Electromyographic responses to constant position errors imposed during voluntary elbow joint movement in human

The role of reflexes in the control of stiffness during human elbow joint movement was investigated for a wide range of movement speeds (1.5–6 rad/s). The electromyographic (EMG) responses of the elbow joint muscles to step position errors (step amplitude 0.15 rad; rise time 100 ms) imposed at the onset of targeted flexion movements (1.0 rad amplitude) were recorded. For all speeds of movement, the step position disturbance produced large modulations of the usual triphasic EMG activity, both excitatory and inhibitory, with an onset latency of 25 ms. In the muscles stretched by the perturbation, the early EMG response (25–60 ms latency) magnitude was greater than 50% of the activity during the unperturbed movements (background activity). In all muscles the EMG responses integrated over the entire movement were greater than 25% of the background activity. The responses were relatively greater for slower movements. Perturbations assisting the movement caused a short-latency (25–60 ms) reflex response (in the antagonist muscle) that increased with movement speed and was constant as a percentage of the background EMG activity. In contrast, perturbations resisting the movement caused a reflex response (in the agonist muscle) that was of the same absolute magnitude at all movement speeds, and thus decreased with movement speed as a percentage of the background EMG activity. There was a directional asymmetry in the reflex response, which produced an asymmetry in the mechanical response during slow movements. When the step perturbation occurred in a direction assisting the flexion movement, the antagonist muscle activity increased, but the main component of this response was delayed until the normal time of onset of the antagonist burst. When the step perturbation resisted the movement the agonist muscles responded briskly at short latency (25 ms). A reflex reversal occurred in two of six subjects. A fixed reflex response occurred in the antagonist muscle, regardless of the perturbation direction. For the extension direction perturbations (resisting movement), this response represented a reflex reversal (50 ms onset latency) and it caused the torque resisting the imposed step (stiffness) to drop markedly (below zero for one subject). Reflex responses were larger when the subject was prevented from reaching the target. That is, when the perturbation remained on until after the normal time of reaching the target, the EMG activity increased, with a parallel increase in stiffness. Similarly, when the perturbations prevented the subject from reaching the target during a 1-rad voluntary cyclic movement, the EMG and stiffness increased markedly. Coactivation of the antagonist muscle with the agonist muscle was not prominent (<30% of antagonist activity) during unperturbed movements. The perturbations were resisted with reciprocal activity, and thus reflex action did not increase the coactivation. However, as a result of the low-pass properties of muscle, substantial cocontraction of the agonist and antagonists muscle forces may have occurred during rapid movements, thus leading to increased stiffness. As the relative changes in normal EMG activity produced by the perturbation were often comparable with the changes in mean muscle torque (stiffness) reported in the first paper of this series, we conclude that the action of reflexes produced a significant portion of the resistance to perturbations. This reflexive portion was greater for slower movements, it was greater when the subject neared the target, and it was variable according to the perturbation direction and the particular subject. Given that the perturbations were of similar frequency content to the movement itself (though of smaller amplitude) and that the reflexes contributed substantially to the resistance to these perturbations, we suggest that in normal unperturbed movements the observed EMG is likewise substantially determined by the reflex activity.     

Relationship between EMG patterns and kinematic properties for flexion movements at the human wrist

Summary EMG patterns associated with voluntary wrist flexion movements were studied in normal human subjects. Initially, subjects were trained to produce movements within five specified velocity ranges while the amplitude of the movement and the opposing load remained constant. In a second set of experiments, subjects were required to produce movements at four different amplitudes, moving as rapidly as possible against a constant load. Finally, with movement velocity and amplitude kept constant, the external load was varied so that different forces were required to generate the movements. The slowest movements were associated with a prolonged burst of EMG activity from the agonist muscle with little or no antagonist activity. With increasing movement velocity, there was a gradual evolution to the characteristic triphasic pattern associated with rapid voluntary movements. As velocity of movement increased further, the amplitude and area of the EMG bursts increased while burst duration and interburst intervals decreased. Increases in movement amplitude were accomplished mainly by changing the timing of the EMG bursts; with larger amplitude movements the antagonist burst occurred later. With movements against larger loads there was an increase in the size of the agonist burst and a decrease in the antagonist burst, but no change in the relative timing of the EMG bursts. These systematic changes in EMG patterns associated with different types of movement provide an indirect method of obtaining information concerning the motor programs which generate the movements.     

