Long-latency Stretch Reflex Research Articles

Assistive Loading Promotes Goal-Directed Tuning of Stretch Reflex Gains.

Voluntary movements are prepared before they are executed. Preparatory activity has been observed across the CNS and recently documented in first-order neurons of the human PNS (i.e., in muscle spindles). Changes seen in sensory organs suggest that independent modulation of stretch reflex gains may represent an important component of movement preparation. The aim of the current study was to further investigate the preparatory modulation of short-latency stretch reflex responses (SLRs) and long-latency stretch reflex responses (LLRs) of the dominant upper limb of human subjects. Specifically, we investigated how different target parameters (target distance and direction) affect the preparatory tuning of stretch reflex gains in the context of goal-directed reaching, and whether any such tuning depends on preparation duration and the direction of background loads. We found that target distance produced only small variations in reflex gains. In contrast, both SLR and LLR gains were strongly modulated as a function of target direction, in a manner that facilitated the upcoming voluntary movement. This goal-directed tuning of SLR and LLR gains was present or enhanced when the preparatory delay was sufficiently long (>250 ms) and the homonymous muscle was unloaded [i.e., when a background load was first applied in the direction of homonymous muscle action (assistive loading)]. The results extend further support for a relatively slow-evolving process in reach preparation that functions to modulate reflexive muscle stiffness, likely via the independent control of fusimotor neurons. Such control can augment voluntary goal-directed movement and is triggered or enhanced when the homonymous muscle is unloaded.

Significantly Delayed Medium-Latency Response of the Stretch Reflex in Delayed-Onset Muscle Soreness of the Quadriceps Femoris Muscles Is Indicative of Sensory Neuronal Microdamage.

Unaccustomed or strenuous eccentric exercise is known to cause delayed-onset muscle soreness. A recent hypothesis postulated that mechano-energetic microinjury of the primary afferent sensory neuron terminals in the muscle spindles, namely a transient Piezo2 channelopathy, could be the critical cause of delayed-onset muscle soreness in the form of a bi-phasic non-contact injury mechanism. This theory includes that this microlesion could delay the medium-latency response of the stretch reflex. Our aim with this study was to investigate this hypothesis. According to our knowledge, no study has examined the effect of delayed-onset muscle soreness on the medium-latency response of the stretch reflex. Our findings demonstrated that a significant delay in the medium-latency stretch reflex could be observed right after a multi-stage fitness test in the quadriceps femoris muscles of Hungarian professional handball players who consequently experienced delayed-onset muscle soreness. The long-latency stretch reflex and most likely short-latency stretch reflex were unaffected by delayed-onset muscle soreness in our study, which is in line with earlier findings. We translate these findings as indicative of proprioceptive Type Ia terminal microdamage in the muscle spindle in line with the aforementioned new acute non-contact compression axonopathy theory of delayed-onset muscles soreness.

The effect of cathodal transspinal direct current stimulation on tibialis anterior stretch reflex components in humans.

Spinal DC stimulation (tsDCS) shows promise as a technique for the facilitation of functional recovery of motor function following central nervous system (CNS) lesion. However, the network mechanisms that are responsible for the effects of tsDCS are still uncertain. Here, in a series of experiments, we tested the hypothesis that tsDCS increases the excitability of the long-latency stretch reflex, leading to increased excitability of corticospinal neurons in the primary motor cortex. Experiments were performed in 33 adult human subjects (mean age 28 ± 7years/14 females). Subjects were seated in a reclining armchair with the right leg attached to a footplate, which could be quickly plantarflexed (100deg/s; 6deg amplitude) to induce stretch reflexes in the tibialis anterior (TA) muscle at short (45ms) and longer latencies (90-95ms). This setup also enabled measuring motor evoked potentials (MEPs) and cervicomedullary evoked potentials (cMEPs) from TA evoked by transcranial magnetic stimulation (TMS) and electrical stimulation at the cervical junction, respectively. Cathodal tsDCS at 2.5 and 4mA was found to increase the long-latency reflex without any significant effect on the short-latency reflex. Furthermore, TA MEPs, but not cMEPs, were increased following tsDCS. We conclude that cathodal tsDCS over lumbar segments may facilitate proprioceptive transcortical reflexes in the TA muscle, and we suggest that the most likely explanation of this facilitation is an effect on ascending fibers in the dorsal columns.

