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Biomedical subjects

O C Lippold

Publications and source records attributed to O C Lippold.

At least 19 recordsLinked to original sources
PubMed2000

Long-latency component of the stretch reflex in human muscle is not mediated by intramuscular stretch receptors.

Reflex responses to mechanical stimulation of muscle (brief imposed movement) were investigated. Reflexes were elicited in the forefinger, recording from the first dorsal interosseous (FDI), and in the foot, recording from soleus. These responses typically consisted of a short-latency component (M1) and a long-latency component (M2) at 33 ms and 53 ms, respectively, after the stimulus in the case of FDI, and 37 ms and 68 ms, respectively, in soleus upon stimulation of the sole of the foot. Normally, when a muscle is stretched by a mechanical stimulus (either naturally or by an experimentally imposed movement), both skin receptors and muscle stretch receptors are activated. It is possible, however, to devise stimulation parameters where this is not the case. Fixating the finger with plasticine enables the effects of skin stimulation to be studied without stretching the FDI muscle. On the other hand, tapping a long tendon allows muscle stretch receptors to be activated without involving skin or subcutaneous structures. Component M1 was always abolished by finger fixation in 40 trials on 10 subjects, with M2 being essentially unchanged in latency, duration, or amplitude. Reflex responses were obtained in soleus muscle in nine experiments by prodding the sole of the foot (thereby stimulating both skin and muscle stretch receptors). Alternatively, the tendo achilles was prodded (which solely activates stretch receptors in the muscle). In the former, M1 and M2 were generated. In the latter, only M1 was produced. It is concluded that the long-latency component of the stretch reflex, M2, originates in skin and/or subcutaneous nerve terminals and that no part of M2 originates in muscle stretch receptors.

Achilles Tendon↗
PubMed1996

Reflex inhibition following electrical stimulation over muscle tendons in man.

Electrical stimulation over selected muscle tendons in alert human subjects produced, in each muscle, a reflex inhibition of muscle activity. This inhibition, when maximal, was seen in the surface EMG as an interval of complete electrical silence during a sustained voluntary contraction. The inhibition was clearly visible in single sweeps and in averaged records. Its onset latency and duration were respectively, 56 +/- 4.9 and 46 +/- 11.8 ms in extensor digitorum communis, 71 +/- 6.1 and 46 +/- 10.5 ms in extensor pollicis brevis, 77 +/- 11.2 and 47 +/- 10.5 ms in extensor pollicis longus, 72 +/- 7.3 and 43 +/- 8.6 ms in abductor digiti minimi, and 97 +/- 3.5 and 43 +/- 2.8 ms in tibialis anterior. The inhibitory response was produced at low stimulus intensities (< 10 mA) without electrical (M wave) or mechanical (muscle twitch) signs of direct muscle stimulation. It therefore did not arise from stimulation of la afferents (muscle spindles). The response arose from tendons since it occurred at lowest threshold when stimulation was applied directly over the tendons of the five different muscles studied. At low stimulus intensities, the response declined sharply when the stimulating electrodes were moved to the skin immediately adjacent to the tendons. The response did not arise from skin afferents since it was also presented when stimuli were delivered to the tendon by subcutaneous needle electrodes and it was not reproduced by stimulation of cutaneous nerves in the region of the tendon. In another series of experiments on extensor pollicis brevis, five skin locations were stimulated while overlying the tendon and again while the skin was stretched so that they were lying 0.6-0.8 cm dorsal to the tendon. In these experiments the response was again greatly attenuated when the stimulation was not directly over the tendon, although the same cutaneous sites were stimulated. The inhibition was followed by a pronounced excitatory component (E1) of peak latency 120-140 ms. The results of the study provide evidence for a powerful autogenic inhibitory reflex in man. The evidence is consistent with the possibility that the response arises from Golgi tendon organ afferents.

Adult↗
PubMed1996

Loss of tendon organ inhibition in Parkinson's disease.

