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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 damage to the primary visual cortex (V1) causes hemianopia, many patients retain some residual vision; known as blindsight. We show that blindsight may be facilitated by an intact white-matter pathway between the lateral geniculate nucleus and motion area hMT+. Visual psychophysics, diffusion-weighted magnetic resonance imaging and fibre tractography were applied in 17 patients with V1 damage acquired during adulthood and 9 age-matched controls. Individuals with V1 damage were subdivided into blindsight positive (preserved residual vision) and negative (no residual vision) according to psychophysical performance. All blindsight positive individuals showed intact geniculo-hMT+ pathways, while this pathway was significantly impaired or not measurable in blindsight negative individuals. Two white matter pathways previously implicated in blindsight: (i) superior colliculus to hMT+ and (ii) between hMT+ in each hemisphere were not consistently present in blindsight positive cases. Understanding the visual pathways crucial for residual vision may direct future rehabilitation strategies for hemianopia patients. Visual information from our eyes projects to a region at the back of the brain called the primary visual cortex, which is where the information is processed to allow us to see the world around us. If a person suffers a stroke that affects this primary visual cortex, he or she can become blind on one side. However, some people can still detect images within this ‘blind’ area, even if they are not consciously aware of it. This phenomenon is known as ‘blindsight’, but it remains unclear which pathways and structures in the brain might allow this information to be detected. Ajina et al. have now examined the brains of a large group of patients with damage to the visual cortex. The results for the patients with blindsight were compared to those without, and to a group of sighted control participants. This analysis identified a pathway that seems to underlie blindsight. This pathway (which runs between an area of the brain called the lateral geniculate nucleus and another called the motion area hMT+) was present in all patients with blindsight, but was missing or disrupted in those patients without blindsight. Ajina et al. then examined other pathways that had previously been suggested to support blindsight and revealed that they were unlikely to do so. This is because the suggested connections were not identifiable in all patients with blindsight, and were often intact in those patients without blindsight. So far, this work has addressed the structure of the pathways rather than their activity. Future work will attempt to determine whether it is possible to strengthen such pathways to improve visual ability.

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. In the 1980s, psychologists made an unexpected discovery while working with individuals who had become blind after sustaining damage to areas of the brain required for vision. These individuals could respond correctly to questions about the shape and location of objects in their visual field, even though they could no longer see the objects. This phenomenon became known as 'blindsight', and it is regarded as a classic example of perception in the absence of conscious awareness. Many researchers who study consciousness believe that everyone is capable of subliminal or unconscious perception: that is, of detecting and processing stimuli without being consciously aware of them. However, studies investigating this phenomenon have produced contradictory results. Peters and Lau have now tested unconscious perception directly, using a recently developed method that overcomes some of the problems faced by previous studies. Human volunteers took part in several trials, in which they were shown two images. Each image was ‘masked’ to prevent the volunteers from consciously registering them. After each image was shown, the volunteers had to state whether a patch of gray and white stripes in the masked image was tilted to the left or to the right. However, one of the two images did not include a gray and white patch. After seeing both images in a trial, the volunteers also had to indicate which of their answers they were most confident about. If the volunteers could perceive the patches without being consciously aware of doing so, their response should show two features. The volunteers should correctly state the tilt direction of the stripes more often than would be expected if they were guessing at random. However, they should also feel no more confident in their responses for the images that did feature a striped patch than for the ‘no patch’ ones. Peters and Lau found no such evidence of unconscious perception. Nevertheless, the volunteers were consistently better at correctly stating the direction the stripes were tilted in than their confidence ratings would suggest. Does this indicate some degree of perception without awareness? Peters and Lau argue that it does not, because a computer model designed to perform the task showed a similar level of performance to the volunteers. These findings suggest that previous reports of unconscious perception may have been contaminated by the problems that Peters and Lau controlled for, and that perhaps unconscious perception doesn’t occur in people without brain damage. Researchers will now need to do more studies using similar approaches to determine whether observers without brain damage can truly experience unconscious perception, and how such unconscious perception might be represented in the brain.

Unilateral damage to the primary visual cortex (V1) leads to clinical blindness in the opposite visual hemifield, yet nonconscious ability to transform unseen visual input into motor output can be retained, a condition known as “blindsight.” Here we combined psychophysics, functional magnetic resonance imaging, and tractography to investigate the functional and structural properties that enable the developing brain to partly overcome the effects of early V1 lesion in one blindsight patient. Visual stimuli appeared in either the intact or blind hemifield and simple responses were given with either the left or right hand, thereby creating conditions where visual input and motor output involve the same or opposite hemisphere. When the V1-damaged hemisphere was challenged by incoming visual stimuli, or controlled manual responses to these unseen stimuli, the corpus callosum (CC) dynamically recruited areas in the visual dorsal stream and premotor cortex of the intact hemisphere to compensate for altered visuomotor functions. These compensatory changes in functional brain activity were paralleled by increased connections in posterior regions of the CC, where fibers connecting homologous areas of the parietal cortex course.

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.

Individuals with Autism Spectrum Disorder (ASD) seem to have difficulties looking others in the eyes, but the substrate for this behavior is not well understood. The subcortical pathway, which consists of superior colliculus, pulvinar nucleus of the thalamus, and amygdala, enables rapid and automatic face processing. A specific component of this pathway – i.e., the amygdala – has been shown to be abnormally activated in paradigms where individuals had to specifically attend to the eye-region; however, a direct examination of the effect of manipulating the gaze to the eye-regions on all the components of the subcortical system altogether has never been performed. The subcortical system is particularly important as it shapes the functional specialization of the face-processing cortex during development. Using functional MRI, we investigated the effect of constraining gaze in the eye-region during dynamic emotional face perception in groups of participants with ASD and typical controls. We computed differences in activation in the subcortical face processing system (superior colliculus, pulvinar nucleus of the thalamus and amygdala) for the same stimuli seen freely or with the gaze constrained in the eye-region. Our results show that when constrained to look in the eyes, individuals with ASD show abnormally high activation in the subcortical system, which may be at the basis of their eye avoidance in daily life.

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.

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 face’s 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 face’s 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.

The spontaneous tendency to synchronize our facial expressions with those of others is often termed emotional contagion. It is unclear, however, whether emotional contagion depends on visual awareness of the eliciting stimulus and which processes underlie the unfolding of expressive reactions in the observer. It has been suggested either that emotional contagion is driven by motor imitation (i.e., mimicry), or that it is one observable aspect of the emotional state arising when we see the corresponding emotion in others. Emotional contagion reactions to different classes of consciously seen and \"unseen\" stimuli were compared by presenting pictures of facial or bodily expressions either to the intact or blind visual field of two patients with unilateral destruction of the visual cortex and ensuing phenomenal blindness. Facial reactions were recorded using electromyography, and arousal responses were measured with pupil dilatation. Passive exposure to unseen expressions evoked faster facial reactions and higher arousal compared with seen stimuli, therefore indicating that emotional contagion occurs also when the triggering stimulus cannot be consciously perceived because of cortical blindness. Furthermore, stimuli that are very different in their visual characteristics, such as facial and bodily gestures, induced highly similar expressive responses. This shows that the patients did not simply imitate the motor pattern observed in the stimuli, but resonated to their affective meaning. Emotional contagion thus represents an instance of truly affective reactions that may be mediated by visual pathways of old evolutionary origin bypassing cortical vision while still providing a cornerstone for emotion communication and affect sharing.

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.