Dynamic Control of Upper Limb Stretch Reflex in Wrestlers.

ABSTRACTPurposeThe objective of this study was to clarify the characteristics of the upper limb stretch reflex in wrestlers.MethodsTen wrestlers and 11 control subjects participated in the study. The experiment was divided into two sessions. In the extension perturbation session, participants either relaxed or flexed the elbow when they felt a perturbation (abrupt elbow extension induced by a dynamometer). This was done 30 times by each subject for both sessions. In the flexion perturbation session, participants also relaxed or extended the elbow when they felt a perturbation (abrupt elbow flexion). During the tasks, the stretch reflex was monitored by recording the surface EMG activities of the right biceps and triceps brachii. The EMG reflex components were divided into three periods based on the time after the perturbation (M1, 20–50 ms; M2, 50–80 ms; and M3, 80–100 ms). The averaged background EMG activity just before the disturbance was subtracted from the EMG activity in each period. The resultant value was integrated to obtain reflex magnitudes of M1 to M3.ResultsFor the triceps brachii, in the relaxation task, the wrestler group showed a significantly smaller value for M2 than did the control group. In the extension task, the wrestler group showed a significantly larger value for M3 than did the control group. There was no difference in M1 between the two groups. For the biceps brachii, there was no significant difference between any reflex components.ConclusionsOur results suggest that high-level wrestlers have specific characteristics of the long-latency stretch reflex in the triceps brachii that are modulated in a situation-specific manner.

Assessing Neural Connectivity and Associated Time Delays of Muscle Responses to Continuous Position Perturbations.

Both linear and nonlinear electromyographic (EMG) connectivity has been reported during the expression of stretch reflexes, though it is not clear whether they are generated by the same neural pathways. To answer this question, we aim to distinguish linear and nonlinear connectivity, as well as their delays in muscle responses, resulting from continuous elbow joint perturbations. We recorded EMG from Biceps Brachii muscle when eight able-bodied participants were performing a steady elbow flexion torque while simultaneously receiving a continuous position perturbation. Using a recently developed phase coupling metric, we estimated linear and nonlinear connectivity as well as their associated delays between Biceps EMG responses and perturbations. We found that the time delay for linear connectivity (24.5 ± 5.4ms) is in the range of short-latency stretch reflex period (< 35ms), while that for nonlinear connectivity (53.8 ± 3.2ms) is in the range of long-latency stretch reflex period (40-70ms). These results suggest that the estimated linear connectivity between EMG and perturbations is very likely generated by the mono-synaptic spinal stretch reflex loop, while the nonlinear connectivity may be associated with multi-synaptic supraspinal stretch reflex loops. As such, this study provides new evidence of the nature of neural connectivity related to the stretch reflex.

Predicting Perturbed Human Arm Movements in a Neuro-Musculoskeletal Model to Investigate the Muscular Force Response.

