implausible. They then offer a positive picture of blindsight as a specific deficit of detection, locating this idea within a framework which distinguishes perceptual from response bias. Here, I explain why neither objection convinces. I then argue that Michel and Lau give us no good reason to prefer their approach to our simpler, conscious-vision-only alternative. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Brain damage or disruption to the primary visual cortex sometimes produces blindsight, a striking condition in which patients lose the ability to consciously detect visual information yet retain the ability to discriminate some attributes without awareness. Although there have been few demonstrations of somatosensory equivalents of blindsight, the lesions that produce “numbsense,” in which patients can make accurate guesses about tactile information without awareness, have been rare and localized to different regions of the brain. Despite transient loss of tactile awareness in the contralateral hand after transcranial magnetic stimulation (TMS) of the primary somatosensory cortex but not TMS of a control site, 12 participants (six female) reliably performed at above-chance levels on a localization task. These results demonstrating TMS-induced numbsense implicate a parallel somatosensory pathway that processes the location of touch in the absence of awareness and highlight the importance of primary sensory cortices for conscious perception.

Consciousness is currently a thriving area of research in psychology and neuroscience. While this is often attributed to events that took place in the early 1990s, consciousness studies today are a continuation of research that started in the late 19th century and that continued throughout the 20th century. From the beginning, the effort built on studies of animals to reveal basic principles of brain organization and function, and of human patients to gain clues about consciousness itself. Particularly important and our focus here is research in the 1950s, 1960s, and 1970s involving three groups of patients—amnesia, split brain, and blindsight. Across all three groups, a similar pattern of results was found—the patients could respond appropriately to stimuli that they denied seeing (or in the case of amnesiacs, having seen before). These studies paved the way for the current wave of research on consciousness. The field is, in fact, still grappling with the implications of the findings showing that the ability to consciously know and report the identity of a visual stimulus can be dissociated in the brain from the mechanisms that underlie the ability to behave in a meaningful way to the same stimulus.

Although sensory processing is pivotal to nearly every theory of emotion, the evaluation of the visual input as ‘emotional’ (e.g. a smile as signalling happiness) has been traditionally assumed to take place in supramodal ‘limbic’ brain regions. Accordingly, subcortical structures of ancient evolutionary origin that receive direct input from the retina, such as the superior colliculus (SC), are traditionally conceptualized as passive relay centres. However, mounting evidence suggests that the SC is endowed with the necessary infrastructure and computational capabilities for the innate recognition and initial categorization of emotionally salient features from retinal information. Here, we built a neurobiologically inspired convolutional deep neural network (DNN) model that approximates physiological, anatomical and connectional properties of the retino-collicular circuit. This enabled us to characterize and isolate the initial computations and discriminations that the DNN model of the SC can perform on facial expressions, based uniquely on the information it directly receives from the virtual retina. Trained to discriminate facial expressions of basic emotions, our model matches human error patterns and above chance, yet suboptimal, classification accuracy analogous to that reported in patients with V1 damage, who rely on retino-collicular pathways for non-conscious vision of emotional attributes. When presented with gratings of different spatial frequencies and orientations never ‘seen’ before, the SC model exhibits spontaneous tuning to low spatial frequencies and reduced orientation discrimination, as can be expected from the prevalence of the magnocellular (M) over parvocellular (P) projections. Likewise, face manipulation that biases processing towards the M or P pathway affects expression recognition in the SC model accordingly, an effect that dovetails with variations of activity in the human SC purposely measured with ultra-high field functional magnetic resonance imaging. Lastly, the DNN generates saliency maps and extracts visual features, demonstrating that certain face parts, like the mouth or the eyes, provide higher discriminative information than other parts as a function of emotional expressions like happiness and sadness. The present findings support the contention that the SC possesses the necessary infrastructure to analyse the visual features that define facial emotional stimuli also without additional processing stages in the visual cortex or in ‘limbic’ areas.This article is part of the theme issue ‘Cracking the laugh code: laughter through the lens of biology, psychology and neuroscience’.

People make rapid inferences about others' thoughts and intentions. For example, they observe facial movements and pupil size of others and unwittingly make use of this information when deciding whether to trust someone or not. However, whether spontaneous mimicry depends on visual awareness of the stimulus and whether these processes underlie trust decisions is still unknown. To investigate whether visual awareness modulates the relationship between emotional expressions, mimicry and trust, participants played a series of trust games and saw either their partners’ faces with a neutral, happy or fearful expression, or their partners' eyes in which the pupil size was large, medium or small. Subjects' trust investments, facial movements and pupil responses were measured. In half of the trials, the stimuli were rendered invisible by continuous flash suppression. Results showed that facial expressions were mimicked and influenced trust decisions during the conscious condition, but not during the unconscious (suppressed) condition. The opposite was found for pupil size, which influenced trust decisions during states of unawareness. These results suggest that the neurobiological pathway linking the observation of facial expressions to mimicry and trust is predominantly conscious, whereas partner pupil size influences trust primarily when presented unconsciously. This article is part of the theme issue ‘Cracking the laugh code: laughter through the lens of biology, psychology and neuroscience’.

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.

