Biomedical subjects

V Dietz

Publications and source records attributed to V Dietz.

At least 199 records · Page 11Linked to original sources

PubMed1986

Stumbling reactions in man: release of a ballistic movement pattern.

Four different modes of perturbation were applied during gait, either alone or in combination, in order to determine the extent to which compensatory reactions in the leg are released as fixed patterns or, alternatively, are generated by feedback mechanisms. The first agonist burst of the usually triphasic pattern evoked by a perturbation was unchanged in amplitude and timing when a second disturbance of an opposite sense was induced a short time later. Following this burst, the remainder of the response evoked by the second disturbance appeared time locked to the second stimulus and was unchanged in form. It is concluded, that the first agonist burst induced by a perturbation is stimulus specific and immutable after release, while the appearance of the following bursts of the triphasic pattern is dependent on the actual conditions. This suggests that a similar mechanism as assumed for ballistic hand and finger movements is operative, with the difference that the compensatory reactions following gait perturbations are induced by peripheral signals.

Adult↗

PubMed1986

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.

Adult↗

PubMed1986

Compensatory movements following gait perturbations: changes in cinematic and muscular activation patterns.

The present study was designed to investigate the neuronal control and biomechanical effects of stumbling reactions. To induce these perturbations, a specially prepared treadmill was used which allowed rapid and powerful changes of treadmill speed. EMG recordings of leg muscles were related to cinematic movement patterns. Following an accelerating impulse, the standing leg was displaced in a posterior direction compared with normal gait, with a premature touchdown of the contralateral, swinging leg, forward of the body axis. This was associated with simultaneous activation of the gastrocnemius and biceps femoris of the ipsilateral and the tibialis anterior muscles of the contralateral leg. Following deceleration, the standing leg was displaced in an anterior direction and the contralateral swinging leg touched the ground prematurely behind the body axis. This was associated with activation of the ipsilateral tibialis anterior and rectus femoris and contralateral tibialis anterior muscles. In both conditions, the activation of the lower leg muscles on both sides occurred with a latency of 60-70 ms, monosynaptic responses being absent. In both cases, early touchdown was associated with a forward extension of the arm. It is concluded that the EMG responses are mediated by a polysynaptic spinal pathway to keep the body center of gravity constant and to prevent falling.

Ankle Joint↗

PubMed1985

Compensatory reactions to gait perturbations in man: short- and long-term effects of neuronal adaptation.

Short- and long-term changes in the cerebral potentials and the electromyographic (EMG) responses in the arms and legs evoked by gait perturbations were followed up over repeated trials in healthy subjects. Two different modes of muscle activation could be discerned. The first adapted to the specific motor task within a few trials and remained constant during the remaining experiments. This 'hard wired' and complex leg muscle reaction was shown to be task specific and necessary for an adequate compensation for the displacement. It was supposed that this reaction is mediated via a spinal pathway. The other mode, which included an early arm extension, disappeared successively as the motor task became familiar. These flexible EMG responses represent the 'protective' part of the reaction and are suggested to be mediated via a transcortical pathway, due to their close relationship to the cerebral potentials evoked by the perturbations.

Adaptation, Physiological↗

PubMed1985

Neuronal control of ballistic finger movements in man: task specific electromyographic patterns.

The electromyographic (EMG) patterns of finger flexor and extensor muscles have been studied during ballistic finger movements in three different conditions: (1) rapid isotonic finger flexion; (2) throwing and (3) catching a tennis ball. In 1 and 2 a three-burst pattern was observed. In the latter, the first agonist burst was shorter and of higher amplitude compared to condition 1. Catching a ball was connected with a coactivation of extensor and flexor muscles prior to and during ball contact and a contribution of segmental stretch reflexes to the flexor activation. The finger flexion movement was 10-15 times faster than in conditions 1 and 2. After ischaemic blocking of group I afferents and in patients with rigidity, a short inhibition of the increased extensor activation became predominant and was the basic mechanism underlying finger flexion for catching a ball. It is concluded that in natural ballistic finger movements, other neuronal mechanisms are of functional significance than those seen in the usual experimental paradigms.

Biomechanical Phenomena↗

PubMed1985

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

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.

Adult↗

PubMed1985

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

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.

Adult↗

PubMed1985

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 Palsy↗

PubMed1984

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.

Adaptation, Physiological↗

PubMed1984

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.

Acceleration↗

PubMed1984

Regulation of muscle stiffness in human locomotion.

The tension development of the triceps surae muscle was analyzed during the stance phase of locomotion at different speeds with respect to its electrical activation and its lengthening and shortening behavior. The main point was the coincidence of maximal dorsiflexion, maximal Achilles tendon tension, transition from amortization to acceleration phase, and projection of the center of gravity to the supporting leg. It is concluded that the stiffness regulation needed for load compensation after impact and pushing off at the end of stance phase depends on modulation and enhancement of a centrally programmed muscle activation by a segmental stretch reflex activity.

