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PubMed1989

The role of joint biomechanics in determining stretch reflex latency at the normal human ankle.

In order to study the influence of biomechanical factors on the timing of stretch reflex activity in the ankle extensor musculature, well defined, small amplitude and relatively rapid dorsiflexing stretch was applied to the ankle of seated normal human subjects at a series of angles within the range of physiological movement. If the ankle musculature was relaxed, a single reflex component appeared in the Triceps surae (TS) EMG with a latency compatible with a predominantly monosynaptic pathway. The latency of this response could be prolonged by applying stretch from an initially plantarflexed position and, similarly, decreased by applying stretch from a dorsiflexed position. A decrease in latency of 5-30 ms could be achieved by altering the pre-displacement ankle angle from 105 to 75 degrees. Intermediate changes in the start angle led to intermediate changes in latency. This trend was highly linear. If stretch was applied while the subject maintained a low level contraction in the TS, however, this shift in latency was abolished, with the earliest reflex components appearing with a latency obtained in the relaxed state at or close to maximum dorsiflexion. It is suggested that this shift in latency results from the properties of the long, compliant tendon through which joint movements are transmitted to the TS muscle. This shift in latency caused by passive alteration in the ankle angle at which a reflex was evoked should be taken into account when classifying reflexes arising from a mechanical input, or when using latency determinations as evidence for the involvement of particular pathways in their genesis.

Adult↗

PubMed1993

The limitations of the tendon jerk as a marker of pathological stretch reflex activity in human spasticity.

The motor disorders associated with human spasticity arise, partly from a pathological increase in the excitability of muscle stretch reflexes. In clinical practice, reflex excitability is commonly assessed by grading the reflex response to a blow delivered to the tendon of a muscle. This is a much simpler response than the complex patterns of activity which may be elicited following muscle stretch caused by active or passive movement. Changes in the biceps brachii tendon jerk response have been followed over the first year after stroke in a group of hemiparetic patients and compared with changes in short and medium latency reflex responses elicited by imposed elbow flexion of initially relaxed spastic muscle and with the development of the late reflex responses which contribute to spastic hypertonia. A progressive increase in tendon jerk responses occurred over the first year following stroke, whereas reflex responses to imposed displacement, in particular the late reflex responses contributing to muscle hypertonia, reached their peak excitability one to three months after stroke, with a subsequent reduction in activity. The tendon jerk reflex therefore provides an incomplete picture of the pathological changes in the reflex responses in spasticity.

Adult↗

PubMed1981

Interaction between pre-activity and stretch reflex in human triceps brachii during landing from forward falls.

1. Electromyographic (e.m.g.) profiles of proximal arm muscles were studied in human subjects falling forward onto a platform. 2. The stretching of the triceps lasted 200-300 msec for deep falls, and immediately after impact angular velocities of the elbow joint up to 1000 degrees sec-1 were reached. 3. For angles of fall between 50 and 90 degrees, more than half of the subjects exhibited marked short-latency e.m.g. responses of the triceps brachii. Such responses began 20-30 msec after touchdown, arising from a more or less plateau-like activity which started about 130 msec before impact. In some cases distinct later responses were found, the second peak having a latency of 60-80 msec after touchdown. 4. The early e.m.g. response even appeared when the subject was blindfolded and when the depth of the fall was randomly varied. 5. It is concluded that both the pre-existing activity and the spinal stretch reflex contribute significantly to the over-all activity of the triceps during stretch after impact.

Adult↗

PubMed2002

Short-latency stretch reflex modulation in response to varying soleus muscle activities.

