How visual attention span and phonological skills contribute to N170 print tuning: An EEG study in French dyslexic students

Developmental dyslexia is a disorder characterized by a sustainable learning deficit in reading. Based on ERP-driven approaches focusing on the visual word form area, electrophysiological studies have pointed a lack of visual expertise for written word recognition in dyslexic readers by contrasting the left-lateralized N170 amplitudes elicited by alphabetic versus non-alphabetic stimuli. Here, we investigated in 22 dyslexic participants and 22 age-matched control subjects how two behavioural abilities potentially affected in dyslexic readers (phonological and visual attention skills) contributed to the N170 expertise during a word detection task. Consistent with literature, dyslexic participants exhibited poorer performance in these both abilities as compared to healthy subjects. At the brain level, we observed (1) an unexpected preservation of the N170 expertise in the dyslexic group suggesting a possible compensatory mechanism and (2) a modulation of this expertise only by phonological skills, providing evidence for the phonological mapping deficit hypothesis

Couplage entre adaptation saccadique et perception visuo-spatiale : études neurophysiologiques chez l’homme

The vast majority of our daily activities (reading a book, driving a car, appreciating a work of art) are guided by active vision, that is, the dynamic and constant interaction between our visual system -which allows us to acquire the representation of the scene around us- and our oculomotor system - which allows us to move our gaze briefly and quickly ('ocular saccade') from one object to another within this scene-. The interaction between these two systems is eminently remarkable. Indeed, despite these ballistic movements of the eyes, we systematically achieve to: (1) direct our gaze precisely on the stimulus of interest and (2) maintain a stable visual representation of the world despite the execution of the saccade (which could generate a blurred or unstable image due to its high speed). These abilities are possible thanks to two processes: (1) a mechanism of sensorimotor plasticity called saccadic adaptation which ensures the permanent control of our eye movements and (2) a predictive system which allows to anticipate the post-saccadic visual image. The objective of this thesis was to better understand how the predictions of our oculomotor actions structure - at least in part - our visual perception through three studies. The first was conducted in a patient with an injury to the posterior parietal cortex. This study enabled us to validate two hypotheses: (1) an eye movement prediction signal is necessary - under certain conditions - to precisely locate a visual target after a saccade and (2) the posterior parietal cortex plays a key role in its integration. Studies 2 and 3 were conducted in a group of healthy volunteers and cerebellar patients, respectively. The aim of these experiments was to understand how a phase of oculomotor plasticity (inducing a systematic discrepancy between the predicted and real image of the post-saccadic visual scene - which necessarily had to be corrected by the adaptation mechanism -) alters our ability to precisely locate an object in space. The results showed that the oculomotor correction of this discrepancy was effective in healthy subjects and led to a perceptual localization bias. In contrast, the lesion of the cerebellum hampered the ability of these patients to correct this discrepancy, which allowed them to maintain precise localization judgments. Finally, two patients showed a dissociation between their adaptive capacity and their spatial localization performance. Taken together, these data suggest that (1) the cerebellum