Lesions Of Visual Cortex Research Articles

Pupil response as a predictor of blindsight in hemianopia

Significantly above-chance detection of stimuli presented within the field defect of patients with postgeniculate lesions is termed "blindsight." It has been proposed that those with blindsight are more likely to benefit from visual rehabilitation by repeated stimulation, leading to increased visual sensitivity within their field defect. Establishing the incidence of blindsight and developing an objective and reliable method for its detection are of great interest. Sudden onsets of a grating pattern in the absence of any change in light flux result in a transient constriction of the pupil, termed "pupil grating response." The existence of pupil grating responses for stimuli presented within the blindfield has previously been reported in a hemianopic patient and two monkeys with removal of the primary visual cortex unilaterally. Here, we have systematically investigated the presence of a spatial channel of processing at a range of spatial frequencies using a psychophysical forced-choice technique and obtained the corresponding pupil responses in the blindfield of 19 hemianopic patients. In addition, in 13 cases we determined the pupil responses in a sighted field location that matched the blindfield eccentricities. Our findings demonstrate that blindfield pupil responses are similar to those for the sighted field, but attenuated in amplitude. Pupillometry correctly characterized the presence or absence of a significant psychophysical response and thus is worth measuring in the cortically blindfields as a predictor of intact psychophysical capacity. The incidence of blindsight where detection performance had been investigated psychophysically over a range of spatial frequencies was 70%.

P 155. Serial anodal tDCS over V1 induces long-term effects on colour discrimination in V4 measured in the unimpaired hemifield of patients with occipital stroke

Question Little is known about the impact of tDCS on higher level visual functions such as colour perception. Previous studies have primarily investigated the effects of anodal and cathodal direct current stimulation over the occipital cortex on basic visual functions (Antal and Paulus, 2008). In a recent single-session tDCS study in healthy young subjects, anodal stimulation was ineffective in transiently improving red/green discrimination (Costa, 2012). One possible explanation for this may be a ceiling effect of red/green discrimination in the healthy visual system. Given the high degree of plasticity in the sensory cortices of adults (Fahle and Poggie, 2002) we examined whether serial anodal tDCS can induce long-lasting improvements in colour discrimination in the unimpaired visual hemifield of patients with occipital stroke. Materials and methods Twelve chronic stroke patients with unilateral visual cortex lesions (mean age 54.0years, 5 male) participated in a within-subject, sham-controlled, double-blind study. MRI-registered anodal(1.5mA, 20min.)or sham tDCS was applied on 5 consecutive days above the ipsilesional calcarine sulcus. Campimetric testing of age matched colour discrimination was performed in the unaffected hemifield before and after each stimulation session and at 14-and 28-day follow-up. After a 14-day interval, an identical stimulation block with the other stimulation parameter was performed. The visual task was a forced choice task involving binocular detection of red circular stimuli, presented for 200ms in one visual field quadrant at 5° offset from fixation against a green background. Results The age matched overall deviation of colour discrimination was entered in a 2-way ANOVA. In order to control for assumable learning effects, a covariate was added to the ANOVA model. The repeated measures ANOVA attained significance for the factor stimulation ( p =0.004) (stimulation∗learning: p =0.006). The factor time reached significance by trend ( p =0.065) (time∗learning: p =0.181).No significant interaction was revealed for the factor stimulation∗time (stimulation∗time∗learning).Due to a positive learning effect post hoc tests were performed within the first block. No significant difference was seen between the baselines of anodal and sham conditions ( p =0.21).In the anodal condition colour discrimination improved compared to sham on day 5 ( p =0.045) and at two ( p =0.066) and four week ( p =0.041) follow-up. Conclusion Long-term modulation in colour perception following serial anodal tDCS may represent evidence of inducible long-term plasticity in distantly connected components of the visual system (V1 and V4) in patients with occipital stroke measured in the unimpaired hemifield. This builds on studies describing the immediate effects of tDCS in the visual system in healthy volunteers. The temporal dynamics of serial anodal tDCS seem to interact with learning processes, and may yield potential support for neuroplastic adaptation processes following cerebral lesions. Future studies should examine the long-term outcomes and dynamics of tDCS-induced neuromodulation.

