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In this article, we will define the principles of loyalty and watchfulness in algorithm’s usage. We will then explore some of the interpretability techniques, which let us explain the decisions of an algorithm and share them with transparency. We will focus on ways to express indecision in order to increase the trust of the users in those systems. The second part is dedicated to a collection of statistical biases, which can be introduced both in the conception and the usage of those algorithmic processes. We will define a methodology to control the possible outputs (decisions) of an algorithm and keep them from conflicting with the interests of the algorithm designer and users.

Decisions are typically made after integrating information about multiple attributes of alternatives in a choice set. The computational mechanisms by which this integration occurs have been a focus of extensive research in humans and other animals. Where observers are obliged to consider attributes in turn, a framework known as “selective integration” can capture salient biases in human choices. The model proposes that successive attributes compete for processing resources and integration is biased towards the alternative with the locally preferred attribute. Quantitative analysis shows that this model, although it discards choice-relevant information, is optimal when the observers’ decisions are corrupted by noise that occurs beyond the sensory stage. Here, we used scalp electroencephalographic (EEG) recordings to test a neural prediction of the model: that locally preferred attributes should be encoded with higher gain in neural signals over posterior cortex. Over two sessions, human observers (of either sex) judged which of two simultaneous streams of bars had the higher (or lower) average height. The selective integration model fit the data better than a rival model without bias. Single-trial analysis showed that neural signals contralateral to the preferred attribute covaried more steeply with the decision information conferred by locally preferred attributes. These findings provide neural evidence in support of selective integration, complementing existing behavioural work.Significance StatementWe often make choices about stimuli with multiple attributes, such as when deciding which car to buy on the basis of price, performance and fuel economy. A model of the choice process, known as selective integration, proposes that rather than taking all of the decision-relevant information equally into account when making choices, we discard or overlook a portion of it. Although information is discarded, this strategy can lead to better decisions when memory is limited. Here, we test and confirm predictions of the model about the brain signals that occur when different stimulus attributes of stimulus are being evaluated. Our work provides the first neural support for the selective integration model.

Over the last decades, psychophysical and electrophysiological studies in patients and animal models of Parkinson’s disease (PD), have consistently revealed a number of visual abnormalities. In particular, specific alterations of contrast sensitivity curves, electroretinogram (ERG), and visual evoked potentials (VEP), have been attributed to dopaminergic retinal depletion. However, fundamental mechanisms of cortical visual processing, such as normalization or “gain-control” computations, have not yet been examined in PD patients. Here we measured electrophysiological indices of gain control in both space (surround suppression) and time (sensory adaptation) in PD patients based on steady-state VEP (ssVEP). Compared to controls, patients exhibited a significantly higher initial ssVEP amplitude that quickly decayed over time, and greater relative suppression of ssVEP amplitude as a function of surrounding stimulus contrast. Meanwhile, EEG frequency spectra were broadly elevated in patients relative to controls. Thus, contrary to what might be expected given the reduced contrast sensitivity often reported in PD, visual neural responses are not weaker; rather, they are initially larger but undergo an exaggerated degree of spatial and temporal gain control and are embedded within a greater background noise level. We conclude that compensatory cortical mechanisms may play a role in determining dysfunctional center-surround interactions at the retinal level.

Over the last decades, psychophysical and electrophysiological studies in patients and animal models of Parkinson’s disease (PD), have consistently revealed a number of visual abnormalities. In particular, specific alterations of contrast sensitivity curves, electroretinogram (ERG), and visual-evoked potentials (VEP), have been attributed to dopaminergic retinal depletion. However, fundamental mechanisms of cortical visual processing, such as normalization or “gain control” computations, have not yet been examined in PD patients. Here, we measured electrophysiological indices of gain control in both space (surround suppression) and time (sensory adaptation) in PD patients based on steady-state VEP (ssVEP). Compared with controls, patients exhibited a significantly higher initial ssVEP amplitude that quickly decayed over time, and greater relative suppression of ssVEP amplitude as a function of surrounding stimulus contrast. Meanwhile, EEG frequency spectra were broadly elevated in patients relative to controls. Thus, contrary to what might be expected given the reduced contrast sensitivity often reported in PD, visual neural responses are not weaker; rather, they are initially larger but undergo an exaggerated degree of spatial and temporal gain control and are embedded within a greater background noise level. These differences may reflect cortical mechanisms that compensate for dysfunctional center-surround interactions at the retinal level.

