J. Quintern

Corrective reactions to stumbling in man: neuronal co-ordination of bilateral leg muscle activity during gait.

Electromyogram (e.m.g.) responses of lower leg muscles, and corresponding movements were studied following a perturbation of the limb during walking, produced by either (a) a randomly timed, short acceleration or decelerating impulse applied to the treadmill, or (b) a unilateral triceps surae contraction induced by tibial nerve stimulation. Bilateral e.m.g. responses following the perturbation were specific for the mode of perturbation and depended on the phase of the gait cycle in which the perturbation occurred. Treadmill deceleration evoked a bilateral tibialis anterior activation; acceleration evoked an ipsilateral gastrocnemius and contralateral tibialis anterior activation (latency in either condition and on both sides was 65‐75 ms, duration about 150 ms). Tibial nerve stimulation at the beginning of a stance phase, was followed by an ipsilateral tibialis anterior activation; during the swing phase it was followed by an ipsilateral tibialis anterior and contralateral gastrocnemius activation (latency about 90 ms, duration about 100 ms). These patterns differed from the response seen after a unilateral displacement during static standing, which evoked a bilateral tibialis anterior activation. These early responses were in most cases followed by late ipsilateral responses, but the e.m.g. pattern of the next step cycle was usually unchanged, or affected only at its onset. The e.m.g. responses were unaltered by ischaemic nerve blockade of group I afferents, by training effects or by pre‐warning of the onset of perturbation (randomly or self‐induced). Despite the different e.m.g. responses following a perturbation during gait, the same basic functional mechanism was obviously at work: the early ipsilateral response achieved a repositioning of the displaced foot and leg, while the early contralateral and late ipsilateral responses provided compensation for body displacement. It is suggested that the e.m.g. responses may be mediated predominantly by peripheral information from group II and group III afferents, which modulate the basic motor pattern of spinal interneuronal circuits underlying the respective motor task.

Afferent control of human stance and gait: evidence for blocking of group I afferents during gait

SummaryThe 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 μV and 9 μV, 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 μV and 40 μV; 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.

Stumbling reactions in man: significance of proprioceptive and pre‐programmed mechanisms.

1. Electromyogram (e.m.g.) responses of the leg musculature and the corresponding joint movements were studied following a perturbation of the limb during walking on a treadmill, produced by a randomly timed treadmill acceleration impulse, either predictable, or unpredictable in its amplitude and rate of acceleration. 2. The rate of rise of ipsilateral gastrocnemius e.m.g. response following a perturbation was dependent on the rate of treadmill acceleration. For a given acceleration rate the amplitude of the e.m.g. response and the timing of its peak was dependent on the amplitude of the impulse and the rate of rise of the gastrocnemius response was the same for impulses of both small and large amplitude. The onset latency was shorter (65 ms) for high accelerations and longer (85 ms) for lower ones. 3. The amplitude of the ipsilateral biceps femoris response was much smaller than the gastrocnemius response but was larger following unpredictable than predictable impulses. 4. The initial gastrocnemius response was followed by a tibialis anterior activation associated with a gastrocnemius depression and sometimes with a second, weak gastrocnemius activation. The gastrocnemius depression ended within a fixed time range relative to the onset of the response. The tibialis anterior activation was most pronounced when unpredictable impulses with high acceleration but a small amplitude were induced. 5. It is concluded that generation of the first gastrocnemius response is obviously under continuous control by muscle proprioceptive information and can be best described in terms of a stretch reflex response. It is suggested that, on the evidence of the diphasic or triphasic e.m.g. pattern, a close interaction occurs between a central programme and muscle proprioceptive input in order to generate the appropriate e.m.g. pattern. 6. On the basis of earlier work (Berger, Dietz & Quintern, 1984a) and on the present results it is suggested that the e.m.g. responses may be mediated mainly by muscle proprioceptive input from group II afferents. This input is modulated and processed by spinal interneuronal circuits, closely connected with spinal locomotor centres. The mode of processing depends on various factors, such as the predictability of the nature of the impulse.

Motor unit involvement in spastic paresis ☆: Relationship between leg muscle activation and histochemistry

In 4 patients with spastic hemiparesis the electromyograms (EMG) of leg muscles were recorded during walking and the gastrocnemius medialis on both sides was investigated by histochemistry and morphometry. During walking a reciprocal mode of muscle activation was preserved on the spastic side, but the EMG amplitude was reduced. In one patient the discharge behaviour of single motor units was investigated during stance. The mean discharge rate on both the spastic and the unaffected side amounted to about 5.5 Hz. Modification of this rate over a wider range by manoeuvres of the trunk was only observed on the unaffected side. Histochemistry and morphometry of the spastic muscle revealed: Increased levels of muscle fibre atrophy (especially type II); A predominance of type I fibres during later stages, when spasticity was established; Structural changes, such as the appearance of target fibres, mainly in type I fibres. These results suggest that the low level of tonic activation in spastic muscle develops tension enough during the stance phase of gait to support the body. The histopathological profile of the spastic gastrocnemius muscle is considered to be indicative of denervation, due to the combined effects of an impaired supraspinal control of the lower motoneurone and a concurrent transsynaptic muscle membrane dysfunction, muscle cell atrophy and fibre type transformation.