The current investigation examined the effect of various types of background muscle contractions on the short-latency stretch reflex (SLR) elicited from the soleus muscle while subjects were in a sitting position. A stretch was applied to the calf muscles while they performed an isometric (pre-ISO), shortening (pre-SHO) and lengthening contraction (pre-LEN) with several pre-contraction levels. The ankle was at a 90 degrees tibio-tarsal joint angle when the perturbation was applied. Subjects developed and maintained a given pre-load level, which was maintained at various percentages of the maximum voluntary isometric plantar flexion torque. This was performed at 80 degrees in pre-SHO, 90 degrees in pre-ISO and 100 degrees in pre-LEN for about 2s before the contractions. The SLRs in trials with 0, 35 and 50% of the maximum voluntary contraction torque level were compared among the three conditions. The main results were as follows. (1) Pre-ISO and pre-SHO showed an equal SLR area and a different SLR waveform in the active muscle. (2) Pre-LEN showed the smallest SLR area of three conditions in the active muscle. (3) Pre-LEN showed shorter SLR latencies than the other conditions. (4) Pre-SHO showed a longer SLR latency in the relaxed muscle than in the active muscle. (5) The SLR area was larger in the active muscle than in the relaxed muscle. These findings demonstrate that the muscle contraction type and the pre-contraction level before a stretch perturbation have a considerable influence on the latency, the area and the waveform of the SLR. In particular, the equal area and the different waveforms of the SLR between pre-ISO and pre-SHO were a unique finding in the present study. They might result from differences in muscle spindle sensitivity and afferent input from various receptors induced by the present motor task.

Adult↗

PubMed1987

Changes in size of the stretch reflex of cat and man attributed to aftereffects in muscle spindles.

1. This is a report of experiments carried out on the cat and on man, which demonstrate that conditioning of a muscle by contraction and movement can lead to changes in amplitude of stretch reflexes elicited in that muscle. 2. In triceps surae of the cat, the reflex response to a brief stretch was recorded after conditioning with a whole-muscle contraction followed by a pause at a length either 5 mm longer or shorter than the length at which the reflex was elicited. Following conditioning at the long length the reflex response was less than half as large as that following conditioning at the short length. 3. The changes in reflex amplitude could be correlated with an altered stretch responsiveness of muscle spindles in the soleus muscle. When the muscle had been held long during conditioning, a subsequent brief stretch applied at an intermediate length elicited fewer impulses in primary endings of spindles than after conditioning at a short length. 4. The same kind of experiment was then carried out on adult human subjects. When a tendon tap was applied to the Achilles tendon after a voluntary contraction and relaxation of triceps surae with the muscle at a long length, (foot dorsiflexed) the reflex was frequently less than half the size it had been after a contraction at a short length (foot plantarflexed). It was concluded that the same kind of spindle aftereffects as observed for cat soleus spindles were responsible for the changes in reflex amplitude. 5. It was found both in the cat and in human subjects that the changes in reflex amplitude after conditioning became progressively less as the test length was made longer. 6. The explanation put forward to account for these observations is that stable cross-bridges form between actin and myosin filaments of passive intrafusal (and extrafusal) fibers. When the muscle is shortened several seconds after a contraction at a long length, the intrafusal fibers, stiffened by the presence of cross-bridges, fall slack. Slack does not develop after a contraction at a short muscle length, as the fiber is stretched to the test length. Since any slack must first be taken up by the test stretch, there is a smaller afferent response and consequently a smaller reflex contraction in response to a tendon tap after conditioning at a long length.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1973

Comparison of the tonic stretch reflex in athetotic patients during rest and voluntary activity.

An electromyographic technique was used to record the tonic stretch reflex (TSR) responses to passive sinusoidal stretching of biceps brachii muscle in athetotic patients. The TSR transmission characteristics measured while the patient was in a relaxed state were compared with those measured while the patient was voluntarily active. The resting TSR and action TSR were found to differ markedly. Sensitivity, pattern, duration, and timing of the TSR responses were all changed during voluntary activity. The results suggest that the TSR in athetosis is functionally reorganized by supraspinal influences during voluntary activity. It is proposed that athetoid movements and action tremor may be a manifestation of abnormal action TSR caused by faulty supra-spinal control during activity.

Adult↗

PubMed1991

Evidence for a contribution of the motor cortex to the long-latency stretch reflex of the human thumb.