Parkinson’s disease (PD) is a neurological disorder characterized by motor deficits as a result of progressive degeneration of dopaminergic neurons. Patients often report visual impairments and exhibit deficits of visual acuity, contrast sensitivity and color vision, suggesting abnormal processing of visual information. Although electrophysiological studies indicate amplitude and latency differences in patients, one of the major challenges is the lack of a conclusive, accurate, non-invasive biomarker for diagnosis and monitoring of therapeutic efficacy. In this study, we used machine learning to model and identify the most relevant signs from the EEG spectra over the span of visual stimulation. First, we used human electroencephalography (EEG) to measure visual evoked responses during steady state (ssVEP) in a visual surround suppression paradigm, in which measures of gain control and temporal aspects of the visual response are simultaneously tracked. We found an excessive response gain profile of the contrast response function, and an abnormally greater background noise level in PD patients compared to healthy controls. Second, performance of three learning models was tested: logistic regression, decision tree and extra tree. Together, these provide powerful insights about the most relevant features that allow classifying patients from controls. These models contribute with new hints on the interpretation of functional abnormalities in PD based on spectral EEG during visual stimulation. Machine learning provides a promising tool for accurate and robust prediction in PD diagnosis, based on EEG signatures during visual information processing.

Summary In dynamic environments, split-second sensorimotor decisions must be prioritized according to potential payoffs to maximize overall rewards. The impact of relative value on deliberative perceptual judgments has been examined extensively [1–6], but relatively little is known about value-biasing mechanisms in the common situation where physical evidence is strong but the time to act is severely limited. In prominent decision models, a noisy but statistically stationary representation of sensory evidence is integrated over time to an action-triggering bound, and value-biases are affected by starting the integrator closer to the more valuable bound. Here, we show significant departures from this account for humans making rapid sensory-instructed action choices. Behavior was best explained by a simple model in which the evidence representation—and hence, rate of accumulation—is itself biased by value and is non-stationary, increasing over the short decision time frame. Because the value bias initially dominates, the model uniquely predicts a dynamic "turn-around" effect on low-value cues, where the accumulator first launches toward the incorrect action but is then re-routed to the correct one. This was clearly exhibited in electrophysiological signals reflecting motor preparation and evidence accumulation. Finally, we construct an extended model that implements this dynamic effect through plausible sensory neural response modulations and demonstrate the correspondence between decision signal dynamics simulated from a behavioral fit of that model and the empirical decision signals. Our findings suggest that value and sensory information can exert simultaneous and dynamically countervailing influences on the trajectory of the accumulation-to-bound process, driving rapid, sensory-guided actions.

In situations in which impending sensory events demand fast action choices, we must be ready to prioritize higher-value courses of action to avoid missed opportunities. When such a situation first presents itself, stimulus–action contingencies and their relative value must be encoded to establish a value-biased state of preparation for an impending sensorimotor decision. Here, we sought to identify neurophysiological signatures of such processes in the human brain (both female and male). We devised a task requiring fast action choices based on the discrimination of a simple visual cue in which the differently valued sensory alternatives were presented 750–800 ms before as peripheral “targets” that specified the stimulus–action mapping for the upcoming decision. In response to the targets, we identified a discrete, transient, spatially selective signal in the event-related potential (ERP), which scaled with relative value and strongly predicted the degree of behavioral bias in the upcoming decision both across and within subjects. This signal is not compatible with any hitherto known ERP signature of spatial selection and also bears novel distinctions with respect to characterizations of value-sensitive, spatially selective activity found in sensorimotor areas of nonhuman primates. Specifically, a series of follow-up experiments revealed that the signal was reliably invoked regardless of response laterality, response modality, sensory feature, and reward valence. It was absent, however, when the response deadline was relaxed and the strategic need for biasing removed. Therefore, more than passively representing value or salience, the signal appears to play a versatile and active role in adaptive sensorimotor prioritization.SIGNIFICANCE STATEMENTIn many situations such as fast-moving sports, we must be ready to act fast in response to sensory events and, in our preparation, prioritize courses of action that lead to greater rewards. Although behavioral effects of value biases in sensorimotor decision making have been widely studied, little is known about the neural processes that set these biases in place beforehand. Here, we report the discovery of a transient, spatially selective neural signal in humans that encodes the relative value of competing decision alternatives and strongly predicts behavioral value biases in decisions made ∼500 ms later. Follow-up manipulations of value differential, reward valence, response modality, sensory features, and time constraints establish that the signal reflects an active, feature- and effector-general preparatory mechanism for value-based prioritization.

Perceptual decisions occur when sensory inputs are converted to discrete categorical variables. The neural and computational mechanisms by which rodents, monkeys, and humans make perceptual decisions have been intensively studied since 1989. Here, we address five questions that continue to raise controversy, summarizing research that has asked (1) how information is integrated to form a categorical choice, (2) what computations are carried out in cortical neurons during perceptual decisions, (3) how perceptual decision-making can be studied using cognitive neuroimaging techniques, (4) how we decide when to draw our decisions to a conclusion, and (5) how perceptual decisions are biased by prior information. Despite considerable progress, these remain key open questions in psychology and the neurosciences.

