Neural dynamics of illusory tactile pulling sensations.

Directional tactile pulling sensations are integral to everyday life, but their neural mechanisms remain unknown. Prior accounts hold that primary somatosensory (SI) activity is sufficient to generate pulling sensations, with alternative proposals suggesting that amodal frontal or parietal regions may be critical. We combined high-density EEG with asymmetric vibration, which creates an illusory pulling sensation, thereby unconfounding pulling sensations from unrelated sensorimotor processes. Oddballs that created opposite direction pulls to common stimuli were compared to the same oddballs after neutral common stimuli (symmetric vibration) and to neutral oddballs. We found evidence against the sensory-frontal N140 and in favor of the midline P200 tracking the emergence of pulling sensations, specifically contralateral parietal lobe activity 264-320ms, centered on the intraparietal sulcus. This suggests that SI is not sufficient to generate pulling sensations, which instead depend on the parietal association cortex, and may reflect the extraction of orientation information and related spatial processing.

Evidence that endpoint feedback facilitates intermanual transfer of visuomotor force learning by a cognitive strategy.

Humans continuously adapt their movement to a novel environment by recalibrating their sensorimotor system. Recent evidence, however, shows that explicit planning to compensate for external changes, i.e., a cognitive strategy, can also aid performance. If such a strategy is planned in external space, it should improve performance in an effector-independent manner. We tested this hypothesis by examining whether promoting a cognitive strategy during a visual-force adaptation task performed in one hand can facilitate learning for the opposite hand. Participants rapidly adjusted the height of visual bar on screen to a target level by isometrically exerting force on a handle using their right hand. Visuomotor gain increased during the task and participants learned the increased gain. Visual feedback was continuously provided for one group, whereas for another group only the endpoint of the force trajectory was presented. The latter has been reported to promote cognitive strategy use. We found that endpoint feedback produced stronger intermanual transfer of learning and slower response times than continuous feedback. In a separate experiment, we found evidence that aftereffects are reduced when only endpoint feedback is provided, a finding that has been consistently observed when cognitive strategies are used. The results suggest that intermanual transfer can be facilitated by a cognitive strategy. This indicates that the behavioral observation of intermanual transfer can be achieved either by forming an effector-independent motor representation or by sharing an effector-independent cognitive strategy between the hands.NEW & NOTEWORTHY The causes and consequences of cognitive strategy use are poorly understood. We tested whether a visuomotor task learned in a manner that may promote cognitive strategy use causes greater generalization across effectors. Visual feedback was manipulated to promote cognitive strategy use. Learning consistent with cognitive strategy use for one hand transferred to the unlearned hand. Our result suggests that intermanual transfer can result from a common cognitive strategy used to control both hands.

On Stopping Voluntary Muscle Relaxations and Contractions: Evidence for Shared Control Mechanisms and Muscle State-Specific Active Breaking.

Control of the body requires inhibiting complex actions, involving contracting and relaxing muscles. However, little is known of how voluntary commands to relax a muscle are cancelled. Action inhibition causes both suppression of muscle activity and the transient excitation of antagonist muscles, the latter being termed active breaking. We hypothesized that active breaking is present when stopping muscle relaxations. Stop signal experiments were used to compare the mechanisms of active breaking for muscle relaxations and contractions in male and female human participants. In experiments 1 and 2, go signals were presented that required participants to contract or relax their biceps or triceps muscle. Infrequent Stop signals occurred after fixed delays (0-500 ms), requiring that participants cancelled go commands. In experiment 3, participants increased (contract) or decreased (relax) an existing isometric finger abduction depending on the go signal, and cancelled these force changes whenever Stop signals occurred (dynamically adjusted delay). We found that muscle relaxations were stopped rapidly, met predictions of existing race models, and had Stop signal reaction times that correlated with those observed during the stopping of muscle contractions, suggesting shared control mechanisms. However, stopped relaxations were preceded by transient increases in electromyography (EMG), while stopped contractions were preceded by decreases in EMG, suggesting a later divergence of control. Muscle state-specific active breaking occurred simultaneously across muscles, consistent with a central origin. Our results indicate that the later stages of action inhibition involve separate excitatory and inhibitory pathways, which act automatically to cancel complex body movements.SIGNIFICANCE STATEMENT The mechanisms of how muscle relaxations are cancelled are poorly understood. We showed in three experiments involving multiple effectors that stopping muscle relaxations involves transient bursts of EMG activity, which resemble cocontraction and have onsets that correlate with Stop signal reaction time. Comparison with the stopping of matched muscle contractions showed that active breaking was muscle state specific, being positive for relaxations and negative for contractions. The two processes were also observed to co-occur in agonist-antagonist pairs, suggesting separate pathways. The rapid, automatic activation of both pathways may explain how complex actions can be stopped at any stage of their execution.

