EMG responses to load perturbations of the upper limb: effect of dynamic coupling between shoulder and elbow motion

Summary Load perturbations were applied to the arm of human subjects under conditions where both limb segments (upper arm and forearm) were free to move. The perturbations consisted of pulses of torque 50 ms in duration and of pseudo-random sequences of such pulses. They were applied to either the forearm or the upper arm. Under all conditions, the perturbations resulted in angular motion at the shoulder and elbow joints and evoked consistent responses in muscles acting about these joints (biceps, triceps, anterior and posterior deltoid). Activity in biceps and triceps was not related simply to angular motion at the elbow joint. For example, activation of biceps could be evoked during elbow flexion (by applying a torque perturbation at the shoulder) as well as during elbow extension (by applying a torque perturbation at the elbow). The effect of varying degrees of dynamic coupling between upper arm and forearm on EMG responses was investigated by applying torque perturbations to the upper arm over a wide range of elbow angles. When the forearm is extended, such a perturbation induces a greater amount of elbow flexion than when the forearm is in a flexed position. The results of these experiments showed that the larger was the amount of flexion of the forearm induced by the perturbation, the larger was the activation of biceps. The results are incompatible with the notion of a negative feedback of total muscle length as being responsible for the EMG activity following the load perturbations. It is suggested that the EMG responses can best be interpreted functionally in terms of parameters more global than muscle length. Among such global parameters, changes in net torque at a joint resulting from the perturbation gave the best correlation with the pattern of EMG activities observed.     

Fast corrective responses are evoked by perturbations approaching the natural variability of posture and movement tasks

A wealth of studies highlight the importance of rapid corrective responses during voluntary motor tasks. These studies used relatively large perturbations to evoke robust muscle activity. Thus it remains unknown whether these corrective responses (latency 20-100 ms) are evoked at perturbation levels approaching the inherent variability of voluntary control. To fill this gap, we examined responses for large to small perturbations applied while participants either performed postural or reaching tasks. To address multijoint corrective responses, we induced various amounts of single-joint elbow motion with scaled amounts of combined elbow and shoulder torques. Indeed, such perturbations are known to elicit a response at the unstretched shoulder muscle, which reflects an internal model of arm intersegmental dynamics. Significant muscle responses were observed during both postural control and reaching, even when perturbation-related joint angle, velocity, and acceleration overlapped in distribution with deviations encountered in unperturbed trials. The response onsets were consistent across the explored range of perturbation loads, with short-latency onset for the muscles spanning the elbow joints (20-40 ms), and long-latency for shoulder muscles (onset > 45 ms). In addition, the evoked activity was strongly modulated by perturbation magnitude. These results suggest that multijoint responses are not specifically engaged to counter motor errors that exceed a certain threshold. Instead, we suggest that these corrective processes operate continuously during voluntary motor control.     

The effect of task instruction on the excitability of spinal and supraspinal reflex pathways projecting to the biceps muscle

There is controversy within the literature regarding the influence of task instruction on the size of the long-latency stretch reflex (M2) elicited by a joint displacement. The aim of this study was to investigate if the previously reported task-dependent modulation of the M2 is specific to the M2 or can be explained by an early release of the intended voluntary response. We took advantage of the fact that the M2 is absent when the duration of the applied perturbation is less than a critical time period. This allowed us to examine modulation of muscle activity with and without the contribution of the M2. In addition, we applied transcranial magnetic stimulation (TMS) over the primary motor cortex to examine the modulation of corticomotor excitability with task instruction. Elbow joint extension displacements were used to elicit a stretch reflex in the biceps muscle. Subjects were instructed to “do not intervene” (DNI) with the applied perturbation, or to oppose the perturbation by activating the elbow flexors in response to the perturbation (FLEX). Electromyographic (EMG) activity in the time period corresponding to the M2 was significantly facilitated in the FLEX task instruction both with and without the presence of the M2. Motor evoked potentials (MEPs) elicited by TMS were also facilitated during the FLEX condition in the absence of the M2. EMG and MEP responses were not facilitated until immediately prior to the onset of the M2. Paired-pulse TMS revealed a significant reduction in short-interval intracortical inhibition (SICI) during the M2 response, but the level of SICI was not altered by the task instruction. We conclude that the task-dependent modulation of the biceps M2 results, at least in part, from an early release of the prepared movement and is accompanied by an increase in corticospinal excitability that is not specific to the M2 pathway. Task-dependent modulation of the response cannot be explained by an alteration in the excitability of intracortical inhibitory circuits.     