1. In normal subjects, transcranial magnetic stimulation of the hand region of the motor cortex evokes motor responses only in contralateral hand muscles at a latency of about 19-24 ms. In contrast, stimulation of the motor cortex of three mirror movement subjects evoked, nearly simultaneously, motor responses in hand muscles on both sides of the body at latencies similar to those of normal subjects. In these subjects no other neuroanatomical pathways appear to be abnormally directed across the mid-line. Thus, their mirror movements are probably due to a projection of the corticospinal tract to homologous motoneurone pools on each side of the body. 2. We reasoned that if the motor cortex contributes to the generation of long-latency stretch reflex responses then in these mirror movement subjects stretching a muscle on one side of the body should produce long-latency reflex responses in the ipsilateral and the homologous contralateral muscle. 3. To test this idea experiments were done on normal human subjects and on the subjects with mirror movements. The electromyographic (EMG) activity of the flexor pollicis longus muscle (FPL) on each side of the body was recorded. Stretch of the distal phalanx of the thumb of one hand produced a series of distinct reflex EMG responses in the ipsilateral FPL. The earliest response, when present, began at 25 ms (S.D. = 3.5 ms) and was followed by responses at 40 (S.D. = 3.9 ms) and 56 ms (S.D. = 4.3 ms). There was no difference, either in timing or intensity, between the ipsilateral FPL EMG responses of normal subjects and those of the mirror movement subjects. 4. No response of any kind was observed in the contralateral (unstretched) FPL of normal subjects. In contrast, we observed in all three mirror movement subjects EMG responses in the contralateral (unstretched) FPL beginning at 45-50 ms. The latency of this response is considerably shorter than the fastest voluntary kinaesthetic reaction time, which was on average 130 ms (S.D. = 11 ms). The contralateral long-latency EMG response observed in the mirror movement subjects was on average 30% (range 5-60%) of that on the ipsilateral side. No short-latency response (25 ms) was ever observed in the contralateral FPL of these subjects. 5. These observations are quite consistent with the idea that the long-latency stretch reflex responses of hand and finger muscles are produced, at least in part, by the motor cortex.

Electromyography↗

PubMed1990

Effects of muscle history on the stretch reflex in cat and man.

1. This is a report of experiments on cat and man which demonstrate effects of a muscle's previous history of contraction and length changes on the size of the stretch reflex. 2. In adult human subjects the size of the tendon jerk was measured in ankle extensor muscles by tapping the Achilles tendon. Muscle conditioning consisted of a maximum voluntary contraction with the foot dorsiflexed or plantarflexed by 30 deg from the test position, after which the subject was asked to relax while the foot was held still for several seconds before being returned to the test position and a tendon tap given. After a contraction of the lengthened muscle the tendon jerk was smaller than after a contraction of the shortened muscle. 3. The experiment was then repeated, but instead of a tendon jerk an H (Hoffmann) reflex was elicited by transcutaneous electrical stimulation of the tibial nerve in the popliteal fossa. The reflex after a conditioning contraction of the lengthened muscle was larger than after a contraction of the shortened muscle. In other words muscle conditioning produced opposite effects on the tendon jerk and H reflex. 4. These findings were confirmed in cats anaesthetized with chloralose. After a conditioning contraction of triceps surae at a length 5 mm longer than the test length (hold-long) a quick tendon stretch produced a smaller reflex response than following a conditioning contraction with the muscle 5 mm shorter than the test length (hold-short). The reverse trend was seen with a reflex elicited by direct electrical stimulation of the muscle nerve, which stimulates the H reflex. 5. One consequence of a conditioning contraction is that it leads to an alteration of the level of resting discharge of muscle spindles. We propose that the larger tendon jerk after a contraction of the shortened muscle is the result of changes in stretch sensitivity of muscle spindles. The reverse effect on the H reflex we attribute to a rise in the level of resting discharge of muscle spindles, which, we propose, leads to reflex inhibition of motoneurones. 6. We support this conclusion with evidence from an experiment in which the size of the conditioning step was systematically altered. Even quite small hold-short conditioning steps led to depression of the H reflex in man and the monosynaptic reflex in cats. Recordings from single afferents showed that such small steps were also accompanied by a detectable rise in spindle resting discharge.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1992

Skeletal muscle tone and the misunderstood stretch reflex.

