Differential effects of a flexor nerve input on the human soleus H-reflex during standing versus walking

1995 ◽  
Vol 73 (4) ◽  
pp. 436-449 ◽  
Author(s):  
C. Capaday ◽  
B. A. Lavoie ◽  
F. Comeau

A conditioning (C) stimulus at group I strength was delivered during standing to the common peroneal (CP) nerve before a test (T) stimulus at several C–T intervals ranging from 0 to 150 ms. At sufficiently long C–T intervals (100–120 ms) the soleus H-reflex was strongly inhibited despite little, or no change, in the background level of EMG activity. This finding indicates that a significant portion of the inhibition occurs at a premotoneuronal level, likely via presynaptic inhibition of the Ia-afferent terminals. During standing, at C–T intervals of 100–120 ms (optimal C–T interval) a conditioning stimulus to the CP nerve of 1.5 times motor threshold (MT) intensity reduced the soleus H-reflex by an average of 45.8% (n = 14 subjects). The conditioning stimulus always produced a clear inhibition of the H-reflex during standing at these C–T intervals. The effects of this conditioning stimulus on the soleus H-reflex were then determined in the early part of the stance phase of walking. In contrast to standing, the conditioning stimulus produced little or no inhibition during the early part of the stance phase of walking (average inhibition 45.8 vs. 11.6%, n = 14 subjects). The soleus background EMG, and the soleus and tibialis anterior M-waves were essentially the same during standing and walking. Furthermore, there was no shift of the optimal C–T interval during walking. The difference in the effects of the conditioning stimulus was not due to differences in the size of the test H-reflex in each task. It appears to be due to a genuine task-dependent change in the input–output properties of the underlying spinal cord circuits. There are at least two, mutually compatible, explanations of these results. Firstly, during walking the intraspinal terminals of the afferent fibres (group Ia and Ib) conducting the conditioning volley may be presynaptically inhibited, or their input gated at the interneuronal level. Secondly, on the assumption that the conditioning stimulus is acting via the presynaptic inhibitory network in the spinal cord, it is possible that during walking this network is saturated as a result of increased central or peripheral synaptic inputs. Finally, it seems unlikely that differences in the refractoriness of the CP nerve between the tasks may be involved; the reasons for this are presented in the discussion.Key words: Ia afferents, motoneurons, presynaptic inhibition, EMG, posture, locomotion, spinal cord.

2003 ◽  
Vol 89 (1) ◽  
pp. 304-314 ◽  
Author(s):  
H. S. Pyndt ◽  
J. B. Nielsen

Transmission in the corticospinal and Ia pathways to soleus motoneurons was investigated in healthy human subjects during bicycling. Soleus H reflexes and motor evoked potentials (MEPs) after transcranial magnetic stimulation (TMS) were modulated similarly during the crank cycle being large during downstroke [concomitant with soleus background electromyographic (EMG) activity] and small during upstroke. Tibialis anterior MEPs were in contrast large during upstroke and small during downstroke. The soleus H reflexes and MEPs were also recorded during tonic plantarflexion at a similar ankle joint position, corresponding ankle angle, and matched background EMG activity as during the different phases of bicycling. Relative to their size during tonic plantarflexion, the MEPs were found to be facilitated in the early part of downstroke during bicycling, whereas the H reflexes were depressed in the late part of downstroke. The intensity of TMS was decreased below MEP threshold and used to condition the soleus H reflex. At short intervals (conditioning-test intervals of −3 to −1 ms), TMS produced a facilitation of the H reflex that is in all likelihood caused by activation of the fast monosynaptic corticospinal pathway. This facilitation was significantly larger in the early part of downstroke during bicycling than during tonic plantarflexion. This suggests that the increased MEP during downstroke was caused by changes in transmission in the fast monosynaptic corticospinal pathway. To investigate whether the depression of H reflexes in the late part of downstroke was caused by increased presynaptic inhibition of Ia afferents, the soleus H reflex was conditioned by stimulation of the femoral nerve. At a short interval (conditioning-test interval: −7 to −5 ms), the femoral nerve stimulation produced a facilitation of the H reflex that is mediated by the heteronymous monosynaptic Ia pathway from the femoral nerve to soleus motoneurons. Within the initial 0.5 ms after its onset, the size of this facilitation depends on the level of presynaptic inhibition of the Ia afferents, which mediate the facilitation. The size of the facilitation was strongly depressed in the late part of downstroke, compared with the early part of downstroke, suggesting that increased presynaptic inhibition was indeed responsible for the depression of the H reflex. These findings suggest that there is a selectively increased transmission in the fast monosynaptic corticospinal pathway to soleus motoneurons in early downstroke during bicycling. It would seem likely that one cause of this is increased excitability of the involved cortical neurons. The increased presynaptic inhibition of Ia afferents in late downstroke may be of importance for depression of stretch reflex activity before and during upstroke.