Low Gain Servo Control During the Kohnstamm Phenomenon Reveals Dissociation Between Low-Level Control Mechanisms for Involuntary vs. Voluntary Arm Movements.

The Kohnstamm phenomenon is a prolonged involuntary aftercontraction following a sustained voluntary isometric muscle contraction. The control principles of the Kohnstamm have been investigated using mechanical perturbations, but previous studies could not dissociate sensorimotor responses to perturbation from effects of gravity. We induced a horizontal, gravity-independent Kohnstamm movement around the shoulder joint, and applied resistive or assistive torques of 0.5 Nm after 20° angular displacement. A No perturbation control condition was included. Further, participants made velocity-matched voluntary movements, with or without similar perturbations, yielding a 2 × 3 factorial design. Resistive perturbations produced an increase in agonist electromyography (EMG), in both Kohnstamm and voluntary movements, while assistive perturbations produced a decrease. While overall Kohnstamm EMGs were greater than voluntary EMGs, the EMG responses to perturbation, when expressed as a percentage of unperturbed EMG activity, were significantly smaller during Kohnstamm movements than during voluntary movements. The results suggest that the Kohnstamm aftercontraction involves a central drive, coupled with low-gain servo control by a negative feedback loop between afferent input and a central motor command. The combination of strong efferent drive with low reflex gain may characterize involuntary control of postural muscles. Our results question traditional accounts involving purely reflexive mechanisms of postural maintenance. They also question existing high-gain, peripheral accounts of the Kohnstamm phenomenon, as well as accounts involving a central adaptation interacting with muscle receptors via a positive force feedback loop.

Experimental investigations of control principles of involuntary movement: a comprehensive review of the Kohnstamm phenomenon.

The Kohnstamm phenomenon refers to the observation that if one pushes the arm hard outwards against a fixed surface for about 30 s, and then moves away from the surface and relaxes, an involuntary movement of the arm occurs, accompanied by a feeling of lightness. Central, peripheral and hybrid theories of the Kohnstamm phenomenon have been advanced. Afferent signals may be irrelevant if purely central theories hold. Alternatively, according to peripheral accounts, altered afferent signalling actually drives the involuntary movement. Hybrid theories suggest afferent signals control a centrally-programmed aftercontraction via negative position feedback control or positive force feedback control. The Kohnstamm phenomenon has provided an important scientific method for comparing voluntary with involuntary movement, both with respect to subjective experience, and for investigating whether involuntary movements can be brought under voluntary control. A full review of the literature reveals that a hybrid model best explains the Kohnstamm phenomenon. On this model, a central adaptation interacts with afferent signals at multiple levels of the motor hierarchy. The model assumes that a Kohnstamm generator sends output via the same pathways as voluntary movement, yet the resulting movement feels involuntary due to a lack of an efference copy to cancel against sensory inflow. This organisation suggests the Kohnstamm phenomenon could represent an amplification of neuromotor processes normally involved in automatic postural maintenance. Future work should determine which afferent signals contribute to the Kohnstamm phenomenon, the location of the Kohnstamm generator, and the principle of feedback control operating during the aftercontraction.

Voluntary motor commands reveal awareness and control of involuntary movement.

