Michael James Grey

Group II muscle afferents probably contribute to the medium latency soleus stretch reflex during walking in humans

1 The objective of this study was to determine which afferents contribute to the medium latency response of the soleus stretch reflex resulting from an unexpected perturbation during human walking. 2 Fourteen healthy subjects walked on a treadmill at approximately 3.5 km h−1 with the left ankle attached to a portable stretching device. The soleus stretch reflex was elicited by applying small amplitude (∼8 deg) dorsiflexion perturbations 200 ms after heel contact. 3 Short and medium latency responses were observed with latencies of 55 ± 5 and 78 ± 6 ms, respectively. The short latency response was velocity sensitive (P < 0.001), while the medium latency response was not (P= 0.725). 4 Nerve cooling increased the delay of the medium latency component to a greater extent than that of the short latency component (P < 0.005). 5 Ischaemia strongly decreased the short latency component (P= 0.004), whereas the medium latency component was unchanged (P= 0.437). 6 Two hours after the ingestion of tizanidine, an α2‐adrenergic receptor agonist known to selectively depress the transmission in the group II afferent pathway, the medium latency reflex was strongly depressed (P= 0.007), whereas the short latency component was unchanged (P= 0.653). 7 An ankle block with lidocaine hydrochloride was performed to suppress the cutaneous afferents of the foot and ankle. Neither the short (P= 0.453) nor medium (P= 0.310) latency reflexes were changed. 8 Our results support the hypothesis that, during walking the medium latency component of the stretch reflex resulting from an unexpected perturbation is contributed to by group II muscle afferents.

Post-activation depression of Soleus stretch reflexes in healthy and spastic humans

Reduced depression of transmitter release from Ia afferents following previous activation (post-activation depression) has been suggested to be involved in the pathophysiology of spasticity. However, the effect of this mechanism on the myotatic reflex and its possible contribution to increased reflex excitability in spastic participants has not been tested. To investigate these effects, we examined post-activation depression in Soleus H-reflex responses and in mechanically evoked Soleus stretch reflex responses. Stretch reflex responses were evoked with consecutive dorsiflexion perturbations delivered at different intervals. The magnitude of the stretch reflex and ankle torque response was assessed as a function of the time between perturbations. Soleus stretch reflexes were evoked with constant velocity (175°/s) and amplitude (6°) plantar flexion perturbations. Soleus H-reflexes were evoked by electrical stimulation of the tibial nerve in the popliteal fossa. The stretch reflex and H-reflex responses of 30 spastic participants (with multiple sclerosis or spinal cord injury) were compared with those of 15 healthy participants. In the healthy participants, the magnitude of the soleus stretch reflex and H-reflex decreased as the interval between the stimulus/perturbation was decreased. Similarly, the stretch-evoked torque decreased. In the spastic participants, the post-activation depression of both reflexes and the stretch-evoked torque was significantly smaller than in healthy participants. These findings demonstrate that post-activation depression is an important factor in the evaluation of stretch reflex excitability and muscle stiffness in spasticity, and they strengthen the hypothesis that reduced post-activation depression plays a role in the pathophysiology of spasticity.

Cortical excitability changes following grasping exercise augmented with electrical stimulation

Rehabilitation with augmented electrical stimulation can enhance functional recovery after stroke, and cortical plasticity may play a role in this process. The purpose of this study was to compare the effects of three training paradigms on cortical excitability in healthy subjects. Cortical excitability was evaluated by analysing the input–output relationship between transcranial magnetic stimulation intensity and motor evoked potentials (MEPs) from the flexor muscles of the fingers. The study was performed with 25 healthy volunteers who underwent 20-min simulated therapy sessions of: (1) functional electrical stimulation (FES) of the finger flexors and extensors, (2) voluntary movement (VOL) with sensory stimulation, and (3) therapeutic FES (TFES) where the electrical stimulation augmented voluntary activation. TFES training produced a significant increase in MEP magnitude throughout the stimulation range, suggesting an increase in cortical excitability. In contrast, neither the FES nor voluntary movement alone had such an effect. These results suggest that the combination of voluntary effort and FES has greater potential to induce plasticity in the motor cortex and that TFES might be a more effective approach in rehabilitation after stroke than FES or repetitive voluntary training alone.

