Effects of artificial and natural baroreceptor stimulation on nociceptive responding and pain

The arterial baroreflex may mediate hypertensive hypoalgesia. Carotid baroreceptors can be artificially stimulated by neck suction and inhibited by compression. Effects of brief neck suction and compression on nociceptive responding and pain were studied in 25 normotensive adults. The sural nerve was electrocutaneously stimulated at threshold intensity during systole or diastole combined with neck suction, neck compression, or no pressure. Nociceptive responding was indexed by electromyographic activity elicited in the biceps femoris. Participants rated the intensity of sural stimulation. Although artificial baroreceptor stimulation (suction) did not affect nociceptive responding, baroreceptor inhibition (compression) reduced pain ratings. In contrast, natural baroreceptor stimulation during systole reduced nociceptive responding compared to diastole, but did not affect pain ratings. The data provide partial support for baroreflex modulation of pain.     

Habituation and conditioning of the human long latency stretch reflex

Summary The effects of stretch repetition rate, prior warning stimuli and self administered stretch were examined on the size of the short and long latency components of the stretch reflex electromyographic EMG response in flexor pollicis longus and the flexor muscles of the wrist and fingers. Stretches of constant velocity and extent were given every 10 s, 5 s, 2 s, or 1 s to either the wrist or thumb during a small background contraction of the flexor muscles. The size of the long latency component of the stretch reflex (measured as the area under the averaged rectified EMG responses) declined dramatically at faster repetition rates, especially in the wrist and finger flexors. The size of the short latency component was relatively unaffected. The size of the electrically elicited H-reflex in forearm muscles also failed to habituate under the same conditions. If each individual trial of a series was examined, the long latency component of the stretch reflex EMG could be seen to decrease in size over the first three to six stretches if stretches were given every 1 s, but not if stretches were given every 10 s. When stretches were given every 5 s to either wrist or thumb, an electrical stimulus applied to the digital nerves of the opposite hand 1 s before stretch reduced the size of the long latency component of the reflex EMG response. The short latency component was unaffected. Self triggering of wrist or thumb stretch by the subject pressing the stimulator button himself with his opposite hand, also decreased the size of the long latency component of the reflex EMG response without affecting the short latency component. It is concluded that factors other than stretch size or velocity can have marked effects on the size of the long latency component of the stretch reflex. These factors must be taken into account when comparing values of reflex size obtained with different stretching techniques and in different disease states in man.     

The human nociceptive flexion reflex threshold is higher during systole than diastole

A baroreflex mechanism may explain hypertensive hypoalgesia. At rest, arterial baroreceptors are stimulated during the systolic upstroke of the pressure pulse wave. This study examined the effects of naturally occurring variations in baroreceptor activity during the cardiac cycle on an objective measure of pain, the nociceptive flexion reflex (NFR). Two interleaved up-down staircase procedures determined separate NFR thresholds during systole and diastole in 36 healthy, normotensive young adults. On odd-numbered trials, the sural nerve was stimulated electrocutaneously at R + 300 ms whereas on even-numbered trials, stimulation was delivered at R + 600 ms. The NFR threshold was higher at R + 300 ms than R + 600 ms. In contrast, stimulus intensity ratings did not differ between R + 300 ms and R + 600 ms. Stimulation of baroreceptors by natural increases in blood pressure during the systolic phase of the cardiac cycle was associated with dampened nociception.     

Relationship between stretch reflex thresholds and voluntary arm muscle activation in patients with spasticity

