Step-tracking movements of the wrist in humans. II. EMG analysis

We asked human subjects to make accurate step-tracking movements of the wrist to targets that required 5 degrees-30 degrees of radial or ulnar deviation. Speed instructions were given prior to each trial. Muscle activity was recorded from extensor carpi radialis longus (ECRL) and extensor carpi ulnaris (ECU) using surface electrodes. The agonist muscle initiated each movement with a brief burst of activity which began approximately 45 msec before movement onset. Then, the antagonist muscle displayed a brief burst of activity which began approximately 10 msec after movement onset. The magnitude, but not the timing, of these bursts was modulated by changes in the task requirements. The area of the initial agonist burst varied with changes in both displacement and intended speed. This burst was most highly correlated with the initial peaks of acceleration and jerk. In contrast, the area of the initial antagonist burst varied with changes in intended speed and was less well modulated by changes in displacement. This burst was highly correlated with the reciprocal of movement duration. Some small, fast movements had the same agonist bursts as some large, slow movements. However, the antagonist bursts for these movements differed greatly. This observation provides clear evidence that the magnitudes of the agonist and antagonist bursts are independently controlled. In a prior paper (Hoffman and Strick, 1986b), we proposed that step-tracking movements of different amplitudes and intended speeds are centrally generated by adjusting 2 kinematic variables: (1) the peak value and (2) the duration of a derivative of displacement. The present results suggest that these 2 kinematic parameters are separately generated by independently modulating the magnitudes of the agonist and antagonist bursts. Thus, the peak displacement of a step-tracking movement must be determined by the appropriate adjustment of both bursts of muscle activity.     

Disturbances in human arm movement trajectory due to mild cerebellar dysfunction.

The temporal structure of arm movements was studied in nine cerebellar patients with mild impairment of the upper limbs and in six age-matched control subjects. The experimental paradigm consisted of visually guided, step tracking movements about the elbow. Movements ranged from 10 degrees to 70 degrees in amplitude and were made under different instructions (fast, fast/accurate, accurate). As in normal subjects, cerebellar patients were able to scale peak velocity with movement amplitude. This relationship was highly linear under all instruction conditions. Similar relationships existed between movement duration and amplitude. In contrast to normal subjects who produced movements with nearly symmetric velocity profiles, movements made by cerebellar patients were characterised by short acceleration and long deceleration durations. The degree of asymmetry was directly related to movement duration but was unaffected by movement peak velocity. Acceleration durations did not increase beyond 300 ms even in movements lasting up to 1s. These findings demonstrate that, despite little or no obvious impairment of the limb during routine examination, the temporal structure of voluntary movements in cerebellar patients is clearly disturbed. This supports the view that the production of an optimal movement trajectory is under cerebellar influence.     

Effects of expected perturbations on the velocity control of fast arm abduction movements

A triphasic electromyographic pattern of sequential activation of agonist, antagonist, and again agonist muscles underlies rapid or ballistic limb movements in humans. The first agonist burst reflects muscular force accelerating the limb, the antagonist burst is mainly related to the braking process of movement, while the second agonist burst is considered a reactive adjustment to the deceleration. The duration of the first agonist burst has been reported to be constant for movements of different amplitudes, thus suggesting that only changes in its amplitude contribute to the velocity control of movement. The present research has been undertaken to investigate the strategy whereby the nervous system increases agonist impulsive force for ballistic performance in response to experimental conditions requiring perceptual and/or provisional processes related to expected changes in load or accuracy constraints. The effects of expected perturbations of different strengths on some kinematic and electromyographic variables of fast arm abduction movements performed in a step-tracking task and in an outer-stop terminated task were analyzed in normal subjects. All motor performances were characterized by triphasic electromyographic patterns. In the absence of expected perturbations, the mean velocity of the movements was markedly higher in the outer-stop terminated task. Correspondingly, greater amplitudes and durations of the first agonist burst were observed. In both types of motor tasks, when expected perturbations were inserted, the velocity of the movement increased as well as the amplitude and the duration of the first agonist burst. These results, in agreement with previous observations, indicate that the normal mechanism, whereby the nervous system increases agonist impulsive force in rapid movements, comprises changes not only in the amplitude but also in the duration of the first agonist burst.     

