Tendon Stimulation Research Articles

Synaptic potentials contributing to reflex inhibition in gastrocnemius following tendon electrical stimulation

Objective To investigate the synaptic potentials underlying reflex inhibition in gastrocnemius following electrical stimulation of the Achilles tendon using single motor unit recordings. Methods Surface electromyography (SEMG) and single motor unit (SMU) action potentials were recorded from the medial head of left gastrocnemius muscle in eight healthy human subjects. The left Achilles tendon was stimulated electrically while subjects maintained a low contraction level sufficient to record one or two motor units. SMU responses were analysed using peri-stimulus time histogram (PSTH) and peri-stimulus frequencygram (PSF) techniques and compared with SEMG results. Results A total of 22 SMU experiments were completed. In all trials, a large reflex inhibition (I1) was observed in both SEMG and PSTH followed by a later inhibition (I2). In 50% of trials, SEMG and PSTH showed that both I1 and I2 were followed by excitation (E1 and E2, respectively). PSF analysis showed only a prolonged reduction in SMU discharge rate. This inhibition had a latency of 38 ms and duration of 130 ms, extending into the E1 period in 14 units and more than 200 ms extending into the E2 period in six units. Conclusions PSF data suggest that tendon electrical stimulation results in a long-lasting inhibition, most likely through the autogenic inhibitory reflex pathway mediated by group I tendon afferents. Significance These findings emphasise the importance of using both probability (SEMG, PSTH) and frequency (PSF) based techniques in error free estimation of synaptic potentials.

Inhibitory mechanisms following electrical stimulation of tendon and cutaneous afferents in the lower limb

Electrical stimulation of the Achilles tendon (TES) produced strong reflex depression (duration>250 ms) of a small background contraction in both heads of gastrocnemius (GA) via large diameter electrodes localized to the tendon. The inhibitory responses were produced without electrical (M wave) or mechanical (muscle twitch) signs of direct muscle stimulation. In this study, the contribution of presynaptic and postsynaptic mechanisms to the depression was investigated by studying conditioning effects of tendon afferent stimulation on the mechanical tendon reflex (TR) and magnetic motor evoked potential (MEP). TES completely inhibited the TR over an ISI of 300 ms that commenced before and continued during and after the period of voluntary EMG depression. Tendon afferent conditioning stimuli also partially inhibited the MEP, but over a short time course confined to the period of voluntary EMG depression. The strength and extended time course of tendon afferent conditioning of the TR and its failure to produce a similar depression of the MEP are consistent with a mechanism involving presynaptic inhibition of Ia terminals. Cutaneous (sural nerve) afferent conditioning partially inhibited the TR and MEP over a short time course (ISI <100 ms) resembling the inhibition seen in the voluntary EMG. This was consistent with the postsynaptic origin of cutaneous inhibition of the motoneurons.

Muscle inhibition following tendon stimulation is reduced in chronic stroke

Electrical tendon stimulation elicits reflex inhibition in the homonymous muscle that is thought to be mediated by group III afferents. The study goals were to: evaluate group III-mediated reflex inhibition in people with post-stroke hemiparesis; determine the presence of heteronymous group III pathways; investigate the relevance of reflex inhibition to arm function. Reflex responses were recorded in wrist, elbow, and shoulder muscles following stimulation of the extensor carpi radialis (ECR) tendon in 16 people with post-stroke hemiparesis and 16 control subjects. In control subjects, reflex inhibition also was compared between static and dynamic muscle activation. Reflex inhibition following ECR tendon stimulation was present in heteronymous muscles of most, but not all, stroke and control subjects. The level of reflex inhibition was significantly reduced in stroke subjects. In the controls, reflex inhibition was greater during dynamic activation of elbow muscles compared to static activation. Evidence that reflex inhibition projects to heteronymous muscles and is modulated during movement suggests a role for the reflex in multi-joint coordination. The reflex is impaired in post-stroke hemiparesis. Abnormalities in the regulation of group III-mediated muscle inhibition in the stroke population may contribute to impaired muscle activation patterns during movement.

