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PubMed1996

Nitrous oxide depresses somatocardiac sympathetic A- and C-reflexes in anesthetized rats.

Effect of nitrous oxide (N2O) on the somatosympathetic A- and C-reflexes was investigated using artificially ventilated rats anesthetized with alpha-chloralose and urethane. Somatocardiac sympathetic A- and C-reflexes were elicited in the inferior cardiac nerve by electrical stimulation of A and C afferent fibers of the tibial nerve, respectively. Both reflexes were depressed by inhalation of N2O for 20 min. The depression was greater in the C-reflex than in the A-reflex. The depressive effects of N2O on both reflexes were unchanged after pretreatment with intravenous naloxone (0.2 or 2.0 mg/kg) or by prolongation of the inhalation of N2O for 2 h. These results suggest that the opioid receptor is not involved and that acute tolerance is not developed in the depressive action of N2O on the somatosympathetic A- and C-reflexes.

Anesthetics, Inhalation↗
PubMed1996

Systemic hypoxia facilitates somato-cardiac sympathetic A- and C-reflexes in anesthetized rats.

In rats anesthetized with urethane, electrical stimuli applied to tibial nerve afferents produced a somato-sympathetic A-reflex of 41 +/- 2 (mean +/- SEM)ms latency and C-reflex of 210 +/- 13 ms latency recorded in the left inferior cardiac sympathetic nerve. Hypoxia was induced by switching room air to nitrogen/oxygen gas mixture in the inspiratory line reducing end-tidal oxygen from about 18% FETO2 to 10% FETO2 and 6% FETO2 for 60s, respectively. During 6% FETO2 hypoxia, the amplitude of the somato-cardiac sympathetic A-reflex increased significantly to 138 +/- 13% of the control, and that of the C-reflex increased to 186 +/- 18% of the control. During 10% FETO2 hypoxia, the A-reflex increased insignificantly to 117 +/- 8%; the amplitude of the C-reflex was augmented significantly to 149 +/- 11% of the control. Peripheral carotid chemoreceptor denervation abolished the facilitatory effects of systemic hypoxia. It is concluded that carotid chemoreceptor stimulation enhances the responsiveness of somato-cardiac sympathetic excitatory reflexes originating in the hind limb receptors.

Animals↗
PubMed1980

Local electrical stimulation: effective needling points for suppressing jaw opening reflex in rat.

Effects of electroacupuncture on the jaw opening reflex after tooth pulp stimulation were investigated in lightly anesthetized rats. Electroacupuncture stimulation (45 Hz, 5 msec) was delivered to 8 meridian points and 6 nonmeridian ones for 15 min so as to compare the degree of suppression elicited from each point. Significant suppressive effects on the reflex were observed in the cases of Yin-Hsiang, Ho-Ku and Shou-Sanli stimulation and these effects were antagonized by naloxone. However, stimulation of Hsia-Kuan, Chu-Chih, Neiting and Taichi, although these points were reported to suppress oro-facial or dental pain in man, scarcely produced suppressive effects. On the other hand, stimulation of some nonmeridian points produced moderate analgesic effects as gauged by the jaw opening reflex. The present study revealed that specificity of the meridian points is not absolute, but relative and that Yin-Hsiang, Ho-Ku and Shou-Sanli points were fairly effective in suppressing pulp-evoked jaw opening reflex in rat, which is presumably a noxious reflex. When the jaw opening reflex was evoked by non-pulpal stimulation, electroacupuncture was less effective on the reflex.

Acupuncture Therapy↗
PubMed1987

Inhibition of the human flexion reflex by low intensity, high frequency transcutaneous electrical nerve stimulation (TENS) has a gradual onset and offset.

