Agonist Burst Research Articles

EMG remains fractionated in Parkinson's disease, despite practice-related improvements in performance.

We studied the ability of patients with Parkinson's disease to improve their performance in a motor task requiring both speed and accuracy in the execution of elbow flexion movements. Our goal was to investigate the changes in electromyographic activity associated with the changes in movement performance. Eleven patients on anti-Parkinsonian medication were tested. The patients were selected for being bradykinetic, having little or no resting tremor or dyskinesias, and being in stages II or III of the Hoehn and Yahr rating scale. The untrained patients displayed multiple bursts of agonist activity, characteristic of Parkinsonian EMG recordings. All patients improved their performance by increasing peak velocity while maintaining movement accuracy within strict boundaries. With practice, the patients' performance changed in a manner similar to that which has been previously observed for performance curves in neurologically normal subjects. As movement duration decreased (i.e. peak velocity increased), we observed a slight decrease in the number of agonist bursts and an increase in the average burst duration. However, the patients continued to generate a fractionated, multi-burst agonist pattern. We conclude that Parkinsonian patients benefit from practice by improving their performance but remain fundamentally impaired in the generation of muscle activation patterns. This study has shown that the generation of fractionated, multiple short bursts of EMG activity that is characteristic of movements made by Parkinsonian patients is not normalized by practice.

Neural factors underlying reduced postural adaptability in children with cerebral palsy.

This study aimed to test mechanisms underlying impairments in balance control in children with cerebral palsy. We hypothesized that balance loss during large/fast perturbations could be due to reduced contraction of agonist muscles, delay in muscle contraction or simultaneous contraction of antagonist muscles, reducing the efficiency of the agonist burst. Electromyograms were recorded as children recovered from balance threats of varying magnitudes/velocities. In typically developing children muscle response magnitudes increased with larger/faster perturbations, while in children with cerebral palsy they did not. There was no difference in muscle onset latency or antagonist co-contraction between groups. Thus the primary constraint on balance recovery in these children is insufficient levels of contraction of agonist postural muscles.

Essential tremor and cerebellar dysfunction: abnormal ballistic movements

Background: Clinical characteristics reminiscent of cerebellar tremor occur in patients with advanced essential tremor. Ballistic movements are known to be abnormal in cerebellar disease. The hypothesis was proposed that ballistic...

Electromyographic responses to an unexpected load in fast voluntary movements: descending regulation of segmental reflexes.

This study examined the effects of unexpected loading on muscle activation during fast goal-oriented movements. We tested the hypothesis that the electromyographic (EMG) response to an unexpected load occurs at a short latency after the difference between the expected and the unexpected movement velocity exceeds a fixed threshold. Subjects performed two movement tasks as follows: 1) 30 degrees fast elbow flexion movement with an inertial load added by a torque motor; and 2) 50 degrees fast elbow flexion movement with no added load. These movement tasks were chosen to have similar timing parameters, such as movement time, time-to-peak velocity, and duration of the first agonist burst, while the magnitudes of the angular displacement, velocity, and acceleration were different. In task 1, in random trials a viscous load was substituted for the inertial load at movement onset. In task 2, the same viscous load was added in random trials. The earliest consistent response to the unexpected load was detected in the agonist (biceps) EMG at the same time, about 200 ms from the EMG onset, in both tasks. However, the velocity errors were different in the two tasks and no velocity error threshold dependency could be found. Therefore we reject the hypothesis that the timing of the EMG response to an unexpected load is related to a velocity error threshold. Instead, we suggest that the timing of the EMG response is primarily determined by descending regulation of segmental reflex gain.

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.

Fatigue induced changes in phasic muscle activation patterns for fast elbow flexion movements.

The present study investigated how muscle fatigue influences single degree-of-freedom elbow flexion movements and their associated patterns of phasic muscle activation. Maximal unfatigued voluntary isometric elbow flexor and extensor joint torque was measured at the beginning of the experiment. Subjects then performed elbow flexion movements over two distances as fast as possible, and movements over the longer distance at an intentionally slower speed. The slower speed was close to what would become the maximal speed in the fatigued state. Subjects then performed a fatiguing protocol of 20 sustained isometric flexion contractions of 25 s duration with 5 s rest at 50% maximal unfatigued voluntary force. After a recovery period they repeated the movements. The fatigue protocol was successful in inducing muscle fatigue, the evidence being decreased isometric maximal joint torque of over 20%. Fatigued movements had lower peak muscle torque and speed. Our principal finding was of changes in the timing of the phasic patterns of fatigued muscle activation. There was an increase in the duration of the agonist burst and a delay in the timing of the antagonist muscle as measured by the centroid of the EMG signals. We conclude that these changes serve as partial but incomplete, centrally driven compensation for fatigue induced changes in muscle function. An additional, unexpected finding was how small an effect fatigue had on movement performance when using a recovery time of 10 min that is long enough to allow muscle membrane conduction velocity to return to normal. This raises questions concerning the behavioral significance of classical laboratory studies of human fatigue mechanisms.