Patients with blindsight are blind due to an early visual cortical lesion, but they can discriminate stimuli presented to the blind visual field better than chance. Studies using transcranial magnetic stimulation (TMS) of early visual cortex have tried to induce blindsight-like behaviour in neurologically healthy individuals, but the studies have yielded varied results. We hypothesized that previous demonstrations of TMS-induced blindsight may result from degraded awareness of the stimuli due to the use of dichotomous visibility scales in measuring awareness. In the present study, TMS was applied to early visual cortex during an orientation discrimination task and the subjective scale measuring awareness was manipulated: The participants reported their conscious perception either using a dichotomous scale or a 4-point Perceptual Awareness Scale. Although the results with the dichotomous scale replicated previous reports of blindsight-like behaviour, there was no evidence of TMS-induced blindsight for orientation when the participants used the lowest rating of the 4-point graded scale to indicate that they were not aware of the presence of the stimulus. Moreover, signal detection analyses indicated that across participants, the individual’s sensitivity to consciously discriminate orientation predicted behaviour on reportedly unconscious trials. These results suggest that blindsight-like discrimination of orientation in neurologically healthy individuals does not occur for completely invisible stimuli, that is, when the observers do not report any kind of consciousness of the stimulus. TMS-induced blindsight for orientation is likely degraded conscious vision.

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.

© 2017 Elsevier Ltd Previous research suggests that the implicit recognition of emotional expressions may be carried out by pathways that bypass primary visual cortex (V1) and project to the amygdala. Some of the strongest evidence supporting this claim comes from case studies of “affective blindsight” in which patients with V1 damage can correctly guess whether an unseen face was depicting a fearful or happy expression. In the current study, we report a new case of affective blindsight in patient MC who is cortically blind following extensive bilateral lesions to V1, as well as face and object processing regions in her ventral visual stream. Despite her large lesions, MC has preserved motion perception which is related to sparing of the motion sensitive region MT+ in both hemispheres. To examine affective blindsight in MC we asked her to perform gender and emotion discrimination tasks in which she had to guess, using a two-alternative forced-choice procedure, whether the face presented was male or female, happy or fearful, or happy or angry. In addition, we also tested MC in a four-alternative forced-choice target localization task. Results indicated that MC was not able to determine the gender of the faces (53% accuracy), or localize targets in a forced-choice task. However, she was able to determine, at above chance levels, whether the face presented was depicting a happy or fearful (67%, p = .006), or a happy or angry (64%, p = .025) expression. Interestingly, although MC was better than chance at discriminating between emotions in faces when asked to make rapid judgments, her performance fell to chance when she was asked to provide subjective confidence ratings about her performance. These data lend further support to the idea that there is a non-conscious visual pathway that bypasses V1 which is capable of processing affective signals from facial expressions without input from higher-order face and object processing regions in the ventral visual stream.

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.

The subcortical visual pathway including the superior colliculus (SC), pulvinar, and amygdala has been implicated in unconscious visual processing of faces, eyes, and gaze direction in blindsight. Our previous studies reported that monkey SC and pulvinar neurons responded preferentially to images of faces while performing a delayed non-matching to sample (DNMS) task to discriminate different visual stimuli (Nguyen et al., 2013, 2014). However, the contribution of SC and pulvinar neurons to the discrimination of the facial images and subsequent behavioral performance remains unknown. Since gamma oscillations have been implicated in sensory and cognitive processes as well as behavioral execution, we hypothesized that gamma oscillations during neuronal responses might contribute to achieving the appropriate behavioral performance (i.e., a correct response). In the present study, we re-analyzed those neuronal responses in the monkey SC and pulvinar to investigate possible relationships between gamma oscillations in these neurons and behavioral performance (correct response ratios) during the DNMS task. Gamma oscillations of SC and pulvinar neuronal activity were analyzed in three phases around the stimulus onset [inter-trial interval (ITI): 1000ms before trial onset; Early: 0-200ms after stimulus onset; and Late: 300-500ms after stimulus onset]. We found that human facial images elicited stronger gamma oscillations in the early phase than the ITI and late phase in both the SC and pulvinar neurons. Furthermore, there was a significant correlation between strengths of gamma oscillations in the early phase and behavioral performance in both the SC and pulvinar. The results suggest that gamma oscillatory activity in the SC and pulvinar contributes to successful behavioral performance during unconscious perceptual and behavioral processes.

The continuous flash suppression (CFS) paradigm is increasingly used to study unconscious visual perception. Our goal was to use CFS and to to compare the results with previous findings from patients with brain lesions, and studies of healthy participants. We used an emotion discrimination task and bilaterally presented whole-body postures expressing fear or anger, rendering the stimuli invisible in either one of the visual fields. We found that the CFS presentation did not yield the classical redundant target effect of response facilitation when the unconsciously seen stimuli had congruent emotions; instead we found a facilitation effect in reaction times by body stimuli of incongruent emotions, especially by the unconscious fearful body facilitating discrimination of conscious angry body. Our results with healthy participants showed similarities to hemianopia patients without blindsight, but not to blindsight or neglect patients, indicating that unconscious visual processing is not a single phenomenon, but is likely to involve multiple mechanisms, processes and brain regions. Further studies are necessary to validate the facilitation effect of fearful bodies on other tasks, and to study the neural substrates of this effect.