Electrical stimulation via skin electrodes placed over human tendons results in a reflex inhibition of voluntary activity in the stimulated muscle, probably due to activation of Golgi tendon organ afferents. The characteristics of this response in the extensor digitorum communis (EDC) muscles of subjects with Parkinson's disease were compared with those in age-matched controls. The threshold of the inhibitory response was significantly increased in the patient population compared with controls (159 +/- 34 V for tremulous patients; 134 +/- 10 V for rigid patients, 90 +/- 5.5 V for age-matched controls and 70 +/- 16 V for all normals). The latency of the inhibitory wave was increased (onset latency was 68.01 +/- 5.5 ms in patients was 51.5 +/- 4.9 ms in controls). The duration of I was also increased in patients (60 +/- 20.8 ms) relative to controls (46 +/- 11.8 ms). This was associated with slow development of the inhibition with the result that maximal inhibition was delayed by approximately 20 ms. Other features of the patient response were its oscillatory character whereby the initial inhibitory and excitatory components were followed by further prominent peaks and troughs which gave the appearance of continuing response cycles. Such behaviour was not seen in normal records. Also electrical stimulation of the extensor muscle tendon produced concurrent records in the forearm flexor muscle, which resembled those from the stimulated muscle. This was in contrast to normal records which showed no response in the flexor. The possible contribution of a disorder of tendon organ reflexes to the rigidity and tremor of Parkinson's disease is discussed.

Aged↗
PubMed1996

Age-related impaired reflex sensitivity in a human hand muscle.

1. The rectified and averaged electromyogram (EMG) was recorded from the first dorsal interosseous muscle (FDI) in normal male and female human subjects, ranging in age from 18 to 67 yr. It was elicited by a brief stretch, given to the outstretched forefinger. 2. The responses to stretch consisted of components W30, the monosynaptic stretch reflex and W60, which is likely to arise in the skin and nonmuscular structures. The figures 30 and 60 refer to the mean latencies, in milliseconds, of the respective waveforms (W). 3. For a group of subjects > 30 yr of age, W30 was significantly smaller than in a group under this age. The size of W60 was not related to age and the W30/W60 ratio was < 0.45 in the older subjects. In the younger group, the ratio was always above 0.5. 4. The fact that the age-related reflex impairment affects only W30 and not W60, indicates that central processing in the motor neuron pool is unlikely to be the mechanism involved in the impairment. 5. Control experiments show that changes in frictional resistance in muscles, joints, and tendons with age, are not large enough to account for these results. 6. Neuromuscular block did not occur in these experiments and could not be implicated in the impaired reflex sensitivity.

Adolescent↗
PubMed1987

Contralateral intramuscular acupuncture-like electrical stimulation differentially changes the short-latency responses to muscle stretch.

Measurements were made from the human first dorsal interosseous and extensor digitorum communis muscles of the surface electromyographic activity reflexly produced by brief stretch of the muscle. For the first dorsal interosseous muscle, reflex EMG activity was also produced by electrical stimulation of the ulnar nerve at the wrist. The procedures were carried out before, during, and after 25 min of nonspecific, low-frequency electrical stimulation to the contralateral arm delivered through intramuscular electrodes. Control stimulation was delivered subcutaneously. The EMG recorded during a maintained contraction was rectified, filtered, and averaged. Two reflex components (M1 and M2) of the EMG response to muscle stretch or ulnar nerve stimulation were investigated. During nonspecific intramuscular stimulation to the contralateral arm, M1 responses of the extensor digitorum communis were depressed, initially by 37%. The effect began to fade during stimulation but extended beyond it. Reflex responses were elicited alternately by brief stretch of the first dorsal interosseus muscle and by electrical stimulation of the ulnar nerve in the same experiment. Nonspecific intramuscular stimulation to the contralateral arm depressed the M1 response to stretch, but had no effect on the M1 response to electrical stimulation. It is concluded that nonspecific intramuscular electrical stimulation reduces the amplitude of the M1 component of the response to brief stretch of contralateral muscle, either through depression of fusimotor activity or inhibition of oligosynaptic pathways that contribute to the early reflex response.

