The irrelevance of fusimotor activity to the Achilles tendon jerk of relaxed humans

In two normal subjects the sciatic nerve was blocked completely using concentrated lidocaine. The muscle afferent and reflex electromyographic responses to reproducible percussion of the Achilles tendon were recorded while the blocks developed. The intensity of percussion was sufficient to produce an Achilles tendon jerk in one subject when at rest and in the other during reinforcement. The block did not alter the muscle afferent response to tendon percussion in either subject. It is concluded that background fusimotor activity is not a prerequisite for the tendon jerk and that, during complete relaxation, there may be no significant fusimotor drive directed to the triceps surae. The varying ease with which tendon jerks can be elicited in different normal subjects or in different muscles of the same subject appears to be related not to fusimotor activity but to differences in the "central excitability state."     

The limitations of the tendon jerk as a marker of pathological stretch reflex activity in human spasticity.

The motor disorders associated with human spasticity arise, partly from a pathological increase in the excitability of muscle stretch reflexes. In clinical practice, reflex excitability is commonly assessed by grading the reflex response to a blow delivered to the tendon of a muscle. This is a much simpler response than the complex patterns of activity which may be elicited following muscle stretch caused by active or passive movement. Changes in the biceps brachii tendon jerk response have been followed over the first year after stroke in a group of hemiparetic patients and compared with changes in short and medium latency reflex responses elicited by imposed elbow flexion of initially relaxed spastic muscle and with the development of the late reflex responses which contribute to spastic hypertonia. A progressive increase in tendon jerk responses occurred over the first year following stroke, whereas reflex responses to imposed displacement, in particular the late reflex responses contributing to muscle hypertonia, reached their peak excitability one to three months after stroke, with a subsequent reduction in activity. The tendon jerk reflex therefore provides an incomplete picture of the pathological changes in the reflex responses in spasticity.     

Electroneurographic correlates of the monosynaptic reflex: experimental studies and normative data.

The neurographic concomitants of the monosynaptic reflex, evoked either by electrical stimulation of the tibial nerve at the popliteal fossa or by percussion of the Achilles tendon, have been recorded from the sciatic nerve in the lower and middle thigh. Neurographic recordings were characterised by two travelling waves (P1 and P2), respectively increasing and decreasing in latency in the proximal direction, that showed the same chronological trend of the propagated action potentials concurrently recorded in the dorsal and ventral spinal roots at the lumbar level. At variance with P2, the speed of propagation of the P1 volley was stimulus-related, being faster on mechanical than on electrical stimulation, probably because in the latter case the latency of the fastest afferents is overestimated. The P2 volley is subserved by alpha-efferent fibres in either case as suggested, inter alia, by the strict parallelism between the P2 volley and the monosynaptic reflex under appropriate experimental conditions. Simultaneous recordings of spinal root and sciatic nerve action potentials allowed the direct assessment of afferent and efferent conduction velocities, both in the proximal (that is from the middle thigh to the spinal recording site and vice-versa) and in the distal (that is from the lower to the middle thigh recording site and vice versa) segments of the reflex arc. As expected, the speed of propagation of impulses was significantly higher in the proximal than in the distal segments, as well as in the afferent than in efferent limb of the monosynaptic pathway. The P1-P2 time interval was longer on mechanical than on electrical stimulation, probably due to the increased spinal delay of the T versus the H reflex. The present study provides a reliable method for the direct assessment of alpha-efferent as well as of Ia afferent group fibres conduction velocity, provided that in the latter case mechanical stimuli be used.     

The time-course of bilateral changes in the reflex excitability of relaxed triceps surae muscle in human hemiparetic spasticity

