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PubMed2001

Mechanisms of reflexes induced by esophageal distension.

We investigated the mechanisms of esophageal distension-induced reflexes in decerebrate cats. Slow air esophageal distension activated esophago-upper esophageal sphincter (UES) contractile reflex (EUCR) and secondary peristalsis (2P). Rapid air distension activated esophago-UES relaxation reflex (EURR), esophago-glottal closure reflex (EGCR), esophago-hyoid distraction reflex (EHDR), and esophago-esophagus contraction reflex (EECR). Longitudinal esophageal stretch did not activate these reflexes. Magnitude and timing of EUCR were related to 2P but not injected air volume. Cervical esophagus transection did not affect the threshold of any reflex. Bolus diversion prevented swallow-related esophageal peristalsis. Lidocaine or capsaicin esophageal perfusion, esophageal mucosal layer removal, or intravenous baclofen blocked or inhibited EURR, EGCR, EHDR, and EECR but not EUCR or 2P. Thoracic vagotomy blocked all reflexes. These six reflexes can be activated by esophageal distension, and they occur in two sets depending on inflation rate rather than volume. EUCR was independent of 2P, but 2P activated EUCR; therefore, EUCR may help prevent reflux during peristalsis. All esophageal peristalsis may be secondary to esophageal stimulation in the cat. EURR, EHDR, EGCR, and EECR may contribute to belching and are probably mediated by capsaicin-sensitive, rapidly adapting mucosal mechanoreceptors. GABA-B receptors also inhibit these reflexes. EUCR and 2P are probably mediated by slowly adapting muscular mechanoreceptors. All six reflexes are mediated by vagal afferent fibers.

Afferent Pathways↗
PubMed1989

Electrophysiological study of micturition reflexes in rats.

Electrophysiological techniques were used to examine the asynchronous and evoked activity on postganglionic nerves to the urinary bladder in the urethananesthetized rat. Distension of the bladder (0.4-0.6 ml) evoked reflex contractions of the bladder (mean intravesical pressure 28 cmH2O) and efferent firing on postganglionic nerves. Electrical stimulation of afferent and efferent axons in the pelvic nerve elicited short-latency (0.3-11 ms) responses and long-latency (45-170 ms) reflexes on the nerves. The short-latency responses consisted of nonsynaptic axonal volleys with conduction velocities ranging from 0.5 to 11 m/s and synaptic responses with latencies of 6-11 ms. Stimulation of the pelvic nerve elicited late supraspinal reflexes (mean latency 122 +/- 28 ms) in 60% of normal rats and an early reflex (mean latency 56 +/- 5 ms) in 25% of those animals in which a late reflex was also identified. Early reflexes (mean latency 50 +/- 9 ms) were elicited in 100% of chronic spinal animals. The conduction time for the afferent and efferent limbs of the reflexes was calculated to be 7 and 58 ms, respectively, with a central delay of 57 ms for the late and less than 5 ms for the early reflex. It is concluded that sacral parasympathetic input to the urinary bladder of the rat is mediated by supraspinal and spinal reflex pathways. It is likely that in normal animals the late-occurring supraspinal reflex mediates micturition. The significance of the spinal reflex in the normal animals is uncertain; however, this reflex is essential for the generation of automatic micturition in chronic spinal preparations.

Afferent Pathways↗
PubMed2004

Latency of pupillary reflex dilation during general anesthesia.

Areas of insensibility produced by neuraxial anesthesia or peripheral nerve blocks can be detected during general anesthesia by failure of noxious stimulation to trigger pupillary reflex dilation. We examined the latency of pupillary reflex dilation and the effect of fentanyl on the latency of reflex dilation during anesthesia in nine volunteers. We hypothesized that the reflex was generated by slowly conducting C nociceptive fibers and would be significantly delayed if a distal dermatome (L(4)) was stimulated compared with a proximal dermatome (C(5)). We also hypothesized that fentanyl would prolong the latency and alter the shape of the reflex. After induction of general anesthesia, pupillary reflex dilation was measured with an infrared pupillometer every 5 min after stimulations of the L(4) and C(5) dermatomes. Fentanyl (3 microg/kg) was then given intravenously. Pupillary reflex dilation latencies were calculated by examining each individual measurement. After 3 h, naloxone (400 microg) was given intravenously; anesthesia was then discontinued. Pupillary reflex dilation had a long latency and consisted of distinct early and late phases. No differences were found between latencies of reflex dilation after simulation of L(4) and C(5) dermatomes either before or after fentanyl administration. Fentanyl at high concentrations essentially eliminated pupillary reflex dilation; but over the 180-min observation period, first early and then late dilation returned. Fentanyl produced a small increase in the latency of the initial early dilation. We conclude that pupillary reflex dilation during anesthesia is not initiated by slowly conducting C fibers and that fentanyl depresses the reflex in a stereotypical manner.