Alterations in membrane and firing properties of layer 2/3 pyramidal neurons following focal laser lesions in rat visual cortex

Focal cortical injuries are well known to cause changes in function and excitability of the surviving cortical areas but the cellular correlates of these physiological alterations are not fully understood. In the present study we employed a well established ex vivo–in vitro model of focal laser lesions in the rat visual cortex and we studied membrane and firing properties of the surviving layer 2/3 pyramidal neurons. Patch-clamp recordings, performed in the first week post-injury, revealed an increased input resistance, a depolarized spike threshold as well as alterations in the firing pattern of neurons in the cortex ipsilateral to the lesion. Notably, the reported lesion-induced alterations emerged or became more evident when an exciting perfusing solution, known as modified artificial cerebrospinal fluid, was used to increase the ongoing synaptic activity in cortical slices. Conversely, application of glutamatergic or GABAA receptor blockers reduced the observed alterations and GABAB receptor blockers abolished the differences completely. All together the present findings suggest that changes in synaptic receptors function, following focal cortical injuries, can modulate membrane and firing properties of layer 2/3 pyramidal neurons. This previously unknown functional interplay between synaptic and membrane properties may constitute a novel cellular mechanism to explain alterations in neuronal network function and excitability following focal cortical injuries.

Long-Term Effects of Serial Anodal tDCS on Motion Perception in Subjects with Occipital Stroke Measured in the Unaffected Visual Hemifield

Transcranial direct current stimulation (tDCS) is a novel neuromodulatory tool that has seen early transition to clinical trials, although the high variability of these findings necessitates further studies in clinically relevant populations. The majority of evidence into effects of repeated tDCS is based on research in the human motor system, but it is unclear whether the long-term effects of serial tDCS are motor-specific or transferable to other brain areas. This study aimed to examine whether serial anodal tDCS over the visual cortex can exogenously induce long-term neuroplastic changes in the visual cortex. However, when the visual cortex is affected by a cortical lesion, up-regulated endogenous neuroplastic adaptation processes may alter the susceptibility to tDCS. To this end, motion perception was investigated in the unaffected hemifield of subjects with unilateral visual cortex lesions. Twelve subjects with occipital ischemic lesions participated in a within-subject, sham-controlled, double-blind study. MRI-registered sham or anodal tDCS (1.5 mA, 20 min) was applied on five consecutive days over the visual cortex. Motion perception was tested before and after stimulation sessions and at 14- and 28-day follow-up. After a 16-day interval an identical study block with the other stimulation condition (anodal or sham tDCS) followed. Serial anodal tDCS over the visual cortex resulted in an improvement in motion perception, a function attributed to MT/V5. This effect was still measurable at 14- and 28-day follow-up measurements. Thus, this may represent evidence for long-term tDCS-induced plasticity and has implications for the design of studies examining the time course of tDCS effects in both the visual and motor systems.

“Sightblind”: Perceptual Deficits in the “Intact” Visual Field

Unilateral visual cortex lesions caused by stroke or trauma lead to blindness in contralateral visual field – a condition called homonymous hemianopia. Although the visual field area processed by the uninjured hemisphere is thought to be “intact,” it also exhibits marked perceptual deficits in contrast sensitivity, processing speed, and contour integration. Such patients are “sightblind” – their blindness reaches far beyond the primary scotoma. Studies showing perceptual deficits in patients’ intact fields are reviewed and implications of these findings are discussed. It is concluded that consequences of partial blindness are greater than previously thought, since perceptual deficits in the “intact” field likely contribute to subjective vision loss in patients with visual field defect. This has important implications for vision diagnosis and rehabilitation.

