Triphasic Electromyographic Pattern Research Articles

Immediate effects of postural repositioning on maximum phonation duration tasks in seated individuals with acquired dysarthria: a pilot study

Purpose To determine the effectiveness of a single 10-min postural repositioning session on the maximum phonation duration (MPD) of the vowel/a/in individuals with acquired dysarthria. Materials and methods A pre-post interventional design was implemented; five patients with dysarthria (PWDs) underwent a single 2-hour experimental session. MPD capacities were assessed before and immediately after a 10-min postural repositioning intervention by a physical and occupational therapist. Five age- and sex-matched individuals without dysarthria were recruited as controls. The main outcome measure was the MPD of the vowel/a/at conversational and louder voice levels, with a speech-and-language therapist standing 1 and 6 m away, respectively. Secondary outcome measures were thoracic expansion, manometry, electromyographic recordings of axial muscles and perceived effort. Results In PWDs, postural repositioning improved the MPD during the/a/–1-m (80.3% increase) and/a/–6-m tasks (18% increase), increased thoracic expansion and manometric measurements, and reduced the perceived effort necessary to perform the tasks. A triphasic electromyographic pattern was observed during both/a/–1-m and/a/–6-m tasks in controls, but was absent in participants with severe dysarthria, even after postural repositioning. Nonetheless, postural repositioning enabled an earlier onset of EMG activity prior to voice production. Conclusions These data suggest the efficacy of postural repositioning in improving phonatory capacities essential for voice production in PWDs.

Progressive resistance exercise restores some properties of the triphasic EMG pattern and improves bradykinesia: the PRET-PD randomized clinical trial.

In Parkinson's disease (PD), the characteristic triphasic agonist and antagonist muscle activation pattern during ballistic movement is impaired: the number of agonist muscle bursts is increased, and the amplitudes of the agonist and antagonist bursts are reduced. The breakdown of the triphasic electromyographic (EMG) pattern has been hypothesized to underlie bradykinesia in PD. Progressive resistance exercise has been shown to improve clinical measures of bradykinesia, but it is not clear whether the benefits for bradykinesia are accompanied by changes in agonist and antagonist muscle activity. This study examined the spatiotemporal changes in agonist and antagonist muscle activity following 24 mo of progressive resistance exercise and the combined relationship between spatiotemporal muscle activity and strength measures and upper limb bradykinesia. We compared the effects of progressive resistance exercise training (PRET) with a nonprogressive exercise intervention, modified Fitness Counts (mFC), in patients with PD. We randomized 48 participants with mild-to-moderate PD to mFC or PRET. At the study endpoint of 24 mo, participants randomized to PRET compared with mFC had significantly faster movement velocity, accompanied by significant increases in the duration, magnitude, and magnitude normalized to duration of the 1st agonist burst and fewer number of agonist bursts before peak velocity. The antagonist muscle activity was increased relative to baseline but did not differ between groups. Spatiotemporal EMG muscle activity and muscle strength were significantly associated with upper limb bradykinesia. These findings demonstrate that progressive resistance exercise improves upper limb movement velocity and restores some aspects of the triphasic EMG pattern.

Control of Arm Movements for Quick Change of Movement Direction

ABSTRACT The authors investigated the control strategy for changing movement direction during arm movements by analyzing the changes in a triphasic electromyographic pattern. Subjects performed a 40° flexion (basic) and a 40° flexion-extension to return to the start position (return) under two conditions: performing a predetermined task (SF) and performing each task in response to a signal (ST). The results revealed the agonist burst for the return task under the ST condition resembled that of the basic task under the SF condition, and the antagonist burst increased after presenting the modification signal. In conclusion, the strategy for quick change of movement direction was to increase the antagonist burst by an additional command from the central nervous system without cancelling the planned movement.

Effects of Transcranial Magnetic Stimulation Over the Cerebellum on Triphasic Electromyographic Pattern

The purpose of this study was to investigate the effects of transcranial magnetic stimulation (TMS) over the cerebellum on the triphasic electromyographic (EMG) pattern. Eight healthy subjects extended the left wrist as fast as possible in response to a start cue. TMS was delivered over the cerebellum 50 ms after the start cue. TMS over the cerebellum produced shortening of the latency in the first agonist burst, and an increase in the EMG activity of the antagonist burst. The triphasic EMG pattern may be partially under the control of the cerebellum.

Recognition of the physiological actions of the triphasic EMG pattern by a dynamic recurrent neural network

Triphasic electromyographic (EMG) patterns with a sequence of activity in agonist (AG1), antagonist (ANT) and again in agonist (AG2) muscles are characteristic of ballistic movements. They have been studied in terms of rectangular pulse-width or pulse-height modulation. In order to take into account the complexity of the EMG signal within the bursts, we used a dynamic recurrent neural network (DRNN) for the identification of this pattern in subjects performing fast elbow flexion movements. Biceps and triceps EMGs were fed to all 35 fully-connected hidden units of the DRNN for mapping onto elbow angular acceleration signals. DRNN training was supervised, involving learning rule adaptations of synaptic weights and time constants of each unit. We demonstrated that the DRNN is able to perfectly reproduce the acceleration profile of the ballistic movements. Then we tested the physiological plausibility of all the networks that reached an error level below 0.001 by selectively increasing the amplitude of each burst of the triphasic pattern and evaluating the effects on the simulated accelerating profile. Nineteen percent of these simulations reproduced the physiological action classically attributed to the 3 EMG bursts: AG1 increase showed an increase of the first accelerating pulse, ANT an increase of the braking pulse and AG2 an increase of the clamping pulse. These networks also recognized the physiological function of the time interval between AG1 and ANT, reproducing the linear relationship between time interval and movement amplitude. This task-dynamics recognition has implications for the development of DRNN as diagnostic tools and prosthetic controllers.