In the natural environment, humans make saccades almost continuously. In many eye movement experiments, however, observers are required to fixate for unnaturally long periods of time. The resulting long and monotonous experimental sessions can become especially problematic when collecting data in a clinical setting, where time can be scarce and subjects easily fatigued. With this in mind, we tested whether the well-studied motor learning process of saccade adaptation could be induced with a dramatically shortened intertrial interval. Observers made saccades to targets that stepped left or right either ∼250 ms or ∼1,600 ms after the saccade landed. In experiment I, we tested baseline saccade parameters to four different target amplitudes (5°, 10°, 15°, and 20°) in the two timing settings. In experiments II and III, we adapted 10° saccades via 2° intrasaccadic steps either backwards or forwards, respectively. Seven subjects performed eight separate adaptation sessions (2 intertrial timings × 2 adaptation direction × 2 session trial lengths). Adaptation proceeded remarkably similarly in both timing conditions across the multiple sessions. In the faster-paced sessions, robust adaptation was achieved in under 2 min, demonstrating the efficacy of our approach to streamlining saccade adaptation experiments. Although saccade amplitudes were similar between conditions, the faster-paced condition unexpectedly resulted in significantly higher peak velocities in all subjects. This surprising finding demonstrates that the stereotyped “main sequence” relationship between saccade amplitude and peak velocity is not as fixed as originally thought.

Interaction with visual objects in the environment requires an accurate correspondence between visual space and its internal representation within the brain. Many clinical conditions involve some impairment in visuo-motor control and the errors created by the lesion of a specific brain region are neither random nor uninformative. Modern approaches to studying the neuropsychology of action require powerful data-driven analyses and error modelling in order to understand the function of the lesioned areas. In the present paper we carried out mixed-effect analyses of the pointing errors of seven optic ataxia patients and seven control subjects. We found that a small parameter set is sufficient to explain the pointing errors produced by unilateral optic ataxia patients. In particular, the extremely stereotypical errors made when pointing toward the contralesional visual field can be fitted by mathematical models similar to those used to model central magnification in cortical or sub-cortical structure(s). Our interpretation is that visual areas that contain this footprint of central magnification guide pointing movements when the posterior parietal cortex is damaged and that the functional role of the posterior parietal cortex is to actively compensate for the under-representation of peripheral vision that accompanies central magnification. Optic ataxia misreaching reveals what would be hand movement accuracy and precision if the human motor system did not include elaborated corrective processes for reaching and grasping to non-foveated targets.

The classic definition of ‘pure’ optic ataxia suggests that these patients’ visuomotor impairments are independent of perceptual or attentional deficits. More recent work suggests that some patients with optic ataxia also have difficulty attending to targets in their ataxic field. Thus, an important question is whether these attentional deficits might be related to the well-known problems in visuomotor control evident in these patients. To investigate this question we had controls (N = 5) and CF, a patient with optic ataxia in his left visual field, perform tasks that required them to detect or reach towards targets presented in either central vision, or at different target eccentricities in the periphery. As expected, CF was less accurate than controls when reaching to targets in his ataxic (left) visual field, and was much slower than controls to detect the presence of targets in his ataxic field. The reaction times to lift the hand in the pointing and the detecting conditions were correlated in the ataxic field of patient CF, suggesting a common attentional deficit in both tasks. Importantly, although CF was slower to detect targets in the ataxic field, and less accurate to reach towards those same targets, the two deficits did not follow the same pattern. Specifically, only reaching errors in the ataxic field were strongly modulated by target eccentricity. These results suggest that dorsal posterior parietal lesions result in attention and visuomotor control problems in optic ataxia that arise from damage to independent mechanisms.