Human movement is generated by a dynamic interplay between the nervous system, the biomechanical structures, and the environment. To investigate this interaction, we propose a neuro-musculoskeletal model of human goal-directed arm movements. Using this model, we simulated static perturbations of the inertia and damping properties of the arm, as well as dynamic torque perturbations for one-degree-of freedom movements around the elbow joint. The controller consists of a feed-forward motor command and feedback based on muscle fiber length and contraction velocity representing short-latency (25 ms) or long-latency (50 ms) stretch reflexes as the first neuronal responses elicited by an external perturbation. To determine the open-loop control signal, we parameterized the control signal resulting in a piecewise constant stimulation over time for each muscle. Interestingly, such an intermittent open-loop signal results in a smooth movement that is close to experimental observations. So, our model can generate the unperturbed point-to-point movement solely by the feed-forward command. The feedback only contributed to the stimulation in perturbed movements. We found that the relative contribution of this feedback is small compared to the feed-forward control and that the characteristics of the musculoskeletal system create an immediate and beneficial reaction to the investigated perturbations. The novelty of these findings is (1) the reproduction of static as well as dynamic perturbation experiments in one neuro-musculoskeletal model with only one set of basic parameters. This allows to investigate the model's neuro-muscular response to the perturbations that—at least to some degree—represent stereotypical interactions with the environment; (2) the demonstration that in feed-forward driven movements the muscle characteristics generate a mechanical response with zero-time delay which helps to compensate for the perturbations; (3) that this model provides enough biomechanical detail to allow for the prediction of internal forces, including joint loads and muscle-bone contact forces which are relevant in ergonomics and for the development of assistive devices but cannot be observed in experiments.

Learning New Feedforward Motor Commands Based on Feedback Responses.

Learning a new motor task modifies feedforward (i.e., voluntary) motor commands and such learning also changes the sensitivity of feedback responses (i.e., reflexes) to mechanical perturbations [1-9]. For example, after people learn to generate straight reaching movements in the presence of an external force field or learn to reduce shoulder muscle activity when generating pure elbow movements with shoulder fixation, evoked stretch reflex responses to mechanical perturbations reflect the learning expressed during self-initiated reaching. Such a transfer from feedforward motor commands to feedback responses is thought to take place because of shared neural circuits at the level of the spinal cord, brainstem, and cerebral cortex [10-13]. The presence of shared neural resources also predicts the transfer from feedback responses to feedforward motor commands. Little is known about such a transfer presumably because it is relatively hard to elicit learning in reflexes without engaging associated voluntary responses following mechanical perturbations. Here, we demonstrate such transfer by leveraging two approaches to elicit stretch reflexes while minimizing engagement of voluntary motor responses in the learning process: applying very short mechanical perturbations [14-19] and instructing participants to not respond to them [20-26]. Taken together, our work shows that transfer between feedforward and feedback control is bidirectional, furthering the notion that these processes share common neural circuits that underlie motor learning and transfer.

Spinal Circuits Mediate a Stretch Reflex Between the Upper Limbs in Humans

Inter-limb reflexes play an important role in coordinating behaviors involving different limbs. Previous studies have demonstrated that human elbow muscles express an inter-limb stretch reflex at long-latency (50–100 ms), a timing consistent with a trans-cortical linkage. Here we probe for inter-limb stretch reflexes in the shoulder muscles of human participants. Unexpected torque pulses displaced one or both shoulders while participants adopted a steady posture against background torques. The results demonstrated inter-limb stretch reflexes occurring at short-latency for both shoulder extensors and flexors; the rapid timing (36–50 ms) must involve a spinal linkage for the two arms. Inter-limb stretch reflexes were also observed at long-latency yet they were opposite to the preceding short-latency; when the short-latency stretch reflex was excitatory then the long-latency stretch reflex was inhibitory and vice versa. Comparing the responses to contralateral arm displacement to those during simultaneous displacement of both arms revealed that inhibitory inter-limb stretch reflexes are independent of within-limb stretch reflexes, but that excitatory inter-limb stretch reflexes are suppressed by within-limb stretch reflexes. Our results provide the first demonstration of short-latency inter-limb stretch reflexes in the upper limb of humans and reveal interacting spinal circuits for within-limb and inter-limb stretch reflexes.

