SEARCH · PubMed Health

Results for “Reflex, Stretch”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources

PubMed1985

Stretch reflex blepharospasm.

We studied a patient with blepharospasm provoked by stretching the orbicularis oculi muscles. With the eyes closed, EMG of the orbicularis oculi at rest revealed spontaneous rhythmic muscle activity that was not visible. When she tried to open her eyes, repetitive jerking blepharoclonus and tonic blepharospasm rendered her functionally blind. Passive stretching of the orbicularis oculi evoked a burst of EMG activity with two components. Touch or pinprick did not elicit such reflex activity. Anesthesia of the supraorbital nerves abolished muscle responses to stretch and improved the blepharospasm.

Aged↗

PubMed1997

Regional variability of stretch reflex amplitude in the cat medial gastrocnemius muscle during a postural task.

The relationship between local fibre stretch velocity (mechanical input) and the corresponding local reflex electromyographic (EMG) amplitude (a measure of the neural output) was assessed to determine the contribution of muscle spindle feedback in postural control. We hypothesized that traditionally measured input variables (e.g., the velocity of an external movement or whole muscle velocity) may not accurately represent the mechanical input to the muscle spindles, especially when the background forces are small. Three cats were trained to stand on pedestals while ankle rotations were applied to the left hindlimb. EMG and fiber movement in both proximal and distal regions of the muscle were recorded in addition to muscle length and tendon force. We found that local muscle velocity was correlated poorly with whole muscle velocity, demonstrating that internal and external muscle movements are often dissimilar, particularly during tasks that involve modest levels of muscle activation. Local EMG reflex amplitudes were correlated well with the corresponding local fiber stretch velocities (R values ranging from 0.5 to 0.8) but not with muscle stretch velocity. The lack of crossed correlations between fiber stretch velocities and reflex EMG amplitudes measured in proximal versus distal regions of the muscle suggests the presence of a local reflex component. It is concluded that changes in local muscle fiber length represent the mechanical input to spindles better than changes in the total muscle length. Additionally, spindles have a specific role in the reflex activation of nearby muscle fibers.

Animals↗

PubMed1981

Activity evoked in hand muscles by the stretch reflex of m. biceps in man.

Experiments were performed on six volunteers, in order to investigate the effect of the activity of the m. biceps branchii on the median and ulnar nerves. The reflex of the m. biceps brachii was evoked by a sudden stretch and the EMG responses of the m. biceps brachii, m. abductor dig. V. and thenar muscles were recorded. Hand muscles produced early EMG potentials, the latency between them, as well as the onset of the electrical response recorded from the m. biceps brachii, being about the same as the conduction time of nerve excitation from biceps to the hand muscles. The possible mechanisms of the origin of the early EMG activity recorded from the hand muscles are discussed.

Action Potentials↗

PubMed1983

Stretch reflexes of triceps surae in patients with upper motor neuron syndromes.

Electromyographic responses of triceps surae to dorsiflexion stretch were studied in 47 patients with a variety of lesions producing an upper motor neuron syndrome. The short latency spinal reflexes, both when the patient was at rest and when he was exerting a voluntary plantarflexion, were frequently enhanced in magnitude and the rate of increase with acceleration was also enhanced. Long-latency reflexes were uncommon at rest. With background force long-latency reflexes were present unless the short latency reflex was very large. Long latency reflexes often were normal, but in some patients they were either excessively larger or even of abnormal shape with prolonged continuous activity. The clinical assessment of the ankle jerk correlated with the magnitude of the short latency reflex. The clinical assessment of tone correlated with the magnitude of the short latency reflex, the magnitude of the long latency reflex and the duration of the long latency reflex. There appear to be multiple physiological mechanisms underlying the clinical phenomenon of spasticity.

Cerebral Cortex↗

PubMed1998

Significance of passively induced stretch reflexes on achilles tendon force enhancement.

An in vivo buckle transducer technique was applied to study the reflex contribution to ATF enhancement during passive dorsiflexion stretches. Single stretches led to a linear ATF increase in the absence of an EMG reflex response, whereas clear ATF enhancement over the passive component occurred 13-15 ms after the onset of EMG responses. To quantify the reflexly induced increase in ATF, the stretched position was maintained. The mean reflex effect was two to four times greater than the passive stretch effect.

Achilles Tendon↗

PubMed1992

Effects of fatigue on the stretch reflex in a human muscle.