Neuro-CognitivePsychology, Bielefeld University, Bielefeld 33501, GermanyA well-known theory in the field of attention today is the premotortheory of attention which suggests that the mechanisms involved ineye movements are the same as those for spatial attention shifts.We tested a parietal damaged patient with unilateral optic ataxiaand 4 controls on a dual saccade/attentional task and showa dissociation between saccadic eye movements and presaccadicperceptual enhancement at the saccade goal. Remarkably, thoughthe patient was able to make the appropriate saccades to the left,impaired visual field (undistinguishable from saccades to his right,intact visual field), he was unable to discriminate the letter at thesaccade goal (whereas his performance was like controls for letterdiscrimination in his right visual field). This suggests that saccadeplanning and presaccadic perceptual facilitation are separable—planning a saccade to a location does not necessitate that theprocessing of this location is enhanced. Based on these results, wesuggest that the parietal cortex is necessary for the couplingbetween saccade planning and presaccadic perceptual facilitation.Keywords: attention, optic ataxia, parietal cortex, saccadesIntroductionEye movements and attention are very closely related.Normally, when we want to pay attention to an object, wemove our eyes so as to foveate on it (i.e., we shift our gaze) andthis is known as overt attention. However, it is also possible toshift attention without moving the eyes. This process is knownas covert attention. Both overt and covert attention have thesame objective: to enhance a location in space for furtherprocessing, either by bringing the object into higher-precisionprocessing pathways associated with central vision (Anstis1998), or by enhancing the efficiency of the processing inperipheral vision selectively at this specific location (Bushnellet al. 1981).According to the premotor theory of attention (Rizzolatti1983; Rizzolatti et al. 1987, 1994), a command to shift attentionis the same as a command to shift gaze. In both cases, attentionis shifted (covertly or overtly). This theory suggests thatpreparing a saccade to a peripheral target location involves thesame process as orienting selective attention to this peripherallocation, except that this process is then followed by the motorexecution. Inversely, any saccade will be associated witha spatially specific enhancement of processing at the locationof the saccade goal, i.e. saccades to a spatial location cannotoccur without a previous shift of attention to the location(Hoffman and Subramaniam 1995; Kowler et al. 1995; Goldberget al. 2006). In a behavioral study, Deubel and Schneider (1996)tested subjects’ ability to discriminate letter symbols atlocations around or at the saccade target location, beforesaccadic execution. They found that letter discrimination wasbest when it was in the same position as the saccade goal. Theability to discriminate a letter at any location other than thegoal of the saccade decreased to chance level. By showing thatwhen a saccade is executed toward a peripheral target, it ispreceded by a phenomenon of ‘‘presaccadic facilitation’’ ofletter discrimination specifically at this precise peripherallocation, this paradigm confirmed the spatial and temporalrelationship between saccades and attention: attention isoriented before saccadic execution toward the specific locationof the saccade goal, and may thus share common mechanismswith saccadic preparation (Schneider and Deubel 2002).Central to this theory is the finding that the same areas in thebrain that are involved in gaze or eye movements are alsoinvolved in attention shifts (Ignashchenkova et al. 2004; Mooreand Fallah 2004; Goldberg et al. 2006). One of the key areasshown to be involved in both attention and saccadic eyemovements is the lateral intraparietal area (LIP) in the monkeyposterior parietal cortex (Goldberg et al. 2006). We thereforetested involvement of the parietal cortex in the couplingbetween presaccadic attentional shifts and eye movements byobserving the performance of a patient with unilateral opticataxia due to damage to the right posterior parietal cortex. Ifsaccade planning and attentional shifts involve the samemechanisms, we should find a similar pattern of performancein target discrimination and saccade execution to the damagedvisual field. On the other hand, a dissociation between saccadicperformance and target discrimination performance couldsuggest that separate neural substrates govern attention andsaccade planning, but those processes could be coupled andoccur simultaneously. A second possibility could be that theparietal cortex mediates the coupling between a network ofareas involved in saccade planning and presaccadic facilitation,such as frontal and temporal areas. In normal behavior, it isimpossible to distinguish between a coupling and a commonsubstrate, however the impaired region/pathways in thispatient may provide valuable insight into these mechanisms.We tested the patient and 4 control subjects on a simplifiedversion of the task used by Deubel and Schneider (1996). In ourtask the saccade was always directed to the same location (at10 visual degrees of eccentricity) leftward or rightward.Subjects were then required to discriminate letters presentedbriefly during the saccade latency either at the saccade goal orat nonsaccade goal locations 3 closer or further away in thesame visual field. This task allowed us to test the presence ofpresaccadic facilitation, 1) at the location of the saccade goaland 2) at surrounding locations, testing for potential spatialdistortions in attentional shifts. Spatial distortions have been

Patients with bilateral optic ataxia fail to show rapid perturbation-induced corrections during manual aiming movements. Based on this, it has been proposed that this pathology results from a disruption of processes of on-line motor control in the posterior parietal cortex (PPC). Here, we show that on-line motor control performance in a patient with unilateral optic ataxia is similar to that of pointing towards stationary targets in peripheral vision, showing the same combination of hand and field effects. We also show that in the patient, manual correction towards his ataxic field was possible only when a preceding saccade (100 msec earlier) rapidly provides foveal information about the new target location. In control subjects, manual correction was often, but not necessarily preceded by a saccade. These results allow us to put forward a model of visuo-manual transformation, which involves updating of the reach plan based on the target–eye error, and rely upon two dissociated spatial representations (of the hand and of the target, respectively) within the PPC. a 2007 Elsevier Masson Srl. All rights reserved.

Visual illusions have been shown to affect perceptual judgements more so than motor behaviour, which was interpreted as evidence for a functional division of labour within the visual system. The dominant perception-action theory argues that perception involves a holistic processing of visual objects or scenes, performed within the ventral, inferior temporal cortex. Conversely, visuomotor action involves the processing of the 3D relationship between the goal of the action and the body, performed predominantly within the dorsal, posterior parietal cortex. We explored the effect of well-known visual illusions (a size-contrast illusion and the induced Roelofs effect) in a patient (IG) suffering bilateral lesions of the dorsal visual stream. According to the perception-action theory, IG's perceptual judgements and control of actions should rely on the intact ventral stream and hence should both be sensitive to visual illusions. The finding that IG performed similarly to controls in three different illusory contexts argues against such expectations and shows, furthermore, that the dorsal stream does not control all aspects of visuomotor behaviour. Assuming that the patient's dorsal stream visuomotor system is fully lesioned, these results suggest that her visually guided action can be planned and executed independently of the dorsal pathways, possibly through the inferior parietal lobule.

