Brain Basis of Blindsight

Author(s):  
Holly Bridge

The sensation of vision arises from the detection of photons of light at the eye, but in order to produce the percept of the world, extensive regions of the brain are required to process the visual information. The majority of information entering the brain via the optic nerve from the eye projects via the lateral geniculate nucleus (LGN) of the thalamus to the primary visual cortex, the largest visual area, having been reorganized such that one side of the brain represents one side of the world. Damage to the primary visual cortex in one hemisphere therefore leads to a loss of conscious vision on the opposite side of the world, known as hemianopia. Despite this cortical blindness, many patients are still able to detect visual stimuli that are presented in the blind region if forced to guess whether a stimulus is present or absent. This is known as “blindsight.” For patients to gain any information (conscious or unconscious) about the visual world, the input from the eye must be processed by the brain. Indeed, there is considerable evidence from functional brain imaging that several visual areas continue to respond to visual stimuli presented within the blind region, even when the patient is unaware of the stimulus. Furthermore, the use of diffusion imaging allows the microstructure of white matter pathways within the visual system to be examined to see whether they are damaged or intact. By comparing patients who have hemianopia with and without blindsight it is possible to determine the pathways that are linked to blindsight function. Through understanding the brain areas and pathways that underlie blindsight in humans and non-human primates, the aim is to use modern neuroscience to guide rehabilitation programs for use after stroke.

2016 ◽  
Vol 23 (5) ◽  
pp. 529-541 ◽  
Author(s):  
Sara Ajina ◽  
Holly Bridge

Damage to the primary visual cortex removes the major input from the eyes to the brain, causing significant visual loss as patients are unable to perceive the side of the world contralateral to the damage. Some patients, however, retain the ability to detect visual information within this blind region; this is known as blindsight. By studying the visual pathways that underlie this residual vision in patients, we can uncover additional aspects of the human visual system that likely contribute to normal visual function but cannot be revealed under physiological conditions. In this review, we discuss the residual abilities and neural activity that have been described in blindsight and the implications of these findings for understanding the intact system.


2016 ◽  
Author(s):  
Dylan R Muir ◽  
Patricia Molina-Luna ◽  
Morgane M Roth ◽  
Fritjof Helmchen ◽  
Björn M Kampa

AbstractLocal excitatory connections in mouse primary visual cortex (V1) are stronger and more prevalent between neurons that share similar functional response features. However, the details of how functional rules for local connectivity shape neuronal responses in V1 remain unknown. We hypothesised that complex responses to visual stimuli may arise as a consequence of rules for selective excitatory connectivity within the local network in the superficial layers of mouse V1. In mouse V1 many neurons respond to overlapping grating stimuli (plaid stimuli) with highly selective and facilitatory responses, which are not simply predicted by responses to single gratings presented alone. This complexity is surprising, since excitatory neurons in V1 are considered to be mainly tuned to single preferred orientations. Here we examined the consequences for visual processing of two alternative connectivity schemes: in the first case, local connections are aligned with visual properties inherited from feedforward input (a ‘like-to-like’ scheme specifically connecting neurons that share similar preferred orientations); in the second case, local connections group neurons into excitatory subnetworks that combine and amplify multiple feedforward visual properties (a ‘feature binding’ scheme). By comparing predictions from large scale computational models with in vivo recordings of visual representations in mouse V1, we found that responses to plaid stimuli were best explained by a assuming ‘feature binding’ connectivity. Unlike under the ‘like-to-like’ scheme, selective amplification within feature-binding excitatory subnetworks replicated experimentally observed facilitatory responses to plaid stimuli; explained selective plaid responses not predicted by grating selectivity; and was consistent with broad anatomical selectivity observed in mouse V1. Our results show that visual feature binding can occur through local recurrent mechanisms without requiring feedforward convergence, and that such a mechanism is consistent with visual responses and cortical anatomy in mouse V1.Author summaryThe brain is a highly complex structure, with abundant connectivity between nearby neurons in the neocortex, the outermost and evolutionarily most recent part of the brain. Although the network architecture of the neocortex can appear disordered, connections between neurons seem to follow certain rules. These rules most likely determine how information flows through the neural circuits of the brain, but the relationship between particular connectivity rules and the function of the cortical network is not known. We built models of visual cortex in the mouse, assuming distinct rules for connectivity, and examined how the various rules changed the way the models responded to visual stimuli. We also recorded responses to visual stimuli of populations of neurons in anaesthetised mice, and compared these responses with our model predictions. We found that connections in neocortex probably follow a connectivity rule that groups together neurons that differ in simple visual properties, to build more complex representations of visual stimuli. This finding is surprising because primary visual cortex is assumed to support mainly simple visual representations. We show that including specific rules for non-random connectivity in cortical models, and precisely measuring those rules in cortical tissue, is essential to understanding how information is processed by the brain.


