Search

We investigated the influence of vestibular (caloric ear irrigation) and visual (optokinetic) stimulation on slow and fast split-belt walking. The velocity of one belt was fixed (1.5 or 5.0-6.0 km/h) and subjects (N = 8 for vestibular and N = 6 for visual experiments) were asked to adjust the velocity of the other belt to a level at which they perceived the velocity of both the belts as equal. Throughout all experiments, subjects bimanually held on to the space-fixed handles along the treadmill, which provided haptic information on body orientation. While the optoki- netic stimulus (displayed on face-mounted virtual reality goggles) had no effect on belt velocity adjustments com- pared to control trials, cold-water ear irrigation during slow (but not fast) walking effectively influenced belt velocity adjustments in seven of eight subjects. Only two of these subjects decreased the velocity of the ipsilateral belt, consistent with the ipsilateral turning toward the irrigated ear in the Fukuda stepping test. The other five subjects, however, increased the velocity of the ipsilateral belt. A straight-ahead sense mechanism can explain both decreased and increased velocity adjustments. Subjects decrease or increase ipsilateral belt velocity depending on whether the vestibular stimulus is interpreted as an indi- cator of the straight-ahead direction (decreased velocity) or as an error signal relative to the straight-ahead direction provided by the haptic input from the space-fixed handles along the treadmill (increased velocity). The missing effect during fast walking corroborates the findings by others that the influence of vestibular tone asymmetry on locomotion decreases at higher gait velocities.

The goal of this study was to investigate changes of H-reflex amplitudes during a motor learning task. Subjects with reduced vision were instructed to step over an obstacle on a treadmill as low as possible, while the soleus H-reflex was elicited. Acoustic warning and feedback signals about performance were provided. Performance improvement was associated with a decrease of muscle activity, needed to step over the obstacle (rectus femoris, biceps femoris, tibialis anterior and gastrocnemius medialis muscles), and of foot clearance, while joint angle trajectories from knee and ankle became more stable. The experiment consisted of five runs, three with normal treadmill walking and two with randomly stepping over the obstacle (100 times). H-reflexes were elicited at early and late stance phase before stepping over the obstacle. H/M ratio, latency and duration were determined. The values of these measures were calculated for the onset and end of a run and their course over time was evaluated using a correlation coefficient. The largest adaptations with a significant increase of reflex amplitude occurred during the first obstacle run. This increase lasted only briefly and the reflex amplitudes decreased to their previous values. During the later obstacle run, no H-reflex modulation occurred. It is concluded that a motor learning task causes adaptational effects not only on performance, but also on H-reflex responses. The results indicate that most of the modulation of H-reflexes is probably due to supraspinal influences on reflex transmission. The observations made are probably less specific for this motor task (stepping over the obstacle), but rather associated with the increased attention required by the motor learning task during the first obstacle run

In walking humans, arm to leg coordination is a well established phenomenon. The origin of this coordination, however, remains a matter for debate. It could derive from the intrinsic organisation of the human CNS, but it could also consist of a movement induced epiphenomenon. In order to establish which of these alternatives applies, we recorded arm and leg movements as well as their muscle activities during walking, creeping on all fours and swimming. The relationship between arm and leg cycle frequency observed under these various conditions was then investigated. We found that during walking, creeping on all fours or swimming, arm and leg movements remain frequency locked with a fixed relationship of 1/1, 2/1, 3/1, 4/1 or 5/1. When movements of the legs are slowed by flippers, the frequency relationship may skip to a different value, but the coordination is preserved. Furthermore, minimising the mechanical interactions between the limbs does not abolish coordination. These findings demonstrate that the arm to leg coordination observed in the walking human is also present during other human locomotor activities. The characteristics of this coordination correspond to those of a system of two coupled oscillators like that underlying quadruped locomotion.

