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Patients with lesions in the visual cortex are blind in corresponding regions of the visual field, but they still may process visual information, a phenomenon referred to as residual vision or “blindsight”. Here we report behavioral and fMRI observations with a patient who reports conscious vision across an extended area of blindness for moving, but not for stationary stimuli. This completion effect is shown to be of perceptual and not of conceptual origin, most likely mediated by spared representations of the visual field in the striate cortex. The neural output to extra‐striate areas from regions of the deafferented striate cortex is apparently still intact; this is, for instance, indicated by preserved size constancy of visually completed stimuli. Neural responses as measured with fMRI reveal an activation only for moving stimuli, but importantly on the ipsilateral side of the brain. In a conceptual model this shift of activation to the “wrong” hemisphere is explained on the basis of an imbalance of excitatory and inhibitory interactions within and between the striate cortices due to the brain injury. The observed neuroplasticity indicated by this shift together with the behavioral observations provide important new insights into the functional architecture of the human visual system and provide new insight into the concept of consciousness. [ABSTRACT FROM AUTHOR]

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]

The primary visual cortex (V1) is one of the most studied regions of the brain and is characterized by its specialized and laminated layer 4 in human and non-human primates. However, studies aiming to harmonize the definition of the cortical layers and borders of V1 across rodents and primates are very limited. This article attempts to identify and harmonize the molecular markers and connectional patterns that can consistently link corresponding cortical layers of V1 and borders across mammalian species and ages. V1 in primates has at least two additional and unique layers (L3b2 and L3c) and two sublayers of layer 4 (L4a and L4b) compared to rodent V1. In all species examined, layers 4 and 3b of V1 receive strong inputs from the (dorsal) lateral geniculate nucleus, and V1 is mostly surrounded by the secondary visual cortex except for one location where V1 directly abuts area prostriata. The borders of primate V1 can also be clearly identified at mid-gestational ages using gene markers. In rodents, a novel posteromedial extension of V1 is identified, which expresses V1 marker genes and receives strong inputs from the lateral geniculate nucleus. This V1 extension was labeled as the posterior retrosplenial cortex and medial secondary visual cortex in the literature and brain atlases. Layer 6 of the rodent and primate V1 originates corticothalamic projections to the lateral geniculate, lateral dorsal, and reticular thalamic nuclei and the lateroposterior–pulvinar complex with topographic organization. Finally, the direct geniculo-extrastriate (particularly the strong geniculo-prostriata) projections are probably major contributors to blindsight after V1 lesions. Taken together, compared to rodents, primates, and humans, V1 has at least two unique middle layers, while other layers are comparable across species and display conserved molecular markers and similar connections with the visual thalamus with only subtle differences. [ABSTRACT FROM AUTHOR]

The nature of subjective conscious experience, which accompanies us throughout our waking lives, and how it is generated, remain elusive. One of the challenges in studying subjective experience is disentangling the brain activity related to the sensory stimulus processing and stimulus-guided behavior from those associated with subjective perception. Blindsight, a phenomenon characterized by the retained visual discrimination performance but impaired visual consciousness due to damage to the primary visual cortex, becomes a special entry point to address this question. However, to fully understand the underlying neural mechanism, relying on studies involving human patients alone is insufficient. In this paper, we tried to address this issue, by first introducing the well-known cases of blindsight, especially the reports on subjective experience in both human and monkey subjects. And then we described how the impaired visual awareness of blindsight monkeys has been discovered and further studied by specifically designed tasks, as verbal reporting is not possible for these animals. Our previous studies also demonstrated that many complex visually guided cognitive processes were still retained despite the impairment of visual awareness. Further investigation needs to be conducted to explore the relationship between visually guided behavior, visual awareness and brain activity in blindsight subjects. • Blindsight is a special entry point to study the mechanism of subjective experience. • We described how impaired visual awareness was discovered in blindsight monkeys. • We propose our future strategies to clarify the metacognition in blindsight monkeys. [ABSTRACT FROM AUTHOR]