The aim of the present review is to discuss the localization of circuits that allow recognition of emotional facial expressions in blindsight patients. Because recognition of facial expressions is function of different centers, and their localization is not always clear, we decided to discuss here three emotional facial expression - smiling, disgust, and fear - whose anatomical localization in the pregenual sector of the anterior cingulate cortex (pACC), anterior insula (AI), and amygdala, respectively, is well established. We examined, then, the possible pathways that may convey affective visual information to these centers following lesions of V1. We concluded that the pathway leading to pACC, AI, and amygdala involves the deep layers of the superior colliculus, the medial pulvinar, and the superior temporal sulcus region. We suggest that this visual pathway provides an image of the observed affective faces, which, although deteriorated, is sufficient to determine some overt behavior, but not to provide conscious experience of the presented stimuli.

Blindsight refers to the observation of residual visual abilities in the hemianopic field of patients without a functional V1. Given the within- and between-subject variability in the preserved abilities and the phenomenal experience of blindsight patients, the fine-grained description of the phenomenon is still debated. Here we tested a patient with established "perceptual" and "attentional" blindsight (c.f. Danckert and Rossetti, 2005). Using a pointing paradigm patient MS, who suffers from a complete left homonymous hemianopia, showed clear above chance manual localisation of 'unseen' targets. In addition, target presentations in his blind field led MS, on occasion, to spontaneous responses towards his sighted field. Structural and functional magnetic resonance imaging was conducted to evaluate the magnitude of V1 damage. Results revealed the presence of a calcarine sulcus in both hemispheres, yet his right V1 is reduced, structurally disconnected and shows no fMRI response to visual stimuli. Thus, visual stimulation of his blind field can lead to "action blindsight" and spontaneous antipointing, in absence of a functional right V1. With respect to the antipointing, we suggest that MS may have registered the stimulation and subsequently presumes it must have been in his intact half field.

Patients with hemianopia can present with the so called blindsight phenomenon: the ability to perform above chance in the absence of acknowledged awareness. Proper awareness reports are, thus, crucial to distinguish pure forms of blindsight from forms of conscious, yet degraded, vision. It has, in fact, been recently shown that 1) dichotomous and graded measures to assess awareness can lead to different behavioural results in patients with hemianopia and that 2) different grades of perceptual clarity show different electrophysiological correlates in healthy participants. Here, in hemianopic patients, we assessed awareness by means of the four-point Perceptual Awareness Scale (PAS) and investigated its neural correlates with Event Related Potentials (ERPs). Results showed that patients, in most of the cases, can rate the clarity of their perceptual experience in a graded manner. Moreover, graded perceptual experiences correlated with the amplitude of deflections in ERPs. These results call for the need to assess perceptual awareness with graded measures and for the importance to use electrophysiological data to correlate behaviour with neural processing., Highlights • Hemianopic patients can grade their phenomenal experience along PAS levels. • The amplitude of VAN is modulated by the perceived clarity of the stimulus. • LP, although present, does not increase in amplitude as a function of awareness.

The human brain has evolved a multifaceted fear system, allowing threat detection to enable rapid adaptive responses crucial for survival. Although many cortical and subcortical brain areas are believed to be involved in the survival circuits detecting and responding to threat, the amygdala has reportedly a crucial role in the fear system. Here, we review evidence demonstrating that fearful faces, a specific category of salient stimuli indicating the presence of threat in the surrounding, are preferentially processed in the fear system and in the connected sensory cortices, even when they are presented outside of awareness or are irrelevant to the task. In the visual domain, we discuss evidence showing in hemianopic patients that fearful faces, via a subcortical colliculo-pulvinar-amygdala pathway, have a privileged visual processing even in the absence of awareness and facilitate responses towards visual stimuli in the intact visual field. Moreover, evidence showing that somatosensory cortices prioritise fearful-related signals, to the extent that tactile processing is enhanced in the presence of fearful faces, will be also reported. Finally, we will review evidence revealing that fearful faces have a pivotal role in modulating responses in peripersonal space, in line with the defensive functional definition of PPS.

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.

Psychophysical studies on confidence construction are often grounded in bidimensional signal detection theory (SDT) and its relatives. However, these studies often stand on oversimplified assumptions of (a) bidimensional variance-equality and (b) bidimensional statistical independence. The present study simulated 2-alternative forced-choice and confidence rating performances, incorporating more empirically plausible variance-covariance structures. One prominent observation is that superior metacognitive accuracy can be achieved when one applies a heuristic in which the response-incongruent dimension of information is ignored. This is because such an heuristic takes advantage of the specific unequal-variance structure, which paradoxically cannot be easily exploited if both dimensions are evaluated together. Furthermore, under a variety of internal statistical structures, this simple heuristic predicts dissociations of objective decision and subjective metacognition, which have been empirically observed. Also, it provides a tentative account of some behavioral features of blindsight. Therefore, this surprisingly simple decision heuristic may inspire novel perspectives on metacognition and consciousness. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

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.