plays a key role both in motor functions and in transmitting predictive signals to the cerebral cortex for visuospatial perception and (2) these two ‘cerebellar’ functions are underpinned by distinct territories. Beyond the fundamental aspect of these studies, the experimental tasks that we used could be useful as biomarkers to identify an early impairment of this predictive coding ; a deficit which has been commonly documented in a psychiatric context, especially in the case of schizophrenia.Une très grande majorité de nos activités quotidiennes (lire un livre, conduire une voiture, apprécier une œuvre d’art) sont guidées par la vision active, c’est-à-dire l’interaction dynamique et constante entre notre système visuel, qui nous permet d’acquérir la représentation de la scène qui nous entoure et notre système oculomoteur, qui nous permet de déplacer notre regard de façon brève et rapide (‘saccades oculaires’) d’un objet à un autre au sein de cette scène. L’interaction entre ces deux systèmes est éminemment remarquable puisque malgré ces déplacements balistiques de l’œil, nous arrivons systématiquement à : (1) diriger notre regard de façon précise sur le stimulus d’intérêt en dépit de perturbations physiologiques ou pathologiques et (2) à maintenir une représentation visuelle stable de l’environnement malgré l’exécution de la saccade qui pourrait générer une image floutée ou instable en raison de sa haute vitesse. Ceci est respectivement permis par deux processus : (1) un mécanisme de plasticité sensori-motrice appelé adaptation saccadique qui assure le contrôle permanent de nos mouvements oculaires et (2) un système prédictif qui permet d’anticiper l’image visuelle post-saccadique. L’objectif de cette thèse était de mieux comprendre comment les prédictions de nos actions oculomotrices structurent -du moins en partie- notre perception visuelle par trois études. La première a été menée auprès d’un patient présentant une lésion du cortex pariétal postérieur. Elle a permis de valider deux hypothèses : (1) un signal de prédiction du mouvement oculaire est -sous certaines conditions- nécessaire pour localiser de façon précise une cible visuelle après une saccade et (2) le cortex pariétal postérieur joue un rôle clé dans son intégration. Les études 2 et 3 ont été menées respectivement auprès d’un groupe de volontaires sains et de patients cérébelleux. Elles visaient à comprendre comment une phase de plasticité oculomotrice (induisant une discordance systématique entre l’image prédite et réelle de la scène visuelle post-saccadique -qui devait nécessairement être corrigée par le mécanisme d’adaptation-) altérait notre capacité à localiser précisément un objet dans l’espace. Les résultats obtenus ont montré que la correction oculomotrice de cette discordance était effective chez le sujet sain et entraînait en contrepartie un biais perceptif de localisation. En revanche, la lésion du cervelet entravait la capacité de ces patients à corriger cette discordance, ce qui leur permettait de maintenir des jugements de localisation précis. Enfin, deux patients présentaient une dissociation entre capacité d’adaptation et performances de localisation spatiale. Dans l’ensemble, ces données suggèrent que le cervelet joue un rôle clé à la fois dans les fonctions motrices mais aussi dans la transmission de signaux prédictifs au cortex cérébral pour la perception visuo-spatiale et que ces deux fonctions sont sous-tendues par des territoires cérébelleux distincts. Au-delà de l’aspect fondamental, les tâches expérimentales que nous avons utilisées dans ces études pourraient s’avérer utiles en tant que biomarqueurs afin d’identifier une atteinte précoce de ce codage prédictif, ce qui a été couramment documenté en contexte psychiatrique, notamment dans le cas de schizophrénie