Load dependent reflex adaptations were studied in healthy subjects walking on a split-belt treadmill. Compensatory reflex responses were elicited in the right leg extensor muscles during mid-stance by a short acceleration of the right treadmill belt. Electromyographic activity (EMG) was recorded from the right medial gastrocnemius (GMR), soleus (SO) and tibialis anterior (TA) muscles of the right leg as well as from the gastrocnemius of the left unperturbed leg (GML). To study the adaptational reflex behavior, multiple measurements were taken during walking with normal (control) and increased body load and after removing the load. In most experiments the compensatory EMG response in the GMR consisted of a short inhibitory and a subsequent excitatory component. Both reflex components were larger when the body was loaded. During the course of continuous loading, divergent reflex adaptations of different degrees and directions were observed in the subjects. In one group of subjects the reflex response increased to a higher level of EMG activity. In a second group EMG activity first increased and afterwards decreased to baseline level. A subsequent removal of body loading resulted in a slow adaptation to the control reflex values in both groups. Neither the EMG activity in the GM nor the reflex responses in the GMR after increasing the load changed differently in the two groups. Our results suggest that load information is not simply used in a fixed input/output relationship of the actual biomechanical conditions of a subject. Load information is rather used to slowly modify the reflex response, to achieve the desired posture during walking.

The modification of the normal locomotor pattern of humans was investigated using a split-belt locomotion protocol (treadmill belt speeds of 4.5 km/h and 1.5 km/h for the right and left legs, respectively) and also by changing afferent input from the legs (30% reduction or increase in body weight by suspending subjects in a parachute harness or by wearing a lead-filled vest). After a control-speed training period (10 min) of symmetrical walking (3 km/h each leg) and a period (10 min) of split-belt walking, the adjustment back to the control speed resulted in a mean speed difference between the right leg and the left leg of 0.85 km/h. Adjustment of belt speed on either side was performed by the hands using a potentiometer. For comparison, also speed adjustment by the feet via feedback derived from changes in the treadmill drive current was studied. No significant difference was obtained when both modes of adjustment were compared. Body unloading or loading during the training period resulted in an improved adjustment of treadmill belt speed. This suggests that load receptor information plays a major role in the programming of a new walking pattern.

The aim of this study was to evaluate the modulation of muscle activity during locomotor-like movements by different walking speeds in subjects with a motor complete spinal cord injury (SCI) compared to actively- and passively-walking control subjects without neurological deficit. Stepping movements on a treadmill were induced and assisted by a driven gait orthosis. Electromyographic (EMG) muscle activity of one leg (rectus and biceps femoris, tibialis anterior and gastrocnemius) was recorded and analyzed at three stepping velocities with similar body weight support in both subject groups. In SCI subjects, the EMG amplitude of biceps femoris, tibialis anterior and gastrocnemius was in general similar or weaker than in passively- and actively-stepping control subjects, but that of rectus femoris was larger. The degree of co-activation between tibialis anterior and gastrocnemius was higher in SCI than in control subjects. A significant velocity-dependent EMG modulation was present in all four-leg muscles in both subject groups. In SCI subjects, this EMG modulation was similar to that in actively stepping control subjects. It is concluded that in complete spastic SCI subjects, spinal neuronal circuits underlying locomotion can to a large extent adequately respond to a change in external drive to adapt the neuronal pattern to a new locomotion speed. The application of various speeds might enhance the effect of locomotor training in incomplete SCI subjects.

Postural responses to head displacements are triggered by the vestibular system; responses to body displacements are triggered by the somatosensory system. We examined the interaction of responses to combinations of head and support surface perturbations. Head displacements were always in the opposite direction of body displacements. The time between head and support surface perturbations was varied. We measured amplitude and latency of gastrocnemius and tibialis anterior EMGs for various head backward/body forward and head forward/body backward displacement combinations. These responses were compared to head-only or body-only displacement trials, which served as controls. Relative to controls, the latency of somatosensory-evoked responses to body displacement was longer and vestibular-evoked responses were absent or of low amplitude for combinations where head and support surface perturbations were presented closely in time (10-50 ms apart). These results illustrate complex integration of vestibular and somatosensory information, suggesting that the vestibulospinal and somatosensory-spinal pathways are not two isolated systems independently driving motor neurons. Rather, these pathways may influence one another at premotoneuronal levels where common circuitry may be shared by both systems.

Recent studies have demonstrated that coordinated stepping movements can be induced in patients with complete para-/tetraplegia, when they were standing on a moving treadmill with their body weight partially unloaded and external assistance. The aim of this study was to determine which part of the spinal cord generated the locomotor pattern. In patients with complete paraplegia due to lesions at different levels of the spinal cord, the locomotor pattern was compared with that of healthy subjects. Any similarities in electromyographic (EMG) activity of gastrocnemius and tibialis anterior muscles between the patients and healthy subjects were reflected by the analysis of the variation ratio and amplitudes of the EMG activity. It was found that the higher the level of spinal cord lesion the more "normal" was the locomotor pattern. This suggests that neuronal circuits underlying locomotor "pattern generation" in man are not restricted to any specific level(s) of the spinal cord, but that an intricate neuronal network contributing to bipedal locomotion extends from thoracolumbal to cervical levels.