Instruction-dependent modulation of the long-latency stretch reflex is associated with indicators of startle

Long-latency responses elicited by postural perturbation are modulated by how a subject is instructed to respond to the perturbation, yet the neural pathways responsible for this modulation remain unclear. The goal of this study was to determine whether instruction-dependent modulation is associated with activity in brainstem pathways contributing to startle. Our hypothesis was that elbow perturbations can evoked startle, indicated by activity in the sternocleidomastoid muscle (SCM). Perturbation responses were compared to those elicited by a loud acoustic stimulus, known to elicit startle. Postural perturbations and startling acoustic stimuli both evoked SCM activity, but only when a ballistic elbow extension movement was planned. Both stimuli triggered SCM activity with the same probability. When SCM activity was present, there was an associated early onset of triceps electromyographic (EMG), as required for the planned movement. This early EMG onset occurred at a time often attributed to long-latency stretch reflexes (75–100 ms). The nature of the perturbation-triggered EMG (excitatory or inhibitory) was independent of the perturbation direction (flexion or extension) indicating that it was not a feedback response appropriate for returning the limb to its original position. The net EMG response to perturbations delivered after a movement had been planned could be explained as the sum of a stretch reflex opposing the perturbation and a startle-evoked response associated with the prepared movement. These results demonstrate that rapid perturbations can trigger early release of a planned ballistic movement, and that this release is associated with activity in the brainstem pathways contributing to startle reflexes.     

Co-contraction modifies the stretch reflex elicited in muscles shortened by a joint perturbation

Simultaneous contraction of agonist and antagonist muscles acting about a joint influences joint stiffness and stability. Although several studies have shown that reflexes in the muscle lengthened by a joint perturbation are modulated during co-contraction, little attention has been given to reflex regulation in the antagonist (shortened) muscle. The goal of the present study was to determine whether co-contraction gives rise to altered reflex regulation across the joint by examining reflexes in the muscle shortened by a joint perturbation. Reflexes were recorded from electromyographic activity in elbow flexors and extensors while positional perturbations to the elbow joint were applied. Perturbations were delivered during isolated activation of the flexor or extensor muscles as well as during flexor and extensor co-contraction. Across the group, the shortening reflex in the elbow extensor switched from suppression during isolated extensor muscle activation to facilitation during co-contraction. The shortening reflex in the elbow flexor remained suppressive during co-contraction but was significantly smaller compared to the response obtained during isolated elbow flexor activation. This response in the shortened muscle was graded by the level of activation in the lengthened muscle. The lengthening reflex did not change during co-contraction. These results support the idea that reflexes are regulated across multiple muscles around a joint. We speculate that the facilitatory response in the shortened muscle arises through a fast-conducting oligosynaptic pathway involving Ib interneurons.     

Short- and long-latency reflex responses during different motor tasks in elbow flexor muscles

 Stretch reflex responses in three elbow flexor muscles – the brachioradialis and the short and long heads of the biceps brachii – were studied during different motor tasks. The motor tasks were iso-velocity (8 deg/s) elbow flexion movements in which the muscles performed shortening or lengthening contractions, or were isometric contractions. Care was taken to maintain constant background electromyographic (EMG) activity in the brachoradialis muscle at a 50-deg elbow angle across the tasks by changing the magnitude of the initial load. During each task, mechanical perturbations (duration 170 ms) were applied at pseudorandom intervals when the elbow angle was 50 deg. The magnitude of the perturbation was varied across tasks in order to induce an elbow extension velocity of 80 deg/s over the first 50 ms after the onset of perturbation. The stretch reflex EMG responses in all muscles varied across the three tasks, despite a constant EMG level and similar perturbation-induced angular velocity in the direction of elbow extension. In particular, both the short- and long-latency reflex EMG components were reduced during the lengthening contractions. Further, the task-dependent variations in the early (M2) and the late (M3) components of the long-latency reflex were different, i.e., the magnitude of M3 was considerably enhanced during the shortening task as compared with that of M2. These findings suggest that central modification was responsible for the task-dependent modulation of late EMG responses. Received: 24 April 1996 / Accepted: 24 January 1997     