Even when brain scans fail to detect a striate lesion, functional evidence for blindsight can be adduced. In the aftermath of an automobile accident, JK became blind. Results of ophthalmic exams indicated that the blindness must be cortical. Nevertheless, multiple MRI scans failed to detect structural damage to the striate cortex. Prior to the accident JK had been an athlete; after the accident he retained some athletic abilities, arousing suspicions that hemight be engaged in fraud. His residual athletic abilities--e.g., hitting a handball or baseball, or catching a Frisbee--coupled with his experienced blindness, suggested blindsight. But due to the apparent absence of striate lesions, we designed a series of tasks for temporal and spatial dimensions in an attempt to detect functional evidence of his disability. Indeed, test results revealed compelling neural evidence that comport with his subjective reports. This spatiotemporal task-related method that includes contrasts with healthy controls, and detailed understanding of the patient's conscious experience, can be generalized for clinical, scientific and forensic investigations of blindsight. [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]

Even when brain scans fail to detect a striate lesion, functional evidence for blindsight can be adduced. In the aftermath of an automobile accident, JK became blind. Results of ophthalmic exams indicated that the blindness must be cortical. Nevertheless, multiple MRI scans failed to detect structural damage to the striate cortex. Prior to the accident JK had been an athlete; after the accident he retained some athletic abilities, arousing suspicions that he might be engaged in fraud. His residual athletic abilities—e.g., hitting a handball or baseball, or catching a Frisbee—coupled with his experienced blindness, suggested blindsight. But due to the apparent absence of striate lesions, we designed a series of tasks for temporal and spatial dimensions in an attempt to detect functional evidence of his disability. Indeed, test results revealed compelling neural evidence that comport with his subjective reports. This spatiotemporal task-related method that includes contrasts with healthy controls, and detailed understanding of the patient's conscious experience, can be generalized for clinical, scientific and forensic investigations of blindsight.

Convolutional Neural Networks (CNN) are a class of machine learning models predominately used in computer vision tasks and can achieve human-like performance through learning from experience. Their striking similarities to the structural and functional principles of the primate visual system allow for comparisons between these artificial networks and their biological counterparts, enabling exploration of how visual functions and neural representations may emerge in the real brain from a limited set of computational principles. After considering the basic features of CNNs, we discuss the opportunities and challenges of endorsing CNNs as in silico models of the primate visual system. Specifically, we highlight several emerging notions about the anatomical and physiological properties of the visual system that still need to be systematically integrated into current CNN models. These tenets include the implementation of parallel processing pathways from the early stages of retinal input and the reconsideration of several assumptions concerning the serial progression of information flow. We suggest design choices and architectural constraints that could facilitate a closer alignment with biology provide causal evidence of the predictive link between the artificial and biological visual systems. Adopting this principled perspective could potentially lead to new research questions and applications of CNNs beyond modeling object recognition. [ABSTRACT FROM AUTHOR]

Some researchers have argued that normal human observers can exhibit blindsight-like behavior: the ability to discriminate or identify a stimulus without being aware of it. However, we recently used a bias-free task to show that what looks like blindsight may in fact be an artifact of typical experimental paradigms susceptibility to response bias. While those findings challenge previous reports of blindsight in normal observers, they do not rule out the possibility that different stimuli or techniques could still reveal perception without awareness. One intriguing candidate is emotion processing, since processing of emotional stimuli (e.g. fearful/happy faces) has been reported to potentially bypass conscious visual circuits. Here we used the bias-free blindsight paradigm to investigate whether emotion processing might reveal featural blindsight, i.e. ability to identify a faces emotion without introspective access to the task-relevant features that led to the discrimination decision. However, we saw no evidence for emotion processing featural blindsight: as before, whenever participants could identify a faces emotion they displayed introspective access to the task-relevant features, matching predictions of a Bayesian ideal observer. These results add to the growing body of evidence that perceptual discrimination ability without introspective access may not be possible for neurologically intact observers.