Adult↗
PubMed2002

Bilateral soleus H-reflexes in humans elicited by simultaneous trains of stimuli: symmetry, variability, and covariance.

Experiments using electrical and mechanical activation of spinal reflexes have contributed important results toward the understanding of neuronal and synaptic dynamics involved in spinal neural circuits as well as their response to different inputs. In this work, data obtained from the simultaneous stimulation of both legs are analyzed to provide information on the degree of symmetry of the respective spinal reflex circuits and on the characteristics of reflex variability. H-reflexes recorded from relaxed muscles show a frequency-dependent amplitude depression when elicited by a train of stimuli. This effect has been attributed to homosynaptic depression. Soleus H-reflexes were recorded in response to trains of simultaneous stimuli applied to both legs in right-handed subjects that were sitting in a relaxed state. The first objective was to verify the existence of asymmetries in H-reflex parameters obtained from the two legs. We measured the mean, variance, and coefficient of variation of the depressed H-reflex amplitudes and the time constant of decay toward the depressed plateau. The second objective was the analysis of the time correlation of subsequent H-reflex amplitudes in a long train of responses recorded from a given leg. The statistical dependence of H-reflex amplitudes in the long trains recorded from both legs was also investigated. Data obtained from preliminary experiments showed that there was no effect of a given stimulus on the contralateral leg applied simultaneously or 1 s before, therefore validating the simultaneous stimulation paradigm. Paired t-tests indicated that several parameters measured bilaterally from soleus H-reflex trains of right-handed subjects were not statistically different in the overall, although individually there were statistically significant asymmetries, toward either the right or left leg. Sequences of H-reflex amplitudes, as measured by the auto-covariance, were either white or had a memory ranging from 2 up to 50 s. This indicates that the random fluctuations in presynaptic inhibition and/or postsynaptic inputs to motoneurons may have either fast or slow time courses. The average auto-covariance sequences of the right and left legs, computed from all subjects, were practically superposable. The cross-covariance between the bilateral H-reflex amplitudes showed a statistically significant peak at zero lag in some experiments, suggesting a correlation between the synaptic inputs to the Ia-motoneuron systems of the soleus muscles of both legs.

Adult↗
PubMed2003

Conditioned H-reflex increase persists after transection of the main corticospinal tract in rats.

The brain shapes spinal cord function throughout life. Operant conditioning of the H-reflex, the electrical analog of the spinal stretch reflex (SSR), is a relatively simple model for exploring the spinal cord plasticity underlying this functional change and may provide a new method for modifying spinal cord reflexes after spinal cord injury. In response to an operant conditioning protocol, rats can gradually increase (i.e., up-training mode) or decrease (i.e., down-training mode) the soleus H-reflex. This study explored the effects of midthoracic transection of the ipsilateral lateral column (LC) (rubrospinal, vestibulospinal, and reticulospinal tracts), the dorsal column corticospinal tract (CST), or the dorsal column ascending tract (DA) on maintenance of an H-reflex increase that has already occurred. Rats were implanted with EMG electrodes in the right soleus muscle and a nerve-stimulating cuff on the right posterior tibial nerve. After initial (i.e., control) H-reflex size was determined, the rats were exposed for 50 days to the up-training mode, in which reward was given when the H-reflex was above a criterion value. H-reflex size gradually rose to 168 +/- 12% (mean +/- SE) of its initial value. Each rat then received an LC, CST, or DA transection and continued under the up-training mode for 50 more days. None of the transections abolished the H-reflex increase. H-reflex size increased further to 197 +/- 19% of its initial value and did not differ significantly among LC, CST, and DA rats (P > 0.78 by ANOVA). Although earlier studies show that the main CST is needed for acquisition of H-reflex up-training and down-training and for maintenance of down-training, this study shows that it is not needed for maintenance of up-training. It adds to the evidence that H-reflex conditioning changes the spinal cord and that the spinal cord plasticity associated with up-training is different from that associated with down-training.