The aim of this study was to investigate visuomotor control during human gait. It was assumed that visual input should modulate transcranially evoked motor potentials (EMPs) during walking. The effect of transcranial magnetic stimulation (TMS) in a visually guided precision stepping task was compared with that during normal gait. EMPs were studied in tibialis anterior (TA), gastrocnemius (GM), and abductor digiti minimi (AD) muscles during treadmill walking. In both stepping tasks, a facilitation of EMPs was observed prior to activation of the respective leg muscle. EMP facilitation proved to be modulated throughout the stride cycle when normalising EMP with respect to the underlying electromyogram (EMG). Facilitation was strongest in TA prior to the swing phase. Significant differences of EMP facilitation between the visual and control tasks were present. In the visual task, maximal facilitation of TA EMPs prior to and during the swing phase was decreased compared to the control task. Conversely, there was increased facilitation of GM EMPs during swing phase of the visual task, prior to the heel strike and prior to the plantarflexion, which was the moment when the target was hit. Thus, the effect of visual input upon EMPs in TA and GM was differential and reciprocal according to the respective functional state. The results support the hypothesis of a conditioning effect of visual or, alternatively volitional, drive on EMPs during stepping.

Transcranial magnetic stimulation (TMS) of the motor cortex was applied during locomotion to investigate the significance of corticospinal input upon the gait pattern. Evoked motor responses (EMR) were studied in the electromyogram (EMG) of tibialis anterior (TA), gastrocnemius (GM) and, for reference, abductor digiti minimi (AD) muscles by applying below-threshold magnetic stimuli during treadmill walking in healthy adults. Averages of 15 stimuli introduced randomly at each of 16 phases of the stride cycle were analysed. Phase-dependent amplitude modulation of EMR was present in TA and GM which did not always parallel the gait-associated modulation of the EMG activity. No variation of onset latency of the EMR was observed. The net modulatory response was calculated by comparing EMR amplitudes during gait with EMR amplitudes obtained (at corresponding background EMG activities) during tonic voluntary muscle contraction. Large net responses in both muscles occurred prior to or during phasic changes of EMG activity in the locomotor pattern. This facilitation of EMR was significantly higher in leg flexor than extensor muscles, with maxima in TA prior to and during late swing phase. A comparison of this facilitation of TA EMR prior to swing phase and prior to a phasic voluntary foot dorsiflexion revealed a similar onset but an increased amount of early facilitation in the gait condition. The modulated facilitation of EMR during locomotion could in part be explained by spinal effects which are different under dynamic and static motor conditions. However, we suggest that changes in corticospinal excitability during gait are also reflected in this facilitation. This suggestion is based on: (1) the similar onset yet dissimilar size of facilitatory effects in TA EMR prior to the swing phase of the stride cycle and during a voluntary dynamic activation, (2) the inverse variation of EMR and EMG amplitudes during this phase, and (3) the occurrence of this inversion at stimulation strengths below motor threshold (motor threshold was determined during weak tonic contraction and EMR were facilitated during gait). It is hypothesized that the facilitation is phase linked to ensure postural stability and is most effective during the phases prior to and during rhythmical activation of the leg muscles resulting in anticipatory adjustment of the locomotor pattern.

Modulation of presynaptic inhibition of Ia afferents projecting monosynaptically to soleus motoneurones was investigated during human gait. Changes in presynaptic inhibition of Ia afferents were deduced from alterations in the amount of heteronymous soleus H-reflex facilitation evoked by a constant femoral nerve stimulation. It has been shown that this facilitation is mediated through a monosynaptic Ia pathway and that during its first 0.5 ms it is still uncontaminated by any polysynaptic effect and can be used to assess ongoing presynaptic inhibition of Ia terminals to soleus motoneurones. During gait, heteronymous facilitation was reduced with respect to its control value (rest during sitting) and modulated during the step cycle: it reached its maximum at mid-stance and decreased to near zero by the end of stance. At the same time the H-reflex amplitude was to some extent similarly modulated. It is argued that this decrease in heteronymous Ia facilitation and in H-reflex amplitude reflects an increased, ongoing presynaptic inhibition of Ia terminals projecting onto soleus motoneurones, which could be from central and/or peripheral origin. D1 inhibition, i.e. the late and long-lasting inhibition of the soleus H-reflex evoked by a train of stimuli to the common peroneal nerve, was used as another method to assess presynaptic inhibition. This D1 inhibition was decreased during gait, and it is argued that this decrease might reflect an occlusion in presynaptic pathways or increased presynaptic inhibition of pathways mediating the conditioning volley.