Responses of mono- and bi-articular muscles to load perturbations of the human arm

Summary We studied the behavior of muscles acting synergistically in elbow flexion in response to load perturbations. The perturbations were applied either proximally or distally to the elbow joint and consisted of single pulses or steps of torque and of pseudorandom sequences of torque pulses. They produced changes in angular position and torque at both the shoulder and elbow joints. The electromyographic (EMG) responses evoked in biceps, brachio-radialis and brachialis muscles were different when elbow and shoulder motion was in the same direction and when the two angular motions were oppositely directed. For example, elbow extension resulted both when a downward force perturbation was applied to the forearm as well as when a posteriorly directed force applied to the upper arm was released. Elbow flexors were activated at a short latency only in the former case and not in the latter. The modulation of EMG activity in elbow flexors evoked by the perturbations was related to the global motion of the limb, including the angular motions at both the shoulder and elbow joints. The time course of the EMG responses in biceps, which acts on both joints, differed from that of brachio-radialis and brachialis muscles, which act only at the elbow. The results are discussed in the context of the possible mechanisms responsible for the muscle responses to the perturbations.     

Spinal mechanisms of the functional stretch reflex

Summary A sudden and rapid angular displacement of the limb evokes, in human and monkey subjects, a segmented pattern of electromyographic activity in muscles which are stretched. While the first segment is acknowledged to represent a tendon jerk, it has been proposed that the second segment, occurring with a shorter latency than a reaction time, is mediated by a transcortical loop. The present experiments were conducted in cats to determine the properties of muscle responses to torque perturbations analogous to those used in the monkey, and to determine if the integrity of supraspinal pathways is required for the individual response segments to occur.Torque perturbations which flexed the forearm evoked a segmented response in the electromyogram of the cat triceps muscle. This response typically consisted of three early segments with latencies of 10, 30 and 60 msec which were similar to the M1, M2, and M3 segments described in the monkey. The M3 and occasionally M2 components were depressed when the cat followed rather than resisted the perturbation. A torque pulse of 10 msec duration was sufficient to elicit a near maximal M1 response while torque pulses in excess of 20 msec were required to evoke the M2 response.To determine if any of these components required mediation by the cerebral cortex, experiments were conducted in decerebrate and spinal cats. Similar torque perturbations produced segmented electromyographic responses in the triceps muscles which were indistinguishable in their timing from those observed in intact cats. The torque required to produce the segmented responses was comparable as well. All three segments were dependent upon the activation of receptors in the homonymous muscle and did not require cutaneous input. These observations show that receptor properties and/or spinal mechanisms involved in the stretch reflex are sufficient to produce a segmented response similar to that observed in intact animals.     

Neural compensation for fatigue-induced changes in muscle stiffness during perturbations of elbow angle in human.

1. The contribution to muscle force regulation provided by reflex pathways was studied in the elbow flexor muscles of seven normal human subjects, with the use of voluntary fatigue to induce a deficit in the force-generating capability of these muscles. To estimate the changes in the mechanical state of the muscle and the compensatory actions taken by reflex pathways to minimize the impact of fatigue, stochastic and "step" angular perturbations were applied to the joint, and the resulting joint stiffness and electromyographic (EMG) responses were compared before and after fatigue. 2. The magnitude of contractile fatigue, induced by repeatedly lifting a weight via a pulley system, was quantified by comparing the slope of the isometric torque-EMG relationship before and after fatigue. The exercise routine was quite effective in producing severe and long-lasting fatigue, with average percentage changes in the isometric torque-EMG slope of 210-306% for biceps and 129-205% for brachioradialis, depending on the point in time examined. 3. The torque response to a rapid step stretch of the elbow joint was quite similar before and after fatigue for the time interval before reflex action (less than 20 ms after stretch onset), suggesting that intrinsic muscle stiffness for a given mean torque level was not changed by fatigue. The steady-state torque level attained after completion of the stretch was always decreased after fatigue, indicating a decrease in the reflex component of joint stiffness, but this decrease was small compared with the change in the isometric torque-EMG relationship and was accompanied by a significantly larger incremental EMG response after fatigue. This increase in incremental EMG after fatigue was found to be of reflex origin, with activation-related reflex gain changes apparently playing a significant role only at low contraction levels. 4. Torque and angle responses recorded during stochastic perturbations were used to identify elbow joint compliance impulse responses. A second-order mechanical model was fit to each impulse response, and the parameters representing joint inertia, elastic stiffness, and viscous stiffness were used to summarize changes in joint mechanical properties as the mean contraction level was varied. For a perturbation with a relatively wide bandwidth (0-25 Hz), fatigue had little or no effect on the form of the compliance impulse response, apparently because the stimulus disabled reflex force generation in elbow flexor muscles, whereas a perturbation with a more restricted bandwidth (0-10 Hz) demonstrated consistent decreases in joint stiffness after fatigue.(ABSTRACT TRUNCATED AT 400 WORDS)     