Couplage entre adaptation saccadique et perception visuo-spatiale : études neurophysiologiques chez l’homme

The vast majority of our daily activities (reading a book, driving a car, appreciating a work of art) are guided by active vision, that is, the dynamic and constant interaction between our visual system -which allows us to acquire the representation of the scene around us- and our oculomotor system - which allows us to move our gaze briefly and quickly ('ocular saccade') from one object to another within this scene-. The interaction between these two systems is eminently remarkable. Indeed, despite these ballistic movements of the eyes, we systematically achieve to: (1) direct our gaze precisely on the stimulus of interest and (2) maintain a stable visual representation of the world despite the execution of the saccade (which could generate a blurred or unstable image due to its high speed). These abilities are possible thanks to two processes: (1) a mechanism of sensorimotor plasticity called saccadic adaptation which ensures the permanent control of our eye movements and (2) a predictive system which allows to anticipate the post-saccadic visual image. The objective of this thesis was to better understand how the predictions of our oculomotor actions structure - at least in part - our visual perception through three studies. The first was conducted in a patient with an injury to the posterior parietal cortex. This study enabled us to validate two hypotheses: (1) an eye movement prediction signal is necessary - under certain conditions - to precisely locate a visual target after a saccade and (2) the posterior parietal cortex plays a key role in its integration. Studies 2 and 3 were conducted in a group of healthy volunteers and cerebellar patients, respectively. The aim of these experiments was to understand how a phase of oculomotor plasticity (inducing a systematic discrepancy between the predicted and real image of the post-saccadic visual scene - which necessarily had to be corrected by the adaptation mechanism -) alters our ability to precisely locate an object in space. The results showed that the oculomotor correction of this discrepancy was effective in healthy subjects and led to a perceptual localization bias. In contrast, the lesion of the cerebellum hampered the ability of these patients to correct this discrepancy, which allowed them to maintain precise localization judgments. Finally, two patients showed a dissociation between their adaptive capacity and their spatial localization performance. Taken together, these data suggest that (1) the cerebellum plays a key role both in motor functions and in transmitting predictive signals to the cerebral cortex for visuospatial perception and (2) these two ‘cerebellar’ functions are underpinned by distinct territories. Beyond the fundamental aspect of these studies, the experimental tasks that we used could be useful as biomarkers to identify an early impairment of this predictive coding ; a deficit which has been commonly documented in a psychiatric context, especially in the case of schizophrenia.Une très grande majorité de nos activités quotidiennes (lire un livre, conduire une voiture, apprécier une œuvre d’art) sont guidées par la vision active, c’est-à-dire l’interaction dynamique et constante entre notre système visuel, qui nous permet d’acquérir la représentation de la scène qui nous entoure et notre système oculomoteur, qui nous permet de déplacer notre regard de façon brève et rapide (‘saccades oculaires’) d’un objet à un autre au sein de cette scène. L’interaction entre ces deux systèmes est éminemment remarquable puisque malgré ces déplacements balistiques de l’œil, nous arrivons systématiquement à : (1) diriger notre regard de façon précise sur le stimulus d’intérêt en dépit de perturbations physiologiques ou pathologiques et (2) à maintenir une représentation visuelle stable de l’environnement malgré l’exécution de la saccade qui pourrait générer une image floutée ou instable en raison de sa haute vitesse. Ceci est respectivement permis par deux processus : (1) un mécanisme de plasticité sensori-motrice appelé adaptation saccadique qui assure le contrôle permanent de nos mouvements oculaires et (2) un système prédictif qui permet d’anticiper l’image visuelle post-saccadique. L’objectif de cette thèse était de mieux comprendre comment les prédictions de nos actions oculomotrices structurent -du moins en partie- notre perception visuelle par trois études. La première a été menée auprès d’un patient présentant une lésion du cortex pariétal postérieur. Elle a permis de valider deux hypothèses : (1) un signal de prédiction du mouvement oculaire est -sous certaines conditions- nécessaire pour localiser de façon précise une cible visuelle après une saccade et (2) le cortex pariétal postérieur joue un rôle clé dans son intégration. Les études 2 et 3 ont été menées respectivement auprès d’un groupe de volontaires sains et de patients cérébelleux. Elles visaient à comprendre comment une phase de plasticité oculomotrice (induisant une discordance systématique entre l’image prédite et réelle de la scène visuelle post-saccadique -qui devait nécessairement être corrigée par le mécanisme d’adaptation-) altérait notre capacité à localiser précisément un objet dans l’espace. Les résultats obtenus ont montré que la correction oculomotrice de cette discordance était effective chez le sujet sain et entraînait en contrepartie un biais perceptif de localisation. En revanche, la lésion du cervelet entravait la capacité de ces patients à corriger cette discordance, ce qui leur permettait de maintenir des jugements de localisation précis. Enfin, deux patients présentaient une dissociation entre capacité d’adaptation et performances de localisation spatiale. Dans l’ensemble, ces données suggèrent que le cervelet joue un rôle clé à la fois dans les fonctions motrices mais aussi dans la transmission de signaux prédictifs au cortex cérébral pour la perception visuo-spatiale et que ces deux fonctions sont sous-tendues par des territoires cérébelleux distincts. Au-delà de l’aspect fondamental, les tâches expérimentales que nous avons utilisées dans ces études pourraient s’avérer utiles en tant que biomarqueurs afin d’identifier une atteinte précoce de ce codage prédictif, ce qui a été couramment documenté en contexte psychiatrique, notamment dans le cas de schizophrénie