Animals↗
PubMed2003

Intrinsic properties and reflex compensation in reinnervated triceps surae muscles of the cat: effect of activation level.

The manner in which activation levels influence intrinsic muscular properties and contributions of the stretch reflex were studied in homogeneous soleus (SOL) and heterogeneous gastrocnemius (G) muscles in the decerebrate cat. Intrinsic mechanical properties were represented by the initial stiffness of the muscle, measured prior to reflex action, and by the tendency of the muscle to yield during stretch in the absence of the stretch reflex. Stiffness regulation by the stretch reflex was evaluated by measuring the extent to which reflex action reduces yielding and the extent to which stiffness depends on background force. Intrinsic mechanical properties were measured in muscles deprived of effective autogenic reflexes using the method of muscular reinnervation. Reinnervated muscles were recruited to force levels comparable to those achieved during natural locomotion. As force declined during crossed-extension reflexes in reinnervated and intact muscles, initial stiffness declined according to similar convex trajectories. The data did not support the hypothesis that, for a given force level, initial stiffness is greatest in populations of predominantly type I motor units. Incremental stiffness (Deltaf/Deltal) of both G and SOL increased in the presence of the stretch reflex. Yielding of SOL (ratio of incremental to initial stiffness) substantially decreased in the presence of the stretch reflex over the full range of forces. In reflexive G, yielding significantly decreased for low to intermediate forces, whereas at higher forces, yielding was similar irrespective of the presence or absence of the stretch reflex. The stretch reflex regulates stiffness in both homogeneous and heterogeneous muscles.

Animals↗
PubMed1998

Direct comparison of heat-evoked activity of nociceptive neurons in the dorsal horn with the hindpaw withdrawal reflex in the rat.

Although the sensory coding of nociceptive neurons in the dorsal horn has been studied extensively, surprisingly little is known about how these neurons contribute to nociceptive reflexes. The objective of the present study was to examine the characteristics of dorsal horn neurons capable of initiating hindpaw withdrawal. To this end, neural and reflex activity were measured simultaneously in response to noxious radiant heat applied to the hindpaw in lightly anesthetized rats. Subsets of both multireceptive (MR; 52/95) and nociceptive-specific (NS; 19/46) neurons showed a consistent burst of activity that preceded the reflex. However, when compared with NS neurons, MR neurons as a group were: more likely to be active before the reflex (55 vs. 41%); more active before the reflex (31 vs. 23 Hz); and active earlier (2.8 vs. 2.3 s before the reflex). Subsets of MR neurons were active before the reflex regardless of receptive field size or location in the dorsal horn. In contrast, NS neurons with small receptive fields or those located outside of superficial laminae were rarely active before the reflex and thus unlikely to be part of the reflex circuit. These results suggest that current classification schemes, in particular MR and NS categories, cannot be used as the sole criterion to predict involvement in nociceptive reflexes. However, simultaneous measurement of neural and reflex activity provides an opportunity to determine the characteristics of nociceptive neurons involved in withdrawal reflexes.

Animals↗
PubMed1997

Differential effects of noxious conditioning stimulation of the cheek by capsaicin on human sensory and inhibitory masseter reflex responses evoked by tooth pulp stimulation.

