558 research outputs found

    What neuroscientific studies tell us about inhibition of return

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    An inhibitory aftermath of orienting, inhibition of return (IOR), has intrigued scholars since its discovery about 40 years ago. Since then, the phenomenon has been subjected to a wide range of neuroscientific methods and the results of these are reviewed in this paper. These include direct manipulations of brain structures (which occur naturally in brain damage and disease or experimentally as in TMS and lesion studies) and measurements of brain activity (in humans using EEG and fMRI and in animals using single unit recording). A variety of less direct methods (e.g., computational modeling, developmental studies, etc.) have also been used. The findings from this wide range of methods support the critical role of subcortical and cortical oculomotor pathways in the generation and nature of IOR

    Temporal Limitations of the Standard Leaky Integrate and Fire Model

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    Itti and Koch’s Saliency Model has been used extensively to simulate fixation selection in a variety of tasks from visual search to simple reaction times. Although the Saliency Model has been tested for its spatial prediction of fixations in visual salience, it has not been well tested for their temporal accuracy. Visual tasks, like search, invariably result in a positively skewed distribution of saccadic reaction times over large numbers of samples, yet we show that the leaky integrate and fire (LIF) neuronal model included in the classic implementation of the model tends to produce a distribution shifted to shorter fixations (in comparison with human data). Further, while parameter optimization using a genetic algorithm and Nelder–Mead method does improve the fit of the resulting distribution, it is still unable to match temporal distributions of human responses in a visual task. Analysis of times for individual images reveal that the LIF algorithm produces initial fixation durations that are fixed instead of a sample from a distribution (as in the human case). Only by aggregating responses over many input images do they result in a distribution, although the form of this distribution still depends on the input images used to create it and not on internal model variability

    Inhibitory control in mind and brain 2.0: blocked-input models of saccadic countermanding.

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    The interactive race model of saccadic countermanding assumes that response inhibition results from an interaction between a go unit, identified with gaze-shifting neurons, and a stop unit, identified with gaze-holding neurons, in which activation of the stop unit inhibits the growth of activation in the go unit to prevent it from reaching threshold. The interactive race model accounts for behavioral data and predicts physiological data in monkeys performing the stop-signal task. We propose an alternative model that assumes that response inhibition results from blocking the input to the go unit. We show that the blocked-input model accounts for behavioral data as accurately as the original interactive race model and predicts aspects of the physiological data more accurately. We extend the models to address the steady-state fixation period before the go stimulus is presented and find that the blocked-input model fits better than the interactive race model. We consider a model in which fixation activity is boosted when a stop signal occurs and find that it fits as well as the blocked input model but predicts very high steady-state fixation activity after the response is inhibited. We discuss the alternative linking propositions that connect computational models to neural mechanisms, the lessons to be learned from model mimicry, and generalization from countermanding saccades to countermanding other kinds of responses

    Different decision deficits impair response inhibition in progressive supranuclear palsy and Parkinson's disease

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    Progressive supranuclear palsy and Parkinson’s disease have distinct underlying neuropathology, but both diseases affect cognitive function in addition to causing a movement disorder. They impair response inhibition and may lead to impulsivity, which can occur even in the presence of profound akinesia and rigidity. The current study examined the mechanisms of cognitive impairments underlying disinhibition, using horizontal saccadic latencies that obviate the impact of limb slowness on executing response decisions. Nineteen patients with clinically diagnosed progressive supranuclear palsy (Richardson’s syndrome), 24 patients with clinically diagnosed Parkinson’s disease and 26 healthy control subjects completed a saccadic Go/No-Go task with a head-mounted infrared saccadometer. Participants were cued on each trial to make a pro-saccade to a horizontal target or withhold their responses. Both patient groups had impaired behavioural performance, with more commission errors than controls. Mean saccadic latencies were similar between all three groups. We analysed behavioural responses as a binary decision between Go and No-Go choices. By using Bayesian parameter estimation, we fitted a hierarchical drift–diffusion model to individual participants’ single trial data. The model decomposes saccadic latencies into parameters for the decision process: decision boundary, drift rate of accumulation, decision bias, and non-decision time. In a leave-one-out three-way classification analysis, the model parameters provided better discrimination between patients and controls than raw behavioural measures. Furthermore, the model revealed disease-specific deficits in the Go/No-Go decision process. Both patient groups had slower drift rate of accumulation, and shorter non-decision time than controls. But patients with progressive supranuclear palsy were strongly biased towards a pro-saccade decision boundary compared to Parkinson’s patients and controls. This indicates a prepotency of responding in combination with a reduction in further accumulation of evidence, which provides a parsimonious explanation for the apparently paradoxical combination of disinhibition and severe akinesia. The combination of the well-tolerated oculomotor paradigm and the sensitivity of the model-based analysis provides a valuable approach for interrogating decision-making processes in neurodegenerative disorders. The mechanistic differences underlying participants’ poor performance were not observable from classical analysis of behavioural data, but were clearly revealed by modelling. These differences provide a rational basis on which to develop and assess new therapeutic strategies for cognition and behaviour in these disorders