Evidence that a disordered servo-like mechanism contributes to tremor in movements during cerebellar dysfunction

The characteristics of discontinuities and tremor that occurred in elbow flexions during cooling of the lateral cerebellar nuclei were investigated in five Cebus monkeys. Discontinuities in movements appeared as rhythmical oscillations (kinetic tremor) when movements were slow or when movements were made with a constant force that loaded the antagonist. These oscillations had similar properties to cerebellar terminal tremor following movements; e.g., their amplitude and frequency were decreased by addition of mass to the handle and they occurred in the absence of visual feedback. The abnormal initial decrease in velocity that initiated oscillations in flexion movements was associated with abnormally early or large antagonist (triceps) electromyogram (EMG) activity. This abnormal EMG activity did not follow the normal inverse relation between initial velocity and antagonist latency from onset of movement. The initial deflection from the expected trajectory was opposed by a second burst of EMG activity in the agonist (biceps). This second burst was not the continuation of a step of EMG activity because its amplitude was often larger than the amplitude of the first agonist burst. The second agonist burst had the properties of a servo-like response: it occurred when biceps shortening was slowed (but biceps was not stretched), its magnitude was proportional to the magnitude or the deflection in velocity, its latency was 50-80 ms from onset of the abnormal decrease in velocity, and it occurred in the absence of visual feedback. However, this servo-like response was disordered because it did not return the limb accurately to the expected trajectory. The servo-like mechanism was studied further by applying torque pulse perturbations during elbow flexions. When the cerebellar nuclei were cooled, agonist responses to the perturbation were proportional to the size of the velocity deflection, but they were prolonged and onset of antagonist activity was delayed. It is suggested that discontinuities and tremor in movements during cerebellar dysfunction result from the same mechanism: alternation between disordered stretch reflexes and disordered servo-assistance mechanisms, both partly involving transcortical pathways.     

Low Frequency Cortico-Muscular Coherence During Voluntary Rapid Movements of the Wrist Joint

Rapid voluntary point-to-point wrist tracking movements are generated by the co-operative action of a large number of wrist muscles activated in a stereotypic pattern. This pattern is composed of a two burst sequence occurring in synergist and antagonist muscles. The time course and duration of these bursts are relatively fixed but the burst magnitude in any one muscle varies in relation to the direction of movement and the preferred directional tuning characteristic of the muscle. This creates a highly adaptive method for generating fast movements to different positions in space. In this study we have examined the extent to which this adaptive burst behaviour can be associated with activity changes occurring in the contralateral motor cortex. Time dependent coherence estimates were obtained from simultaneous recordings of the electroencephalogram (EEG) made from the contralateral sensorimotor cortex and the electromyogram (EMG) from various wrist flexor and extensor muscles during fast point-to-point wrist tracking movements. Using the onset of movement as a trigger, event related coherence estimates reveal the presence of short lasting periods of low frequency (<12 Hz) coherence during the execution of fast wrist movements. The onset and duration of the periods of low frequency coherence vary with direction of movement and the temporal burst profile of a particular muscle's EMG activity. It is therefore likely that a significant low frequency activation of the motor cortex plays a part in the generation of the EMG burst patterns that underpin rapid point-to-point movements of the human wrist.     

Influence of ipsilateral transcranial magnetic stimulation on the triphasic EMG pattern accompanying fast ballistic movements in humans

