Dataset Information

Behavioral Consequences and Cortical Reorganization in Homonymous Hemianopia.

ABSTRACT: The most common visual defect to follow a lesion of the retrochiasmal pathways is homonymous hemianopia (HH), whereby, in each eye, patients are blind to the contralesional visual field. From a behavioral perspective, in addition to exhibiting a severe deficit in their contralesional visual field, hemianopic patients can also present implicit residual capacities, now usually referred to collectively as blindsight. It was recently demonstrated that HH patients can also suffer from a subtle deficit in their ipsilesional visual field, called sightblindness (the reverse case of blindsight). Furthermore, the nature of the visual deficit in the contralesional and ipsilesional visual fields, as well as the pattern of functional reorganization in the occipital lobe of HH patients after stroke, all appear to depend on the lesion side. In addition to their contralesional and ipsilesional visual deficits, and to their residual capacities, HH patients can also experience visual hallucinations in their blind field, the physiopathological mechanisms of which remain poorly understood. Herein we review blindsight in terms of its better-known aspects as well as its less-studied clinical signs such as sightblindness, hemispheric specialization and visual hallucinations. We also discuss the implications of recent experimental findings for rehabilitation of visual field defects in hemianopic patients.

SUBMITTER: Chokron S

PROVIDER: S-EPMC4923162 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Behavioral Consequences and Cortical Reorganization in Homonymous Hemianopia.

Chokron Sylvie S Perez Céline C Peyrin Carole C

Frontiers in systems neuroscience 20160628

The most common visual defect to follow a lesion of the retrochiasmal pathways is homonymous hemianopia (HH), whereby, in each eye, patients are blind to the contralesional visual field. From a behavioral perspective, in addition to exhibiting a severe deficit in their contralesional visual field, hemianopic patients can also present implicit residual capacities, now usually referred to collectively as blindsight. It was recently demonstrated that HH patients can also suffer from a subtle defici ...[more]

PMID: 27445717

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Project description:While prisms are commonly prescribed for homonymous hemianopia to extend or expand the visual field, they cause potentially troubling visual side effects, including nonveridical location of perceived images, diplopia, and visual confusion. In addition, the field behind a prism at its apex is lost to an apical scotoma equal in magnitude to the amount of prism shift. The perceptual consequences of apical scotomas and the other effects of various designs were examined to consider parameters and designs that can mitigate the impact of these effects.Various configurations of sector and peripheral prisms were analyzed, in various directions of gaze, and their visual effects were illustrated using simulated perimetry. A novel "percept" diagram was developed that yielded insights into the patient's view through the prisms. The predictions were verified perimetrically with patients.The diagrams distinguish between potentially beneficial field expansion via visual confusion and the pericentrally disturbing and useless effect of diplopia, and their relationship to prism power and gaze direction. They also illustrate the nonexpanding substitution of field segments of some popular prism designs.Yoked sector prisms have no effect at primary gaze or when gaze is directed toward the seeing hemifield, and they introduce pericentral field loss when gaze is shifted into them. When fitted unilaterally, sector prisms also have an effect only when the gaze is directed into the prism and may cause a pericentral scotoma and/or central diplopia. Peripheral prisms are effective at essentially all gaze angles. Since gaze is not directed into them, they avoid problematic pericentral effects. We derive useful recommendations for prism power and position parameters, including novel ways of fitting prisms asymmetrically.Clinicians will find these novel diagrams, diagramming techniques, and analyses valuable when prescribing prismatic aids for hemianopia and when designing new prism devices for patients with various types of field loss.

Project description:Exposure to prolonged stress is a major risk-factor for psychiatric disorders such as generalized anxiety and major depressive disorder. Human imaging studies have identified structural and functional abnormalities in the prefrontal cortex of subjects with depression and anxiety disorders, particularly Brodmann's area 25 (BA25). Further, deep brain stimulation of BA25 reduces symptoms of treatment-resistant depression. The rat homolog of BA25 is the infralimbic cortex (IL), which is critical for cognitive appraisal, executive function, and physiological stress reactivity. Previous studies indicate that the IL undergoes stress-induced changes in excitatory/inhibitory balance culminating in reduced activity of glutamate output neurons. However, the regulatory role of IL glutamate output in mood-related behaviors after chronic variable stress (CVS) is unknown. Here, we utilized a lentiviral-packaged small-interfering RNA to reduce translation of vesicular glutamate transporter 1 (vGluT1 siRNA), thereby constraining IL glutamate output. This viral-mediated gene transfer was used in conjunction with a quantitative anatomical analysis of cells expressing the stable immediate-early gene product FosB/ΔFosB, which accumulates in response to repeated neural activation. Through assessment of FosB/ΔFosB-expressing neurons across the frontal lobe in adult male rats, we mapped regions altered by chronic stress and determined the coordinating role of the IL in frontal cortical plasticity. Specifically, CVS-exposed rats had increased density of FosB/ΔFosB-expressing cells in the IL and decreased density in the insula. The latter effect was dependent on IL glutamate output. Next, we examined the interaction of CVS and reduced IL glutamate output in behavioral assays examining coping, anxiety-like behavior, associative learning, and nociception. IL glutamate knockdown decreased immobility during the forced swim test compared to GFP controls, both in rats exposed to CVS as well as rats without previous stress exposure. Further, vGluT1 siRNA prevented CVS-induced avoidance behaviors, while also reducing risk aversion and passive coping. Ultimately, this study identifies the necessity of IL glutamatergic output for regulating frontal cortical neural activity and behavior following chronic stress. These findings also highlight how disruption of excitatory/inhibitory balance within specific frontal cortical cell populations may impact neurobehavioral adaptation and lead to stress-related disorders.

Project description:Hemianopia patients have lost vision from the contralateral hemifield, but make behavioural adjustments to compensate for this field loss. As a result, their visual performance and behaviour contrast with those of hemineglect patients who fail to attend to objects contralateral to their lesion. These conditions differ in their ocular fixations and perceptual judgments. During visual search, hemianopic patients make more fixations in contralesional space while hemineglect patients make fewer. During line bisection, hemianopic patients fixate the contralesional line segment more and make a small contralesional bisection error, while hemineglect patients make few contralesional fixations and a larger ipsilesional bisection error. Hence, there is an attentional failure for contralesional space in hemineglect but a compensatory adaptation to attend more to the blind side in hemianopia. A challenge for models of visual attentional processes is to show how compensation is achieved in hemianopia, and why such processes are hindered or inaccessible in hemineglect. We used a neurophysiology-derived computational model to examine possible cortical compensatory processes in simulated hemianopia from a V1 lesion and compared results with those obtained with the same processes under conditions of simulated hemineglect from a parietal lesion. A spatial compensatory bias to increase attention contralesionally replicated hemianopic scanning patterns during visual search but not during line bisection. To reproduce the latter required a second process, an extrastriate lateral connectivity facilitating form completion into the blind field: this allowed accurate placement of fixations on contralesional stimuli and reproduced fixation patterns and the contralesional bisection error of hemianopia. Neither of these two cortical compensatory processes was effective in ameliorating the ipsilesional bias in the hemineglect model. Our results replicate normal and pathological patterns of visual scanning, line bisection, and differences between hemianopia and hemineglect, and may explain why compensatory processes that counter the effects of hemianopia are ineffective in hemineglect.

Dataset Information

Behavioral Consequences and Cortical Reorganization in Homonymous Hemianopia.

Publications

Behavioral Consequences and Cortical Reorganization in Homonymous Hemianopia.

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