Acupuncture Therapy↗
PubMed1986

Long-term potentiation and depression in hippocampal slices.

Antidromic stimulation of hippocampal CA 1 cells, in the presence of Mg2+ to eliminate synaptic transmission and with a pattern of impulses which when applied via a synaptic pathway produced long-term potentiation, was found to decrease the response of the CA 1 cells to subsequent synaptic activation. It was found that stimulation via synapses with the same pattern of stimuli caused long-term potentiation in normal conditions but not in the presence of 25 mM Mg2+.

Animals↗
PubMed1986

Reflex origin for the slowing of motoneurone firing rates in fatigue of human voluntary contractions.

During fatigue from a sustained maximal voluntary contraction (m.v.c.) the mean motoneurone discharge rates decline. In the present experiments we found no recovery of firing rates after 3 min of rest if the fatigued muscle was kept ischaemic, but near full recovery 3 min after the blood supply was restored. Since 3 min is thus sufficient time for recovery of any central changes in excitability, the results support the hypothesis that, during fatigue, motoneurone firing rates may be regulated by a peripheral reflex originating in response to fatigue-induced changes within the muscle.

Biomechanical Phenomena↗
PubMed1985

Intramuscular acupuncture-like electrical stimulation inhibits stretch reflexes in contralateral finger extensor muscles.

Electro-acupuncture is one of many physical measures used to relieve musculoskeletal pain and to improve the associated restricted range of motion. Experiments were designed to determine whether or not acupuncture-like stimulation inhibits stretch reflexes in an arm extensor muscle in human volunteers. Surface electromyographic recordings were made on the right extensor digitorum communis muscle and averaging techniques were used to study the reflex responses to brief deflection of the finger with a solenoid-driven probe. The ratio M1:M2 of two components of the reflex was reduced during continuous acupuncture-like stimulation of the contralateral first dorsal interosseus and extensor digitorum communis muscles near their motor points (acupuncture points LI 4 and LI 11). Concomitant changes in skin temperature were observed on the forehead and in the arm in which acupuncture-like stimulation was used. In control experiments, when the acupuncture needles were inserted subcutaneously and stimulated with the same current parameters at distinctly uncomfortable intensities, no change in the reflexes occurred. These findings show that acupuncture-like stimulation exerts physiologic effects on the central nervous system, mediated presumably by muscle afferent fibers. The effects may be relevant to relief of muscle spasm and musculoskeletal pain, and restoration of mobility.

Arm↗
PubMed1985

Long-latency spinal reflexes in humans.

Stretching human muscles with a mechanical device gave rise to multiple peaks in the rectified and averaged electromyogram. In the first dorsal interosseous the latency of the first peak (M1) was 32.4 +/- 2.4 ms (SD) and the latency of the second peak (M2) was 55.1 +/- 11.3 ms, in both cases measured from the time of the stimulus to the take-off point of the peak. Often a third peak (M3) was seen, having a considerably longer latency. The origin of peak M1 was considered to be in the stretch reflex arc because of its latency and its invariable association with muscle movement. Peak M2 was due to stimulation of afferent terminals in the skin and/or subcutaneous tissues by the mechanical device producing the muscle stretch. The conduction velocity of the pathway involved in the generation of the M1 component is the same as that for M2. This implies that central processing in the spinal cord delays the M2 response. The M2 mechanism does not involve a transcortical (long-loop) pathway because in foot muscles the M1-M2 delay remains the same as is found for hand muscles, although M1 latency is prolonged (to 39.4 +/- 6.2 ms for extensor digitorum longus). This indicates that there is not time for M2 impulses to traverse a pathway any longer than that passing to and from the spinal cord.

Afferent Pathways↗
PubMed1984

Proprioceptors and normal tremor.