The relative contribution of vestibular and somatosensory information to triggering postural responses to external body displacements may depend on the task and on the availability of sensory information in each system. To separate the contribution of vestibular and neck mechanisms to the stabilization of upright stance from that of lower body somatosensory mechanisms, responses to displacements of the head alone were compared with responses to displacements of the head and body, in both healthy subjects and in patients with profound bilateral vestibular loss. Head displacements were induced by translating two 1-kg weights suspended on either side of the head at the level of the mastoid bone, and body displacements were induced translating the support surface. Head displacements resulted in maximum forward and backward head accelerations similar to those resulting from body displacements, but were not accompanied by significant center of body mass, ankle, knee, or hip motions. We tested the effect of disrupting somatosensory information from the legs on postural responses to head or body displacements by sway-referencing the support surface. The subjects' eyes were closed during all testing to eliminate the effects of vision. Results showed that head displacements alone can trigger medium latency (48–84 ms) responses in the same leg and trunk muscles as body displacements. Nevertheless, it is unlikely that vestibular signals alone normally trigger directionally specific postural responses to support surface translations in standing humans because: (1) initial head accelerations resulting from body and head displacements were in opposite directions, but were associated with activation of the same leg and trunk postural muscles; (2) muscle responses to displacements of the head alone were only one third of the amplitude of responses to body displacements with equivalent maximum head accelerations; and (3) patients with profound bilateral vestibular loss showed patterns and latencies of leg and trunk muscle responses to body displacements similar to those of healthy subjects. Altering somatosensory information, by sway-referencing the support surface, increased the amplitude of ankle muscle activation to head displacements and reduced the amplitude of ankle muscle activation to body displacements, suggesting context-specific reweighting of vestibular and somatosensory inputs for posture. In contrast to responses to body displacements, responses to direct head displacements appear to depend upon a vestibulospinal trigger, since trunk and leg muscle responses to head displacements were absent in patients who had lost vestibular function as adults. Patients who lost vestibular function as infants, however, had near normal trunk and leg response to head displacements, suggesting a substitution of upper trunk and neck somatosensory inputs for missing vestibular inputs during development.

With subjects standing on a treadmill moving sinusoidally backward and forward, recordings of electromyographic (EMG) leg and trunk muscle activity, head and joint movements and platform torque were made with the subjects' eyes open or closed. The sinusoidal frequency was changed, stepwise and randomly, between 0.5, 0.3 and 0.25 Hz. The amplitude of the deflection was constant at ±12 cm. During an adapted sinus cycle, the maximum leg muscle EMG activity was recorded in the tibialis anterior around the posterior turning point and in the gastrocnemius around the anterior turning point in the treadmill cycle. This activity was associated with a forward inclination of the body around the posterior point and a straightening of the body at the anterior point. Both the degree of body inclination and the corresponding EMG activity were dependent upon the sinusoidal frequency. The programmed adjustment of the body inclination was such that the result of inertial and gravitational forces acting on the body coincided with the axis of the body at the posterior turning point. At the anterior point, the adjustment was achieved mainly by strong activation of the leg extensors. The latencies of the compensatory muscle responses to a change in treadmill frequency were significantly shorter at the posterior point for the gastrocnemius than for the tibialis anterior, and at the anterior point for the tibialis anterior than for the gastrocnemius. No correlated changes were seen in the corresponding head and joint movements. The difference in latency can best be attributed to the different body postures during the sinusoid. Early activation of the gastrocnemius is required due to the forward-directed impulse to the inclined body at the posterior point, and of the tibialis anterior muscle due to the backward-directed impulse to the erect body at the anterior point. It is suggested that afferent input from extensor load receptors provides information about the position of the body's centre of gravity relative to the support surface and determines the generation of the EMG responses. Adaptation of both the EMG and biomechanical patterns to a new sinusoidal frequency of the treadmill occurred within four cycles after the change. Biomechanically, this was reflected as a change in the body posture. Vision did not significantly affect these changes. In conclusion, standing on a sinusoidally moving platform, the nervous system acts to control the position of the body's centre of gravity relative to the feet. Body posture is adjusted in such a way that the forces acting on the body during the treadmill movements become minimised. After adaptation, body equilibrium becomes predominantly controlled by positive feedback from programmed leg muscle activation.