In this study, we investigated whether selective activation of nociceptive primary afferent fibers by capsaicin would induce modulations on tooth-pulp-evoked sensory or inhibitory masseter reflex responses in healthy human subjects. The contribution of central N-methyl-D-aspartate (NMDA) receptor mechanisms in capsaicin-induced effects on sensory or reflex responses was evaluated by dextromethorphan, an NMDA-receptor antagonist. The inhibitory masseter reflex was evoked by electrical stimulation (constant current, single pulses) of the upper incisor while the subject was biting at 10% of his maximal force. The sensation of the tooth pulp stimulation was evaluated by visual analogue scale (VAS). The magnitude, duration, and the the latency of the reflex were determined by bite force measurements. The inhibitor masseter reflex could be induced by non-painful tooth pulp stimulation, and the inhibition was enhanced as a function of increasing stimulus intensity. Capsaicin (1%) applied topically to the skin of the cheek produced a spontaneous burning pain sensation. During capsaicin treatment, the VAS ratings for the sensation induced by tooth pulp stimulation were significantly reduced, whereas no significant changes were found in the tooth-pulp-induced masseter reflex responses. Double-blind treatment with dextromethorphan at a dose of 100 mg (= the highest does without side-effects) had no effect on sensory or reflex responses. These data indicate that noxious stimulation of the facial skin by capsaicin induces differential effects on tooth-pulp-evoked sensory and inhibitory masseter reflex responses: Sensory responses are strongly attenuated, while masseter reflex responses are not significantly changed. Dextromethorphan at a clinically applicable dose does not influence tooth-pulp-evoked sensory or reflex responses or their modulation by capsaicin. Furthermore, the lack of modulation of the masseter reflex response by capsaicin differs from the capsaicin-induced enhancement of a nocifensive limb flexion reflex described earlier.

Administration, Cutaneous↗
PubMed1992

Lateralization of the grasp reflex in male and female human newborns.

The lateralization of the grasp reflex was studied in male and female newborns. The mean grasp-reflex strength of the right hand was found to be higher than that of the left hand in males, but the difference was not significant. The mean grasp-reflex strength of the right hand was found to be significantly higher than that of the left hand in females. There was no significant difference between the mean grasp-reflex strengths of the right hand in the male and female subjects. The mean reflex strength of the left hand was found to be higher in males than females; the difference was only marginally significant. The right minus left (R - L) reflex strength showed a significant positive linear relation to the right-and left-reflex strengths in both sexes. This was, however, much more pronounced for the right-reflex than the left-reflex. There was a significantly positive linear correlation between the reflex strengths of the right and left hands and the body weight in males. The females did not show such a relationship between reflex strength and body weight. These sex-related differences in the grasp reflex in newborns were discussed in light of cerebral lateralization and its hormonal modulation.

Body Weight↗
PubMed1992

[Localization of level of lesions in internuclear ophthalmoplegia through assessment of masseter and blink reflex].

The masseter and blink reflexes were investigated in 100 patients with internuclear ophthalmoplegia due to multiple sclerosis (58 patients) or lacunar brainstem infarction (42 patients). In unilateral internuclear ophthalmoplegia, 38 of 60 patients (63.3%) had masseter reflex abnormalities, two patients (3.3%) showed changes of the blink reflex R1 component, and 13 patients (21.7%) combined alterations of the masseter reflex and the blink reflex R1 component. 46 (86.8%) of these 53 patients with electrophysiological abnormalities had unilateral changes, which were ipsilateral to the medial longitudinal fasciculus lesion in 42 patients (91.3%). In bilateral internuclear ophthalmoplegia, 24 of 40 patients (60.0%) had abnormalities of the masseter reflex, two (5.0%) showed changes of the blink reflex R1, and nine (22.5%) combined alterations of the masseter reflex and the blink reflex R1 component. 20 (57.1%) of these 35 patients with electrophysiological abnormalities had bilateral changes. Thus, masseter reflex abnormalities indicating midbrain lesions were seen in 63.3% and 60.0%, respectively, of unilateral and bilateral internuclear ophthalmoplegia. Blink reflex R1 component changes with or without impairment of the masseter reflex indicating rostral pontine to midpontine lesions occurred in 25.0% and 27.5%, respectively. These figures correspond to the results of postmortem examinations and to theoretical considerations based on the length of the medial longitudinal fasciculus.

Adult↗
PubMed1989

Selective inhibitory effects of ethylketocyclazocine on reflex pathways to the external urethral sphincter of the cat.