2017 ◽  
Vol 372 (1715) ◽  
pp. 20160504 ◽  
Author(s):  
Megumi Kaneko ◽  
Michael P. Stryker

Mechanisms thought of as homeostatic must exist to maintain neuronal activity in the brain within the dynamic range in which neurons can signal. Several distinct mechanisms have been demonstrated experimentally. Three mechanisms that act to restore levels of activity in the primary visual cortex of mice after occlusion and restoration of vision in one eye, which give rise to the phenomenon of ocular dominance plasticity, are discussed. The existence of different mechanisms raises the issue of how these mechanisms operate together to converge on the same set points of activity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.


1998 ◽  
Vol 78 (2) ◽  
pp. 467-485 ◽  
Author(s):  
CHARLES D. GILBERT

Gilbert, Charles D. Adult Cortical Dynamics. Physiol. Rev. 78: 467–485, 1998. — There are many influences on our perception of local features. What we see is not strictly a reflection of the physical characteristics of a scene but instead is highly dependent on the processes by which our brain attempts to interpret the scene. As a result, our percepts are shaped by the context within which local features are presented, by our previous visual experiences, operating over a wide range of time scales, and by our expectation of what is before us. The substrate for these influences is likely to be found in the lateral interactions operating within individual areas of the cerebral cortex and in the feedback from higher to lower order cortical areas. Even at early stages in the visual pathway, cells are far more flexible in their functional properties than previously thought. It had long been assumed that cells in primary visual cortex had fixed properties, passing along the product of a stereotyped operation to the next stage in the visual pathway. Any plasticity dependent on visual experience was thought to be restricted to a period early in the life of the animal, the critical period. Furthermore, the assembly of contours and surfaces into unified percepts was assumed to take place at high levels in the visual pathway, whereas the receptive fields of cells in primary visual cortex represented very small windows on the visual scene. These concepts of spatial integration and plasticity have been radically modified in the past few years. The emerging view is that even at the earliest stages in the cortical processing of visual information, cells are highly mutable in their functional properties and are capable of integrating information over a much larger part of visual space than originally believed.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Jan C. Frankowski ◽  
Andrzej T. Foik ◽  
Alexa Tierno ◽  
Jiana R. Machhor ◽  
David C. Lyon ◽  
...  

AbstractPrimary sensory areas of the mammalian neocortex have a remarkable degree of plasticity, allowing neural circuits to adapt to dynamic environments. However, little is known about the effects of traumatic brain injury on visual circuit function. Here we used anatomy and in vivo electrophysiological recordings in adult mice to quantify neuron responses to visual stimuli two weeks and three months after mild controlled cortical impact injury to primary visual cortex (V1). We found that, although V1 remained largely intact in brain-injured mice, there was ~35% reduction in the number of neurons that affected inhibitory cells more broadly than excitatory neurons. V1 neurons showed dramatically reduced activity, impaired responses to visual stimuli and weaker size selectivity and orientation tuning in vivo. Our results show a single, mild contusion injury produces profound and long-lasting impairments in the way V1 neurons encode visual input. These findings provide initial insight into cortical circuit dysfunction following central visual system neurotrauma.


Author(s):  
Mark Edwards ◽  
Stephanie C. Goodhew ◽  
David R. Badcock

AbstractThe visual system uses parallel pathways to process information. However, an ongoing debate centers on the extent to which the pathways from the retina, via the Lateral Geniculate nucleus to the visual cortex, process distinct aspects of the visual scene and, if they do, can stimuli in the laboratory be used to selectively drive them. These questions are important for a number of reasons, including that some pathologies are thought to be associated with impaired functioning of one of these pathways and certain cognitive functions have been preferentially linked to specific pathways. Here we examine the two main pathways that have been the focus of this debate: the magnocellular and parvocellular pathways. Specifically, we review the results of electrophysiological and lesion studies that have investigated their properties and conclude that while there is substantial overlap in the type of information that they process, it is possible to identify aspects of visual information that are predominantly processed by either the magnocellular or parvocellular pathway. We then discuss the types of visual stimuli that can be used to preferentially drive these pathways.


