1. The stretch reflex in the elbow flexor musculature was studied in 23 human subjects. The subjects were required to establish an initial force equivalent to 10% maximum at a prescribed initial length; mechanical disturbances delivered at random times increased load force to 15% or reduced it to 5%. We measured arm force, displacement, and EMG (usually biceps); acceleration was calculated from displacement, and average responses from sets of 10 like trials. 2. Modification of the stretch reflex was studied by comparing average responses obtained with different instructions, but with the same disturbance. The usual introductions were "compensate for arm deflection" and "do not intervene voluntarily". The initial response did not depend on instruction; changes in response that depended on instruction began abruptly after a latent period which ranged from 70 to 320 ms (measured from force and acceleration), depending on conditions and subject. The latency became longer (10-50 ms) and more variable when the subject did not know the direction of disturbance in advance. This and other observations indicate that modifications of the stretch reflex are not produced by servo actions. They are produced by triggered reactions, which occur at both short and long latencies and which have properties resembling the movements produced in a reaction-time task. 3. We confirmed that most subjects can suppress triggered reactions when the instruction calls for no intervention, leaving an unmodified reflex response. This response consists of a compliant deflection of the arm in the direction of the disturbance. 4. The compensatory actions associated with unmodified stretch (and unloading) reflexes were assessed from EMG responses of biceps. During a 300-ms transient phase, EMG changes were notably asymmetric when responses to symmetric disturbances were compared. Increased force stretched biceps and produced a prominent increase in EMG, whereas decreased force allowed biceps to shorten and produced either an EMG decrease of smaller magnitude or an actual increase. These asymmetric reflex actions produced quite symmetric mechanical responses (arm displacements and forces), which implies the existence of and compensation for nonlinear muscle mechanical properties. This result is discussed in relation to the hypothesis that the function of the stretch reflex is to compensate for variations in muscle properties, thus maintaining stiffness. 5. Effective control of muscle length or joint position does not result from servo action by the stretch reflex. Errors in position are corrected only when triggered reactions are superimposed on the reflex response.

Regulatory actions of human stretch reflex

Central feedback pathways for motor control were studied by recording EMG responses to sudden upper limb displacements in humans and monkeys using a precision torque motor to generate step load changes. Normal human subjects showed three short-latency EMG responses (M1, M2 and M3) which appear to correspond to those recorded from trained monkeys. The M2 and M3 components, thought to represent feedback in supraspinal pathways, were significantly increased when the subjects were instructed to actively compensate for the load changes. Parkinsonian patients with rigidity showed evidence of markedly increased feedback over the interval for the M2 and M3 responses and appeared to have lost the ability to modulate feedback according to the motor task being performed. The results are discussed with reference to recent research on motor control mechanisms in primates and a tentative model for the basis of Parkinsonian rigidity is proposed.

/pdf/motor-responses-to-sudden-limb-displacements-in-primates-fenir0dty2.pdf

Motor responses to sudden limb displacements in primates with specific CNS lesions and in human patients with motor system disorders.

Since the early 1950s when Merton (44) first introduced his "follow-up servo hypothesis" of movement control, the dominant opinion has held that stretch and unloading reflexes function to control the length of a muscle in opposition to changes in mechanical load, thus providing load compensa­ tion. In this article I review recent evidence indicating that this notion is wrong, or at least incomplete, and proceed to develop an alternative idea (47) that neither muscle length nor force are regulated as individual vari­ ables, but that a property called stiffness (the ratio of force change to length change) is maintained relatively constant by skeletomotor reflexes. This leads to a discussion of the actions of descending motor commands on the segmental system, from which I conclude that these may be much less versatile than was formerly believed. The reader is referred to another review (55) and to Matthews' mono­ graph (42) for additional information.

https://physio.northwestern.edu/docs/Houk/Houk79.pdf

Regulation of Stiffness by Skeletomotor Reflexes

1. Monkeys were trained to react to an arm perturbation according to an instruction delivered prior to the perturbation. There were two possible instructions (push or pull), and monkeys learned to respond accordingly regardless of the direction (push or pull) of the triggering perturbation. 2. Pyramidal tract neurons (PTNs) in contralateral motor cortex arm area responded to the triggering perturbation with two dissociable components: 1) a relatively short-latency (20-25 ms) reflex component which depended on the direction of the perturbation, and 2) a longer latency (40-50 ms) intended component which depended on the prior instruction. 3. Intended PTN discharge could occur in arm area with latencies of 50 ms even following arm perturbations whose initial reflex effects on the PTN were inhibitory. 4. Intended PTN responses triggered by perturbations of the appropriate body part occur at shorter latencies than intended PTN responses triggered by auditory or visual stimuli. These short-latency intended PTN responses may play a role in thsshort-latency but volitionally controlled limb movements occurring in response to limb perturbations.

Reflex and intended responses in motor cortex pyramidal tract neurons of monkey

To test the hypothesis that a transcortical reflex contributes to the stretch-evoked long-latency electromyographic (e.m.g.) response we documented the responses of identified corticomotoneuronal (c.m.) cells and their target muscles to perturbations of active wrist movements. Macaque monkeys performed ramp-and-hold wrist movements against elastic loads, alternating between flexion and extension zones; brief (25 ms) torque pulses were intermittently applied during the hold period. C.m. cells were identified by a clear post-spike facilitation in spike-triggered averages of forelimb muscle e.m.g. activity. Activity of c.m. cells and twelve wrist and digit flexor and extensor muscles was recorded during: (a) active ramp-and-hold wrist movements, (b) passive ramp-and-hold wrist movements, and (c) torque perturbations applied during the hold phase of active flexion and extension which either lengthened or shortened the c.m. cell's target muscles. Muscle-lengthening perturbations evoked a reproducible pattern of average e.m.g. activity in the stretched muscles, consisting of two peaks: the first response (M1) had an onset latency of 11.2 +/- 2.1 ms (mean +/- S.D.), and the second (M2) began at 27.9 +/- 5.1 ms. Torque perturbations which shortened the active muscles also evoked a characteristic e.m.g. response consisting of an initial cessation of activity at 13.5 +/- 3.4 ms followed by a peak beginning at 33.9 +/- 3.0 ms. The responses of twenty-one c.m. cells which facilitated wrist muscles were documented with torque pulse perturbations applied during active muscle contraction. Twenty of twenty-one c.m. cells responded at short latency (23.4 +/- 8.8 ms) to torque perturbations which stretched their target muscles. For each c.m. cell-target muscle pair, transcortical loop time was calculated as the sum of the onset latency of the c.m. cell's response to lengthening perturbations (afferent time) and the onset latency of post-spike facilitation (efferent time). The mean transcortical loop time was 30.4 +/- 10.2 ms, comparable to the mean onset latency of the M2 peak (27.9 +/- 5.1). The duration of a c.m. cell's response to torque perturbations provides a further measure of the extent of its potential contribution to the M2 muscle response. In all cases but two, the c.m. cell response, delayed by the latency of the post-spike facilitation, overlapped the M2 e.m.g. peak.

W.W. Chambers

Papers

The effect of postcentral cortical lesions on motor responses to sudden upper limb displacements in monkeys

Induction of spinal seizures by natural stimulation in cats.