In this review, we approach Parkinson's disease (PD) in the context of an evolutionary mismatch of central nervous system functions. The neurons at risk have hyperbranched axons, extensive transmitter release sites, display spontaneous spiking, and elevated mitochondrial stress. They function in networks largely unchanged throughout vertebrate evolution, but now connecting to the expanded human cortex. Their breakdown is favoured by longevity. At the cellular level, mitochondrial dysfunction starts at the synapses, then involves axons and cell bodies. At the behavioural level, network dysfunctions provoke the core motor syndrome of parkinsonism including freezing and failed gait automatization, and non-motor deficits including inactive blindsight and autonomic dysregulation. The proposed evolutionary re-interpretation of PD-prone cellular phenotypes and of prototypical clinical symptoms allows a new conceptual framework for future research.

Blindsight is the ability of patients with primary visual cortex (V1) damage to process information in their clinically blind visual field in the absence of conscious awareness. In addition to those with localized V1 lesions, some patients exhibiting this phenomenon have had a cerebral hemisphere removed or disconnected from the rest of the brain for the treatment of drug-resistant epilepsy (hemispherectomy). Research into the underlying neural substrates of blindsight has long implicated the intact visual cortex in maintaining residual vision and supporting visuo-guided responses to stimuli presented ipsilaterally within the blind visual field while operating outside the geniculo-striate pathway. A recent study demonstrated functional reorganization in the dorsal visual areas of the intact hemisphere, thereby supporting its compensatory role in non-conscious vision. In this study, we used cortical thickness analysis to examine anatomical differences in the visual cortex of the intact hemisphere of three subjects with varying degrees of cortical damage and well documented blindsight: two with a right hemispherectomy (complete and partial), and one with a left V1 lesion. T1-weighted MRI data were obtained for the subjects while control data were chosen from publicly available NKI-dataset to match closely the acquisition parameters of our blindsight cases. Our results show significant increases in cortical thickness in the visual cortex of all blindsight subjects compared to healthy controls, irrespective of age-onset, etiology, and extent of the damage. Our findings add to accumulating evidence from behavioral, functional imaging, and tractography studies of cerebral compensation and reorganization., Highlights • Examined anatomical changes in the intact visual cortex of rare blindsight patients. • First comparison of hemispherectomy and lesion patients to a large control sample. • Blindsight subjects show significant increases in peri-calcarine cortical thickness. • Similar changes observed despite differences in etiology and age at time of lesion. • Increases are possible morphological signs of compensation underlying blindsight.

Podeu consultar les dades primàries associades a l'article a: http://hdl.handle.net/2445/136617, The assessment of task-independent functional connectivity (FC) after a lesion causing hemianopia remains an uncovered topic and represents a crucial point to better understand the neural basis of blindsight (i.e. unconscious visually triggered behavior) and visual awareness. In this light, we evaluated functional connectivity (FC) in 10 hemianopic patients and 10 healthy controls in a resting state paradigm. The main aim of this study is twofold: first of all we focused on the description and assessment of density and intensity of functional connectivity and network topology with and without a lesion affecting the visual pathway, and then we extracted and statistically compared network metrics, focusing on functional segregation, integration and specialization. Moreover, a study of 3-cycle triangles with prominent connectivity was conducted to analyze functional segregation calculated as the area of each triangle created connecting three neighboring nodes. To achieve these purposes we applied a graph theory-based approach, starting from Pearson correlation coefficients extracted from pairs of regions of interest. In these analyses we focused on the FC extracted by the whole brain as well as by four resting state networks: The Visual (VN), Salience (SN), Attention (AN) and Default Mode Network (DMN), to assess brain functional reorganization following the injury. The results showed a general decrease in density and intensity of functional connections, that leads to a less compact structure characterized by decrease in functional integration, segregation and in the number of interconnected hubs in both the Visual Network and the whole brain, despite an increase in long-range inter-modules connections (occipito-frontal connections). Indeed, the VN was the most affected network, characterized by a decrease in intra- and inter-network connections and by a less compact topology, with less interconnected nodes. Surprisingly, we observed a higher functional integration in the DMN and in the AN regardless of the lesion extent, that may indicate a functional reorganization of the brain following the injury, trying to compensate for the general reduced connectivity. Finally we observed an increase in functional specialization (lower between-network connectivity) and in inter-networks functional segregation, which is reflected in a less compact network topology, highly organized in functional clusters. These descriptive findings provide new insight on the spontaneous brain activity in hemianopic patients by showing an alteration in the intrinsic architecture of a large-scale brain system that goes beyond the impairment of a single RSN.

The presence of above-chance unconscious behavioral responses following stimulus presentation to the blind hemifield of hemianopic patients (blindsight) is a well-known phenomenon. What is still lacking is a systematic study of the neuroanatomical bases of two distinct aspects of blindsight: the unconscious above chance performance and the phenomenological aspects that may be associated. Here, we tested 17 hemianopic patients in two tasks i.e. movement and orientation discrimination of a visual grating presented to the sighted or blind hemifield. We classified patients in four groups on the basis of the presence of above chance unconscious discrimination without or with perceptual awareness reports for stimulus presentation to the blind hemifield. A fifth group was represented by patients with interruption of the Optic Radiation. In the various groups we carried out analyses of lesion extent of various cortical areas, probabilistic tractography as well as assessment of the cortical thickness of the intact hemisphere. All patients had lesions mainly, but not only, in the occipital lobe and the statistical comparison of their extent provided clues as to the critical anatomical substrate of unconscious above-chance performance and of perceptual awareness reports, respectively. In fact, the two areas that turned out to be critical for above-chance performance in the discrimination of moving versus non-moving visual stimuli were the Precuneus and the Posterior Cingulate Gyrus while for perceptual awareness reports the crucial areas were Intracalcarine, Supracalcarine, Cuneus, and the Posterior Cingulate Gyrus. Interestingly, the proportion of perceptual awareness reports was higher in patients with a spared right hemisphere. As to probabilistic tractography, all pathways examined yielded higher positive values for patients with perceptual awareness reports. Finally, the cortical thickness of the intact hemisphere was greater in patients showing above-chance performance than in those at chance. This effect is likely to be a result of neuroplastic compensatory mechanisms.