1997 ◽  
Vol 78 (6) ◽  
pp. 2975-2984 ◽  
Author(s):  
John E. Misiaszek ◽  
Keir G. Pearson

Misiaszek, John E. and Keir G. Pearson. Stretch of quadriceps inhibits the soleus H reflex during locomotion in decerebrate cats. J. Neurophysiol. 78: 2975–2984, 1997. Previously, it has been demonstrated that afferent signals from the quadriceps muscles can suppress H reflexes in humans during passive movements of the leg. To establish whether afferent input from quadriceps contributes to the modulation of the soleus H reflex during locomotion, the soleus H reflex was conditioned with stretches of the quadriceps muscle during bouts of spontaneous treadmill locomotion in decerebrate cats. We hypothesized that 1) in the absence of locomotion such conditioning would lead to suppression of the soleus H reflex and 2) this would be retained during periods of locomotor activity. In the absence of locomotion, slow sinusoidal stretches (0.2 Hz, 8 mm) of quadriceps cyclically modulated the amplitude of the soleus H reflex. The H reflex amplitude was least during the lengthening of the quadriceps and greatest as quadriceps shortened. Further, low-amplitude vibrations (48–78 μm) applied to the patellar tendon suppressed the reflex, indicating that the muscle spindle primaries were the receptor eliciting the effect. During bouts of locomotion, ramp stretches of quadriceps were applied during the extensor phase of the locomotor rhythm. Soleus H reflexes sampled at two points during the stance phase were reduced compared with phase-matched controls. The background level of the soleus electromyographic activity was not influenced by the applied stretches to quadriceps, either during locomotion or in the absence of locomotion. This indicates that the excitability of the soleus motoneuron pool was not influenced by the stretching of quadriceps, and that the inhibition of the soleus H reflex is due to presynaptic inhibition. We conclude that group Ia afferent feedback from quadriceps contributes to the regulation of the soleus H reflex during the stance phase of locomotion in decerebrate cats. This afferent mediated source of regulation of the H reflex, or monosynaptic stretch reflex, would allow for rapid alterations in reflex gain according to the dynamic needs of the animal. During early stance, this source of regulation might suppress the soleus stretch reflex to allow adequate yielding at the ankle and facilitate the movement of the body over the foot.


2007 ◽  
Vol 107 (4) ◽  
pp. 553-562 ◽  
Author(s):  
Jan H. Baars ◽  
Michael Benzke ◽  
Falk von Dincklage ◽  
Josephine Reiche ◽  
Peter Schlattmann ◽  
...  

Background Reduced spinal excitability contributes to the suppression of movement responses to noxious stimuli during the anesthetic state. This study examines and compares presynaptic and postsynaptic effects of two anesthetics in the human spinal cord. Methods The authors tested two parameters during the administration of 0.8 vol% sevoflurane or 40 vol% nitrous oxide compared with control states before and after drug administration: (1) the size of the soleus H reflex (integrating presynaptic and postsynaptic effects) at increasing stimulus intensities (recruitment curve) and (2) the amount of presynaptic inhibition on Ia afferents of the quadriceps femoris, evaluated by the heteronymous facilitation of the soleus H reflex caused by a conditioning stimulation of the femoral nerve. The study was performed in 10 subjects for each drug. Results At the chosen concentrations, the maximum H reflex was reduced by 26.3 +/- 8.4% (mean +/- SD) during sevoflurane and by 33.5 +/- 15.6% during nitrous oxide administration. The averaged recruitment curves were similarly depressed under the influence of the two drugs. The reduction of H-reflex facilitation was significantly stronger for sevoflurane (28.8 +/- 20.0%) than for nitrous oxide administration (6.2 +/- 26.4%). Conclusions These results demonstrate in humans presynaptic effects of the volatile anesthetic sevoflurane but not of nitrous oxide. A possible explanation for this difference may be the different potency of the respective drugs in enhancing gamma-aminobutyric acid type A receptor-mediated inhibition, because presynaptic inhibition in the spinal cord involves this receptor subtype.