Humans and monkeys occasionally report the presence of a stimulus that has not occurred. A new study by Carnevale et al. (2015) sheds light on the nature and timing of the neural mechanisms that give rise to false detections.

Surround suppression is a well-known example of contextual interaction in visual cortical neurophysiology, whereby the neural response to a stimulus presented within a neuron's classical receptive field is suppressed by surrounding stimuli. Human psychophysical reports present an obvious analog to the effects seen at the single-neuron level: stimuli are perceived as lower-contrast when embedded in a surround. Here we report on a visual paradigm that provides relatively direct, straightforward indices of surround suppression in human electrophysiology, enabling us to reproduce several well-known neurophysiological and psychophysical effects, and to conduct new analyses of temporal trends and retinal location effects. Steady-state visual evoked potentials (SSVEP) elicited by flickering “foreground” stimuli were measured in the context of various static surround patterns. Early visual cortex geometry and retinotopic organization were exploited to enhance SSVEP amplitude. The foreground response was strongly suppressed as a monotonic function of surround contrast. Furthermore, suppression was stronger for surrounds of matching orientation than orthogonally-oriented ones, and stronger at peripheral than foveal locations. These patterns were reproduced in psychophysical reports of perceived contrast, and peripheral electrophysiological suppression effects correlated with psychophysical effects across subjects. Temporal analysis of SSVEP amplitude revealed short-term contrast adaptation effects that caused the foreground signal to either fall or grow over time, depending on the relative contrast of the surround, consistent with stronger adaptation of the suppressive drive. This electrophysiology paradigm has clinical potential in indexing not just visual deficits but possibly gain control deficits expressed more widely in the disordered brain.

The question of how sensory information is encoded and integrated for goal-directed movements is a major topic in action research. Here we studied the influence of the direction of gaze on a task in which healthy individuals were required to point to their own unseen fingertip. An effect of the position of gaze on pointing, leading to pointing errors in the direction opposite to the gaze position, was obtained in the range of 11° but vanished for 22°. These results suggest that targets of aiming movements performed with an unseen arm may be encoded in retinal coordinates even when the target is encoded in a nonvisual modality and remains unseen.

International audience; The rapid point-to-point movements of the eyes called saccades are the most commonly made movement by humans, yet differ from nearly every other type of motor output in that they are completed too quickly to be adjusted during their execution by visual feedback. Saccadic accuracy remains quite high over a lifetime despite inevitable changes to the physical structures controlling the eyes, indicating that the oculomotor system actively monitors and adjusts motor commands to achieve consistent behavioral production. Indeed, it seems that beyond the ability to compensate for slow, age-related bodily changes, saccades can be modified following traumatic injury or pathology that affects their production, or in response to more short-term systematic alterations to post-saccadic visual feedback in a laboratory setting. These forms of plasticity rely on the visual detection of accuracy errors by a unified set of mechanisms that support the process known as saccade adaptation. Saccade adaptation has been mostly studied as a phenomenon in its own right, outside of motor learning in general. Here, we highlight the commonalities between eye and arm movement adaptation by reviewing the literature across these fields wherever there are compelling overlapping theories or data. Recent exciting findings are challenging previous interpretations of the underlying mechanisms of saccade adaptation with the incorporation of concepts including prediction, reinforcement and contextual learning. We review the emerging ideas and evidence with particular emphasis on the important contributions made by Josh Wallman in this sphere over the past 15 years.

We review evidence showing a right-hemispheric dominance for visuo-spatial processing and representation in humans. Accordingly, visual disorganization symptoms (intuitively related to remapping impairments) are observed in both neglect and constructional apraxia. More specifically, we review findings from the intervening saccade paradigm in humans—and present additional original data—which suggest a specific role of the asymmetrical network at the temporo-parietal junction (TPJ) in the right hemisphere in visual remapping: following damage to the right dorsal posterior parietal cortex (PPC) as well as part of the corpus callosum connecting the PPC to the frontal lobes, patient OK in a double-step saccadic task exhibited an impairment when the second saccade had to be directed rightward . This singular and lateralized deficit cannot result solely from the patient's cortical lesion and, therefore, we propose that it is due to his callosal lesion that may specifically interrupt the interhemispheric transfer of information necessary to execute accurate rightward saccades towards a remapped target location. This suggests a specialized right-hemispheric network for visuo-spatial remapping that subsequently transfers target location information to downstream planning regions, which are symmetrically organized.