Afferents contributing to autogenic inhibition of gastrocnemius following electrical stimulation of its tendon

Electrical stimulation of the Achilles tendon produced strong reflex inhibition of the ongoing voluntary EMG activity in the two heads of the gastrocnemius (GA) muscle in all tested subjects. The inhibition was seen clearly in both averaged and single sweep surface EMG records. The inhibitory response was produced without electrical (M wave) or mechanical, (muscle twitch) signs of direct muscle stimulation. The onset latency and duration for the first period of inhibition (I 1) were 47–49 ms and 67 ms, respectively. A second inhibition (I 2) had an onset latency of 187–193 ms and duration under 40 ms. Non-noxious stimuli in the range of 2.6–7.6 × mean perceptual threshold, when delivered to four locations over the GA tendon, all produced clear inhibition of the voluntary muscle activity. The inhibition was maximal when the cathode was a large metal plate located near the musculotendinous junction and decreased approximately linearly with distances more distal to that site. The effect of passive muscle stretch on the electrically induced tendon reflex inhibition (TRE) was tested at ankle joint angles incremented in steps of 20°. It was found that TRE is strongly dependent on joint angle, being maximal in the fully stretched muscle. TRE was lost completely after partial tibial nerve block. In comparison, GA inhibition produced by cutaneous (sural) nerve stimulation was of a higher threshold, longer latency and persisted after partial tibial nerve block. We thus demonstrated a powerful autogenic inhibition in the lower limb arising from tendon afferents in conscious subjects that is increased by passive muscle stretch and likely to originate from group I tendon afferents.

Reflex Inhibition of Normal Cramp Following Electrical Stimulation of the Muscle Tendon

Muscle cramp was induced in one head of the gastrocnemius muscle (GA) in eight of thirteen subjects using maximum voluntary contraction when the muscle was in the shortened position. Cramp in GA was painful, involuntary, and localized. Induction of cramp was indicated by the presence of electromyographic (EMG) activity in one head of GA while the other head remained silent. In all cramping subjects, reflex inhibition of cramp electrical activity was observed following Achilles tendon electrical stimulation and they all reported subjective relief of cramp. Thus muscle cramp can be inhibited by stimulation of tendon afferents in the cramped muscle. When the inhibition of cramp-generated EMG and voluntary EMG was compared at similar mean EMG levels, the area and timing of the two phases of inhibition (I(1), I(2)) did not differ significantly. This strongly suggests that the same reflex pathway was the source of the inhibition in both cases. Thus the cramp-generated EMG is also likely to be driven by spinal synaptic input to the motorneurons. We have found that the muscle conditions that appear necessary to facilitate cramp, a near to maximal contraction of the shortened muscle, are also the conditions that render the inhibition generated by tendon afferents ineffective. When the strength of tendon inhibition in cramping subjects was compared with that in subjects that failed to cramp, it was found to be significantly weaker under the same experimental conditions. It is likely that reduced inhibitory feedback from tendon afferents has an important role in generating cramp.

Recalcitrant Patellar Tendinosis in Elite Athletes

Background Recalcitrant patellar tendinosis is difficult to treat, and results are varied. Hypothesis Surgical removal of necrotic tissue, surgical stimulation of remaining tendon, and aggressive and specific rehabilitation after patellar tendonectomy will allow athletes to return to sports. Study Design Case series; Level of evidence, 4. Methods From December 1996 to July 2002, 16 high-level athletes (4 professional, 2 Olympic, 9 collegiate, 1 preparatory), aged 16 to 25 years (mean, 19.7 years), with 22 symptomatic patellar tendons had failed nonoperative care of their patellar tendinosis symptoms and were unable to compete effectively in their sports. Magnetic resonance imaging showed confirmation of disease, with typical findings being necrosis in the posterior half of an abnormally thick patellar tendon, often in conjunction with partial tearing of the posterior half with a compensatory enlargement of the anterior half. Each patient then underwent tendonectomy of the necrotic portion in conjunction with stimulation of the remaining tendon by making multiple longitudinal cuts in the tendon. Patients participated in a postoperative rehabilitation protocol that included immediate range of motion, full flexion, and immediate high-repetition, low-resistance quadriceps muscle exercise. Results Subjective improvement was noted in all athletes. Return to the same sport at prior level of intensity was accomplished by 14 of 16 patients (87.5%) at a mean of 8.1 months (range, 3-12 months). Conclusion Overall, tendonectomy, surgical tendon stimulation, and aggressive postoperative rehabilitation were found to be a safe, effective way to return high-level athletes to their sports.

