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Monkeys can change the amplitude of the spinal stretch reflex without change in initial alpha motor neuron tone, as measured by EMG, or in initial muscle length. Change is apparent in 5-10 days, continues to develop over weeks, and persists during inactive periods. Spinal stretch reflex change may be a valuable system for studying the neuronal and synaptic bases of an adaptive change in primate CNS function.
Despite considerable speculation it remains unclear as to whether stretch reflexes perform a functional role in speech articulator muscles. Recent research, however, has shown that long loop stretch reflex mechanisms are brought into play during voluntary contraction of limb muscles and a functional role in oscillatory damping has been suggested. It was decided, therefore, to use a method and a technique of analysis similar to that used in limb muscles to search for tonic stretch reflex (TSR) responses in lip, tongue and jaw muscles during sustained voluntary contraction. The term 'action TSR' is used to differentiate stretch reflex responses measured from voluntary activity from those measured at rest. Simultaneous electromyogram (EMG) recordings were taken from the lip, tongue and jaw musculature in normal, stutterer and cerebral spastic subjects. Subjects were instructed to hold the appropriate articulator in a fixed position while the experiment applied an irregular, continuously changing, stretching force. The stretch and EMG signals were analyzed using a cross correlation and spectral analysis technique. This provided a sensitive means of detecting any EMG fluctuations which covaried with applied stretch and might therefore be classified as reflex. No suggestion of such action TSR responses could be found in lip or tongue muscles of any of the subjects tested, including the cerebral spastic subjects with dysarthric speech. It is therefore concluded that action TSR mechanisms are not operative in control of lip and tongue muscles in man. Furthermore, dysarthric speech in cerebral spasticity cannot be attributed to exaggerated tone of lip and tongue muscles resulting from hypersensitivity of TSR mechanisms. In contrast, clear action TSR responses were demonstrable in jaw closing muscles while in jaw opening muscles, small amplitude responses were detected but were not substantial in comparison with background activity. Since the action TSR is present in jaw and limb muscles, but absent in lip and tongue muscles, the suggestion of a functional role of this reflex in damping mechanical oscillations associated with inertial loads is further supported.
OBJECTIVES: To study the correlation between spasticity and motor dysfunction in the wrist-hand unit of adult hemiplegic patients, and to investigate the correlation between clinical spasticity and hyperactive stretch reflexes. STUDY DESIGN: A survey study with a sequential case series of subjects. SETTING: Neuromuscular Research Laboratory, School of Physical Therapy, Texas Woman's University, Houston, TX. SUBJECTS: Sequential sample recruited from local stroke support groups: 10 patients with chronic hemiplegia caused by cerebral vascular accident who had various degrees of spasticity in the wrist joint. OUTCOME MEASURES: Modified Ashworth Scale, amplitudes of stretch reflexes for wrist flexors, grip strength, active range of motion of the wrist joint, and Fugl-Meyer test. RESULTS: Strong reverse correlation was found between spasticity and grip strength, the Fugl-Meyer test scores, and the Box and Blocks test scores (p = .001 to .005). Results also indicated a strong and consistent correlation between spasticity and reflexive electromyographic activities of the stretch reflex recorded from active muscles (p = .005 and .007), but not between spasticity and torque response of the stretch reflex. CONCLUSIONS: The degree of wrist spasticity is associated with impaired hand function in hemiplegic patients, and hyperactive electromyographic response of the stretch reflex, recorded from active muscles, is a valid indicator of spasticity.
The effects of muscle spindle secondary ending activity on the stretch reflex were studied in unanesthetized decerebrate cats. Activation of secondary endings was accomplished by reducing the muscle temperature. This has been shown to cause a sustained asynchronous discharge from secondary endings. Cooling of the medial gastrocnemius or lateral gastrocnemius-soleus muscles caused an increase in the phasic and tonic components of their stretch reflexes. Cooling of the relaxed medial gastrocnemius muscle caused similar increases in the components of the stretch reflex of the synergistic lateral gastrocnemius-soleus muscle and an increase in its monosynaptic reflex. It was concluded that the facilitatory autogenetic and synergistic effects of muscle cooling on the stretch and monosynaptic reflexes were brought about by activity in group II afferents from muscle spindle secondary endings and could not be ascribed to any other type of muscle receptor. These results support the concept of an excitatory role for the secondary endings of the muscle spindle in the stretch reflex of the decerebrate cat.