Recordings of electromyographic (EMG) leg muscle activity, head and joint movements and platform torque were taken in healthy subjects within three age groups (approximately 6, 10 and greater than 22 years) standing upright upon a sinusoidally moving treadmill. The sinusoidal frequency was randomly changed between 0.5, 0.33 and 0.25 Hz, while the amplitude of the deflection was constant (+/- 12 cm). During an adapted sinus, forward inclination of the body at the posterior turning point was associated with a slowly increasing tibialis anterior and decreasing gastrocnemius activity, while straightening of the body at the anterior turning point was associated with a sharply increasing gastrocnemius and decreasing tibialis anterior activity. The angle of forward inclination was greatest in the groups of children and was dependent upon both the sinus frequency and the child's height. The presumed programmed adjustment of the body inclination was such that the net effect of both inertial and gravitational forces acting on the body coincided approximately with the axis of the body at the posterior turning point. Changes of sinusoidal frequency were followed by compensatory responses, the amplitude of which depended upon the velocity of the body's displacement and the height of the subjects. In all three subject groups the response latencies were significantly shorter at the posterior turning point for the gastrocnemius response to a change from 0.5 to 0.25 Hz (105 ms for children and 119 ms for adults) than for the tibialis anterior response to a change from 0.25 to 0.5 Hz for which the values were 162 and 169 ms, respectively. This difference could be attributed to the forward inclination of the body at the posterior turning point which requires an earlier onset of compensatory extensor activity in order to maintain equilibrium. Adaptation to a new sinusoidal frequency occurred within 4 cycles following a change in sinus frequency. The phase shifts between treadmill position and the biomechanical and EMG signals that occurred during the adaptational process suggest that the position of the body's centre of gravity is the variable controlled by the programmed leg muscle activation. In young children the phase shifts during adaptation were absent, which may contribute to their greater instability. It is concluded that posture is continually adjusted in such a way that the resulting torque acting on the body during the treadmill movement becomes minimized. For this regulation load receptors in addition to the classical afferent impulses from visual, vestibular and muscle stretch receptors could play a major role.

To investigate whether phase-dependent reversals in reflex responses on electromyography (EMG) are accompanied by movement reversals, a series of human volunteers were studied for their behavioural responses to sural nerve stimulation during running or walking on a treadmill. Low-intensity stimulation (less than 2.5 x perception threshold, T) of the sural nerve yielded facilitatory responses in the tibialis anterior muscle (TA), correlated with an induced ankle dorsiflexion (mean maximum 4 degrees) in early swing. The same stimuli yielded primarily TA suppression and weak ankle plantar flexion (mean maximum 1 degree) at end swing. The correlated induced knee angle changes did not precede the ankle changes, and they were relatively small. Mean maximum flexion in early swing was 6.2 degrees, while mean maximum extension was 3.7 degrees. High-intensity stimulation of the sural nerve (greater than 2.5 x T) always gave rise to suppression of the ongoing activity. This resulted in a second type of movement reversal. During late stance and early swing the responses in TA were suppressive (i.e. below background activity) and related to ankle plantar flexion. In contrast, the responses during early and middle stance consisted of suppression in extensor activity (gastrocnemius medialis and soleus) and ankle dorsiflexion. The data are discussed in terms of a new hypothesis, which states that the responses to electrical stimulation of cutaneous nerves during locomotion do not correspond directly to corrections for stumbling following mechanical perturbations during the step cycle. Instead, the data invite a reinterpretation in terms of the opening and closing of reflex pathways, presumably by a central pattern generator for locomotion.

