Neural correlates of motion-induced blindness in the human brain

Motion-induced blindness (MIB) is a visual phenomenon in which highly salient visual targets spontaneously disappear from visual awareness (and subsequently reappear) when superimposed on a moving background of distracters. Such fluctuations in awareness of the targets, although they remain physically present, provide an ideal paradigm to study the neural correlates of visual awareness. Existing behavioral data on MIB are consistent both with a role for structures early in visual processing and with involvement of high-level visual processes. To further investigate this issue, we used high field functional MRI to investigate signals in human low-level visual cortex and motion-sensitive area V5/MT while participants reported disappearance and reappearance of an MIB target. Surprisingly, perceptual invisibility of the target was coupled to an increase in activity in low-level visual cortex plus area V5/MT compared with when the target was visible. This increase was largest in retinotopic regions representing the target location. One possibility is that our findings result from an active process of completion of the field of distracters that acts locally in the visual cortex, coupled to a more global process that facilitates invisibility in general visual cortex. Our findings show that the earliest anatomical stages of human visual cortical processing are implicated in MIB, as with other forms of bistable perception

The integration of bottom-up and top-down signals in human perception in health and disease

To extract a meaningful visual experience from the information falling on the retina, the visual system must integrate signals from multiple levels. Bottom-up signals provide input relating to local features while top-down signals provide contextual feedback and reflect internal states of the organism. In this thesis I will explore the nature and neural basis of this integration in two key areas. I will examine perceptual filling-in of artificial scotomas to investigate the bottom-up signals causing changes in perception when filling-in takes place. I will then examine how this perceptual filling-in is modified by top-down signals reflecting attention and working memory. I will also investigate hemianopic completion, an unusual form of filling-in, which may reflect a breakdown in top-down feedback from higher visual areas. The second part of the thesis will explore a different form of top-down control of visual processing. While the effects of cognitive mechanisms such as attention on visual processing are well-characterised, other types of top-down signal such as reward outcome are less well explored. I will therefore study whether signals relating to reward can influence visual processing. To address these questions, I will employ a range of methodologies including functional MRI, magnetoencephalography and behavioural testing in healthy participants and patients with cortical damage. I will demonstrate that perceptual filling-in of artificial scotomas is largely a bottom-up process but that higher cognitive functions can modulate the phenomenon. I will also show that reward modulates activity in higher visual areas in the absence of concurrent visual stimulation and that receiving reward leads to enhanced activity in primary visual cortex on the next trial. These findings reveal that integration occurs across multiple levels even for processes rooted in early retinotopic regions, and that higher cognitive processes such as reward can influence the earliest stages of cortical visual processing

Predictive masking of an artificial scotoma is associated with a system-wide reconfiguration of neural populations in the human visual cortex

The visual brain has the remarkable capacity to complete our percept of the world even when the information extracted from the visual scene is incomplete. This ability to predict missing information based on information from spatially adjacent regions is an intriguing attribute of healthy vision. Yet, it gains particular significance when it masks the perceptual consequences of a retinal lesion, leaving patients unaware of their partial loss of vision and ultimately delaying diagnosis and treatment. At present, our understanding of the neural basis of this masking process is limited which hinders both quantitative modelling as well as translational application. To overcome this, we asked the participants to view visual stimuli with and without superimposed artificial scotoma (AS). We used fMRI to record the associated cortical activity and applied model-based analyses to track changes in cortical population receptive fields and connectivity in response to the introduction of the AS. We found that throughout the visual field and cortical hierarchy, pRFs shifted their preferred position towards the AS border. Moreover, extrastriate areas biased their sampling of V1 towards sections outside the AS projection zone, thereby effectively masking the AS with signals from spared portions of the visual field. We speculate that the signals that drive these system-wide population modifications originate in extrastriate visual areas and, through feedback, also reconfigure the neural populations in the earlier visual areas

Highly accurate retinotopic maps of the physiological blind spot in human visual cortex

The physiological blind spot is a naturally occurring scotoma corresponding with the optic disc in the retina of each eye. Even during monocular viewing, observers are usually oblivious to the scotoma, in part because the visual system extrapolates information from the surrounding area. Unfortunately, studying this visual field region with neuroimaging has proven difficult, as it occupies only a small part of retinotopic cortex. Here, we used functional magnetic resonance imaging and a novel data-driven method for mapping the retinotopic organization in and around the blind spot representation in V1. Our approach allowed for highly accurate reconstructions of the extent of an observer’s blind spot, and out-performed conventional model-based analyses. This method opens exciting opportunities to study the plasticity of receptive fields after visual field loss, and our data add to evidence suggesting that the neural circuitry responsible for impressions of perceptual completion across the physiological blind spot most likely involves regions of extrastriate cortex—beyond V1

Neural correlates of lateral modulation and perceptual filling-in in center-surround radial sinusoidal gratings: an fMRI study

We investigated lateral modulation effects with functional magnetic resonance imaging. We presented radial sinusoidal gratings in random sequence: a scotoma grating with two arc-shaped blank regions (scotomata) in the periphery, one in the left and one in the right visual field, a center grating containing pattern only in the scotoma regions, and a full-field grating where the pattern occupied the whole screen. On each trial, one of the three gratings flickered in counterphase for 10 s, followed by a blank period. Observers were instructed to perform a fixation task and report whether filling-in was experienced during the scotoma condition. The results showed that the blood-oxygen-level-dependent signal was reduced in areas corresponding to the scotoma regions in the full-field compared to the center condition in V1 to V3 areas, indicating a lateral inhibition effect when the surround was added to the center pattern. The univariate analysis results showed no difference between the filling-in and no-filling-in trials. However, multivariate pattern analysis results showed that classifiers trained on activation pattern in V1 to V3 could differentiate between filling-in and no-filling-in trials, suggesting that the neural activation pattern in visual cortex correlated with the subjective percept