Some neurological patients with primary visual cortex (V1) lesions can guide their behavior based on stimuli presented to their blind visual field. One example of this phenomenon is the ability to discriminate colors in the absence of awareness. These so-called patients with blindsight must have a neural pathway that bypasses V1, explaining their ability to unconsciously process stimuli. The pathways that have been most often hypothesized to be the cause of blindsight connect lateral geniculate nucleus (LGN) or superior colliculus (SC) to extrastriate cortex, most likely V5, and parietal areas. To test if similar pathways function in neurologically healthy individuals or if unconscious processing depends on early visual cortex, we disturbed the visibility of a chromatic stimulus with metacontrast masking (Experiment 1) or neuronavigated transcranial magnetic stimulation (TMS) of early visual cortex, exact target being retinotopically mapped V1 (Experiment 2). We measured unconscious processing using the redundant target effect (RTE), which is the speeding up of reaction times in response to dual stimuli compared with one stimulus, when the task is to respond to any number of stimuli. An unconscious chromatic RTE was found when the visibility of the redundant chromatic stimulus was suppressed with a visual mask. When TMS was targeted to the correct retinotopic location of V1, and conscious perception of the redundant chromatic stimulus suppressed, the RTE was eliminated. Whether the elimination of unconscious RTE during TMS was exclusively due to disruption of V1 activity, or whether it was due to the possible interference with processing in V2 or even V3, is discussed. Based on our results and converging evidence from previous studies, we conclude that unconscious processing of chromatic information depends on the early visual cortex, in neurologically healthy participants.

© 2020 Elsevier Ltd Some patients who are considered cortically blind due to the loss of their primary visual cortex (V1) show a remarkable ability to act upon or discriminate between visual stimuli presented to their blind field, without any awareness of those stimuli. This phenomenon is often referred to as blindsight. Despite the range of spared visual abilities, the identification of the pathways mediating blindsight remains an active and contentious topic in the field. In this review, we discuss recent findings of the candidate pathways and their relative contributions to different forms of blindsight across the lifespan to illustrate the varied nature of unconscious visual processing.

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.

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.

Cognitive neuropsychological evidence is widely viewed as inherently flawed or weak, despite well-reasoned arguments to the contrary by many theorists. Rather than attempting yet another defence of cognitive neuropsychology on logical grounds, we point out through examples that in practice, cognitive neuropsychological evidence is widely accepted as valid and important, and has had a major impact on cognitive theory and research. Objections offered in the abstract rarely arise in the context of actual studies. We develop these points through examples from the domain of vision, discussing cerebral achromatopsia and akinetopsia, selective impairment and sparing of face recognition, perception-action dissociations, and blindsight.

To what extent does functional brain organization rely on sensory input? Here, we show that for the penultimate visual-processing region, ventral-temporal cortex (VTC), visual experience is not the origin of its fundamental organizational property, category selectivity. In the fMRI study reported here, we presented 14 congenitally blind participants with face-, body-, scene-, and object-related natural sounds and presented 20 healthy controls with both auditory and visual stimuli from these categories. Using macro-anatomical alignment, response mapping, and surface-based multi-voxel pattern analysis, we demonstrated that VTC in blind individuals shows robust discriminatory responses elicited by the four categories and that these patterns of activity in blind subjects could successfully predict the visual categories in sighted controls. These findings were confirmed in a subset of blind participants born without eyes and thus deprived from all light perception since conception. The sounds also could be decoded in primary visual and primary auditory cortex, but these regions did not sustain generalization across modalities. Surprisingly, although not as strong as visual responses, selectivity for auditory stimulation in visual cortex was stronger in blind individuals than in controls. The opposite was observed in primary auditory cortex. Overall, we demonstrated a striking similarity in the cortical response layout of VTC in blind individuals and sighted controls, demonstrating that the overall category-selective map in extrastriate cortex develops independently from visual experience.

