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.

Prism adaptation in M1

Panico F.;Trojano L.;
2020

Abstract

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.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11591/448244
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