The present study examines the inhibitory effect of segmentally applied TENS on the nociceptive component of the flexion reflex elicited in various lower limb muscles, in an attempt to gain some insight into the underlying mechanism. The flexion reflex from 11 normal subjects was recorded electromyographically from the biceps femoris (BF), the tibialis anterior (TA), and in 2 subjects, the hip flexor (HF), in the manner described in a previous paper [9]. Amplitude and area values of the flexion reflex of each muscle were computerized prior to, during, and 50 min after the application of placebo or low intensity TENS at 100 Hz, for 30 min to the low back, at levels of segmental innervation (L4-S1) similar to those of the muscles under study. In the majority of subjects, we found that: Low intensity TENS caused a significant inhibition of the flexion reflex in proximal limb flexors. Thus, the BF measured 64% and 52%, and the HF 45% and 51%, of their respective mean control amplitude and area values at the time of maximum inhibition during TENS. Moreover, less reduction of the mean values of the flexion reflex was observed in the TA, a distal limb (ankle) flexor. It is noteworthy that in both the BF and HF, the time to peak maximum inhibitory effect took 30 and 20 min respectively after the onset of TENS, and the flexion reflex often did not return to control values even at 40-50 min after TENS. In contrast, placebo TENS application resulted in no significant change of the flexion reflex in all the muscles examined. These findings showed that prolonged stimulation of large diameter fibers by conventional TENS application to the lumbosacral level, exerts a progressive and long latency inhibitory influence on a number of lower limb flexor motoneurons. In keeping with functional demand, this effect was found to be more prominent on the proximal than distal limb muscles. Furthermore, a gradual onset and offset of this inhibitory action is consistent with the results of some investigators demonstrating the possible involvement of endogenous opioids.

Electric Stimulation Therapy↗
PubMed1996

Suppression of an inhibitory jaw reflex by the anticipation of pain in man.

Electromyographic recordings (EMGs) were made from the active masseter muscle, of the inhibitory reflex evoked by application of electrical stimuli to the skin of the upper lip in 15 human subjects. In control sequences, the reflex had a mean latency and duration (+/- S.E.M.) of 45.4 +/- 1.3 msec and 47.9 +/- 2.8 msec, respectively. Significant decreases in the reflex as well as increases in heart rate and anxiety levels assessed by a visual analogue scale, occurred when the subjects were stressed by the anticipation of receiving painful electrical stimuli above the ankle (P < 0.00005; Student's t-tests). During such sequences, the magnitude of the reflex measured by integration of the EMG, was reduced by 47.7 +/- 5.6%. This effect involved a reduction in both the duration and depth of the inhibitory wave. It occurred regardless of whether the painful stimuli were applied during or after the recording of the reflex and of whether the baseline activity in the muscle was inadvertently raised or lowered during the stressful sequences. It is concluded that stress induced by the anticipation of pain, can markedly reduce an inhibitory jaw reflex in man by exerting an influence on the reflex pathway prior to the motoneurones.

Adult↗
PubMed1985

Effects of glutamate, substance P and eledoisin-related peptide on solitary tract neurones involved in respiration and respiratory reflexes.

Recent studies have implicated glutamate and substance P in synaptic transmission in the nuclei tractus solitarii and in central regulation of cardiorespiratory functions. Consequently, in chloralose-anaesthetized cats that were artificially ventilated, we examined the effects of the microiontophoretic application of both chemicals (and the substance P homologue, eledoisin-related peptide) on single neurones of the nuclei tractus solitarii implicated in the control of respiration and respiratory tract reflexes. These neurones were functionally identified as either respiratory neurones or presumed reflex interneurones, and showed functional properties comparable to those previously documented for each of these two types. The iontophoretic application of glutamate produced an excitation of rapid onset in 23 or 25 reflex interneurones tested, but the respiratory neurones showed a differential sensitivity: one type (n = 32) was "glutamate-sensitive" and showed rapid excitation with glutamate applications of less than 30 nA, the other type of respiratory neurone (n = 26) was termed "glutamate-insensitive" since it either showed excitation only with applications of 60 nA or more or showed no response even with currents up to 94 nA. Each neurone studied was clearly of one type or the other. Glutamate could increase the number of spikes per rhythmic burst and the burst duration of respiratory neurones, it facilitated evoked activity in the reflex interneurones and in those respiratory neurones having a superior laryngeal nerve or vagus nerve afferent input, and the magnitude of the excitatory responses to glutamate varied directly with the amount of ejecting current. Substance P and eledoisin-related peptide also had excitatory effects on respiratory neurones and reflex interneurones, but compared with glutamate-induced effects the excitation was slower in onset and more prolonged in after-discharge. Both rhythmic and evoked activity could be facilitated, and the magnitude of the effect varied directly with the magnitude of the ejecting current. In showing that both glutamate and substance P (and its analogue, eledoisin-related peptide) have excitatory effects on the activity of respiratory neurones and reflex interneurones, this study provides evidence suggesting that these neurones have receptors for these neural chemicals, supportive of a role for each chemical in the regulation of respiration and respiratory tract reflexes.