Control of movement distance in Parkinson's disease

Studies of electromyographic (EMG) patterns during movements in Parkinson's disease (PD) have often yielded contradictory results, making it impossible to derive a set of rules to explain how muscles are activated to perform different movement tasks. We sought to clarify the changes in modulation of EMG parameters associated with control of movement distance during fast movements in patients with PD. Specifically, we studied surface EMG activity during rapid elbow flexion movements over a wide range of distances (5-72 degrees) in 14 patients with relatively mild symptoms of PD and 14 control subjects of similar age, sex, height, and weight. The PD group exhibited several changes in EMG modulation including impaired modulation of agonist burst duration; increased number of agonist bursts; reduced scaling of agonist EMG magnitude in the more severely impaired subjects; and increased temporal overlap of the antagonist and agonist signals in the most severely impaired subjects. These findings suggest that progressive motor dysfunction in PD is accompanied by increasing deficits in modulating muscle activation. These results help clarify previous disparate and sometimes contradictory results of EMG patterns in subjects with PD.

Influence of Strategy on Muscle Activity During Impact Movements

Participants (N = 10) made flexions or extensions about the elbow. Movements either were pointing (i.e., self-terminated) or terminated by impact on a barrier. The author examined how the trajectory and the electromyographic (EMG) patterns varied according to the distance moved, the instruction provided concerning speed, or the type of termination. Variations in kinematics induced by changes in the target distance or the instruction regarding speed were the same for impact and pointing movements. In comparison with a pointing movement of similar distance and speed instruction, an impact movement (a) accelerated longer and reached a higher velocity, (b) had a longer agonist EMG burst, and (c) had a low level of contraction that started slightly after the agonist burst and continued throughout the movement but had little or no antagonist burst. Because the different types of movements required different forces from the muscles, there were systematic, task-specific differences in EMG patterns that reflected task-specific differences in central control. The results of this experiment demonstrate that impact movements share some of the rules used in the control of other tasks, such as pointing and reversing movements. The sharing is not imposed by mechanical or physiological constraints but, rather, represents the imposition of internal constraints.

Neuromuscular Control Mechanisms and Strategy in Arm Movements of Attempted Supranormal Speed

Rapid, goal-directed elbow flexion movements were examined under interacting conditions of inertial loading and resistance to movement initiation. The resistance ceased when movement began, resulting in quick release movements. Inertial load slowed the movement and lengthened the agonist and antagonist electromyographic (EMG) burst durations. The quick release resulted in larger accelerations but only minimal changes in peak velocity. Most aspects of the triphasic EMG pattern were little affected by the quick release, but the build up of agonist EMG and the corresponding rate of static force development differed markedly between load and quick release conditions. These and other data suggest that the specific pattern of agonist muscle activation is set according to neuromuscular constraints of the antagonist muscle and the expectation of movement dynamics.

The time course of changes in motor cortex excitability associated with voluntary movement.

The excitability of the motor cortex is modulated before and after voluntary movements. Transcranial magnetic stimulation studies showed increased corticospinal excitability from about 80 and 100 ms before EMG onset for simple reaction time and self-paced movements, respectively. Following voluntary movements, there are two phases of increased corticospinal excitability from 0 to approximately 100 ms and from approximately 100 to 160 ms after EMG offset. The first phase may correspond to the frontal peak of motor potential in movement-related cortical potentials studies and the movement-evoked magnetic field I (MEFI) in magnetoencephalographic (MEG) studies, and likely represents a time when decreasing output from the motor cortex falls below that required for activation of spinal motoneurons, but is still above resting levels. The second phase of increased corticospinal excitability may be due to peripheral proprioceptive inputs or may be centrally programmed representing a subthreshold, second agonist burst. This may correspond to the MEFII in MEG studies. Corticospinal excitability was reduced below baseline levels from about 500 to 1,000 ms after EMG offset, similar to the timing of increase in the power (event-related synchronization, ERS) of motor cortical rhythm. Similarly, motor cortex excitability is reduced at the time of ERS of motor cortical rhythm following median nerve stimulation. These findings support the hypothesis that ERS represents an inactive, idling state of the cortex. The time course of cortical activation is abnormal in movement disorders such as Parkinson's disease and dystonia, reflecting abnormalities in both movement preparation and in cortical excitability following movement.