    Infant and toddler precursors of attentional processes in Fragile X syndrome: A neurodevelopmental perspective

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    With the recent sequencing of the human genome, the following question has attracted much interest: can the function of single genes be linked to specific neural and cognitive processes? Within this context, developmental disorders of known genetic origins have been used as naturally-occurring models to link the function (and dysfunction) of genes with cognition. Fragile X syndrome (FXS) is a genetically inherited disorder associated with the silencing of a single gene involved in experience-dependent changes at glutamatergic synapses. In adulthood, it is associated with core attentional difficulties accompanied by seemingly proficient visuo-perception, but the profile of infants and toddlers has not been investigated. In this thesis, fragile X syndrome is used as a tool to investigate how initial changes in a generalised property of all cortical neurones can nonetheless result, in the adult, in core difficulties in the control of attention. I argue that, even in disorders associated with the silencing of a single gene like FXS, the answer requires a developmental approach. Chapter 1 delineates a theoretical distinction between endogenous and exogenous influences on attentional control, whereas Chapter 2 defines methodological issues in assessing atypical attention, such as tools for the assessment of general developmental level and choices of control groups. Part II focuses on tasks tapping endogenous attention control. In particular, Chapters 3 and 4 examine the control of eye-movements and manual response conflict in infants and toddlers with FXS and in typically developing controls. In contrast, Part III concentrates on the exogenous effects of sudden peripheral onsets on visual orienting (Chapter 5) and of the perceptual salience of targets during visual search (Chapter 6). Finally, Part IV traces longitudinal changes in visual search performance. The findings suggest that, like adults with the syndrome, infant and toddlers with FXS display striking deficits in endogenous attention. However, unlike adults, infants are also characterised by atypical exogenous influences on attention and longitudinal changes in performance point to complex developmental relationships between early and later measures of attention. The findings are discussed in terms of their theoretical implications for fragile X syndrome and other developmental disorders affecting attention. They challenge the notion of direct genotype-phenotype mappings that fail to take development into account

    Change blindness: eradication of gestalt strategies

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    Arrays of eight, texture-defined rectangles were used as stimuli in a one-shot change blindness (CB) task where there was a 50% chance that one rectangle would change orientation between two successive presentations separated by an interval. CB was eliminated by cueing the target rectangle in the first stimulus, reduced by cueing in the interval and unaffected by cueing in the second presentation. This supports the idea that a representation was formed that persisted through the interval before being 'overwritten' by the second presentation (Landman et al, 2003 Vision Research 43149–164]. Another possibility is that participants used some kind of grouping or Gestalt strategy. To test this we changed the spatial position of the rectangles in the second presentation by shifting them along imaginary spokes (by ±1 degree) emanating from the central fixation point. There was no significant difference seen in performance between this and the standard task [F(1,4)=2.565, p=0.185]. This may suggest two things: (i) Gestalt grouping is not used as a strategy in these tasks, and (ii) it gives further weight to the argument that objects may be stored and retrieved from a pre-attentional store during this task

    Functional Organization of the Human Brain: How We See, Feel, and Decide.

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    The human brain is responsible for constructing how we perceive, think, and act in the world around us. The organization of these functions is intricately distributed throughout the brain. Here, I discuss how functional magnetic resonance imaging (fMRI) was employed to understand three broad questions: how do we see, feel, and decide? First, high-resolution fMRI was used to measure the polar angle representation of saccadic eye movements in the superior colliculus. We found that eye movements along the superior-inferior visual field are mapped across the medial-lateral anatomy of a subcortical midbrain structure, the superior colliculus (SC). This result is consistent with the topography in monkey SC. Second, we measured the empathic responses of the brain as people watched a hand get painfully stabbed with a needle. We found that if the hand was labeled as belonging to the same religion as the observer, the empathic neural response was heightened, creating a strong ingroup bias that could not be readily manipulated. Third, we measured brain activity in individuals as they made free decisions (i.e., choosing randomly which of two buttons to press) and found the activity within fronto-thalamic networks to be significantly decreased compared to being instructed (forced) to press a particular button. I also summarize findings from several other projects ranging from addiction therapies to decoding visual imagination to how corporations are represented as people. Together, these approaches illustrate how functional neuroimaging can be used to understand the organization of the human brain

    Visual Attention-Related Processing: Perspectives from Ageing, Cognitive Decline and Dementia

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    Visual attention is essential for environmental interactions, but our ability to respond to stimuli gradually declines across the lifespan, and such deficits are even more pronounced in various states of cognitive impairment. Examining the integrity of related components, from elements of attention capture to executive control, will improve our understanding of related declines by helping to explain behavioural and neural effects, which will ultimately contribute towards our knowledge of the extent of dysfunctional attention processes and their impact upon everyday life. Accordingly, this Special Issue represents a body of literature that fundamentally advances insights into visual attention processing, featuring studies spanning healthy ageing, mild cognitive impairment, and dementi
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