Animals↗
PubMed1989

Topical versus systemic capsaicin desensitization: specific and unspecific effects as indicated by modification or reflex micturition in rats.

The aim of this study was to determine the acute and delayed effect of topical application of high concentrations of capsaicin on the rat urinary bladder on micturition reflex and compare the effects of "topical" bladder desensitization with those produced by systemic (subcutaneous administration) capsaicin desensitization. On acute application, capsaicin (1-3%) produced a transient bladder contraction, not observed in capsaicin-pretreated rats. After a transient increase in excitability of the micturition reflex, topical capsaicin suppressed micturition and overflow incontinence ensued which was reverted by intravenous injection of 4-aminopyridine. Topical capsaicin also abolished reflex micturition in rats which had been systemically treated with capsaicin as adults (50 mg/kg, 7 days before) and reduced significantly the neurogenic bladder contractions produced by intravenous dimethylphenylpiperazinium or neurokinin A, while the direct (myogenic) response to neurokinin A was unaffected. In rats whose bladder was pre-exposed to 1-3% topical capsaicin (7 days before) the micturition reflex was affected in a manner which is qualitatively and quantitatively similar to that observed in rats treated with capsaicin as adults, e.g. increase in bladder capacity with no change in voiding efficiency. Topical capsaicin desensitization of the rat urinary bladder was shown to produce a selective impairment of bladder sensory nerves without any sign of desensitization in other areas of the body using both functional (hot plate, wiping, plasma extravasation) and neurochemical (determination of substance P-like immunoreactivity) assays. Systemically administered capsaicin (7 days before) had little effect on reflex micturition at 12.5 mg/kg but the change in bladder capacity produced at a dose of 25 mg/kg was comparable with that produced at 350 mg/kg. These findings provide evidence that selective desensitization of peripheral terminals of capsaicin-sensitive nerves of the rat urinary bladder inactivates their sensory and "efferent" function in a manner similar to that observed after systemic capsaicin desensitization in adult rats. The functional deficit of reflex micturition produced in this way can be overcome by increasing the stimulus to void. By contrast, neonatal capsaicin desensitization produced a long lasting abolition of reflex micturition. These data are in keeping with the hypothesis that adult versus neonatal capsaicin desensitization may be used as a tool to distinguish between two sets of sensory nerves in the rat urinary bladder.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗
PubMed1992

Serotonergic fibers induce a long-lasting inhibition of monosynaptic reflex in the neonatal rat spinal cord.