Premovement silence in agonist muscles preceding maximum efforts

Electromyographic silent periods (premovement silence) preceding the initial agonist burst were studied in 11 healthy subjects who performed rapid forearm flexions and extensions. Premovement silence occurred with higher frequency during self-paced movements when subjects produced maximum power efforts than during a reaction time paradigm. The occurrence and duration were significantly correlated with the peak acceleration of the movement. Premovement silence occurred specifically in those muscles involved in the intended movement, often in several synergists with different latencies and durations. The shortest latency of premovement silence was considerably briefer than that of the earliest voluntary increase in EMG. The findings suggest that premovement silence may increase peak muscular force by bringing motoneurons into a nonrefractory state prior to their activation. The fact that it occurred on some, but not all, trials within single subjects and had a variable duration from trial to trial suggests that it may be a learned, rather than automatic, motor response.     

Fast voluntary neck movements in patients with cervical dystonia: a kinematic study before and after therapy with botulinum toxin type A.

OBJECTIVE: To study fast voluntary neck movements in patients with cervical dystonia (CD) before and after therapy with botulinum toxin type-A (BTX-A). METHODS: A selected sample of 15 patients with CD (with prevalent torticollis) and 13 age-matched control subjects performed both right and left rotational, and flexion and extension neck movements as fast as possible. Movements were recorded with a motion analysis system (SMART, BTS). Movement time, angular amplitude, and peak angular velocity were analyzed. In patients, rotational neck movements were pooled as "pro-dystonic" (toward the dystonic side) and "anti-dystonic" (toward the non-dystonic side). Results obtained in patients before BTX-A treatment were compared with those of control subjects. The effect of BTX-A treatment was evaluated by comparing movement performance before and after treatment. RESULTS: Before receiving BTX-A, patients performed pro- and anti-dystonic movements with lower peak angular velocity than control subjects. Pro-dystonic movements had a reduced angular amplitude. Anti-dystonic movements showed an abnormally long movement time. Flexion and extension movements required longer movement times, but the other kinematic variables were normal. After BTX-A injections, pro-dystonic movement amplitude and anti-dystonic movement peak angular velocity increased, whereas flexion and extension movements remained unchanged. CONCLUSIONS: Before BTX-A injection patients with CD perform fast voluntary neck movements abnormally and BTX-A injections improved their peak velocity and amplitude. SIGNIFICANCE: Kinematic studies can detect specific neck movement disturbance in patients with CD, and can quantify both the severity of clinical picture and the effect of BTX-A injections in these patients.     

Could bradykinesia in Parkinson's disease simply be compensation?

Even normal movements can be slow and hesitant. To distinguish between bradykinesia and the simple slow inefficiency sometimes seen in normal movement, we matched the movement durations of 12 patients with Parkinson's disease (PD) and 12 age-matched controls and examined end-point accuracy, number of submovements, force inefficiency, and relative duration of acceleration and deceleration phases of movement. Subjects used an electronic pen which sampled pen-tip position at 200 Hz, and performed a sequence of drawing movements to nine targets (0.5, 1, or 2 cm diameter) upon a WACOM SD420 graphics tablet. Patients could be trained to move at the preferred speed of controls (and vice versa). When moving at the same fast speed as controls, patient's movements were less accurate (increased end-point spread). Even when moving at their own preferred speed, patients' movements were less efficient (more submovements, more zero crossings in acceleration function) than controls moving at the same speed. If bradykinesia simply reflected increased caution and visual guidance, we would expect patients to exhibit prolongeddecelerative phases of movement associated with terminal guidance. However, patients consistently required prolongedaccelerative phases of movement, suggesting that there was a problem in generating appropriate movement forces to produce the required end-point accuracy. It is hypothesised that bradykinesia is not simply a compensation for defective preparatory processes, but may reflect a defective internal cue in PD which disrupts and impairs the outflow of motor responses.     

Interaction between eye and hand movements in multiple sclerosis patients with intention tremor.

Deficient eye and hand movements are present in patients with multiple sclerosis. In the present study, eye and hand movements were simultaneously measured during visually guided wrist step-tracking tasks in 16 patients with intention tremor and 15 healthy controls. The coupling between eye and hand movements was analyzed during simultaneous eye-hand tracking, and interactions were studied by comparing the coordinated eye-hand condition with isolated eye- or hand-tracking conditions. Despite movement abnormalities, the onset of eye and hand movements was highly correlated and an invariant coupling between the saccadic completion time and hand peak velocity was found, suggesting that the temporal coupling was very much preserved. The differences between the experimental tracking conditions suggest that, in MS patients with intention tremor, the ocular system influenced the hand movements. Intention tremor amplitude was reduced when there was no preceding saccadic eye movement, whereas conversely, eye movements were not affected by different hand tremor severity.     

Effect of medication on EMG patterns in individuals with Parkinson's disease.