According to recent observations, influence of body load has to be taken into account for the neuronal control of upright stance in addition to the systems known to be involved in this regulation (e.g. afferent input from vestibular canals, visual and muscle stretch receptors). The modulation of compensatory leg muscle electromyographic (EMG) responses observed during horizontal body posture indicates the existence of a receptor system which responds to loading of the body against the supporting platform. This receptor should be located within the extensor muscles because a compensatory EMG response and a loading effect on this response was only present following translational, but not rotational impulses. As the EMG responses were identical to those obtained during upright stance, it is argued that these load receptors activate postural reflexes. According to recent observations in the spinal cat, this afferent input probably arises from Golgi tendon organs and represents a newly discovered function of these receptors in the regulation of stance and gait.

Phase-dependent reflex modulation was studied by recording the electromyographic (EMG) responses in soleus (SOL) and gastrocnemius medialis (GM) to a 20 ms train of 5 electrical pulses, applied to the sural or tibial nerve at the ankle, in 14 volunteers walking or running on a treadmill. Although both the spontaneous activity and the reflex responses were usually similar for both muscles, instances were identified in which separate control was evident. During walking (4 km/h), activity in SOL started earlier in the stance phase than GM activity. Correspondingly, the amplitude of the reflex responses was larger in SOL than in GM in early stance, both ipsi- and contralateral to the side of stimulation. In some cases, the same stimulus could elicit contralaterally a suppression of GM in synchrony with a facilitation of SOL. These crossed extensor reflexes had a low threshold (1.2 × T) and a latency ranging from 72 to 105 ms. During running (8 km/h or more), responses were seen selectively in GM instead, without concomitant responses in SOL. Such responses had a latency ranging from 82 to 158 ms and they appeared during the first extension phase, at the end of the swing phase. In addition, selective GM responses, with latencies above 200 ms, were seen near the transition from stance to swing during running. These instances of separate reflex control of SOL and GM were correlated with step cycle periods during which the motoneurones of either one of these muscles received more spontaneous activation than the other. Nevertheless, it is argued that premotoneuronal gating must also be involved since the increased amplitude of the crossed SOL responses (in early stance) and of GM responses (at end swing) was not strictly linked to an elevated amount of spontaneous activity during these parts of the step cycle as compared to other parts.

Amplitude modulation of the quadriceps H reflex was investigated during the early part of the stance phase of gait in normal human subjects. Stability of the M wave was used to ensure constancy of the effective stimulus strength. In all subjects there was a progressive decrease in the reflex amplitude throughout the early knee flexion (yield of the knee), whereas the quadriceps EMG activity remained constant or even increased. At an equal stimulus strength and EMG level, the reflex was often larger at the onset of the stance phase of gait than during voluntary contraction, whereas it was always smaller during the knee extension following the yield of the knee. It is argued that changes in presynaptic inhibition of quadriceps Ia terminals could account for this amplitude modulation of the monosynaptic reflex during gait. The possible role of changes in the gain of the quadriceps stretch reflex during bipedal gait is discussed.

Sudden tilts of the head to the front or rear were induced during stance, balancing, gait and during perturbations of gait. The most prominent response in the leg muscle electromyogram (e.m.g.) to head tilt occurred in the tibialis anterior muscle (latency about 55 ms) following a backward tilt induced during balancing. During stance and gait, the e.m.g. activity related to head tilt was only a minor component of the leg muscle activity normally occurring during gait. When the head tilt was induced shortly after a perturbation of gait (treadmill acceleration impulse), the compensatory reaction in the leg muscles did not significantly differ from that seen after the gait perturbation alone. In addition, the rate of acceleration of the head was tested against the compensatory e.m.g. responses: No correlation of influence could be discerned. The results indicate that sudden head tilts and the resulting head acceleration have little influence on the e.m.g. patterns that occur during gait and perturbations of gait. It is assumed that these patterns are regulated by central programs, and that the compensation for leg perturbation is achieved mainly by spinal reflex mechanisms. It is discussed whether the lack of head tilt responses is the result of an antagonistic vestibular-neck interaction, or whether it indicates a reduced effectiveness of vestibulo- and cervico-spinal reflexes during gait.

While subjects were standing and balancing on two separate seesaws, the EMG of the leg muscles and the positions of the two seesaws were recorded. The spontaneous balancing movements with predominant oscillations of 4–5 Hz, and the accompanying bursts of EMG activity in the leg muscles occurred quite symmetrically on the two sides. After a displacement, induced either by stimulating the tibial nerves, or by a brisk anterior tilt of one seesaw, the EMG responses of the tibialis anterior muscles started with the same latency (about 50 ms) on both sides, and with similar amplitudes, even when only one side was displaced. It is concluded that this symmetrical leg muscle activation is mediated by a spinal coordinating mechanism the function of which depends on the actual motor task.