In the ventral horn of the sacral spinal cord of the cat, opioid terminals are preferentially localized in Onuf's nucleus, an area containing motor neurons that innervate the striated muscle of the external urethral sphincter. The present study was undertaken to 1) compare the effects of selective opioid agonists on sphincter reflex pathways with the effects of these drugs on hindlimb reflexes and urinary bladder reflexes and 2) determine if the physiological inhibition of sphincter reflexes, which accompany bladder contractions, is mediated by endogenous opioids. The effects of intrathecal (i.t.) and i.v. drug administration on bladder activity, sphincter reflexes and reflexes to the hindlimb musculature were monitored in chloralose-anesthetized cats. Ethylketocyclazocine (0.05-500 micrograms i.t.) produced a dose-dependent, naloxone-sensitive, inhibition of sphincter reflexes to less than 10% of control amplitude while having no consistent effects on hindlimb reflexes or bladder activity. D-Ser2-leu5-enkephalin-thr6 (DSLET; 0.1-2.0 micrograms i.t.) abolished rhythmic bladder activity, while having no effects on sphincter or hindlimb reflexes. Larger doses of DSLET (5.0-10 micrograms i.t.) produced a modest reduction of sphincter reflexes (to 60% of control amplitude), without affecting hindlimb reflexes. Naloxone (50 micrograms i.t.) reversed DSLETs marked inhibition of bladder activity, whereas large doses (greater than 250 micrograms i.t.) only partially antagonized DSLETs weak inhibition of sphincter reflexes. Morphine (5-500 micrograms i.t.) had no consistent effect on any of the measures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Morphine microinjected into the nucleus tractus solitarius and rostral ventrolateral medullary nucleus enhances somatosympathetic A- and C- reflexes in anesthetized rats.

The modulatory effects of morphine microinjected into localized areas of the brainstem on somatosympathetic A- and C-reflexes were examined in urethane-anesthetized rats. Somatosympathetic A- and C-reflexes were elicited in a branch of the inferior cardiac nerve by electrical stimulation of myelinated (A) and unmyelinated (C) afferent fibers in the tibial nerve. Morphine (0.002-0.2 microgram/50 nl) was microinjected into the rostral, intermediate and caudal parts of the nucleus tractus solitarius (NTS), the rostral ventrolateral medullary nucleus (RVLM), the caudal ventrolateral medullary nucleus (CVLM), the locus coeruleus (LC), the raphe magnus (RM), the periaqueductal gray (PAG), and the accumbens nucleus (Acb). Microinjections of morphine (0.2 microgram) into the intermediate and caudal NTS produced significant augmentations of the A- and C-reflexes, C-reflexes being more markedly enhanced than A-reflexes. Microinjection of morphine (0.2 microgram) into the RVLM produced a prominent increase in the C-reflex, the threshold dose for a significant increase being 0.02 microgram morphine. Microinjection of morphine up to 0.2 micrograms/50 nl into the other areas mentioned above had no significant effect on either reflex component. All opiate-induced increases of the reflex discharges could be reversed by intravenous application of naloxone (2 mg/ kg). The reflex augmentation induced by microinjection of morphine into the NTS may be caused by suppressing inhibitory baroreceptor information or by enhancing excitatory chemoreceptor information in the NTS. Augmentation of the C-reflex induced by microinjection of morphine into the RVLM may be caused by facilitating C-reflex pathways or by suppressing inhibitory neural circuits involved in the C-reflex within the RVLM.

Afferent Pathways↗
PubMed1989

Topical anesthetics: effects on the Achilles tendon and H-reflexes. I. Able-bodied subjects.

Achilles tendon reflexes (ATR) and H-reflexes were monitored to determine changes in motor responses after the application of a benzocaine spray or an air spray to normal individuals. There was no change in ATR after application of the spray or the benzocaine, even when the sequence of reflex elicitation was reversed. The only significant change (p less than 0.05) in the H-reflex was an increase in its amplitude from baseline at all posttest times following (1) the placebo application when the H-reflex preceded the ATR (0.264 +/- 0.054V, ten minutes; 0.290 +/- 0.054V, 20 minutes; and 0.322 +/- 0.058V, 30 minutes), and (2) the benzocaine spray when the ATR preceded the H-reflex (0.277 +/- 0.084V, ten minutes; 0.309 +/- 0.152V, 20 minutes; and 0.329 +/- 0.131V, 30 minutes). Within-group comparisons revealed that a significantly greater H-reflex (p less than 0.05) was obtained at 20 and 30 minutes after air spray when H-reflex/ATR test sequence was used, whereas at 30 minutes after application of the benzocaine spray a significantly greater H-reflex was seen using the ATR/H-reflex test sequence. Changes in H-reflex amplitude appear to be as much a function of the reflex testing sequence as whether an air or benzocaine spray is used.