Summary Short, rapid dorsiflexion of the normal human ankle induces a single, synchronised reflex EMG response in the initially relaxed triceps surae muscle (TS). In subjects in whom hemiparesis is present as a result of a unilateral ischaemic cerebral lesion, a reflex EMG response can be elicited on either side with timing identical to that of the normal response. The magnitude of the response in hemiparetic subjects, however, differs from the normal on both the side contralateral and that ipsilateral to the causative lesion. Furthermore, the magnitude of this response varies over the time-course of spasticity. Contralaterally to the lesion, a gradual increase in the magnitude of the response to imposed displacement occurs. One year after stroke, the response has reached a level significantly larger than normal. Changes in the magnitude of the contralateral Achilles tendon jerk reflex EMG are apparent earlier than changes in the response to imposed displacement, with exaggerated tendon jerks already being apparent between 1 and 3 months after stroke. On the side ipsilateral to the lesion, a profound depression of the response to imposed displacement is visible as early as a month after stroke. This depression diminishes over the 1st year, but the response has not even then returned to normal values. These changes are not reflected in the ipsilateral tendon jerk response, which remains normal throughout this period. It is thus concluded that at least two processes are at work in determining the reflex excitability of the TS in hemiparetic humans: firstly, a unilateral increase in excitability at a low spinal level on the side contralateral to the lesions, appearing in the 1st month after stroke and producing the exaggerated tendon jerk response on this side; secondly, a bilateral depression mediated unlike the tendon jerk response, over a predominantly polysynaptic pathway and affecting the response to imposed displacement. This depression appears in the 1st month after stroke and gradually becomes less marked over the following year. On the contralateral side, owing to the increase in excitability at a lower level, this does not appear as a reduction in the magnitude of the response to imposed displacement, but rather is evident in the slower time-course of the development of hyperexcitability in this response, relative to that of the tendon jerk reflex.     

Observations on the variability of the H reflex in human soleus

H reflexes were evoked in human soleus by stimulating the tibial nerve at a constant intensity. Each trial was then assigned to one of three groups on the basis of the amplitude of its H reflex; all trials in each group were then full-wave rectified and reaveraged. There was a strong positive relationship between the amplitude of the H reflex and the level of electromyographic activity in the muscle at the time of onset of the H reflex, which reflects the activity of the motoneuronal pool when the afferent volley arrived. Thus, much of the variability of the H reflex is due to small changes in the level of activation of the motoneuronal pool during repeated trials. The steady torque preceding the H reflex was a poor predictor of the H-reflex amplitude, presumably because of the delay between the changes in the electrical activity of motoneurons and the mechanical outcome thereof.     

Tendon vibration-induced inhibition of human and cat triceps surae group I reflexes: evidence of selective Ib afferent fiber activation

In humans, prolonged vibration of the Achilles tendon produced transient depression or abolition of the soleus H-reflex. Recovery of the electrical reflex threshold to previbration values at a constant lower stimulus intensity usually occurred between 10 to 55 min. Electrical stimulation at higher multiples of the reflex threshold produced reflex EMG amplitudes more immediately comparable to previbration controls. When postvibration H-reflexes were completely abolished, poststimulus averaging of voluntarily maintained tonic EMG activity showed evidence of inhibition at a 46-ms latency in contrast to a 32-ms previbration H-reflex latency. In cat, observation of H-reflexes were rare, but stimulus-evoked changes in EMG activity mimicked the postvibration depression seen in humans. Ventral root postvibration reflexes from triceps surae varied in magnitude but were usually depressed or abolished at 1.0 to 1.2 times the electrical reflex threshold. These responses returned to previbration control amplitudes within 20 to 35 min. Magnitude of depression and time to recovery were dependent on the intensity of the electrical stimulus. In five experiments, depression of postvibration reflex activity and recovery were accompanied by gradual recovery in amplitude of the group I volley to previbration amplitudes. Elevated group Ia axonal electrical thresholds, monitored from seven isolated units, were observed to recover to previbration values in parallel with postvibration reflex recovery to control amplitudes. At electrical stimulus intensities greater than 1.4 times the reflex threshold, postvibration reflex responses were often potentiated, probably reflecting posttetanic potentiation of group Ia pathways activated at their higher axonal thresholds. In two observations, postvibration Ib axonal electrical thresholds did not change. Overall, the findings supported the proposal that postvibration depression of soleus H-reflexes in humans or cats is caused by both disfacilitation and autogenetic inhibition due to withdrawal of Ia afferent activation and increased selectivity of Ib afferent fiber stimulation, respectively.     