Couplage entre adaptation saccadique et perception visuo-spatiale : études neurophysiologiques chez l’homme

The vast majority of our daily activities (reading a book, driving a car, appreciating a work of art) are guided by active vision, that is, the dynamic and constant interaction between our visual system -which allows us to acquire the representation of the scene around us- and our oculomotor system - which allows us to move our gaze briefly and quickly ('ocular saccade') from one object to another within this scene-. The interaction between these two systems is eminently remarkable. Indeed, despite these ballistic movements of the eyes, we systematically achieve to: (1) direct our gaze precisely on the stimulus of interest and (2) maintain a stable visual representation of the world despite the execution of the saccade (which could generate a blurred or unstable image due to its high speed). These abilities are possible thanks to two processes: (1) a mechanism of sensorimotor plasticity called saccadic adaptation which ensures the permanent control of our eye movements and (2) a predictive system which allows to anticipate the post-saccadic visual image. The objective of this thesis was to better understand how the predictions of our oculomotor actions structure - at least in part - our visual perception through three studies. The first was conducted in a patient with an injury to the posterior parietal cortex. This study enabled us to validate two hypotheses: (1) an eye movement prediction signal is necessary - under certain conditions - to precisely locate a visual target after a saccade and (2) the posterior parietal cortex plays a key role in its integration. Studies 2 and 3 were conducted in a group of healthy volunteers and cerebellar patients, respectively. The aim of these experiments was to understand how a phase of oculomotor plasticity (inducing a systematic discrepancy between the predicted and real image of the post-saccadic visual scene - which necessarily had to be corrected by the adaptation mechanism -) alters our ability to precisely locate an object in space. The results showed that the oculomotor correction of this discrepancy was effective in healthy subjects and led to a perceptual localization bias. In contrast, the lesion of the cerebellum hampered the ability of these patients to correct this discrepancy, which allowed them to maintain precise localization judgments. Finally, two patients showed a dissociation between their adaptive capacity and their spatial localization performance. Taken together, these data suggest that (1) the cerebellum plays a key role both in motor functions and in transmitting predictive signals to the cerebral cortex for visuospatial perception and (2) these two ‘cerebellar’ functions are underpinned by distinct territories. Beyond the fundamental aspect of these studies, the experimental tasks that we used could be useful as biomarkers to identify an early impairment of this predictive coding ; a deficit which has been commonly documented in a psychiatric context, especially in the case of schizophrenia.Une très grande majorité de nos activités quotidiennes (lire un livre, conduire une voiture, apprécier une œuvre d’art) sont guidées par la vision active, c’est-à-dire l’interaction dynamique et constante entre notre système visuel, qui nous permet d’acquérir la représentation de la scène qui nous entoure et notre système oculomoteur, qui nous permet de déplacer notre regard de façon brève et rapide (‘saccades oculaires’) d’un objet à un autre au sein de cette scène. L’interaction entre ces deux systèmes est éminemment remarquable puisque malgré ces déplacements balistiques de l’œil, nous arrivons systématiquement à : (1) diriger notre regard de façon précise sur le stimulus d’intérêt en dépit de perturbations physiologiques ou pathologiques et (2) à maintenir une représentation visuelle stable de l’environnement malgré l’exécution de la saccade qui pourrait générer une image floutée ou instable en raison de sa haute vitesse. Ceci est respectivement permis par deux processus : (1) un mécanisme de plasticité sensori-motrice appelé adaptation saccadique qui assure le contrôle permanent de nos mouvements oculaires et (2) un système prédictif qui permet d’anticiper l’image visuelle post-saccadique. L’objectif de cette thèse était de mieux comprendre comment les prédictions de nos actions oculomotrices structurent -du moins en partie- notre perception visuelle par trois études. La première a été menée auprès d’un patient présentant une lésion du cortex pariétal postérieur. Elle a permis de valider deux hypothèses : (1) un signal de prédiction du mouvement oculaire est -sous certaines conditions- nécessaire pour localiser de façon précise une cible visuelle après une saccade et (2) le cortex pariétal postérieur joue un rôle clé dans son intégration. Les études 2 et 3 ont été menées respectivement auprès d’un groupe de volontaires sains et de patients cérébelleux. Elles visaient à comprendre comment une phase de plasticité oculomotrice (induisant une discordance systématique entre l’image prédite et réelle de la scène visuelle post-saccadique -qui devait nécessairement être corrigée par le mécanisme d’adaptation-) altérait notre capacité à localiser précisément un objet dans l’espace. Les résultats obtenus ont montré que la correction oculomotrice de cette discordance était effective chez le sujet sain et entraînait en contrepartie un biais perceptif de localisation. En revanche, la lésion du cervelet entravait la capacité de ces patients à corriger cette discordance, ce qui leur permettait de maintenir des jugements de localisation précis. Enfin, deux patients présentaient une dissociation entre capacité d’adaptation et performances de localisation spatiale. Dans l’ensemble, ces données suggèrent que le cervelet joue un rôle clé à la fois dans les fonctions motrices mais aussi dans la transmission de signaux prédictifs au cortex cérébral pour la perception visuo-spatiale et que ces deux fonctions sont sous-tendues par des territoires cérébelleux distincts. Au-delà de l’aspect fondamental, les tâches expérimentales que nous avons utilisées dans ces études pourraient s’avérer utiles en tant que biomarqueurs afin d’identifier une atteinte précoce de ce codage prédictif, ce qui a été couramment documenté en contexte psychiatrique, notamment dans le cas de schizophrénie