The transmitter mechanism of a long-lasting descending inhibition of the monosynaptic reflex was investigated in the isolated spinal cord of the neonatal rat. The monosynaptic reflex elicited by dorsal root stimulation was recorded extracellularly from a lumbar ventral root (L3-L5). Electrical stimulation of the upper thoracic part of the hemisected cord caused an inhibition lasting about 40 s of the monosynaptic reflex. This descending inhibition was markedly attenuated by perfusing the spinal cord with reserpine (1 microM) or 5,7-dihydroxytryptamine (10 microM) for 2-6 h. The perfusion with reserpine (1 microM) for 4 h significantly decreased the contents of 5-hydroxytryptamine, dopamine, and norepinephrine of the neonatal rat spinal cord, whereas the perfusion with 5,7-dihydroxytryptamine (10 microM) for 4 h decreased the contents of 5-hydroxytryptamine and dopamine. The descending inhibition was markedly potentiated by a 5-hydroxytryptamine uptake blocker, citalopram (10 nM), and was blocked by a 5-hydroxytryptamine antagonist, ketanserin (10-100 nM). Application of 5-hydroxytryptamine to the spinal cord induced an inhibition of the monosynaptic reflex, a later part of which was blocked by ketanserin. Ketanserin also moderately blocked inhibitions of the monosynaptic reflex caused by norepinephrine and dopamine. Phentolamine (10 microM) abolished the depressant actions of norepinephrine and dopamine, but did not affect that of 5-hydroxytryptamine or the descending inhibition. These results strongly suggest the involvement of 5-hydroxytryptamine, but not dopamine nor norepinephrine, in the descending inhibition. Besides ketanserin, the descending inhibition was blocked by ritanserin, haloperidol, and pipamperone, which have affinities to 5-hydroxytryptamine2 receptors, and also by spiperone and methiothepin, which are antagonists at both 5-hydroxytryptamine1 and 5-hydroxytryptamine2 receptors (all 1 microM). On the other hand, a 5-hydroxytryptamine1C and 5-hydroxytryptamine2 antagonist, mesulergine (1 microM), and 5-hydroxytryptamine3 antagonists, ICS 205-930 and quipazine (both 1 microM), did not depress either the descending inhibition or the 5-hydroxytryptamine-evoked inhibition of the monosynaptic reflex. The results with these antagonists favor the involvement of 5-hydroxytryptamine2 receptors although the results with mesulergine disagree with this notion. 5-Hydroxytryptamine1 agonists, such as 8-hydroxy-2-(di-n-propylamino)tetralin, buspirone, and 5-carboxyamidotryptamine, and a 5-hydroxytryptamine3 agonist, 2-methyl-5-hydroxytryptamine, induced a long-lasting inhibition of the monosynaptic reflex, which was blocked by ketanserin whereas a 5-hydroxytryptamine2 agonist, S-(+)-alpha-methyl-5-hydroxytryptamine, evoked a biphasic inhibition, in which only the later component was blocked by ketanserin.(ABSTRACT TRUNCATED AT 400 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1995

NK1-tachykinin receptors and prolonged, stimulus-evoked alterations in the excitability of withdrawal reflexes in the decerebrated and spinalized rabbit.

Intense natural or electrical stimulation of afferents from the toes or the heel results in prolonged changes in the excitability of the heel withdrawal reflex pathway in the rabbit. This study has investigated the roles played by tachykinin NK1 receptors in mediating these effects. Reflexes were evoked by electrical stimulation of the sural nerve and recorded from the gastrocnemius medialis muscle nerve. High-intensity electrical stimulation of the common peroneal nerve, or application of a crush stimulus to the toes, resulted in suppression of gastrocnemius reflex responses to between 30 and 50% of controls, from which recovery was complete in 15-25 min. In contrast, intense electrical stimulation of the sural nerve, or application of mustard oil to the heel, facilitated the sural to gastrocnemius reflex to two to four times control values. Recovery was rarely complete within 30 min of these stimuli. Administration of the NK1 receptor antagonist CP-96,345, but not its enantiomer CP-96,344, reduced gastrocnemius reflex responses to sural nerve stimulation per se; significantly decreased the time to recovery after common peroneal nerve stimulation and toe crush (but did not affect maximum inhibition); and significantly reduced the facilitation of reflexes resulting from sural nerve stimulation or mustard oil applied to the heel in the first 3-5 min after the application of the stimuli. Both CP-96,345 and CP-96,344 reduced blood pressure and heart rate. These data show that: (i) blockade of NK1-receptors reduces excitatory drive from sural nerve afferents to GM motoneurones; (ii) NK1-receptors are involved in the generation of the early excitatory events which follow stimulation of nociceptive afferents from the heel; and (iii) have a role in the later stages of prolonged, opioid-mediated inhibition of reflexes resulting from activation of fine afferents from the toes. We believe that (ii) and (iii) reflect a role for tachykinins as transmitters from small diameter primary afferent fibres.

