Prism Adaptation (PA) is a behavioral task to assess visuo-motor plasticity and to ameliorate the symptoms of unilateral spatial neglect. Several studies have addressed the effects of PA on both ...sensory-motor and cognitive processing and the contribution of different brain regions to PA, although via non standardized procedures. The aim of the present review is to gather findings from the neuro-imaging and neuro-stimulation fields and put forward an interpretative framework for PA. The available evidence supports that sensory-motor effects of PA would mainly relate to the activation of a cerebello-parietal network, while the effects on spatial cognition would be mediated by bottom-up activation of temporal and prefrontal regions. The consolidation of PA effects would rely on activity of the motor cortex. The use of standardized PA procedures is strongly recommended for a systematic and accurate investigation of the neural mechanisms of PA.
Prism Adaptation in M1 Panico, Francesco; Fleury, Lisa; Trojano, Luigi ...
Journal of cognitive neuroscience,
04/2021, Volume:
33, Issue:
4
Journal Article
Peer reviewed
During prism adaptation (PA), active exposure to an optical shift results in sustained modifications of the sensorimotor system, which have been shown to expand to the cognitive level and serve as a ...rehabilitation technique for spatial cognition disorders. Several models based on evidence from clinical and neuroimaging studies offered a description of the cognitive and the neural correlates of PA. However, recent findings using noninvasive neurostimulation call for a reexamination of the role of the primary motor cortex (M1) in PA. Specifically, recent studies demonstrated that M1 stimulation reactivates previously vanished sensorimotor changes 1 day after PA, induces after-effect strengthening, and boosts therapeutic effects up to the point of reversing treatment-resistant unilateral neglect. Here, we articulate findings from clinical, neuroimaging, and noninvasive brain stimulation studies to show that M1 contributes to acquiring and storing PA, by means of persisting latent changes after the behavioral training is terminated, consistent with studies on other sensorimotor adaptation procedures. Moreover, we describe the hierarchical organization as well as the timing of PA mechanisms and their anatomical correlates, and identify M1 as an anatomo-functional interface between low- and high-order PA-related mechanisms.
We investigated the contributions of the cerebellum and the motor cortex (M1) to acquisition and retention of human motor memories in a force field reaching task. We found that anodal transcranial ...direct current stimulation (tDCS) of the cerebellum, a technique that is thought to increase neuronal excitability, increased the ability to learn from error and form an internal model of the field, while cathodal cerebellar stimulation reduced this error-dependent learning. In addition, cathodal cerebellar stimulation disrupted the ability to respond to error within a reaching movement, reducing the gain of the sensory-motor feedback loop. By contrast, anodal M1 stimulation had no significant effects on these variables. During sham stimulation, early in training the acquired motor memory exhibited rapid decay in error-clamp trials. With further training the rate of decay decreased, suggesting that with training the motor memory was transformed from a labile to a more stable state. Surprisingly, neither cerebellar nor M1 stimulation altered these decay patterns. Participants returned 24hours later and were re-tested in error-clamp trials without stimulation. The cerebellar group that had learned the task with cathodal stimulation exhibited significantly impaired retention, and retention was not improved by M1 anodal stimulation. In summary, non-invasive cerebellar stimulation resulted in polarity-dependent up- or down-regulation of error-dependent motor learning. In addition, cathodal cerebellar stimulation during acquisition impaired the ability to retain the motor memory overnight. Thus, in the force field task we found a critical role for the cerebellum in both formation of motor memory and its retention.
•We applied tDCS to the brain during force field learning.•Anodal stimulation of the cerebellum increased learning from error.•Cathodal cerebellar stimulation impaired learning from error and feedback control.•Cathodal cerebellar stimulation during acquisition impaired subsequent overnight retention.•Anodal motor cortex stimulation had no effect on learning from error and retention.
The sensorimotor system sets up plastic alterations to face new demands. Terms such as adaptation and learning are broadly used to describe a variety of processes underlying this aptitude. The ...mechanisms whereby transformations acquired to face a perturbation generalize to other situations or stay context-dependent remain weakly understood. Here, we compared the performance of hand pointing vs throwing to visual targets while facing an optical shift of the visual field (prismatic deviation). We found that the transfer of compensations was conditioned by the task performed during exposure to the perturbation: compensations transferred from pointing to throwing but not at all from throwing to pointing. Additionally, expertise on the task performed during exposure had a marked influence on the amount of transfer to the non-exposed task: throwing experts (dart players) remarkably transferred compensations to the pointing task. Our results reveal that different processes underlying these distinct transfer properties may be at work to face a given perturbation. Their solicitation depends on mastery for the exposed task, which is responsible for different patterns of inter-task transfer. An important implication is that transfer properties, and not only after-effects, should be included as a criterion for adaptation. At the theoretical level, we suggest that tasks may need to be mastered before they can be subjected to adaptation, which has new implications for the distinction between learning and adaptation.