This review presents a revision of long-accepted tenets regarding the genesis of muscle tone in humans. Most discussions liken muscle tone in humans to the reflex tone described by Sherrington in decerebrate animals. That tradition presumes that muscle tone is fully determined by the monosynaptic stretch reflex, that tonic fusimotor activity is necessary for its production in normal humans, and that tonic muscle tone in antigravity leg muscles is responsible for the maintenance of posture. Data reviewed here show that nonreflex, mechanical mechanisms are involved in the maintenance of resting muscle tone; that spinal cord reflex responses are not stereotyped responses, but depend upon the ongoing activity in interneurons upon which inputs from a variety of peripheral sensory receptors and descending fiber systems converge; that long-latency transcortical responses are elicited when a muscle is stretched, and these responses effectively deal with large displacements; and that inertial components and viscoelastic muscle forces can counterbalance small amounts of body sway during quiet standing. In sum, the response to muscle stretch is not fixed and inflexible, but can be adjusted according to the demands of the moment.

Action Potentials↗

PubMed1983

Adaptive plasticity in primate spinal stretch reflex: initial development.

Description of the neuronal and synaptic bases of memory in the vertebrate central nervous system (CNS) requires a CNS stimulus-response pathway that is defined and accessible, has the capacity for adaptive change, and clearly contains the responsible substrates. This study was an attempt to determine whether the spinal stretch reflex (SSR), the initial, purely spinal, portion of the muscle stretch response, which satisfies the first requirement, also satisfies the second, capacity for adaptive change. Monkeys prepared with chronic fine-wire biceps electromyographic (EMG) electrodes were trained to maintain elbow position and a given level of biceps background EMG activity against constant extension torque. At random times, a brief additional extension torque pulse extended the elbow and elicited the biceps SSR. Under the control mode, reward always followed. Under the SSR increases or SSR decreases mode, reward followed only if the absolute value of biceps EMG from 14 to 24 ms after stretch onset (the SSR interval) was above or below a set value. Animals performed 3,000-6,000 trials/day over data-collection periods of up to 15 mo. Background EMG and the initial 30 ms of pulse-induced extension remained stable throughout data collection. Under the SSR increases or SSR decreases mode, SSR amplitude (EMG amplitude in the SSR interval minus background EMG amplitude) changed appropriately. Change was evident in 5-10 days and progressed over at least 4 wk. The SSR increased (SSR increases) to 140-190% control amplitude or decreased (SSR decreases) to 22-79%. SSR change did not regress over 12-day gaps in task performance. A second pair of biceps electrodes, monitored simultaneously, supplied comparable data, indicating that SSR amplitude change occurred throughout the muscle. Beyond 40 ms after pulse onset, elbow extension was inversely correlated with SSR amplitude. The delay between the SSR and its apparent effect on movement is consistent with expected motor-unit contraction time. The data demonstrate that the SSR is capable of adaptive change. At present the most likely site(s) of the mechanism of SSR amplitude change are the Ia synapse and/or the muscle spindle. Available related evidence suggests persistent segmental change may in fact come to mediate SSR amplitude change. If so, such segmental change would constitute a technically accessible fragment of a memory.

Adaptation, Physiological↗

PubMed1984

Adaptive plasticity in the primate spinal stretch reflex: evidence for a two-phase process.

Monkeys can slowly increase or decrease the amplitude of the purely spinal, largely monosynaptic portion of the response to sudden muscle stretch, the spinal stretch reflex (SSR), when confronted by a task requiring such change (Wolpaw, J.R., V.A. Kieffer, R.F. Seegal, D.J. Braitman, and M.G. Sanders (1983) Brain Res. 267: 196-200; Wolpaw, J.R., D.J. Braitman, and R.F. Seegal (1983) J. Neurophysiol. 50: 1296-1311). Change occurs without alteration in initial muscle length or in background activity of agonist, antagonist, or synergist muscles. This study uses composite curves to describe in detail the development of SSR amplitude change. It reveals important, previously unexpected features of this development. SSR increase or decrease appears to occur in two distinct phases. Phase I, a nearly immediate 8% change, occurs within the first 6 hr. Phase II, a 2%/day change, continues for at least 2 months. Although phase II is much slower than phase I, its final magnitude is far greater. Phase I indicates a nearly immediate change in suprasegmental influence of the segmental arc of the SSR. Because stretch onset time is unpredictable and the SSR occurs before any other possible response, this change in descending activity must be tonic; it must be present continually, day after day, for the 5 to 7 hr/day the animal spends at the task. Phase I produces a rapid and significant increase in reward probability. Thus, it may be readily interpreted as an example of operant conditioning, provoked by the reward contingency.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2000