Afferent Pathways↗
PubMed1992

Altered postural reflexes in Parkinson's disease: a reverse hypothesis.

In subjects standing on a movable platform, sudden dorsiflexion of the ankle joint elicits a set of reflexes in leg muscles. These responses include a short latency (SL) and medium latency (ML) stretch reflex in the gastrocnemius muscle and a distal to proximal innervation sequence of long latency (LL) reflexes in the shortened tibialis anterior and vastus lateralis muscles. Because of their role in maintaining upright stance these responses have been termed postural reflexes. In patients with Parkinson's disease (PD), the following abnormalities have been described: 1) enhanced ML-amplitudes; 2) a reversed LL innervation sequence; and 3) delayed onset latencies. These abnormalities are thought to be due to defective motor programming and disturbed control of spinal and supraspinal reflex centers by basal ganglia circuits. The altered reflexes have been held responsible for some of the clinical features of PD, including balance impairment and rigidity. In this paper, we argue the reverse hypothesis that postural reflexes are essentially normal in PD, and that the observed alterations are at least in part consequence rather than cause of balance impairment, the stooped parkinsonian posture and rigidity of PD patients.

Humans↗
PubMed1995

Soleus H reflex extinction in controls and spastic patients: ordered occlusion or diffuse inhibition?

Extinction of the soleus H reflex at higher stimulus intensities is commonly attributed to retrograde conduction of action potentials in motor axons. This study was designed to gain further insight into the mechanisms underlying the extinction. The decrease of the H reflex was quantified in a group of controls and spastic patients, with and without depression of the H response by continuous tendon vibration. Response amplitudes were normalized as a percentage of the maximal M wave amplitude. Stimuli were normalized as a multiple of the M wave threshold. After normalization, the mean M recruitment curves, and similarly the fractions of motor axons activated, were equal in each group. In contrast, the mean H reflex amplitudes at the M threshold were different. The mean H reflex decrease, between 1.0 and 1.5 times the M threshold, was found to be the same fraction of the maximal H reflex amplitude in each group. The largest motor fibres, belonging to the largest motoneurones, are traditionally thought to have the lowest threshold for electrical excitation. Collision or retrograde inactivation should therefore preferentially affect the largest motoneurones, employed in only the largest H reflexes, at the lowest stimulus intensities. Our results are contrary to this hypothesis. Renshaw and/or Ib inhibition is likely to play a role in the initial decrease of the H reflex at higher stimulus intensities.

Adolescent↗
PubMed2005

Somatotopic arrangement of sudomotor axon reflex sweating in humans.

BACKGROUND: Impaired sweating may be one of the first symptoms in neuropathies, and therefore the evaluation of sweating might facilitate their early detection. Sudomotor axon reflexes can be quantified by two different methods: quantitative sudomotor axon reflex testing (QSART) measures the amount of local sweating, whereas staining with the iodine starch reaction assesses the extension of the sudomotor axon reflex area. The aim of our study was to compare both tests at three different sites on the leg: foot, lower leg and thigh. METHODS: QSART and iodine starch staining after iontophoretic stimulation with acetylcholine were performed on 15 male volunteers (mean age: 25; range 24-27 years) on the left resp. the right leg during a single session. RESULTS: QSART response, measured as area under the curve (AUC), was maximal at the lower leg (911 AUC), smaller at the dorsum of the foot (585 AUC) and even smaller at the thigh (480 AUC). The difference between lower leg and thigh was significant (p < 0.02). The sudomotor axon reflex area was also biggest on the lower leg (39 cm(2)) followed by the foot dorsum (28 cm(2)), and then the thigh (16 cm(2)). The differences between lower leg and thigh as well as between lower leg and foot were significant (p < 0.01, resp. p < 0.04). The size of the sudomotor axon reflex areas and QSART responses were correlated (p < 0.01). CONCLUSIONS: QSART and sudomotor axon reflex areas had similar somatotopic arrangements in human skin. The bigger the axon reflex area was the stronger the QSART response was. This indicates that the size of the innervation territories of sudomotor fibres covaries with the amount of local sweat production. The latter is a surrogate for increased sweat gland density or capacity in skin areas of dense sudomotor innervation.