Optic ataxia, following dorsal stream lesions, is characterised by impaired visuomotor guidance. Recent studies have found concurrent perceptual deficits, but it is unclear whether these are functionally related to the visuomotor symptoms. We studied the ability of a well-documented patient (IG) with bilateral optic ataxia to react to sudden target jumps by correcting ongoing reaches or by explicitly reporting the jump direction. IG showed deficient reach corrections, especially for target jumps to the visual periphery, and was similarly slow to discriminate the same jumps perceptually. Across six test conditions, in which the retinal locations of target jumps were varied, her perceptual slowing mirrored her reaching deficit precisely. These findings confirm perceptual impairments after dorsal stream lesions, and imply a shared functional basis with the classical visuomotor symptoms of optic ataxia. Additionally, we show that the online correction deficit is determined dually by the retinal location to which the reach must be diverted, and the location to which it is initially directed. We suggest that this deficit, and its perceptual counterpart, can be traced to a slowed contralesional orienting of attention in optic ataxia.

The pre-motor theory of attention suggests that the mechanisms involved in target selection for eye movements are the same as those for spatial attention shifts. The pre-saccadic facilitation of perceptual discrimination at the location of a saccadic goal (paradigm of Deubel and Schneider, 1996) has been considered as an argument for this theory. We compared letter discrimination performance in a saccade (overt attention - pre-saccadic facilitation) and a fixation (covert attention) task in a patient with right posterior parietal damage and 4 controls. In the overt attention condition, the patient was instructed by a central cue to make a saccade to a target located at a peripheral location. During the saccade latency (in a period of time of 250 msec following the presentation of the cue), a letter was presented at the target location. Accuracy of leftward saccades was impaired compared to rightward saccades. To evaluate letter discrimination performance in this saccade task (i.e., the presence of pre-saccadic facilitation), we selected only those leftward saccades that were equivalent in accuracy (and latency) to the rightward ones. Within these selected trials, the patient was able to discriminate letters equally well in both visual fields. In contrast, he performed at chance level during the fixation task (covert attention condition) for letters presented at the same peripheral location with the same timing with respect to the cue presentation. The patient could thus discriminate the letter presented at 8° of visual eccentricity while he was preparing a saccade, whereas he was unable to perceive the letter in the fixation task. Remarkably, in the left visual field, letter discrimination was impossible even when a letter was presented as close as 2.5° of visual eccentricity in the fixation task. Altogether, these results suggest that pre-saccadic perceptual facilitation does not rely on the same processes as those of covert attention, as tested by fixation task. Instead, we propose that pre-saccadic perceptual facilitation results from a form of attention specific to action, which could correspond to a pre-saccadic remapping process.

The main aim of this study is to determine the reference frame of the pointing errors that characterize patients with unilateral optic ataxia (OA). The reaching errors of seven patients with unilateral OA when pointing on a 2D matrix in peripheral vision were investigated in order to better qualify the reference frame of their deficit. Patients were asked to fixate a central target and then to point at one of 24 visual targets presented in their left or right peripheral visual fields, with their left or right hands. The four left and the three right hemisphere lesion patients with OA exhibited an identical pattern of results. In the contralesional visual field, error vectors were systematically directed toward the fixation point, rather than horizontally toward the side of the lesion. OA results from a deficit in transforming targets' eye-centred coordinates into appropriate motor commands.

Optic ataxia (OA) is one of the symptoms pertaining to Balint's Syndrome. It has been described clinically for nearly 80 years before it became a cornerstone of the most popular dual stream theory of the visual brain. Over the last 10 years a regain of interest for this neurological condition lead to a number of precise analyses of the deficits found in optic ataxia, giving rise to a renewed outline of its very definition and hence of the function(s) of the occipito-parietal (dorsal) stream. In absence of concomitant clinical symptoms, we review evidence that misreaching errors in central vision result from the "hand effect": an erroneous dynamic spatial processing of proprioceptive information from the hand. When visual feedback of the hand is provided (closed-loop condition), pure optic ataxia is restricted to peripheral vision. This central versus peripheral vision distinction is repeatedly used to argue that action and perception are not unique and dissociated systems. New assessments of optic ataxia patients are provided, confirming on one hand that their visuomotor deficit is specific to peripheral vision (i.e. when the gaze and the hand goals are dissociated), on the other hand that they disclose perceptual deficits in peripheral vision. These results are coherent with the recent demonstration that optic ataxia patients exhibit a general contralesional deficit for dynamic visuo-spatial processing, affecting both hand and eye movements [Gaveau, V., Pelisson, D., Blangero, A., Urquizar, C., Prablanc, C.,Vighetto, A., et al. (2008). A common parietal module for saccade and reach: Eye-hand coordination and saccadic control in optic ataxia. Neuropsychologia, 46, 475-486]. Such module(s) within the dorsal stream could be used for both action and perception in the periphery. It is concluded that optic ataxia cannot be considered as a unitary and specific visuo-manual deficit, and that the modular organisation of the dorsal stream allows for numerous dorsal-ventral interactions for perception and action.