Effects of Age and ACL Reconstruction on Quadriceps Gamma Loop Function

Both aging and anterior cruciate ligament (ACL) reconstruction are associated with strength deficits, which can in turn influence performance of activities of daily living. Thus it is informative to understand mechanisms underlying strength deficits. Age-related declines in strength follow reductions in muscle fiber numbers and size, whereas strength deficits following ACL reconstruction may be caused by the loss of intraligamentous mechanoreceptors. A common link between these conditions is the gamma spindle system, or the gamma loop. Appropriately applied vibration can affect the gamma loop by causing disruption of afferent feedback to a muscle and result in decreased force capabilities. We investigated the effect of age and ACL reconstruction on gamma loop function. Maximal isometric strength (MVC) and electromyography (EMG) of the quadriceps were quantified before and after vibration stimulation of the infrapatellar tendon of 3 groups: young healthy (n=4; mean age=23.8 yrs), young ACL reconstructed (n=7; mean age=22.4 yrs), and older healthy (n=4; mean age=66.1 yrs) individuals. The quadriceps MVC, vastus lateralis EMG, vastus medialis EMG, and rectus femoris EMG declined significantly in the young healthy group following vibration stimulation to the infrapatellar tendon, which indicated an intact gamma loop. There were no changes in these variables for the old healthy and ACL reconstructed groups. Gamma loop function was impaired in both the older and ACL reconstructed groups possibly due to either decreased muscle spindle sensitivity or the loss of mechanoreceptors.

A portable vibrator for muscle performance enhancement by means of direct muscle tendon stimulation

Combining vibration stimulation with conventional resistance training has gained in popularity. However, no portable vibrator capable of directly stimulating muscle tendon appears to feature in the literature. The aim of this study was the development of such a unit. The unit developed makes use of a rotating eccentric mass system to produce desired amplitude and frequency range capable of investigating the diverse vibration characteristics used in previous research studies. The effects of strapping force, joint angle and day-to-day repeatability on these vibration characteristics were investigated. In addition, muscle electromyography (EMG) activity was subsequently used to identify the optimum vibration amplitude and frequency. Finally, the repeatability of these EMG responses and effect of joint angle were examined. The unit was able to produce desired vibration characteristics (amplitude: 0.2–2 mm; frequency: 30–200 Hz). Test day, strapping force and joint angle had no significant effect on these characteristics ( p > 0.05). Both amplitudes (0.5 and 1.2 mm) and all three frequencies (30, 65 and 100 Hz) tested, significantly enhanced EMG activity ( p < 0.05), with 1.2 mm and both 65 and 100 Hz resulting in significantly greater enhancements ( p < 0.05). Joint angle had no significant effect on these EMG results ( p > 0.05). The day-to-day repeatability of EMG response was shown to be high ( r = 0.76–0.90).

Loss of reflex inhibition following muscle tendon stimulation in essential tremor.