Coupling between saccadic adaptation and visuo-spatial perception : neurophysiological studies in human

Une très grande majorité de nos activités quotidiennes (lire un livre, conduire une voiture, apprécier une œuvre d’art) sont guidées par la vision active, c’est-à-dire l’interaction dynamique et constante entre notre système visuel, qui nous permet d’acquérir la représentation de la scène qui nous entoure et notre système oculomoteur, qui nous permet de déplacer notre regard de façon brève et rapide (‘saccades oculaires’) d’un objet à un autre au sein de cette scène. L’interaction entre ces deux systèmes est éminemment remarquable puisque malgré ces déplacements balistiques de l’œil, nous arrivons systématiquement à : (1) diriger notre regard de façon précise sur le stimulus d’intérêt en dépit de perturbations physiologiques ou pathologiques et (2) à maintenir une représentation visuelle stable de l’environnement malgré l’exécution de la saccade qui pourrait générer une image floutée ou instable en raison de sa haute vitesse. Ceci est respectivement permis par deux processus : (1) un mécanisme de plasticité sensori-motrice appelé adaptation saccadique qui assure le contrôle permanent de nos mouvements oculaires et (2) un système prédictif qui permet d’anticiper l’image visuelle post-saccadique. L’objectif de cette thèse était de mieux comprendre comment les prédictions de nos actions oculomotrices structurent -du moins en partie- notre perception visuelle par trois études. La première a été menée auprès d’un patient présentant une lésion du cortex pariétal postérieur. Elle a permis de valider deux hypothèses : (1) un signal de prédiction du mouvement oculaire est -sous certaines conditions- nécessaire pour localiser de façon précise une cible visuelle après une saccade et (2) le cortex pariétal postérieur joue un rôle clé dans son intégration. Les études 2 et 3 ont été menées respectivement auprès d’un groupe de volontaires sains et de patients cérébelleux. Elles visaient à comprendre comment une phase de plasticité oculomotrice (induisant une discordance systématique entre l’image prédite et réelle de la scène visuelle post-saccadique -qui devait nécessairement être corrigée par le mécanisme d’adaptation-) altérait notre capacité à localiser précisément un objet dans l’espace. Les résultats obtenus ont montré que la correction oculomotrice de cette discordance était effective chez le sujet sain et entraînait en contrepartie un biais perceptif de localisation. En revanche, la lésion du cervelet entravait la capacité de ces patients à corriger cette discordance, ce qui leur permettait de maintenir des jugements de localisation précis. Enfin, deux patients présentaient une dissociation entre capacité d’adaptation et performances de localisation spatiale. Dans l’ensemble, ces données suggèrent que le cervelet joue un rôle clé à la fois dans les fonctions motrices mais aussi dans la transmission de signaux prédictifs au cortex cérébral pour la perception visuo-spatiale et que ces deux fonctions sont sous-tendues par des territoires cérébelleux distincts. Au-delà de l’aspect fondamental, les tâches expérimentales que nous avons utilisées dans ces études pourraient s’avérer utiles en tant que biomarqueurs afin d’identifier une atteinte précoce de ce codage prédictif, ce qui a été