Individuals with Parkinson's disease show dramatic improvements in their ability to move when medicated. However, the neural cause of this improvement is unclear. One hypothesis is that neural activation patterns, as measured by surface electromyography (EMG), are normalized by medication. We tested this hypothesis by investigating the effect of medication on the electromyographic (EMG) patterns recorded when individuals with idiopathic Parkinson's disease performed elbow flexion movements over three movement distances while off and on antiparkinsonian medication. When the subjects were off medication, they lacked the ability to modulate the agonist EMG burst duration with changes in movement distance. The ability to modulate agonist EMG burst duration is characteristic of the EMG patterns observed in healthy subjects. Also, multiple agonist bursts were exhibited during the acceleration phase. As expected, medication diminished the clinical signs of Parkinson's disease, increased movement speed, and increased the magnitude of the first agonist burst. Medication did not restore agonist burst duration modulation with movement distance, did not change the frequency of agonist bursting, and did not alter the timing of the antagonist activation. These results show that medication does not alter the temporal profile of EMG activation.     

Temporal movement control in patients with Parkinson''s disease.

Patients with Parkinson's disease (PD) have been reported to be unable to modify their movement velocity to adapt to changing environmental demands. For example, when movement amplitude is varied, PD patients usually exhibit a nearly constant peak velocity, whereas elderly subjects show an increase of their peak velocity with increased amplitude. The experiment examined the ability of PD patients to vary the duration of their movement (four different percentages of their maximum) under conditions where temporal, but not spatial, control was emphasised. PD patients had longer movement times than control subjects, but were able to vary the duration of their movement with comparable temporal accuracy to that of elderly subjects. For both groups, the agonist EMG activity increased with decreased movement duration. For the PD patients, the number of agonist bursts increased with increased movement duration.     

Jaw movement dysfunction related to Parkinson's disease and partially modified by levodopa.

OBJECTIVES--To test the hypotheses that Parkinson's disease can differentially produce deficits in voluntary and rhythmic jaw movements, which involve different neuronal circuits, and that levodopa treatment improves specific components of the motor deficit. METHODS--Patients with idiopathic Parkinson's disease and control subjects were tested on a series of jaw motor tasks that included simple voluntary movement, isometric clenching, and natural and paced rhythmic movements. Jaw movements were measured by changes in electromagnetic fields and EMG activity. Patients with Parkinson's disease with fluctuations in motor responses to levodopa were tested while off and on. RESULTS--During the off state, patients with Parkinson's disease were significantly worse than the control subjects on most tasks. The deficits included a decrease in amplitude and velocity during jaw opening and closing, aberrant patterns and low amplitude of EMG activity during clenching, and low vertical amplitude and prolonged durations of occlusion during rhythmic movements. No decrements were found in the amplitude of voluntary lateral jaw movements or the frequency of rhythmic movements. During the on state, improvements occurred in the patterns and level of EMG activity during clenching and in the vertical amplitude and duration of occlusion during rhythmic movements, although a significant decrement occurred in the lateral excursion of the jaw. CONCLUSIONS--Parkinson's disease affects the central programming of functionally related muscles involved in voluntary and rhythmic jaw movements and levodopa replacement influences only certain aspects of jaw movement, most likely those requiring sensory feedback.     

The coordination of arm movements: an experimentally confirmed mathematical model

This paper presents studies of the coordination of voluntary human arm movements. A mathematical model is formulated which is shown to predict both the qualitative features and the quantitative details observed experimentally in planar, multijoint arm movements. Coordination is modeled mathematically by defining an objective function, a measure of performance for any possible movement. The unique trajectory which yields the best performance is determined using dynamic optimization theory. In the work presented here, the objective function is the square of the magnitude of jerk (rate of change of acceleration) of the hand integrated over the entire movement. This is equivalent to assuming that a major goal of motor coordination is the production of the smoothest possible movement of the hand. Experimental observations of human subjects performing voluntary unconstrained movements in a horizontal plane are presented. They confirm the following predictions of the mathematical model: unconstrained point-to-point motions are approximately straight with bell-shaped tangential velocity profiles; curved motions (through an intermediate point or around an obstacle) have portions of low curvature joined by portions of high curvature; at points of high curvature, the tangential velocity is reduced; the durations of the low-curvature portions are approximately equal. The theoretical analysis is based solely on the kinematics of movement independent of the dynamics of the musculoskeletal system and is successful only when formulated in terms of the motion of the hand in extracorporal space. The implications with respect to movement organization are discussed.     

Ballistic and corrective movements on an aiming task. Intention tremor and parkinsonian movement disorders compared.

