Different mechanisms underlie the long‐latency stretch reflex response of active human muscle at different joints.

Thilmann, A. F.; Schwarz, Michael; Töpper, Rudolf; Fellows, S J; Noth, Johannes

doi:10.1113/jphysiol.1991.sp018898

Cited by 99 publications

(65 citation statements)

References 26 publications

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“…Transcranial magnetic brain stimuli delivered over motor cortex and timed to coincide with the LLSR are facilitated, also suggesting a transcortical contribution (Pruszynski et al, 2011b). However, evidence from patients with motor disorders suggests that the transcortical route for the LLSR may be less important in elbow muscles compared with the hand (Thilmann et al, 1991;Fellows et al, 1996). The tonic vibration reflex, which may relate to the LLSR, relies on the brainstem reticular formation (Gillies et al, 1971).…”

Section: Discussionmentioning

confidence: 99%

“…It is likely therefore that the large torque generated by the motor rapidly accelerated the arm to a terminal velocity, in which friction in the gears and bearings was equal and opposite to the motor torque. These perturbations evoked consistent shortand long-latency reflexes (Thilmann et al, 1991;Trumbower et al, 2013) in the recorded muscles. Subjects were told to return the arm to the central target after each perturbation, but were not required to do this within any time constraints.…”

Section: Methodsmentioning

confidence: 99%

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

2016

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The long-latency stretch reflex (LLSR) in human elbow muscles probably depends on multiple pathways; one possible contributor is the reticulospinal tract. Here we attempted to induce plastic changes in the LLSR by pairing noninvasive stimuli that are known to activate reticulospinal pathways, at timings predicted to cause spike timing-dependent plasticity in the brainstem. In healthy human subjects, reflex responses in flexor muscles were recorded following extension perturbations at the elbow. Subjects were then fitted with a portable device that delivered auditory click stimuli through an earpiece, and electrical stimuli around motor threshold to the biceps muscle via surface electrodes. We tested the following four paradigms: biceps stimulus 10 ms before click (Bi-10ms-C); click 25 ms before biceps (C-25ms-Bi); click alone (C only); and biceps alone (Bi only). The average stimulus rate was 0.67 Hz. Subjects left the laboratory wearing the device and performed normal daily activities. Approximately 7 h later, they returned, and stretch reflexes were remeasured. The LLSR was significantly enhanced in the biceps muscle (on average by 49%) after the Bi-10ms-C paradigm, but was suppressed for C-25ms-Bi (by 31%); it was unchanged for Bi only and C only. No paradigm induced LLSR changes in the unstimulated brachioradialis muscle. Although we cannot exclude contributions from spinal or cortical pathways, our results are consistent with spike timing-dependent plasticity in reticulospinal circuits, specific to the stimulated muscle. This is the first demonstration that the LLSR can be modified via paired-pulse methods, and may open up new possibilities in motor systems neuroscience and rehabilitation.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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

2016

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“…There is compelling evidence that the M2 response in thenar, finger and wrist muscles is mediated, in part, by a transcortical pathway that traverses the primary motor cortex (Marsden et al 1973(Marsden et al , 1977Capaday et al 1991;Day et al 1991;Palmer and Ashby 1992;Tsuji and Rothwell 2002). There has been no evidence to date for such a transcortical loop in more proximal upper limb muscles, including the biceps (Lenz et al 1983;Cohen et al 1991;Thilmann et al 1991;Fellows et al 1996). Task-dependent modulation of the M2 in distal muscles has been shown to be smaller than the effect seen in proximal muscles (Rothwell et al 1980).…”

Section: Generalizability Across Joints and Motor Tasksmentioning

confidence: 99%

The effect of task instruction on the excitability of spinal and supraspinal reflex pathways projecting to the biceps muscle