In order to investigate the neuronal mechanisms underlying the compensatory movements following stance disturbance, leg muscle e.m.g. responses and cerebral potentials evoked by a treadmill acceleration impulse were analysed. It was found that the displacement was followed by a cerebral potential of a latency of 40–45 ms and EMG responses in the calf muscles at a latency of 65–70 ms. The e.m.g. responses represented specific compensatory reactions to the mode of perturbation (with a gastrocnemius activation following positive acceleration but a tibialis ant. activation following negative acceleration). The cerebral potentials, however, showed a common pattern to both conditions. In addition, the leg muscle e.m.g. reactions were not altered by learning effects and by forewarning of displacement onset, while the amplitude of the cerebral potentials was significantly smaller in these conditions compared to those produced in response to randomly induced perturbations. It was therefore concluded that the leg muscle e.m.g. reactions are mediated by a polysynaptic spinal reflex pathway which depends on a supraspinal control. The cerebral potentials seem to represent afferent signals which can be supposed to be subjected to modification and processing by supraspinal motor centres, according to the actual requirements.

While subjects balanced on a seesaw consisting of a platform with a curved base, the antero-posterior sway of head and body as well as changes in the angle of the ankle joint were recorded and analysed for their frequency power spectrum. The EMG of leg muscles and the position of the resultant force exerted by the seesaw on a force-measuring platform were simultaneously registered and analysed. Balancing oscillations of 4–5 Hz were observed under this condition. They were accompanied by short, reciprocally organized bursts of EMG activity in the leg muscles. When stimulating the tibialis nerves to produce a displacement, the delay until the counterbalancing EMG activity started (about 40 ms) was in the time range of a fast-conducting segmental reflex. After partial ischaemic blocking of group I afferents from the leg muscles or fixation of the ankle joints, the predominant sway frequency was lacking, bursts of EMG activity became longer and stronger, and body balance was more unstable. Altering the height of the seesaw showed that a threshold change in the ankle angle was the determining factor in the production of spinal stretch reflex activity for fast regulation of balance.

The cerebral potentials (c.p.) evoked by electrical stimulation of the tibial nerve during stance and in the various phases of gait of normal subjects were compared with the c.p. and leg muscle e.m.g. responses evoked by perturbations of stance and gait. Over the whole step cycle of gait the c.p. evoked by an electrical stimulus were of smaller amplitude (3 microV and 9 microV, respectively) than that seen in the stance condition, and appeared with a longer latency (mean times to first positive peak: 63 and 43 ms, respectively). When the electrical stimulus was applied during stance after ischaemic blockade of group I afferents, the c.p. were similar to those evoked during gait. The c.p. evoked by perturbations were larger in amplitude than those produced by the electrical stimulus, but similar in latencies in both gait and stance (mean 26 microV and 40 microV; 65 ms and 42 ms, respectively) and configurations. The large gastrocnemius e.m.g. responses evoked by the stance and gait perturbations arose with a latency of 65 to 70 ms. Only in the stance condition was a smaller, shorter latency (40 ms) response seen. It is concluded that during gait the signals of group I afferents are blocked at both segmental and supraspinal levels which was tested by tibial nerve stimulation. It is suggested that the e.m.g. responses induced in the leg by gait perturbations are evoked by group II afferents and mediated via a spinal pathway. The c.p. evoked during gait most probably reflect the processing of this group II input by supraspinal motor centres for the coordination of widespread arm and trunk muscle activation, necessary to restablish body equilibrium.

After minimizing proprioceptive input from the legs by ischemia without degradation of muscle force and excluding visual stabilization by eye closure, a characteristic anterior-posterior postural sway around 1 Hz was observed in three normal subjects. This is similar to the instability seen in two tabes dorsalis patients. From the spectral analysis of head and hip movements, displacements of the center of force and of ankle angle as well as from EMG recordings of the anterior tibial and gastrocnemius muscle it is concluded that the oscillations around 1 Hz are due to the long latency and high threshold of vestibularly induced leg muscle discharges (200-300 ms) arriving in the counterbalancing phase of the trunk, which causes an overshoot in body sway.