Latency Stretch Reflex Research Articles

Stretch reflex oscillations and essential tremor.

Using a computer-controlled torque motor and manipulandum, 50 ms torque pulses and 70 second trains of binary pseudorandom torque disturbances were applied to the wrists of 10 adult controls and 22 patients with essential tremor in order to study the interaction between mechanically-induced stretch-reflex oscillations and essential tremor. These two oscillations were separated by applying inertial and spring loads to the wrist. There was no evidence of increased or unstable stretch-reflex activity in the essential tremor patients, and stretch-reflex latencies did not correlate with the frequency of essential tremor. Essential tremor and mechanically-induced stretch-reflex oscillations are separate phenomena capable of complex interaction.

Changes in short and long latency stretch reflexes prior to movement initiation

The amplitudes of both short (M 1) and long (M 2) latency stretch reflexes mechanically elicited in the triceps brachii muscle were investigated prior to its voluntary activation. The results obtained from 14 healthy subjects indicated that the amplitude of the M 2 response increased steadily as the perturbation was delivered closer to the movement suggesting that the M 2 changes are associated with the preparation to respond to the visual stimulus. In contrast, the amplitude of the M 1 response showed no systematic variations over the same time period. This dissociation of the M 1 and M 2 reflex responses prior to movement may be attributable to selective gain modulation in supraspinal stretch reflex pathways or to descending projections to polysynaptic spinal pathways.

Habituation and conditioning of the human long latency stretch reflex.

The effects of stretch repetition rate, prior warning stimuli and self administered stretch were examined on the size of the short and long latency components of the stretch reflex electromyographic EMG response in flexor pollicis longus and the flexor muscles of the wrist and fingers. Stretches of constant velocity and extent were given every 10 s, 5 s, 2 s, or 1 s to either the wrist or thumb during a small background contraction of the flexor muscles. The size of the long latency component of the stretch reflex (measured as the area under the averaged rectified EMG responses) declined dramatically at faster repetition rates, especially in the wrist and finger flexors. The size of the short latency component was relatively unaffected. The size of the electrically elicited H-reflex in forearm muscles also failed to habituate under the same conditions. If each individual trial of a series was examined, the long latency component of the stretch reflex EMG could be seen to decrease in size over the first three to six stretches if stretches were given every 1 s, but not if stretches were given every 10 s. When stretches were given every 5 s to either wrist or thumb, an electrical stimulus applied to the digital nerves of the opposite hand 1 s before stretch reduced the size of the long latency component of the reflex EMG response. The short latency component was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral potentials and electromyographic responses evoked by stretch of wrist muscles in man.

The cerebral evoked potential produced by rapid extension of the wrist was recorded from scalp electrodes in normal subjects while they exerted a small background flexor torque (0.24 Nm) against an electric motor. The initial part of the response consisted of a negative deflection (N1) with an average latency of 24.7 ms. This was followed by a biphasic P1/P2 (32 ms) response and a large later negative wave (N2) (76 ms). Passive wrist extension also evoked reflex EMG responses in the forearm flexor muscles which could be resolved into a short latency (25 ms) and long-latency (52 ms) component. The cerebral responses persisted almost unchanged during complete ischaemic anaesthesia of the hand produced by a pressure cuff around the wrist, and were reduced if the stretch was given during voluntary wrist flexion. The primary component (N1-P1/P2) of the cerebral response probably represents the arrival at the cortex of the muscle afferent volley. However, the significance of the secondary component (P1/P2-N2) is unknown. Under certain conditions, its size was related to the size of the long latency stretch reflex evoked by stretch of the flexor muscles. Thus, increasing the velocity of stretch or decreasing the repetition rate (from 1.0 to 0.15 Hz) at which stretches were applied, increased the size of both the muscle reflex and the cerebral response. The secondary component also could be changed by voluntary reaction to wrist stretch. Changes in the size of the secondary component of the evoked response may represent the earliest cortical sign of interaction between sensory input and motor output.

Role of reflex responses of knee musculature during the swing phase of walking in man.