Six patients with Parkinson's disease, six patients with essential or intention tremor, and nine controls were tested on a step-tracking task using a joystick control and oscilloscope display. Tremor subjects resembled controls in making an initial ballistic movement followed by (defective) corrections, and took longer than the controls to reach the target with small amplitude jumps, but not with larger ones. The reverse was true for parkinsonian subjects, who acquired the target with slow corrective movements only. This suggests that two kinds of movement available to normal people are selectively impaired in these disorders; ballistic movements in Parkinson's disease and small amplitude corrective movements in the other disorders.     

Monkey pyramidal tract neurons and changes of movement parameters in visual tracking

During a single-step visual tracking task of monkeys, parametric changes of the wrist extension-flexion movement and related discharge rate changes of pyramidal tract neurons (PTNs) of hand-arm motor area were studied. The task consisted of preparatory, precontraction, contraction and target periods. If the displacement amplitude was changed from narrow (10–20°) to moderate (40°) range, peak velocity, peak acceleration and contraction period increased linearly but precontraction period decreased slightly. In 61 movement-related PTNs, no linear relationships were found between PTN discharge rate during precontraction or contraction period and displacement amplitude, velocity, acceleration, precontraction period or contraction period. In less than 20% of PTNs, however, correlations between PTN discharge rate during precontraction period and velocity or acceleration were found in the moderate range task. It occurred less frequently in narrow range task. It is said in a visual tracking task that PTN activity is not dependent upon factors related to the task parameters, such as velocity, acceleration. Possible related factors were discussed.     

Theta‐burst stimulation over primary motor cortex degrades early motor learning

Theta‐burst stimulation (TBS) is currently used for inducing long‐lasting changes in primary motor cortex (M1) excitability. More information is needed on how M1 is involved in early motor learning (practice‐related improvement in motor performance, motor retention and motor consolidation). We investigated whether inhibitory continuous TBS (cTBS) is an effective experimental approach for modulating early motor learning of a simple finger movement in healthy humans. In a short task, 11 subjects practised 160 movements, and in a longer task also testing motor consolidation ten subjects practised 600 movements. During both experiments subjects randomly received real or sham cTBS over the left M1. Motor evoked potentials were tested at baseline and 7 min after cTBS. In the 160‐movement experiment to test motor retention, 20 movements were repeated 30 min after motor practice ended. In the 600‐movement experiment motor retention was assessed 15 and 30 min after motor practice ended, motor consolidation was tested by performing 20 movements 24 h after motor practice ended. Kinematic variables – movement amplitude, peak velocity and peak acceleration – were measured. cTBS significantly reduced the practice‐related improvement in motor performance of finger movements in the experiment involving 160 movements and in the first part of the experiment involving 600 movements. After cTBS, peak velocity and peak acceleration of the 20 movements testing motor retention decreased whereas those testing motor consolidation remained unchanged. cTBS over M1 degrades practice‐related improvement in motor performance and motor retention, but not motor consolidation of a voluntary finger movement.     

Parkinsonian arm movements as altered by task difficulty

A discrete elbow movement to targets with different indexes of difficulty (ID) was used to determine the kinematic organization of arm movements in a young, an elderly and a Parkinson's disease (PD) group (n = 14). Target size and movement amplitude changes led to expected modifications of the kinematics in all three groups according to Fitts' law. Increased task demands by changing target size produced not only differences between the age-groups, but affected the modulation of velocity and acceleration in the parkinsonian patients differentially. For large amplitude movements, the PD patients were less able to increase velocity and acceleration magnitudes when target accuracy constraints were reduced. These findings, when taken together with the observation that speed scaling was preserved for small movement amplitudes, suggest that a reduced capability to initiate and regulate force is the cause for the observed slowness in PD.     

Impairment of individual finger movements in Parkinson's disease.

By analyzing the kinematics of repetitive, constant-amplitude, finger oppositions, we compared the impairment of individual and nonindividual finger movements in patients with Parkinson's disease. In one task, subjects tapped only the index finger against the thumb (individual oppositions); in the other task, they tapped all four fingers together against the thumb pad (nonindividual oppositions). We used an optoelectronic motion analysis system to record movements in three-dimensional space and recorded three 5-second trials for each task. We counted how many finger oppositions subjects performed during each trial and measured the duration and amplitude of the flexions and extensions. We also calculated the duration of the pauses after flexion and extension. We assessed the deterioration of motor performance in patients by investigating the changes in speed and amplitude with task completion. During both tasks, normal subjects and patients performed finger flexions faster than extensions, and they invariably paused longer after flexion than after extension. Patients performed individual and nonindividual finger movements slowly and with reduced amplitude. Patients were disproportionately slow during flexion and in switching from flexion to extension. Movement slowness increased as finger oppositions progressed but predominantly when patients had to move fingers individually. In conclusion, in patients with Parkinson's disease, the motor performance deteriorated with task completion more during individual than during nonindividual finger movements. Parkinson's disease, therefore, impairs individual finger movements more than gross hand movements. This distinction reflects the finer cortical control needed to promote and sustain this highly fractionated type of motor output.     