Electrical stimulation of human upper limb muscle tendons produces a reflex inhibition (I(1)) in the same muscles. This inhibition is reduced in Parkinson's disease (PD), prompting a similar study of essential tremor (ET). In essential tremor, two of eight subjects had no discernible inhibition, even following supramaximal stimulation (< 80 mA) of the tendons from extensor digitorum communis and extensor pollicis brevis. In the remaining six subjects, the mean thresholds for I(1) in these muscles were increased by 270 and 320%, respectively, relative to controls. The maximal amplitude of the inhibition was significantly reduced in the ET group, as was the following excitation (E(1)). The latency and duration of I(1) were not different in ET subjects and controls. The maximal duration of I(1) was correlated with tremor frequency in individuals, and tendon stimulation was effective in initiating ongoing tremor cycles. These results disclose a peripheral reflex abnormality in ET that is mediated by tendon afferents and can be linked to the coexistent tremor. The response in ET was distinguished from that in PD by its different time-course and by failure of the response to appear in the antagonist muscle. The abnormality may prove a useful marker for ET, which currently lacks a definitive pathological or neurophysiological marker to support objective clinical diagnosis.

Decreased EMG inhibition following electrical stimulation over muscle tendons in myopathies

Objective: To assess the central EMG inhibitory action of tendon afferent input in muscle diseases. Methods: The EMG inhibition elicited by electrical stimulation over muscle tendons was tested in 13 healthy voluntary subjects and 8 patients who had a primary muscle disease with a mild force deficit. Electrical stimuli were delivered to the tendon of the extensor carpi radialis muscle at the wrist during tonic voluntary isometric contraction at 50% of the maximum EMG level. The EMG signal was recorded by surface electrodes over the extensor carpi radialis muscle. Results: The prestimulus background EMG level was reduced in 7 out 8 of the patients. Both groups had the same phases of EMG modulation following tendon stimulation (TE1, TI1, TE2) and their latency and amplitude did not differ significantly. Conversely, the area of TI1 was significantly larger (i.e. the inhibition decreased) in patients ([mean±SD] absolute area: controls=4.1±1.6 mVms, patients=6.9±2.9 mVms, P<0.05). Conclusions: In muscle dysfunction there are serial ‘upstream’ changes of central inhibitory systems, probably to maximize the residual muscle power of the affected muscle.

Continuous, bilateral Achilles’ tendon vibration is not detrimental to human walk

Sensory feedback from the moving limbs contributes to the regulation of animal and human locomotion. However, the question of the specific role of the various modalities is still open. Further, functional loss of leg afferent fibres due to peripheral neuropathy does not always lead to major alteration in the gait pattern. In order to gain further insight on proprioceptive control of human gait, we applied vibratory tendon stimulation, known to recruit spindle primary afferent fibres, to both triceps surae muscles during normal floor walk. This procedure would disturb organisation and execution of walking, especially if spindles fire continuously and subjects are blindfolded. Vibration induced significant, though minor, changes in duration and length of stance and swing phase, and on speed of walking and kinematics of lower limb segments. No effect was induced on angular displacement of the ankle joint or trunk and head kinematics. This paucity of effects was at variance with the perception of the subjects, who reported illusion of leg stiffness and gait imbalance. These findings would speak for a selective gating of Ia input during locomotion and emphasise the notion that the central nervous system can cope with an unusual continuous input along the Ia fibres from a key muscle like the soleus.

Impaired EMG inhibition elicited by tendon stimulation in dystonia.

to test the effects of tendon stimulation on isometric voluntary contraction. Twenty patients with dystonia (12 patients with generalized and eight with task-specific dystonia) and 10 normal healthy subjects participated in the study. The tendon of the extensor carpi radialis muscle was stimulated with electrical stimuli at the wrist, and the electromyogram (EMG) signal was recorded during an isometric voluntary contraction. In normal subjects, tendon stimulation elicited an excitatory phase (TE1), followed by a pronounced inhibitory phase (TI1) and a second excitatory phase (TE2). The three phases had similar perceptive thresholds, latencies, and durations in patients and control subjects. In patients with generalized dystonia, the TI1 area exceeded the control values (controls [mean +/- SE], 40.3 +/- 5.4; patients, 66.9 +/- 5.5; p = 0.0048, Mann-Whitney U: test). In the patients with task-specific dystonia, the TI1 area was similar to control values (controls [mean +/- SE], 40.3 +/- 5.4; patients, 54.2 +/- 4.8; p = 0.7396, Mann-Whitney U: test). The EMG suppression (TI1) after tendon stimulation is reduced in generalized dystonia, indicating a decreased group III-elicited presynaptic inhibition of Ia fibers. The impaired group III presynaptic inhibitory action from tendon afferents could contribute to the motor abnormalities present in dystonia. Dystonia causes widespread dysfunction of presynaptic inhibitory mechanisms in the spinal cord, involving Group I and III afferents.