The capacity to inhibit actions is central to voluntary motor control. However, the control mechanisms and subjective experience involved in voluntarily stopping an involuntary movement remain poorly understood. Here we examined, in humans, the voluntary inhibition of the Kohnstamm phenomenon, in which sustained voluntary contraction of shoulder abductors is followed by involuntary arm raising. Participants were instructed to stop the involuntary movement, hold the arm in a constant position, and 'release' the inhibition after ∼2s. Participants achieved this by modulating agonist muscle activity, rather than by antagonist contraction. Specifically, agonist muscle activity plateaued during this voluntary inhibition, and resumed its previous increase thereafter. There was no discernible antagonist activation. Thus, some central signal appeared to temporarily counter the involuntary motor drive, without directly affecting the Kohnstamm generator itself. We hypothesise a form of "negative motor command" to account for this novel finding. We next tested the specificity of the negative motor command, by inducing bilateral Kohnstamm movements, and instructing voluntary inhibition for one arm only. The results suggested negative motor commands responsible for inhibition are initially broad, affecting both arms, and then become focused. Finally, a psychophysical investigation found that the perceived force of the aftercontraction was significantly overestimated, relative to voluntary contractions with similar EMG levels. This finding is consistent with the hypothesis that the Kohnstamm generator does not provide an efference copy signal. Our results shed new light on this interesting class of involuntary movement, and provide new information about voluntary inhibition of action.

Sensorimotor organization of a sustained involuntary movement.

Involuntary movements share much of the motor control circuitry used for voluntary movement, yet the two can be easily distinguished. The Kohnstamm phenomenon (where a sustained, hard push produces subsequent involuntary arm raising) is a useful experimental model for exploring differences between voluntary and involuntary movement. Both central and peripheral accounts have been proposed, but little is known regarding how the putative Kohnstamm generator responds to afferent input. We addressed this by obstructing the involuntary upward movement of the arm. Obstruction prevented the rising EMG pattern that characterizes the Kohnstamm. Importantly, once the obstruction was removed, the EMG signal resumed its former increase, suggesting a generator that persists despite peripheral input. When only one arm was obstructed during bilateral involuntary movements, only the EMG signal from the obstructed arm showed the effect. Upon release of the obstacle, the obstructed arm reached the same position and EMG level as the unobstructed arm. Comparison to matched voluntary movements revealed a preserved stretch response when a Kohnstamm movement first contacts an obstacle, and also an overestimation of the perceived contact force. Our findings support a hybrid central and peripheral account of the Kohnstamm phenomenon. The strange subjective experience of this involuntary movement is consistent with the view that movement awareness depends strongly on efference copies, but that the Kohnstamm generator does not produces efference copies.

On the bimanual integration of proprioceptive information.

Proprioception can be defined as the sense for body movement and position. While most sensory information can be successfully integrated across hemispheres, little is known about the bilateral integration of proprioceptive information. In two behavioural experiments, we investigated whether estimates of the position of one hand are influenced by simultaneous proprioceptive information from the other hand. We further investigated whether such putative bimanual proprioceptive integration would differ between expert dancers and non-dancer controls. Either one hand or both hands were passively moved to novel positions, and participants indicated the perceived location of the index finger tip of the designated target hand, by orienting a visible laser beam mounted on a cap. Synchronized bimanual movements compared to unimanual movements significantly improved proprioceptive position sense. In particular, we found a bias reduction to perceive the target hand's index finger tip as shifted away from the midline in the bimanual condition, compared to the unimanual condition. Expert dancers, in contrast, did not show this change in proprioceptive position sense after bimanual movements. We suggest that bimanual movements may improve proprioception due to interhemispheric integration in controls, but not in expert dancers.

Sleep deprivation reduces default mode network connectivity and anti-correlation during rest and task performance.

Sleep deprivation (SD) can alter extrinsic, task-related fMRI signal involved in attention, memory and executive function. However, its effects on intrinsic low-frequency connectivity within the Default Mode Network (DMN) and its related anti-correlated network (ACN) have not been well characterized. We investigated the effect of SD on functional connectivity within the DMN, and on DMN-ACN anti-correlation, both during the resting state and during performance of a visual attention task (VAT). 26 healthy participants underwent fMRI twice: once after a normal night of sleep in rested wakefulness (RW) and once following approximately 24h of total SD. A seed-based approach was used to examine pairwise correlations of low-frequency fMRI signal across different nodes in each state. SD was associated with significant selective reductions in DMN functional connectivity and DMN-ACN anti-correlation. This was congruent across resting state and VAT analyses, suggesting that SD induces a robust alteration in the intrinsic connectivity within and between these networks.