Movement amplitude choice reaction time performance in Parkinson''s disease may be independent of dopaminergic status.

The effect of circulating levels of plasma levodopa on reaction time performance was studied in patients with Parkinson's disease and untreated normal controls when instructed to move either a shorter or longer distance. On half the movements, subjects were pre-cued on the direction and amplitude of an impending movement. On the remaining movements, only the direction was pre-specified, and the amplitude was determined only when the cue to move was presented. Reaction time performance of patients was evaluated at three infusion levels of levodopa so that the patients were optimally, moderately, or minimally medicated. Parkinsonian patients were always slower to react and move than normal subjects. Clinical state correlated with movement time, but not with reaction time. These results contrast with those in which reaction time was related to plasma levodopa levels when movement direction and initiation were processed concomitantly, but the movement amplitude was pre-cued. It is possible that specification of the amount of muscle activity is partially independent of dopaminergic transmission.     

Cerebellare Bewegungsstörungen im Tierversuch

The effects of short reversible cooling of the dentate nucleus in two groups of 3 and 4 cebus monkeys, with two different types of ipsilateral elbow movements, have been studied. One group was trained to turn a moving handle back and forth rapidly between two mechanical stops, while the second group was trained to move the handle between two target zones. Brief blocking of the dentate nucleus caused a delayed termination of contraction of the agonistic muscles (hypermetria) near the mechanical stop for very rapid, ballistic, alternating arm movements and, consequently, delayed initiation of the antagonistic return movement. The resulting increase of the duration of a single movement was not caused by a reduction of the peak acceleration of the movement. For the slower target movements, dentate nucleus cooling caused shortening of agonistic muscular contraction (hypometria) with corresponding, saccadic movement corrections. The frequency of the "movement tremor" lay between 3 and 5 Hz. The average velocity maxima during dentate cooling did not change. The findings indicate that different types of movements exhibit different disturbances of the movement pattern during the period of functional elimination of the same anatomical structure. The results indicate that the dentate nucleus and cerebellar hemispheres take part in preprogramming movement duration (Kornhuber) for rapid ballistic movements. In slower target movements, the dentate nucleus may be involved in sectional preprogramming of step movements.     

Physiological analysis of simple rapid movements in patients with cerebellar deficits.

Patients with cerebellar deficits made elbow flexion movements as rapidly as possible for three different angular distances. Electromyographic activity of biceps and triceps and the kinematics of the movements were analysed. Results were compared with those of normal subjects making both rapid and slow movements. In the patients, the first agonist burst of the biceps was frequently prolonged regardless of the distance or speed of the movement. The most striking kinematic abnormality was prolonged acceleration time. The pattern of acceleration time exceeding deceleration time was common in patients but uncommon in normal subjects. The best kinematic correlate of the duration of the first agonist burst was acceleration time. Altered production of appropriate acceleration may therefore be an important abnormality in cerebellar dysfunction for attempted rapid voluntary movements.     

The relation between EMG activity and kinematic parameters strongly supports a role of the action tremor in parkinsonian bradykinesia.

The kinematics characteristics of an upper arm extension of large amplitude (90 degrees) performed in the horizontal plane and the simultaneous activity of the shoulder muscles were recorded in 12 parkinsonian patients and in six normal control subjects. The movement, triggered by an acoustic "go" signal, was preceded by an isometric adduction. Within the whole population of individuals (n = 18) a strong, positive correlation was observed between the root mean square value of agonist EMG activity, evaluated during the acceleration phase of the movement, and both peak velocity and acceleration. In six patients tremor bursts at the frequency of 8-14 Hz (action tremor) were observed during the movement phase in the anterior, middle, and posterior deltoid: all these patients showed low root mean square values and were bradykinetic with respect to the control subjects. The remaining six patients did not show this action tremor during the movement phase. All but one had an agonist activation of normal duration and amplitude, showed high root mean square values, and performed well in the range of control subjects. We conclude that the inability to suppress the activity of pathological oscillator(s) responsible for the action tremor plays a fundamental role in the bradykinesia associated with Parkinson's disease.