• Neurologically healthy humans can initiate and guide saccadic responses unconsciously. • Unconscious saccadic responses were observed in the minority of trials. • The reduced visibility of stimuli was associated with slower and less precise gaze shift. • Unconscious saccadic responses may be based on weak conscious experiences. Some patients with a visual field loss due to a lesion in the primary visual cortex (V1) can shift their gaze to stimuli presented in their blind visual field. The extent to which a similar "blindsight" capacity is present in neurologically healthy individuals remains unknown. Using retinotopically navigated transcranial magnetic stimulation (TMS) of V1 (Experiment 1) and metacontrast masking (Experiment 2) to suppress conscious vision, we examined neurologically healthy humans' ability to make saccadic eye movements toward visual targets that they reported not seeing. In the TMS experiment, the participants were more likely to initiate a saccade when a stimulus was presented, and they reported not seeing it, than in trials which no stimulus was presented. However, this happened only in a very small proportion (∼8%) of unseen trials, suggesting that saccadic reactions were largely based on conscious perception. In both experiments, saccade landing location was influenced by unconscious information: When the participants denied seeing the target but made a saccade, the saccade was made toward the correct location (TMS: 68%, metacontrast: 63%) more often than predicted by chance. Signal detection theoretic measures suggested that in the TMS experiment, saccades toward unseen targets may have been based on weak conscious experiences. In both experiments, reduced visibility of the target stimulus was associated with slower and less precise gaze shifts. These results suggest that saccades made by neurologically healthy humans may be influenced by unconscious information, although the initiation of saccades is largely based on conscious vision. [ABSTRACT FROM AUTHOR]

Convolutional Neural Networks (CNN) are a class of machine learning models predominately used in computer vision tasks and can achieve human-like performance through learning from experience. Their striking similarities to the structural and functional principles of the primate visual system allow for comparisons between these artificial networks and their biological counterparts, enabling exploration of how visual functions and neural representations may emerge in the real brain from a limited set of computational principles. After considering the basic features of CNNs, we discuss the opportunities and challenges of endorsing CNNs as in silico models of the primate visual system. Specifically, we highlight several emerging notions about the anatomical and physiological properties of the visual system that still need to be systematically integrated into current CNN models. These tenets include the implementation of parallel processing pathways from the early stages of retinal input and the reconsideration of several assumptions concerning the serial progression of information flow. We suggest design choices and architectural constraints that could facilitate a closer alignment with biology provide causal evidence of the predictive link between the artificial and biological visual systems. Adopting this principled perspective could potentially lead to new research questions and applications of CNNs beyond modeling object recognition.

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'. [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]

In the contemporary discussions concerning unconscious perception it is not uncommon to postulate that content and phenomenal character are 'orthogonal', i.e., there is no type of content which is essentially conscious, but instead, every representational content can be either conscious or not. Furthermore, this is not merely treated as a thesis justified by theoretical investigations, but as supported by empirical considerations concerning the actual functioning of the human cognition. In this paper, I address unconscious color perception and argue for a negative thesis—that the main experimental paradigms used in studying unconscious color perception do not provide support for the position that conscious and unconscious color representations have the same type of content. More specifically, I claim that there is no significant support for the claim that unconscious vision categorically represents surface colors. [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.