2012 ◽  
Vol 108 (4) ◽  
pp. 1176-1185 ◽  
Author(s):  
Rinaldo André Mezzarane ◽  
André Fabio Kohn ◽  
Erika Couto-Roldan ◽  
Lourdes Martinez ◽  
Amira Flores ◽  
...  

Crossed effects from group I afferents on reflex excitability and their mechanisms of action are not yet well understood. The current view is that the influence is weak and takes place indirectly via oligosynaptic pathways. We examined possible contralateral effects from group I afferents on presynaptic inhibition of Ia terminals in humans and cats. In resting and seated human subjects the soleus (SO) H-reflex was conditioned by an electrical stimulus to the ipsilateral common peroneal nerve (CPN) to assess the level of presynaptic inhibition (PSI_control). A brief conditioning vibratory stimulus was applied to the triceps surae tendon at the contralateral side (to activate preferentially Ia muscle afferents). The amplitude of the resulting H-reflex response (PSI_conditioned) was compared to the H-reflex under PSI_control, i.e., without the vibration. The interstimulus interval between the brief vibratory stimulus and the electrical shock to the CPN was −60 to 60 ms. The H-reflex conditioned by both stimuli did not differ from that conditioned exclusively by the ipsilateral CPN stimulation. In anesthetized cats, bilateral monosynaptic reflexes (MSRs) in the left and right L7 ventral roots were recorded simultaneously. Conditioning stimulation applied to the contralateral group I posterior biceps and semitendinosus (PBSt) afferents at different time intervals (0–120 ms) did not have an effect on the ipsilateral gastrocnemius/soleus (GS) MSR. An additional experimental paradigm in the cat using contralateral tendon vibration, similar to that conducted in humans, was also performed. No significant differences between GS-MSRs conditioned by ipsilateral PBSt stimulus alone and those conditioned by both ipsilateral PBSt stimulus and contralateral tendon vibration were detected. The present results strongly suggest an absence of effects from contralateral group I fibers on the presynaptic mechanism of MSR modulation in relaxed humans and anesthetized cats.


Author(s):  
M. Verrier ◽  
S. MacLeod ◽  
P. Ashby

SUMMARY:The effect of diazepam on presynaptic inhibition in man has been examined in 5 patients with complete spinal transections and 7 patients with incomplete lesions. The inhibition of the H reflex by vibration applied to the tendo Achilles was used to assess presynaptic inhibition of the la monosynaptic pathway. Diazepam increased this inhibition in the patients with incomplete lesions, but had no significant effect on the inhibition in the patients with complete spinal transections.Evidently diazepam can enhance presynaptic inhibition in man. The effect, however, cannot be demonstrated in patients with longstanding complete spinal lesions possibly because of some alteration in the segmental presynaptic inhibitory mechanism in this group.


1994 ◽  
Vol 72 (5) ◽  
pp. 2090-2104 ◽  
Author(s):  
J. Fung ◽  
H. Barbeau

1. The modulation of the soleus H-reflex by a conditioning cutaneomuscular stimulation was investigated in 10 normal and 10 spastic paretic subjects who suffered from incomplete spinal cord lesions. The different motor tasks examined were standing, locomotion, and the maintenance of static limb postures to mimic critical gait events. The test soleus H-reflex was obtained by stimulating the tibial nerve in the popliteal fossa with a single 1-ms pulse at an intensity that produced a barely detectable M wave. The conditioning stimulus, consisting of an 11-ms train of three 1-ms pulses at 200 Hz, was delivered to the ipsilateral medial plantar arch, stimulating predominantly the medial plantar nerve, at an innocuous intensity of 2.5–3.0 X sensory threshold and at a conditioning-test delay of 45 ms. 2. During quiet standing, the H-reflex amplitude was inhibited only marginally by the conditioning cutaneomuscular stimulation, not reaching statistical significance in either the normal or spastic group of subjects. Although there was a trend of reflex inhibition in the normal subjects as the conditioning intensity was increased, a reversed trend of reflex facilitation was observed in the spastic patients. 3. During treadmill walking, the conditioned H-reflex was inhibited significantly during all phases in all the normal subjects and in one mildly impaired patient. In the moderately and severely impaired patients, cutaneomuscular stimulation selectively inhibited the soleus H-reflex in the early stance and swing phases, thereby producing a near normal phasic modulation pattern. Such modulatory effects were not present under static gait-mimicking conditions. 4. The task-specific and phase-dependent effects of cutaneomuscular stimulation on the soleus H-reflex in the spinal cord-injured patients revealed strong inhibitory influence on Ia afferents from cutaneomuscular inputs. It is plausible that inhibition occurs at both pre- and postsynaptic levels. 5. It is concluded that normal Ia modulatory mechanisms during locomotion are deficient in spastic spinal cord-injured patients and can partially and artificially be restored by cutaneomuscular stimulation applied to the sole of the foot. This can be used as a functional electrical stimulation (FES) regime in gait rehabilitation.