Loss of set in muscle responses to limb perturbations during cerebellar dysfunction

The properties of electromyograph (EMG) responses that enabled the arm to return accurately to target following limb perturbations were investigated in five Cebus monkeys. In particular, factors that affected the timing and magnitude of an early antagonist response that occurred prior to stretch of the antagonist muscle were examined. The early antagonist response was large and early (latency, 60 ms) when the perturbation was brief and a constant force assisted the return movement. In this situation, early contraction of the antagonist muscle was required to prevent the return movement from overshooting the target. To determine whether this early antagonist response was influenced by prior instruction (which in this case was the type of perturbation the monkey had previously received), two types of perturbations requiring different EMG responses were studied. When torque steps (duration, 2,000 ms) were expected and were applied, monkeys generated M1, M2, and M3 responses and later activity only in the agonist (the initially stretched) muscle. When torque pulses (duration, 40 ms) were expected and were applied, monkeys generated M1 and M2 responses in the agonist and an early antagonist response. EMG responses to torque pulses and steps were then compared when the type of perturbation was expected and when it was unexpected. These comparisons revealed that the early antagonist response only occurred when the monkey expected a torque pulse. Therefore, this response was dependent on set. Expectation of a torque step caused enhancement of the agonist M2 and M3 responses. These agonist and antagonist EMG responses that were dependent on set were also influenced by changes in afferent drive. Cerebellar nuclear cooling through probes implanted lateral and medial to the dentate abolished that component of EMG responses attributed to set. The residual EMG responses in agonists and antagonists appeared to be driven by stretch of their respective muscles. The results suggest that when the nature of an arm perturbation is correctly predicted, the cerebellum provides accuracy in repositioning the limb a) by adjusting the magnitude of the M2 agonist response and b) by enabling activity after a latency of 60 ms (e.g., the M3 and early antagonist response) to be switched to the agonist or antagonist as appropriate, irrespective of which muscle is being stretched. This latter mechanism provides the motor system with predictive ability.     

Neural control: novel evaluation of stretch reflex sensitivity

We evaluated the stretch reflex activities of the elbow flexor and extensor muscles considering the relationship between the reflex electromyographic (EMG) responses and their corresponding standardized muscle stretch velocities. Specifically, muscular stretch velocity was estimated by using ultrasonograms. Stretch reflex EMG responses were elicited in the biceps brachii, brachioradialis and triceps brachii with a ramp-and-hold rotation at the elbow joint, which consisted of various angular velocities for the extension- or flexion-direction. The whole muscle stretch velocity induced by each ramp-and-hold rotation was calculated on the basis of fibre length changes associated with the elbow joint angle. A linear regression equation was fitted to the relation between the whole muscle stretch velocity and the reflex EMG responses, and the variables from the equation were used to quantify sensitivity of each reflex EMG component. The reflex EMG responses were increased as the ramp-and-hold rotational velocity increased. There were no significant differences in the recorded magnitudes of reflex EMG responses with equivalent joint rotational velocity between the brachioradialis and the triceps brachii medial head. These muscles showed the highest reflex responses in the flexor and extensor muscles, respectively. To the contrary, the reflex EMG response elicited by the standardized muscle stretches was significantly greater in the extensor muscles, indicating a higher reflex sensitivity. This was because of the lower muscle stretch velocity of the triceps brachii with an equivalent elbow joint rotation. The stretch reflex sensitivity in both the elbow flexor and extensor muscles might be regulated so as to make the reflex responses the same when the equivalent joint rotational velocity is applied to these muscles.     