Shift from phasic to tonic GABAergic transmission following laser-lesions in the rat visual cortex

Reduction in the strength of GABAergic neurotransmission has often been reported following brain lesions. This weakened inhibition is believed to influence neurological deficits, neuronal hyperexcitability and functional recovery after brain injuries. Uncovering the mechanisms underlying the altered inhibition is therefore crucial. In the present study we used an ex vivo-in vitro model of laser lesions in the rat visual cortex to characterize the cellular correlates of changes in GABAergic transmission in the tissue adjacent to the injury. In the first week post-injury the number of VGAT positive GABAergic terminals as well as the expression level of the GABA synthesizing enzymes GAD67 and GAD65 remained unaltered. However, a reduced frequency of miniature inhibitory postsynaptic currents (mIPSCs) together with an increased paired-pulse ratio (PPR) of evoked IPSCs suggested a functional reduction of phasic GABA release. In parallel, we found an enhancement in the GABAA receptor-mediated tonic inhibition. On the basis of these findings, we propose that cortical lesions provoke a shift in GABAergic transmission, decreasing the phasic and reinforcing the tonic component. We therefore suggest that it is not, as traditionally assumed, the overall inhibitory strength to be primarily compromised by a cortical lesion but rather the temporal accuracy of the GABAergic synaptic signaling.

Unconscious processing of emotional faces and its probable neural mechanism

With the advancement of techniques in probing unconscious visual processing, an increasing number of researches have demonstrated that unconscious visual information could have an impact on human being’s cognition and behavior. This review mainly introduces those studies regarding processing of fearful faces which are rendered subconscious through weak bottom-up inputs rather than insufficient top-down attentional resources. Studies that adopted backward masking, binocular rivalry, and interocular suppression paradigms and those conducted on patients who suffered from visual cortex lesion have shown converging evidence that some subcortical structures, like superior colliculus, thalamus, and amygdala, and the functional connectivity between these regions contribute to the unconscious processing of fearful faces. It is thus suggested that the human brain is able to process unconscious emotional faces through a rapid subcortical route bypassing early visual cortex. However, this route still needs further studies to delineate its causal instead of correlational relationship with unconscious processing. In addition, how the highly efficient subcortical route adds to the conscious processing of emotional faces is worthy of future investigations.

Transient enhancement of inhibition following visual cortical lesions in the mouse superior colliculus

Numerous studies have investigated the effects of lesions of the primary visual cortex (V1) on visual responses in neurons of the superficial layer of the superior colliculus (sSC), which receives visual information from both the retina and V1. However, little is known about the changes in the local circuit dynamics of the sSC after receiving V1 lesions. Here, we show that surround inhibition of sSC neurons is transiently enhanced following V1 lesions in mice and that this enhancement may be attributed to alterations in the balance between excitatory and inhibitory inputs to sSC neurons. Extracellular recordings in vivo revealed that sSC neuronal responses to large visual stimuli were transiently reduced at about 1 week after visual cortical lesions compared with normal mice and that this reduction was partially recovered at about 1 month after the lesions. By using whole-cell patch-clamp recordings from sSC neurons in slice preparations obtained from mice that had received visual cortical lesions at 1 week prior to the recordings, we found cell type-dependent changes in the balance between excitation and inhibition. In non-GABAergic cells, inhibition predominated over excitation, whereas the excitation-inhibition balance did not change in GABAergic neurons. These results suggest that enhanced inhibition may be partially responsible for the reduced responses to large visual stimuli in some sSC neurons. Thus, we propose that the enhanced surround inhibition shortly after visual cortical lesions may prevent hyperexcitability in the sSC local circuit, contributing to reconstructing the finely tuned receptive field organization of sSC neurons after the visual cortical lesions.