Item does not contain fulltext Intense visual training can lead to partial recovery of visual field defects caused by lesions of the primary visual cortex. However, the standard visual detection and discrimination tasks, used to assess this recovery process tend to ignore the complexity of the natural visual environment, where multiple stimuli continuously interact. Visual competition is an essential component for natural search tasks and detecting unexpected events. Our study focused on visual decision-making and to what extent the recovered visual field can compete for attention with the 'intact' visual field. Nine patients with visual field defects who had previously received visual discrimination training, were compared to healthy age-matched controls using a saccade target-selection paradigm, in which participants actively make a saccade towards the brighter of two flashed targets. To further investigate the nature of competition (feed-forward or feedback inhibition), we presented two flashes that reversed their intensity difference during the flash. Both competition between recovered visual field and intact visual field, as well as competition within the intact visual field, were assessed. Healthy controls showed the expected primacy effect; they preferred the initially brighter target. Surprisingly, choice behaviour, even in the patients' supposedly 'intact' visual field, was significantly different from the control group for all but one. In the latter patient, competition was comparable to the controls. All other patients showed a significantly reduced preference to the brighter target, but still showed a small hint of primacy in the reversal conditions. The present results indicate that patients and controls have similar decision-making mechanisms but patients' choices are affected by a strong tendency to guess, even in the intact visual field. This tendency likely reveals slower integration of information, paired with a lower threshold. Current rehabilitation should therefore also include training focused on improving visual decision-making of the defective and the intact visual field.

Summary Object constancies are central constructs in theories of visual phenomenology. A powerful example is "size constancy," in which the perceived size of an object remains stable despite changes in viewing distance [1–4]. Evidence from neuropsychology [5], neuroimaging [6–11], transcranial magnetic stimulation [12, 13], single-unit and lesion studies in monkey [14–20], and computational modeling [21] suggests that re-entrant processes involving reciprocal interactions between primary visual cortex (V1) and extrastriate visual areas [22–26] play an essential role in mediating size constancy. It is seldom appreciated, however, that object constancies must also operate for the visual guidance of goal-directed action. For example, when reaching out to pick up an object, the hand's in-flight aperture scales with size of the goal object [27–30] and is refractory to the decrease in retinal-image size with increased viewing distance [31–41] (Figure 1), a phenomenon we call "grip constancy." Does grip constancy, like perceptual constancy, depend on V1 or can it be mediated by pathways that bypass it altogether? We tested these possibilities in an individual, M.C., who has bilateral lesions encompassing V1 and much of the ventral visual stream. We show that her perceptual estimates of object size co-vary with retinal-image size rather than real-world size as viewing distance varies. In contrast, M.C. shows near-normal scaling of in-flight grasp aperture to object size despite changes in viewing distance. Thus, although early visual cortex is necessary for perceptual object constancy, it is unnecessary for grip constancy, which is mediated instead by separate visual inputs to dorsal-stream visuomotor areas [42–48].

The development of visual function takes place over many months or years in primate infants. Visual sensitivity is very poor near birth and improves over different times courses for different visual functions. The neural mechanisms that underlie these processes are not well understood despite many decades of research. The puzzle arises because research into the factors that limit visual function in infants has found surprisingly mature neural organization and adult-like receptive field properties in very young infants. The high degree of visual plasticity that has been documented during the sensitive period in young children and animals leaves the brain vulnerable to abnormal visual experience. Abnormal visual experience during the sensitive period can lead to amblyopia, a developmental disorder of vision affecting ∼3% of children. This review provides a historical perspective on research into visual development and the disorder amblyopia. The mismatch between the status of the primary visual cortex and visual behavior, both during visual development and in amblyopia, is discussed, and several potential resolutions are considered. It seems likely that extrastriate visual areas further along the visual pathways may set important limits on visual function and show greater vulnerability to abnormal visual experience. Analyses based on multiunit, population activity may provide useful representations of the information being fed forward from primary visual cortex to extrastriate processing areas and to the motor output.This article is based on a Presidential Lecture presented at the 2016 Annual Meeting.

We investigated whether healthy participants can spontaneously adopt effective eye movement strategies to compensate for information loss similar to that experienced by patients with damage to visual cortex (hemianopia). Visual information in 1 hemifield was removed or degraded while participants searched for an emotional face among neutral faces or a line tilted 45° to the right among lines of varying degree of tilt. A bias to direct saccades toward the sighted field was observed across all 4 experiments. The proportion of saccades directed toward the "blind" field increased with the amount of information available in that field, suggesting fixations are driven toward salient visual stimuli rather than toward locations that maximize information gain. In Experiments 1 and 2, the sighted-field bias had a minimal impact on search efficiency, because the target was difficult to find. However, the sighted-field bias persisted even when the target was visually distinct from the distractors and could easily be detected in the periphery (Experiments 3 and 4). This surprisingly inefficient search behavior suggests that eye movements are biased to salient visual stimuli even when it comes at a clear cost to search efficiency, and efficient strategies to compensate for visual deficits are not spontaneously adopted by healthy participants. (PsycINFO Database Record

The relationship between visual loss and psychosis is complex: congenital visual loss appears to be protective against the development of a psychotic disorder, particularly schizophrenia. In later life, however, visual deprivation or visual loss can give rise to hallucinosis, disorders of visual insight such as blindsight or Anton syndrome, or, in the context of neurodegenerative disorders, more complex psychotic presentations. We draw on a computational psychiatric approach to consider the foundational role of vision in the construction of representations of the world and the effects of visual loss at different developmental stages. Using a Bayesian prediction error minimization model, we describe how congenital visual loss may be protective against the development of the kind of computational deficits postulated to underlie schizophrenia, by increasing the precision (and consequent stability) of higher-level (including supramodal) priors, focusing on visual loss-induced changes in NMDA receptor structure and function as a possible mechanistic substrate. In simple terms, we argue that when people cannot see from birth, they rely more heavily on the context they extract from the other senses, and the resulting model of the world is more impervious to the false inferences, made in the face of inevitably noisy perceptual input, that characterize schizophrenia. We show how a Bayesian prediction error minimization framework can also explain the relationship between later visual loss and other psychotic symptoms, as well as the effects of visual deprivation and hallucinogenic drugs, and outline experimentally testable hypotheses generated by this approach.

