Automatic postural responses following rapid displacement of a light touch contact during standing.

Responses elicited by the rapid displacement of a light touch contact surface were investigated during standing with the eyes closed. During quiet standing the touch surface was moved with an imperceptible slow (0.5Hz), small (0.5cm) oscillation to entrain the participant's sway. Periodically, a rapid displacement (1.25cm, 12.5cm/s peak velocity, 187.5cm/s/s peak acceleration) of the rod was applied, either forward or backward, at either the fore or aft position of the entrained sway. Each participant received 10 unexpected displacements of the same direction, with 20 participants receiving forward displacements and 6 participants receiving backward displacements. Electromyographic recordings from 4 arm and 2 ankle muscles were sampled along with center of pressure and joint kinematics. Rapid displacement of the touch surface consistently resulted in short-latency (<120ms) responses in the muscles of the arm or ankle in 21 of 26 participants. However, the first exposure to the touch displacement resulted in a distinct response in the muscles about the ankle in 13 participants, while responses in arm muscles were observed in 11 participants. Participants that responded with activation of muscles at the ankle displayed a corresponding shift in the center of pressure. Trials 2 through 10 were characterized by an absence of responses in the ankle muscles, but more consistent responses in the arm muscles. The rapid onset of ankle muscle activity following the unexpected slip of a touch surface in some instances suggests that tactile cues provide a potential sensory cue for triggering balance reactions. The importance of this sensory cue in balance control is likely dependent in part on the relevance of the tactile inputs in the context of the perceived task.

Effects of ankle extensor muscle afferent inputs on hip abductor and adductor activity in the decerebrate walking cat.

Electrical stimulation of the lateral gastrocnemius-soleus (LGS) nerve at group I afferent strength leads to adaptations in the amplitude and timing of extensor muscle activity during walking in the decerebrate cat. Such afferent feedback in the stance leg might result from a delay in stance onset of the opposite leg. Concomitant adaptations in hip abductor and adductor activity would then be expected to maintain lateral stability and balance until the opposite leg is able to support the body. As many hip abductors and adductors are also hip extensors, we hypothesized that stimulation of the LGS nerve at group I afferent strength would produce increased activation and prolonged burst duration in hip abductor and adductor muscles in the premammillary decerebrate walking cat. LGS nerve stimulation during the extensor phase of the locomotor cycle consistently increased burst amplitude of the gluteus medius and adductor femoris muscles, but not pectineus or gracilis. In addition, LGS stimulation prolonged the burst duration of both gluteus medius and adductor femoris. Unexpectedly, long-duration LGS stimulus trains resulted in two distinct outcomes on the hip abductor and adductor bursting pattern: 1) a change of burst duration and timing similar to medial gastrocnemius; or 2) to continue rhythmically bursting uninterrupted. These results indicate that activation of muscle afferents from ankle extensors contributes to the regulation of activity of some hip abductor and adductor muscles, but not all. These results have implications for understanding the neural control of stability during locomotion, as well as the organization of spinal locomotor networks.

Compensatory balance reactions during forward and backward walking on a treadmill.

Previous work suggests that balance perturbations to the body opposing the direction of progression during walking lead to larger amplitude corrective reactions than perturbations concurrent with walking direction. To test this hypothesis, subjects received forward and backward perturbations applied to the pelvis through a padded harness, while walking forwards or backwards on a treadmill. Contrary to our hypothesis, the greatest responses were associated with backward perturbations regardless of the direction of walking.

Contribution of hindpaw cutaneous inputs to the control of lateral stability during walking in the cat.

