Influence of joint interactional effects on the coordination of planar two-joint arm movements

We have examined EMG-movement relations in two-joint planar arm movements to determine the influence of interactional torques on movement coordination. Explicitly defined combinations of elbow movements (ranging from 20 to 70°) and wrist movements (ranging from 20 to 40°) were performed during a visual, step-tracking task in which subjects were specifically required to attend to the initial and final angles at each joint. In all conditions the wrist and elbow rotated in the same direction, that is, flexion-flexion or extension-extension. Elbow movement kinematics were only slightly influenced by motion about the wrist. In contrast, the trajectory of the wrist movement was significantly influenced by uncompensated reaction torques resulting from movement about the elbow joint. At any given wrist amplitude, wrist movement duration increased and peak velocity decreased as elbow amplitude increased. In addition, as elbow amplitude increased, wrist movement on-set was progressively delayed relative to this elbow movement. Surprisingly, the changes between joint movement onsets were not accompanied by corresponding changes between agonist EMG onsets at the elbow and wrist joints. The mean difference in onset times between elbow and wrist agonists (22–30 ms) remained unchanged across conditions. In addition, a basic pattern of muscle activation that scaled with movement amplitude was observed at each joint. Phasic agonist activity at the wrist and elbow joints remained remarkably similar across conditions and thus the changes in joint movement onset could not be attributed to changes in the motor commands. Rather, the calculated torques from the averaged data showed that the difference in timing of joint movement onsets was influenced by joint interactional torques. These findings suggest that during simple two-joint planar movements of the elbow and the wrist joint, the central nervous system does not alter the basic motor commands at each joint and as a result the actual trajectory of each joint is determined by interactional torques.     

Adjustments of fast goal-directed movements in response to an unexpected inertial load

Summary Subjects made fast goal-directed elbow flexion movements against an inertial load. Target distance was 8 or 16 cm, randomly chosen. To exert a force in the direction of the movement subjects had to activate flexors of both shoulder and elbow, but shoulder flexors did not change appreciably in length during the movement. In 20% of the trials the inertial load was increased or decreased without knowledge of the subjects. Until 90–110 ms after the onset of the agonist muscle activity (about 65–85 ms after the start of movement) EMG activity was very similar in all conditions tested. The changes that occured in the EMG from that moment on were effectively a later cessation of the agonist activity and a later start of the antagonist activity if the load was increased unexpectedly. If the load was reduced unexpectedly, the agonist activity ceased earlier and the antagonist activity began earlier. The latency at which EMGs started to change was the same for muscles around shoulder and elbow, for agonists and antagonists and for both distances. All adjustments had the same latency (37 ms) relative to the point where the angular velocity of the elbow in the unexpectedly loaded movements differed by 0.6 rad/s from the expected value. We discuss why simple reflex- or servo-mechanisms cannot account for the measured EMG changes. We conclude that appropriate adjustments of motor programmes for fast goal-directed arm movements start within 40 ms of the detection of misjudgment of load.     

Patterns of facilitation and suppression of antagonist forelimb muscles from motor cortex sites in the awake monkey

Patterns of excitatory and inhibitory effects were produced in antagonistic forelimb muscles by single intracortical microstimuli (S-ICMS) applied to motor cortex sites in macaque monkeys performing ramp-and-hold wrist movements. Stimulus-triggered averages (stimulus-TAs) of rectified electromyographic (EMG) activity revealed poststimulus facilitation and/or suppression in identified flexor and extensor muscles of the wrist and fingers. At 22 cortical sites the action potentials of single cells were also recorded and used to compute spike-triggered averages (spike-TAs) of covarying muscles. The set of muscles activated during the movement in which the cell was active are referred to here as "agonists"; those muscles active during wrist movement in the opposite direction are called "antagonists." (At sites where cells were not isolated the muscles showing poststimulus facilitation were called agonists.) Poststimulus effects in agonist muscles typically consisted of facilitation in a subset of the agonists. For 48 sites from which poststimulus effects were tested on both flexors and extensors, the following combinations of effects were observed: 1) pure facilitation of agonist muscles with no effect on antagonists; 2) facilitation of both agonists and antagonists; 3) facilitation of agonist muscles with reciprocal suppression of antagonists; 4) "mixed" facilitation and suppression of synergist muscles; and 5) pure suppression of some muscles with no effect on their antagonists. The suppression effects appeared most commonly in flexor muscles; conversely, facilitation was generally stronger in extensors. Cortical sites eliciting pure suppression of flexor muscles with no facilitation of extensor muscles were found in two monkeys. These purely suppressive effects were observed not only in stimulus-TAs but also in spike-TAs computed from single cells at these sites. Some of these cells increased their activity during wrist extension (but had no detectable effect on the extensor muscles); others discharged during flexion. Several observations suggest that the cortically evoked suppression is mediated by polysynaptic relays. The mean onset latency of the postspike suppression (7.4 ms) produced by inhibitory cells was longer than the mean onset latency of postspike facilitation (6.7 ms) produced by CM cells. Similarly, the mean onset latency of poststimulus suppression (8.9 ms) was longer than that of poststimulus facilitation (8.0 ms). Moreover, suppression was usually weaker than facilitation in the spike-TAs, as well as in stimulus-TAs compiled for the same stimulus intensity.(ABSTRACT TRUNCATED AT 400 WORDS)     