couramment documenté en contexte psychiatrique, notamment dans le cas de schizophrénie.The vast majority of our daily activities (reading a book, driving a car, appreciating a work of art) are guided by active vision, that is, the dynamic and constant interaction between our visual system -which allows us to acquire the representation of the scene around us- and our oculomotor system - which allows us to move our gaze briefly and quickly ('ocular saccade') from one object to another within this scene-. The interaction between these two systems is eminently remarkable. Indeed, despite these ballistic movements of the eyes, we systematically achieve to: (1) direct our gaze precisely on the stimulus of interest and (2) maintain a stable visual representation of the world despite the execution of the saccade (which could generate a blurred or unstable image due to its high speed). These abilities are possible thanks to two processes: (1) a mechanism of sensorimotor plasticity called saccadic adaptation which ensures the permanent control of our eye movements and (2) a predictive system which allows to anticipate the post-saccadic visual image. The objective of this thesis was to better understand how the predictions of our oculomotor actions structure - at least in part - our visual perception through three studies. The first was conducted in a patient with an injury to the posterior parietal cortex. This study enabled us to validate two hypotheses: (1) an eye movement prediction signal is necessary - under certain conditions - to precisely locate a visual target after a saccade and (2) the posterior parietal cortex plays a key role in its integration. Studies 2 and 3 were conducted in a group of healthy volunteers and cerebellar patients, respectively. The aim of these experiments was to understand how a phase of oculomotor plasticity (inducing a systematic discrepancy between the predicted and real image of the post-saccadic visual scene - which necessarily had to be corrected by the adaptation mechanism -) alters our ability to precisely locate an object in space. The results showed that the oculomotor correction of this discrepancy was effective in healthy subjects and led to a perceptual localization bias. In contrast, the lesion of the cerebellum hampered the ability of these patients to correct this discrepancy, which allowed them to maintain precise localization judgments. Finally, two patients showed a dissociation between their adaptive capacity and their spatial localization performance. Taken together, these data suggest that (1) the cerebellum plays a key role both in motor functions and in transmitting predictive signals to the cerebral cortex for visuospatial perception and (2) these two ‘cerebellar’ functions are underpinned by distinct territories. Beyond the fundamental aspect of these studies, the experimental tasks that we used could be useful as biomarkers to identify an early impairment of this predictive coding ; a deficit which has been commonly documented in a psychiatric context, especially in the case of schizophrenia

The posterior parietal cortex processes visuo-spatial and extra-retinal information for saccadic remapping: A case study

International audienc

A triple distinction of cerebellar function for oculomotor learning and fatigue compensation.