038 Tremor: a clinical and neurophysiological study

IntroductionTremor is a common clinical problem seen in a number of diseases. Robust classification and diagnosis of tremor remains controversial due to overlap in clinical features and lack of established biomarkers. This hampers effective research including therapeutic trials. We present our research protocol for a cross-sectional study which aims to find more robust methods of tremor classification and diagnosis.MethodsAdults with upper limb tremor of varying aetiologies, diagnosed using current clinical criteria (including essential tremor, Parkinsonian tremor, and dystonic tremor), and age-matched controls are eligible for recruitment. Participants undergo a clinical and neurophysiological assessment, including accelerometry, surface electromyography, long-latency stretch reflexes, temporal discrimination, and tonic vibration reflexes. Data will be analysed using a cluster analysis to identify robust tremor syndromes and biomarkers associated with them. We aim to recruit 100 participants prior to analysis.ResultsAt time of writing, 13 participants with upper limb tremor have been studied (6 with essential tremor, 5 with dystonic tremor, and 2 with indeterminate tremor; mean age 66 years, range 18–85). Participants tolerated the clinical and neurophysiological studies well with 100% completion rate after recruitment. With current rates of recruitment we anticipate completion of recruitment and commencement of data analysis in October 2019.ConclusionsOur protocol aims to identify robust tremor phenotypes and biomarkers for them. This will allow patients with tremor to be classified into more biologically homogeneous diagnostic categories, aiding future research into the mechanism of tremor and more rational clinical trial design.

The intelligent reflex

ABSTRACTThe seeming distinction between motor and cognitive skills has hinged on the fact that the former are automatic and non-propositional (knowing-how), whereas the latter are slow and deliberative (knowing-that). Here, the physiological and behavioral phenomenon of long-latency stretch reflexes is used to show that “knowing-that” can be incorporated into “knowing-how,” either immediately or through learning. The experimental demonstration that slow computations can, with practice, be cached for fast retrieval, without the need for re-computation, dissolves the intellectualist/anti-intellectualist distinction: All complex human tasks, at any level of expertise, are a combination of intelligent reflexes and deliberative decisions.

Modification of Spastic Stretch Reflexes at the Elbow by Flexion Synergy Expression in Individuals With Chronic Hemiparetic Stroke

ObjectiveTo systematically characterize the effect of flexion synergy expression on the manifestation of elbow flexor stretch reflexes poststroke, and to relate these findings to elbow flexor stretch reflexes in individuals without neurologic injury. DesignControlled cohort study. SettingAcademic medical center. ParticipantsParticipants (N=20) included individuals with chronic hemiparetic stroke (n=10) and a convenience sample of individuals without neurologic or musculoskeletal injury (n=10). InterventionsParticipants with stroke were interfaced with a robotic device that precisely manipulated flexion synergy expression (by regulating shoulder abduction loading) while delivering controlled elbow extension perturbations over a wide range of velocities. This device was also used to elicit elbow flexor stretch reflexes during volitional elbow flexor activation, both in the cohort of individuals with stroke and in a control cohort. In both cases, the amplitude of volitional elbow flexor preactivation was matched to that generated involuntarily during flexion synergy expression. Main Outcome MeasuresThe amplitude of short- and long-latency stretch reflexes in the biceps brachii, assessed by electromyography, and expressed as a function of background muscle activation and stretch velocity. ResultsIncreased shoulder abduction loading potentiated elbow flexor stretch reflexes via flexion synergy expression in the paretic arm. Compared with stretch reflexes in individuals without neurologic injury, paretic reflexes were larger at rest but were approximately equal to control muscles at matched levels of preactivation. ConclusionsBecause flexion synergy expression modifies stretch reflexes in involved muscles, interventions that reduce flexion synergy expression may confer the added benefit of reducing spasticity during functional use of the arm.

Spike Timing-Dependent Plasticity in the Long-Latency Stretch Reflex Following Paired Stimulation from a Wearable Electronic Device.

This report is the first demonstration that the long-latency stretch reflex can be modified by repeated, precisely timed pairing of stimuli known to activate brainstem pathways. Furthermore, pairing was achieved with a portable electronic device capable of delivering many more stimulus repetitions than conventional laboratory studies. Our findings open up new possibilities for basic research into these underinvestigated pathways, which are important for motor control in healthy individuals. They may also lead to paradigms capable of enhancing rehabilitation in patients recovering from damage, such as after stroke or spinal cord injury.