Load-dependent muscle strategy during plantarflexion in humans

This study analyses the relative contribution of the triceps surae and tibialis anterior (TA) muscles to tension development with reference to voluntary plantarflexion at two articular positions of the knee joint (extended and flexed at 90°) for various inertial loads. Subjects were instructed to perform plantarflexions at various sub-maximal and maximal velocities with no intention of stopping the movement. Whereas in one series of experiments the subjects were informed of the load countering the movement, in the other they were not. The average electromyographic (EMG) activity of the different muscles was recorded. The main results were that with loading: (a) greater maximal plantarflexion velocities were recorded in flexed as compared to extended-knee positions; (b) greater durations and amplitudes of agonist and antagonist EMG bursts were recorded; (c) the co-activation of the TA and triceps surae muscles was enhanced; (d) unexpected sub-maximal loads induced greater EMG activity and speed of movement. It is concluded that increasing the load during plantarflexion in humans brings about changes in neuromuscular strategies that contribute to the efficiency of contractile activity during rapid movements. The results also indicate that unexpected sub-maximal loading induces a potentiated neuromuscular activity which increases the speed of movement.

Time course of corticospinal excitability in reaction time and self-paced movements.

We used transcranial magnetic stimulation (TMS) to study the time course of corticospinal excitability before and after brisk thumb abduction movements, either in a simple reaction time (RT) paradigm or self-paced. Premovement increase in corticospinal excitability began about 20 msec earlier for self-paced compared with simple RT movements. For both simple RT and self-paced movements after electromyographic (EMG) offset, there was a first period of increased excitability from 0 to 100 msec, followed by a second period from 100 to 160 msec. Corticospinal excitability was decreased from about 500 to 1,000 msec after EMG offset for both types of movements. Our results show that motor preparation that begins 1.5 to 2 seconds before self-paced movement is not associated with increased corticospinal excitability. The first phase of increased corticospinal excitability after EMG offset may be due to activity of motor cortex neuron subthreshold for activating spinal motor neurons, and the second phase may reflect a subthreshold second agonist burst. The period of decreased corticospinal excitability after movement corresponds to the onset of event-related synchronization (ERS) of electroencephalographic signals in the 20-Hz band, and supports the hypothesis that ERS may be related to an inactive, idling state of the motor cortex.

Motor unit recruitment and discharge behavior in movements and isometric contractions.

The purpose of this study was to contrast the discharge patterns of the same motor units during movements and during isometric contractions that were produced with comparable torque-time characteristics. Subjects performed elbow flexion and extension movements with predetermined acceleration characteristics. The average acceleration and deceleration profiles for the movements were reproduced in the isometric setting by presenting the kinematic profiles as templates for torque production. Trained subjects were able to match the first agonist (AG1) and antagonist (ANT) electromyographic (EMG) bursts, but tended to produce a smaller second agonist burst (AG2) in the isometric contraction. Twenty-five motor units from triceps brachii were studied. The same motor units (with one exception) were recruited and subsequently discharged in a similar fashion in both the isometric and movement tasks in the AG1 and ANT EMG bursts, with fewer motor unit discharges in the AG2 burst in the isometric contraction. The central control mechanisms appear to be the same for the acceleration phase of movement and isometric contraction, but differ during the deceleration phase.

Motor cortex excitability during ballistic forearm and finger movements.

In a ballistic forearm flexion movement, a centrally programmed triphasic pattern of electromyogram (EMG) is seen with two bursts in biceps and a single burst in triceps. Rapid abduction of the index finger, in contrast, is achieved with a single agonist burst. Transcranial magnetic and electrical stimuli, triggered at the onset of the EMG burst, have been used to probe cortical and spinal cord excitability during and after self-paced ballistic finger and forearm movements. The first phase is coincident with the initial agonist burst. The second phase in biceps is associated with the second agonist burst, but in the finger movement, the raised motor cortical excitability is not associated with any EMG. It is argued that the motor program for the two movements may be similar, despite there being large differences in the EMG pattern generated.

Single-joint rapid arm movements in normal subjects and in patients with motor disorders.

