Impact of Experimental Tonic Pain on Corrective Motor Responses to Mechanical Perturbations

Movement is altered by pain, but the underlying mechanisms remain unclear. Assessing corrective muscle responses following mechanical perturbations can help clarify these underlying mechanisms, as these responses involve spinal (short-latency response, 20-50 ms), transcortical (long-latency response, 50-100 ms), and cortical (early voluntary response, 100-150 ms) mechanisms. Pairing mechanical (proprioceptive) perturbations with different conditions of visual feedback can also offer insight into how pain impacts on sensorimotor integration. The general aim of this study was to examine the impact of experimental tonic pain on corrective muscle responses evoked by mechanical and/or visual perturbations in healthy adults. Two sessions (Pain (induced with capsaicin) and No pain) were performed using a robotic exoskeleton combined with a 2D virtual environment. Participants were instructed to maintain their index in a target despite the application of perturbations under four conditions of sensory feedback: (1) proprioceptive only, (2) visuoproprioceptive congruent, (3) visuoproprioceptive incongruent, and (4) visual only. Perturbations were induced in either flexion or extension, with an amplitude of 2 or 3 Nm. Surface electromyography was recorded from Biceps and Triceps muscles. Results demonstrated no significant effect of the type of sensory feedback on corrective muscle responses, no matter whether pain was present or not. When looking at the effect of pain on corrective responses across muscles, a significant interaction was found, but for the early voluntary responses only. These results suggest that the effect of cutaneous tonic pain on motor control arises mainly at the cortical (rather than spinal) level and that proprioception dominates vision for responses to perturbations, even in the presence of pain. The observation of a muscle-specific modulation using a cutaneous pain model highlights the fact that the impacts of pain on the motor system are not only driven by the need to unload structures from which the nociceptive signal is arising.

Short-term pressure induced suppression of the short-latency response: a new methodology for investigating stretch reflexes

During experiments involving ischemic nerve block, we noticed that the short-latency response (SLR) of evoked stretches in m. soleus decreased immediately following inflation of a pneumatic cuff surrounding the lower leg. The present study aimed to investigate this short-term effect of pressure application in more detail. Fifty-eight healthy subjects were divided into seven protocols. Unilateral stretches were applied to the calf muscles to elicit a SLR, and bilateral stretches to evoke a subsequent medium-latency response (MLR). Furthermore, H-reflexes and sensory nerve action potentials (SNAPs) were recorded. Additionally, stretches were applied with different velocities and amplitudes. Finally, the SLR was investigated during hopping and in two protocols that modified the ability of the muscle-tendon complex distal to the cuff to stretch. All measurements were performed with deflated and inflated cuff. Results of the protocols were as follows: 1) inflation of the cuff reduced the SLR but not the MLR; 2) the H-reflex, the M-wave, and, 3) SNAPs of n. tibialis remained unchanged with deflated and inflated cuff; 4) the SLR was dependent on the stretch velocity with deflated and also inflated cuff; 5 and 6) the reduction of the SLR by the cuff was dependent on the elastic properties of the muscle-tendon complex distal to the cuff; and 7) the cuff reduced the SLR during hopping. The present results suggest that the cuff did not affect the reflex arc per se. It is proposed that inflation restricted stretch of the muscles underlying the cuff so that most of the length change occurred in the muscle-tendon complex distal to the cuff. As a consequence, the muscle spindles lying within the muscle may be less excited, resulting in a reduced SLR. Due to its applicability in functional tasks, the introduced method can be a useful tool to study afferent feedback in motor control.

Temporal Evolution of “Automatic Gain-Scaling”

The earliest neural response to a mechanical perturbation, the short-latency stretch response (R1: 20–45 ms), is known to exhibit “automatic gain-scaling” whereby its magnitude is proportional to preperturbation muscle activity. Because gain-scaling likely reflects an intrinsic property of the motoneuron pool (via the size-recruitment principle), counteracting this property poses a fundamental challenge for the nervous system, which must ultimately counter the absolute change in load regardless of the initial muscle activity (i.e., show no gain-scaling). Here we explore the temporal evolution of gain-scaling in a simple behavioral task where subjects stabilize their arm against different background loads and randomly occurring torque perturbations. We quantified gain-scaling in four elbow muscles (brachioradialis, biceps long, triceps lateral, triceps long) over the entire sequence of muscle activity following perturbation onset—the short-latency response, long-latency response (R2: 50–75 ms; R3: 75–105 ms), early voluntary corrections (120–180 ms), and steady-state activity (750–1250 ms). In agreement with previous observations, we found that the short-latency response demonstrated substantial gain-scaling with a threefold increase in background load resulting in an approximately twofold increase in muscle activity for the same perturbation. Following the short-latency response, we found a rapid decrease in gain-scaling starting in the long-latency epoch (∼75-ms postperturbation) such that no significant gain-scaling was observed for the early voluntary corrections or steady-state activity. The rapid decrease in gain-scaling supports our recent suggestion that long-latency responses and voluntary control are inherently linked as part of an evolving sensorimotor control process through similar neural circuitry.