Achilles Tendon↗
PubMed1989

Modulation of spinal reflexes by pyramidal tract stimulation in an in vitro brainstem-spinal cord preparation from the hamster.

Electrophysiological evidence is presented showing that the pyramidal tract (PT) of the hamster modulates spinal reflexes in an in vitro brainstem-spinal cord preparation. Three spinal reflexes were studied. Stimulation of a dorsal root (DR) while recording from a ventral root (VR) of the same spinal segment evoked two reflexes: the monosynaptic reflex, and a long latency polysynaptic reflex. Stimulation of a DR while recording from a DR immediately rostral to it elicited a volley of antidromic discharges characteristic of the dorsal root reflex (DRR). The effect of PT stimulation on reflex transmission was tested by stimulating the PT at varying intervals prior to evoking a reflex. The results show that the amplitude of the monosynaptic reflex is progressively inhibited when preceded at shorter delays by a train of PT stimuli. Similarly, PT stimulation also suppresses the long latency reflex. In contrast, the PT facilities the DRR and repeated stimulation of the PT may evoke antidromic discharges recorded from the DRs. These data from the in vitro brainstem-spinal cord preparation indicate that the PT of the hamster exerts both inhibitory and facilitatory effects on reflex transmission in the spinal cord. The present study shows that it is possible to examine the descending control of spinal circuitry using an in vitro brainstem-spinal cord preparation.

Action Potentials↗
PubMed1990

Amplitude modulation of the human quadriceps tendon jerk reflex during gait.

Amplitude modulation of the quadriceps tendon jerk reflex was investigated during the step cycle in normal human subjects. Reflex amplitude was compared with that obtained during a control stance condition, with "equivalent" levels of EMG activity and limb position. During gait there was a progressive decrease in the reflex amplitude early in the stance phase, i.e. during yielding of the knee, and it remained reduced throughout the step cycle. This pattern of changes in reflex amplitude correlated with neither the quadriceps EMG activity nor with the knee joint movements. The behavior of the tendon reflex was similar to that described for the modulation of the quadriceps H-reflex during the early stages of the stance phase of gait. In the latter study it was argued that changes in presynaptic inhibition of quadriceps la terminals could account for the amplitude modulation. We conclude that there is no dramatic change in the gamma drive to quadriceps muscle spindles: tendon reflexes are modulated during the step cycle in much the same way as H-reflexes, in spite of the peripheral and central differences between them. Similar behavior has been described for the soleus H-reflex and Achilles tendon reflex during gait although the modulation of these reflexes followed a different pattern than that seen in the quadriceps.

Achilles Tendon↗
PubMed2002

Afferent mechanisms for the reflex response to imposed ankle movement in chronic spinal cord injury.

We have reported earlier that externally imposed ankle movements trigger ankle and hip flexion reflexes in individuals with spinal cord injury (SCI). In order to examine the afferent mechanisms underlying these movement-triggered reflexes, controlled ankle movements were imposed in 17 SCI subjects. In 13 of these subjects, reflex torques were recorded at the hip, knee and ankle in response to 5 ankle movement ranges, and 4 movement speeds. Subjects were tested using both ankle plantarflexion and dorsiflexion movements. The principal outcome measure, peak hip flexion torque of the induced reflexes, was used for comparing the effects of movement range and speed on the reflex response. We found that movement-triggered reflexes were sensitive to the angular range of ankle deflection, but insensitive to the velocity of the movement. Movement amplitudes sufficient to trigger hip and ankle flexion were routinely associated with increases in ankle passive force, suggesting that force-sensitive receptors participated in the reflex response. However, increases in angular range also corresponded to increases in muscle length, making it difficult to distinguish whether the response was triggered by a load-sensitive receptor (e.g., Golgi tendon organ or muscle free nerve ending) or a position-sensitive receptor responsive to absolute ankle angle (e.g., muscle spindle secondary afferent). The absence of velocity dependence of the reflex suggested that spindle Ia afferents were not major contributors. These results suggest movement-triggered reflexes originate in muscle receptors that are sensitive to either absolute muscle length, to muscle force or to both. Although receptors that are sensitive to absolute muscle length cannot be excluded with certainty, the finding that reflex responses require that ankle movements elicit an increase in passive force argues for a prominent role of nonspindle mechanoreceptors, such as group III/IV muscle afferents. These afferents are activated preferentially as muscles are stretched to near maximum length, and they appear to have potent reflex effects in spinal cord injury.