2006

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There is controversy within the literature regarding the influence of task instruction on the size of the long-latency stretch reflex (M2) elicited by a joint displacement. The aim of this study was to investigate if the previously reported task-dependent modulation of the M2 is specific to the M2 or can be explained by an early release of the intended voluntary response. We took advantage of the fact that the M2 is absent when the duration of the applied perturbation is less than a critical time period. This allowed us to examine modulation of muscle activity with and without the contribution of the M2. In addition, we applied transcranial magnetic stimulation (TMS) over the primary motor cortex to examine the modulation of corticomotor excitability with task instruction. Elbow joint extension displacements were used to elicit a stretch reflex in the biceps muscle. Subjects were instructed to "do not intervene" (DNI) with the applied perturbation, or to oppose the perturbation by activating the elbow flexors in response to the perturbation (FLEX). Electromyographic (EMG) activity in the time period corresponding to the M2 was significantly facilitated in the FLEX task instruction both with and without the presence of the M2. Motor evoked potentials (MEPs) elicited by TMS were also facilitated during the FLEX condition in the absence of the M2. EMG and MEP responses were not facilitated until immediately prior to the onset of the M2. Paired-pulse TMS revealed a significant reduction in short-interval intracortical inhibition (SICI) during the M2 response, but the level of SICI was not altered by the task instruction. We conclude that the taskdependent modulation of the biceps M2 results, at least in part, from an early release of the prepared movement and is accompanied by an increase in corticospinal excitability that is not specific to the M2 pathway. Task-dependent modulation of the response cannot be explained by an alteration in the excitability of intracortical inhibitory circuits.

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“…Such matters remain of concern. Just as new evidence has convinced even the sceptics that there can be a transcortical component to the reflex, further findings fortify the view that other mechanisms may also be involved (Matthews, 1991;Thilmann, Schwarz, Topper, Fellows & Noth, 1991;Rothwell, Colebatch, Britton, Priori, Thompson, Day & Marsden, 1991). Moreover, inhibitory as well as excitatory mechanisms must be expected to be active, but their contribution to the overall response remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Interaction between short‐ and long‐latency components of the human stretch reflex during sinusoidal stretching.

Matthews¹

1993

The Journal of Physiology

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SUMMARY1. Using wrist muscles, the subdivision of the human stretch reflex into separate components was examined with small amplitude sinusoidal stretching of relatively high frequency (10-40 Hz). The reflex was evoked by angular rotation of the wrist (below 1 deg amplitude), applied via the hand during maintained voluntary contraction of the muscle studied; both flexors and extensors were tested.2. The reflex response was recorded electromyographically rather than mechanically. For each condition, the surface EMG was rectified and averaged to give a cycle average showing the mean response evoked by a cycle of stretching. The cycle average was fitted with a sinusoid, the amplitude and phase of which were used to assess the reflex; their value reflects the combined action of its various subcomponents. Fourier analysis gave similar results (the EMG was then rectified but not averaged).3. The amplitude of the reflex response typically fell to a minimum in the region of 20-25 Hz. The phase lag of the response in relation to the stimulus increased approximately linearly with frequency, except in the region of the amplitude minimum. Here the lag tended to remain constant, or to decrease slightly; this created a discontinuity between the upper and lower limbs of the phase plot.4. Such effects are attributed to an interaction between two components of the reflex that differ in latency by 20-25 ms. These would progressively change their relative phase as the frequency increased. At first they would come to interfere with each other, but then the more delayed reflex produced by a given cycle of stretching would begin to sum with the shorter latency reflex evoked by the next stretch.5. At high and low frequencies the cycle averages were normally well fitted by a single sinusoid. Around 20-25 Hz, however, they typically showed appreciable harmonic distortion, with the second harmonic larger than the fundamental. The cycle average then showed two separate responses per cycle of stretching. These were considered to represent the uncancelled non-linear residua of separate components of the reflex response. Their relative timing shifted appropriately with change of frequency.6. These 'double responses' are unlikely to be due to mechanical resonance. First, the relative sizes of the two components could be altered by the reflex action of cutaneous afferents. Second, the same pattern of behaviour was found when the MS 1143 P. B. C. MATTHEWS mechanical stimuli were applied directly to the tendon of flexor carpi radialis while the hand remained fixed.7. Sinusoidal stretching thus provides an alternative to ramp stretching for fractionating the stretch reflex into components of different latency. A longer latency component has thereby been found to persist at frequencies above those at which muscle can respond mechanically; its central machinery can thus be expected to take part in the moment to moment control of muscle action.

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Different mechanisms underlie the long‐latency stretch reflex response of active human muscle at different joints.

Cited by 99 publications

References 26 publications

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

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

The effect of task instruction on the excitability of spinal and supraspinal reflex pathways projecting to the biceps muscle

Interaction between short‐ and long‐latency components of the human stretch reflex during sinusoidal stretching.

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