Fast ballistic flexion movements of the wrist are produced by a triphasic pattern of electromyographic (EMG) activity in flexor and extensor muscle. Whereas it is generally accepted that the primary motor cortex generates the first agonist burst (AG1), its contribution to the following antagonist burst (ANT) and second agonist burst (AG2) is unresolved. We applied single pulses of suprathreshold transcranial magnetic stimulation (TMS) at different times to the motor cortex ipsilateral to wrist flexion. This produced interhemispheric inhibition of the opposite motor cortex and a silent period in the ballistic EMG pattern that started about 30 ms after the stimulus and lasted for a further 30 ms. If the silence was timed to start within the first 30 ms of AG1, then timing of the subsequent ANT and AG2 bursts was delayed. However, if the silence began later, then the timing of the ANT burst was not changed. A similar effect on the onset latency of the AG2 was seen if the silence began in the first part of the ANT burst. The results are compatible with a model in which the triphasic pattern is not triggered as a single entity. Instead we suggest that each burst has its own trigger that occurs about 30–40 ms after the start of AG1 (or ANT). If AG1 (or ANT) is interrupted within this time period then this trigger, and hence later bursts, are delayed. If the interruption occurs after 30–40 ms it has no effect on the onset of later bursts since they have already been triggered.     

Arm movement performance during reversible basal ganglia lesions in the monkey

Summary Arm motor performance of eight Cebus monkeys was examined during reversible cooling in the ventral lateral region of the putamen and globus pallidus (primarily the external segment), where neurons discharging during arm movements have been found (DeLong 1972).When attempting to hold a handle stationary during basal ganglia cooling, all monkeys developed flexion at the wrist and some developed a slow flexion drift of the arm at the elbow. The prominence of wrist flexion emphasizes that the basal ganglia may normally influence distal musculature.During basal ganglia cooling an increase in segmental stretch reflexes (15–30 ms) was sometimes observed following arm perturbations, but no consistent increase occurred in the later EMG responses (30–95 ms) in contrast to results obtained in Parkinsonian patients (Tatton and Lee 1975).No major changes were observed in the time of onset of the earliest EMG activity in the agonist muscle in a simple reaction time elbow movement task during basal ganglia cooling.Basal ganglia lesions produced major disorders in both flexion and extension movements including slowing of movements and rebound of the arm towards its initial position after onset of movement. These disorders were accompanied by an increase in tonic activity of both flexors and extensors while holding and by increased levels of cocontraction of agonists and antagonists during attempted movements.It is suggested that this basal ganglia disorder is due to a failure to achieve the correct balance of activity between agonists and antagonists that is appropriate for a particular motor act.This study was supported by the Canadian MRC PG-1     

Ballistic reactions under different motor sets

In preparation for performing task specific ballistic movements, subjects may choose among different possibilities for setting up their motor apparatus, ranging from quiet resting to different types of muscle activation. In the study presented here, we investigated whether differences in the motor set modify either the reaction time or the kinematic characteristics of the movement. Subjects wearing surface EMG recording electrodes in the wrist extensor (WE) and wrist flexor (WF) muscles were requested to react to the presentation of a visual stimulus by performing a ballistic wrist extension movement of an amplitude of about 50° in the following experimental conditions: resting quietly, which was considered as the control condition (CC); isometric contraction (IC), in which subjects were required to activate WE and WF muscles isometrically; rapid oscillations (RO), in which subjects were requested to make a fast oscillatory wrist movement; and slow oscillations (SO), in which subjects were maintaining a slow oscillatory motion of the wrist. To constrain the movement to the wrist joint and limit the action of postural muscles, the subjects forearm and hand were attached to joined non-resistive metallic platforms, allowing for free non-frictional displacement. In the EMG recordings, we measured the size of the EMG bursts in agonist and antagonist muscles, and the inter-burst intervals. In movement recordings, we measured movement onset latency and the velocity profile. Movement onset was delayed in SO with respect to all other conditions. Conversely, peak velocity was larger in all test conditions in comparison to CC. There were no differences in the size of the first EMG burst of the agonist muscle, but significant changes occurred in the subsequent bursts recorded in the agonist and antagonist muscles. Our study indicates that the motor program used to execute a ballistic voluntary movement is influenced by the conditions of the motor system. The configuration of the motor set should be specifically considered in the search for improving the speed of the reaction and the kinematics of ballistic movements.JMC and MTS were funded by the Spanish Ministry of Education, Culture and Sport, with grant numbers PR 2003-0212 and AP2000-0913     