Vibratory stimulation of proximal muscles does not affect cortical components of somatosensory evoked potential following distal nerve stimulation

Objectives: The effects of the proprioceptive activity of the proximal muscles on somatosensory evoked potentials (SEPs) were investigated, using vibratory stimulation of proximal muscle tendons. Methods: SEPs were recorded following electrical median nerve stimulation at the wrist during vibratory stimulation of tendon of pronator teres, biceps and trapezius muscles and fingers in 8 normal subjects. Results: The cortical SEP components, N20, P25 and N33 recorded from the parietal area, and P20 and N30 recorded from frontal area contralateral to the stimulated side, were markedly attenuated by vibratory stimulation applied to the fingers, but unaffected by vibratory stimulation of the proximal muscles. Conclusion: The proprioceptive afferent, especially group Ia muscle spindle afferent, in the relaxed proximal muscles is not likely to contribute to the gating of SEP following distal nerve stimulation.

Electroencephalographic measurement of motor cortex control of muscle activity in humans

Objective: To detect and measure correlation between cortical and muscle activities, coherence analysis was used. Methods: The electroencephalogram (EEG) and electromyogram (EMG) were recorded in 9 normal volunteers during tonic contraction of upper and lower limb muscles on the right side. Coherence between EEG and EMG was computed to analyze their linear association. Results: EEG over the contralateral sensorimotor area was coherent with EMG, with peak coherence at 11–36 Hz (mean, 22 Hz). For the abductor pollicis brevis (APB) muscle, peak coherence, as determined by functional brain mapping with focal transcranial magnetic stimulation (TMS), was over or slightly posterior to the hand area on the primary motor cortex determined by focal transcranial magnetic stimulation (TMS). Peak coherence over the scalp was somatotopically organized. The temporal relation between EEG and EMG was analyzed with a new model for interpreting the phase shift (‘constant phase shift plus constant time lag’ model). For the APB muscle, the phase relation between cortical and muscular oscillations differed in the frequency ranges of 3–13 Hz and 14–50 Hz, respectively, suggesting that different coupling mechanisms operate in different bands. Only the phase shift between cortical and motoneuronal firing at 14–50 Hz was reliably estimated by a linear model. At 14–50 Hz, motoneuronal firing was led by surface-negative cortical activity with a constant time lag that depended on the cortical-muscular distance. For the APB muscle, the time lag was slightly shorter than the cortical-muscular conduction time determined by TMS. Vibratory stimulation (100 Hz) of a muscle tendon during tonic contraction had no significant effect on cortical-muscular coherence, indicating that cortical oscillation reflected motor rather than sensory activity. Conclusions: The present findings suggest temporal coding of the oscillatory motor control system (3–13 Hz vs. 14–50 Hz), and confirm the functional importance of cortical beta and gamma rhythms in the motor efferent command. Cortical-muscular synchronization is most likely mediated by the direct corticospinal pathway within the frequency range of 14–50 Hz.

Electrical stimulation over muscle tendons in humans. Evidence favouring presynaptic inhibition of Ia fibres due to the activation of group III tendon afferents.