The cerebellum implements error-based motor learning via synaptic gain adaptation of an inverse model, i.e. the mapping of a spatial movement goal onto a motor command. Recently, we modeled the motor and perceptual changes during learning of saccadic eye movements, showing that learning is actually a threefold process. Besides motor recalibration of (1) the inverse model, learning also comprises perceptual recalibration of (2) the visuospatial target map and (3) of a forward dynamics model that estimates the saccade size from corollary discharge. Yet, the site of perceptual recalibration remains unclear. Here we dissociate cerebellar contributions to the three stages of learning by modeling the learning data of eight cerebellar patients and eight healthy controls. Results showed that cerebellar pathology restrains short-term recalibration of the inverse model while the forward dynamics model is well informed about the reduced saccade change. Adaptation of the visuospatial target map trended in learning direction only in control subjects, yet without reaching significance. Moreover, some patients showed a tendency for uncompensated oculomotor fatigue caused by insufficient upregulation of saccade duration. According to our model, this could induce long-term perceptual compensation, consistent with the overestimation of target eccentricity found in the patients' baseline data. We conclude that the cerebellum mediates short-term adaptation of the inverse model, especially by control of saccade duration, while the forward dynamics model was not affected by cerebellar pathology

Neural substrates of saccadic adaptation: plastic changes versus error processing and forward versus backward learning

International audiencePrevious behavioral, clinical, and neuroimaging studies suggest that the neural substrates of adaptation of saccadic eye movements involve, beyond the central role of the cerebellum, several, still incompletely determined, cortical areas. Furthermore, no neuroimaging study has yet tackled the differences between saccade lengthening (“forward adaptation”) and shortening (“backward adaptation”) and neither between their two main components, i.e. error processing and oculomotor changes.The present fMRI study was designed to fill these gaps. Blood-oxygen-level-dependent (BOLD) signal and eye movements of 24 healthy volunteers were acquired while performing reactive saccades under 4 conditions repeated in short blocks of 16 trials: systematic target jump during the saccade and in the saccade direction (forward: FW) or in the opposite direction (backward: BW), randomly directed FW or BW target jump during the saccade (random: RND) and no intra-saccadic target jump (stationary: STA). BOLD signals were analyzed both through general linear model (GLM) approaches applied at the whole-brain level and through sensitive Multi-Variate Pattern Analyses (MVPA) applied to 34 regions of interest (ROIs) identified from independent 'Saccade Localizer’ functional data. Oculomotor data were consistent with successful induction of forward and backward adaptation in FW and BW blocks, respectively. The different analyses of voxel activation patterns (MVPAs) disclosed the involvement of 1) a set of ROIs specifically related to adaptation in the right occipital cortex, right and left MT/MST, right FEF and right pallidum; 2) several ROIs specifically involved in error signal processing in the left occipital cortex, left PEF, left precuneus, Medial Cingulate cortex (MCC), left inferior and right superior cerebellum; 3) ROIs specific to the direction of adaptation in the occipital cortex and MT/MST (left and right hemispheres for FW and BW, respectively) and in the pallidum of the right hemisphere (FW). The involvement of the left PEF and of the (left and right) occipital cortex were further supported and qualified by the whole brain GLM analysis: clusters of increased activity were found in PEF for the RND versus STA contrast (related to error processing) and in the left (right) occipital cortex for the FW (BW) versus STA contrasts [related to the FW (BW) direction of error and/or adaptation].The present study both adds complementary data to the growing literature supporting a role of the cerebral cortex in saccadic adaptation through feedback and feedforward relationships with the cerebellum and provides the basis for improving conceptual frameworks of oculomotor plasticity and of its link with spatial cognition

Neural substrates of saccadic adaptation: plastic changes versus error processing and forward versus backward learning