Coordination of multiple muscles in two degree of freedom elbow movements

The present study quantifies electromyographic (EMG) magnitude, timing, and duration in one and two degree of freedom elbow movements involving combinations of flexion-extension and pronation-supination. The aim is to understand the organization of commands subserving motion in individual and multiple degrees of freedom. The muscles tested in this study fell into two categories with respect to agonist burst magnitude: those whose burst magnitude varied with motion in a second degree of freedom at the elbow, and those whose burst magnitude depended on motion in one degree of freedom only. In multiarticular muscles contributing to motion in two degrees of freedom at the elbow, we found that the magnitude of the agonist burst was greatest for movements in which a muscle acted as agonist in both degrees of freedom. The burst magnitudes for one degree of freedom movements were, in turn, greater than for movements in which the muscle was agonist in one degree of freedom and antagonist in the other. It was also found that, for movements in which a muscle acted as agonist in two degrees of freedom, the burst magnitude was, in the majority of cases, not different from the sum of the burst magnitudes in the component movements. When differences occurred, the burst magnitude for the combined movement was greater than the sum of the components. Other measures of EMG activity such as burst onset time and duration were not found to vary in a systematic manner with motion in these two degrees of freedom. It was also seen that several muscles which produced motion in one degree of freedom at the elbow, including triceps brachii (long head), triceps brachii (lateral head), and pronator quadratus displayed first agonist bursts whose magnitude did not vary with motion in a second degree of freedom. However, for the monoarticular elbow flexors brachialis and brachioradialis, agonist burst magnitude was affected by pronation or supination. Lastly, it was observed that during elbow movements in which muscles acted as agonist in one degree of freedom and antagonist in the other, the muscle activity often displayed both agonist and antagonist components in the same movement. It was found that, for pronator teres and biceps brachii, the timing of the bursts was such that there was activity in these muscles concurrent with activity in both pure agonists and pure antagonists. The empirical summation of EMG burst magnitudes and the presence in a single muscle of both agonist and antagonist bursts within a movement suggest that central commands associated with motion in individual degrees of freedom at the elbow may be superimposed to produce elbow movements in two degrees of freedom.     

Movement and electromyographic disorders associated with cerebellar dysmetria

The objective of these experiments was to determine whether dysmetric elbow flexions, which occurred during cerebellar dysfunction, had the same kinematic and electromyographic characteristics as movements of the same amplitude and velocity performed under normal conditions. Reversible cerebellar lesions were produced by cooling through two probes implanted on either side of the dentate nucleus in five Cebus albifrons monkeys. Normal, fast, and accurate elbow flexions had single-peaked velocities and a bi- or triphasic EMG pattern in agonist and antagonist muscles. During cerebellar dysfunction movements became ataxic. Ataxic movements were classified into two categories: those with oscillations (tremor) during the movement and those without oscillations. A terminal tremor occurred after both types of movements. Oscillations during movements were more likely to occur when a constant force loaded the antagonist. Addition of mass to the handle attenuated or abolished the oscillations. Movements with oscillations reached the target with increased variability of end position, whereas movements without oscillations were often hypermetric. The movement parameters and EMG patterns associated with flexions without oscillations during the movement were studied in detail. A characteristic of these movements was that the acceleration and deceleration phases were asymmetric. Compared with control movements of the same peak velocity, they had smaller magnitudes of acceleration and larger magnitudes of deceleration. The large deceleration was abnormal because it initiated the terminal tremor. The disorder in acceleration was associated with agonist EMG activity that was less abrupt in onset, smaller in magnitude, and more prolonged in duration. The disorder in deceleration was associated with delayed onset of phasic antagonist EMG activity. The results show that hypermetric arm movements without oscillations have different properties than those of normal movements of similar velocity and amplitude. Thus it is unlikely that dysmetria results from inappropriate selection or triggering of an otherwise normal motor program. We conclude that normal function of the cerebellum is necessary for the generation of agonist and antagonist muscle activity that is both of the appropriate magnitude and timing to control the dynamic phase of arm movements.     