Inhibition of the achilles tendon reflex by antagonist long-latency postural responses in humans

The present study demonstrated inhibition of the Achilles tendon reflex in freely standing humans during platform perturbations which elicited a long-latency postural response (90 to 110 ms) in the stretched antagonist tibialis anterior musculature. The inhibition was apparent under those conditions in which the long-latency postural response had adapted to subthreshold within the antagonist motoneuron pool. The inhibition was also apparent under those conditions in which the long-latency postural response occurred in the ankle muscles shortened rather than stretched by the perturbation, and therefore did not require prior activation of antagonist muscle spindle afferent neurons. This modulation was more efficacious than equivalent phasic or tonic voluntary activation of the antagonist musculature and this implied that pathways activated during long-latency postural responses and voluntary responses were not equivalent. The experiments also demonstrated that the myotatic stretch reflex (40 to 45 ms latency) remained in the homonymous muscle under conditions in which the long-latency postural response adapted to subthreshold. This finding supports the hypothesis that postural response adaptation involves mechanisms other than presynaptic inhibition of the Ia afferent fibers or inhibition of the homonymous motoneuron pool.     

Muscle afferent potential (`A-wave'') in the surface electromyogram of a phasic stretch reflex in normal humans

The experiments reported in this paper tested the hypothesis that the afferent potential elicited by a tendon tap in an isometrically recorded phasic stretch reflex can be detected in the surface EMG of normal humans when appropriate techniques are used. These techniques involved (1) training the subjects to relax mentally and physically so that the EMG was silent before and immediately after the diphasic MAP which reflects a highly synchronous discharge of afferent impulses from low threshold muscle stretch receptors after a tendon tap, and (2) using a data retrieval computer to summate stimulus-locked potentials in the EMG over a series of 16 samples using taps of uniform peak force and duration on the Achilles tendon to elicit the tendon jerk in the calf muscles. A discrete, diphasic potential (`A-wave') was recorded from EMG electrodes placed on the surface of the skin over the medial gastrocnemius muscle. The `A-wave' afferent potential had the opposite polarity to the corresponding efferent MAP. Under control conditions of relaxation the `A-wave' had a latency after the onset of the tap of 2 msec, the peak to peak amplitude was of the order of 5 μV and the duration was in the range of 6 to 10 msec. Further experiments were conducted to show that the `A-wave' (1) was not an artefact of the instrumentation used, (2) had a threshold at low intensities of stimulation, and (3) could be reliably augmented by using a Jendrassik manoeuvre compared with the potential observed during control (relaxation) conditions. The results support the conclusion that the `A-wave' emanates from the pool of muscle spindles which discharges impulses along group Ia nerve fibres in response to the phasic stretch stimulus because the primary ending of the spindles is known to initiate the stretch reflex and the spindles can be sensitized by fusimotor impulses so that their threshold is lowered as a result of a Jendrassik manoeuvre. The finding has important implications for the investigation of the fusimotor system in intact man.     

Stretch reflexes of triceps surae in normal man.

In order to learn more about stretch reflex behaviour of triceps surae, normal human subjects sat in a chair with one foot on a platform attached to a torque motor that produced phasic dorsiflexion displacements on the ankle. EMG activity was recorded from triceps surae and responses were obtained for various conditions. When the subjects's foot was relaxed, stretch of triceps surae produced a single EMG component at short-latency which increased in magnitude with increasing velocity of stretch. The response was not altered if the subject was asked to plantarflex or dorsiflex the ankle voluntarily when he felt the perturbation. It was reduced by vibration of the Achilles tendon. If the triceps surae was stretched while the subject plantarflexed his ankle, the short-latency response was followed by one and sometimes two long-latency responses. Like the short-latency reflex when the foot was relaxed, none of these responses was altered by the subject's planned movement after feeling the perturbation. All of the responses were suppressed to a similar degree by vibration. The long-latency reflexes depended on long-duration of stretching and relatively slow acceleration of stretch. The reflexes persisted after anaesthesia to the foot suggesting that muscle afferents were responsible. Interactions between H-reflexes and stretch-reflexes revealed that the afferent volley producing a stretch reflex acted like the afferent volley producing a small H-reflex. Responses at an interval of 30 ms to both an electrical stimulus for an H-reflex and a stretch stimulus were possible if the electrical stimulus produced only a small H-reflex and if the subject had been plantarflexing the ankle. The short-latency reflex when the foot was relaxed or exerting a background force appears to be the monosynaptic, Ia mediated stretch reflex. The physiological properties of the long latency reflexes are similar to those of the short-latency reflex, and they may represent, at least to a certain extent, response of the motor neuron pool to successive Ia bursts.     