Previous studies have shown that deficits in agonist–antagonist muscle activation in the single-joint elbow system in patients with spastic hemiparesis are directly related to limitations in the range of regulation of the thresholds of muscle activation. We extended these findings to the double-joint, shoulder-elbow system in these patients. Ten non-disabled individuals and 11 stroke survivors with spasticity in upper limb muscles participated. Stroke survivors had sustained a single unilateral stroke 6–36 months previously, had full pain-free passive range of motion of the affected shoulder and elbow and had some voluntary control of the arm. EMG activity from four elbow and two shoulder muscles was recorded during quasi-static (<5°/s) stretching of elbow flexors/extensors and during slow voluntary elbow flexion/extension movement through full range. Stretches and active movements were initiated from full elbow flexion or extension with the shoulder in three different initial positions (60°, 90°, 145° horizontal abduction). SRTs were defined as the elbow angle at which EMG signals began to exceed 2SD of background noise. SRT angles obtained by passive muscle stretch were compared with the angles at which the respective muscles became activated during voluntary elbow movements. SRTs in elbow flexors were correlated with clinical spasticity scores. SRTs of elbow flexors and extensors were within the biomechanical range of the joint and varied with changes in the shoulder angle in all subjects with hemiparesis but could not be reached in this range in all healthy subjects when muscles were initially relaxed. In patients, limitations in the regulation of SRTs resulted in a subdivision of all-possible shoulder-elbow arm configurations into two areas, one in which spasticity was present (“spatial spasticity zone”) and another in which it was absent. Spatial spasticity zones were different for different muscles in different patients but, taken together, for all elbow muscles, the zones occupied a large part of elbow-shoulder joint space in each patient. The shape of the boundary between the spasticity and no-spasticity zones depended on the state of reflex inter-joint interaction. SRTs in single- and double-joint flexor muscles correlated with the positions at which muscles were activated during voluntary movements, for all shoulder angles, and this effect was greater in elbow flexor muscles (brachioradialis, biceps brachii). Flexor SRTs correlated with clinical spasticity in elbow flexors only when elbow muscles were at mid-length (90°). These findings support the notion that motor impairments after CNS damage are related to deficits in the specification and regulation of SRTs, resulting in the occurrence of spasticity zones in the space of elbow-shoulder configurations. It is suggested that the presence of spatial spasticity zones might be a major cause of motor impairments in general and deficits in inter-joint coordination in particular in patients with spasticity.     

Dependence of stretch reflexes on amplitude and bandwidth of stretch in human wrist muscle

The tonic stretch reflex was investigated using small-amplitude displacements (<4.2°) of the wrist while subjects maintained average contraction levels of 25% of maximum in flexor carpi radialis. The wrist displacements were designed to preclude voluntary following but at the same time were confined to the frequency range most relevant to voluntary movements. They included a broad-frequency band (0–12 Hz) signal as well as sets of narrow-band signals spanning the range from 0 to 10 Hz. The maximum frequency was set so as to remain within the linear encoding bandwidth of the reflex system and thereby minimize distortion. The effects of frequency bandwidth and amplitude of the displacement perturbations were tested in separate experiments. The coherence square, gain and phase between the EMG and angular displacement were calculated in order to characterize the stretch reflex under these conditions. It was found that the phase of the reflex response was dependent on both bandwidth and amplitude. For narrow-band displacements, the phase advance was about 30° greater over the frequency range tested than for broad-band displacements, suggesting that the reflex response may be influenced by the predictability of the perturbation. At the smallest amplitude of 0.3°, the peak phase advance was about 20° greater than at the largest amplitude of 4.2°. The gain was also higher and rose more steeply with frequency at smaller amplitudes. In the frequency range up to 12 Hz, the tonic stretch reflex responds most effectively to smaller-amplitude, more regular, higher-frequency inputs and this is consistent with a role for the reflex in counteracting small-amplitude oscillations, tremors and errors of voluntary movement. Received: 19 October 1998 / Accepted: 23 May 1999     

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° amplitude, 230–350°/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.     

Evidence for a supraspinal contribution to the human quadriceps long-latency stretch reflex

In sitting humans a rapid unexpected lengthening of the knee extensors elicits a stretch reflex (SR) response as recorded by the electromyogram (EMG) which comprises multiple bursts. These are termed short latency responses (SLR), medium latency responses (MLR) and long latency responses (LLR). The aim of this study was to determine if a transcortical pathway contributes to any of these bursts. Flexion perturbations (amplitude =4°, velocity=150°/s) were imposed on the right knee joint of sitting subjects (n=11). The effect of the perturbation on the electromyographic (EMG) response of the pre-contracted quadriceps muscle to magnetic stimulation of the contralateral motor cortex was quantified. Transcranial magnetic stimulation (TMS) was applied to elicit a compound motor evoked potential (MEP) in the target muscle rectus femoris (RF), in the vastus lateralis (VL), vastus medialis (VM) and biceps femoris (BF). The MEP and SR were elicited either in combination or separately. When applied in combination the delay between the SR and the MEP varied from 0 to 150 ms in steps of 4, 5 and 10 ms. Somatosensory evoked potentials (SEPs) were recorded from four subjects during the imposed stretch to quantify the latency of the resulting afferent volley. Onset latencies of responses in RF were 25±2 ms for the SR and 20±4 ms for the MEP. The average SEP latency was 24±2 ms. A transcortical pathway thus has the potential to contribute to the RF SR no earlier than 54±6 ms (SEP + MEP + 10 ms central processing delay) following the stretch onset. The duration of the total reflex burst was 85±6 ms. Significant facilitation of the MEP commenced at 78 ms, coinciding with the LLR component of the stretch response. No such facilitation was observed in the synergists VL and VM, or in the antagonist BF. Our results indicate that the LLR of the RF likely involves supraspinal pathways. More importantly, of the investigated muscles, this involvement of higher centers in the shaping of the LLR is specific to the RF muscle during the investigated task.     