Activity of neurons in putamen during active and passive movements of wrist

Recent studies have shown that many neurons in the basal ganglia have patterns of activity that are closely related to various parameters of active movements of the arm. The topographical distribution of these cells suggests that they are influenced by afferents from primary motor and sensory areas of the cerebral cortex. Although there is abundant evidence that information from peripheral receptors is relayed to the basal ganglia, relatively little information is available on whether neurons related to active movement are influenced by peripheral inputs. The present study was undertaken to provide information on this problem by comparing responses of putamen neurons to active and passive movements of the wrist. Two monkeys were trained to place their hand in a manipulandum and actively extend and flex their wrist against opposing torque loads. Additionally, they were trained to accept 1) passive step displacements of the wrist by the experimenter, which were comparable in amplitude, duration, and velocity to active movements, and 2) brief rapid displacements generated by a pulse of torque applied to the manipulandum by a motor. An extensive electromyographic (EMG) study was made prior to unit recording to characterize patterns of muscle activity during active and passive movements. A sample of 82 neurons was isolated in the putamen on the basis of a phasic burst of spikes associated with active movement of the wrist. Most (80%) of these cells showed directionally specific responses. The onset latency of unit firing in 91% of the cells lagged behind the onset of EMG activity in forearm agonist muscles. Phasic unit discharge during active movement increased with increasing opposing torque loads in 59% of the sample. The rate-torque curves for most of these cells were curvilinear (plateau occurred at heavy torque loads), although some cells showed a linear relationship. A comparison of these neuronal activity patterns with EMG activity-torque curves suggests that most of the cells were related to activity in forearm muscles and not to activity in proximal or axial muscles. The functional significance of these findings is interpreted in light of recent physiological and anatomic studies of the basal ganglia. A substantial proportion (44%) of the units that were related to active wrist movements showed an excitatory response during passive step displacements of the wrist in the absence of phasic EMG activity.(ABSTRACT TRUNCATED AT 400 WORDS)     

Reprogramming of muscle activation patterns at the wrist in compensation for elbow reaction torques during planar two-joint arm movements

The relationship between wrist kinematics, dynamics and the pattern of muscle activation were examined during a two-joint planar movement in which the two joints moved in opposite directions, i.e. elbow flexion/wrist extension and elbow extension/wrist flexion. Elbow movements (ranging from 10 to 70 deg) and wrist movements (ranging from 10 to 50 deg) were performed during a visual, step-tracking task in which subjects were required to attend to the initial and final angles at each joint. As the elbow amplitude increased, wrist movement duration increased and the wrist movement trajectories became quite variable. Analysis of the torques acting at the wrist joint showed that elbow movements produced reaction torques acting in the same direction as the intended wrist movement. Distinct patterns of muscle activation were observed at the wrist joint that were dependent on the relative magnitude of the elbow reaction torque in relation to the net wrist torque. When the magnitude of the elbow reaction torque was quite small, the wrist agonist was activated first. As the magnitude of the elbow reaction torque increased, activity in the wrist agonist decreased significantly. In conditions where the elbow reaction torque was much larger than the net wrist torque, the wrist muscle torque reversed direction to oppose the intended movement. This reversal of wrist muscle torque was directly associated with a change in the pattern of muscle activation where the wrist antagonist was activated prior to the wrist agonist. Our findings indicate that motion of the elbow joint is an important consideration in planning wrist movement. Specifically, the selection of muscle activation patterns at the wrist is dependent on the relative magnitude and direction of the elbow reaction torque in relation to the direction of wrist motion.     

Movement-related phasic muscle activation. I. Relations with temporal profile of movement