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)     

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.     

Influence of globus pallidus on arm movements in monkeys. I. Effects of kainic acid-induced lesions

The role of basal ganglia output via the globus pallidus (GP) was examined in monkeys trained to make rapid arm-reaching movements to a visual target in a reaction-time task. When neurons in the globus pallidus were destroyed by injection of kainic acid (KA) during task execution, contralateral arm movement times (MT) were increased significantly, with little or no change in reaction times (RT). The slowed movements were associated with a generalized depression in the amplitude and rate of rise of electromyographic (EMG) activity in all the contralateral muscles studied at the wrist, elbow, shoulder, and back, but there was no change in the sequential activation of these muscles. The most profound and persistent increases in movement time occurred when neurons were destroyed in the ventrolateral and caudal aspects of the internal as well as external pallidal segment. These results suggest a role for globus pallidus output in scaling the magnitude and/or buildup of EMG activity without affecting the initiation or the sequential organization of the programmed motor output.     

Activity patterns of upper arm muscles in relation to direction of rapid wrist movement in man

Summary Adjustment of arm posture associated with rapid wrist movements was studied by EMG analysis. Seven healthy adults, seated and holding their right arm with the shoulder in a neutral position with the elbow in 90° flexion and the wrist position neutral, were instructted to flex or extend the wrist as fast as possible. To examine whether the activity patterns of the upper arm muscles were related to the prime mover or the direction of the movement in space, the forearm was in two postures, supinate and pronate. The surface EMGs of biceps brachii, brachialis, triceps brachii and the prime movers were recorded along with the angular displacement of the wrist. The sequences of the upper arm muscle activities changed in relation to the direction of the movement. The earliest activities of the upper arm muscles were considered to counteract the dynamic perturbation induced by the rapid wrist movement. The onsets of the earliest activity of the upper arm muscles preceded the movement onset by 50–60 ms. These results revealed that the activity patterns of the arm muscles associated with the rapid wrist movements were functionally compatible with the anticipatory postural adjustment and were controlled according to the direction of the movement in space.     

Vibration-induced changes in movement-related EMG activity in humans

The effect of muscle tendon vibration during voluntary arm movement was studied in normal humans. Subjects made alternating step flexion and extension movements about the elbow. A small vibrator was mounted over either the biceps or the triceps muscle and vibration was applied during flexion or extension movements. The vibrator was turned off between movements. After a period of practice, subjects learned the required movements and were able to make them with their eyes closed. Application of vibration to the muscle antagonist to the movement being performed produced an undershoot of the required end-movement position. The undershoot was 20-30% of the total movement amplitude. In contrast, vibration of the muscle agonist to the movement resulted in no change in movement end position. The vibration-induced undershoot was associated with an increase in the EMG activity of the vibrated (antagonist) muscle and a resultant increase in the ratio of the antagonist to agonist EMG activity. The increase in antagonist EMG produced by the vibration occurred with a latency of approximately 60 ms from vibration onset. The observed results are consistent with vibration-induced activation of muscle spindle receptors in the lengthening muscle during movement. It is suggested that, during movement, the sensitivity of the spindle receptors in the shortening muscle is decreased and the information concerning limb position during movement comes primarily from the lengthening muscle.     