Gordon's reflex phenomenon in huntington's disease

Summary The patellar tendon jerk was examined quantitatively in 8 cases of Huntington's disease and in 27 controls using surface electrodes over the quadriceps femoris and biceps femoris muscles. The purpose was to investigate whether Gordon's patellar phenomenon was caused by a lack of antagonistic innervation or by late agonistic tonic reflex activity in Huntington's disease. Specific results could indicate that the patellar tendon jerk could be used as a diagnostic aid, as is the long loop reflex of hand muscles. A late tonic stretch response was found, appearing between 160 and 260 ms after the tendon tap. This response appeared in 6 out of the 8 Huntington's cases, even when Gordon's phenomenon was not observed. Therefore, it could be assumed that the tonic quadriceps activation gives rise to the clinically observed Gordon's phenomenon.     

Characteristics of the vibratory reflex in humans with reduced suprasegmental influence due to spinal cord injury

The tonic stretch reflex elicited by vibration of a muscle or tendon provides a means of studying segmental reflex activity in humans with impaired volitional motor activity due to spinal cord injury (SCI). Vibration applied to the achilles or patellar tendon in a group of 51 SCI subjects elicited motor unit activity different from that found in 12 healthy subjects. Four distinct features of motor unit responses to vibration of a single tendon (achilles or patellar) could be seen in the SCI subjects: (i) a rapid onset, tonic response, frequently beginning with a single burst analogous to a tendon jerk, in 72% of vibrated sites; (ii) repetitive, phasic bursts of activity or vibratory-induced clonus in 23% of the tonic responses; (iii) spread of activity to muscles distant from the vibration in 44% of the tonic responses; and vibratory-induced withdrawal reflexes (VWR) which occurred after vibration of 37% of the sites. Overall, 81% of stimulated sites responded to vibration in SCI subjects. In contrast, only 54% of vibrated sites responded in control subjects, always with a gradual onset tonic response, never accompanied by a VWR. The VWR in SCI subjects was typically of much larger amplitude than the tonic responses and involved a mean of 5 muscles (41% bilaterally). Features of these responses provide an insight into underlying neurocontrol mechanisms which may provide guidance in the selection of appropriate intervention or management strategies.     

Effects of the Jendrassik manoeuvre on muscle spindle activity in man.

Twenty-eight mechanoreceptive units identified as primary or secondary spindle afferents were sampled from muscle nerve fascicles in the median, peroneal, and tibial nerves of healthy adult subjects. The responses of these units to sustained passive muscle stretch, to passive stretching movements, to tendon taps, and electrically-induced muscle twitches were studied while the subject performed repeated Jendrassik manoeuvres involving strong voluntary contractions in distant muscle groups. The manoeuvres had no effect upon the afferent spindle discharges as long as there were no EMG signs of unintentional contractions occurring in the receptor-bearing muscle and no mechanotransducer signs of unintentional positional changes altering the load on that muscle. Unintentional contractions in the receptor-bearing muscle frequently occurred during the manoeuvres, however, and then coactivation of the spindle afferents was observed. Multiunit afferent responses to Achilles tendon taps, led off from tibial nerve fascicles, were in a similar way uninfluenced by the Jendrassik manoeuvres, even when these resulted in marked reinforcement of the calf muscle tendon jerk. The results provide no evidence for fusimotor sensitization of spindles in muscles remaining relaxed during the Jendrassik manoeuvre, and reflex reinforcement occurring without concomitant signs of active tension rise in the muscles tested is presumed to depend upon altered processing of the afferent volleys within the cord.     