Contributions of altered stretch reflex coordination to arm impairments following stroke

Patterns of stereotyped muscle coactivation, clinically referred to as synergies, emerge following stroke and impair arm function. Although researchers have focused on cortical contributions, there is growing evidence that altered stretch reflex pathways may also contribute to impairment. However, most previous reflex studies have focused on passive, single-joint movements without regard to their coordination during volitional actions. The purpose of this study was to examine the effects of stroke on coordinated activity of stretch reflexes elicited in multiple arm muscles following multijoint perturbations. We hypothesized that cortical injury results in increased stretch reflexes of muscles characteristic of the abnormal flexor synergy during active arm conditions. To test this hypothesis, we used a robot to apply position perturbations to impaired arms of 10 stroke survivors and dominant arms of 8 healthy age-matched controls. Corresponding reflexes were assessed during volitional contractions simulating different levels of gravitational support, as well as during voluntary flexion and extension of the elbow and shoulder. Reflexes were quantified by average rectified surface electromyogram, recorded from eight muscles spanning the elbow and shoulder. Reflex coordination was quantified using an independent components analysis. We found stretch reflexes elicited in the stroke group were significantly less sensitive to changes in background muscle activation compared with those in the control group (P < 0.05). We also observed significantly increased reflex coupling between elbow flexor and shoulder abductor-extensor muscles in stroke subjects relative to that in control subjects. This increased coupling was present only during volitional tasks that required elbow flexion (P < 0.001), shoulder extension (P < 0.01), and gravity opposition (P < 0.01), but not during the "no load" condition. During volitional contractions, reflex amplitudes scaled with the level of impairment, as assessed by Fugl-Meyer scores (r(2) = 0.63; P < 0.05). We conclude that altered reflex coordination is indicative of motor impairment level and may contribute to impaired arm function following stroke.     

Electromyographic responses to constant position errors imposed during voluntary elbow joint movement in human

The role of reflexes in the control of stiffness during human elbow joint movement was investigated for a wide range of movement speeds (1.5–6 rad/s). The electromyographic (EMG) responses of the elbow joint muscles to step position errors (step amplitude 0.15 rad; rise time 100 ms) imposed at the onset of targeted flexion movements (1.0 rad amplitude) were recorded. For all speeds of movement, the step position disturbance produced large modulations of the usual triphasic EMG activity, both excitatory and inhibitory, with an onset latency of 25 ms. In the muscles stretched by the perturbation, the early EMG response (25–60 ms latency) magnitude was greater than 50% of the activity during the unperturbed movements (background activity). In all muscles the EMG responses integrated over the entire movement were greater than 25% of the background activity. The responses were relatively greater for slower movements. Perturbations assisting the movement caused a short-latency (25–60 ms) reflex response (in the antagonist muscle) that increased with movement speed and was constant as a percentage of the background EMG activity. In contrast, perturbations resisting the movement caused a reflex response (in the agonist muscle) that was of the same absolute magnitude at all movement speeds, and thus decreased with movement speed as a percentage of the background EMG activity. There was a directional asymmetry in the reflex response, which produced an asymmetry in the mechanical response during slow movements. When the step perturbation occurred in a direction assisting the flexion movement, the antagonist muscle activity increased, but the main component of this response was delayed until the normal time of onset of the antagonist burst. When the step perturbation resisted the movement the agonist muscles responded briskly at short latency (25 ms). A reflex reversal occurred in two of six subjects. A fixed reflex response occurred in the antagonist muscle, regardless of the perturbation direction. For the extension direction perturbations (resisting movement), this response represented a reflex reversal (50 ms onset latency) and it caused the torque resisting the imposed step (stiffness) to drop markedly (below zero for one subject). Reflex responses were larger when the subject was prevented from reaching the target. That is, when the perturbation remained on until after the normal time of reaching the target, the EMG activity increased, with a parallel increase in stiffness. Similarly, when the perturbations prevented the subject from reaching the target during a 1-rad voluntary cyclic movement, the EMG and stiffness increased markedly. Coactivation of the antagonist muscle with the agonist muscle was not prominent (<30% of antagonist activity) during unperturbed movements. The perturbations were resisted with reciprocal activity, and thus reflex action did not increase the coactivation. However, as a result of the low-pass properties of muscle, substantial cocontraction of the agonist and antagonists muscle forces may have occurred during rapid movements, thus leading to increased stiffness. As the relative changes in normal EMG activity produced by the perturbation were often comparable with the changes in mean muscle torque (stiffness) reported in the first paper of this series, we conclude that the action of reflexes produced a significant portion of the resistance to perturbations. This reflexive portion was greater for slower movements, it was greater when the subject neared the target, and it was variable according to the perturbation direction and the particular subject. Given that the perturbations were of similar frequency content to the movement itself (though of smaller amplitude) and that the reflexes contributed substantially to the resistance to these perturbations, we suggest that in normal unperturbed movements the observed EMG is likewise substantially determined by the reflex activity.     