Here, we report on a previously unknown form of thalamocortical plasticity observed following lesions of the primary visual area (V1) in marmoset monkeys. In primates, lateral geniculate nucleus (LGN) neurons form parallel pathways to the cortex, which are characterized by the expression of different calcium-binding proteins. LGN projections to the middle temporal (MT) area only originate in the koniocellular layers, where many neurons express calbindin. In contrast, projections to V1 also originate in the magnocellular and parvocellular layers, where neurons express parvalbumin but not calbindin. Our results demonstrate that this specificity is disrupted following long-term (1 to 3 y) unilateral V1 lesions, indicating active rearrangement of the geniculocortical circuit. In lesioned animals, retrograde tracing revealed MT-projecting neurons scattered throughout the lesion projection zone (LPZ, the sector of the LGN that underwent retrograde degeneration following a V1 lesion). Many of the MT-projecting neurons had large cell bodies and were located outside the koniocellular layers. Furthermore, we found that a large percentage of magno- and parvocellular neurons expressed calbindin in addition to the expected parvalbumin expression and that this coexpression was present in many of the MT-projecting neurons within the LPZ. These results demonstrate that V1 lesions trigger neurochemical and structural remodeling of the geniculo-extrastriate pathway, leading to the emergence of nonkoniocellular input to MT. This has potential implications for our understanding of the neurobiological bases of the residual visual abilities that survive V1 lesions, including motion perception and blindsight, and reveals targets for rehabilitation strategies to ameliorate the consequences of cortical blindness. [ABSTRACT FROM AUTHOR]

Blindsight regroups the different manifestations of preserved discriminatory visual capacities following the damage to the primary visual cortex. Blindsight types differentially impact objective and subjective perception, patients can report having no visual awareness whilst their behaviour suggests visual processing still occurs at some cortical level. This phenomenon hence presents a unique opportunity to study consciousness and perceptual consciousness, and for this reason, it has had an historical importance for the development of this field of research. From these studies, two main opposing models of the underlying mechanisms have been established: (a) blindsight is perception without consciousness or (b) blindsight is in fact degraded vision, two views that mirror more general theoretical options about whether unconscious cognition truly exists or whether it is only a degraded form of conscious processing. In this article, we want to re-examine this debate in the light of recent advances in the characterization of blindsight and associated phenomena. We first provide an in-depth definition of blindsight and its subtypes, mainly blindsight type I, blindsight type II and the more recently described blindsense. We emphasize the necessity of sensitive and robust methodology to uncover the dissociations between perception and awareness that can be observed in brain-damaged patients with visual field defects at different cognitive levels. We discuss these different profiles of dissociation in the light of both contending models. We propose that the different types of dissociations reveal a pattern of relationship between perception, awareness and metacognition that is actually richer than what is proposed by either of the existing models. Finally, we consider this in the framework of current theories of consciousness and touch on the implications the findings of blindsight have on these. [ABSTRACT FROM AUTHOR]

Following lesions of the primary visual cortex (V1), the lateral geniculate nucleus (LGN) undergoes substantial cell loss due to retrograde degeneration. However, visually responsive neurons remain in the degenerated sector of LGN, and these have been implicated in mediation of residual visual capacities that remain within the affected sectors of the visual field. Using immunohistochemistry, we compared the neurochemical characteristics of LGN neurons in V1-lesioned marmoset monkeys (Callithrix jacchus) with those of non-lesioned control animals. We found that GABAergic neurons form approximately 6.5% of the neuronal population in the normal LGN, where most of these cells express the calcium-binding protein parvalbumin. Following long-term V1 lesions in adult monkeys, we observed a marked increase (~ sevenfold) in the proportion of GABA-expressing neurons in the degenerated sector of the LGN, indicating that GABAergic cells are less affected by retrograde degeneration in comparison with magno- and parvocellular projection neurons. In addition, following early postnatal V1 lesions and survival into adulthood, we found widespread expression of GABA in putative projection neurons, even outside the degenerated sectors (lesion projection zones). Our findings show that changes in the ratio of GABAergic neurons in LGN need to be taken into account in the interpretation of the mechanisms of visual abilities that survive V1 lesions in primates. [ABSTRACT FROM AUTHOR]