Patterns of muscle activation in human hopping

In the present study, we examined the electromyogram (EMG) patterns of the soleus and medial gastrocnemius (MG) muscles during rhythmical, two-legged hopping to investigate the contributions of the monosynaptic short- and long-latency stretch reflexes during such a natural movement in human. During rhythmical hopping, soleus muscle is activated reflexly at near-monosynaptic latency by stretch resulting from passive ankle flexion upon landing. Soleus muscle also contracts voluntarily in order to launch the body into the next hop. This is part of the rhythmical bursts of activity producing the hops. Depending on the hopping interval, this phase of activation can follow the short-latency phase or precede landing at very short hopping intervals. In MG, there is an initial phase of activity that stiffens the muscle in preparation for landing, and continues through the contact phase. The monosynaptic reflex response to landing is usually superimposed on this activity. Depending on the hopping interval, both of these responses may be overlaid with activity that is time-locked to the take-off into the next hop, and serves to launch the body into the next hop. However, no evidence for a long-latency stretch reflex was found. In addition, the preferred hopping frequency for all subjects was about 2 Hz. This frequency is associated with a pattern of EMG activity the timing of which indicates that it balances the requirement for a comfortable landing from a hop with the optimal muscle activation required for launching the following hop. Electronic Publication     

Enhanced stretch reflex excitability of the soleus muscle in experienced swimmers

The purpose of this study was to investigate effects of long-term participation to swimming on adaptations of spinal reflex excitability. To this end, mechanically induced stretch reflex (SR) and electrically induced Hoffmann (H-) reflex of the soleus muscle were investigated between swimmers with experience of more than 10 years and non-trained individuals while sitting at rest. The amplitude and the gain (stretch velocity vs. amplitude of the reflex response) of the SR were significantly greater in the swimming group than in the non-trained control group. Similarly, the responses of the H-reflex were also significantly greater in the swimming group than in the non-trained control group. Results of this study demonstrated that the spinal reflex excitability in experienced swimmers was far more enhanced than in non-trained individuals.     

Position dependence of stretch reflex dynamics at the human ankle

Summary The purpose of this study was to examine the effect of ankle position on the human ankle stretch reflexes during tonically-maintained contractions over most of the range of motion. The ankle was placed at randomly selected mean positions. Target levels of triceps surae (TS) or tibialis anterior (TA) tonic contractions were generated while the ankle was displaced by small amplitude, stochastic perturbations. System identification techniques were used to identify the stretch reflex dynamics at each combination of tonic level and ankle angle. As shown previously, the TS stretch reflex was characterized by an unidirectional, velocity-sensitive impulse response function whereas the TA stretch reflex was characterized by a linear impulse response function between ankle velocity and TA EMG. TS stretch reflexes showed a strong dependence on ankle position while TA stretch reflexes did not. Thus the TS stretch reflex magnitude increased greatly as the ankle was progressively dorsiflexed. In contrast, ankle mean position had only a minor effect on the TA stretch reflex magnitude. Our results indicate that the position-dependent facilitation of the TS stretch reflex is not due to changes in the level of skeletal motoneuron excitability. Rather, this effect may be accounted for by mechanisms that modulate the efficacy of the stochastic ankle perturbation. Such mechanisms could include position-induced: (1) modulation of monosynaptic and polysynaptic afferent inputs to skeletal motoneurons, (2) alterations in the extent of fusimotor drive and (3) changes in the transmission of the joint perturbation to spindle receptors. Such mechanisms are discussed in terms of the differences between TS and TA stretch reflexes. Finally, the functional significance of position-dependent reflex responses are considered.     