Postural responses in the cat to unexpected rotations of the supporting surface: evidence for a centrally generated synergic organization

Summary Postural reactions to disruptions of stance are rapid and automatic in both quadrupeds and bipeds. Current evidence suggests that these postural responses are generated by the central nervous system as patterns involving muscle synergies. This study attempted to test this hypothesis of a centrally generated postural mechanism by determining whether the same postural response could be evoked in the freely-standing cat under two different biomechanical conditions. The present work is an extension of previous experiments in which the stance of cats was perturbed by a horizontal translation of the supporting surface in the anterior and posterior directions (Rushmer et al. 1983). We now tested whether simple rotation of the metacarpo- and metatarsophalangeal (M-P) joints that mimics the digit rotation occurring during platform translation, was sufficient to evoke the translation postural response. The rotational perturbations were biomechanically different from translations in that the rotation did not cause displacement of the centre of mass of the animal, nor did it result in any significant movement about any but the M-P joints. Even so, rotational perturbations did evoke the appropriate translational muscle synergies in all four animals. Both plantar flexion rotation and headward translation activated the posterior hindlimb synergy (which included gluteus medius, semitendinosus and lateral gastrocnemius). Similarly, dorsiflexion rotation and tailward translation both activated the same anterior hindlimb synergy (iliopsoas, vastus lateralis and tibialis anterior) together with the forelimb synergy. The postural responses elicited by rotational perturbations were biomechanically inappropriate, and caused the animal to displace its own centre of mass away from the stable, control position. The most striking finding was that the group of muscles in which the medium latency postural response was evoked was different than the group from which short latency reflex responses were elicited. These data support the hypothesis that postural reactions are not merely reflex responses to local sensory inputs associated with the perturbation but, instead, represent a centrally generated response, with the muscle synergy being the controlled unit.Supported by NIH grants NS19484 and RR05593 as well as Good Samaritan Hospital     

Joint receptors modulate short and long latency muscle responses in the awake cat