Acetylcholine↗
PubMed2006

Pre- and post-alpha motoneuronal control of the soleus H-reflex during sinusoidal hip movements in human spinal cord injury.

The aim of this study was to establish the contribution of hip-mediated sensory feedback to spinal interneuronal circuits during dynamic conditions in people with incomplete spinal cord injury (SCI). Specifically, we investigated the effects of synergistic and antagonistic group I afferents on the soleus H-reflex during imposed sinusoidal hip movements. The soleus H-reflex was conditioned by stimulating the common peroneal nerve (CPN) at short (2, 3, and 4 ms) and long (80, 100, and 120 ms) conditioning test (C-T) intervals to assess the reciprocal and pre-synaptic inhibition of the soleus H-reflex, respectively. The soleus H-reflex was also conditioned by medial gastrocnemius (MG) nerve stimulation at C-T intervals ranging from 4 to 7 ms to assess changes in autogenic Ib inhibition during hip movement. Sinusoidal hip movements were imposed to the right hip joint at 0.2 Hz by the Biodex system while subjects were supine. The effects of sinusoidal hip movement on five leg muscles along with hip, knee, and ankle joint torques were also established during sensorimotor conditioning of the reflex. Phase-dependent modulation of antagonistic and synergistic muscle afferents was present during hip movement, with the reciprocal, pre-synaptic, and Ib inhibition to be significantly reduced during hip extension and reinforced during hip flexion. Reflexive muscle and joint torque responses--induced by the hip movement--were entrained to specific phases of hip movement. This study provides evidence that hip-mediated input acts as a controlling signal of pre- and post-alpha motoneuronal control of the soleus H-reflex. The expression of these spinal interneuronal circuits during imposed sinusoidal hip movements is discussed with respect to motor recovery in humans after SCI.

Adult↗
PubMed2006

Effects of long-term food restriction on genital reflexes in paradoxically sleep-deprived male rats.

The purpose was to ascertain whether the different schedules of long-term food restriction (FR) exert influence on genital reflexes (penile erection-PE and ejaculation-EJ) induced by paradoxical sleep deprivation (PSD) in male rats. Diet restriction began at weaning with 6 g/day and food was increased by 1 g per week until reaching 15 g/day by adulthood. Rats submitted to FR and those fed ad libitum were distributed into PSD or maintained as control groups and challenged with saline or cocaine. The results indicated that PSD+saline induced PE and EJ in both ad libitum and FR groups, but cocaine only potentiated reflexes in ad libitum group. In an attempt to revert the effects of FR on genital reflexes, we provided food ad libitum to the restricted group during the PSD period (4 days). When compared to FR rats, an increase in the frequency of PE was observed in the FR group fed ad libitum during PSD (both groups were challenged with cocaine). Further, we sought to investigate motivational behavior by placing food within the behavioral cage during the evaluation of genital reflexes. The FR PSD+saline group challenged with food did not display genital reflexes but when injected with cocaine the responses were similar to those observed in FR PSD+cocaine rats not challenged with food. Our data suggest that the facilitatory effect of PSD on genital reflexes did not override the inhibitory effect of FR on erectile function, but different schedules of FR produce distinct effects on genital reflexes. Further studies are warranted to dissect the effect of food restriction on sexual behavior.

Animals↗
PubMed2004

Cutaneous reflexes from the foot during gait in hereditary spastic paraparesis.