• TMS of early visual cortex impaired visual awareness of orientation. • Unconscious visual processing of orientation was not observed when nothing was seen. • TMS-induced blindsight-like performance depended on awareness. 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. [ABSTRACT FROM AUTHOR]

• Mouse and Monkey Vision. • Object vision in neocortex/cerebellum. • Visuomotor coding schemes. We conduct a comparative evaluation of the visual systems from the retina to the muscles of the mouse and the macaque monkey noting the differences and similarities between these two species. The topics covered include (1) visual-field overlap, (2) visual spatial resolution, (3) V1 cortical point-image [i.e., V1 tissue dedicated to analyzing a unit receptive field], (4) object versus motion encoding, (5) oculomotor range, (6) eye, head, and body movement coordination, and (7) neocortical and cerebellar function. We also discuss blindsight in rodents and primates which provides insights on how the neocortex mediates conscious vision in these species. This review is timely because the field of visuomotor neurophysiology is expanding beyond the macaque monkey to include the mouse; there is therefore a need for a comparative analysis between these two species on how the brain generates visuomotor responses. [ABSTRACT FROM AUTHOR]

Through phylogeny, novel neural circuits are added on top of ancient circuits. Upon injury of a novel circuit which enabled fine control, the ancient circuits can sometimes take over its function for recovery; however, the recovered function is limited according to the capacity of the ancient circuits. In this review, we discuss two examples of functional recovery after neural injury in nonhuman primate models. The first is the recovery of dexterous hand movements following damage to the corticospinal tract. The second is the recovery of visual function after injury to the primary visual cortex (V1). In the former case, the functions of the direct cortico-motoneuronal pathway, which specifically developed in higher primates for the control of fractionated digit movements, can be partly compensated for by other descending motor pathways mediated by rubrospinal, reticulospinal, and propriospinal neurons. However, the extent of recovery depends on the location of the damage and which motor systems take over its function. In the latter case, after damage to V1, which is highly developed in primates, either the direct pathway from the lateral geniculate nucleus to extrastriate visual cortices or that from the midbrain superior colliculus–pulvinar–extrastriate/parietal cortices partly takes over the function of V1. However, the state of visual awareness is no longer the same as in the intact state, which might reflect the limited capacity of the compensatory pathways in visual recognition. Such information is valuable for determining the targets of neuromodulatory therapies and setting treatment goals after brain and spinal cord injuries.

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. [ABSTRACT FROM AUTHOR]

• 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]

There are no qualia. The phenomenological difference between seeing and visualizing something is that the propositions which the experient begins to believe in the first case are only entertained in the second. We can know what it's like to be a bat by knowing that their echolocation informs them non-inferentially of the shapes, sizes, and directional distances away of nearby surfaces. The terms for secondary qualities like colours, though, are names of the type-properties they designate, tracing back causally to a verbal 'baptism,' and so experients don't know the character of colour experiences until they study brain physiology. [ABSTRACT FROM AUTHOR]

Many believe that humans can 'perceive unconsciously' - that for weak stimuli, briefly presented and masked, above-chance discrimination is possible without awareness. Interestingly, an online survey reveals that most experts in the field recognize the lack of convincing evidence for this phenomenon, and yet they persist in this belief. Using a recently developed bias-free experimental procedure for measuring subjective introspection (confidence), we found no evidence for unconscious perception; participants' behavior matched that of a Bayesian ideal observer, even though the stimuli were visually masked. This surprising finding suggests that the thresholds for subjective awareness and objective discrimination are effectively the same: if objective task performance is above chance, there is likely conscious experience. These findings shed new light on decades-old methodological issues regarding what it takes to consider a neurobiological or behavioral effect to be 'unconscious,' and provide a platform for rigorously investigating unconscious perception in future studies.

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.