Uncoupling of human short and long latency stretch reflex responses with operant conditioning.

Purpose: Successful operant conditioning of the biceps brachii spinal stretch reflex (SSR) has resulted in concurrent changes in the magnitude of long latency reflex responses (LLRRs). This finding suggests a coupling of the SSR and LLRR. The purpose of the present study was to downtrain the LLRR using operant conditioning and to observe any concurrent change in the SSR. Methods: Fourteen, able-bodied, human subjects were randomly assigned to either the control group or the training group. The LLRR and SSR responses were measured as magnitude of electromyographic response to a quick stretch of the elbow flexors, delivered by a torque motor. All the subjects attended fourteen sessions. The first six sessions were baseline sessions during which no conditioning or feedback occurred. The next eight sessions were the same as the baseline sessions (extended baseline sessions) for the control group; no feedback or operant conditioning of the LLRR occurred. The next eight sessions for the training group comprised the operant conditioning. Results: Operant conditioning of the LLRR resulted in a statistically significant reduction of that response within the training group and between the two groups. Also, operant conditioning of the biceps brachii LLRR did not result in concurrent changes in the magnitude of the SSR suggesting an uncoupling of these responses. Conclusions: The LLRR of the biceps brachii could be operantly conditioned without significant changes in the SSR which suggests that these two responses can be volitionally uncoupled.

Journal Article↗

PubMed2004

Characterisation of the quadriceps stretch reflex during the transition from swing to stance phase of human walking.

The main objective of this study was to characterize the stretch reflex response of the human thigh muscles to an unexpected knee flexion at the transition from stance to swing during walking. Eleven healthy subjects walked on a treadmill at their preferred speed. Reliable and constant knee flexions (6-12 degrees amplitude, 230-350 degrees /s velocity, 220 ms duration) were applied during the late swing and early stance phase of human walking by rotating the knee joint with a specifically designed portable stretch apparatus affixed to the left knee. Responses from rectus femoris (RF), vastus lateralis (VL), vastus medialis (VM), biceps femoris (BF), medial hamstrings (MH) and medial gastrocnemius (GM) were recorded via bipolar surface electromyograms (EMG). The onset of the response in the RF, VL and VM, remained stable and independent of the time in the step cycle when the stretch was applied. Across all subjects the response onset (mean +/- SD) occurred at 23+/-1, 24+/-1 and 23+/-1 ms for RF, VL and VM, respectively. The duration of the initial response was 90-110 ms, at which time the EMG signal returned towards baseline levels. Three reflex response windows, labelled the short latency reflex (SLR), the medium latency reflex (MLR) and the late latency reflex response (LLR), were analysed. The medium and late reflex responses of all knee extensors increased significantly ( p=0.008) as the gait cycle progressed from swing to stance. This was not related to the background EMG activity. In contrast, during standing at extensor EMG levels similar to those attained during walking the reflex responses were dependent on background EMG. During walking, LLR amplitudes expressed as a function of the background activity were on average two to three times greater than SLR and MLR reflex amplitudes. Distinct differences in SLR and LLR amplitude were observed for RF, VL and VM but not in the MLR amplitude. This may be related to the different pathways mediating the SLR, MLR and LLR components of the stretch response. As for the knee extensor antagonists, they exhibited a response to the stretch of the quadriceps at latencies short enough to be monosynaptic. This is in agreement with the suggestion by Eccles and Lundberg (1958) that there may be functional excitatory connections between the knee extensors and flexors in mammals.