To delineate the role of cutaneous feedback from the paws in the regulation of balance during walking, we compared the corrective responses of cats to lateral support surface translation before and after cutaneous denervation of the hindpaws. In addition, we compared characteristics of undisturbed walking before and after denervation. Electromyographic and kinematic data were collected from three cats trained to walk across a walkway, the central portion of which could be unexpectedly translated laterally in either direction. Following denervation, all of the cats changed their step width, lowered their pelvis, and spent more time with the hindlegs in double-support when walking across the walkway. When displaced by lateral support surface translations, the denervated cats made larger lateral steps and required more than a single step to regain balance. However, none of the cats fell following the denervation. The appearance and latency of the responses evoked in the hindleg muscles by the perturbations were unaffected by the denervation. However, the amplitude of these responses was affected by the loss of cutaneous inputs. Responses evoked at paw contact were significantly reduced in most muscles in the absence of cutaneous input, whereas responses evoked at end of stance revealed significant increases in gluteus medius activity with little influence on the activity of other muscles. Therefore the loss of cutaneous inputs leads to instability during gait. Although cutaneous feedback from the hindpaws is not essential for triggering corrective responses to support surface disturbances, it appears that cutaneous inputs are important for scaling the responses initiated by other cues.

Reflex pathways connect receptors in the human lower leg to the erector spinae muscles of the lower back.

Reflex pathways connect all four limbs in humans. Presently, we tested the hypothesis that reflexes also link sensory receptors in the lower leg with muscles of the lower back (erector spinae; ES). Taps were applied to the right Achilles' tendon and electromyographic activity was recorded from the right soleus and bilaterally from ES. Reflexes were compared between sitting and standing and between standing with the eyes open versus closed. Reflexes were evoked bilaterally in ES and consisted of an early latency excitation, a medium latency inhibition, and a longer latency excitation. During sitting but not standing, the early excitation was larger in the ES muscle ipsilateral to the stimulation (iES) than in the contralateral ES (cES). During standing but not sitting, the longer latency excitation in cES was larger than in iES. This response in cES was also larger during standing compared to sitting. Responses were not significantly different between the eyes open and eyes closed conditions. Taps applied to the lateral calcaneus (heel taps) evoked responses in ES that were not significantly different in amplitude or latency than those evoked by tendon taps, despite a 75-94% reduction in the amplitude of the soleus stretch reflex evoked by the heel taps. Electrical stimulation of the sural nerve, a purely cutaneous nerve at the ankle, evoked ES reflexes that were not significantly different in amplitude but had significantly longer latencies than those evoked by the tendon and heel taps. These results support the hypothesis that reflex pathways connect receptors in the lower leg with muscles of the lower back and show that that the amplitude of these reflexes is modulated by task. Responses evoked by stimulation of the sural nerve establish that reflex pathways connect the ES muscles with cutaneous receptors of the foot. In contrast, the large volley in muscle spindle afferents induced by the tendon taps compared to the heel taps did not alter the ES responses, suggesting that the reflex connection between triceps surae muscle spindles and the ES muscles may be relatively weak. These heteronymous reflexes may play a role in stabilizing the trunk for maintaining posture and balance.

Phase-specific modulation of the soleus H-reflex as a function of threat to stability during walking.

The purpose of the present study was to determine whether the soleus H-reflex is modulated with changes in the level of postural threat during walking. H-reflexes were tested at four points in the step cycle when subjects walked in 5 conditions representing different levels of postural threat. H-reflexes were significantly increased in amplitude at heelstrike in conditions of increased postural threat compared to normal treadmill walking with only minimal changes in H-reflex amplitude at other step cycle points. Conversely when subjects walked while holding stable handles, to decrease postural threat, the amplitude of the H-reflex was significantly smaller at heelstrike and midstance compared to normal walking. The changes in the amplitude of the H-reflex between walking conditions were not accompanied by changes in ongoing electromyographic activity or movements. Our findings suggest that the amplitude of the reflex is adjusted in a phase-specific manner, related to the postural uncertainty of the task. These adaptations in reflex amplitude may be related to changes in the amplitude of corrective responses following perturbations during walking. The adaptations in the amplitude of the H-reflex specific to heelstrike may be important in the control of foot placement at ground contact.

