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      Beyond eye gaze: What else can eyetracking reveal about cognition and cognitive development?

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          Highlights

          • •

            Eyetracking measures provide non-invasive and rich indices of brain function and cognition.

          • •

            Gaze analysis reveals current attentional focus and cognitive strategies.

          • •

            Pupil dilation is modulated by norepinephrine and reflects mental effort.

          • •

            Spontaneous blink rate is modulated by dopamine, which is involved in learning and goal-oriented behavior.

          • •

            Ocular measures can provide insights regarding cognition and cognitive development.

          Abstract

          This review provides an introduction to two eyetracking measures that can be used to study cognitive development and plasticity: pupil dilation and spontaneous blink rate. We begin by outlining the rich history of gaze analysis, which can reveal the current focus of attention as well as cognitive strategies. We then turn to the two lesser-utilized ocular measures. Pupil dilation is modulated by the brain’s locus coeruleus-norepinephrine system, which controls physiological arousal and attention, and has been used as a measure of subjective task difficulty, mental effort, and neural gain. Spontaneous eyeblink rate correlates with levels of dopamine in the central nervous system, and can reveal processes underlying learning and goal-directed behavior. Taken together, gaze, pupil dilation, and blink rate are three non-invasive and complementary measures of cognition with high temporal resolution and well-understood neural foundations. Here we review the neural foundations of pupil dilation and blink rate, provide examples of their usage, describe analytic methods and methodological considerations, and discuss their potential for research on learning, cognitive development, and plasticity.

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          Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications.

          Rita Goldstein, Nora D. Volkow (2011)
          The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.
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            The debate over dopamine's role in reward: the case for incentive salience.

            Kent C. Berridge (2007)
            Debate continues over the precise causal contribution made by mesolimbic dopamine systems to reward. There are three competing explanatory categories: 'liking', learning, and 'wanting'. Does dopamine mostly mediate the hedonic impact of reward ('liking')? Does it instead mediate learned predictions of future reward, prediction error teaching signals and stamp in associative links (learning)? Or does dopamine motivate the pursuit of rewards by attributing incentive salience to reward-related stimuli ('wanting')? Each hypothesis is evaluated here, and it is suggested that the incentive salience or 'wanting' hypothesis of dopamine function may be consistent with more evidence than either learning or 'liking'. In brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic 'liking' for sensory pleasures. Other recent evidence indicates that dopamine is not needed for new learning, and not sufficient to directly mediate learning by causing teaching or prediction signals. By contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. Dopamine appears necessary for normal 'wanting', and dopamine activation can be sufficient to enhance cue-triggered incentive salience. Drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Such drugs interact with incentive salience integrations of Pavlovian associative information with physiological state signals. That interaction sets the stage to cause compulsive 'wanting' in addiction, but also provides opportunities for experiments to disentangle 'wanting', 'liking', and learning hypotheses. Results from studies that exploited those opportunities are described here. In short, dopamine's contribution appears to be chiefly to cause 'wanting' for hedonic rewards, more than 'liking' or learning for those rewards.
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              Inverted-U-shaped dopamine actions on human working memory and cognitive control.

              Roshan Cools, Mark D'Esposito (2011)
              Brain dopamine (DA) has long been implicated in cognitive control processes, including working memory. However, the precise role of DA in cognition is not well-understood, partly because there is large variability in the response to dopaminergic drugs both across different behaviors and across different individuals. We review evidence from a series of studies with experimental animals, healthy humans, and patients with Parkinson's disease, which highlight two important factors that contribute to this large variability. First, the existence of an optimum DA level for cognitive function implicates the need to take into account baseline levels of DA when isolating the effects of DA. Second, cognitive control is a multifactorial phenomenon, requiring a dynamic balance between cognitive stability and cognitive flexibility. These distinct components might implicate the prefrontal cortex and the striatum, respectively. Manipulating DA will thus have paradoxical consequences for distinct cognitive control processes, depending on distinct basal or optimal levels of DA in different brain regions. Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Silvia A. Bunge
                Journal
                Journal ID (nlm-ta): Dev Cogn Neurosci
                Journal ID (iso-abbrev): Dev Cogn Neurosci
                Title: Developmental Cognitive Neuroscience
                Publisher: Elsevier
                ISSN (Print): 1878-9293
                ISSN (Electronic): 1878-9307
                Publication date PMC-release: 11 November 2016
                Publication date Collection: June 2017
                Publication date (Electronic): 11 November 2016
                Volume: 25
                Pages: 69-91
                Affiliations
                [a ]Department of Psychology, University of California at Berkeley, United States
                [b ]Helen Wills Neuroscience Institute, University of California at Berkeley, United States
                Author notes
                [* ]Corresponding author at: University of California, Berkeley, 134 Barker Hall, Berkeley, CA 94720, United States. sbunge@ 123456berkeley.edu
                Article
                Publisher ID: S1878-9293(16)30084-6
                DOI: 10.1016/j.dcn.2016.11.001
                PMC ID: 6987826
                PubMed ID: 27908561
                SO-VID: 1a7a8f5a-ec7a-4b2c-b042-8932e369c6fd
                Copyright © © 2016 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 1 June 2016
                Date revision received : 26 October 2016
                Date accepted : 7 November 2016
                Categories
                Subject: Article

                ScienceOpen disciplines: Neurosciences
                Keywords: eyetracking,saccades,pupillometry,pupil dilation,blink rate,children
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: eyetracking, saccades, pupillometry, pupil dilation, blink rate, children

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