Adult↗

PubMed1994

A re-examination of the effects of instruction on the long-latency stretch reflex response of the flexor pollicis longus muscle.

We re-examined the issue of how a subject's intention to react to a joint perturbation may modulate the long-latency M2 stretch reflex response. The experiments were done on the flexor pollicis longus muscle (FPL) of the human thumb, for which there is evidence that its M2 reflex response is mediated, at least in part, by a pathway that traverses the motor cortex. The participation of the cerebral cortex in the genesis of the M2 reflex response may allow for a modulation of its amplitude, based on the intention of the subject. To test whether the M2 response is genuinely modulated by the subject's intention, we examined the magnitude of this response as a function of the FPL background level of activation, measured by the surface rectified and filtered EMG. The subject was instructed either to oppose the perturbation as quickly as possible, not to react, or to relax as quickly as possible after the onset of the perturbation. The time integral of the long latency FPL EMG response, computed between 40 and 70 ms following the onset of stretch, was plotted against the mean torque produced by the distal inter-phalangeal joint of the thumb, or against the mean background FPL EMG. There were no significant differences in the FPL M2 EMG responses for different instructions. The amplitude of the reflex response was dependent only--in an approximately linear manner--on the background level of muscle activation. The total joint stiffness (intrinsic plus reflex) was also calculated for each combination of instruction and background torque.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2006

The tonic stretch reflex and spastic hypertonia after spinal cord injury.

The operational definition of spasticity is focused on increased resistance of joints to passive rotation and the possible origin of this increased resistance in the induced tonic stretch reflex (TSR). This term is applied in the context of both cerebral and spinal injury, implying that a similar reflex mechanism underlies the two disorders. From recent studies it is clear that increased passive joint resistance in resting limbs following stroke is highly correlated with the induced TSR, but this evidence is lacking in spinal injury. The contribution of the TSR to hypertonia in spinal cord injury (SCI) is unclear and it is possible that hypertonia has a different origin in SCI. The contribution of resting and activated TSR activity to joint stiffness was compared in SCI and normal subjects. The magnitude of the TSR in ankle dorsiflexors (DF) and plantarflexors (PF) and mechanical ankle resistive torque were measured at rest and over a range of contraction levels in normal subjects. Similar measures were made in 13 subjects with SCI to the limits of their range of voluntary contraction. Normals and SCI received a pseudo-sinusoidal stretch perturbation of maximum amplitude +/- 20 degrees and frequency band 0.1-3.5 Hz that was comparable to that used in manual clinical testing of muscle tone. Elastic resistance and resonant frequency of the ankle joint, after normalization for limb volume, were significantly lower in complete and incomplete SCI than normal subjects. No reflex response related to stretch velocity was observed. Resting DF and PF TSR gain, when averaged over the tested band of frequencies, were significantly lower in complete SCI than in resting normal subjects (<0.5 microV/deg). Linear regression analysis found no significant relationship between TSR gain and resting joint stiffness in SCI. Mean TSR gain of DFs and PFs at rest was not correlated with the subject variables: age, time since SCI, level of injury, Frankel score, number of spasms per day, Ashworth score or anti-spastic medication. DF and PF reflex gain were linearly related to voluntary contraction level and regression analysis produced similar slopes in incomplete SCI and normal subjects. Hence TSR loop gain was not significantly increased in SCI at any equivalent contraction level. Extrapolation of the regression lines to zero contraction level predicted that reflex threshold was not reduced in SCI. Low frequency passive stretches did not induce significant TSR activity in the resting limbs of any member of this SCI group. The TSR thus did not contribute to their clinical hypertonia. Other reflex mechanisms must contribute to hypertonia as assessed clinically. This result contrasts with our similar study of cerebral spasticity after stroke, where a comparable low frequency stretch perturbation produced clear evidence of increased TSR gain that was correlated with the hypertonia at rest. We conclude that a low frequency stretch perturbation clearly distinguished between spasticity after stroke and SCI. Spasticity in the two conditions is not equivalent and care should be taken in generalizing results between them.

Adult↗

PubMed1979

Modulation of the tonic stretch reflex by monoamines.