The effects of fatigue on the electromyographic (EMG) reflex activities were compared during sustained voluntary contractions and contractions evoked by electrical stimulation (30 Hz) in the human first dorsal interosseus (FDI). Short latency (SL), medium latency (ML) and long latency (LL) reflex responses to a ramp-and-hold stretch of the muscle were recorded and analysed in 27 healthy subjects of both sexes. The amplitude of the reflex components was normalized as function of the amplitude of the surface action potential (SAP) recorded in response to the supramaximal stimulation of the motor nerve. The results indicate that for a similar reduction of force, SL and ML are significantly reduced after fatigue induced by voluntary contractions but they are not when the fatigue test is performed by electrical stimulation at the motor point. In voluntary fatigue experiments, the LL component showed no significant decrease below control values, but an enhancement was observed during electrically evoked contraction. This enhancement remained above control values for at least 15 min during the recovery period, whereas SL and ML decreases returned to control within 5 min after the fatigue tests. The electrical stimulation applied to the skin overlying the FDI at an intensity lower than the motor threshold did not affect SL and ML, but enhanced LL for about 15 min. On the contrary, the anaesthesia of the skin overlying the FDI induced a decrease in LL without significant change of SL and ML. It is concluded that muscle reflex fatigue is present during sustained voluntary contractions and decreases SL and ML responses to quick stretches.(ABSTRACT TRUNCATED AT 250 WORDS)

Electric Stimulation↗

PubMed1998

Evidence that a transcortical pathway contributes to stretch reflexes in the tibialis anterior muscle in man.

1. In human subjects, stretch applied to ankle dorsiflexors elicited three bursts of reflex activity in the tibialis anterior (TA) muscle (labelled M1, M2 and M3) at mean onset latencies of 44, 69 and 95 ms, respectively. The possibility that the later of these reflex bursts is mediated by a transcortical pathway was investigated. 2. The stretch evoked a cerebral potential recorded from the somatosensory cortex at a mean onset latency of 47 ms in nine subjects. In the same subjects a compound motor-evoked potential (MEP) in the TA muscle, evoked by magnetic stimulation of the motor cortex, had a mean onset latency of 32 ms. The M1 and the M2 reflexes thus had too short a latency to be caused by a transcortical pathway (minimum latency, 79 ms (47 + 32)), whereas the later part of the M2 and all of the M3 reflex had a sufficiently long latency. 3. When the transcranial magnetic stimulation was timed so that the MEP arrived in the TA muscle at the same time as the M1 or M2 reflexes, no extra increase in the potential was observed. However, when the MEP arrived at the same time as the M3 reflex a significant (P < 0.01) extra-facilitation was observed in all twelve subjects investigated. 4. Peaks evoked by transcranial magnetic stimulation in the post-stimulus time histogram of the discharge probability of single TA motor units (n = 28) were strongly facilitated when they occurred at the same time as the M3 response. This was not the case for the first peaks evoked by electrical transcranial stimulation in any of nine units investigated. 5. We suggest that these findings are explained by an increased cortical excitability following TA stretch and that this supports the hypothesis that the M3 response in the TA muscle is - at least partly - mediated by a transcortical reflex.

Adult↗

PubMed1990

On the localization of the stretch reflex of intrinsic hand muscles in a patient with mirror movements.

1. The patient studied showed the typical mirror movements of the Klippel-Feil syndrome. Earlier intensive electrophysiological analysis suggests that many of her corticospinal axons branch abnormally to supply motoneurones on both sides of the spinal cord. Thus, in her, a long-latency reflex utilizing the motor cortex should manifest itself bilaterally. 2. EMG recordings were made simultaneously from the first dorsal interosseous (FDI) muscles of both hands while they were being voluntarily activated by the subject. The FDI of one hand was then briefly stretched by forcibly adducting the index finger. Similar but more limited studies were made using flexor pollicis brevis. 3. The reflex response of the stretched muscle consisted of a typical mixture of early (M1) and late (M2) components, with mean latencies of 32 and 49 ms respectively. 4. Unlike normal controls, the contralateral muscle responded on stretch of the ipsilateral muscle. However, its response consisted solely of a long-latency reflex. This was comparable in size, latency and waveform to the ipsilateral late component. (Mean size, 84% of the ipsilateral M2 response; mean latency 46 ms, or 3 ms less than the ipsilateral response due to the absence of M1). 5. The short-latency response did not spread to the homologous contralateral muscle even when it was large ipsilaterally. The long-latency response elicited from FDI did not spread to the abductor digiti minimi muscle of either hand. 6. Reducing the duration of the stretch reduced the duration of the crossed response by an equivalent amount. Unloading the ipsilateral muscle produced a delayed reduction of EMG activity contralaterally. Thus her long-latency pathway can act tonically as well as phasically. 7. These findings strongly support the hypothesis that delayed components of the human stretch reflex are relayed via the motor cortex and the corticospinal tract.