The laser lesion of the mouse visual cortex as a model to study neural extracellular matrix remodeling during degeneration, regeneration and plasticity of the CNS

CNS lesions generally result in impaired function because regeneration of the adult CNS of mammals is poor. A variety of lesion models has been described that serve to further the understanding of the pathophysiology of the damaged tissue. A central cause of aborted regeneration is the glial scar that expresses a plethora of extracellular matrix molecules. Some of these are considered inhibitors of axon growth and regeneration. The laser lesion of the cortex offers the advantage that a circumscribed lesion of defined energy can be delivered to the cortex non-invasively through the intact dura mater and a thinly drilled wet translucent remnant of the skull. Previously, we have shown that distinct ECM is up-regulated in the penumbra of laser lesions in the rat visual cortex. We propose to transfer this model to the mouse, in view of the availability of a large number of genetical models in this small rodent. Here, we discuss this model and the lesion-related ECM that forms the focus of our analysis.

Interactive processes in viual perception: Evidence from neuropsychology

Event Abstract Back to Event Interactive processes in viual perception: Evidence from neuropsychology Glyn Humphreys1* 1 Oxford University, Experimental Psychology, United Kingdom Lesions of extra-striate visual cortex are associated with a range of perceptual problems, including deficits in visual object recognition in which patients can be selectively impaired at responding either to the local or global properties of objects. Standard ‘subtraction’ accounts of neuropsychological cases suggest that such impairments reflect the simple loss of a visual process. Here I will present evidence from two contrasting patients, with complementary lesions of extra-striate cortex, which indicate that, rather than there being a simple loss of visual processing, there is a dynamic change in processing produced by the lesion. Neuropsychological fMRI demonstrates that, following impairments to local processing regions in ventral extra-striate cortex, there is an enhanced response to global shape in dorsal extra-striate cortex. Similarly, following damage to dorsal extra-striate cortex, there is an enhanced response to local shape. The data indicate the important role of interactions between visual areas in determining visual perception. Acknowledgements Stroke Association (UK) Keywords: local-global perception, fMRI, Agnosia, ventral visual cortex, dorsal visual cortex Conference: Belgian Brain Council, Liège, Belgium, 27 Oct - 27 Oct, 2012. Presentation Type: Oral Presentation (only for invited speakers) Topic: Higher Brain Functions in health and disease: cognition and memory Citation: Humphreys G (2012). Interactive processes in viual perception: Evidence from neuropsychology. Conference Abstract: Belgian Brain Council. doi: 10.3389/conf.fnhum.2012.210.00097 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 03 Sep 2012; Published Online: 12 Sep 2012. * Correspondence: Prof. Glyn Humphreys, Oxford University, Experimental Psychology, Oxford, OX1 3UD, United Kingdom, glyn.humphreys@frontiersin.org Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Glyn Humphreys Google Glyn Humphreys Google Scholar Glyn Humphreys PubMed Glyn Humphreys Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Changes in NMDA-Receptor Function in the First Week Following Laser-Induced Lesions in Rat Visual Cortex

Focal brain injuries are accompanied by processes of functional reorganization that partially compensate the functional loss. In a previous study, extracellular recordings at the border of a laser-induced lesion in the visual cortex of rats showed an enhanced synaptic plasticity, which was mediated by the activity of NR2B-contaning NMDA-receptors (NMDARs) shedding light on the potential cellular mechanisms underlying this reorganization. Given the potentially important contribution of NMDARs in processes of functional reorganization, in the present study, we used the same lesion model to further investigate lesion-induced changes in function and localization of NMDARs in the vicinity of the lesion. The most important finding was a lesion-mediated functional reexpression of nonpostsynaptic, but according to our data, presynaptic or peri-/extrasynaptic NMDARs (preNMDARs), which were undetectable in age-matched (>P21) sham-operated controls. Notably, preNMDARs were able to boost both spontaneous and evoked synaptic glutamatergic transmission. At the postsynaptic site, we also disclosed an increase in the decay time constant of NMDARs mediated currents, which was accompanied by a decreased NR2A/NR2B ratio, as revealed by Western blot analysis. All together these findings provide new insights into the role of NMDARs activity during processes of functional reorganization following a focal lesion in the cerebral cortex.