An examination of the startle response during upper limb stretch perturbations

Unexpected presentation of a startling auditory stimulus (SAS>120 decibels) in a reaction time (RT) paradigm results in the startle reflex and an early release (<100ms) of the preplanned motor response (StartReact effect). Mechanical perturbations applied to the upper limbs elicit short- (M1) and long-latency (M2) stretch reflexes and have also been shown to initiate intended motor responses early (<100ms). Ravichandran et al. (2013) recently proposed that unexpected delivery of a perturbation could also elicit a startle response and therefore the StartReact effect may be responsible for the early trigger of a preplanned response. To investigate this further, we examined startle incidence, RT, and stretch reflex modulation for both expected and unexpected perturbations. In Experiment 1, participants performed active (ACT) and passive (DNI) conditions to an expected large perturbation (similar to previous studies examining M2). The startle response was not observed; however, the perturbation still elicited the voluntary response at short latency (<100ms) and goal-dependent modulation of the M2 response was observed. In Experiment 2, participants performed ACT and DNI conditions to a weak auditory stimulus or a small wrist perturbation. On unexpected trials we probed startle circuitry with a large perturbation or SAS. The SAS consistently elicited a startle response in both ACT and DNI conditions, but startle-like activity was only observed on 17.4% of ACT perturbation probe trials. Our findings suggest that while unexpected upper limb perturbations can be startling, startle triggering of the preplanned voluntary response is not the primary mechanism responsible for goal-dependent modulation of the M2 response.

Increased long-latency reflex activity as a sufficient explanation for childhood hypertonic dystonia: a neuromorphic emulation study

Objective. Childhood dystonia is a movement disorder that interferes with daily movements and can have a devastating effect on quality of life for children and their families. Although injury to basal ganglia is associated with dystonia, the neurophysiological mechanisms leading to the clinical manifestations of dystonia are not understood. Previous work suggested that long-latency stretch reflex (LLSR) is hyperactive in children with hypertonia due to secondary dystonia. We hypothesize that abnormal activity in motor cortices may cause an increase in the LLSR leading to hypertonia. Approach. We modeled two possibilities of hyperactive LLSR by either creating a tonic involuntary drive to cortex, or increasing the synaptic gain in cortical neurons. Both models are emulated using programmable very-large-scale-integrated-circuit hardware to test their sufficiency for producing dystonic symptoms. The emulation includes a joint with two Hill-type muscles, realistic muscle spindles, and 2,304 Izhikevich-type spiking neurons. The muscles are regulated by a monosynaptic spinal pathway with 32 ms delay and a long-latency pathway with 64 ms loop-delay representing transcortical/supra-spinal connections. Main results. When the limb is passively stretched, both models produce involuntary resistance with increased antagonist EMG responses similar to human data; also the muscle relaxation is delayed similar to human data. Both models predict reduced range of motion in voluntary movements. Significance. Although our model is a highly simplified and limited representation of reflex pathways, it shows that increased activity of the LLSR is by itself sufficient to cause many of the features of hypertonic dystonia.

Arm dominance affects feedforward strategy more than feedback sensitivity during a postural task.

Handedness is a feature of human motor control that is still not fully understood. Recent work has demonstrated that the dominant and nondominant arm each excel at different behaviors and has proposed that this behavioral asymmetry arises from lateralization in the cerebral cortex: the dominant side specializes in predictive trajectory control, while the nondominant side is specialized for impedance control. Long-latency stretch reflexes are an automatic mechanism for regulating posture and have been shown to contribute to limb impedance. To determine whether long-latency reflexes also contribute to asymmetric motor behavior in the upper limbs, we investigated the effect of arm dominance on stretch reflexes during a postural task that required varying degrees of impedance control. Our results demonstrated slightly but significantly larger reflex responses in the biarticular muscles of the nondominant arm, as would be consistent with increased impedance control. These differences were attributed solely to higher levels of voluntary background activity in the nondominant biarticular muscles, indicating that feedforward strategies for postural stability may differ between arms. Reflex sensitivity, which was defined as the magnitude of the reflex response for matched levels of background activity, was not significantly different between arms for a broad subject population ranging from 23 to 51 years of age. These results indicate that inter-arm differences in feedforward strategies are more influential during posture than differences in feedback sensitivity, in a broad subject population. Interestingly, restricting our analysis to subjects under 40 years of age revealed a small increase in long-latency reflex sensitivity in the nondominant arm relative to the dominant arm. Though our subject numbers were small for this secondary analysis, it suggests that further studies may be required to assess the influence of reflex lateralization throughout development.