In normal subjects the execution of single rapid one-joint movements is characterized by an electromyographic (EMG) pattern composed of three discrete bursts of activity; two bursts (first and second agonist bursts, or AG1 and AG2) are present in the agonist muscle separated by an almost complete period of electrical silence. During this pause, another burst (antagonist burst, or ANT) occurs in the antagonist muscle. If a rapid movement is executed during tonic activation of the agonist muscle, tonic activity is inhibited just prior to AG1 onset (agonist inhibition). Similarly, if the movement is performed during tonic activation of the antagonist muscle, such activity is also inhibited prior to AG1 onset (antagonist inhibition). Antagonist inhibition also starts prior to AG1 onset and lasts until ANT onset. A general descriptor of the kinematic features related to the EMG pattern described above is a symmetrical and unimodal velocity profile that is bell-shaped and shows an acceleration time roughly equal to the deceleration time. This holds true for movements performed under low accuracy constraints; as accuracy demands become stricter and stricter, the peak velocity decreases but, as long as the movement is made with one continuous trajectory, the velocity profile remains roughly symmetrical. In general terms, the function of AG1 is to provide the impulsive force to start the movement; the function of ANT is to halt the movement at the desired end-point; and the function of AG2 is to dampen out the oscillations which might occur at the end of the movement. The timing and size of the bursts vary according to the speed and amplitude of the movement. The origin of the EMG pattern is a central programme, but afferent inputs can modulate the voluntary activity. In this paper, we also review the EMG and kinematic abnormalities that are present during the execution of single-joint, rapid arm movements in patients with Parkinson's disease, Huntington's disease, Sydenham's chorea, dystonia, athetosis, cerebellar deficits, upper motor neuron syndrome, essential tremor and large-fibre sensory neuropathy. The data from these studies lead us to the following conclusions: (i) the basal ganglia have a role in scaling the size of AG1, reinforcing the voluntary command and inhibiting inappropriate EMG activity; (ii) the cerebellum has a role in timing the voluntary bursts and probably in implementing muscle force phasically; (iii) the corticospinal tract has a role in determining spatial and temporal recruitment of motor units; (iv) proprioceptive feedback is not necessary to produce the triphasic pattern but it contributes to the accuracy of both the trajectory and the end-point of rapid movements.

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.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain mechanisms of the mind: information synthesis in dominant cortical areas

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°–80° were made under two instructions: “move at own speed” and “move fast and accurate.” In a second experiment, 5 elderly subjects practiced 30° 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. This greater movement variability may result from: 1) changes in motor neuron population and motor unit properties with aging and the associated effects on muscle force output and joint torques and 2) abnormal control of phasic and tonic antagonist muscle activity. The ability to improve performance with practice, however, is clearly not lost in the elderly.

EMG activities of mono- and bi-articular muscles during goal-directed ballistic movement

Eight subjects, who were seated with the upper arm supported in a horizontal position, performed a series of elbow flexion and extension movements in which a visual target was provided together with an elbow angle signal by vertically moving horizontal lines on an oscilloscope. Five loading conditions were employed, which differed in the number of steel plates attached to the subject's wrist: 0, 0.65, 1.30, 1.95 and 2.60 kg. The electromyographic (EMG) activity of the bi-articular biceps brachii (BB) was compared with the mono-articular brachioradialis (BR) for each of three EMG components; the first and the second agonist burst (AG1, AG2) during flexion movements, and the antagonist burst (ANT) during extension movements. The magnitude relations for each EMG component between the two muscles were evaluated by the BR/BB ratio. The results showed that there were significant differences ( p < 0.05) among the three EMG components in all but the no-loading condition. Further a post-hoc test revealed that there were significant BR/BB differences ( p < 0.05) between AG1 vs. AG2 in 0.65 and 1.3 kg loading conditions and between AG1 vs. ANT in all but the no-loading condition. These results may suggest that different neural processes underlie the activation of mono- and bi-articular muscles in the organization and the control of movements.

Essential Tremor Entrains Rapid Voluntary Movements

The effect of essential tremor on the timing of rapid wrist flexion was examined in 10 patients with moderate to severe disability. The mean reaction time and motor time of the patients did not differ from the mean values of 10 healthy age- and sex-matched controls. The latencies of the triphasic agonist and antagonist EMG bursts did not differ between patients and controls. The initiation of movement was time-locked to the tremor cycle in all patients. The initial agonist muscle activation occurred in phase with the rhythmic bursts of EMG, but the onset of rapid wrist flexion occurred when the momentum of essential tremor opposed the volitional movement. Essential tremor has subtle effects on motor control that transcend oscillation per se. These effects probably contribute to the impaired performance of fine motor tasks in patients with advanced disease.

Control of fast elbow movement: a study of electromyographic patterns during movements against unexpectedly decreased inertial load.

Predictions of three models of single-joint motor control were compared with experimental observations of the changes in electromyographic (EMG) patterns during fast voluntary movements against an unexpectedly reduced inertial load. The subjects performed elbow flexions over 40 degrees "as fast as possible" in two series. During the first series, an approximately 40% decrease in inertia, simulated by a torque-motor, might occur unpredictably on half of the trials (unloaded trials). During the second series, all the trials were unloaded. The major findings are: (1) no differences in the antagonist burst latency in unexpectedly unloaded and unperturbed trials; (2) a decrease in the antagonist latency during expected unloadings; (3) a small, statistically non significant decrease in the first agonist burst EMG integral; and (4) a larger, statistically significant increase in the antagonist burst EMG integral in unexpectedly unloaded trials as compared to unperturbed trials. The data are in good correspondence with a version of the equilibrium-point hypothesis that assumes central programming of the beginning of the antagonist burst and incorporates the possibility of reflex-induced changes in EMG amplitudes.