Electromyography↗

PubMed1990

Pathological stretch reflexes on the "good" side of hemiparetic patients.

The reflex EMG responses from a tendon tap or an imposed, medium amplitude (30 degrees), stretch at a range of stretch velocities have been recorded from the triceps and biceps muscles of normal human subjects and in both the affected and "unaffected" arms of hemiparetic patients under relaxed conditions. In the hemiparetic arm, exaggerated tendon jerks were, as expected, observed in both muscles. The response of the biceps to elbow extension was also exaggerated compared with normal values and displayed both an additional earlier component and a much reduced velocity threshold. The triceps, in contrast, showed depressed responses to elbow flexion, with a much higher velocity threshold than normal subjects. Furthermore, on the supposedly "unaffected" side of the hemiparetic subjects, the reciprocal pattern was seen, with depression of the biceps response and a raising of its threshold, along with considerably exaggerated responses in the triceps including earlier components not seen in the normal subjects. The increased excitability of the flexor musculature on the spastic side may be paralleled by increases in activity in the segmental pathways responsible for modulation of agonist/antagonist activity in the ipsi and contralateral limb, leading to an inhibition of the ipsilateral extensors and contralateral flexors and excitatory input to the contralateral extensors. Thus the "good" side of hemiparetic patients also receives pathological changes, and studies of the mechanisms of spasticity should avoid the use of the "unaffected" side of hemiparetic subjects as a control for monitoring pathological reflexes.

Adult↗

PubMed1991

Quantitative assessment of the effect of basal ganglia lesions on the stretch reflex in primates.

The effect of basal ganglia stereotactic lesions on motor tone in 3 primates was quantitated. The elastic and neurogenic forces generated with a controlled stretch of each animal's upper extremities were measured pre- and postlesion, and compared to previous studies. The techniques were sensitive to subtle changes in motor tone that were not clinically apparent. The results suggest that the basal ganglia, through the outflow path of the globus pallidus, is important in controlling the sensitivity of both flexors and extensors to stretch. These quantification techniques also have promise in evaluating treatment regimens for spasticity, rigidity, and other conditions with abnormal motor tone.

Animals↗

PubMed1997

Medium-latency stretch reflexes of foot and leg muscles analysed by cooling the lower limb in standing humans.

1. In standing subjects, an ankle-dorsiflexing perturbation of the supporting surface evokes a short-latency response (SLR) and a medium-latency response (MLR) to stretch in both soleus (Sol) and flexor digitorum brevis (FDB) muscles. The SLR is the counterpart of the monosynaptic reflex, whilst the MLR might be either mediated by Ia fibres, the delay being due to a long-loop central circuit, or by fibres of slower conduction velocity. Since small afferents are slowed more than large ones by low temperature, a greater latency increment for the MLR than the SLR induced by cooling of the limb would point to a peripheral origin of the MLR. 2. In nine subjects, one limb was cooled by circulating water in a tube wrapped around it for about 120 min. Perturbations were delivered to the same limb prior to and during cooling, and after rewarming. EMG was recorded by surface electrodes from the Sol and FDB muscles. 3. The mean increase in latency of MLRs was significantly greater than that of SLRs in both muscles. On average, the Sol SLR increased from 42.4 to 47.0 ms and the Sol MLR from 72.0 to 82.3 ms. The FDB SLR increased from 58.1 to 66.5 ms and the FDB MLR from 94.9 to 110.5 ms. The mean difference (MLR minus SLR) increased from 29.6 to 35.2 ms for Sol, and from 36.8 to 43.9 ms for FDB at the end of cooling. After 30 min of rewarming, the responses of both muscles recovered towards control values. 4. The greater latency increment of the MLRs than of the SLRs favours the hypothesis of a slower conduction velocity of the responsible afferent fibres. The most likely candidate fibres are the spindle group II afferents.

Adult↗

PubMed1987

Long-latency stretch reflexes of the human elbow extensors during voluntary relaxation: differences between agonistic muscles.

Reflex electromyographic (EMG) responses of elbow extensor muscles to unexpected elbow flexion were recorded in the absence of initial tonic activity from subjects instructed not to resist the stretch. The monosynaptic component M1 was present only in the anconeus muscle and only for high accelerations. The acceleration value at which the long-latency components M2 and M3 appeared was lower for anconeus than for triceps brachii. Increases in peak acceleration of stretch resulted in decreases in M2 and M3 latencies and increases in M2 and M3 magnitudes in both muscles. However, M2 and M3 latencies for anconeus were shorter than those of triceps brachii, except at high acceleration values. Furthermore, the magnitude of M2 and M3 components of anconeus activity increased faster for low accelerations than for high accelerations, whereas those of triceps brachii increased in proportion to the acceleration. These differences between anconeus and triceps brachii were similar to those described earlier for voluntary movements. It is suggested that the motoneurons of all elbow extensor muscles may be recruited as a single motoneuron pool following Henneman's size principle, irrespective of whether the activity is voluntary or reflex in origin.