Muscle receptors close to the myotendinous junction play a role in eliciting exercise pressor reflex during contraction

Although a muscle mechanosensitive reflex contributes to regulation of the cardiovascular responses during exercise, the precise location of muscle mechanoreceptors responding to contraction has not been identified yet. We have recently reported that mechanosensitive receptors located at or close to the myotendinous junction play a role in eliciting the cardiovascular responses to passive stretch of skeletal muscle. The mechanoreceptors located at or near the myotendinous junction are hypothesized to respond to static contraction as well. To test this hypothesis, we had two interventions for the reflex cardiovascular responses to static contraction of the triceps surae muscle with the same tension development in decerebrate or pentobarbital-anesthetized rats; cutting the Achilles tendon and local injection of lidocaine into the myotendinous junction. The cardiovascular responses were evoked by static contraction regardless of the achillotomy, suggesting that mechanoreceptors terminating in the more distal part of the cut Achilles tendon did not contribute to the reflex cardiovascular responses. Lidocaine (volume, 0.04-0.1 ml) injected into the myotendinous junction blunted the reflex cardiovascular responses, indicating that muscle afferent fibers terminating at or passing through the myotendinous junction contribute to the exercise pressor reflex. The achillotomy did not affect the cardiovascular responses to passive stretch with the same tension as static contraction, but the localized injection of lidocaine similarly blunted the responses to passive stretch as contraction. We conclude that the mechanosensitive receptors eliciting the reflex cardiovascular responses may at least partly locate close to the myotendinous junction, to monitor tension development during muscular activity.     

Measurement of the Achilles tendon reflex for the diagnosis of lumbosacral root compression syndromes.

The Hoffmann reflex and the Achilles tendon reflex were measured in a group of 194 subjects suspected of having a lumbosacral root compression syndrome. The Achilles tendon reflex was elicited manually with a metal hammer. There was a high correlation between the H-M interval and the Achilles tendon reflex-M interval. The usefulness of the Achilles tendon reflex was evaluated in a selected sub-group of 61 patients with proven L5 or S1 root compression. Neither the H-reflex nor the Achilles tendon reflex appeared to be of any value in detecting L5 root compression. Both the H-reflex and the Achilles tendon reflex proved to be useful for diagnosis of S1 root compression syndromes, the latter being the more sensitive method.     

Depression of involuntary activity in muscles paralyzed by spinal cord injury

Involuntary muscle contractions are common after spinal cord injury (SCI). Increased sensitivity to Ia muscle afferent input may contribute to the development of these spasms. Since tendon vibration results in a period of postactivation depression of the Ia synapse, we sought to determine whether Achilles tendon vibration (80 HZ for 2 s) altered involuntary contractions evoked by superficial peroneal nerve (SPN) stimulation (5 pulses at 300 HZ) in paralyzed leg muscles of subjects with chronic (>1 year) SCI. Responses to SPN stimulation that were conditioned by vibration were reduced in 66% of trials (by 33+/-12% in tibialis anterior and 40+/-16% in soleus). These reductions in electromyographic activity are unlikely to be mediated by changes at the Ia synapse or motoneuron because vibration did not alter the magnitude of the soleus H reflex. The electromyographic reductions may involve long-lasting neuromodulatory effects on spinal inhibitory interneurons or synapses involved in the flexor reflex pathway. Vibration-evoked depression of electromyographic activity may be clinically useful in controlling involuntary muscle contractions after SCI.     

Vibration insensitivity of a short latency reflex linking the lower leg and the active knee extensor muscles in humans.

The study indirectly investigated the afferent source of a human lower limb reflex that spans two joints and may link limb muscular activity during movement. Low threshold (motor nerve threshold (MT) to 1.6 MT) single, 1 msec, pulses were delivered to the common peroneal nerve at caput fibula. Heteronymous excitatory responses were observed in the elctromyogram of the knee extensor muscle vastus medialis (VM), when the latter was prior contracted. The briefest latency for the VM reflex was 24.2 msec. The distal belly and tendon of the tibialis anterior muscle were vibrated for 20 min at a frequency of 105 Hz, amplitude 1-2 mm, to inhibit the reflex potential evoked by group Ia afferent fibres from that muscle. This significantly reduced the amplitude of the group Ia mediated Hoffmann (H) reflex in TA. Such vibration did not depress the amplitude of the heteronymous reflex to VM, when initially the latter was at peak amplitude or at its mid-range for amplitude. Reflex latency, threshold, and stimulation current for peak expression suggested that group II fibres were unlikely to be the major initiators of the reflex. The results support the view that this human reflex is primarily Ib mediated.     