We studied the effects of longitudinal tendon vibration on the stretch reflex of the soleus and gastrocnemius muscles in 11 decerebrate cats. Vibration was applied at amplitudes (40-80 micrometer) and frequencies (120-250 HZ) sufficient to provide a strong tonic vibration reflex. In keeping with previous reports, we found that during an established tonic vibration reflex, the force and emg response to superimposed ramp and hold stretch are largely suppressed. This suppression is most obvious during the dynamic phase of stretch where it gives rise to a complex force response resembling that of active areflexic muscle. If stretch initiation is delayed until after vibration is terminated, the suppressed effects of vibration persist for 5 s or more. These suppressive effects are marked in the first 200 ms, and then decay gradually over the ensuing time period, paralleling the decline in emg and force which follows vibration offset. Simultaneous recordings from homonymous Ia afferents showed that this suppression persists even though the stretch responsiveness of primary spindle endings has returned to normal immediately following the end of vibration. When stretch is initiated shortly after vibration commences, the suppressive effects are first evident at 50-100 ms latency, but are not well established until 1 s or more after vibration onset. Tests of monosynaptic transmission using small amplitude tendon taps or electrical stimulation of synergist nerves to activate Ia fibers revealed that reductions in the magnitude of the response following vibration are usually modest (12% mean reduction at 50 ms, n = 5), and they are quite sensitive to the initial level of excitation of the motoneuron pool. These reductions were also rather shortlived, being largely completed within 500 ms of vibration offset. Although the relative contributions of presynaptic and postsynaptic inhibition are not readily dissociated in this type of experiment, it is likely that the magnitude of presynaptic inhibition is quite small. We argue that the effects of vibration on the stretch reflex are best explained by invoking an excitatory autogenetic projection from Ia interneurons to extensor motor neurons, which lies in parallel with the Ia monosynaptic projection. In order to account for the vibratory suppression, we propose that these interneurons are driven to saturation by vibration. When vibration ceases, the discharge rate of these interneurons declines with a prolonged time-course that coincides with the recovery of stretch responsiveness. This recovery would contribute to the return of stretch reflex force.
Experiments with tick-paralyzed dogs and woodchucks have shown impairment of stretch reflexes in addition to partial paralysis at the neuromuscular junction. Stretch reflexes disappear very early during paralysis, whereas nociceptive reflexes do not appear to be directly affected. The early incoordination and the ascending nature of the paralysis may be related to impairment of stretch reflex pathways.
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.
1. A cat preparation was used to study the modulation of stretch reflexes during locomotion. The brain stem was transected and locomotion was induced by electrical stimulation of the mesencephalic locomotor region below the level of transection. Three legs walked normally on a treadmill, while the fourth leg, which was denervated except for the soleus muscle, was held fixed. Brief length perturbations were applied to the soleus muscle at various phases of the stepping cycle.2. The stretch reflex in this muscle was deeply modulated during the step cycle, and reached its peak at or before the peak in soleus e.m.g. activity associated with the locomotion. A similar variation was observed when the sciatic nerve was stimulated electrically at a strength which elicited reflex activity (H wave), but did not directly elicit motor nerve activity (M wave). Variation in the reflex during electrical stimulation could not be accounted for by cyclic variation in fusimotor activity or in the afferent volley, but must be due to post-synaptic changes in alpha-motoneurones or in the presynaptic inputs to them.3. Large changes were also observed in intrinsic muscle stiffness during the step cycle. The maximum stiffness occurred near the time the limb would normally strike the ground during locomotion. A high stiffness would be useful in reducing the amount that the limb would yield under the weight of the body during the extension phase of the step cycle. The variation of the stretch reflex in parallel with stiffness suggests that reflexes could assist in this load compensation. The variation is not consistent with the idea that the stretch reflex is used to compensate for changes in intrinsic muscle properties, so that the total system behaves more like a spring of constant stiffness than does muscle alone.
Stretch reflexes play a vital role in fine-tuning movements and in automatically maintaining posture. This article briefly reviews the operation of the stretch reflex in the human masticatory system. The conventional approach of stretching muscles in an open-loop manner has yielded much valuable information on the operation of this reflex. In particular, it has revealed that stretching the jaw-closing muscles evokes a reflex response with two major components. The short-latency reflex is favoured when stretches are brisk, but slower stretches evoke an additional long-latency component. In the hand muscles, the long-latency response is transcortical: in the masticatory muscles, it is not. In addition to its role in servo-control of muscle length during chewing, the stretch reflex in the jaw-closing muscles maintains the vertical position of the mandible during vigorous head movements such as those that occur during running, jumping, hopping and other vigorous whole-body movements in which the head moves briskly up and down. This is an interesting model system in which to investigate stretch reflexes with natural stimuli under unrestrained, physiological conditions.