Distinguishing active from passive components of ankle plantar flexor stiffness in stroke, spinal cord injury and multiple sclerosis

OBJECTIVE Spasticity is a common manifestation of lesion of central motor pathways. It is essential for correct anti-spastic treatment that passive and active contributions to increased muscle stiffness are distinguished. Here, we combined biomechanical and electrophysiological evaluation to distinguish the contribution of active reflex mechanisms from passive muscle properties to ankle joint stiffness in 31 healthy, 10 stroke, 30 multiple sclerosis and 16 spinal cord injured participants. The results were compared to routine clinical evaluation of spasticity. METHODS A computer-controlled robotic device applied stretches to the ankle plantar flexor muscles at different velocities (8-200deg/s; amplitude 6°). The reflex threshold was determined by soleus EMG. Torque and EMG data were normalized to the maximal torque and EMG evoked by supramaximal stimulation of the tibial nerve. Passive resistance (the torque response to stretches) was confirmed to be a good representation of the passive stiffness also at higher velocities when transmission in the tibial nerve was blocked by ischemia. RESULTS Passive torque tended to be larger in the neurological than in the healthy participants, but it did not reach statistical significance, except in the stroke group (p<0.05). Following normalization to the maximal stimulus-evoked torque, the passive torque was found to be significantly larger in neurological participants identified with spasticity than in non-spastic participants (p<0.01). There was no significant difference in the reflex threshold between the healthy and the neurological participants. The reflex evoked torque and EMG were significantly larger in all neurological groups than in the healthy group (p<0.001). Twenty three participants with evidence of hypertonia in the plantar flexors (Ashworth score⩾1) showed normal reflex torque without normalization. With normalization this was only the case in 11 participants. Increased reflex mediated stiffness was detected in only 64% participants during clinical examination. CONCLUSION The findings confirm that the clinical diagnosis of spasticity includes changes in both active and passive muscle properties and the two can hardly be distinguished based on routine clinical examination. SIGNIFICANCE The data suggest that evaluation techniques which are more efficient in distinguishing active and passive contributions to muscle stiffness than routine clinical examination should be considered before anti-spastic treatment is initiated.

Load Rather Than Length Sensitive Feedback Contributes to Soleus Muscle Activity During Human Treadmill Walking

Walking requires a constant adaptation of locomotor output from sensory afferent feedback mechanisms to ensure efficient and stable gait. We investigated the nature of the sensory afferent feedback contribution to the soleus motoneuronal drive and to the corrective stretch reflex by manipulating body load and ankle joint angle. The volunteers walked on a treadmill ( approximately 3.6 km/h) connected to a body weight support (BWS) system. To manipulate the load sensitive afferents the level of BWS was switched between 5 and 30% of body weight. The effect of transient changes in BWS on the soleus stretch reflex was measured by presenting dorsiflexion perturbations ( approximately 5 degrees, 360-400 degrees/s) in mid and late stances. Short (SLRs) and medium latency reflexes (MLRs) were quantified in a 15 ms analysis window. The MLR decreased with decreased loading (P = 0.045), but no significant difference was observed for the SLR (P = 0.13). Similarly, the effect of the BWS was measured on the unload response, i.e., the depression in soleus activity following a plantar-flexion perturbation ( approximately 5.6 degrees, 203-247 degrees/s), quantified over a 50 ms analysis window. The unload response decreased with decreased load (P > 0.001), but was not significantly affected (P = 0.45) by tizanidine induced depression of the MLR (P = 0.039, n = 6). Since tizanidine is believed to depress the group II afferent pathway, these results are consistent with the idea that force-related afferent feedback contributes both to the background locomotor activity and to the medium latency stretch reflex. In contrast, length-related afferent feedback may contribute to only the medium latency stretch reflex.

Contribution of afferent feedback and descending drive to human hopping

During hopping an early burst can be observed in the EMG from the soleus muscle starting about 45 ms after touch‐down. It may be speculated that this early EMG burst is a stretch reflex response superimposed on activity from a supra‐spinal origin. We hypothesised that if a stretch reflex indeed contributes to the early EMG burst, then advancing or delaying the touch‐down without the subjects knowledge should similarly advance or delay the burst. This was indeed the case when touch‐down was advanced or delayed by shifting the height of a programmable platform up or down between two hops and this resulted in a correspondent shift of the early EMG burst. Our second hypothesis was that the motor cortex contributes to the first EMG burst during hopping. If so, inhibition of the motor cortex would reduce the magnitude of the burst. By applying a low‐intensity magnetic stimulus it was possible to inhibit the motor cortex and this resulted in a suppression of the early EMG burst. These results suggest that sensory feedback and descending drive from the motor cortex are integrated to drive the motor neuron pool during the early EMG burst in hopping. Thus, simple reflexes work in concert with higher order structures to produce this repetitive movement.

Involvement of the corticospinal tract in the control of human gait.

