Search PubMed⌕ Search

Biomedical subjects

J D Cooke

Publications and source records attributed to J D Cooke.

At least 37 records · Page 2Linked to original sources
PubMed1985

Initial agonist burst duration changes with movement amplitude in a deafferented patient.

Changes in the duration of the initial agonist burst were studied in a deafferented human. The patient had been functionally deafferented for five years, having no touch, vibration, pressure or kinesthetic sensation nor any tendon reflexes in the four limbs. Pain and temperature sensation were intact and motor fibres were unaffected. The subject made visually guided step-tracking movements using flexion/extension movements about the elbow. Initial agonist burst duration increased with movement amplitude. Burst duration was approximately 65 ms in small movements (6-12 deg) increasing to 136 ms in intermediate (36 deg) and 200 ms in large (54 and 60 deg) movements. Similar changes in initial burst duration with movement amplitude were seen when the subject made non-visually guided movements. It is concluded that the duration of the initial agonist burst is centrally determined.

Adult↗
PubMed1985

Matching of movements made independently by the two arms in normal humans.

Comparisons were made of voluntary movements of the right and left arms in normal human subjects. A series of movements of different amplitudes, made at the subject' own speed, was performed with one limb. After a rest period, the same series was repeated with the contralateral limb. The relation between movement peak velocity and movement amplitude was linear and was the same for both arms. With repeated testing over periods up to two months, the slope of the peak velocity-amplitude relation decreased during the first week, thereafter remaining unchanged. In a second series of experiments, six normal subjects continuously wore a 1 lb (0.45 kg) weight strapped to their left (non-dominant) forearm for up to 1 week. This resulted in an increase in the slope of the peak-velocity/amplitude relation in this arm. A parallel change occurred in movements made independently by the right (non-loaded) arm. A similar matching of movement performance of the two limbs was seen following removal of the weight. The data is interpreted as proving support for the hypothesis that there is a single movement "command" which is applied to both limbs. The interaction of this command with the limbs which have similar second-order mechanical properties yields similar movements even when they are made independently.

Journal Article↗
PubMed1984

Initial agonist burst duration depends on movement amplitude.

The initial burst of EMG activity associated with arm movements made by normal human subjects was studied. Subjects made visually guided, steptracking movements of different amplitudes and speeds. The duration of the initial agonist burst was greater for large than for small amplitude movements. The burst duration was not continuously graded but was either short (70 ms) for small amplitude movements (less than 20 deg) or long (140 ms) for large amplitude ones (greater than 50 deg). Movements of intermediate amplitudes (30-40 deg) were made with both short and long duration bursts. The increase in the duration of the initial agonist burst for large movements was produced by the appearance of a second component in the burst. Both components were of the same duration and occurred before movement peak velocity was reached. Intramuscular recording showed that both components originate from the same muscle. Similar observations were made in both fast and slow movements and in both the biceps and triceps muscles when they were being used as agonists. The data show that the central nervous system has two mechanisms for generation of large amplitude movements: modulation of the magnitude of the initial agonist burst and generation of a second component or pulse of agonist activity at the start of movement.

Arm↗
PubMed1984

Rapid error correction during human arm movements: evidence for central monitoring.

Studies were made of rapid error correction movements in eight subjects performing a visually guided tracking task involving flexion-extension movements about the elbow. Subjects were required to minimize reaction times in this two-choice task. Errors in initial movement direction occurred in about 3% of the trials. Error correction times (time from initiation to reversal of movement in incorrect direction) ranged from 30-150 ms. The first sing of correction of the error movement was a suppression of the electromyographic (EMG) activity in the muscle producing the error movement. This suppression started as early as 20-40 ms after the initiation of the error-related EMG activity and as much as 50 ms before any overt sign of limb movement. The correction of the error movement was also accompanied by an increase in the drive to the muscle which moved the arm in the correct direction. This increased activity always occurred after the initiation of the error movement. it is concluded that the first step in the error correction, suppression of drive to the muscle producing the error movement, cannot be based on information from the moving limb. It is thus suggested that this earliest response to the error movement is based on central monitoring of the commands for movement.

Journal Article↗
PubMed1983

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.

Electromyography↗
PubMed1983

The effects of cutaneous mechanoreceptor stimulation on the stretch reflex.