© 2017 Elsevier Ltd Injury to the primary visual cortex (V1, striate cortex) and the geniculostriate pathway in adults results in cortical blindness, abolishing conscious visual perception. Early studies by Larry Weiskrantz and colleagues demonstrated that some patients with an occipital-lobe injury exhibited a degree of unconscious vision and visually-guided behaviour within the blind field. A more recent focus has been the observed phenomenon whereby early-life injury to V1 often results in the preservation of visual perception in both monkeys and humans. These findings initiated a concerted effort on multiple fronts, including nonhuman primate studies, to uncover the neural substrate/s of the spared conscious vision. In both adult and early-life cases of V1 injury, evidence suggests the involvement of the Middle Temporal area (MT) of the extrastriate visual cortex, which is an integral component area of the dorsal stream and is also associated with visually-guided behaviors. Because of the limited number of early-life V1 injury cases for humans, the outstanding question in the field is what secondary visual pathways are responsible for this extraordinary capacity? Here we report for the first time a case of a child (B.I.) who suffered a bilateral occipital-lobe injury in the first two weeks postnatally due to medium-chain acyl-Co-A dehydrogenase deficiency. At 6 years of age, B.I. underwent a battery of neurophysiological tests, as well as structural and diffusion MRI and ophthalmic examination at 7 years. Despite the extensive bilateral occipital cortical damage, B.I. has extensive conscious visual abilities, is not blind, and can use vision to navigate his environment. Furthermore, unlike blindsight patients, he can readily and consciously identify happy and neutral faces and colors, tasks associated with ventral stream processing. These findings suggest significant re-routing of visual information. To identify the putative visual pathway/s responsible for this ability, MRI tractography of secondary visual pathways connecting MT with the lateral geniculate nucleus (LGN) and the inferior pulvinar (PI) were analysed. Results revealed an increased PI-MT pathway in the left hemisphere, suggesting that this pulvinar relay could be the neural pathway affording the preserved visual capacity following an early-life lesion of V1. These findings corroborate anatomical evidence from monkeys showing an enhanced PI-MT pathway following an early-life lesion of V1, compared to adults.

ObjectiveTo compare recognition of facial expression (FE) vs recognition of facial identity (FI) in posterior cortical atrophy (PCA), with the hypothesis that FE recognition would be relatively preserved in PCA.MethodsIn this observational study, FI and expression recognition tasks were performed by 194 participants in 4 groups, including 39 with Alzheimer disease (AD) (non-PCA), 49 with behavioral variant frontotemporal dementia (bvFTD), 15 with PCA, and 91 healthy controls. Between-group differences in test scores were compared.ResultsPatients with PCA performed worse than healthy controls in FI and emotion recognition tasks (p < 0.001 for all). Patients with PCA also performed worse than AD and bvFTD groups in FI recognition, with no difference in FE recognition.ConclusionsPatients with PCA have relatively preserved FE recognition compared to FI recognition, as seen in affective blindsight.

Blindsight refers to the ability of some patients with destruction of the primary visual cortex (V1) to respond to stimuli presented in their clinically blind visual field despite lack of visual awareness. Here we tested a rare and well-known patient with blindsight following hemispherectomy, DR, who has had the entire cortex in the right hemisphere removed, and in whom the right superior colliculus is the only post-chiasmatic visual structure remaining intact. Compared to more traditional cases of blindsight after damage confined to V1, the study of blindsight in hemispherectomy has offered the invaluable opportunity to examine directly two outstanding questions: the contribution of the intact hemisphere to visual processing without awareness, and the nature of plastic and compensatory changes in these remaining contralesional visual areas. Population receptive field (pRF) mapping was used to define retinotopic maps, delineate the boundaries between the visual areas, examine changes in the sizes of receptive field centres within each visual area, and their variability as a function of eccentricity. Aside from the dorsal visual areas showing blurred borders between V2d and V3d, not otherwise detected with perimetric mapping, the retinotopic maps of DR did not differ substantially from those of three matched healthy controls. Interestingly, those dorsal compartments showed a significant increase in the RF sizes toward values typical of higher-order processing cortices, while no differences were observed in the corresponding ventral visual areas. Findings showed that whereas receptive field sizes at foveal and parafoveal eccentricities (≤ 4°) were not measurably altered, the pRF size increased by ~ 270% at 4-6° of eccentricity, and the size difference reached ~ 300% between 8° and 10°. We interpret these findings to suggest that an increase in pRF sizes could be indicative of cerebral plasticity involving the retinotopic reorganization of the dorsal visual areas.