Single cell studies of the primate putamen

The major goal of this study was to determine whether the activity of single cells in the primate putamen was better related to the direction of limb movement or to the underlying pattern of muscular activity. In addition, the neural responses to load application were studied in order to determine whether the same neurons were also responsive to somatosensory stimuli. Two rhesus monkeys were trained to perform a visuomotor arm tracking task which required elbow flexion/extension movements with assisting and opposing loads in order to dissociate the direction of elbow movement from the pattern of muscular activity required for the movement. Neurons in the putamen were selected for study only if they were related both to the task and to arm movements outside the task. Most (96%) of the cells studied responded to load application: 36% of these showed short-latency (less than 50 ms), "sensory" responses. Forty-four percent of neurons had significant relations to the level of static load as the animal held the arm stationary against the steady loads: in general, static load effects were relatively weak. During the elbow flexion/extension movements in the task, 76% of cells had significant relations to the direction of movement, and 52% of neurons had significant dynamic relations to the level of load. Half of all neurons studied were primarily related to the direction of movement independent of the load. Only thirteen percent of cells in the putamen had a pattern of activity similar to that of muscles. These results indicate that neuronal activity in the putamen is predominantly related to the direction of limb movement rather than to the activity of particular muscles and that the basal ganglia may play a role in the specification of parameters of movement independent of the activity of specific muscles. These results also indicate that the basal ganglia receive proprioceptive input which may be used in the control of ongoing movement.     

Sequential activation of neurons in primate motor cortex during unrestrained forelimb movement

We trained monkeys to perform an unrestrained, reaching movement of the arm. Electromyogram (EMG) recordings of forelimb muscles revealed sequential activation, proximal to distal, of muscle groups involved in the task. The delay in onset of EMG activity between proximal (shoulder and elbow) and distal (wrist and finger) muscles was approximately 60 ms. We identified the neurons in the forelimb area of the contralateral motor cortex as controlling particular joints by previously defined criteria involving responses to somatosensory stimulation and effects of intracortical microstimulation. Many cells discharged prior to the onset of EMG activity acting on the appropriate joint, whereas others began firing at a later phase of the movement. The population of all proximal cells altered discharge patterns approximately 60 ms earlier than the population of distal cells. A small percentage of cells showed an initial inhibitory change in discharge frequency, and this inhibition typically occurred prior to the excitatory changes seen in the majority of cells. The results are discussed in terms of the "nested-zone" model of the forelimb motor cortex. The data support one of the predictions of this model, namely that discharges of identified cells within the cortical zones are causally related to voluntary movement at appropriate forelimb joints.     

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.     

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.     

Complex-spike activity of cerebellar Purkinje cells related to wrist tracking movement in monkey

Four rhesus monkeys were trained to perform visually guided wrist tracking movements (50). While they performed tasks by wrist flexion or extension from a neutral position, simple-spike (SS) and complex-spike (CS) discharges of a single Purkinje cell (P-cell) were recorded from intermediate and lateral parts of cerebellar hemispheres (lobules IV to VI) ipsilateral to the task-performing wrist. Of approximately 400 P-cells observed, 215 (54%) significantly increased or decreased their SS discharge rate during task performance (task-related P-cells). Of these, 161 were selected for analysis of CS activity; in these P-cells, we could reliably discriminate between CS and background SS by a spike discriminator. The 161 P-cells were further classified into response locked (n = 65) and poorly locked (n = 96) cells according to temporal coupling of the SS frequency modulation to the onset of wrist movements. About 60% of the response-locked P-cells showed a phasic increase (statistical significance level: P less than 0.01) of CS firing rate at the onset of wrist tracking movement. In a few P-cells, a phasic decrease (statistically insignificant) of CS firing rate was observed with the wrist movement. In most P-cells, an increase of CS firing rate was observed with both rapid- and slow-tracking wrist movements. The increase was larger with faster step-tracking movement than with slower ramp-tracking movement. In most P-cells, the CS activity increased with both wrist flexion and extension; in some cells, however, it increased only with either flexion or extension. In most of the response-locked P-cells, the increase of CS firing rate occurred during motor time, i.e., after the onset of the EMG change in prime movers and before the beginning of wrist tracking movement. The increase occurred phasically at the onset and/or at the recovery phase of SS frequency modulation. At neutral wrist position, the maintained frequency of the CS was 0.72 +/- 0.29 CS/s (mean and SD for 161 task-related P-cells). Compared with the frequency at neutral position, the CS frequency did not change tonically during maintained flexed or extended wrist position in any response-locked P-cells. There was no increase of CS firing rate when the monkey returned the handle to center position after completing the tracking task, even in P-cells that had shown a significant increase of CS activity during tracking.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effects of unexpected perturbations on trajectories and EMG patterns of rapid wrist flexion movements in humans