Achilles Tendon↗

PubMed1984

Interlimb coordination of posture in patients with spastic paresis. Impaired function of spinal reflexes.

Activation of leg musculature on both sides following a unilateral displacement was studied during stance on separate see-saws, or on stable force-measuring platforms, in patients with spastic hemiparesis and paraparesis. During balancing the movements on the spastic side were damped and the degree of muscle activation reduced. Whereas in healthy subjects the tibialis anterior muscles of both sides were activated, following a unilateral displacement, with the same strength and latency (see-saws 55 ms, platforms 85 ms), in hemispastic patients the EMG responses were delayed (by about 20 to 30 ms) and of reduced strength on the spastic leg, irrespective of whether the unaffected or the spastic side was displaced. In addition, the compensatory movements on the spastic side were damped in both conditions, although the amplitude of displacement was the same bilaterally. Although there was no correlation between the delay and the reduction in EMG response, the latter was correlated with the severity of paresis. In patients with spastic paraparesis quite similar results were obtained with delayed and reduced EMG responses on both sides. It is concluded that in spasticity the impaired regulation of quick compensatory movements is due to a dysfunction of a spinal interneuronal system by which the early EMG responses are mediated. This could be explained by loss of supraspinal control. In addition to the impaired neural activation of leg muscles, changes in the mechanical properties of muscle can be assumed to contribute to the damped movements on the spastic side.

Adult↗

PubMed1984

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.

Adult↗

PubMed1984

Tension development and muscle activation in the leg during gait in spastic hemiparesis: independence of muscle hypertonia and exaggerated stretch reflexes.

In 15 patients with spastic hemiparesis the development of tension of calf muscles in relation to their electrical activation and their stretching period was studied on both sides during locomotion. Only in the spastic leg did isolated small biphasic potentials appear in the gastrocnemius E.M.G. with monosynaptic latency at the beginning of the stance phase, while the remaining gastrocnemius activation was reduced compared to the unaffected side. Perturbations of gait were followed in the spastic leg by a large monosynaptic response, while the polysynaptic reflex response was reduced. In the unaffected leg only a strong polysynaptic response appeared, which suggests a reciprocal modulation of monosynaptic and polysynaptic reflex responses. Tension development paralleled the gastrocnemius E.M.G. in the unaffected leg, while in the spastic leg tension was more closely correlated to muscle stretch. It is concluded that in spasticity the exaggerated monosynaptic reflexes represent only a small part of leg extensor activation during gait and that the tension development does not depend on these reflexes.

Adult↗

PubMed1984

Normal and impaired development of children's gait.

The development of bipedal locomotion was studied electrophysiologically in 50 children, ages varying between 6 months and 7 years. The typical features of the immature gait were: A co-activation of antagonistic leg muscles during the stance phase. With the development of free walking the activity pattern gradually became more reciprocally organized. Up to an age of 4 years, large solitary biphasic potentials in gastrocnemius with segmental latency after the muscle was stretched as the forefoot reached the ground. A reduced magnitude of gastrocnemius-EMG at the early stages of stepping. While the magnitude of tibialis anterior EMG did not change substantially with the maturation of gait, the final magnitude of gastrocnemius activity was established around 4-5 years. In the early stages of gait development, preprogrammed leg muscle EMG in form of the co-activation, and segmental stretch reflex activity appear separately. It is conjectured that during the course of maturation, the integration of the stretch-reflex activity into the preprogrammed leg muscle EMG corresponds to an increase of gastrocnemius activity with optimal adaptation to the environment. The locomotor pattern of older children with cerebral palsy showed a striking similarity to the early stages of gait development in healthy children.

Adolescent↗

PubMed1983

Normal and impaired regulation of muscle stiffness in gait: a new hypothesis about muscle hypertonia.

The activation of leg muscles was analyzed in respect to ankle joint movement and the changes in tension produced by the triceps surae muscle during slow gait in spastic adults and children with cerebral palsy. In normal subjects the increase in tension of the triceps surae in the stance phase of gait is mainly due to an increase in gastrocnemius and soleus EMG. In spastic patients the abnormally high tension development in triceps surae is due more to passive muscle stretch, for the reciprocally organized leg muscle EMG is reduced. It is concluded that the leg extensor muscles in spastic patients exhibit a pseudostretch-reflex behavior due to their mechanical properties, and that this is mainly responsible for muscle hypertonia. The coactivation of the leg muscles seen in children with cerebral palsy, which also is seen in the stepping of the newborn, suggests impaired maturation of the neuronal locomotor pattern.

Adult↗

PubMed1982

Spinal coordination of bilateral leg muscle activity during balancing.

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.

Electromyography↗

PubMed1982

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.

Adolescent↗