Adult↗

PubMed1997

Load compensation tasks evoke tremor in cerebellar patients: the possible role of long latency stretch reflexes.

'Tremor' is one of the clinical signs of cerebellar dysfunction. Its nature remains subject to debate, one hypothesis being that of a predominant role of peripheral afferences in its genesis. This study was designed to study whether load compensating tasks, evoking sudden stretch, and thus stimulation of peripheral afferences induced tremor in cerebellar patients. We study the kinematics and EMG pattern of a load compensating task which consists of maintaining a constant elbow position despite the onset and cessation of a 2 Nm torque loading the elbow flexors in eight cerebellar patients and six controls. Angular position and velocity, and EMG of the biceps and triceps are recorded at a sampling rate of 1 kHz. In normal subjects, trajectories are simple with little overshoot of the aimed position. EMG analysis shows a long latency stretch response (LLSR) which initiates a phasic and then tonic voluntary activity. In cerebellar patients, the two prominent cinematic features are hypermetria and tremor. The stretch response is of the same latency, but the EMG pattern is modified with bursts of activity related to the tremor. These results show severe perturbations of load compensating tasks in cerebellar patients. We discuss the possible role of the exaggeration of LLSR in both hypermetria and tremor.

Case-Control Studies↗

PubMed1986

Observations on the genesis of the stretch reflex in Parkinson's disease.

Using surface electromyography the reflex response of flexor carpi radialis elicited by forcibly dorsiflexing the wrist was compared with that elicited by applying vibration percutaneously to its tendon. This was done both in patients with Parkinson's disease and in normal subjects. The reflexes were elicited on top of a pre-existing voluntary contraction of the muscle of about 20 per cent maximum. The responses in parkinsonism were qualitatively similar to the normal, but differed quantitatively in certain respects. The response to 'stretch' of the muscle by wrist dorsiflexion normally continued at a high level up to at least 80 ms from the beginning of the movement, commonly with an apparent separation into 'short' and 'long' latency responses. On average, the later components of the response were enhanced in parkinsonian patients in comparison with the normals, confirming other workers' findings; they were also prolonged. The short-latency responses were unchanged. Vibration, in contrast, elicited solely a short-latency response with the initial reflexly-evoked augmentation of EMG activity coming to an end 40 to 50 ms from the beginning of the stimulation, even though the vibration was continuing. Such an absence of the later components that were so prominent with stretch was found whatever the size of the initial short-latency response evoked by vibration, including when it was comparable to that evoked by stretch in the same subject. This purely short-latency vibration response was on average unchanged in parkinsonism. The findings support the hypothesis, already advanced for the long flexor of the thumb, that the long-latency components of response are largely attributable to a spinal excitatory action of the spindle group II afferents with the delay arising from the slowness of their conduction. They are not readily compatible with either of the two major alternative hypotheses, namely the 'long-loop' (or transcortical) hypothesis and the 'resonance' hypothesis, both of which attribute the late response, as well as the initial response, to the spindle Ia afferents. The enhancement of the later components of response in parkinsonism thus now seems likely to be due to an increase in the postulated spindle group II excitatory action, possibly related to a reduction in opposing inhibition, rather than to any change in the reflex excitability of the higher centres on Ia activation. However, the rigidity of parkinsonism cannot be uniquely ascribed to an enhancement of group II action, because over the population as a whole clinically similar degrees of rigidity could be accompanied by quite different long-latency responses, and vice versa.

Adult↗

PubMed1984

Tension development and muscle activation in the leg during gait in spastic hemiparesis: independence of muscle hypertonia and exaggerated stretch reflexes.

In 15 patients with spastic hemiparesis the development of tension of calf muscles in relation to their electrical activation and their stretching period was studied on both sides during locomotion. Only in the spastic leg did isolated small biphasic potentials appear in the gastrocnemius E.M.G. with monosynaptic latency at the beginning of the stance phase, while the remaining gastrocnemius activation was reduced compared to the unaffected side. Perturbations of gait were followed in the spastic leg by a large monosynaptic response, while the polysynaptic reflex response was reduced. In the unaffected leg only a strong polysynaptic response appeared, which suggests a reciprocal modulation of monosynaptic and polysynaptic reflex responses. Tension development paralleled the gastrocnemius E.M.G. in the unaffected leg, while in the spastic leg tension was more closely correlated to muscle stretch. It is concluded that in spasticity the exaggerated monosynaptic reflexes represent only a small part of leg extensor activation during gait and that the tension development does not depend on these reflexes.