Electrical stimulation over muscle tendons produces a transient suppression of voluntary EMG activity; its onset latency is approximately 55 ms in the forearm extensor muscles. This phenomenon has been attributed to the activation of a polysynaptic inhibitory pathway originating from Ib afferent fibres. To clarify its origin we conducted several experiments in 10 normal healthy subjects. The EMG silence after tendon stimulation appeared at relatively high stimulus intensities (> 50 mA); conditioning cutaneous stimulation left it unchanged, and the inhibition had a short recovery cycle (50 ms). Tendon stimulation still evoked EMG suppression during an ischaemic block of fast-conducting afferents. The motor potentials evoked by transcranial magnetic stimulation of the motor cortex during the EMG silence remained almost unchanged, whereas the H reflex was strongly inhibited. Hence we conclude that tendon stimulation activates slow-conducting tendon afferents, possibly group III fibres, connected not through a polysynaptic pathway originating from Ib afferents but through an oligo- or disynaptic inhibitory circuit. The EMG suppression after tendon stimulation probably represents a dysfacilitation of the alpha-motor neurons due to presynaptic inhibition of Ia fibres produced by tendon afferent input to the spinal cord.

Mechanical stimulation of cartilage, ligment and tendon

Mechanical stimulation of cartilage, ligment and tendon

Physiological characterization of spinohypothalamic tract neurons in the lumbar enlargement of rats.

1. Ninety-six neurons in the lumbar enlargement of urethananesthetized rats were antidromically activated from the contralateral hypothalamus. The antidromic stimulating electrode was moved systematically within the hypothalamus until antidromic activation could be produced with currents of less than or equal to 50 microA (18.6 +/- 10.8 microA; mean +/- SD). The points at which antidromic activation thresholds were lowest were found in several regions of the hypothalamus but were concentrated in the optic tract and the supraoptic decussation. 2. The recording locations of 79 spinohypothalamic tract (SHT) neurons were marked and recovered. Twenty-nine were located in the superficial dorsal horn (SDH), 42 in the deep dorsal horn (DDH), 4 in the intermediate zone, and 2 in the gray matter surrounding the central canal. Two additional marks were located in the dorsal lateral funiculus (DLF). 3. The responses of 46 SHT neurons were examined during innocuous and noxious mechanical stimulation of their receptive fields. Forty-eight percent of recorded SHT neurons responded to both innocuous and noxious stimuli (wide dynamic range, WDR) and 39% responded only to noxious stimuli (high threshold, HT). Therefore 87% of SHT neurons responded preferentially or exclusively to noxious mechanical stimulation. Nine percent of SHT neurons responded exclusively to innocuous manipulation of joints and muscles. Four percent of SHT neurons responded only to innocuous tactile stimul (low threshold, LT). WDR, HT, and LT neurons were recorded widely throughout the dorsal horn; no relationship was found between the locations of recording sites in the dorsal horn and the response types of the neurons. SHT neurons that responded to stimulation of muscle, tendon, or joint were recorded deep in the gray matter. 4. The effects of heating the receptive fields were determined for 25 SHT neurons. Fourteen (56%) responded to thermal stimuli. Six (43%) of the responsive neurons responded at low frequencies to innocuous warming (38-41 degrees C) but more vigorously to noxious (greater than or equal to 45 degrees C) heating. The other eight responded only to noxious heat. Eighteen percent (3/17) of tested SHT neurons were activated by noxious cooling of their receptive fields. 5. Cutaneous receptive fields of most recorded SHT neurons were small, typically involving areas as small as two or three toes on the ipsilateral hindlimb; the largest receptive fields covered the entire paw. These findings indicate that relatively precise information about the location of innocuous and noxious stimuli is conveyed directly to the hypothalamus by SHT neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Proprioceptive control of goal-directed movements in man, studied by means of vibratory muscle tendon stimulation.

The purpose of this study was to investigate the role of propriomuscular feedback in the control of pluriarticular pointing movements, performed without visual feedback toward visual targets. The proprioceptive inputs were distorted during movements by applying vibration to the distal tendon of the biceps muscle. Various movement and vibration durations were imposed. The results show that vibration affects the spatial outcome of the movements. The effects of vibration were movement time-independent when the durations were shorter than 450 ms and became movement time-dependent with longer durations. Moreover, the effects of vibration became more marked when a short vibration was applied at the end rather than at the beginning of a slow movement. These studies suggest that at least two types of proprioceptive control loops may be involved in correcting this kind of movement, depending on the execution time. In slow movements, the final phase might be a privileged period for on-line, propriomuscular-based corrections. Lastly, it emerged that the regulation of a goal-directed movement on the basis of proprioceptive feedback processing can take place within at most 200 ms.