Muscle activation patterns of the quadriceps and hamstrings were studied in normal human subjects walking at comfortable speed on a treadmill. In addition knee angular velocity patterns and swing and stance phases of the step cycle were recorded. Data were collected from normal paces and from paces in which a momentary unexpected resistance was applied to the leg during swing. The application of the resistance caused an advance in the onset of both quadriceps and hamstrings activity. The latency of the onset of activity following the resistance in the quadriceps was 78.2 +/- 26.4 ms and this was considered to indicate a long latency stretch reflex. There was a close association between the onset of quadriceps and hamstrings activity both in the normal and resistance paces. The changes observed in knee angular velocity upon application of the resistance indicate tight control of angular velocity patterns. The results have important implications regarding neural control of muscle during purposive movement and the regulation of sensitivity of muscle receptors during such movements, especially during the periods when the muscle is normally inactive.

Anticipatory changes of long-latency stretch responses during preparation for directional hand movements

We have investigated, in 9 normal subjects, the time course of amplitude changes in the automatic long latency stretch reflex of wrist flexors during the preparatory period as a function of the precued direction of hand movement. Subjects maintained right hand position against a weak force and learned to compensate precisely for brief ramp stretch (250 deg./s, 50 ms) which imposed wrist extension. This probe stretch was applied randomly at different times during the 1 s preparatory period of a reaction time task. The warning signal gave directional advance information (DAI) about the voluntary movement that had to be performed. The EMG activity, recorded between 20 and 80 ms after the stretch started, was measured in terms of 3 successive components, M1, M2 and M3, identified on the basis of their respective latency. There was no significant change in the M1 component. Following a warning signal which precued an extension movement, M2 was depressed prior to the response signal. The time course of M3 was clearly different according to DAI: it increased following a warning signal which precued a flexion movement and decreased in the alternative case. This difference reached statistical significance 400 ms before the response signal. In fast-performing subjects the differential development of M3 was more marked than for slow-performing subjects. This underlines its preparatory significance. These results suggest that the neuronal pathways involved in the M3 response to stretch: i, are partly different from those conveying the earlier components, and ii, include structures which take part in the pre-programming of rapid movements.

Organization of stabilizing reflex responses in tibialis anterior muscles following ankle flexion perturbations of standing man

Reflex activity in human ankle muscles in response to 36 deg./s dorsi-flexion rotations of the feet was investigated in subjects standing upright and when leaning back so as to preactivate ankle flexor muscles. Short latency stretch reflex activity in soleus and inhibition in tibialis anterior muscles occured at 50 ms from ankle rotation onset. Two prominent bursts of tibialis activity followed at 83 and 131 ms, and preceded large stabilizing ankle torques. Head movements commenced 20 ms after foot rotations and acquired accelerations exceeding 100 deg./s 2 within 60 ms. It is suggested that the tibialis anterior activity is either a vestibulospinal reflex resulting rom the head movement, or a strethc reflex only present standing, since this activity was not observed when seated subjects received identical foot rotations.

The behaviour of the long-latency stretch reflex in patients with Parkinson's disease.

The size of the long-latency stretch reflex was measured in a proximal (triceps) and distal (flexor pollicis longus) muscle in 47 patients with Parkinson's disease, and was compared with that seen in a group of 12 age-matched normal control subjects. The patients were classified clinically into four groups according to the degree of rigidity at the elbow or tremor. Stretch reflexes were evaluated while the subject was exerting a small force against a constant preload supplied by a torque motor, and the size of the reflex response was measured as fractional increase over basal levels of activity. When stretches were given at random intervals by increasing the force exerted by the motor by a factor of 2 or 3, there was a clear trend for the more severely affected patients to have larger long latency responses in the triceps muscle, although there was no change in the size of the short-latency, spinal component of the response. In contrast, there was no change in the size of the long-latency response of the flexor pollicis longus in any group of patients with Parkinson's disease. Despite any differences in reflex size, the inherent muscle stiffness of both muscles appeared to be normal in all groups of patients with Parkinson's disease, since the displacement trajectory of the limb following the force increase was the same as control values in the short (25 ms) period before reflex compensation could intervene. In 20 of the patients and in seven of the control subjects, servo-controlled, ramp positional disturbances were given to the thumb. Up to a velocity of 300°/s, the size of the long-latency stretch reflex was proportional to the log velocity of stretch. This technique revealed, in both moderately and severely rigid patients, increases in the reflex sensitivity of the flexor pollicis longus, which had not been clear using step torque stretches alone. However, whether using ramp or step displacements, long latency stretch reflex gain was not closely related to rigidity; reflex size was within the normal range in many patients with severe rigidity. Enhanced long latency stretch reflexes thus contribute to, but may not be solely responsible for, rigidity in Parkinson's disease.