The ipsilateral motor cortex does not contribute to long‐latency stretch reflex amplitude at the wrist

BackgroundA capacity for modulating the amplitude of the long-latency stretch reflex (LLSR) allows us to successfully interact with a physical world with a wide range of different mechanical properties. It has recently been demonstrated that stretch reflex modulation is impaired in both arms following monohemispheric stroke, suggesting that reflex regulation may involve structures on both sides of the motor system.MethodsWe examined the involvement of both primary motor cortices in healthy reflex regulation by eliciting stretch reflexes during periods of suppression of the motor cortices contra-and ipsilateral to the extensor carpi radialis in the nondominant arm.ResultsLLSRs were significantly attenuated during suppression of the contralateral, but not ipsilateral, motor cortex. Modulation of the LLSR was not affected by suppression of either primary motor cortex.ConclusionOur results confirm the involvement of the contralateral motor cortex in the transmission of the LLSR, but suggest that the ipsilateral motor cortex plays no role in reflex transmission and that neither motor cortex is involved in stability-dependent modulation of the LLSR. The implications of these results for reflex impairments following stroke are discussed.

Acceleration dependence and task-specific modulation of short- and medium-latency reflexes in the ankle extensors

Involuntary responses to muscle stretch are often composed of a short-latency reflex (SLR) and more variable responses at longer latencies such as the medium-latency (MLR) and long-latency stretch reflex (LLR). Although longer latency reflexes are enhanced in the upper limb during stabilization of external loads, it remains unknown if they have a similar role in the lower limb. This uncertainty results in part from the inconsistency with which longer latency reflexes have been observed in the lower limb. A review of the literature suggests that studies that only observe SLRs have used perturbations with large accelerations, possibly causing a synchronization of motoneuron refractory periods or an activation of force-dependent inhibition. We therefore hypothesized that the amplitude of longer latency reflexes would vary with perturbation acceleration. We further hypothesized that if longer latency reflexes were elicited, they would increase in amplitude during control of an unstable load, as has been observed in the upper limb. These hypotheses were tested at the ankle while subjects performed a torque or position control task. SLR and MLR reflex components were elicited by ankle flexion perturbations with a fixed peak velocity and variable acceleration. Both reflex components initially scaled with acceleration, however, while the SLR continued to increase at high accelerations, the MLR weakened. At accelerations that reliably elicited MLRs, both the SLR and MLR were reduced during control of the unstable load. These findings clarify the conditions required to elicit MLRs in the ankle extensors and provide additional evidence that rapid feedback pathways are downregulated when stability is compromised in the lower limb.

Instruction-dependent modulation of the long-latency stretch reflex is associated with indicators of startle