To investigate how motor programs can be modified by sensory inputs we recorded kinematic and EMG patterns from normal human subjects performing well-practised wrist flexion movements in response to an auditory tone. On random trials unexpected wrist perturbations were introduced at varying times after the signal to move had been given. Extension perturbations delivered before agonist EMG onset resulted in an increased maximum velocity (MV) during the wrist flexion movement and in an increased target overshoot even though the wrist was further from the target than expected by the subject at the onset of the movement. The first agonist EMG burst and the antagonist burst were both increased in magnitude in these perturbed trials. Flexion perturbations delivered before the agonist EMG onset moved the hand nearer to the target just prior to movement onset. These resulted in a reduced MV, but the expected increased target overshoot did not occur. The first agonist burst was reduced in magnitude, and the antagonist burst was increased in magnitude. Perturbations delivered after agonist EMG onset produced less change in the first agonist and antagonist EMG burst, and less compensation for the perturbation was evident in wrist position and velocity recordings. These results indicate that, at least in some situations, motor programs for rapid voluntary movements can be modified by afferent inputs. This interaction between central motor commands and sensory feedback might occur at the cortical or spinal level, depending on when perturbations occur relative to onset of EMG and movement. The timing of the EMG changes suggest that both reflex mechanisms and longer latency 'voluntary' adjustments contribute to the compensatory changes in movement trajectory.     

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.     

Oscillatory activity in forelimb muscles of behaving monkeys evoked by microstimulation in the cerebellar nuclei

Coherent 20-35 Hz (beta) oscillations are a prominent feature of activity in primary motor cortex and muscles of monkeys and humans performing voluntary movements. We found that coherent beta oscillations are also present in the cerebellar nuclei (CN). Two monkeys were operantly conditioned to perform a wrist flexion/extension step-tracking task while we recorded neuronal activity or microstimulated in CN and recorded EMG activity from forelimb muscles. Coherent beta oscillations were found between discharges of some CN neurons and tonically active shoulder, elbow and wrist/finger flexion and extension muscles. Similarly, localized microstimulation pulses in CN evoked transient beta oscillations in widespread forelimb muscles. We conclude that coherent motor system beta oscillations are present in CN and that CN may be an important nodal point for the generation and/or propagation of beta oscillations throughout the motor system.     

Response of rubromotoneuronal cells identified by spike-triggered averaging of EMG activity in awake monkeys

Red nucleus neurons were recorded in awake monkeys during alternating ramp-and-hold wrist movements into flexion and extension position zones. Spike-triggered averages (STAs) of rectified EMG activity of wrist flexor and extensor muscles were computed to document effects of single RN cells on the activity of forelimb motoneurons. Some red nucleus cells produced a transient short-latency post-spike facilitation (PSF) of motor unit firing probability, indicative of underlying rubromotoneuronal (RM) connections. We, therefore, termed these RM cells. The discharge of wrist-related red nucleus cells was more strongly correlated with the dynamic than static component of wrist movement.     

The effect of muscle pain on elbow flexion and coactivation tasks

The effects of muscle pain on movement can easily be observed in daily life routines. However, the influence of muscle pain on motor control strategies has not been fully clarified. In this human experimental study it was hypothesized that muscle pain affects the motor control of elbow flexion movements, in different combinations of range of motion and target size, by decreased agonistic muscle activity and increased antagonistic muscle activity with consequent implications on kinematic parameters. The effects of experimentally induced muscle pain on movement strategy for: (1) small and large range of motion (ROM) elbow flexion movements towards a wide target, (2) large ROM flexion movements towards a narrow and wide target, and (3) subsequent coactivation of agonistic and antagonistic muscles to elbow flexion were assessed. Muscle pain induced by injections of hypertonic saline (1 ml, 5.8%) in either m. biceps brachii or m. triceps brachii caused similar effects on the movements. For low accurate movements the initial (100 ms) integrated electromyographic (EMG) activity of m. biceps brachii was decreased during muscle pain. In contrast, integrated EMG of the entire m. biceps brachii burst was decreased by muscle pain only for small ROM at a low accuracy, which also showed decreased EMG activity of m. triceps brachii and m. brachioradialis, together with increased activity of m. trapezius. Finally, high accurate movements and post-movement coactivation were generally not modulated by muscle pain. In summary, the present study shows that acute muscle pain can perturb the motor control strategy, which might be highly important in occupational settings where such a change may need compensatory actions from other muscles and thereby eventually contribute to the development of musculoskeletal pain problems.     