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

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

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.

Pathophysiology of chorea and bradykinesia in Huntington's disease

This article reviews the neurophysiological abnormalities described in Huntington's disease. Among the typical features of choreic movements are variable and random patterns of electromyographic (EMG) activity, including cocontraction of agonist and antagonist muscles. Studies of premotor potentials show that choreic movements are not preceded by a Bereitschaftspotential, therefore demonstrating that choreic movement is involuntary. Early cortical median-nerve somatosensory-evoked potentials have reduced amplitudes and the reduction correlates with reduced glucose consumption in the caudate nucleus. Long-latency stretch reflexes evoked in the small hand muscles are depressed. These findings may reflect failed thalamocortical relay of sensory information. In Huntington's disease, the R2 response of the blink reflex has prolonged latencies, diminished amplitudes, and greater habituation than normal. These abnormalities correlate with the severity of chorea in the face. Patients with Huntington's disease perform simple voluntary movements more slowly than normal subjects and with an abnormal triphasic EMG pattern. Bradykinesia is also present during their performance of simultaneous and sequential movements. Eye movements show abnormalities similar to those seen in arm movements. In Huntington's disease, arm movement execution is associated with reduced PET activation of cortical frontal areas. Studies using transcranial magnetic stimulation show that patients with Huntington's disease have normal corticospinal conduction but some patients have a prolonged cortical silent period. Bradykinesia results from degeneration of the basal ganglia output to the supplementary motor areas concerned with the initiation and maintenance of sequential movements. The coexisting hyperkinetic and hypokinetic movement disorders in patients with Huntington's disease probably reflect the involvement of direct and indirect pathways in the basal ganglia-thalamus-cortical motor circuit.

Afferent feedback in the triphasic EMG pattern of leg muscles associated with rapid body sway.

Electromyographic (EMG) patterns of leg muscles associated with rapid body sway were studied in relation to displacement of the center of foot pressure (CFP). Standing subjects were instructed to shift the CFP by swaying their bodies, pivoting at the ankle as rapidly and accurately as possible after an auditory signal. CFP position was designated as N when the subject maintained a relaxed bending posture and as F when a maximally forward-leaning posture was maintained. A serial, stereotyped triphasic EMG pattern was observed in the rapid shift of CFP from N to F: cessation of EMG activity in the gastrocnemius (GC) muscle was followed by a burst in the tibialis anterior (TA) muscle (acceleration phase), and then resumed discharge occurred in the GC muscle with cessation of activity in the TA muscle (deceleration and stop). When the subject shifted the CFP from N to F to different degrees, the duration and amount of EMG activity in the TA muscle during acceleration and the GC muscle in deceleration were proportionate to the amount of CFP displacement associated with forward body sway. To determine the functional roles of sensory inputs from the foot on the triphasic EMG pattern, body sway was studied under the condition of sensory block in the feet induced by ischemia from tourniquets placed bilaterally just above the ankle joints. The triphasic EMG pattern persisted during ischemia. The time of GC cessation and the onset of TA burst at acceleration remained unchanged, but the times of TA cessation and resumption of GC discharge at deceleration were altered during ischemia. Moreover, subjects were unable to stop at F and eventually fell. These results indicate that both amount and duration of EMG activity associated with rapid body sway are functions of the amount of CFP displacement. Somatic sensation from the feet is important for control of burst and cessation timing and duration in leg muscle activity.

The relation between posture and movement: A study of a simple synergy in a two-joint task

Human subjects performed fast, discrete elbow or wrist flexion or extension movements in a sagittal plane under the instruction to move one of the joints “as fast as possible”. We hypothesize that, when an instruction requires voluntary movement in only one joint, the muscles controlling the other, postural joint will display changes in their levels of activation tightly coupled to the primary movement, i.e. a postural synergy. Joint angles and electromyographic (EMG) signals from two flexor and two extensor muscles were recorded and analyzed. Both muscle pairs demonstrated commonly observed tri-phasic EMG patterns. The elbow flexor and the wrist flexor tended to demonstrate simultaneous EMG bursts, while the elbow extensor and the wrist extensor also showed similar patterns of activation. This was confirmed by both visual analysis and also cross-correlation analysis of the EMG pairs. The timing of the antagonist burst in postural muscles frequently coincided with shortening of the muscle and thus could not be attributed to the action of the local reflexes to muscle stretch. We consider the EMG patterns in postural muscles to be primarily of a central origin. We suggest that the formation of postural synergies (postural anticipation) may be not a separate process, but a separate peripheral pattern of a single control process that may involve a number of joints and muscles.

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

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

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

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

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 previsional 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 aggrement 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.

Effects of applied vibration on triphasic electromyographic patterns in neurologically ballistic head movements

Vibration of agonist or antagonist muscle tendon produced changes in the triphasic electromyographic pattern of neck muscles; EMG signals were rectified, averaged, and also integrated by planimetry. The triphasic EMG envelopes obtained during fast horizontal head rotation showed unmodified early agonist pulse, the action pulse (PA), under all conditions; increased antagonist pulse, the braking pulse (PB), only with antagonist muscle vibration; and increase of late agonist pulse, the clamping pulse (PC), only with agonist muscle vibration. Vibration experiments can be considered as a model for studying interactions between central and peripheral effects on control of normal movements.