Summary Nerve cuff electrodes were chronically implanted around multiple peripheral nerves in adult cats, including the medial and posterior articular nerves (MAN and PAN) to the knee while EMG electrodes were implanted into seven hindlimb muscles. Randomized load perturbations producing mid-range knee flexions at varying angular velocities were subsequently applied to awake cats. Recordings were initially obtained with knee joint innervation intact and then after local anaesthetic or saline control solution was injected into the knee. Averaged neurogram and EMG responses to the imposed movements were utilized to assess the contribution of joint mechanoreceptor activity to the evoked muscle responses. Additionally, spike-triggered averaging techniques and peri-stimulus time histograms of single joint afferent units isolated from the articular nerve cuffs were utilized to characterize unitary joint receptor responses. The averaged whole nerve response to knee joint perturbations on each of the cuffed articular nerves revealed phasic increases in activity relative to constant background levels. The earliest phasic responses on the articular nerves were initiated at latencies that were too short to be voluntary, occurring in the short latency (reflex) period. Detectable joint receptors were not recruited until after the earliest excitatory responses of agonist/antagonist muscle pairs acting across the knee had occurred, presumably resulting in mechanical loading of the knee joint capsule and subsequent activation of articular mechanoreceptors. Introduction of local anaesthetic into the knee was accompanied by marked diminution in joint afferent activity. Perturbation-evoked muscle responses were characterized by increased activity above background levels in all seven muscles studied, including antagonist muscle pairs. Local anaesthetic-mediated loss of knee joint mechanoreceptor input altered the latency, amplitude and duration of EMG responses in each muscle. The effect of joint anaesthesia in the short latency period was a generalized decrease in all muscle responses relative to normal and saline controls. The loss of afferent input after joint anaesthesia was also associated with altered muscle responses during the long latency period, when both reflex and voluntary mechanisms could potentially contribute to the generation of EMG activity. Interestingly, long latency activity after joint anaesthesia was characterized by unbalancing in the EMG responses of some antagonist muscle pairs. This alteration of normal antagonist pair co-contraction patterns served to increase the magnitude of the imposed perturbations, rather than to bring the movements under control. Analysis of single joint afferents isolated from whole joint nerve recordings demonstrated that some joint afferent units were tonically active at quiescent, mid-range knee positions. Additionally, isolated afferents demonstrated different time courses of response to imposed perturbations. Some afferents responded with decreased or absent firing activity (TONIC units) while other joint afferents responded with phasic bursts of activity which were greatly increased above their relatively low levels of tonic, background activity (TONIC-PHASIC units). In addition to TONIC and TONIC-PHASIC units, other joint afferents were identified which were only active after imposition of passive knee movements (PHASIC units). In conclusion, data obtained from whole joint nerve recordings as well as data from isolated, single joint afferents demonstrate that joint receptors can modulate short and long latency muscle responses to passively-imposed knee movements in the awake cat.Supported by Medical Research Council of Canada (MRC) grant MT5218. KWM is an MRC fellow     

Effect of Muscle Biomechanics on the Quantification of Spasticity

The impact of muscle biomechanics on spasticity was assessed by comparison of the reflex responses of the elbow and metacarpophalangeal (MCP) flexor muscles in individuals with chronic spastic hemiplegia following stroke. Specifically, methods were developed to quantify reflex responses and to normalize these responses for comparison across different muscle groups. Stretch reflexes were elicited in the muscles of interest by constant velocity ramp-and-hold stretches at the corresponding joint. The muscles were initially passive, with the joint placed in a midrange position. Estimates of biomechanical parameters were used to convert measured reflex joint torque and joint angle into composite flexor muscle stress and stretch. We found that the stretch reflex response for the MCP muscle group had a 74% greater mean stiffness modulus than that for the elbow muscle group, and that the reflex threshold was initiated at an 80% shorter mean muscle stretch. However, we determined that initial normalized fiber length was significantly greater for the experiments involving the MCP muscles than for those involving the elbow muscles. Increasing the initial composite fiber length of the elbow flexors produced significant reduction of the reflex threshold (p < 0.001), while decreasing the initial length of the MCP flexors significantly reduced their measured reflex stiffness (p < 0.001). Thus, biomechanical parameters of muscle do appear to have an important effect on the stretch reflex in individuals with impairment following stroke, and this effect should be accounted for when attempting to quantify spasticity. © 2001 Biomedical Engineering Society. PAC01: 8719Rr     

Transient reversal of the stretch reflex in human arm muscles.