2005 ◽  
Vol 94 (2) ◽  
pp. 1133-1142 ◽  
Author(s):  
Roth-Visal Ung ◽  
Marie-Andrée Imbeault ◽  
Christian Ethier ◽  
Laurent Brizzi ◽  
Charles Capaday

When untrained subjects walk backward on a treadmill, an unexpectedly large amplitude soleus H-reflex occurs in the midswing phase of backward walking. We hypothesized that activity in the corticospinal tract (CST) during midswing depolarizes the soleus α-motoneurons subliminally and thus brings them closer to threshold. To test this hypothesis, transcranial magnetic stimulation (TMS) was applied to the leg area of the motor cortex (MCx) during backward walking. Motor-evoked potentials (MEPs) were recorded from the soleus and tibialis anterior (TA) muscles in untrained subjects at different phases of the backward walking cycle. We reasoned that if soleus MEPs could be elicited in midswing, while the soleus is inactive, this would be strong evidence for increased postsynaptic excitability of the α-motoneurons. In the event, we found that in untrained subjects, despite the presence of an unexpectedly large H-reflex in midswing, no soleus MEPs were observed at that time. The soleus MEPs were in phase with the soleus electromyographic (EMG) activity during backward walking. Soleus MEPs increased more rapidly as a function of the EMG activity during voluntary activity than during backward walking. Furthermore, a conditioning stimulus to the motor cortex facilitated the soleus H-reflex at rest and during voluntary plantarflexion but not in the midswing phase of backward walking. With daily training at walking backward, the time at which the H-reflex began to increase was progressively delayed until it coincided with the onset of soleus EMG activity, and its amplitude was considerably reduced compared with its value on the first experimental day. By contrast, no changes were observed in the timing or amplitude of soleus MEPs with training. Taken together, these observations make it unlikely that the motor cortex via the CST is involved in control of the H-reflex during the backward step cycle of untrained subjects nor in its progressive adaptation with training. Our observations raise the possibility that the large amplitude of H-reflex in untrained subjects and its adaptation with training are mainly due to control of presynaptic inhibition of Ia-afferents by other descending tracts.


2021 ◽  
Vol 12 ◽  
Author(s):  
Timothy S. Pulverenti ◽  
Morad Zaaya ◽  
Monika Grabowski ◽  
Ewelina Grabowski ◽  
Md. Anamul Islam ◽  
...  

Neurophysiological changes that involve activity-dependent neuroplasticity mechanisms via repeated stimulation and locomotor training are not commonly employed in research even though combination of interventions is a common clinical practice. In this randomized clinical trial, we established neurophysiological changes when transcranial magnetic stimulation (TMS) of the motor cortex was paired with transcutaneous thoracolumbar spinal (transspinal) stimulation in human spinal cord injury (SCI) delivered during locomotor training. We hypothesized that TMS delivered before transspinal (TMS-transspinal) stimulation promotes functional reorganization of spinal networks during stepping. In this protocol, TMS-induced corticospinal volleys arrive at the spinal cord at a sufficient time to interact with transspinal stimulation induced depolarization of alpha motoneurons over multiple spinal segments. We further hypothesized that TMS delivered after transspinal (transspinal-TMS) stimulation induces less pronounced effects. In this protocol, transspinal stimulation is delivered at time that allows transspinal stimulation induced action potentials to arrive at the motor cortex and affect descending motor volleys at the site of their origin. Fourteen individuals with motor incomplete and complete SCI participated in at least 25 sessions. Both stimulation protocols were delivered during the stance phase of the less impaired leg. Each training session consisted of 240 paired stimuli delivered over 10-min blocks. In transspinal-TMS, the left soleus H-reflex increased during the stance-phase and the right soleus H-reflex decreased at mid-swing. In TMS-transspinal no significant changes were found. When soleus H-reflexes were grouped based on the TMS-targeted limb, transspinal-TMS and locomotor training promoted H-reflex depression at swing phase, while TMS-transspinal and locomotor training resulted in facilitation of the soleus H-reflex at stance phase of the step cycle. Furthermore, both transspinal-TMS and TMS-transspinal paired-associative stimulation (PAS) and locomotor training promoted a more physiological modulation of motor activity and thus depolarization of motoneurons during assisted stepping. Our findings support that targeted non-invasive stimulation of corticospinal and spinal neuronal pathways coupled with locomotor training produce neurophysiological changes beneficial to stepping in humans with varying deficits of sensorimotor function after SCI.