The effects of cutaneous stimulation on tonic and phasic responses to stretch were studied in the triceps surae complex of unanesthetized, decerebrate cats. The tonic response was produced by a maintained stretch of the muscle group to 80-85% of its maximum length. Stretch was applied directly to the isolated tendon at the calcaneus. Phasic responses were elicited by a ramp stretch of 1.0 to 2.0 mm superimposed on the maintained stretch. Mild, brief, electrical or mechanical stimulation of the plantar cushion caused a sequence of inhibitory and excitatory changes in the tonic EMG activity in the soleus muscle. Mild stimuli, applied 0.01 to 5 ms before the start of ramp stretch, decreased the size of the phasic response to stretch and converted it into a biphasic response. It is suggested that stimulation of cutaneous mechanoreceptors may be responsible for variations in the initial burst of EMG activity seen in the agonist muscle during the response to perturbation or fast voluntary movement in animals and man.

Animals↗
PubMed1981

Responses to force perturbations preceding voluntary human arm movements.

Brief force perturbations were applied 30-120 ms prior to onset of step-tracking forearm movements by normal humans. The perturbations altered the first agonist burst of the movement-related triphasic EMG pattern. Perturbations opposing the movement resulted in an increase in the magnitude of the late part of the first agonist burst, the early part being unchanged. Conversely, in movements which would be assisted by the perturbation, EMG magnitude decreased during the late part of the burst. No reflex EMG responses were elicited during the period following the perturbation and preceding onset of the first agonist burst.

Arm↗
PubMed1981

The effects of muscle vibration on the attainment of intended final position during voluntary human arm movements.

Muscle tendon vibration was applied during voluntary step-tracking arm target-movements performed by normal human subjects. Vibration (freq. = 120 Hz) was applied over either the biceps or triceps tendons. During non-visually guided (eyes closed) trials, vibration of the muscle antagonistic to the movement being performed resulted in an undershoot of the required target. Thus, biceps vibration produced an undershoot of the extension target and triceps vibration an undershoot of the flexion target. The same effect occurred if the vibration was applied continuously over several movements or only during the course of individual movements. In contrast, vibration of the muscle acting as the prime mover had no effect on the correct attainment of the required target. It is suggested that the central nervous system may monitor muscle afferent activity of the lengthening (antagonist) muscle during simple, step movements.

Arm↗
PubMed1981

Amplitude- and instruction-dependent modulation of movement-related electromyogram activity in humans.

1. Studies were made of the electromyogram (EMG) patterns associated with the performance of visually guided, step-tracking arm movements by normal humans. Subjects were instructed to make movement either 'accurately', 'as fast as possible' or 'fast and accurately'. Movements of 16, 32, 48 and 64 deg of arc were made with each instruction. Movements had durations of approximately 250-600 msec. 2. A 'triphasic' pattern of EMG activity was associated with all movements in this study. All bursts in this pattern were more clearly defined in faster movements whether the increased speed of movement was a result of increased movement amplitude or of the instruction-related 'intent' of the subject. 3. The magnitudes of the two agonist EMG bursts showed identical linear dependencies on movement amplitude. The slope of this relation was instruction-dependent, being greatest for 'fast' and least for 'accurate' movements. 4. The duration and time of onset of the initial agonist burst relative to the start of the movement were not dependent on movement amplitude or on instruction. In contrast, the time of onset of the second agonist burst depended on both movement amplitude and instruction, occurring earlier when movements were made faster. 5. The magnitude of the antagonist activity was instruction- but not amplitude-dependent. Duration and onset of this burst varied with both instruction and movement amplitude.

Arm↗
PubMed1978

Increased dependence on visual information for movement control in patients with Parkinson's disease.

Studies were made of visually and non-visually guided movements by patients with Parkinson's disease. The subjects moved a light, horizontal handle using rotation primarily about the elbow. During visually guided trials both handle and target positions were displayed to the subject; during non-visually guided trials only the handle position was displayed. During non-visually guided trials all patients showed a tendency for an overall flexion drift, although there was no change in average movement amplitude. The overall error in position by the end of the non-visually guided trials was greatly in excess of the reported values for passive displacement thresholds in normal subjects. It is suggested that the data indicate an increased dependence on visual information for control of motor activity in Parkinson's patients.

Aged↗
PubMed1977

Long-loop reflexes in the tranquilized monkey.