Walking delays anticipatory postural adjustments but not reaction times in a choice reaction task.

During standing, anticipatory postural adjustments (APAs) and focal movements are delayed while performing a choice reaction task, compared with a simple reaction task. We hypothesized that APAs and focal movements of a choice reaction task would be similarly delayed during walking. Furthermore, reaction times are delayed during walking compared with standing. We further hypothesized that APAs and focal movements would be delayed during walking, compared with standing, for both simple and choice reaction tasks. Subjects either walked or stood on a treadmill while holding on to stable handles. They were asked to push or pull on the handles in response to a visual cue. Muscle activity was recorded from muscles of the leg (APA) and arm (RT). Our results were in agreement with previous work showing APA onset was delayed in the choice reaction task compared with the simple reaction task. In addition, the interval between the onset of APA and focal movement activity increased with choice reaction tasks. The task of walking did not delay the onset of focal movement for either the simple or choice reaction tasks. Walking did delay the onset of the APA, but only during choice reaction tasks. The results suggest the added demand of walking does not significantly modify the control of focal arm movements. However, additional attentional demands while walking may compromise anticipatory postural control.

Chemical ablation of sensory afferents in the walking system of the cat abolishes the capacity for functional recovery after peripheral nerve lesions.

Weakening the ankle extensor muscles of cats by denervation of the synergists of the medial gastrocnemius (MG) muscle results in transient increase in yield at the ankle during early stance. Recovery of ankle function occurs over a period of 1-2 weeks, is use-dependent, and is associated with increases in the strength of reflexes from MG group I muscle afferents and an increase in the magnitude of bursts in the MG muscles during stance. These observations have led to the hypothesis that feedback from large muscle afferents is necessary for functional recovery. In this investigation we have tested this hypothesis by examining functional recovery in animals treated with pyridoxine, a drug known to destroy large muscle afferents. In four adult animals we confirmed that pyridoxine abolished the group I-mediated tendon-tap reflex in the ankle extensor muscle, and subsequently found that group I afferents from MG were either destroyed or non-conducting. Immediately after pyridoxine treatment the animals showed severe locomotor dysfunction but all recovered significantly over a period of 1 or 2 months and showed only minor kinematics deficits at the time of the muscle denervations. In all four pyridoxine-treated animals, weakening of the ankle extensors by denervation of the synergists of the MG muscle resulted in a large increase in yield at the ankle that persisted almost unchanged for a month after the operation. The magnitude of burst activity in the MG muscle during early stance of the pyridoxine-treated animals either did not increase or increased only slightly after the denervation of synergists. These observations are consistent with the hypothesis that feedback from group I afferents is necessary for functional recovery in untreated animals.

Adaptive changes in locomotor activity following botulinum toxin injection in ankle extensor muscles of cats.

The present study investigated the adaptations made in motor behavior following a temporary reduction in ankle extensor activity in the walking cat. Temporary muscle weakness was induced by injecting botulinum toxin into the lateral gastrocnemius (LG), plantaris (PL), and soleus (SOL) muscles, or SOL alone. The medial gastrocnemius (MG) muscle was not injected. Adaptations in the level of muscle activity were recorded using chronically implanted electromyographic (EMG) electrodes. Serial recordings were made prior to botulinum toxin injections and for several days following the injections. Kinematic analysis of ankle joint movements was made from video records to assess the impact of the botulinum toxin injections on the function of the ankle joint during walking. Following injection of the LG, PL, and SOL muscles with botulinum toxin, the amplitude of the MG burst increased over a period of a few days to a week. This increase was similar to the previously reported changes produced in MG following transection of the nerves serving LG, PL, and SOL. Following the weakening of the ankle extensor muscles, there was a temporary deficit in ankle function during walking as evidenced by a marked increase in the amount of ankle flexion that occurred at stance onset. This functional deficit recovered relatively quickly and was not associated with a return of the EMG pattern to the preinjection pattern. After recovery from the initial injections, a second injection of botulinum toxin into SOL alone was performed. No functional deficits were observed in the ankle movements during walking following this second injection. However, weakening SOL produced increases in the burst amplitudes of the MG, LG, and PL muscles over a period of a few days. This suggests that normal movements at the ankle during walking can be generated with more than one pattern of ankle extensor activity and that there is flexibility in how the necessary torque is produced. A final procedure, transection of the nerves serving LG, PL, and SOL, failed to produce any functional deficits in ankle movements. The implication is that adaptations to the neural control of ankle extensor activity that were induced by the initial procedure persisted after the recovery of the injected muscles and were sufficient to compensate for the subsequent challenges.