Striatal neuronal activity during the initiation and execution of hand movements made in response to visual and vibratory cues

Summary Recordings were obtained from 146 neurons in the neostriatum of rhesus monkeys while they performed wrist movements in response to visual and vibratory cues. Of these, 75 putamen and 29 caudate neurons exhibited changes in firing rate that were temporally related to the onset of the wrist movements and that began prior to movement onset. This premovement activity (PMA) usually was directionally specific, in that the magnitude or direction of change in firing rates was different during flexion trials as compared to trials involving wrist extension. PMA onset usually preceded movement onset by more than 100 ms and in most instances preceded the average onset of task-related changes in electromyographic (EMG) activity in muscles of the wrist and forelimb. For most neurons. the changes in neuronal activity that began prior to movement were maintained during movement execution. However, approximately one-third of the neurons that exhibited PMA changed their firing rate in the opposite direction, relative to their PMA and to their baseline rate of activity, once the movement began. Several other neurons either exhibited PMA only or they altered their discharge rates during movement execution but did not exhibit PMA. These observations suggest that, despite the close temporal relationship between the onset of PMA and the onset of wrist movement, the neuronal mechanisms mediating the PMA may differ from those that occur during movement execution. The PMA onset of neostriatal neurons occurred earlier in visually cued than in vibratory cued trials. These differences were statistically significant only for flexion trials, however, in which movements were made against a load and in the same direction as the palmar vibratory stimulus. For trials involving wrist extension, PMA onsets for visually cued as compared with vibratory cued trials were not statistically different. These findings contrast with data obtained previously from somatosensory cortical neurons during performance of the same behavioral task. On average, PMA in the putamen began earlier, relative to movement onset, than it did in the somatosensory cortex. Moreover, in the somatosensory cortex, PMA onset occurred earlier in vibratory cued than in visually cued trials, irrespective of movement direction (Nelson 1988; Nelson and Douglas 1989). For putamen neurons, but not for caudate or cortical neurons, the onset of PMA also occurred significantly earlier during extension trials than flexion trials, irrespective of the modality of the go-cue. These modality-dependent and direction-dependent differences in the PMA onset of neostriatal neurons may reflect the responsiveness of these neurons to somatosensory inputs (e.g., load conditions and vibratory stimulation) that were associated with the behavioral task. These data confirm observations made by other investigators that a substantial proportion of neurons in the putamen exhibit movement-related changes in discharge rate that are initiated prior to task-related changes in EMG activity, and they further suggest that this PMA may be initiated sufficiently early to influence even the earliest task-related activity of cortical neurons.     

Movement discrimination by single cells in the human pallidum characterised by hidden Markov models

In patients undergoing pallidotomy for Parkinson's disease, we recorded extracellularly from single neurons in the two internal segments (GPii, GPie) and the external segment (GPe) of the globus pallidus (GP) in response to active (cued) movements of the contralateral wrist, elbow or ankle. The patterns of cell activity occurring both before and after movement onset were analysed using hidden Markov models (HMMs) and clustered by movement type using the generative topographical mapping algorithm. Cluster separation was quantified in order to measure a cell's ability to discriminate between movements. Statistical analysis of variance indicated a significant regional gradient (GPii > GPie > GPe) of movement discrimination, while cells in all regions differentiated better between movements of different joints (wrist, elbow or ankle) than between flexion and extension of the same joint. We found that GP cells generally showed distinguishable firing patterns corresponding to more than one type of movement per cell, in support of the hypothesis that cells in these regions of the basal ganglia are not involved in preparation or execution of a single type of movement but participate in many different movements, analogous to the hidden units of a neural network. Our results also indicate that cell activity both preceding a movement and during its execution may be modelled by HMMs with only a small number of states.