EMG responses to sudden displacement of the forelimb were studied in Cebus monkeys tranquilized with Atravet, a phenothiazine tranquilizer. The monkey's forearm was strapped firmly to a manipulandum handle. A torque motor attached at the pivot point of the handle, under servo control, provided reproducible limb displacements. In response to a sudden maintained displacement three periods of EMG activation in biceps muscle occurred with peak latencies of approximately 25, 45 and 85 msec. These correspond to the latencies of the M1, M2 and M3 responses in the alert animal. Similar responses were observed in 'naive' animals which had not previously been used in experimentation. All three responses increased in magnitude with increasing background activity and all appeared to be associated with suppression of EMG activity in the antagonist muscle. M1 and M2 responses were position dependent, M1 being greater in extension than in flexion and M2 the opposite. The position-dependence of the M2 response was produced by a depression of activity following the M1. This depression of activity lasted up to 30 msec following M1 and was directly dependent on the M1 magnitude.

Animals↗
PubMed1976

Modulation of the functional stretch reflex by the segmental reflex pathway.

Electromyographic (EMG) reflex responses were examined in the biceps muscle of awake Cebus monkeys trained to resist perturbations of a handle with their forearm. In particular responses at latencies of 15-20 msec (M1) and 40-55 msec (M2), thought to correspond to segmental and suprasegmental reflex pathways respectively, were studied. The experiments demonstrated that the magnitude of the M1 response was large, as compared to M2, only when the muscle was tonically active and small perturbations were applied. For larger perturbations the magnitude of M1 saturated and the M2 response became functionally significant, its magnitude being directly related to the magnitude of the perturbation. By means of delayed reductions in torque, the magnitude of this M2 response was also shown to be very sensitive to changes in facilitatory drive provided by segmental pathways.

Afferent Pathways↗
PubMed1976

Forearm oscillation during cooling of the dentate mucleus in the monkey.

A study was made of oscillations in arm acceleration in monkeys performing a self-paced manual step-tracking task. Power spectral density analyses of segments of arm acceleration data from normal monkeys containing both flexion and extension movements and intermovement holding periods showed three major peaks at 1-1.5 Hz, 3-5 Hz and 5-7 Hz. Cooling of the dentate nucleus produced a marked increase in the relative magnitude of the 3-5 Hz spectral band. The spectral peak in this frequency range was larger than the other two which were also present during cooling. Autocorrelation functions from long segments of data containing flexion and extension movements and intermovement holding periods showed regular periodic variations in both normal and cooled animals. This suggests that the ongoing oscillations were not changed in phase by the occurrence of the self-initiated arm movements.

Animals↗
PubMed1973

Transmitter release by mammalian motor nerve terminals in response to focal polarization.

1. A method is described by which mammalian motor nerve terminals may be uniformly polarized by focally applied current, and the extra-cellular potential in the synaptic cleft, corresponding to any current, estimated.2. The relationship between log m.e.p.p. frequency and local extra-cellular field is flat for hyperpolarization and ascends linearly with depolarization. With depolarization, m.e.p.p. frequency is multiplied about tenfold for every - 18 mV. This characteristic becomes steeper the closer the polarizing electrode to the nerve terminal with a limiting value of ten-fold per - 15 mV.3. There exists a population of small m.e.p.p.s which are generated at the same end-plate as normal m.e.p.p.s.4. Following a prolonged depolarizing pulse there is an increase of m.e.p.p. frequency which continues for periods of up to several minutes.5. With hyperpolarizing pulses m.e.p.p. frequency may increase in a characteristic ;bursty' manner. Similar bursts of m.e.p.p.s also occur spontaneously, but far less frequently, without polarization.6. During a depolarizing pulse, m.e.p.p. frequency becomes maximal or near maximal within 2 sec. There is little subsequent alteration of m.e.p.p. frequency. Numbers of m.e.p.p.s occurring during depolarizing pulses follow the Poisson distribution.7. Following a depolarizing pulse, numbers of m.e.p.p.s released by a subsequent pulse may be either increased or diminished.8. Comparison of the response of m.e.p.p. frequency to raised [K] and to extrinsic presynaptic polarization leads to the conclusion that the presynaptic transmembrane potential change corresponding to any focal current pulse is about two thirds of the local extracellular potential field. Hence the slope of the linear portion of the presynaptic transfer function is about tenfold per 10 mV presynaptic depolarization.

Animals↗