Animal experiments suggest that an increase in sympathetic outflow can depress muscle spindle sensitivity and thus modulate the stretch reflex response. The results are, however, controversial, and human studies have failed to demonstrate a direct influence of the sympathetic nervous system on the sensitivity of muscle spindles. We studied the effect of increased sympathetic outflow on the short-latency stretch reflex in the soleus muscle evoked by tapping the Achilles tendon. Nine subjects performed three maneuvers causing a sustained activation of sympathetic outflow to the leg: 3 min of static handgrip exercise at 30% of maximal voluntary contraction, followed by 3 min of posthandgrip ischemia, and finally during a 3-min mental arithmetic task. Electromyography was measured from the soleus muscle with bipolar surface electrodes during the Achilles tendon tapping, and beat-to-beat changes in heart rate and mean arterial blood pressure were monitored continuously. Mean arterial pressure was significantly elevated during all three maneuvers, whereas heart rate was significantly elevated during static handgrip exercise and mental arithmetic but not during posthandgrip ischemia. The peak-to-peak amplitude of the short-latency stretch reflex was significantly increased during mental arithmetic (P < 0.05), static handgrip exercise (P < 0.001), and posthandgrip ischemia (P < 0.005). When expressed in percent change from rest, the mean peak-to-peak amplitude increased by 111 (SD 100)% during mental arithmetic, by 160 (SD 103)% during static handgrip exercise, and by 90 (SD 67)% during posthandgrip ischemia. The study clearly indicates a facilitation of the short-latency stretch reflex during increased sympathetic outflow. We note that the enhanced stretch reflex responses observed in relaxed muscles in the absence of skeletomotor activity support the idea that the sympathetic nervous system can exert a direct influence on the human muscle spindles.
Averaging of EEG recorded monopolarly from C3, contralateral to the activated limb, in the stretch reflex shows the presence of somatosensory evoked potential (SSEP) with characteristic shape: four constant waves--P29, N84, P202 and N294, and four inconstant waves--N31, P74, P99 and N123. Comparison of this SSEP with the SSEP in children, evoked in the stretch reflex, shows shorter latencies of the waves in adults. On the basis of data from the different series of experiments, it is assumed that kinesthetic signalization plays a dominant role in the genesis of SSEP of the T-reflex. Studies have shown that SSEP of the T-reflex is succeptible to habituation upon long repetition of the stretch reflex.
The present study was carried out to investigate the long-latency soleus stretch reflexes M2 (peak latency of approximately 85 ms) and M3 (peak latency of approximately 115 ms) during walking in healthy and spastic multiple sclerosis (MS) patients. An 8 degrees stretch was applied to the ankle extensors of the left leg in 8 healthy subjects during normal walking speed and 9 spastic MS patients and 10 age-matched healthy subjects during slow walking. When present in walking healthy subjects, M2 and M3 were modulated in a similar way and with the same amplitudes as previously described for the short latency soleus stretch reflex (M1). The spastic patients' soleus M1 was significantly less modulated during walking. The patients' M2 long-latency response was modulated in the same way as the age-matched healthy subjects. All patients' M3 responses were absent or much suppressed during walking. The origin and functional importance of the short- and long-latency stretch reflexes in healthy and spastic persons are discussed in relation to the above findings and the behaviour of the stretch reflexes during matched isometric contractions. M3 is argued to be part of a transcortical reflex in healthy subjects.
The short- and long-latency (SLSR, LLSR) components of the stretch reflex response were investigated in the forearm using a paired transcranial magnetic stimulation (TMS)-stretch reflex protocol. Responses to TMS were recorded in the flexor and extensor carpi radialis muscles (FCR, ECR) after conditioning with a rapid wrist extension movement. The cortical stimuli were timed to elicit a motor-evoked potential (MEP) at either the SLSR or LLSR onset in the FCR muscle. Responses were also collected in TMS-alone and stretch reflex-alone conditions. Six intensities of magnetic stimulation were applied in all conditions. In the FCR muscle, MEP amplitude when timed to arrive at the LLSR onset was significantly greater than the sum of the MEP and stretch reflex responses when given separately. MEP amplitudes at the SLSR onset in the FCR muscle and in the ECR muscle at both SLSR and LLSR onset were not significantly different from that expected from the sum of the two stimuli given separately. This indicates heightened corticospinal excitability at a time corresponding to the passage of an afferent volley induced by the stretch, and raises the possibility of a transcortical loop of the LLSR in the forearm. The extent of MEP facilitation was generally consistent across all stimulus intensities tested. A reduced component of the LLSR was evident when the stretch response was timed to arrive during the silent period following the cortical stimulus, suggesting both cortical and sub-cortical components to the reflex response.
Evidence has recently been presented indicating that muscle stretch reflexes have a large supraspinal component. The finding introduces the possibility that stretch reflex parameters may be modifiable by stimuli involving other modalities besides stretch. In this investigation, the effects of a visual cue on the reflex portions of the EMG activity following a sudden muscle stretch were examined. The results, obtained from the flexor carpi radialis muscles of six normal awake subjects, failed to show any significant change in the EMG parameters as a result of visual cues occurring at the instant of onset of muscle stretch. This was interpreted as indicating that visual inputs do not reach the areas of brain involved in the supraspinal reflex in sufficient time to modify the reflex.
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