Comte argued against the Cartesian conception of the mind that the thinker cannot simultaneously think or perceive and observe itself so doing. Based on insights from cognitive neuroscience, Dehaene has recently given a contemporary answer to Comte's challenge. He has extended some ideas of Helmholtz on unconscious inferences and argued that we can resolve Comte's problem by reformulating it in terms of the brain. Since the brain consists of different parts having different functions, it is possible that some parts are involved in observing (they unconsciously process information) while other parts integrate the received information resulting in conscious experiences to which we have access. Dehaene's answer is criticized and the alternative neo-Aristotelian resolution of Comte's challenge is discussed. Explanations of blindsight are used to illustrate the differences between the two responses to Comte's challenge. [ABSTRACT FROM AUTHOR]

The existence of unconscious visually triggered behavior in patients with cortical blindness (e.g., homonymous hemianopia) has been amply demonstrated and the neural bases of this phenomenon have been thoroughly studied. However, a crosstalk between the two hemispheres as a possible mechanism of unconscious or partially conscious vision has not been so far considered. Thus, the aim of this study was to assess the relationship between structural and functional properties of the corpus callosum (CC), as shown by probabilistic tractography (PT), behavioral detection/discrimination performance and level of perceptual awareness in the blind field of patients with hemianopia. Twelve patients were tested in two tasks with black-and-white visual square-wave gratings, one task of movement and the other of orientation. The stimuli were lateralized to one hemifield either intact or blind. A PT analysis was carried out on MRI data to extract fiber properties along the CC (genu, body, and splenium). Compared with a control group of participants without brain damage, patients showed lower FA values in all three CC sections studied. For the intact hemifield we found a significant correlation between PT values and visual detection/discrimination accuracy. For the blind hemifield the level of perceptual awareness correlated with PT values for all three CC sections in the movement task. Importantly, significant differences in all three CC sections were found also between patients with above-vs. chance detection/discrimination performance while differences in the genu were found between patients with and without perceptual awareness. Overall, our study provides evidence that the properties of CC fibers are related to the presence of unconscious stimulus detection/discrimination and to hints of perceptual awareness for stimulus presentation to the blind hemifield. These results underline the importance of information exchange between the damaged and the healthy hemisphere for possible partial or full recovery from hemianopia. • We reported the existence of unconscious visual discrimination and hints of awareness in hemianopia. • These residual capacities depended on the structure integrity of the Corpus Callosum. • Crosstalk between hemispheres is crucial for possible recovery of partial or full vision in hemianopia. [ABSTRACT FROM AUTHOR]

Phillips argues that blindsight is due to response criterion artifacts under degraded conscious vision. His view provides alternative explanations for some studies, but may not work well when one considers several key findings in conjunction. Empirically, not all criterion effects are decidedly nonperceptual. Awareness is not completely abolished for some stimuli, in some patients. But in other cases, it is clearly impaired relative to the corresponding visual sensitivity. This relative dissociation is what makes blindsight so important and interesting. [ABSTRACT FROM AUTHOR]

Blindsight is a neuropsychological condition defined by residual visual function following destruction of primary visual cortex. This residual visual function is almost universally held to include capacities for voluntary discrimination in the total absence of awareness. So conceived, blindsight has had an enormous impact on the scientific study of consciousness. It is held to reveal a dramatic disconnect between performance and awareness and used to motivate diverse claims concerning the neural and cognitive basis of consciousness. Here I argue that this orthodox understanding of blindsight is fundamentally mistaken. Drawing on models from signal detection theory in conjunction with a wide range of behavioral and first-person evidence, I contend that blindsight is severely and qualitatively degraded but nonetheless conscious vision, unacknowledged due to conservative response biases. Psychophysical and functional arguments to the contrary are answered. A powerful positive case for the qualitatively degraded conscious vision hypothesis is then presented, detailing a set of distinctive predictions borne out by the data. Such data are further used to address the question of what it is like to have blindsight, as well as to explain the conservative and selectively unstable response criteria exhibited by blindsight subjects. On the view defended, blindsight does not reveal any dissociation between performance and awareness, nor does it speak to the neural or cognitive requirements for consciousness. A foundation stone of consciousness science requires radical reconsideration. [ABSTRACT FROM AUTHOR]