Contribution of the retino‐tectal pathway to visually guided saccades after lesion of the primary visual cortex in monkeys

Previous reports on 'blindsight' have shown that some patients with lesions of the primary visual cortex (V1) could localize visual targets in their scotoma with hand and/or eye movements without visual awareness. A role of the retino-tectal pathway on residual vision has been proposed but the direct evidence for this still remains sparse. To examine this possibility, we inactivated the superior colliculus (SC) of unilateral V1-lesioned monkeys using microinjections of muscimol, and analysed the effects on visually guided saccades. Following muscimol injections into the contralesional SC, the monkeys performed the visually guided saccade task with relatively minor deficits. The effects of ipsilesional SC inactivation were more severe. After injections, the monkeys failed to localize the target within the visual field represented at the injection site on the SC map. The effects of ipsilesional SC inactivation may result from sensory deficits, motor deficits or a combination of both. To examine these possibilities, we tested the effects of SC inactivation on the motor system by investigating spontaneous saccades. After inactivation of the ipsilesional SC, spontaneous saccades toward the injection site were not abolished, suggesting that impairment of visually guided saccades following inactivation of the ipsilesional SC could not be explained solely by a motor deficit and was primarily due to a visual deficit, presumably by interfering with processing in the superficial layer. We conclude that the retino-tectal pathway plays an essential role in residual vision after V1 lesion. The results suggest that this pathway may be involved in mediating unconscious vision in blindsight patients.

Lesion of Primary Visual Cortex in Monkey Impairs the Inhibitory but Not the Facilitatory Cueing Effect on Saccade

Prior visual stimulus presentation induces immediate facilitation and subsequent inhibition of orienting to an ensuing target at the same location. Recent studies revealed that the superior colliculus (SC) is involved in these facilitatory and inhibitory cueing effects on saccade; however, as the SC receives inputs both directly from the retina (retino-tectal pathway) and indirectly from visual cortices (geniculostriate pathway), it is unclear which visual pathway contributes to the effects. We investigated this issue using monkeys with lesions in the primary visual cortex (V1), thus depriving the SC of the geniculostriate pathway and leaving the retino-tectal pathway intact. We found that the inhibitory cueing effect was selectively impaired and the facilitatory cueing effect was spared after V1 lesions. The results suggest that the geniculostriate and the retino-tectal pathways are differentially involved in the generation of cueing effects on saccade: The former is critically involved in the inhibitory effect whereas the latter alone can induce the facilitatory effect. The results provide the first direct evidence for the involvement of the geniculostriate pathway in the inhibitory cueing effect and further imply that the more recent evolution of the geniculostriate pathway in higher mammals improves the efficiency of visual search by inhibiting orienting to a previously attended location.

Metaplasticity of horizontal connections in the vicinity of focal laser lesions in rat visual cortex

Focal cortical injuries are accompanied by a reorganization of the adjacent neuronal networks. An increased synaptic plasticity has been suggested to mediate, at least in part, this functional reorganization. Previous studies showed an increased long-term potentiation (LTP) at synapses formed by ascending fibres projecting onto layers 2/3 pyramidal cells following lesions in rat visual cortex. This could be important to establish new functional connections within a vertical cortical column. Importantly, horizontal intracortical connections constitute an optimal substrate to mediate the functional reorganization across different cortical columns. However, so far little is known about their potential implication in the functional rewiring post-lesion. Here, we investigated possible alterations of synaptic plasticity of horizontal connections in layers 2/3 in an 'ex vivo-in vitro' model of focal laser lesion in rat visual cortex. LTP at these synapses was found to be enhanced post-lesion, whereas long-term depression (LTD) was impaired, revealing a metaplastic shift toward strengthening of these synapses. Furthermore, we disclosed a prolonged decay-time constant of NMDAR-dependent currents, which can contribute to the enhanced LTP. Taken together these data revealed that a laser lesion-induced focal damage of the visual cortex is accompanied by a facilitated potentiation of horizontal synaptic connections in the vicinity of the focal injury. This specific strengthening of synaptic plasticity at horizontal connections in layers 2/3 might be one important cellular mechanism to compensate focal injury-mediated dysfunction in the cerebral cortex.