2020 ◽  
Author(s):  
Nicolò Meneghetti ◽  
Chiara Cerri ◽  
Elena Tantillo ◽  
Eleonora Vannini ◽  
Matteo Caleo ◽  
...  

AbstractGamma band is known to be involved in the encoding of visual features in the primary visual cortex (V1). Recent results in rodents V1 highlighted the presence, within a broad gamma band (BB) increasing with contrast, of a narrow gamma band (NB) peaking at ∼60 Hz suppressed by contrast and enhanced by luminance. However, the processing of visual information by the two channels still lacks a proper characterization. Here, by combining experimental analysis and modeling, we prove that the two bands are sensitive to specific thalamic inputs associated with complementary contrast ranges. We recorded local field potentials from V1 of awake mice during the presentation of gratings and observed that NB power progressively decreased from low to intermediate levels of contrast. Conversely, BB power was insensitive to low levels of contrast but it progressively increased going from intermediate to high levels of contrast. Moreover, BB response was stronger immediately after contrast reversal, while the opposite held for NB. All the aforementioned dynamics were accurately reproduced by a recurrent excitatory-inhibitory leaky integrate-and-fire network, mimicking layer IV of mouse V1, provided that the sustained and periodic component of the thalamic input were modulated over complementary contrast ranges. These results shed new light on the origin and function of the two V1 gamma bands. In addition, here we propose a simple and effective model of response to visual contrast that might help in reconstructing network dysfunction underlying pathological alterations of visual information processing.Significance StatementGamma band is a ubiquitous hallmark of cortical processing of sensory stimuli. Experimental evidence shows that in the mouse visual cortex two types of gamma activity are differentially modulated by contrast: a narrow band (NB), that seems to be rodent specific, and a standard broad band (BB), observed also in other animal models.We found that narrow band correlates and broad band anticorrelates with visual contrast in two complementary contrast ranges (low and high respectively). Moreover, BB displayed an earlier response than NB. A thalamocortical spiking neuron network model reproduced the aforementioned results, suggesting they might be due to the presence of two complementary but distinct components of the thalamic input into visual cortical circuitry.


Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 334-334
Author(s):  
Gereon Nelles ◽  
Guido Widmann ◽  
Joachim Esser ◽  
Anette Meistrowitz ◽  
Johannes Weber ◽  
...  

102 Introduction: Restitution of unilateral visual field defects following occipital cortex lesions occurs rarely. Partial recovery, however, can be observed in patients with incomplete lesion of the visual cortex. Our objective was to study the neuroplastic changes in the visual system that underlie such recovery. Methods and Results: Six patients with a left PCA-territory cortical stroke and 6 healthy control subjects were studied during rest and during visual stimulation using a 1.5 T fMRI with a 40 mT gradient. Visual stimuli were projected with a laptop computer onto a 154 x 115 cm screen, placed 90 cm in front of the gantry. Subjects were asked to fixate a red point in the center of the screen during both conditions. During stimulation, a black-and-white checkerboard pattern reversal was presented in each hemifield. For each side, 120 volumes of 48 contiguous axial fMRI images were obtained during rest and during hemifield stimulation in alternating order (60 volumes for each condition). Significant differences of rCBF between stimulation and rest were assessed as group analyses using statistical parametric mapping (SPM 99; p<0.01, corrected for multiple comparison). In controls, strong increases of rCBF (Z=7.6) occurred in the contralateral primary visual cortex V1 (area 17) and in V3a (area 18) and V5 (area 19). No differences were found between the right and left side in controls. During stimulation of the unaffected (left) visual field in hemianopic patients, activation occurred in contralateral V1, but the strongest increases of rCBF (Z>10) were seen in contralateral V3a (area 18) and V5 (area 19). During stimulation of the hemianopic (right) visual field, no activation was found in the primary visual cortex of either hemisphere. The most significant activation (Z=9.2) was seen in the ipsilateral V3a and V5 areas, and contralateral (left) V3a. Conclusions: Partial recovery from hemianopia is associated with strong ipsilateral activation of the visual system. Processing of visual stimuli in the hemianopic side spares the primary visual cortex and may involve recruitment of neurons in ipsilateral (contralesional) areas V3a and V5.


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