Given the inherent mechanical complexity of human bipedal locomotion, and that complete spinal cord lesions in human leads to paralysis with no recovery of gait, it is often suggested that the corticospinal tract (CST) has a more predominant role in the control of walking in humans than in other animals. However, what do we actually know about the contribution of the CST to the control of gait? This chapter will provide an overview of this topic based on the premise that a better understanding of the role of the CST in gait will be essential for the design of evidence-based approaches to rehabilitation therapy, which will enhance gait ability and recovery in patients with lesions to the central nervous system (CNS). We review evidence for the involvement of the primary motor cortex and the CST during normal and perturbed walking and during gait adaptation. We will also discuss knowledge on the CST that has been gained from studies involving CNS lesions, with a particular focus on recent data acquired in people with spinal cord injury.

Within-step modulation of leg muscle activity by afferent feedback in human walking

To maintain smooth and efficient gait the motor system must adjust for changes in the ground on a step‐to‐step basis. In the present study we investigated the role of sensory feedback as 19 able‐bodied human subjects walked over a platform that mimicked an uneven supporting surface. Triceps surae muscle activation was assessed during stance as the platform was set to different inclinations (±3 deg, ±2 deg and 0 deg rotation in a parasagittal plane about the ankle). Normalized triceps surae muscle activity was significantly increased when the platform was inclined (2 deg: 0.153 ± 0.051; 3 deg: 0.156 ± 0.053) and significantly decreased when the platform was declined (−3 deg: 0.133 ± 0.048; −2 deg: 0.132 ± 0.049) compared with level walking (0.141 ± 0.048) for the able‐bodied subjects. A similar experiment was performed with a subject who lacked proprioception and touch sensation from the neck down. In contrast with healthy subjects, no muscle activation changes were observed in the deafferented subject. Our results demonstrate that the ability to compensate for small irregularities in the ground surface relies on automatic within‐step sensory feedback regulation rather than conscious predictive control.

Afferent-mediated modulation of the soleus muscle activity during the stance phase of human walking

The aim of this study was to investigate the contribution of proprioceptive feedback to the amplitude modulation of the soleus muscle activity during human walking. We have previously shown that slow-velocity, small-amplitude ankle dorsiflexion enhancements and reductions applied during the stance phase of the step cycle generate, respectively, increments and decrements on the ongoing soleus activity. We have also shown that the increments in soleus activity are at least partially mediated by feedback from group Ia fibres. In the present study, we further investigated the afferent-mediated contribution from muscle group II afferents, cutaneous and proprioceptive afferents from the foot, and load-sensitive afferents to the soleus EMG. Slow-velocity, small-amplitude ankle trajectory modifications were combined with the pharmaceutical depression of group II polysynaptic pathways with tizanidine hydrochloride, anaesthetic blocking of sensory information from the foot with injections of lidocaine hydrochloride, and modulation of load feedback by increasing and decreasing the body load. The depression of the group II afferents significantly reduced the soleus response to the ankle trajectory modifications. Blocking sensory feedback from the foot did not have an effect on the soleus muscle activity. Changes in body load affected the ongoing soleus activity level; however, it did not affect the amplitude of the soleus EMG responses to the ankle trajectory modifications. These results suggest that the feedback from group II afferents, and possibly from load-sensitive afferents, contribute to the amplitude modulation of the soleus muscle activity during the stance phase of the step cycle. However, feedback from cutaneous afferents and instrinsic proprioceptive afferents from the foot does not seem to contribute to this muscle activation.

Sudden Drop in Ground Support Produces Force-Related Unload Response in Human Overground Walking

Humans maneuver easily over uneven terrain. To maintain smooth and efficient gait the motor system needs to adapt the locomotor output to the walking environment. In the present study we investigate the role of sensory feedback in adjusting the soleus muscle activity during overground walking in 19 healthy volunteers. Subjects walked unrestrained over a hydraulically actuated platform. On random trials the platform was accelerated downward at 0.8 g, unloading the plantar flexor muscles in midstance or late stance. The drop of the platform resulted in a significant depression of the soleus muscle activity of -17.9% (SD 2) and -21.4% (SD 2), with an onset latency of 49 ms (SD 1) and 45 ms (SD 1) in midstance and late stance, respectively. Input to the vestibular apparatus (i.e., the head acceleration) occurred at a latency 10.0 ms (SD 2.4) following the drop and ankle dorsiflexion velocity was decreased starting 22 ms (SD 15) after the drop. To investigate the role of length- and velocity-sensitive afferents on the depression in soleus muscle activity, the ankle rotation was arrested by using an ankle foot orthotic as the platform was dropped. Preventing the ankle movement did not significantly change the soleus depression in late stance [-18.2% (SD 15)], whereas the depression in midstance was removed [+4.9% (SD 13)]. It is concluded that force feedback from ankle extensors increases the locomotor output through positive feedback in late stance. In midstance the effect of force feedback was not observed, suggesting that spindle afferents may have a more significant effect on the output during this phase of the step cycle.