1. The role of phasic muscle activation in determining the temporal properties of human arm movements was studied. The experiments show that subjects can modulate the triphasic electromyographic (EMG) pattern to produce movements of varied temporal structures. 2. Subjects performed horizontal forearm movements in which they varied movement accelerations and decelerations. All movements were of the same amplitude, duration, and peak velocity. A phase-plane (velocity vs. position) template of the desired movement was presented to the subject, who had to reproduce the template by appropriate movement of the forearm. 3. The ratio of the durations of acceleration to deceleration (termed the symmetry ratio, SR) was used as a measure of the temporal structure of the movements. Movements with SRs ranging from 0.4 (short acceleration-long deceleration) to 2.0 (long acceleration-short deceleration) were studied. 4. Subjects modulated the components of the triphasic EMG pattern to produce movements with different temporal profiles. As the SR was increased (increasing acceleration duration-decreasing deceleration duration), the following changes occurred: 1) the duration of the initial agonist burst (AG1) increased while its magnitude decreased; 2) the antagonist burst (ANT1) was progressively delayed relative to movement onset. ANT1 magnitude increased while its duration remained constant; and 3) the magnitude of the second agonist burst (AG2) increased and its duration decreased. 5. The triphasic EMG pattern can be modified to produce movements whose velocity profiles are not the same under simple scaling of duration or magnitude. It is concluded that previously described relations between components of the triphasic EMG pattern and movement parameters, such as amplitude, speed, and duration, are secondary to associated changes in their acceleration and deceleration characteristics.     

Reciprocal facilitation of motor evoked potentials immediately before voluntary movements in Parkinson's disease.

Changes of motor evoked potentials (MEPs) from the agonist and antagonist forearm muscles were investigated in 13 patients with Parkinson's disease and age-matched controls, in whom transcranial magnetic stimulation (TCMS) was delivered to the cortical hand motor area immediately before voluntary wrist flexion. MEPs recorded from the agonist muscles, namely the wrist flexors, were gradually facilitated in accordance with a shortening of the interval between TCMS and wrist flexion in both groups. In contrast, MEPs recorded from the antagonist muscles, namely the wrist extensors, were gradually facilitated as the intervals were shortened only in parkinsonian patients. The reciprocal facilitation of the antagonist MEPs was statistically significant when TCMS was delivered within 80 msec before the voluntary movements, suggesting the presence of the same underlying mechanism of symptomatic cocontraction observed in patients with Parkinson's disease.     

Control of simple arm movements in elderly humans

Eight elderly subjects (aged 68-95 years) and 6 young adults (aged 21-24 years) performed elbow flexion and extension movements in a visual step-tracking paradigm. Movement amplitudes ranging from 10 degrees-80 degrees were made under two instructions: "move at own speed" and "move fast and accurate." In a second experiment, 5 elderly subjects practiced 30 degrees movements for a total of 180 flexion and 180 extension movements under the instruction to increase movement speed, while maintaining accuracy, during practice. Movement trajectories became more variable as both movement amplitude and speed increased. Trajectory variability was greater in the elderly subjects for both the acceleratory and deceleratory phases of movements. This was due primarily to a greater rate of increase in trajectory variability during the acceleration phase in the elderly. With practice, elderly subjects could substantially reduce trajectory variability with little change in movement speed. The agonist burst initiating movements was qualitatively normal in the elderly subjects. However, there was considerable tonic cocontraction of agonist and antagonist muscles prior to and during movement. Phasic antagonist EMG activity was obviously abnormal in many elderly subjects. There was often no clear antagonist burst associated with deceleration of the movements or, if present, it was timed inappropriately early. With practice, combined agonist-antagonist EMG variability decreased. A clear antagonist burst also developed during practice in most elderly subjects, but its inappropriate timing remained in all but one subject. The results show that movement trajectories are less accurately controlled in the elderly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Neural compensation for compliant loads during rhythmic movement

An experiment was performed to characterise the movement kinematics and the electromyogram (EMG) during rhythmic voluntary flexion and extension of the wrist against different compliant (elastic-viscous-inertial) loads. Three levels of each type of load, and an unloaded condition, were employed. The movements were paced at a frequency of 1 Hz by an auditory metronome, and visual feedback of wrist displacement in relation to a target amplitude of 100 degree was provided. Electromyographic recordings were obtained from flexor carpi radialis (FCR) and extensor carpi radialis brevis (ECR). The movement profiles generated in the ten experimental conditions were indistinguishable, indicating that the CNS was able to compensate completely for the imposed changes in the task dynamics. When the level of viscous load was elevated, this compensation took the form of an increase in the rate of initial rise of the flexor and the extensor EMG burst. In response to increases in inertial load, the flexor and extensor EMG bursts commenced and terminated earlier in the movement cycle, and tended to be of greater duration. When the movements were performed in opposition to an elastic load, both the onset and offset of EMG activity occurred later than in the unloaded condition. There was also a net reduction in extensor burst duration with increases in elastic load, and an increase in the rate of initial rise of the extensor burst. Less pronounced alterations in the rate of initial rise of the flexor EMG burst were also observed. In all instances, increases in the magnitude of the external load led to elevations in the overall level of muscle activation. These data reveal that the elements of the central command that are modified in response to the imposition of a compliant load are contingent, not only upon the magnitude, but also upon the character of the load.     