1. Load perturbation responses can violate the law of reciprocal innervation between antagonist muscles under particular conditions. Thus flexor and extensor muscles of wrist and elbow joints are reflexly coactivated by the impact of a ball on the hand during a catching task. The aim of this study was to determine whether reflex coactivation can be preset within the central nervous system (CNS) or whether it is entirely due to the peripheral stimulus. To this end, we studied the behavior of stretch reflex responses of arm muscles evoked by torque motor perturbations applied before and during the catching task. 2. Subjects were instructed to catch a ball dropped from 1.6 m. A torque motor delivered perturbations to the elbow joint, resulting in angular motion at both elbow and wrist joints because of their dynamic mechanical coupling. Two series of experiments were performed that differed in the perturbation waveform. In the first series, a single torque pulse could be randomly applied at different times during the task. The corresponding responses were recovered by subtracting the average of the unperturbed trials from the averages of perturbed trials. In the second series of experiments, a train of pseudorandom pulses was applied continuously during each trial. The time-varying impulse responses were computed at 20-ms intervals by cross-correlation methods. 3. The pattern of the short-latency electromyographic responses evoked by either single pulses or pseudorandom perturbations obeyed the law of reciprocal innervation of antagonist muscles under basal conditions. However, the pattern of the responses evoked by the same perturbations around the time of ball impact on the hand consisted of a substantial coactivation of both stretched and shortening muscles. Reflex coactivation resulted from response patterns that differed at different joints. At the elbow, reflex coactivation resulted from a transient reversal of the direction of the short-latency responses of flexor muscles, with little changes of the responses of extensor muscles. At the wrist, instead, reflex coactivation resulted from simultaneous changes in the response waveform of both flexor and extensor muscles. 4. The peripheral conditions associated with the applied perturbations were constant before the time of ball impact. Thus, because the changes of the stretch reflex responses began before that time, they must have been generated within the CNS. It is here hypothesized that the reversal of the reflex responses is centrally gated by switching from the pathways of reciprocal inhibition to those of coactivation of antagonist alpha-motoneurons.(ABSTRACT TRUNCATED AT 400 WORDS)     

Modulation of dorsal spinocerebellar responses to limb movement. II. Effect of sensory input

Dorsal spinocerebellar tract (DSCT) neurons receive converging sensory inputs from muscle, skin, and joint receptors and their cerebellar projection is a product of the spinal sensory processing of movement-related information. We concluded earlier that DSCT activity relates to global rather than to local parameters of hindlimb postures and movement, specifically to a kinematic representation of the limb endpoint. The waveforms of principal components (PCs) derived from an ensemble of DSCT movement responses were found to correlate with either the waveform of the limb axis length or orientation trajectories. It was not clear, however, whether these global representations resulted from neural processing or from biomechanical factors. In this study, we perturbed the limb biomechanical factors by decoupling limb geometry from endpoint position during passively applied limb trajectories patterned after a step cycle. We used two types of perturbations: mechanical constraints that limited joint rotations and electrical stimulation of hindlimb muscles. We found that about half of the 89 cells studied showed statistically different response patterns during the perturbations. We compared the PCs of the altered responses with the PCs of the control responses, and found two basic results. With the joint constraints, >85% of the total variance in both control and changed responses was accounted for by the same five PCs that were also observed in the earlier study. The differences between altered and control responses could be fully accounted for by changes in the PC weighting, suggesting a modulation of global response components rather than an explicit representation of local parameters. With the muscle stimulation, only the first and third PCs were the same for the control and altered responses. The second PC was modified, and additional PCs were also required to account for the altered responses. This suggests that the stimulus parameters were specifically represented in the responses. The changes induced by both types of perturbation affected primarily the weighting or waveform of the second PC, which relates to the limb axis length trajectory. The results are consistent with the suggestion that information about limb orientation and length may be separately modulated.     

Movement and muscle activity during contact placing of the forelimb and their relations to other postural reactions in the cat

Forelimb trajectory and the activity of eight muscles operating at the elbow, wrist and digit joints were compared during the contact placing reaction, during the swing phase of locomotion and during reactions induced by swing perturbations, to verify the hypothesis that common neural mechanisms are involved in these reactions. Both the patterns of muscle activation and forelimb kinetics during the placing reaction greatly differed from those during the swing phase of locomotion. Both similarities and differences have been found between the placing reaction and the reaction to swing perturbations. Similar latencies, patterns of muscle activation and trajectories have been found for elbow movements while considerable differences were seen in the movements of distal joints. Both reactions started with a backward and upward movement at the proximal joints which was accompanied by a locking at the elbow. At the distal joints, tactile stimuli evoked first a wrist ventroflexion during the placing reaction, whereas they induced wrist dorsiflexion to swing perturbations. A further difference between these two reactions appeared at the beginning of the extension which was highly passive during the reaction to swing perturbation and active during contact placing. These results suggest that some common, most likely spinal, reflexes are involved at the beginning of the two reactions while their extension phases are controlled in a different way.