Implicit visual processing of emotional stimuli has been widely investigated since the classical studies on affective blindsight, in which patients with primary visual cortex lesions showed discriminatory abilities for unseen emotional stimuli in the absence of awareness. In addition, more recent evidence from hemianopic patients showed response facilitation and enhanced early visual encoding of seen faces, only when fearful faces were presented concurrently in the blind field. However, it is still unclear whether unseen fearful faces specifically facilitate visual processing of facial stimuli, or whether the facilitatory effect constitutes an adaptive mechanism prioritizing the visual analysis of any stimulus. To test this question, we tested a group of hemianopic patients who perform at chance in forced-choice discrimination tasks of stimuli in the blind field. Patients performed a go/no-go task in which they were asked to discriminate simple visual stimuli (Gabor patches) presented in their intact field, while fearful, happy and neutral faces were concurrently presented in the blind field. The results showed a reduction in response times to the Gabor patches presented in the intact field, when fearful faces were concurrently presented in the blind field, but only in patients with left hemispheric lesions. No facilitatory effect was observed in patients with right hemispheric lesions. These results suggest that unseen fearful faces are implicitly processed and can facilitate the visual analysis of simple visual stimuli presented in the intact field. This effect might be subserved by activity in the spared colliculo-amygdala-extrastriate pathway that promotes efficient visual analysis of the environment and rapid execution of defensive responses. Such a facilitation is observed only in patients with left lesions, favouring the hypothesis that the right hemisphere mediates implicit visual processing of fear signals.

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 V1 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.

Blindsight, the residual abilities of patients with cortical blindness to respond proficiently to stimuli they do not consciously acknowledge, offers a unique opportunity to study the functional and anatomical mechanisms sustaining visual awareness. Over decades, the phenomenon has been documented in a wide number of different patients, across independent laboratories, and for a variety of tasks and stimulus properties. Nevertheless, the functional neuroanatomy of blindsight remains elusive and alternative proposals have been put forth. To tackle this issue from a novel perspective, we performed a quantitative Activation Likelihood Estimation (ALE) meta-analysis on the neuroimaging literature available on blindsight. Significant activity was reported in subcortical structures, such as the superior colliculus, pulvinar and amygdala, as well as in cortical extrastriate areas along the dorsal and ventral visual stream. This data-driven functional network collectively defines the extant neural fingerprint of blindsight. To further characterize the unique combination of segregation and integration in brain networks engaged in blindsight, we measured the relationship between active areas and experimental features in the original studies, their clustering and hierarchical organization. Results support a network-based organization in the functional neuroanatomy of blindsight, which likely reflects the intersection of different stimulus properties and behavioural tasks examined. We suggest that the conceptualization of blindsight as a constellation of multiple nonconscious visual abilities is better apt as a summary of present-day wisdom, thereby mirroring the variety of existing V1-independent pathway and their different functional roles.

The human brain can process facial expressions of emotions rapidly and without awareness. Several studies in patients with damage to their primary visual cortices have shown that they may be able to guess the emotional expression on a face despite their cortical blindness. This non-conscious processing, called affective blindsight, may arise through an intact subcortical visual route that leads from the superior colliculus to the pulvinar, and thence to the amygdala. This pathway is thought to process the crude visual information conveyed by the low spatial frequencies of the stimuli.In order to investigate whether this is the case, we studied a patient (TN) with bilateral cortical blindness and affective blindsight. An fMRI paradigm was performed in which fearful and neutral expressions were presented using faces that were either unfiltered, or filtered to remove high or low spatial frequencies. Unfiltered fearful faces produced right amygdala activation although the patient was unaware of the presence of the stimuli. More importantly, the low spatial frequency components of fearful faces continued to produce right amygdala activity while the high spatial frequency components did not. Our findings thus confirm that the visual information present in the low spatial frequencies is sufficient to produce affective blindsight, further suggesting that its existence could rely on the subcortical colliculo-pulvino-amygdalar pathway.

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.

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.

Hemianopic patients retain some abilities to integrate audiovisual stimuli in the blind hemifield, showing both modulation of visual perception by auditory stimuli and modulation of auditory perception by visual stimuli. Indeed, conscious detection of a visual target in the blind hemifield can be improved by a spatially coincident auditory stimulus (auditory enhancement of visual detection), while a visual stimulus in the blind hemifield can improve localization of a spatially coincident auditory stimulus (visual enhancement of auditory localization). To gain more insight into the neural mechanisms underlying these two perceptual phenomena, we propose a neural network model including areas of neurons representing the retina, primary visual cortex (V1), extrastriate visual cortex, auditory cortex and the Superior Colliculus (SC). The visual and auditory modalities in the network interact via both direct cortical-cortical connections and subcortical-cortical connections involving the SC; the latter, in particular, integrates visual and auditory information and projects back to the cortices. Hemianopic patients were simulated by unilaterally lesioning V1, and preserving spared islands of V1 tissue within the lesion, to analyze the role of residual V1 neurons in mediating audiovisual integration. The network is able to reproduce the audiovisual phenomena in hemianopic patients, linking perceptions to neural activations, and disentangles the individual contribution of specific neural circuits and areas via sensitivity analyses. The study suggests i) a common key role of SC-cortical connections in mediating the two audiovisual phenomena; ii) a different role of visual cortices in the two phenomena: auditory enhancement of conscious visual detection being conditional on surviving V1 islands, while visual enhancement of auditory localization persisting even after complete V1 damage. The present study may contribute to advance understanding of the audiovisual dialogue between cortical and subcortical structures in healthy and unisensory deficit conditions.