The tremor of the hand, rotating about the wrist joint, was measured using an accelerometer, and groups of muscle action potentials were simultaneously recorded from the wrist extensor muscles using surface electrodes. The accelerometer signal and the rectified, demodulated electromyogram were submitted to Fourier analysis in order to quantify the tremor in terms of its frequency components and the amplitudes of those components. The amplitudes of the 8-12 Hz peak in the frequency spectrum obtained from muscle electrical activity were compared (a) when the hand was held raised against gravity (i.e. the contraction was isotonic) with (b) when it was held raised, with the same force and in the same position against a rigid bar (i.e. the contraction was isometric). In the isotonic condition (a) a prominent 8-12 Hz peak was observed in the spectrum. In the isometric condition (b) the peak was small or absent. The conclusion is drawn that the grouping (synchronization) of motor unit action potentials underlying tremor cannot be due to any process in the central nervous system generating them and they depend on cyclic alterations in muscle length activating proprioceptors.

Action Potentials↗
PubMed1983

The 4-6 HZ tremor during sustained contraction in normal human subjects.

Continuous elevation of the middle finger for 15-60 min gave rise to modulation of the e.m.g. at 4-6 Hz. A marked peak (50-150% of the amplitude of the coexisting 8-12 Hz peak) at 4-6 Hz was produced in sixteen out of twenty-one subjects. The 8-12 Hz peak was also enhanced (2-14 times with respect to its initial amplitude in eighteen subjects) during the course of the prolonged contraction but its frequency did not change. The 4-6 Hz and the 8-12 Hz peaks were present simultaneously; it is concluded that the two phenomena are separate entities. A step-function mechanical perturbation of the finger generates, time-locked to the stimulus, a train of waves at the frequency of the slow tremor, which can be abolished by local ischaemia. It is proposed that this slow tremor is due to an oscillatory process, possibly involving the reflex arc, but entailing a longer neuronal delay than that responsible for 8-12 Hz tremor.

Adolescent↗
PubMed1983

Changes in motoneurone firing rates during sustained maximal voluntary contractions.

Tungsten micro-electrodes have been used to record the electrical activity of single motor units in the human adductor pollicis during maximal voluntary contractions. The potentials were characteristic of those from single muscle fibres. In brief maximal contractions, the firing rates of over 200 motor units were obtained from five normal subjects. Four subjects had a similar range (mean 26.4 +/- 6.5 Hz) while the fifth was slightly higher (35 +/- 7.4 Hz). When maximal voluntary force was sustained for 40-120 s, there was a progressive decline in the range and mean rate of motor-unit discharge. In the first 60 s, mean rates fell from about 27 Hz to 15 Hz. There was some evidence to suggest that those units with the highest initial frequencies changed rate most rapidly. It is suggested that this decline in motor unit discharge rates is not responsible for force loss, but that it may enable effective modulation of voluntary strength by rate coding to continue during fatigue.

Action Potentials↗
PubMed1983

Contractile speed and EMG changes during fatigue of sustained maximal voluntary contractions.

Measurements were made from the human adductor pollicis muscle of force, contractile speed, and electromyographic activity (EMG) before, during, and after maximal isometric voluntary contractions sustained for 60 s. The use of brief test periods of maximal nerve stimulation with single shocks or trains of shocks enabled various muscle mechanical properties to be studied throughout each contraction. Electrical activity was measured after rectification and smoothing of the surface potentials and also by counting the total number of potentials per unit time from a population of motor units using fine wire intramuscular electrodes. During a 60-s maximal voluntary contraction, the force fell by 30-50%. Throughout the experiment the voluntary force matched that produced by supramaximal tetanic nerve stimulation. This indicated that, with sufficient practice, full muscle activation could be maintained by voluntary effort. However, the amplitude of the smoothed, rectifed EMG and the rate of spike counts declined. Since no evidence for neuromuscular block was found, the decline in EMG and spike counts was attributed to a progressive reduction of the neural drive from the central nervous system, despite maintained maximum effort. After the prolonged voluntary contractions twitch duration was prolonged, mainly as a result of slowing in relaxation rate. Twitch summation in unfused tetani increased. Both the maximum rate of relaxation and the time course of force decay declined by 50-70%. Similar changes were seen in both voluntary contractions and in test periods of stimulation. The percentage change in muscle contractile speed measured by these parameters approximately equaled the percentage change in the surface EMG measured simultaneously. It is concluded that 1) during a 60-s sustained maximal voluntary contraction there is a progressive slowing of contraction speed such that the excitation rate required to give maximal force generation is reduced, 2) the simultaneous decline in EMG may be due to a continuous reduction in motoneuron discharge rate, and 3) the EMG decline may not necessarily contribute to force loss.