Long-latency responses elicited by postural perturbation are modulated by how a subject is instructed to respond to the perturbation, yet the neural pathways responsible for this modulation remain unclear. The goal of this study was to determine whether instruction-dependent modulation is associated with activity in brainstem pathways contributing to startle. Our hypothesis was that elbow perturbations can evoked startle, indicated by activity in the sternocleidomastoid muscle (SCM). Perturbation responses were compared to those elicited by a loud acoustic stimulus, known to elicit startle. Postural perturbations and startling acoustic stimuli both evoked SCM activity, but only when a ballistic elbow extension movement was planned. Both stimuli triggered SCM activity with the same probability. When SCM activity was present, there was an associated early onset of triceps electromyographic (EMG), as required for the planned movement. This early EMG onset occurred at a time often attributed to long-latency stretch reflexes (75-100 ms). The nature of the perturbation-triggered EMG (excitatory or inhibitory) was independent of the perturbation direction (flexion or extension) indicating that it was not a feedback response appropriate for returning the limb to its original position. The net EMG response to perturbations delivered after a movement had been planned could be explained as the sum of a stretch reflex opposing the perturbation and a startle-evoked response associated with the prepared movement. These results demonstrate that rapid perturbations can trigger early release of a planned ballistic movement, and that this release is associated with activity in the brainstem pathways contributing to startle reflexes.

Anodal Transcranial Direct Current Stimulation (tDCS) Decreases the Amplitudes of Long-Latency Stretch Reflexes in Cerebellar Ataxia

Recent studies suggest that the neuromodulation of the cerebellum using transcranial direct current stimulation (tDCS) could represent a new therapeutic strategy for the management of cerebellar disorders. Anodal tDCS of the cerebellum increases the excitability of the cerebellar cortex. We tested the effects of anodal tDCS applied over the cerebellum in ataxic patients. We studied (a) stretch reflexes (SR) in upper limb (SLSR: short-latency stretch reflexes; LLSR: long-latency stretch reflexes), (b) a coordination functional task in upper limbs based on mechanical counters (MCT: mechanical counter test), and (c) computerized posturography. tDCS did not change the amplitude of SLSR, but reduced significantly the amplitudes of LLSR. tDCS did not improve the MCT scores and did not modify posture. We suggest that anodal tDCS of the cerebellum reduces the amplitudes of LLSR by increasing the inhibitory effect exerted by the cerebellar cortex upon cerebellar nuclei. The absence of effect upon upper limb coordination and posture suggests that the cerebello-cerebral networks subserving these functions are less responsive to anodal tDCS of the cerebellum. Anodal tDCS of the cerebellum represents a novel experimental tool to investigate the effects of the cerebellar cortex on the modulation of the amplitudes of LLSR.

Involvement of SMAp in the intention-related long latency stretch reflex modulation: A TMS study

When our movement is perturbed by environmental forces, the Long Latency Stretch Reflex (LLSR), generated by a transcortical loop through the primary motor cortex (M1), is the fastest reaction adapted according to our prior intent. We investigated the involvement of the caudal part of the Supplementary Motor Area (SMAp) in this intention-related LLSR modulation. Subjects were instructed either to not react (i.e. to ‘let-go’) or to resist a mechanical perturbation extending the wrist and Transcranial Magnetic Stimulation (TMS) was used to transiently inactivate SMAp, either at the time of the LLSR generation (TMS was applied 50ms before the perturbation), or at the end of the preparation period (TMS was applied 150ms before the perturbation). The effect of SMAp transient inactivation on the LLSR modulation was compared to the effect of transient inactivation of M1 or of a Control area. Compared to the Control condition, the intention-related LLSR modulation decreased when TMS was applied either over SMAp or over M1 50ms before perturbation occurrence, suggesting that SMAp, as M1, is involved in the LLSR modulation. Moreover, the LLSR modulation also decreased when TMS was applied over SMAp 150ms before the perturbation, indicating that anticipatory processes taking place in SMAp participate to the LLSR modulation. In addition, TMS applied over SMAp elicited Motor-Evoked Potentials (MEPs) whose latency and shape were similar to MEPs evoked by TMS over M1, suggesting that they are due to direct corticospinal projections from SMAp. Interestingly, the SMAp MEPs amplitude was modulated depending on the subject’s intention to resist or to let-go. Taken together these results strongly favor the idea that, during the expectation of a perturbation, SMAp is the seat of anticipatory processes that are specific to the subject’s intent and that preset M1 in order to adapt the LLSR to this intention.