Optimal control of redundant muscles in step-tracking wrist movements

An important question in motor neuroscience is how the nervous system controls the spatiotemporal activation patterns of redundant muscles in generating accurate movements. The redundant muscles may not only underlie the flexibility of our movements but also pose the challenging problem of how to select a specific sequence of muscle activation from the huge number of possible activations. Here, we propose that noise in the motor command that has an influence on task achievement should be considered in determining the optimal motor commands over redundant muscles. We propose an optimal control model for step-tracking wrist movements with redundant muscles that minimizes the end-point variance under signal-dependent noise. Step-tracking wrist movements of human and nonhuman primates provide a detailed data set to investigate the control mechanisms in movements with redundant muscles. The experimental EMG data can be summarized by two eminent features: 1) amplitude-graded EMG pattern, where the timing of the activity of the agonist and antagonist bursts show slight variations with changes in movement directions, and only the amplitude of activity is modulated; and 2) cosine tuning for movement directions exhibited by the agonist and antagonist bursts, and the discrepancy found between a muscle's agonist preferred direction and its pulling direction. In addition, it is also an important observation that subjects often overshoot the target. We demonstrate that the proposed model captures not only the spatiotemporal activation patterns of wrist muscles but also trajectory overshooting. This suggests that when recruiting redundant muscles, the nervous system may optimize the motor commands across the muscles to reduce the negative effects of motor noise.     

Effects of reversible blockade of basal ganglia on a voluntary arm movement.

1. The effects of a reversible blockade of basal ganglia were examined in two monkeys trained to perform a visually guided, step-tracking arm movement around the elbow joint. To block glutamatergic excitation, kynurenate (a glutamate antagonist) was locally injected into the putamen and the external segment (GPe) and the internal segment (GPi) of the globus pallidus contralateral to the arm tested. Muscimol [a gamma-aminobutyric acid (GABA) agonist] was also used to suppress neuronal activity in these structures. The drugs were injected in the arm area of the putamen, which was identified by microstimulation or by recording neural activity. For the GPe and GPi, injections were made into the area medioventral to the arm area of the putamen. 2. The blockade of the putamen caused abnormal braking of the arm movements. The first step of the movement became hypometric, and multiple steps were necessary to reach the target. The electromyographic (EMG) analysis revealed an increase of burst activity in the antagonist muscles and a decrease of that in the agonist muscles at the fast movements. The tonic activity increased in the extensor muscles during a holding period. 3. The blockade of the GPi caused dysmetric movements. Amplitude and peak velocity of the first step of movement largely fluctuated among trials. It became difficult for the animal to brake and adjust its arm onto the target. 4. The blockade of the GPe caused a flexion posture at the elbow joint of the contralateral arm. The tonic activity of the flexor muscles increased. Cocontraction of the agonist and antagonist muscles was also observed. 5. These results suggest that the putaminopallidal system of the basal ganglia contributes to both of two motor functions: 1) static control to maintain the posture with tonic muscle activity, and 2) dynamic control to enable fast movements.     