Adult↗
PubMed1982

The absence of neuromuscular transmission failure in sustained maximal voluntary contractions.

1. Muscle mass action potentials (M waves) were evoked by supramaximal single shocks to the ulnar nerve given at 5-10 s intervals throughout sustained isometric maximal voluntary contractions (m.v.c.) of the adductor pollicis and first dorsal interosseous muscles. Both muscles were fatigued simultaneously. Recordings were made from the muscle surface and also intramuscularly. 2. During a maximal contraction lasting for 60 s there was 30-50% loss of force. No decline was observed in intramuscularly recorded M wave amplitude, while the areas of the total and half M wave forms increased due to a slowing in conduction velocity. The area measured over a fixed time period declined. No evidence was obtained that these M wave potentials were contaminated by electrical activity arising in adjacent muscles. The size of the single unit potentials appeared to remain unaltered during maximal voluntary activity. 3. We conclude that neuromuscular block is not a cause of force loss during this type of fatiguing voluntary contraction.

Action Potentials↗
PubMed1980

Finger tremor and cigarette smoking.

1 Finger tremor was recorded with a strain gauge and an accelerometer. 2 Records were subjected to frequency analysis and the amplitude or power at frequencies up to 25 Hz were computed. 3 Comparison was made between the tremor during a control period, during sham smoking and during smoking a cigarette. 4 Smoking significantly increases tremor amplitude by at least twofold over all frequencies from 1 Hz to 25 Hz.

Adolescent↗
PubMed1979

Prolonged changes in excitability of pyramidal tract neurones in the cat: a post-synaptic mechanism.

1. Prolonged changes in the excitability of cortical neurones can be produced by altering their firing rates for brief periods. In the anaesthetized cat, increased firing of pyramidal tract cells induced by trains of antidromic conditioning shocks led to increases in cell excitability, as measured by the size of the mass response at the medullary pyramid to test shocks applied to the cortical surface. We have shown in two ways that post-synaptic mechanisms could be responsible. 2. In one experimental design, MgCl2 solution (1 mole/l.) was applied to the cortical surface in order to block synaptic activity throughout the cortical depth. Following antidromic conditioning trains, cell excitability was increased; the size of the mass response was up to 30% larger than the control values. This persisted undiminished for up to 3 hr. 3. In the second experimental design, synaptic activity was not blocked, but we compared the effects of antidromic plus synaptic activation of pyramidal tract cells with the effects of synaptic activation alone. Antidromic plus synaptic activation was obtained by applying conditioning trains to the pyramidal tract at the medulla ipsilateral to the cortical test shock; prolonged increases in the ipsilateral response to the test shock were produced. Synaptic activation alone was obtained by the same conditioning trains, but in those cells whose axons projected into the contralateral pyramidal tract; prolonged increases in the contralateral response to the cortical test shock were never seen. In many instances prolonged decreases in excitability were found. 4. We conclude that prolonged increases in excitability of pyramidal tract cells can occur in the absence of any synaptic input, demonstrating that the underlying mechanism is post-synaptic; this does not preclude the action of synaptic mechanisms when synaptic transmission is not blocked.

Animals↗