Impact of Rhythmic Oral Activity on the Timing of Muscle Activation in the Swallow of the Decerebrate Pig

The pharyngeal swallow can be elicited as an isolated event but, in normal animals, it occurs within the context of rhythmic tongue and jaw movement (RTJM). The response includes activation of the multifunctional geniohyoid muscle, which can either protract the hyoid or assist jaw opening; in conscious nonprimate mammals, two bursts of geniohyoid EMG activity (GHemg) occur in swallow cycles at times consistent with these two actions. However, during experimentally elicited pharyngeal swallows, GHemg classically occurs at the same time as hyoglossus and mylohyoid activity (short latency response) but, when the swallow is elicited in the decerebrate in the absence of RTJM, GHemg occurs later in the swallow (long latency response). We tested the hypothesis that it was not influences from higher centers but a brain stem mechanism, associated with RTJM, which caused GHemg to occur earlier in the swallow. In 38 decerebrate piglets, RTJM occurred sporadically in seven animals. Before RTJM, GHemg had a long latency, but, during RTJM, swallow related GHemg occurred synchronously with activity in hyoglossus and mylohyoid, early in the swallow. Both early and late responses were present during the changeover period. During this changeover period, duplicate electrodes in the geniohyoid could individually detect either the early or the late burst in the same swallow. This suggested that two sets of geniohyoid task units existed that were potentially active in the swallow and that they were differentially facilitated or inhibited depending on the presence or absence of rhythmic activity originating in the brain stem.

Proactive and Reactive Mechanisms Play a Role in Stepping on Inverting Surfaces During Gait

Ankle inversions have been studied extensively during standing conditions. However, inversion traumas occur during more dynamic conditions, like walking. Therefore in this study sudden ankle inversions were elicited in 12 healthy subjects who stepped on a trap door while walking on a treadmill. First, 10 control trials (0° of rotation) were presented. Then, 20 stimulus (25° of rotation) and control trials were presented randomly. EMG recordings were made of six lower leg muscles. All muscles showed a short-latency response (SLR) of about 40 ms and a late-latency response (LLR) of about 90 ms. The peroneal muscles showed the largest amplitudes in both responses. The functionally more important, larger, and more consistent LLR response was too late to resist the induced stretch during the inversion. The functional relevance of this response must lie after the inversion. During the first trial a widespread “startle-like” coactivation of the LLR was observed. The last trials showed only a recruitment of the peroneal muscles and, to a lesser extent, the gastrocnemius lateralis, which is seen as a switch from reactive control to more proactive adaptive strategies. These proactive strategies were investigated separately by comparing trials in which inversion was expected (but did not occur) with those in which subjects knew that no inversion would occur. Anticipation of a possible inversion was expressed in decreased tibialis anterior activity before initial contact, consistent with a more cautious and stable foot placement. Furthermore, immediately after landing, the peroneal muscles were activated to counteract the upcoming stretch.

Vestibulo-autonomic control in man: Short- and long-latency vestibular effects on cardiovascular function

We examined the hypothesis that vestibular signals may exert a rapid control on the heart adjusting cardiovascular function to maintain homoestasis during changes in body posture. Short- and long-latency effects of vestibular stimulation on heart rate (HR), systolic blood pressure (SP), diastolic pressure (DP) and digital blood flow (BF) were studied in fourteen normal controls (NC) and nine labyrinthine-defective subjects (LDS) exposed to abrupt head accelerations. Subjects lay supine with their head suspended in a sling whose 'release' was triggered at delays of 170 ms and 570 ms after an R-spike of the ECG. Release caused the head to fall with an acceleration ∼0.8 g for approximately 140 ms. Three additional NC underwent head drops at 170 ms, 370 ms, 470 ms and 570 ms to determine response latencies with precision. In NC, the short-latency response to head drops timed 170 to 470 ms after an R-spike was to shorten the time to the next R-spike in comparison to pre-drop heartbeat cycles. Drops at 570 ms delay shortened only the succeeding post-stimulus RR-interval. In LDS, head drops timed 170 ms after a heartbeat failed to shorten the ongoing cardiac cycle. For both delays only the succeeding cardiac cycle was significantly shortened. In all subjects, SP rose slightly by approximately 1–3% and BF decreased by 7–24% after 3–4 heartbeats post-drop. The results are evidence for an excitatory vestibulo-cardiac reflex in man which accelerates heart rate at a latency circa 500–600 ms. SP and BF are affected at longer latencies of several heart beats. A delayed increase of heart rate in response to postural challenge may contribute to the autonomic distress experienced by patients with vestibular loss.