Understanding the function of a tool is an essential step in learning to use a tool. This aspect of interaction with tools has hitherto been neglected. Unlike acquiring the expertise in handling a new tool, which involves practice, understanding its function usually only requires a single observation of the tool being used. The present study uncovers the neural areas involved in this transient understanding effect as a left-lateralized pattern involving prefrontal and mediotemporal areas. We suggest that activation in this network reflects the conceptual encoding of the function of new tools as it is independent from the well-known tool-related networks. We demonstrate that understanding the function of a new tool does not rely on known semantic or motor networks involved in processing tool use.

Optic ataxia (OA) is classically defined as a deficit of visually guided movements that follows lesions of the posterior part of the posterior parietal cortex (PPC). Since the formalisation of the double stream of visual information processing [Milner, A. D., & Goodale, M. A. (1995). The visual brain in action. Oxford: Oxford University Press] and the use of OA as an argument in favour of the involvement of the posterior parietal cortex (dorsal stream) in visually guided movements, many studies have looked at the visuomotor deficits of these patients. In parallel, the development of neuroimaging methods have led to increasing information about the role of the posterior parietal cortex in visually guided actions. In this article, we discuss the similarities and differences in the results that emerged from these two complementary viewpoints by combining a meta-analysis of neuroimaging data on reaching with lesion studies from OA patients and results of our own fMRI study on reaching in the ipsi- and contra-lateral visual field. We identified four bilateral parietal foci from the meta-analysis and found that the more posterior foci showed greater lateralisation for contralateral visual stimulation than more anterior ones Additionally, the more anterior foci showed greater lateralisation for the use of the contralateral hand than the more posterior ones. Therefore, we can demonstrate that they are organised along a postero-anterior gradient of visual-to-somatic information integration. Furthermore, from the combination of imaging and lesion data it can be inferred that a lesion of the three most posterior foci responsible for the target-hand integration could explain the hand and field effect revealed in OA reaching behaviour.

The classic definition of 'pure' optic ataxia suggests that these patients' visuomotor impairments are independent of perceptual or attentional deficits. More recent work suggests that some patients with optic ataxia also have difficulty attending to targets in their ataxic field. Thus, an important question is whether these attentional deficits might be related to the well-known problems in visuomotor control evident in these patients. To investigate this question we had controls (N=5) and CF, a patient with optic ataxia in his left visual field, perform tasks that required them to detect or reach towards targets presented in either central vision, or at different target eccentricities in the periphery. As expected, CF was less accurate than controls when reaching to targets in his ataxic (left) visual field, and was much slower than controls to detect the presence of targets in his ataxic field. The reaction times to lift the hand in the pointing and the detecting conditions were correlated in the ataxic field of patient CF, suggesting a common attentional deficit in both tasks. Importantly, although CF was slower to detect targets in the ataxic field, and less accurate to reach towards those same targets, the two deficits did not follow the same pattern. Specifically, only reaching errors in the ataxic field were strongly modulated by target eccentricity. These results suggest that dorsal posterior parietal lesions result in attention and visuomotor control problems in optic ataxia that arise from damage to independent mechanisms.

The aim of this work was to investigate ocular control in patients with optic ataxia (OA). Following a lesion in the posterior parietal cortex (PPC), these patients exhibit a deficit for fast visuo-motor control of reach-to-grasp movements. Here, we assessed the fast visuo-motor control of saccades as well as spontaneous eye-hand coordination in two bilateral OA patients and five neurologically intact controls in an ecological "look and point" paradigm. To test fast saccadic control, trials with unexpected target-jumps synchronised with saccade onset were randomly intermixed with stationary target trials. Results confirmed that control subjects achieved visual capture (foveation) of the displaced targets with the same timing as stationary targets (fast saccadic control) and began their hand movement systematically at the end of the primary saccade. In contrast, the two bilateral OA patients exhibited a delayed visual capture, especially of displaced targets, resulting from an impairment of fast saccadic control. They also exhibited a peculiar eye-hand coordination pattern, spontaneously delaying their hand movement onset until the execution of a final corrective saccade, which allowed target foveation. To test whether this pathological behaviour results from a delay in updating visual target location, we had subjects perform a second experiment in the same control subjects in which the target-jump was synchronised with saccade offset. With less time for target location updating, the control subjects exhibited the same lack of fast saccadic control as the OA patients. We propose that OA corresponds to an impairment of fast updating of target location, therefore affecting both eye and hand movements.

International audience; Earlier research has suggested that optic ataxia, a deficit in reaching in peripheral vision, can be isolated from Balint's syndrome as it is primarily a visuomotor disorder, independent of perceptual or attentional deficits. Yet almost no research has examined the attentional abilities of these patients. We examined peripheral visual attention in two patients with unilateral optic ataxia. Results indicated that both patients were slower to respond to targets in their ataxic visual field, irrespective of cuing condition (i.e. validly, invalidly, and no cue conditions), consistent with an overall decrease in the salience of stimuli in the ataxic field. Attentional deficits in peripheral vision are therefore an important factor to consider when examining visuomotor control deficits in optic ataxia.