The reflex hammer]

When Erb began to study the knee jerk around 1870 he was able to use the percussion hammer for this purpose. Whereas percussion nowadays is performed with bare fingers, every physician carries a reflex hammer in his bag. Many varieties of reflex hammer have been developed. Their distribution today depends on their use by different schools. The origins and development of the most popular contemporary reflex hammers in English, French and German speaking countries are described.     

Stretch reflex of quadriceps femoris and its relation to rigidity in Parkinson''s disease

Much evidence suggests that parkinsonian rigidity is due to hyperactivity of a reflex arc. While tendon jerk and H reflex are not modified in Parkinson's disease (PD), the long-latency component of stretch reflex (LLR) shows an increased size in PD. It has been proposed that this modification could account for rigidity. We studied in 14 PD patients and 8 normal subjects the stretch reflex of the quadriceps femoris. The muscle was stretched by a torque motor in two experimental sets: at rest and with voluntary background activity. Latency, duration and size of the reflex were compared in two groups; correlation between size of the reflex and rigidity was investigated. A lower threshold for the reflex was found in PD patients in trials at rest, and LLR showed increased size and duration in trials with background activity. No clear relationships between these data and rigidity were demonstrated.     

N-methyl-D-aspartate antagonist applied to the spinal cord hindlimb enlargement reduces the amplitude of flexion reflex in the turtle

APV (D(-)-2-amino-5-phosphonovalerate), an NMDA (N-methyl-D-aspartate) antagonist, was applied in situ onto segments of the hindlimb enlargement of the turtle spinal cord. APV reduced the response amplitude of the flexion reflex. In contrast, APV did not alter the responsiveness of the rostral scratch reflex. Afferents for the flexion reflex enter the spinal cord via the dorsal roots of the middle segment of the hindlimb enlargement; afferents for the rostral scratch reflex enter the spinal cord via dorsal roots located anterior to the hindlimb enlargement. The results are consistent with the hypothesis that sensory interneuron NMDA receptors, synaptically activated either directly or indirectly by nearby cutaneous afferent axons, play a role in the spinal cord processing of cutaneous information.     

Tonic descending inhibition of the spinal cardio-sympathetic reflex in the cat

Electrical stimulation of the left inferior cardiac nerve elicited a two-component reflex potential (spinal and supraspinal reflexes) in the ipsilateral white ramus T3 from which recordings were made in chloralose-anaesthetised cats. Reversible interruption of all spinal pathways achieved by cooling the spinal cord at C2/C3 produced an enhancement of the spinal reflex and abolished the supraspinal reflex, the latter usually being the more prominent reflex potential prior to spinal cord block. The spinal cord block-induced increase in the amplitude of the spinal reflex was, however, less than the increase observed during stimulation of the somatic intercostal nerve T4. Recordings of the afferent volley following cardiac nerve stimulation and analysis of the stimulus-reflex response relationship in neuraxis-blocked cats indicated that the spinal reflex as determined here was activated by A delta afferent fibres. However, if stimulus strength was raised above C-fibre threshold, spinal cord block revealed in addition a late spinal reflex response. In some cases, the appearance of this late potential was accompanied by a secondary decline of the earlier spinal reflex potential, possibly indicating C-fibre-mediated afferent inhibition. Neither baroreceptor activation nor denervation had any effect on spinal reflex amplitudes. Pharmacologically, clonidine given i.v. to cats with a blocked neuraxis reduced the spinal reflex amplitudes to pre-block values, an action which could be antagonised by the subsequent administration of the alpha 2-adrenoceptor antagonist rauwolscine. When given to non-pretreated cats with intact neuraxis, however, neither rauwolscine nor its analog yohimbine were capable of inducing a persistent release from tonic inhibition. The results suggest that both purely visceral and somato-visceral reflexes are subject to tonic descending inhibition, but they do not support the hypothesis that a catecholamine is the responsible transmitter mediating this inhibition.