Adolescent↗
PubMed2000

Low frequency depression of H-reflexes in humans with acute and chronic spinal-cord injury.

We measured low-frequency depression of soleus H-reflexes in individuals with acute (n=5) and chronic (n=7) spinal-cord injury and in able-bodied controls (n=7). In one acute subject, we monitored longitudinal changes in low-frequency depression of H-reflexes over 44 weeks and examined the relationship between H-reflex depression and soleus-muscle fatigue properties. Soleus H-reflexes were elicited at 0.1, 0.2, 1, 5, and 10 Hz. The mean peak-to-peak amplitude of ten reflexes at each frequency was calculated, and values obtained at each frequency were normalized to 0.1 Hz. H-reflex amplitude decreased with increasing stimulation frequency in all three groups, but H-reflex suppression was significantly larger in the able-bodied and acute groups than in the chronic group. The acute subject who was monitored longitudinally displayed reduced low-frequency depression with increasing time post injury. At 44 weeks post injury, the acute subject's H-reflex depression was similar to that of chronic subjects, and his soleus fatigue index (assessed with a modified Burke fatigue protocol) dropped substantially, consistent with transformation to faster muscle. There was a significant inverse correlation over the 44 weeks between the fatigue index and the mean normalized H-reflex amplitude at 1, 5, and 10 Hz. We conclude that: (1) the chronically paralyzed soleus muscle displays impaired low-frequency depression of H-reflexes, (2) attenuation of rate-sensitive depression in humans with spinal-cord injury occurs gradually, and (3) changes in H-reflex excitability are generally correlated with adaptation of the neuromuscular system. Possible mechanisms underlying changes in low-frequency depression and their association with neuromuscular adaptation are discussed.

Acute Disease↗
PubMed2001

[Reevaluation of physiological mechanisms generating the stretch reflex: new hypotheses on the physiopathology of spasticity].

INTRODUCTION: Spasticity has been defined as tendon reflex exaggeration and increased muscle reflex contraction in response to its stretch (Lance, 1980). It has been generally admitted that stretch reflex exaggeration was due to myotatic reflex hyperexcitability (Ia fibre-motoneurone synapses). This interpretation has been recently revisited taking into account neurophysiological data obtained in cat and recent data obtained in spastic patients. PROBLEMATICS: Myotatic reflex has been described in decerebrate cat in 1924 by Liddel and Sherrington. In 1943, Lloyd demonstrated that myotatic reflex was due to monosynaptic Ia fibre motoneurone alpha synapses. Almost all the following studies of stretch reflexes were devoted to monosynaptic reflexes both in animal and humans. In fact, the existence of group II fibres coming also from spindles and some restricted experiments performed in man have led to discuss the role of group II fibres in the static component of the stretch reflexes. RESULTS: Recent studies performed in humans have shown that group II fibres play an important role in the development of stretch reflexes in leg muscles and that in spastic hemiplegic patients group II fibres facilitatory effects was deeply increased. DISCUSSION: Results obtained both in humans and animals suggest that group II fibres play also a role in a stretch reflex and led to consider that the pathophysiological modifications of group II effects could contribute to spasticity. CONCLUSION: Modifications of network fed by group II fibres and modifications of muscular fibres intrinsic properties are likely to play a role in the developments of spasticity in humans.

Animals↗