Movement-related phasic muscle activation. II. Generation and functional role of the triphasic pattern

1. Electromyographic (EMG) activity of arm movements made at constant velocity was studied in humans. In these movements, acceleration was temporally separated from deceleration by a period of constant velocity (zero acceleration) lasting up to 600 ms. 2. Agonist (AG1) and antagonist (ANT1) bursts were associated with acceleration. AG1 began before acceleration onset. ANT1 started after the onset of AG1 and was often partially coextensive with AG1. The initial phasic activity was followed by tonic EMG activity during the constant-velocity phase of the movements. Movement deceleration was associated with an antagonist burst (ANT2) and an agonist (AG2) burst. 3. Subjects could alter the magnitudes of the acceleration- and deceleration-related activities independently, with resulting independent changes in the movement acceleration and deceleration. 4. When the duration of the constant-velocity phase was decreased, the agonist/antagonist burst pairs occurred progressively closer in time. When movement duration was decreased to the point at which the velocity profile resembled that of step-tracking movements, the four periods of phasic EMG activity formed the classic triphasic pattern. 5. Triphasic EMG patterns were occasionally seen at the beginning or end of long-duration, constant-velocity movements. When they occurred, these triphasic patterns were associated with an acceleration/deceleration pattern similar to that seen in step-tracking movements. 6. The data indicate that paired agonist/antagonist activation is the basic unit of movement control. The AG1/ANT1 burst pair determines the increase and decrease of acceleration, respectively, and the ANT2/AG2 burst pair the increase and decrease of deceleration. These muscle activation pairs can be combined as needed to produce movements having different temporal characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)     

Adaptation to destabilizing dynamics by means of muscle cocontraction

Adaptive control of wrist mechanics was investigated by means of destabilizing dynamics created by a torque motor. Subjects performed a 20 degrees movement to a 3 degrees target under the constraint that no motion should occur outside of the target zone once 800 ms had elapsed from movement onset. This constraint served as the minimum acceptable level of postural stability. The ability of subjects to modify their muscle activation patterns in order to successfully achieve this stability was investigated by creating three types of destabilizing dynamics with markedly different features: negative stiffness, negative damping, and square-wave vibration. Subjects performed sets of trials with the first type of destabilizing dynamics and were then required to adapt to the second and third. The adaptive response was quantified in terms of the rms electromyographic (EMG) activity recorded during various phases of the task. Surface EMG activity was recorded from three muscles contributing to wrist flexion and three muscles contributing to wrist extension. With negative stiffness, a significant compensatory increase in cocontraction of wrist flexor and extensor muscles was observed for slow movements, but there was little change in the muscle activity for rapid movements. With negative damping, muscle cocontraction was elevated to stabilize rapid movements, declining only gradually after the target was reached. For slow movements, cocontraction occurred only when negative damping was high. The response to square-wave vibration (10 Hz, +/-0.5 Nm), beginning at movement onset, was similar to that of negative damping, in that it resulted in elevated cocontraction. However, because the vibration persisted after the target was reached, there was no subsequent decrease in muscle activity. When the frequency was reduced to 5.5 Hz, but with the same torque impulse, cocontraction increased. This is consistent with greater mechanical instability. In summary, agonist-antagonist cocontraction was adapted to the stability of the task. This generally resulted in less of a change in muscle activity during the movement phase, when the task was performed quickly compared with slowly. On the other hand, the change in muscle activity during stabilization depended more on the nature of the instability than the movement speed.     

EMG responses to an unexpected load in fast movements are delayed with an increase in the expected movement time

When moving an object, the motor system estimates the dynamic properties of the object and then controls the movement using a combination of predictive feedforward control and proprioceptive feedback. In this study, we examined how the feedforward and proprioceptive feedback processes depend on the expected movement task. Subjects made fast elbow flexion movements from an initial position to a target. The experimental protocol included movements made over a short and a long distance against an expected light or heavy inertial load. In each task in a few randomly chosen trials, a motor applied an unexpected viscous load that produced a velocity error, defined as the difference between the expected and unexpected velocities, and electromyographic (EMG) responses. The EMG responses appeared not earlier than 170-250 ms from the agonist EMG onset. Our main finding is that the onset of the EMG responses was correlated with the expected time of peak velocity, which increased for longer distances and larger loads. An analysis of the latency of the EMG responses with respect to the velocity error suggested that the EMG responses were due to segmental reflexes. We conclude that segmental reflex gains are centrally modulated with the time course dependent on the expected movement task. According to this view, the control of fast point-to-point movement is feedforward from the agonist EMG onset until the expected time of peak velocity after which the segmental reflex feedback is briefly facilitated.