International audiencePrevious behavioral, clinical, and neuroimaging studies suggest that the neural substrates of adaptation of saccadic eye movements involve, beyond the central role of the cerebellum, several, still incompletely determined, cortical areas. Furthermore, no neuroimaging study has yet tackled the differences between saccade lengthening (“forward adaptation”) and shortening (“backward adaptation”) and neither between their two main components, i.e. error processing and oculomotor changes.The present fMRI study was designed to fill these gaps. Blood-oxygen-level-dependent (BOLD) signal and eye movements of 24 healthy volunteers were acquired while performing reactive saccades under 4 conditions repeated in short blocks of 16 trials: systematic target jump during the saccade and in the saccade direction (forward: FW) or in the opposite direction (backward: BW), randomly directed FW or BW target jump during the saccade (random: RND) and no intra-saccadic target jump (stationary: STA). BOLD signals were analyzed both through general linear model (GLM) approaches applied at the whole-brain level and through sensitive Multi-Variate Pattern Analyses (MVPA) applied to 34 regions of interest (ROIs) identified from independent 'Saccade Localizer’ functional data. Oculomotor data were consistent with successful induction of forward and backward adaptation in FW and BW blocks, respectively. The different analyses of voxel activation patterns (MVPAs) disclosed the involvement of 1) a set of ROIs specifically related to adaptation in the right occipital cortex, right and left MT/MST, right FEF and right pallidum; 2) several ROIs specifically involved in error signal processing in the left occipital cortex, left PEF, left precuneus, Medial Cingulate cortex (MCC), left inferior and right superior cerebellum; 3) ROIs specific to the direction of adaptation in the occipital cortex and MT/MST (left and right hemispheres for FW and BW, respectively) and in the pallidum of the right hemisphere (FW). The involvement of the left PEF and of the (left and right) occipital cortex were further supported and qualified by the whole brain GLM analysis: clusters of increased activity were found in PEF for the RND versus STA contrast (related to error processing) and in the left (right) occipital cortex for the FW (BW) versus STA contrasts [related to the FW (BW) direction of error and/or adaptation].The present study both adds complementary data to the growing literature supporting a role of the cerebral cortex in saccadic adaptation through feedback and feedforward relationships with the cerebellum and provides the basis for improving conceptual frameworks of oculomotor plasticity and of its link with spatial cognition

Neural substrates of saccadic adaptation: plastic changes versus error processing and forward versus backward learning

International audiencePrevious behavioral, clinical, and neuroimaging studies suggest that the neural substrates of adaptation of saccadic eye movements involve, beyond the central role of the cerebellum, several, still incompletely determined, cortical areas. Furthermore, no neuroimaging study has yet tackled the differences between saccade lengthening (“forward adaptation”) and shortening (“backward adaptation”) and neither between their two main components, i.e. error processing and oculomotor changes.The present fMRI study was designed to fill these gaps. Blood-oxygen-level-dependent (BOLD) signal and eye movements of 24 healthy volunteers were acquired while performing reactive saccades under 4 conditions repeated in short blocks of 16 trials: systematic target jump during the saccade and in the saccade direction (forward: FW) or in the opposite direction (backward: BW), randomly directed FW or BW target jump during the saccade (random: RND) and no intra-saccadic target jump (stationary: STA). BOLD signals were analyzed both through general linear model (GLM) approaches applied at the whole-brain level and through sensitive Multi-Variate Pattern Analyses (MVPA) applied to 34 regions of interest (ROIs) identified from independent 'Saccade Localizer’ functional data. Oculomotor data were consistent with successful induction of forward and backward adaptation in FW and BW blocks, respectively. The different analyses of voxel activation patterns (MVPAs) disclosed the involvement of 1) a set of ROIs specifically related to adaptation in the right occipital cortex, right and left MT/MST, right FEF and right pallidum; 2) several ROIs specifically involved in error signal processing in the left occipital cortex, left PEF, left precuneus, Medial Cingulate cortex (MCC), left inferior and right superior cerebellum; 3) ROIs specific to the direction of adaptation in the occipital cortex and MT/MST (left and right hemispheres for FW and BW, respectively) and in the pallidum of the right hemisphere (FW). The involvement of the left PEF and of the (left and right) occipital cortex were further supported and qualified by the whole brain GLM analysis: clusters of increased activity were found in PEF for the RND versus STA contrast (related to error processing) and in the left (right) occipital cortex for the FW (BW) versus STA contrasts [related to the FW (BW) direction of error and/or adaptation].The present study both adds complementary data to the growing literature supporting a role of the cerebral cortex in saccadic adaptation through feedback and feedforward relationships with the cerebellum and provides the basis for improving conceptual frameworks of oculomotor plasticity and of its link with spatial cognition