Responses of neurons in VPL and VPL-VL region of the cat to algesic stimulation of muscle and tendon.

1. The responses evoked by electrical stimulation of cutaneous and muscle nerves, by noxious and innocuous mechanical stimulation of muscle, tendon, and cutaneous tissues, and by intra-arterial (ia) injection of algesic substances (potassium, bradykinin) into arteries supplying the gastrocnemius-soleus muscle (GS) were studied in single neurons located in the ventroposterolateral nucleus (VPL) and in the transitional zone between VPL and the ventrolateral nucleus (VL) of cats lightly anesthetized with thiopenthal. Such chemical stimulation of the muscles has been shown to activate muscular groups III and IV axons specifically (43, 44) and presumably is nociceptive in character (14, 17, 31). 2. One hundred eight neurons were tested. Eighty-three of the units responded only to various types of cutaneous stimulation of the hindlimb. The other 25 responded to algesic stimulation of muscle and/or tendon. Of these latter 25, 7 had no apparent cutaneous receptive field although 4 of them responded to electrical stimulation of the common peroneal and/or sural nerve. Thus, only three neurons responded exclusively to algesic chemical and noxious mechanical stimulation of the muscle. Of the other 18 neurons, 14 had cutaneous receptive fields restricted to the hindlimb and often responded to non-noxious repetitive light stroking and to noxious pinching with a high-frequency discharge. Four cells (two of which had cutaneous input only from low-threshold mechanoreceptors) had complex and large receptive fields extending to more than one limb. 3. Potassium was a more potent muscle receptor stimulant than bradykinin, the latter only weakly exciting 3 neurons of 24 tested with both substances. The responses to potassium were rapid (approximately 4.0 s in latency) and tended to be greater (have higher response rates) for the units that responded to cutaneous as well as muscle/tendon stimulation. 4. Most neurons that responded to noxious deep stimulation had a threshold for the GS nerve volley in the group III fiber range. The few neurons with thresholds slightly below the group III range did not respond to activation of group I or II muscle spindle afferents by intra-arterial application of succinylcholine or by stretching the muscle. 5. Neurons with responses to any of the muscle, tendon, or cutaneous nociceptive stimuli were located at the ventral and dorsal periphery of VPL and in the VPL-VL transitional zone. 6. These results strongly suggest that there exist regions within the lateral diencephalon of cats that are capable of processing nociceptive information and that these regions are located at the periphery of VPL.

Ventilatory responses to muscular vibrations in healthy humans.

In healthy humans, we studied the effect of high-frequency mechanical vibrations applied unilaterally to the tendon of the biceps or triceps brachialis on ventilation and the breathing pattern. This stimulus preferentially activates the muscle spindle afferents. Increase of respiratory frequency and changes in the ventilatory timing started at the first or second inspiration during tendon stimulation, and no adaptation occurred as long as the vibrations continued. The tidal volume and mean inspiratory flow rate were only enhanced in individuals having high-frequency breathing during eupnea. The changes in ventilatory variables were observed when the motor response to vibrations was tested under isometric or isotonic conditions. Various experimental procedures enabled us to induce a tonic reflex contraction in either the vibrated muscle or the antagonist of no reflex contraction in either group of muscles. In all cases the increase in minute ventilation was identical. These changes in breathing pattern was not associated with a significant decrease in alveolar CO2 pressure and did not seem to be responsible for important variations in respiratory gas exchanges. The response to high-frequency vibrations was also studied after ventilation was increased with added dead space. The magnitude of hyperventilation an the pattern of ventilatory response produced by tendon stimulation did not change with increased ventilation. In conclusion, the stimulation of muscle spindles in human induces changes in ventilation and pattern of breathing , and the occurrence of a reflex muscular contraction does not seem necessary in order to obtain such effects.