Right brain injury causes visual neglect - lost awareness of left space. During prism adaptation therapy, patients adapt to a rightward optical shift by recalibrating right arm movements leftward. ...This can improve left neglect, but the benefit of a single session is transient (~1 day). Here we show that tonic disinhibition of left motor cortex during prism adaptation enhances consolidation, stabilizing both sensorimotor and cognitive prism after-effects. In three longitudinal patient case series, just 20 min of combined stimulation/adaptation caused persistent cognitive after-effects (neglect improvement) that lasted throughout follow-up (18-46 days). Moreover, adaptation without stimulation was ineffective. Thus stimulation reversed treatment resistance in chronic visual neglect. These findings challenge consensus that because the left hemisphere in neglect is pathologically over-excited it ought to be suppressed. Excitation of left sensorimotor circuits, during an adaptive cognitive state, can unmask latent plastic potential that durably improves resistant visual attention deficits after brain injury.
Data and theory from prism adaptation are reviewed for the purpose of identifying control methods in applications of the procedure. Prism exposure evokes three kinds of adaptive or compensatory ...processes: postural adjustments (visual capture and muscle potentiation), strategic control (including recalibration of target position), and spatial realignment of various sensory-motor reference frames. Muscle potentiation, recalibration, and realignment can all produce prism exposure aftereffects and can all contribute to adaptive performance during prism exposure. Control over these adaptive responses can be achieved by manipulating the locus of asymmetric exercise during exposure (muscle potentiation), the similarity between exposure and post-exposure tasks (calibration), and the timing of visual feedback availability during exposure (realignment).
Following the princeps investigations of Marc Jeannerod on action–perception, specifically, goal-directed movement, this review article addresses visual and non-visual processes involved in guiding ...the hand in reaching or grasping tasks. The contributions of different sources of correction of ongoing movements are considered; these include visual feedback of the hand, as well as the often-neglected but important spatial updating and sharpening of goal localization following gaze-saccade orientation. The existence of an automatic online process guiding limb trajectory toward its goal is highlighted by a series of princeps experiments of goal-directed pointing movements. We then review psychophysical, electrophysiological, neuroimaging and clinical studies that have explored the properties of these automatic corrective mechanisms and their neural bases, and established their generality. Finally, the functional significance of automatic corrective mechanisms–referred to as motor flexibility–and their potential use in rehabilitation are discussed.
•Fast online corrections of an ongoing movement occur even without feedback.•Non-awareness of perturbation is not a pre-requisite for automatic corrections.•The automatic correction process generalizes from reach to grasp.•Clinical, TMS, and neuroimaging approaches argue for some underlying substrates.
Prism adaptation does not only induce short-term sensorimotor plasticity, but also longer-term reorganization in the neural representation of space. We used event-related fMRI to study dynamic ...changes in brain activity during both early and prolonged exposure to visual prisms. Participants performed a pointing task before, during, and after prism exposure. Measures of trial-by-trial pointing errors and corrections allowed parametric analyses of brain activity as a function of performance. We show that during the earliest phase of prism exposure, anterior intraparietal sulcus was primarily implicated in error detection, whereas parieto-occipital sulcus was implicated in error correction. Cerebellum activity showed progressive increases during prism exposure, in accordance with a key role for spatial realignment. This time course further suggests that the cerebellum might promote neural changes in superior temporal cortex, which was selectively activated during the later phase of prism exposure and could mediate the effects of prism adaptation on cognitive spatial representations.
Three timescales in prism adaptation Inoue, Masato; Uchimura, Motoaki; Karibe, Ayaka ...
Journal of neurophysiology,
2015-Jan-01, Volume:
113, Issue:
1
Journal Article
Peer reviewed
It has been proposed that motor adaptation depends on at least two learning systems, one that learns fast but with poor retention and another that learns slowly but with better retention (Smith MA, ...Ghazizadeh A, Shadmehr R. PLoS Biol 4: e179, 2006). This two-state model has been shown to account for a range of behavior in the force field adaptation task. In the present study, we examined whether such a two-state model could also account for behavior arising from adaptation to a prismatic displacement of the visual field. We first confirmed that an "adaptation rebound," a critical prediction of the two-state model, occurred when visual feedback was deprived after an adaptation-extinction episode. We then examined the speed of decay of the prism aftereffect (without any visual feedback) after repetitions of 30, 150, and 500 trials of prism exposure. The speed of decay decreased with the number of exposure trials, a phenomenon that was best explained by assuming an "ultraslow" system, in addition to the fast and slow systems. Finally, we compared retention of aftereffects 24 h after 150 or 500 trials of exposure: retention was significantly greater after 500 than 150 trials. This difference in retention could not be explained by the two-state model but was well explained by the three-state model as arising from the difference in the amount of adaptation of the "ultraslow process." These results suggest that there are not only fast and slow systems but also an ultraslow learning system in prism adaptation that is activated by prolonged prism exposure of 150-500 trials.
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