Adult↗

PubMed1988

Long-latency stretch reflexes as co-ordinated functional responses in man.

1. Reflex activity in human arm muscles has been measured in response to torque perturbations around the elbow joint in the flexion-extension direction and/or the supination-pronation direction. Intramuscular fine-wire electrodes were used to record electromyographic (EMG) activity in the muscles. A pre-load was applied in the same direction as or in a different direction to the perturbation. The subjects were instructed to 'hold on', which means that they had to actively resist the perturbation without unduly co-activating their muscles. 2. The EMG activity showed segmented reflex responses with short-latency (25-50 ms) and long-latency (50-75 ms) components, followed by other bursts of activity which probably originated from the subject's voluntary or triggered reactions. 3. Motor units in m. triceps gave short-latency and long-latency responses to imposed elbow extension but only long-latency responses were seen to imposed pronation, which does not stretch m. triceps. Motor units in m. brachialis gave short-latency and long-latency excitatory (inhibitory) responses to imposed extension (flexion) torques. However, only long-latency inhibitory responses were observed to imposed pronation torques. Motor units in m. biceps gave short-latency and long-latency excitatory responses to imposed pronation torques. 4. These results show that the long-latency reflex cannot be the result of a simple feed-back mechanism that controls muscle length only. We argue that the long-latency reflex activity reflects the co-ordinated activation of muscles which is necessary for an adequate response. This hypothesis is supported by the fact that the distribution of long-latency reflex activity over muscles was found to be similar to the distribution of activation found during a voluntary exerted torque in the direction opposite to the applied perturbation.

Action Potentials↗

PubMed2004

The effects of muscle history on short latency stretch reflex response of soleus muscle.

The purpose of the present study was to investigate the combined effects of muscle history, activation and stretching velocity on short latency stretch response (SLR). Stretches (70, 120 and 200 deg s-1) were elicited to both passive and active (10-25% MVC) triceps surae muscle with constant (ISO), lengthened (LEN) or shortened (SHO) muscle length. Under the passive SHO pre-condition both SLR amplitude and reflex torque (RT) decreased where as latency increased compared with the passive ISO pre-condition. Such observations were absent in active trials. Stretches applied to a lengthening passive muscle (LEN) resulted in smaller SLR amplitude and RT compared with passive ISO. In active muscle the stretch response increased with stretching velocity in ISO and SHO. However, in LEN there was large interindividual variability and no velocity dependent increase in SLR amplitude was observed. Smaller amplitude and longer latency of passive SLR in SHO could result from increased slack in the intrafusal fibres, which may be compensated by fusimotor activation during the active condition. The mechanism behind the smaller amplitude in passive LEN and the lack of velocity dependence in active LEN may be related to changes in motoneuron pool excitability or changes in the spindle sensitivity to stretch.

Adaptation, Physiological↗

PubMed1991

Evidence that low-threshold muscle afferents evoke long-latency stretch reflexes in human hand muscles.

1. The aim of the present study was to identify the type of spinal afferents involved in the generation of the long-latency response in intrinsic human hand muscles. Position-controlled extensions were imposed on the index finger or on the wrist of healthy subjects who were exerting a steady voluntary flexion force at the relevant joint. Averaged surface electromyographic (EMG) responses of the first dorsal interosseus muscle (FDI) or of the wrist flexors were evaluated with respect to latency and size. 2. Small transient angular displacements of the index finger (1 degree, as measured at the metacarpophalangeal joint), which are supposed to excite primary rather than secondary afferents, evoked two clearly discernible EMG responses with mean latencies of 32.3 ms (M1 response) and 54.7 ms (M2 response), respectively. The size of the M2 response exceeded the size of the M1 response by 60%. In the wrist flexors, transient stretch (1 degree) gave rise to a large M1 response (latency 22.8 ms) and a small, inconstent M2 response. 3. Small-amplitude vibration of the index finger elicited EMG responses in the FDI that were qualitatively and quantitatively similar to those seen in response to small transient stretches of the index finger. This was also true for fast ramp-and-hold stretches (stretch velocity 400 degrees/s, amplitude 5 degrees), whereas slow ramp-and-hold stretches (125 degrees/s, 5 degrees) elicited predominantly M2 responses. 4. In the FDI, the mechanical threshold of the M1 and M2 response to the transient angular displacement was approximately 0.15 degrees, with a tendency for the M2 response to appear at a lower threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