Vibration-induced inhibition of the early components of the tibial nerve somatosensory evoked potential is mediated at a spinal synapse.

OBJECTIVES: To investigate whether afferent-induced suppression of cortical somatosensory evoked potentials (SEPs) occurs at a spinal site along the transmission route of afferent signals from the tibial nerve to the primary somatosensory cortex. METHODS: Evoked potentials were recorded at 4 points (sciatic nerve, L5, C1, and cortex) along the path of transmission following electrical stimulation of the tibial nerve in halothane-anesthetized cats. The amplitudes of evoked potentials sampled during vibration of quadriceps were compared to evoked potentials sampled without the vibration. RESULTS: The spinal SEP recorded at C1 and the cortical SEP were both substantially reduced by patellar tendon vibration. The L5 spinal SEP and the sciatic nerve potential were unaffected. Vibration of quadriceps did not influence the latency of the evoked potentials. CONCLUSIONS: These results indicate that afferent-induced suppression of the initial complex of the SEP can be mediated at a spinal synapse.

Use-dependent gain change in the reflex contribution to extensor activity in walking cats.

Denervation of the synergists of the medial gastrocnemius (MG) muscle in the cat hind leg results in a progressive increase in the magnitude of burst activity in the MG muscle during walking. The increase in burst magnitude is associated with an increase in the slope of the relationship between the magnitude of individual MG bursts and the amplitude of ankle flexion during stance. This finding is consistent with the hypothesis that the increase in MG burst magnitude is due to an increase in gain of reflex pathways reinforcing the activation of MG. The increase in slope is use-dependent since it was not observed when the leg was released from a cast that immobilized the leg for 6 days.

Functional role of muscle reflexes for force generation in the decerebrate walking cat.

To quantify the importance of reflexes due to muscle length changes in generating force during walking, we studied high decerebrate cats that walked on a treadmill. One leg was denervated except for the triceps surae and a few other selected muscles. The triceps surae muscles are ankle extensor muscles that attach to the Achilles' tendon which was cut and connected to a muscle puller. In some steps the EMG activity triggered the puller to move the muscle through the pattern of length changes that are normally produced by ankle movements in intact cats walking over ground (simulated walking). In other steps the muscles were held isometrically. The EMG and force produced during the two types of steps were compared. On average about 50 % more EMG was generated during the E2 part of the simulated stance phase in the triceps surae muscles, but not in other muscles studied. Force was increased significantly over the entire stance phase by about 20 %, when muscle stretches simulating walking were applied. However, during much of the stance phase the triceps surae muscles are shortening and so would produce less force. The effect of shortening was assessed in control experiments in which these muscles were stimulated at a constant frequency, either isometrically or during simulated walking movements. By combining data from the walking and control experiments, we estimate that about 35 % of the force produced in the cat ankle extensors during stance is produced by reflexes due to muscle length changes. Other sensory inputs may also contribute to force production, but the total reflex contribution will vary under different conditions of speed, length, loading, task difficulty, etc. Since a substantial percentage of the force in the stance phase of walking is normally produced by muscle reflexes, this force can be continuously adjusted up or down, if the muscles receive extra stretch or unloading during a particular step cycle.

Early corrective reactions of the leg to perturbations at the torso during walking in humans.