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. This variable was calculated over a time interval (from 75 to 105 ms) that included the torque due to the M2 reflex response superimposed on the background torque, but was well before any voluntary reaction. Again, there were no significant differences in joint stiffness as a result of the instruction. We therefore conclude that, despite a cortical contribution to the M2 stretch reflex response, this response is not influenced by the intention of the subject on how to react to a perturbation.     

Variation of magnitude and timing of wrist flexor stretch reflex across the full range of voluntary activation

This paper reports an investigation of the magnitude and timing of the stretch reflex over the full range of activation of flexor carpi radialis. While it is well established that the magnitude of the reflex increases with the level of muscle activation, there have been few studies of reflex magnitude above 50% of maximum voluntary contraction (MVC) and virtually no study of the timing of the response in relation to activation level. Continuous small amplitude (~2°) perturbations were applied to the wrist of 12 normal subjects while they maintained contraction levels between 2.5–95% MVC, monitored via surface electromyography (EMG). Both narrow band (4–5 Hz) and broad band (0–10 Hz) stretch perturbations were employed. The gain (EMG output/stretch input) and phase advance of the reflex varied with the level of muscle activation in a similar manner for both types of stretch, but there were significant differences in the patterns of change due to stretch bandwidth. Consistent with previous studies, the group average reflex gain initially increased with muscle activation level and then saturated. Inspection of individual data, however, revealed that the gain reached a peak at about 60% MVC and then decreased at higher contraction levels, the pattern across the full range of activation being well described by quadratic functions (mean r²=0.82). This quadratic pattern has not been reported previously for the neural reflex response in any muscle but is consistent with the pattern that has been reliably observed in studies of the mechanical reflex response in lower limb muscles. In contrast to the pattern for reflex gain, the phase advance of the reflex (at a stretch frequency of 4.5 Hz) decreased linearly from ~130° at the lowest contraction levels to ~50° as maximum voluntary contraction was reached (mean r²=0.69). This decrease corresponds to a delay of 49 ms introduced centrally in reflex pathways. All subjects showed clearly defined quadratic functions relating reflex gain and linear functions relating reflex phase to activation level, but there were considerable individual differences in the slopes of these functions which point to systematic differences in synaptic behaviour of the motoneuron pool. Thus, there was wide inter-subject variation in both the contraction level at which the reflex gain reached a peak (31–69% MVC) and the highest target contraction level that could be sustained during reflex measurement (47–95% MVC). A high correlation between these variables (r²=0.78) suggests a linear relation between afferent support of contraction and muscle fatigability. The decline in reflex gain at high levels of muscle activation signals a failure of muscle afferent input and subjects in whom the gain reached a peak and declined early were unable to sustain higher target contraction levels. The results of the study show that both the timing and magnitude of the stretch reflex vary markedly over the full range of voluntary muscle activation. The pattern of variation may account for why the stretch reflex contributes most effectively to muscle mechanics over the lower half of the range of activation, while progressive reductions in both gain and phase advance at higher levels render the reflex mechanically less effective and make tremor more likely.     

Recovery of stretch reflex responses following mechanical stimulation

Summary The recovery behaviour of mechanically evoked stretch responses was investigated. Stimuli which promoted identical dorsiflexing movements around the ankle joint were applied to ten subjects in two positions, seated and upright. The experimental sets comprised single as well as double dorsiflexing displacements. In the latter the stimuli were elicited for durations of either 100, 200 or 400 ms. Stretch responses following the first displacements were related to the stretch velocity but not to the amplitude. The responses of the plantar flexors following the second mechanical dorsiflexion were reduced with respect to the delay time between the first and second displacement. In addition, the magnitudes of these responses depended on the functional task: the stretch responses recovered much faster in the standing position when the triceps surae muscle was only slightly activated, whereas in the relaxed sitting position the reflexes remained suppressed. Both reciprocal inhibition, as well as the time course of the reformation of intrafusal cross-bridge links, may help to explain the depression of the monosynaptic stretch reflex.     

Identification of the stretch reflex using pseudorandom excitation: Electromyographic response to displacement of the human forearm

System identification techniques are applied to the human stretch reflex by crosscorrelating a random displacement of the forearm with a surface electromyographic signal obtained from biceps muscle. Since the random forcing function is too fast to be tracked by the subject, the resulting responses reflect components of the limb control system which are automatic. Clear responses are obtained for small displacement amplitudes, typically 0·5 mm at the wrist, with a test duration of about 1 minute. The results, which are highly reproducible, are compared with simulations based upon a linear model of the stretch reflex.     

