Improving Human Plateaued Motor Skill with Somatic Stimulation

Procedural motor learning includes a period when no substantial gain in performance improvement is obtained even with repeated, daily practice. Prompted by the potential benefit of high-frequency transcutaneous electrical stimulation, we examined if the stimulation to the hand reduces redundant motor activity that likely exists in an acquired hand motor skill, so as to further upgrade stable motor performance. Healthy participants were trained until their motor performance of continuously rotating two balls in the palm of their right hand became stable. In the series of experiments, they repeated a trial performing this cyclic rotation as many times as possible in 15 s. In trials where we applied the stimulation to the relaxed thumb before they initiated the task, most reported that their movements became smoother and they could perform the movements at a higher cycle compared to the control trials. This was not possible when the dorsal side of the wrist was stimulated. The performance improvement was associated with reduction of amplitude of finger displacement, which was consistently observed irrespective of the task demands. Importantly, this kinematic change occurred without being noticed by the participants, and their intentional changes of motor strategies (reducing amplitude of finger displacement) never improved the performance. Moreover, the performance never spontaneously improved during one-week training without stimulation, whereas the improvement in association with stimulation was consistently observed across days during training on another week combined with the stimulation. The improved effect obtained in stimulation trials on one day partially carried over to the next day, thereby promoting daily improvement of plateaued performance, which could not be unlocked by the first-week intensive training. This study demonstrated the possibility of effectively improving a plateaued motor skill, and pre-movement somatic stimulation driving this behavioral change

The cerebro-cerebellum: Could it be loci of forward models?

AbstractIt is widely accepted that the cerebellum acquires and maintain internal models for motor control. An internal model simulates mapping between a set of causes and effects. There are two candidates of cerebellar internal models, forward models and inverse models. A forward model transforms a motor command into a prediction of the sensory consequences of a movement. In contrast, an inverse model inverts the information flow of the forward model. Despite the clearly different formulations of the two internal models, it is still controversial whether the cerebro-cerebellum, the phylogenetically newer part of the cerebellum, provides inverse models or forward models for voluntary limb movements or other higher brain functions. In this article, we review physiological and morphological evidence that suggests the existence in the cerebro-cerebellum of a forward model for limb movement. We will also discuss how the characteristic input–output organization of the cerebro-cerebellum may contribute to forward models for non-motor higher brain functions

Releasing dentate nucleus cells from Purkinje cell inhibition generates output from the cerebrocerebellum.

The cerebellum generates its vast amount of output to the cerebral cortex through the dentate nucleus (DN) that is essential for precise limb movements in primates. Nuclear cells in DN generate burst activity prior to limb movement, and inactivation of DN results in cerebellar ataxia. The question is how DN cells become active under intensive inhibitory drive from Purkinje cells (PCs). There are two excitatory inputs to DN, mossy fiber and climbing fiber collaterals, but neither of them appears to have sufficient strength for generation of burst activity in DN. Therefore, we can assume two possible mechanisms: post-inhibitory rebound excitation and disinhibition. If rebound excitation works, phasic excitation of PCs and a concomitant inhibition of DN cells should precede the excitation of DN cells. On the other hand, if disinhibition plays a primary role, phasic suppression of PCs and activation of DN cells should be observed at the same timing. To examine these two hypotheses, we compared the activity patterns of PCs in the cerebrocerebellum and DN cells during step-tracking wrist movements in three Japanese monkeys. As a result, we found that the majority of wrist-movement-related PCs were suppressed prior to movement onset and the majority of wrist-movement-related DN cells showed concurrent burst activity without prior suppression. In a minority of PCs and DN cells, movement-related increases and decreases in activity, respectively, developed later. These activity patterns suggest that the initial burst activity in DN cells is generated by reduced inhibition from PCs, i.e., by disinhibition. Our results indicate that suppression of PCs, which has been considered secondary to facilitation, plays the primary role in generating outputs from DN. Our findings provide a new perspective on the mechanisms used by PCs to influence limb motor control and on the plastic changes that underlie motor learning in the cerebrocerebellum

Characteristics of the SR-evoked potentials in area 3a.

<p>(A) Percent responses evoked by DR and SR stimulations in area 3a. (B) Percent responses evoked by DR and SR stimulations in area 3b/1. (C) Amplitude of the DR- and SR-evoked potentials in area 3a. (D) Latency of the DR- and SR-evoked potentials in area 3a. Error bars in A–D indicated S.E. Asterisk in A–D indicates statistical significance at <i>P</i> < 0.05 using two-sample <i>t</i>-test.</p

Schematic drawing of experimental setting and surface map of the recording sites.

<p>(A) Stimulation of deep radial (DR) and superficial radial (SR) nerves. Three nerve cuffs were implanted: one on the radial nerve trunk (R) at the left forearm, one on the DR, representing primarily muscle afferent input, and one on the SR, representing primarily input from the skin. The DR and SR cuffs were used for electrical stimulation, and the R cuff was used for recording incoming volleys. The nerves were stimulated with biphasic constant-current pulses, 100 μs/phase, at twice the threshold (2T). The electrical stimulation-evoked field potential was recorded from the forearm region at the posterior bank of the CS of the right hemisphere. (B) Cortical surface map of the recording sites in each monkey. The electrode was inserted 8–15 mm at the anterior–posterior level. Gray lines indicate the approximate location of the CS on the cortical surface. Recording sites of the SR- or DR-evoked potentials are indicated by filled circles. Open circles indicate electrode insertions in which intracortical microstimulations were applied and no SEPs were recorded. Body parts activated at the lowest current of the microstimulation are indicated by capital letters. Values indicate the lowest microstimulation current (μA) evoking the movement. “n” indicates no effect up to 200 μA. A: anterior, P: posterior, M: medial, L: lateral.</p

Examples of DR- and SR-evoked potential distribution in area 3a.

<p>(A) Amplitude plots of the DR-evoked potentials at the anterior-posterior 10-mm level in monkey SO where the largest DR-evoked potential was observed in this animal. The circle size indicates the amplitude. A bar indicates no significant activation. (B) Latency plots of the DR-evoked potential indicated by colors. (C, D) same as (A, B), but for the SR-evoked potentials. (E–H) Same as A-D but for monkey TA. The data in A11 were from where the largest DR-evoked potential was observed in this monkey. The scale bar indicates 5 mm, separated by black and gray every 1 mm.</p