The contribution of afferent feedback to the regulation of locomotion in humans is not well understood. Animal experiments have suggested that loading of the leg during the stance phase may enhance the magnitude of extensor burst activity and delay the onset of swing phase. The aim of the present study was to determine whether transient loading of the leg at the end of stance would enhance extensor-muscle activity and delay the onset of swing in walking humans. To test this hypothesis, we applied loads to the hips of subjects so that the load was applied along the long axis of the leg at the end of stance (down-back unsupported, DBU). This resulted in an unexpectedly complex reaction characterised by rapid co-contraction of antagonist pairs of muscles around the ankle and knee and a prolongation of the stance phase. We speculated that the complexity of the reaction was, in part, due to a disturbance in equilibrium. To address this possibility, two additional perturbation paradigms were tested: (1) subjects held a rail during the loading paradigm (down-back supported, DBS), or (2) subjects received only a posteriorly directed perturbation of the hips, which added no additional load to the leg (backward unsupported, BU). As predicted, the DBS perturbation resulted in an enhancement of the ongoing soleus-muscle activity, and the unexpected tibialis anterior burst that was observed during the DBU paradigm was absent. Allowing the subjects to hold a rail substantially reduced the change in the timing of the step cycle observed in the DBU paradigm. The BU perturbation prolonged the stance phase duration and, as expected, resulted in a burst of activity in tibialis activity. This was usually accompanied by a reduction in the ongoing soleus activity. Two important conclusions are drawn from the present study. First, loading of the leg at the end of stance phase enhances the ongoing extensor-muscle activity. We suggest that afferent feedback responding to the increase load supported by the leg leads to rapid enhancement of the active extensor muscles to compensate for the increased load and prevent collapse of the leg. Interestingly, the duration of the stance phase was only marginally increased when loading was applied without a postural disturbance (DBS). Second, posterior perturbation of the centre of mass at the end of stance phase evokes an "automatic postural response" in tibialis anterior. Of particular interest, this evoked postural response can occur simultaneously with an enhanced activation of soleus. This indicates that the DBU perturbation employed in this study elicited two responses, one to prevent the collapse of the leg and the other to stabilise the centre of mass.

Stretch and H reflexes in triceps surae are similar during tonic and rhythmic contractions in high decerebrate cats.

During locomotion in decerebrate and spinal cats the group Ia afferents from hind leg muscles are depolarized rhythmically. An earlier study concluded that this locomotor-related primary afferent depolarization (PAD) does not contribute to modulation of monosynaptic reflex pathways during locomotion. This finding indicated that the neural network generating the locomotor rhythm, the central pattern generator (CPG), does not presynaptically inhibit monosynaptic reflexes. In this investigation we tested this prediction in decerebrate cats by measuring the magnitude of reflexes evoked in ankle extensor muscles during periods of tonic contractions and during sequences of rhythmic contractions. The latter occurred when the animal was induced to walk on a treadmill. At the similar levels of activity in the soleus muscle there was no significant difference in the magnitude of the soleus H reflex in these two behavioral situations. Similar results were obtained for reflexes evoked by brief stretches of the soleus muscle. We also examined the reflexes evoked by ramp-and-hold stretches during periods of rhythmic and tonic activity of the isolated medial gastrocnemius (MG) muscle. At similar levels of background activity, the reflexes evoked in the MG muscle were the same during rhythmic and tonic contractions. Our failure to observe a reduction in the magnitude of H reflexes and stretch reflexes during rhythmic contractions, compared with reflexes evoked at the same level of background activity during tonic contractions, is consistent with the notion that the CPG for stepping does not presynaptically inhibit monosynaptic reflexes during the extension phase of locomotor activity. Our results indicate that presynaptic inhibition of the monosynaptic reflex associated with normal locomotion in cats or humans arises from sources other than the extensor burst generating system of the central pattern generator.

Adaptive changes in motor activity associated with functional recovery following muscle denervation in walking cats.