2021 ◽  
Vol 23 (11) ◽  
pp. 285-296
Author(s):  
Mohaimen A. Ridha ◽  

Background: Baclofen and tizanidine are both used for the treatment of muscle spasticity of spinal origin. patients and methods: This study was conducted in Ibn Al-Quf hospital for spinal cord injuries from the period December 2011 to June 2012. All of the participants gave written consent to participate in the study. The patients were divided into 2 groups: Group (I): Baclofen with physiotherapy treatment group; and Group (II): Tizanidine with physiotherapy treatment groups .H-reflex measurements were performed. parameters were studied: H-reflex latency, M wave latency, H-reflex conduction velocity, H-reflex duration, H-reflex amplitude. Results: All the patients had symptoms of spasticity at any time during the day with a Modified Ashworth Scale (MAS) before performing the H-reflex study. highly significant improvement in the H/M ratio when comparing positive controls to the two groups while the H/M ratio in the negative controls shows no significant difference with group I and group II. A significant correlation was noticed between the height of control subjects & H-reflex latency (P= 0.002), significant positive correlation was also found (P=0.028) between the height & M wave latency in the control subjects, The results revealed that the type of treatment did not affect the H-reflex and F wave parameters except for the H/M ratio. conclusion: H-reflex can provide information regarding neural function after spinal cord injury and the H/M ratio can be used as a good indicator for both spasticity assessment and response to treatment. Tizanidine hydrochloride is useful in the management of spasticity caused by SCI and can be used as a routine drug treatment although liver function tests should be periodically monitored.


2020 ◽  
Author(s):  
Guillaume Caron ◽  
Jadwiga N. Bilchak ◽  
Marie-Pascale Côté

ABSTRACTSpinal cord injury (SCI) results in the disruption of supraspinal control of spinal networks and an increase in the relative influence of afferent feedback to sublesional neural networks, both of which contribute to enhancing spinal reflex excitability. Hyperreflexia occurs in ~75% of individuals with chronic SCI and critically hinders functional recovery and quality of life. It is suggested to result from an increase in motoneuronal excitability and a decrease in presynaptic and postsynaptic inhibitory mechanisms. In contrast, locomotor training decreases hyperreflexia by restoring presynaptic inhibition.Primary afferent depolarization (PAD) is a powerful presynaptic inhibitory mechanism that selectively gates primary afferent transmission to spinal neurons to adjust reflex excitability and ensure smooth movement. However, the effect of chronic SCI and step-training on the reorganization of presynaptic inhibition evoked by hindlimb afferents, and the contribution of PAD has never been demonstrated. The objective of this study is to directly measure changes in presynaptic inhibition through dorsal root potentials (DRPs) and its association to plantar H-reflex inhibition. We provide direct evidence that H-reflex hyperexcitability is associated with a decrease in transmission of PAD pathways activated by PBSt afferents after chronic SCI. More precisely, we illustrate that PBSt group I muscle afferents evoke a similar pattern of inhibition onto both L4-DRPs and plantar H-reflexes evoked by the tibial nerve in Control and step-trained animals, but not in chronic SCI rats. These changes are not observed after step-training, suggesting a role for activity-dependent plasticity to regulate PAD pathways activated by flexor muscle group I afferents.Key point summaryPresynaptic inhibition is modulated by supraspinal centers and primary afferents in order to filter sensory information, adjust spinal reflex excitability, and ensure smooth movements.After SCI, the supraspinal control of primary afferent depolarization (PAD) interneurons is disengaged, suggesting an increased role for sensory afferents. While increased H-reflex excitability in spastic individuals indicates a possible decrease in presynaptic inhibition, it remains unclear whether a decrease in sensory-evoked PAD contributes to this effect.We investigated whether the PAD evoked by hindlimb afferents contributes to the change in presynaptic inhibition of the H-reflex in a decerebrated rat preparation. We found that chronic SCI decreases presynaptic inhibition of the plantar H-reflex through a reduction in PAD evoked by PBSt muscle group I afferents.We further found that step-training restored presynaptic inhibition of the plantar H-reflex evoked by PBSt, suggesting the presence of activity-dependent plasticity of PAD pathways activated by flexor muscle group I afferents.


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