The effects of L-DOPA and 5-HTP on the tonic stretch reflex (TSR) in the decerebrate rat were studied. L-DOPA facilitated the TSR in a dose-dependent manner. The facilitation of the TSR was blocked by pimozide. A sensitive electromygraphic (EMG) technique capable of recording single motor unit discharges was used. The EMG results suggest that gamma motoneuron sensitivity was increased to a greater degree than alpha motoneuron sensitivity during the facilitation by L-DOPA. The L-DOPA-induced facilitation persisted in animals partly depleted of 5-hydroxytryptamine (5-HT) by reserpine, p-chlorophenylalanine or 5,6-dihydroxytryptamine. 5-HTP inhibited the TSR in a dose-dependent manner. It is concluded that DA not 5-HT is the amine which normally mediates facilitation of the TSR after L-DOPA and that gamma motoneuron activation is more likely to be involved to a greater degree than alpha motoneuron activation in the neural mechanisms of the facilitation.

5-Hydroxytryptophan↗

PubMed1995

The effects of baclofen on the stretch reflex parameters of the cat.

Experiments were done in cats decerebrated at the precollicular postmammillary level to determine how a tonic increase of presynaptic inhibition of the intraspinal terminals of muscle spindle afferents changes the mechanical properties of the soleus stretch reflex (s.r.). Baclofen, a specific GABAB receptor agonist, was injected i.v. (1-2 mg/kg) so as to induce a tonic increase in presynaptic inhibition. The effects of baclofen on the stiffness and threshold of the s.r. were determined, respectively, from plots of stiffness vs background force and force vs length (length-tension plot). Baclofen, at these doses, had no effect on the excitation-contraction coupling properties of muscle or on the intrinsic stiffness-force relation. Changes of the soleus background force, required to obtain the stiffness vs force plots, were produced by stimulation of the contralateral common peroneal nerve or the posterior tibial nerve and occasionally by electrical stimulation in the area of the red nucleus. The stiffness of the s.r. as a function of the background force level was determined by stretching the muscle with a square pulse of 1-2 mm amplitude and 200-300 ms duration. The stiffness at each force level was calculated by dividing the change in force by the change in length, at a point where the force trace had stabilized. The length-tension relation of the s.r. was determined by stretching the muscle 12-17 mm at a constant rate of 1-2 mm/s. At all force levels, baclofen produced a significant decrease (40% or more) in the s.r. stiffness, within 10-15 min of injection as determined from the stiffness-force plots. The length-tension plus revealed that the decrease of s.r. stiffness was always accompanied by an increase in the s.r. threshold (typically 2-3 mm). It is suggested, therefore, that the s.r. threshold is not an independent variable, depending on the membrane potential of the alpha-motoneurons, and additionally on the level of presynaptic inhibition of the muscle spindle afferent terminals. The present results also imply that it may be possible for the CNS to adaptively modify the s.r. stiffness via presynaptic inhibition of the intraspinal terminals of muscle afferents. However, any such change of s.r. stiffness will be accompanied by a change in the s.r. threshold.

Afferent Pathways↗

PubMed2002

Capsaicin-induced muscle pain alters the excitability of the human jaw-stretch reflex.

The pathophysiology of painful temporomandibular disorders is not fully understood, but evidence suggests that muscle pain modulates motor function in characteristic ways. This study tested the hypothesis that activation of nociceptive muscle afferent fibers would be linked to an increased excitability of the human jaw-stretch reflex and whether this process would be sensitive to length and velocity of the stretch. Capsaicin (10 micro g) was injected into the masseter muscle to induce pain in 11 healthy volunteers. Short-latency reflex responses were evoked in the masseter and temporalis muscles by a stretch device with different velocities and displacements before, during, and after the pain. The normalized reflex amplitude increased with an increase in velocity at a given displacement, but remained constant with different displacements at a given velocity. The normalized reflex amplitude was significantly higher during pain, but only at faster stretches in the painful muscle. Increased sensitivity of the fusimotor system during acute muscle pain could be one likely mechanism to explain the findings.

Adult↗