Perceptual organization and consciousness

With chapter written by leading researchers in the field, this is the state-of-the-art reference work on this topic, and will be so for many years to come

Lateral modulation, divisive inhibition, and neural mechanism of perceptual filling-in

Lateral modulation refers to the phenomenon that the percept of a test stimulus can be modified by a surrounding pattern. Lateral modulation is ubiquitous throughout the visual system. Thus, understanding the underlying mechanism of lateral modulation can not only unveil the fundamental properties of visual system but also have the potential to increase our understanding of how eye diseases such as macular degeneration that leads to scotoma impact on visual perception. The purpose of this project is to study lateral modulation by investigating visual phenomena such as perceptual filling-in and orientation-specific lateral inhibition by means of psychophysics, computational modeling, and neuroimaging techniques. To address the missing pieces of this puzzling phenomenon, this project defines three goals: 1) To study multiple lateral modulation effects such as center-surround interaction and perceptual filling-in with new paradigms; 2) to analyze the observed lateral modulation effects with a computational model; and 3) to understand the neural mechanism underlying perceptual filling-in. Three studies have been conducted. Within the first two studies, we established an orientation adaption paradigm in which center-surround sinusoidal gratings are used as adapters to estimate the amount of tilt-aftereffect (TAE) induced onto the percept of the subsequent target. In Study 1, we selectively adapted the center, the surround, and both the center and surround regions and measured the tilt-aftereffect on the subsequently presented target. The TAE was the strongest in the center-only condition, intermediate in the center plus surround condition, and the weakest in the surround only condition. The difference between the center and both center and surround conditions indicated a lateral inhibition effect from the surround. Perceptual filling-in arose in the surround-only condition thus allowed us to investigate the filling-in effect. The TAE occurred even when no physical stimulus was presented at the target location during adaptation, and the TAE was more pronounced when filling-in was reported. In Study 2, we independently manipulated the adapter center and surround orientations and measured the TAE. We discovered that the lateral inhibition we found in Study 1 was orientation specific. We developed a divisive inhibition model that could explain both the adaptation effect and the lateral modulation effects in the empirical data of Study 1 and 2. In the third study, we implemented functional magnetic resonance imaging to study lateral modulation by presenting radial sinusoidal gratings that activates either the center, the surround, or both the center and surround regions in both left and right visual fields. When the surround pattern was added to the central pattern, the blood-oxygen level-dependent signal decreased in V1 to V3 regions, suggesting a lateral inhibition effect. The multivariate pattern analysis revealed that trained linear classifiers could differentiate between filling-in and non-filling-in trials, indicating that the neural activation pattern was different between the two percepts although the stimuli were the same. The current PhD project demonstrated effective paradigms that provided new evidence in lateral modulation in human vision. Our computational model captured both the adaptation and lateral modulation aspects in the data. The empirical findings and modeling results provide new evidence in the neural mechanism of perceptual filling-in. These paradigms and model have the potential to improve the understanding of how the brain adapts to eye diseases that could potentially lead to better detection techniques and rehabilitation programs

Illusory Stimuli Can Be Used to Identify Retinal Blind Spots

Background. Identification of visual field loss in people with retinal disease is not straightforward as people with eye disease are frequently unaware of substantial deficits in their visual field, as a consequence of perceptual completion ("filling-in'') of affected areas. Methodology. We attempted to induce a compelling visual illusion known as the induced twinkle after-effect (TwAE) in eight patients with retinal scotomas. Half of these patients experience filling-in of their scotomas such that they are unaware of the presence of their scotoma, and conventional campimetric techniques can not be used to identify their vision loss. The region of the TwAE was compared to microperimetry maps of the retinal lesion. Principal Findings. Six of our eight participants experienced the TwAE. This effect occurred in three of the four people who filled-in their scotoma. The boundary of the TwAE showed good agreement with the boundary of lesion, as determined by microperimetry. Conclusion. For the first time, we have determined vision loss by asking patients to report the presence of an illusory percept in blind areas, rather than the absence of a real stimulus. This illusory technique is quick, accurate and not subject to the effects of filling-in

Brain Plasticity associated with Predictive Masking and Glaucoma

Glaucoma is a disease resulting from damage at the optic nerve, the “highway” through which visual information travels from the retina towards the visual brain. Such lesion deprives the visual cortex of the regular input, causing interruptions within the visual field – scotoma. However, even when such lesions occur, perception remains stable as the human visual system perceptually masks the insult with the visual features of nearby regions of the visual field. To unravel the neural mechanisms by which this remarkable capacity occurs in glaucomatous individuals, we used functional magnetic resonance imaging (fMRI) and neural modelling to track changes in cortical population receptive fields (pRFs). We found that visual neurons from early visual areas (V1-3) expanded their pRFs both inside and at the vicinity of the lesion. V1 pRFs also shifted their preferred central position towards the outside of the scotoma. By doing so, neural populations were able to process information from spared visual field, consistent with the notion of predictive masking. In contrast, well-sighted observers did not show similar patterns of neural activity in response to the introduction of an artificial scotoma (AS). Our findings provide evidence of enduring cortical reorganization underlying the predictive spatial masking of scotomas in glaucoma, meeting the contemporary view that early visual areas of the adult human brain retain plastic mechanisms. Furthermore, the involvement of the brain suggests that glaucoma pathogenesis goes beyond the eye