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. This variable was calculated over a time interval (from 75 to 105 ms) that included the torque due to the M2 reflex response superimposed on the background torque, but was well before any voluntary reaction. Again, there were no significant differences in joint stiffness as a result of the instruction. We therefore conclude that, despite a cortical contribution to the M2 stretch reflex response, this response is not influenced by the intention of the subject on how to react to a perturbation.     

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 GABA_B 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 plots 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 - 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.     

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

Summary 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.     

Modulation of the functional stretch reflex by the segmental reflex pathway

Summary 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.Supported in part by grants from the Medical Research Council of Canada (MT-4465) and the National Institutes of Health (NS-10311)Post-doctoral Fellow supported by the Medical Research Council of Canada     

Identification of time-varying dynamics of the human triceps surae stretch reflex

We examined the time-varying dynamics of the human triceps surae stretch reflex before, during, and after a large stretch was imposed upon the ankle joint, during a constant voluntary contraction of 15% of maximum voluntary contraction. Stretch reflex dynamics were estimated by superimposing a small stochastic displacement on many such stretches and using an ensemble-based time-varying identification procedure to compute impulse response functions relating the perturbation to the evoked electromyogram (EMG) at each point throughout the task. We found that stretch reflex magnitude (relating joint velocity to EMG) varied directly with baseline EMG activity during steady-state conditions before and after the large imposed stretch. Following the large stretch and the reflex activity it evoked, both background EMG and stretch reflex magnitude declined for up to 100 ms; changes in the stretch reflex were substantially greater in magnitude and followed a different time course from the corresponding changes in background EMG, however, indicating that stretch reflex properties were modulated independently of motoneuron pool activation level. Based on timing and the invariance of stretch reflex dynamics across time, it is argued that this behavior is largely mediated via peripheral neural mechanisms. This peripheral modulation of the stretch reflex presumably supplements various descending influences to adjust reflex properties.     

Prolonged time course for vibratory suppression of stretch reflex in the decerebrate cat

Summary We studied the effects of longitudinal tendon vibration on the stretch reflex of the soleus and gastrocnemius muscles in 11 decerebrate cats. Vibration was applied at amplitudes (40–80 m) and frequencies (120–250 Hz) sufficient to provide a strong tonic vibration reflex. In keeping with previous reports, we found that during an established tonic vibration reflex, the force and emg response to superimposed ramp and hold stretch are largely suppressed. This suppression is most obvious during the dynamic phase of stretch where it gives rise to a complex force response resembling that of active areflexic muscle.If stretch initiation is delayed until after vibration is terminated, the suppressive effects of vibration persist for 5 s or more. These suppressive effects are marked in the first 200 ms, and then decay gradually over the ensuing time period, paralleling the decline in emg and force which follows vibration offset. Simultaneous recordings from homonymous Ia afferents showed that this suppression persists even though the stretch responsiveness of primary spindle endings has returned to normal immediately following the end of vibration.When stretch is initiated shortly after vibration commences, the suppressive effects are first evident at 50–100 ms latency, but are not well established until 1 s or more after vibration onset.Tests of monosynaptic transmission using small amplitude tendon taps or electrical stimulation of synergist nerves to activate Ia fibers revealed that reductions in the magnitude of the response following vibration are usually modest (12% mean reduction at 50 ms, n = 5), and they are quite sensitive to the initial level of excitation of the motoneuron pool. These reductions were also rather shortlived, being largely completed within 500 ms of vibration offset. Although the relative contributions of presynaptic and postsynaptic inhibition are not readily dissociated in this type of experiment, it is likely that the magnitude of presynaptic inhibition is quite small.We argue that the effects of vibration on the stretch reflex are best explained by invoking an excitatory autogenetic projection from Ia interneurons to extensor motor neurons, which lies in parallel with the Ia monosynaptic projection. In order to account for the vibratory suppression, we propose that these interneurons are driven to saturation by vibration. When vibration ceases, the discharge rate of these interneurons declines with a prolonged time-course that coincides with the recovery of stretch responsiveness. This recovery would contribute to the return of stretch reflex force.