The primary visual cortex, and feedback to it, are not necessary for conscious vision

A compelling single case report of visual awareness (visual qualia) without primary visual cortex would be sufficient to refute the hypothesis that the primary visual cortex and the back-projections to it are necessary for conscious visual experience. In a previous study, we emphasized the presence of crude visual awareness in Patient G.Y., with a lesion of the primary visual cortex, who is aware of, and able to discriminate, fast-moving visual stimuli presented to his blind field. The visual nature of Patient G.Y.'s blind field experience has since been questioned and it has been suggested that the special circumstances of repeated testing over decades may have altered Patient G.Y.'s visual pathways. We therefore sought new evidence of visual awareness without primary visual cortex in patients for whom such considerations do not apply. Three patients with hemianopic field defects (Patient G.N. and Patient F.B. with MRI confirmed primary visual cortex lesions, Patient C.G. with an inferred lesion) underwent detailed psychophysical testing in their blind fields. Visual stimuli were presented at different velocities and contrasts in two- and four-direction discrimination experiments and the direction of motion and awareness reported using a forced-choice paradigm. Detailed verbal reports were also obtained of the nature of the blind field experience with comparison of the drawings of the stimulus presented in the blind and intact fields, where possible. All three patients reported visual awareness in their blind fields. Visual awareness was significantly more likely when a moving stimulus was present compared to no stimulus catch trials (P < 0.01 for each subject). Psychophysical performance in Patient F.B. and Patient G.N. was consistent with the Riddoch syndrome, with higher levels of visual awareness for moving compared to static stimuli (P < 0.001) and intact direction discrimination (P < 0.0001 for two- and four-direction experiments). Although the blind field experience of all three subjects was degraded, it was clearly visual in nature. We conclude that the primary visual cortex or back-projections to it are not necessary for visual awareness.

Guidance of gaze based on color saliency in monkeys with unilateral lesion of primary visual cortex

Guidance of gaze based on color saliency in monkeys with unilateral lesion of primary visual cortex

Role of different salient features in guiding gaze of monkeys with unilateral lesion of primary visual cortex

Role of different salient features in guiding gaze of monkeys with unilateral lesion of primary visual cortex

Reflections on blindsight: Neuroimaging and behavioural explorations clarify a case of reversed localisation in the blind field of a patient with hemianopia.

Blindsight refers to residual visual abilities of patients with primary visual cortex lesions. Most of this research uses single case studies, most famously patient GY. We examined a patient (DC) after surgical resection of V1 who demonstrated robust but reversed blind field target localisation, mislocalising midline blind field targets to the periphery and vice versa. This pattern was reliable across multiple sessions and was not because of extraocular light scatter. We then used functional magnetic resonance imaging to examine neural responses to blind field motion stimuli with no evidence of motion-selective activation in DC's extrastriate cortex in the damaged hemisphere, in stark contrast to GY who showed robust bilateral activation in response to blind field stimuli. This suggests that DC's blind field performance may not represent true blindsight. Follow-up testing with the target--background contrast reversed (i.e., black targets/white background), eliminated DC's reversed localisation, strongly suggesting that she was employing an unusual decision criterion based on intraocular light scatter. DC's failure to demonstrate true blindsight may be related to the age at which she acquired her lesion--much later in life than GY.

Saliency-based guidance of gaze in monkeys with unilateral lesion of primary visual cortex

Saliency-based guidance of gaze in monkeys with unilateral lesion of primary visual cortex

Investigation of spontaneous saccades based on the saliency model in monkeys with unilateral lesion of primary visual cortex

Investigation of spontaneous saccades based on the saliency model in monkeys with unilateral lesion of primary visual cortex