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 (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 (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. [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]

Humans can respond rapidly to viewed expressions of fear, even in the absence of conscious awareness. This is demonstrated using visual masking paradigms in healthy individuals and in patients with cortical blindness due to damage to the primary visual cortex (V1) - so called affective blindsight. Humans have also been shown to implicitly process facial expressions representing important social dimensions. Two major axes, dominance and trustworthiness, are proposed to characterize the social dimensions of face evaluation. The processing of both types of implicit stimuli is believed to occur via similar subcortical pathways involving the amygdala. However, we do not know whether unconscious processing of more subtle expressions of facial traits can occur in blindsight, and if so, how. To test this, we studied 13 patients with unilateral V1 damage and visual field loss. We assessed their ability to detect and discriminate faces that had been manipulated along two orthogonal axes of trustworthiness and dominance to generate five trait levels inside the blind visual field: dominant, submissive, trustworthy, untrustworthy, and neutral. We compared neural activity and functional connectivity in patients classified as blindsight positive or negative for these stimuli. We found that dominant faces were most likely to be detected above chance, with individuals demonstrating unique interactions between performance and face trait. Only patients with blindsight (n = 8) showed significant preference in the superior colliculus and amygdala for face traits in the blind visual field, and a critical functional connection between the amygdala and superior colliculus in the damaged hemisphere. We also found a significant correlation between behavioral performance and fMRI activity in the amygdala and lateral geniculate nucleus across all participants. Our findings confirm that affective blindsight involving the superior colliculus and amygdala extends to the processing of socially salient but emotionally neutral facial expressions when V1 is damaged. This pathway is distinct from that which supports motion blindsight, as both types of blindsight can exist in the absence of the other with corresponding patterns of residual connectivity.

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.

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. [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]

The paper discusses and provides support for diverse processes of brain plasticity in visual function after damage in infancy and childhood in comparison with injury that occurs in the adult brain. We provide support and description of neuroplastic mechanisms in childhood that do not seemingly exist in the same way in the adult brain. Examples include the ability to foster the development of thalamocortical connectivities that can circumvent the lesion and reach their cortical destination in the occipital cortex as the developing brain is more efficient in building new connections. Supporting this claim is the fact that in those with central visual field defects we can note that the extrastriatal visual connectivities are greater when a lesion occurs earlier in life as opposed to in the neurologically mature adult. The result is a significantly more optimized system of visual and spatial exploration within the ‘blind’ field of view. The discussion is provided within the context of “blindsight” and the “Sprague Effect”.

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.

The relationship between attention and awareness is a topic of great interest in cognitive neuroscience. Some studies in healthy participants and hemianopic patients have shown dissociation between these two processes. In contrast, others confirmed the classic notion that the two processes are mutually exclusive. To try and cast further light on this fascinating dilemma, in the present study we have investigated the neural mechanisms of visual spatial attention when perceptual awareness is totally lacking. To do that, we monitored with steady-state visual evoked potentials (SSVEPs) the neurophysiological correlates of endogenous spatial attention to unseen stimuli presented to the blind field of hemianopic patients. Behaviourally, stimulus detection (a brief change in the orientation of a gabor grating) was absent in the blind hemifield while in the sighted field there was a lower, but non-significant, performance in hit rate with respect to a healthy control group. Importantly, however, in both blind and sighted hemifield of hemianopics (as well as in healthy participants) SSVEP recordings showed an attentional effect with higher frequency power in the attended than unattended condition. The scalp distribution of this effect was broadly in keeping with the location of the dorsal system of endogenous spatial attention. In conclusion, the present results provide evidence that the neural correlates of spatial attention are present regardless of visual awareness and this is in accord with the general hypothesis of a possible dissociation between attention and awareness.