OBJECTIVE: It is known that P2 cutaneous reflexes from the foot show phase-dependent modulation during gait. The role of the motor cortex and the cortico-spinal tract in these reflexes and their modulation is unknown. Patients with hereditary spastic paraparesis (HSP) have a lesion in the cortico-spinal tract and may show deficits in P2 reflexes and/or their modulation. METHODS: Reflex responses of tibialis anterior and biceps femoris after sural nerve stimulation in 10 HSP-patients were compared with those in 10 healthy subjects. The reflexes were studied at two different moments in the step cycle during walking on a treadmill. RESULTS: Both patients and controls showed a phase-dependent modulation of P2 responses. For the individual muscles, no significant difference in reflex activity was observed between HSP-patients and the controls. However, when all muscles were taken together, the reflex activity for the controls was significantly higher than for the patients. CONCLUSIONS: The results of this study suggest that the cortico-spinal tract is involved in the regulation of the amplitude of the P2 responses and their phase-dependent modulation.

Adult↗
PubMed2004

Stretch reflexes in the human masticatory muscles: a brief review and a new functional role.

Stretch reflexes play a vital role in fine-tuning movements and in automatically maintaining posture. This article briefly reviews the operation of the stretch reflex in the human masticatory system. The conventional approach of stretching muscles in an open-loop manner has yielded much valuable information on the operation of this reflex. In particular, it has revealed that stretching the jaw-closing muscles evokes a reflex response with two major components. The short-latency reflex is favoured when stretches are brisk, but slower stretches evoke an additional long-latency component. In the hand muscles, the long-latency response is transcortical: in the masticatory muscles, it is not. In addition to its role in servo-control of muscle length during chewing, the stretch reflex in the jaw-closing muscles maintains the vertical position of the mandible during vigorous head movements such as those that occur during running, jumping, hopping and other vigorous whole-body movements in which the head moves briskly up and down. This is an interesting model system in which to investigate stretch reflexes with natural stimuli under unrestrained, physiological conditions.

Electromyography↗
PubMed2006

Effects of postural anxiety on the soleus H-reflex.

Previous research has proposed that spinal reflex modulation may mediate anxiety-related changes in postural control. This study investigated how soleus H-reflex amplitude was influenced by standing at heights that induced different levels of anxiety. H-reflexes were elicited in 15 participants standing at the center and edge of a platform raised from a low to a high height (with and without vision). Increased skin conductance confirmed the anxiety effect of elevated surface heights. When standing at the edge of the platform with vision, H-reflex amplitude was attenuated in the high compared to low height condition. Changes in background muscle activity could not explain observed H-reflex changes, suggesting the potential involvement of pre-synaptic inhibition or fusimotor drive on anxiety-related changes in reflex modulation. This study reveals that healthy participants reduce spinal reflex excitability in the presence of increased postural anxiety and a postural threat imposed by standing at the edge of a raised platform. These findings have implications for understanding control of standing balance in individuals with postural instability and/or fear of falling, such as the elderly or stroke.

Adult↗
PubMed2006

Role of reflex dynamics in spinal stability: intrinsic muscle stiffness alone is insufficient for stability.

Spinal stability is related to both the intrinsic stiffness of active muscle as well as neuromuscular reflex response. However, existing analyses of spinal stability ignore the role of the reflex response, focusing solely on the intrinsic muscle stiffness associated with voluntary activation patterns in the torso musculature. The goal of this study was to empirically characterize the role of reflex components of spinal stability during voluntary trunk extension exertions. Pseudorandom position perturbations of the torso and associated driving forces were recorded in 11 healthy adults. Nonlinear systems-identification analyses of the measured data provided an estimate of total systems dynamics that explained 81% of the movement variability. Proportional intrinsic response was less than zero in more than 60% of the trials, e.g. mean value of P(INT) during the 20% maximum voluntary exertion trunk extension exertions -415+/-354N/m. The negative value indicated that the intrinsic muscle stiffness was not sufficient to stabilize the spine without reflex response. Reflexes accounted for 42% of the total stabilizing trunk stiffness. Both intrinsic and reflex components of stiffness increased significantly with trunk extension effort. Results reveal that reflex dynamics are a necessary component in the stabilizing control of spinal stability.

Humans↗