In this investigation we examined the changes in the pattern of activity in the medial gastrocnemius (MG) muscle in walking cats following transection of the nerves innervating synergist muscles (lateral gastrocnemius, soleus, and plantaris). Immediately following the nerve transections, there was a large increase in ankle flexion during early stance (from approximately 10 to approximately 30 degrees ) and a marked increase in the magnitude of the MG bursts during stance. We attribute this increase in the magnitude of the MG bursts to an increase in afferent feedback from the abnormally stretched MG muscle. During the week after the nerve transections, there was a progressive decrease in ankle yield. This improvement in ankle function was correlated with an increase in magnitude of two components of the MG bursts; the initial component starting during late swing and ending approximately 40 ms after ground contact, and a late component associated with stance. The time courses of the increases in the initial and late components of the MG bursts were different. Large and significant increases in the late component occurred the day after the nerve transections, whereas increases in the initial component occurred more gradually. This difference in time course was reflected in the kinematics of ankle movement. Over the first few days after the nerve transections, improvement in ankle movement occurred primarily late in the stance phase, and there was little change in ankle yield during early stance. At 1 wk, however, there was a significant reduction in ankle yield during early stance. This decreased yield was most likely due to an increase in stiffness of the MG muscle at the time of ground contact resulting from the increase in magnitude of the initial component of the MG bursts. The increases in the magnitude of the initial and late components of the MG bursts, as well as the improvement in ankle function, depended on use of the leg. All these changes were delayed by immobilizing the leg for 6 days in an extended position. We discuss possible mechanisms underlying the increase in the magnitude of the MG bursts and propose that proprioceptive signals from the stretched MG muscles provide an error signal for rescaling the magnitude of the centrally generated initial component. Our data support the concept that proprioceptive feedback functions to scale the magnitude of feed-forward motor commands to ensure they are appropriate for the biomechanical properties of the musculoskeletal system.

Movement-induced modulation of soleus H reflexes with altered length of biarticular muscles.

Passive pedaling movements of the leg results in the phasic modulation of the soleus H reflex of that leg. In contrast, the H reflex of the contralateral leg is attenuated tonically. The phasic modulation of the reflex ipsilaterally can be attributed to the afferent discharge associated with the cyclic lengthening of the extensor muscles. We hypothesized that the tonic attenuation of the contralateral reflex could be explained if the afferent feedback arising from the lengthening of the biarticular muscles had an increased importance in regulating the amplitude of the contralateral reflex. To test this, the passive pedaling movements were reduced to those about either the knee or hip alone. Despite the alteration in the pattern of stretching of the biarticular muscles, the contralateral soleus H reflex was tonically attenuated during both forms of single joint movements. We suggest that the same phasic afferent discharge responsible for the modulation of the ipsilateral soleus H reflex initiates the tonic attenuation contralaterally, but that the signal undergoes a complex transformation in crossing the cord. These results do not rule out the possibility that the stretching of the biarticular muscles contributes to the attenuation of the ipsilateral soleus H reflex, which is subsequently masked by a powerful influence from the stretching of the uniarticular extensor muscles. To test this possibility, a second experiment manipulated the lengths of the muscles of the leg by altering the positions of the static joints during isolated rotation of either the knee or hip and measuring the amplitude of the ipsilateral soleus H reflex. From the results, it was clear that stretching the uniarticular extensor muscles produced the most dramatic effects. However, the stretch of the biarticular muscles yielded mild inhibitory influences if these muscles were near their maximal lengths.

Crossed inhibition of the soleus H reflex during passive pedalling movement.