Prism adaptation (PA) alleviates some neglect symptoms, however, the mechanisms underlying these effects are unclear. One brain area that may be important in generating these beneficial effects is the superior parietal lobe (SPL), a region not typically damaged in neglect, and known to be important for attention, visuomotor control, and eye movements. We examined the effects of rightward PA on covert attention in CF, a patient with bilateral SPL lesions, compared to a group of controls (N = 26) who underwent sham adaptation. In contrast to previous work in neglect, there was no reduction in CF’s leftward disengage deficit, or rightward attentional bias following PA. These results suggest that the SPL plays an important role in generating the beneficial after-effects of prisms on attention.

International audience; Optic ataxia is considered to be a specific visuo-manual guidance deficit, which combines pointing errors due to the use of the contralesional hand ("hand effect") and to the presentation of the visual target in the contralesional field ("field effect"). The nature of the hand effect has not been identified. The field effect is acknowledged as an impaired spatial integration of visual target location. However, spatial integration of proprioceptive information from the arm has never been experimentally tested in these patients. Here, we specifically investigated the capacity of two patients with unilateral optic ataxia in tasks requiring different levels of proprioceptive integration from primary information processing to proprioceptivo-motor integration. In a first experiment -proprioceptive pointing with the ipsilesional hand toward the index finger of the contralesional hand- revealed a large mislocalisation of the ataxic hand accounting for the hand effect. In a second experiment -proprioceptive pointing with the ataxic arm toward the finger of the ipsilesional hand- revealed reaching errors for non-visual targets, i.e. optic ataxia is not specific to 'optic' targets. Altogether, the present results call for a redefinition of this neurological condition in the framework of parietal functions.

Visual illusions have been shown to affect perceptual judgements more so than motor behaviour, which was interpreted as evidence for a functional division of labour within the visual system. The dominant perception-action theory argues that perception involves a holistic processing of visual objects or scenes, performed within the ventral, inferior temporal cortex. Conversely, visuomotor action involves the processing of the 3D relationship between the goal of the action and the body, performed predominantly within the dorsal, posterior parietal cortex. We explored the effect of well-known visual illusions (a size-contrast illusion and the induced Roelofs effect) in a patient (IG) suffering bilateral lesions of the dorsal visual stream. According to the perception-action theory, IG's perceptual judgements and control of actions should rely on the intact ventral stream and hence should both be sensitive to visual illusions. The finding that IG performed similarly to controls in three different illusory contexts argues against such expectations and shows, furthermore, that the dorsal stream does not control all aspects of visuomotor behaviour. Assuming that the patient's dorsal stream visuomotor system is fully lesioned, these results suggest that her visually guided action can be planned and executed independently of the dorsal pathways, possibly through the inferior parietal lobule.

Corrigendum to “Do visual illusions probe the visual brain? Illusions in action without a dorsal visual stream” [Neuropsychologia 45 (2007) 1849–1858] Yann Coello a,∗, James Danckert b, Annabelle Blangero c, Yves Rossetti c,d a Unit de Recherche sur l’Evolution des Comportements et l’Apprentissage, UPRES EA 1059 and UMR-CNRS 8163 STL, Universite Charles de Gaulle, Lille, BP 60149, F.59653 Villeneuve d’Ascq Cedex, France b Department of Psychology, University of Waterloo, Waterloo, Ontario N2L 3G1, Canada c INSERM UMR-S 534, Institut National de la Sante et de la Recherche Medicale, Universite Claude Bernard, Lyon, Bron, France d Mouvement et Handicap, Institut Federatif des Neurosciences de Lyon, Hospices Civils de Lyon, France

In the haptic domain, a double dissociation can be proposed on the basis of neurological deficits between tactile information for action, represented by tactile apraxia, and tactile information for perception, represented by tactile agnosia. We suggest that this dissociation comes from different networks, both involving the anterior intraparietal area of the posterior parietal cortex.

Patients with optic ataxia (OA), who are missing the caudal portion of their superior parietal lobule (SPL), have difficulty performing visually-guided reaches towards extra-foveal targets. Such gaze and hand decoupling also occurs in commonly performed non-standard visuomotor transformations such as the use of a computer mouse. In this study, we test two unilateral OA patients in conditions of 1) a change in the physical location of the visual stimulus relative to the plane of the limb movement, 2) a cue that signals a required limb movement 180° opposite to the cued visual target location, or 3) both of these situations combined. In these non-standard visuomotor transformations, the OA deficit is not observed as the well-documented field-dependent misreach. Instead, OA patients make additional eye movements to update hand and goal location during motor execution in order to complete these slow movements. Overall, the OA patients struggled when having to guide centrifugal movements in peripheral vision, even when they were instructed from visual stimuli that could be foveated. We propose that an intact caudal SPL is crucial for any visuomotor control that involves updating ongoing hand location in space without foveating it, i.e. from peripheral vision, proprioceptive or predictive information.