Pathophysiology of gait in children with cerebral palsy

The surface electromyogram (EMG) of leg muscles was recorded together with the changes of the angle at the ankle joint during slow gait in 10 normal children and 10 with cerebral palsy. The characteristic pattern of muscle activity recorded from the spastic legs mainly consisted of a co-activation of antagonistic leg muscles during the stance phase of a gait cycle and a general reduction in amplitude of EMG activity. The tension of the Achilles tendon, measured in 2 hemiparetic children during gait, increased much more steeply in the spastic leg than in the normal one at the beginning of the stance phase, when the electrically almost silent triceps surae was stretched. It is suggested that muscle hypertonia during gait in spastic children is mainly due to changed muscle fibre mechanical properties, as recently discussed also for spastic adults. While in the latter the reciprocal EMG activity of antagonistic leg muscles was preserved it is proposed that muscle co-activation recorded in spastic children is due to an impaired maturation of the locomotor pattern with an early neuronal adaptation to altered muscle fibre mechanical characteristics.

Corrective reactions to stumbling in man: Functional significance of spinal and transcortical reflexes

Stumbling reactions were studied in terms of bilateral leg muscle electromyographic (EMG) responses during locomotion on a treadmill. At random times, but fixed points in the stepping cycle, short impulses were applied to the treadmill, either accelerating or decelerating its progress. It was found that acceleration was compensated for by a strong ipsilateral gastrocnemius and contralateral tibialis anterior activation, and deceleration by a bilateral tibialis anterior activation. In both muscles the responses appeared with a latency of about 70 msec and lasted for about 150 msec. It is concluded that sudden displacements induced by acceleration or deceleration during gait are compensated for by a polysynaptic spinal pathway, with an associated depression of monosynaptic responses.

Cerebral potentials and leg muscle e.m.g. responses associated with stance perturbation

SummaryIn 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.

Stance and gait perturbations in children: Developmental aspects of compensatory mechanisms

The leg muscle EMG responses following perturbations during stance and gait were analysed in children between 1 and 8 years of age in order to study the development of those reflex systems responsible for the compensatory movements necessary to maintain body equilibrium. Single monosynaptic reflex potentials followed by a long-lasting (about 500 msec) polysynaptic gastrocnemius EMG response, along with coactivation of all antagonistic leg muscles, were characteristic of the EMG reactions following a treadmill acceleration impulse in early infancy. From 4 years of age on, the monosynaptic reflex potentials disappeared when perturbations were induced during gait. In addition, the polysynaptic reflex response became shorter (about 100 msec) and a reciprocal mode of leg muscle activation occurred, with a consequently more rapid and effective compensation of perturbation impulses. In older children with a disorder of the motor system acquired at an early age, a partial persistence of the immature motor responses could be observed, irrespective of whether the impairment was a cerebral lesion or a muscular dystrophy. It is concluded that the coactivation pattern is due to the immaturity of those nervous structures mediating afferent information necessary for the control of bipedal stance and gait. Furthermore, the existence of mutual inhibition of monosynaptic and polysynaptic spinal reflex responses, dependent on the function of supraspinal motor centres, can be assumed.

Cerebral evoked potentials associated with the compensatory reactions following stance and gait perturbation

We have studied the gastrocnemius electromyographic (EMG) responses and the cerebral potentials evoked in normal subjects by perturbations of stance and gait in the form of short treadmill acceleration impulses. In the stance condition a small EMG response (LM1; latency around 40 ms) was followed by a strong muscle activation (LM2; latency 75-90 ms). Following perturbation during gait, LM1 was lacking and LM2 appeared a little earlier (65-75 ms). In the stance condition, the cerebral potentials appeared with shorter latency (42 ms as compared to 83 ms) and a larger amplitude (41 microV as compared to 21 microV) than those seen in the gait condition. These changes can be explained by a presynaptic inhibition of group I afferent signals during gait, which are assumed to be responsible for the early EMG and EEG responses. It is suggested that the LM2 and the cerebral responses evoked by gait perturbation are mediated by signals from group II and III afferents.

Task-dependent gating of somatosensory transmission in two different motor tasks in man: Falling and writing

The cerebral potentials induced by an electrical stimulus (median nerve or finger) were recorded over the central region of the scalp and were analysed during falling onto the extended arms or during writing to investigate the influence of different motor tasks on the transmission of a synchronous afferent volley to the brain. During both falling (before landing) and writing, the first peaks (20-40 ms) were reduced. Later peaks (60-200 ms) were enhanced during writing but reduced during falling. A reduction of the first peak was also obtained after ischaemic blockade of group I afferents, suggesting that the cerebral transmission of group I afferents is inhibited during falling and writing. The subjects reported a corresponding reduction in the perception of the stimulus during falling. During writing, however, the large late waves indicate a task specific processing of the remaining afferent volley. Such a gating of sensory information to the brain is assumed to play a functional role in the respective motor tasks.