We hypothesized that sensory input from the moving leg induces presynaptic inhibition of the soleus H reflex pathway in the contralateral stationary leg. The results showed a crossed inhibition during passive pedalling movement of the leg, which was not removed by low levels of tonic contraction of soleus in the stationary leg. The inhibition was correlated exponentially to the rate of the movement (R2 = 0.934, P < 0.05) and was not dependent on the quadrants through which the moving leg was passing. Static flexion of the stationary leg caused ipsilateral inhibition of the reflexes (t = 5.590, P < 0.05), independent of the orientations of the other leg. We concluded that sensory inflow from the moving leg induces presynaptic inhibition in the stationary leg, that a complex transformation of the sensory input in the spinal cord or brain underlies the tonic crossed inhibition and phasic ipsilateral inhibition, and that descending motor commands exert a powerful control over these sensorimotor modulatory mechanisms.

Enhancement and resetting of locomotor activity by muscle afferents.

The generation of the normal motor pattern for walking in mammals requires feedback from muscle proprioceptors. Two characteristics of the motor pattern particularly dependent on proprioceptive signals are (1) the magnitude of activity in knee and ankle extensor muscles and (2) the duration of extensor bursts during stance. Sensory regulation of these characteristics ensures that the level of activity in extensor muscles during stance is appropriate for the load carried by the leg and that the swing phase is not initiated when a leg is loaded. Many different groups of afferents from flexor and extensor muscles can influence the locomotor pattern. Most attention has focused on the action of group I afferents from ankle extensors. Electrical stimulation of these afferents during extension increases the duration and the magnitude of extensor activity. The prolongation of extensor activity depends in part on excitation of the extensor half-center by group Ib afferents from Golgi tendon organs. The enhancement of the magnitude of extensor bursts is produced primarily via disynaptic and polysynaptic pathways opened only during locomotion. The involvement of the proprioceptive signals in the generation of locomotor activity means that the gains in reflex pathways must be constantly calibrated according to the biomechanical properties of the locomotor system. Alteration of these properties by weakening ankle extensor muscles has recently been found to produce compensatory changes in proprioceptive influences on the locomotor pattern.

Modulation of H reflexes in human tibialis anterior muscle with passive movement.

Significant movement-induced gain changes in H reflexes have been observed in soleus muscle following passive movement of the lower limb. Hypotheses from these concepts were tested on magnitudes of H reflexes in tonically contracted tibialis anterior. From eleven subjects at rates of 20 and 60 r.p.m. passive leg movement, statistically significant attenuation from controls and phasic modulation occurred. The results make more general the conclusions from soleus H reflexes. However, the functional effect should be much smaller, as tibialis anterior H reflexes are smaller compared to those in soleus.

Movement-induced gain modulation of somatosensory potentials and soleus H-reflexes evoked from the leg. I. Kinaesthetic task demands.

Movement-related gating of cerebral somatosensory evoked potentials (SEPs) occurs during active and passive movements of both the upper and the lower limbs. The general hypothesis was tested that the brain participates in setting the gain of the ascending path from somatosensory receptors of the human leg to the somatosensory cortex. In experiment 1, SEPs from Cz' and soleus H-reflexes were evoked by electrical stimulation of the tibial nerve in the popliteal fossa during passive movement about the right ankle. Early SEPs and H-reflexes sampled during simple passive movement were significantly attenuated when compared with stationary controls (P<0.05). The additional requirement of tracking the passive ankle movement with the other foot led to a significant relative facilitation of mean SEP, but not H-reflex amplitude, compared with means from passive movement alone (P<0.05). In experiment 2, SEPs were evoked in the active (tracking) leg during a forewarned reaction-time task. Subjects were required to move in a preferred direction or to track the passive movement of their right foot with their left. Significant attenuation of early SEP components occurred 100 ms prior to EMG onset (P<0.05), with no apparent effect due to tracking. In the 3rd experiment, SEPs and H-reflexes were evoked in the passively moved leg (the target for active movement of the left leg) during the same forewarned reaction-time task. During the warning period, SEPs were significantly attenuated compared with stationary controls for non-tracking movements, but not for movements involving tracking (P<0.05). It is concluded that centrifugal factors are important in modulating SEP gain required by the kinaesthetic demands of the task.