Erratum: Does anodal cerebellar tDCS boost transfer of after-effects from throwing to pointing during prism adaptation?

[This corrects the article DOI: 10.3389/fpsyg.2022.909565.].

Does anodal cerebellar tDCS boost transfer of after-effects from throwing to pointing during prism adaptation?

Prism Adaptation (PA) is a useful method to study the mechanisms of sensorimotor adaptation. After-effects following adaptation to the prismatic deviation constitute the probe that adaptive mechanisms occurred, and current evidence suggests an involvement of the cerebellum at this level. Whether after-effects are transferable to another task is of great interest both for understanding the nature of sensorimotor transformations and for clinical purposes. However, the processes of transfer and their underlying neural substrates remain poorly understood. Transfer from throwing to pointing is known to occur only in individuals who had previously reached a good level of expertise in throwing (e.g., dart players), not in novices. The aim of this study was to ascertain whether anodal stimulation of the cerebellum could boost after-effects transfer from throwing to pointing in novice participants. Healthy participants received anodal or sham transcranial direction current stimulation (tDCS) of the right cerebellum during a PA procedure involving a throwing task and were tested for transfer on a pointing task. Terminal errors and kinematic parameters were in the dependent variables for statistical analyses. Results showed that active stimulation had no significant beneficial effects on error reduction or throwing after-effects. Moreover, the overall magnitude of transfer to pointing did not change. Interestingly, we found a significant effect of the stimulation on the longitudinal evolution of pointing errors and on pointing kinematic parameters during transfer assessment. These results provide new insights on the implication of the cerebellum in transfer and on the possibility to use anodal tDCS to enhance cerebellar contribution during PA in further investigations. From a network approach, we suggest that cerebellum is part of a more complex circuitry responsible for the development of transfer which is likely embracing the primary motor cortex due to its role in motor memories consolidation. This paves the way for further work entailing multiple-sites stimulation to explore the role of M1-cerebellum dynamic interplay in transfer.

Visual Feedback Modulates Aftereffects and Electrophysiological Markers of Prism Adaptation.

Prism adaptation (PA) is both a model for visuomotor learning and a promising treatment for visuospatial neglect after stroke. The task involves reaching for targets while prism glasses horizontally displace the visual field. Adaptation is hypothesized to occur through two processes: strategic recalibration, a rapid self-correction of pointing errors; and spatial realignment, a more gradual adjustment of visuomotor reference frames that produce prism aftereffects (i.e., reaching errors upon glasses removal in the direction opposite to the visual shift). While aftereffects can ameliorate neglect, not all patients respond to PA, and the neural mechanisms underlying successful adaptation are unclear. We investigated the feedback-related negativity (FRN) and the P300 event-related potential (ERP) components as candidate markers of strategic recalibration and spatial realignment, respectively. Healthy young adults wore prism glasses and performed memory-guided reaching toward vertical-line targets. ERPs were recorded in response to three different between-subject error feedback conditions at screen-touch: view of hand and target (Experiment 1), view of hand only (Experiment 2), or view of lines to mark target and hand position (view of hand occluded; Experiment 3). Conditions involving a direct view of the hand-produced stronger aftereffects than indirect hand feedback, and also evoked a P300 that decreased in amplitude as adaptation proceeded. Conversely, the FRN was only seen in conditions involving target feedback, even when aftereffects were smaller. Since conditions producing stronger aftereffects were associated with a phase-sensitive P300, this component may index a "context-updating" realignment process critical for strong aftereffects, whereas the FRN may reflect an error monitoring process related to strategic recalibration.

Prism Adaptation Alters Electrophysiological Markers of Attentional Processes in the Healthy Brain.

Neglect patients typically show a rightward attentional orienting bias and a strong disengagement deficit, such that they are especially slow in responding to left-sided targets after right-sided cues (Posner et al., 1984). Prism adaptation (PA) can reduce diverse debilitating neglect symptoms and it has been hypothesized that PA's effects are so generalized that they might be mediated by attentional mechanisms (Pisella et al., 2006; Redding and Wallace, 2006). In neglect patients, performance on spatial attention tasks improves after rightward-deviating PA (Jacquin-Courtois et al., 2013). In contrast, in healthy subjects, although there is evidence that leftward-deviating PA induces neglect-like performance on some visuospatial tasks, behavioral studies of spatial attention tasks have mostly yielded negative results (Morris et al., 2004; Bultitude et al., 2013). We hypothesized that these negative behavioral findings might reflect the limitations of behavioral measures in healthy subjects. Here we exploited the sensitivity of event-related potentials to test the hypothesis that electrophysiological markers of attentional processes in the healthy human brain are affected by PA. Leftward-deviating PA generated asymmetries in attentional orienting (reflected in the cue-locked N1) and in attentional disengagement for invalidly cued left targets (reflected in the target-locked P1). This is the first electrophysiological demonstration that leftward-deviating PA in healthy subjects mimics attentional patterns typically seen in neglect patients. Significance statement: Prism adaptation (PA) is a promising tool for ameliorating many deficits in neglect patients and inducing neglect-like behavior in healthy subjects. The mechanisms underlying PA's effects are poorly understood but one hypothesis suggests that it acts by modulating attention. To date, however, there has been no successful demonstration of attentional modulation in healthy subjects. We provide the first electrophysiological evidence that PA acts on attention in healthy subjects by mimicking the attentional pattern typically reported in neglect patients: both a rightward attentional orienting bias (reflected in the cue-locked N1) and a deficit in attentional disengagement from the right hemispace (reflected in the target-locked P1). This study makes an important contribution to refining current models of the mechanisms underlying PA's cognitive effects.