Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “REFLEX”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,099 records · Page 61Linked to original sources

Endogenously released 5-hydroxytryptamine depresses the spinal monosynaptic reflex via 5-HT1D receptors.

In the spinal cord, various 5-hydroxytryptamine (5-HT) receptor subtypes are involved in the modulation of motor output. Previously, we have shown that 5-HT1B receptors mediate the monosynaptic reflex depression induced by exogenously applied 5-HT that was formed from the precursor L-5-hydroxytryptophan in spinalized rats. In this study, we determined the effects of endogenous 5-HT, which was released from serotonergic terminals by DL-p-chloroamphetamine, on spinal reflexes. DL-p-chloroamphetamine depressed the monosynaptic reflex and increased the polysynaptic reflex. The depletion of 5-HT abolished the monosynaptic reflex depression, but the increase in polysynaptic reflexes was maintained, suggesting that endogenous 5-HT released by DL-p-chloroamphetamine mediates depression of the monosynaptic reflex in the spinal cord. The depression of the monosynaptic reflex was antagonized by GR127935 (N-[methoxy-3-(4-methyl-l-piperazinyl)phenyl]-2'-methyl-4'-(5-methyl-1,2,4-oxadiazol-3-yl)[1,1-biphenyl]-4-carboxamide; 5-HT1B/1D receptor antagonist) and BRL15572 (3-[4-(4-chlorophenyl)piperazin-1-yl]-1,1-diphenyl-2-propanol; 5-HT1D receptor antagonist) but not by isamoltane (5-HT(1B) receptor antagonist). These results suggest that 5-HT released from serotonergic terminals depresses monosynaptic reflex transmission via 5-HT1D receptors.

Animals↗

Hip-phase-dependent flexion reflex modulation and expression of spasms in patients with spinal cord injury.

The flexion reflex in human spinal cord injury (SCI) is believed to incorporate interneuronal circuits that consist elements of the stepping generator while ample evidence suggest that hip proprioceptive input is a controlling signal of locomotor output. In this study, we examined the expression of the non-nociceptive flexion reflex in response to imposed sinusoidal passive movements of the ipsilateral hip in human SCI. The flexion reflex was elicited by low-intensity stimulation (300 Hz, 30 ms pulse train) of the right sural nerve at the lateral malleolus, and recorded from the tibialis anterior (TA) muscle. Sinusoidal hip movements were imposed to the right hip joint at 0.2 Hz by a Biodex system while subjects were supine. The effects of leg movement on five leg muscles along with hip, knee, and ankle joint torques were established simultaneously with the modulation pattern of the flexion reflex during hip oscillations. Phase-dependent modulation of the flexion reflex was present during hip movement, with the reflex to be significantly facilitated during hip extension and suppressed during hip flexion. The phase-dependent flexion reflex modulation coincided with no changes in TA pre- and post-stimulus background ongoing activity during hip extension and flexion. Reflexive muscle and joint torque responses, induced by the hip movement and substantiated by excitation of flexion reflex afferents, were entrained to specific phases of hip movement. Joint torque responses were consistent with multi-joint spasmodic muscle activity, which was present mostly during the transition phase of the hip from flexion to extension and from mid- to peak extension. Our findings provide further evidence on the interaction of hip proprioceptors with spinal interneuronal circuits engaged in locomotor pathways, and such interaction should be considered in rehabilitation protocols employed to restore sensorimotor function in people with SCI.

Adult↗

Short-term effects of spinal manipulation on H-reflex amplitude in healthy and symptomatic subjects.

OBJECTIVES: The purpose of this study is to assess Hoffman (H) reflex after spinal manipulation (1) as a function of experimental position in healthy subjects and (2) in patients with low back pain. METHODS: An intervention study was performed to evaluate the effects of sacroiliac (SI) joint manipulation on motoneuron excitability, as measured by the H-reflex. Manual treatment of the SI joint was performed. Hoffman reflex amplitudes before and after SI joint manipulations were measured with subjects lying on the right side (n = 12 healthy subject) or with subjects lying supine (n = 5 healthy subjects), which required turning of subjects onto their sides for SI joint manipulation. Hoffman reflex amplitudes were also measured in 15 patients with low back pain. RESULTS: No significant changes in H-reflex amplitude in healthy subjects receiving manipulation to the SI joint were observed, provided that H-reflex testing and treatments were performed in the same position, that is, the subject was not moved during the experimental procedure. However, changes in motoneuron excitability after SI joint manipulation were observed in patients with low back pain. CONCLUSIONS: It appears that H-reflex responses after spinal manipulation are sensitive to movement/repositioning, and that the H-reflex depressions after manipulation documented in previous studies were movement artifacts rather than treatment effects. The relationship between etiology of low back pain and changes in H-reflex amplitude after spinal manipulation is not clear and needs further investigation.

Adult↗

Soleus and vastus medialis H-reflexes: similarities and differences while standing or lying during varied knee flexion angles.

The H-reflex may be a useful measure to examine the lower extremity muscles activation and inhibition following an injury. Recording the vastus medialis H-reflex amplitudes in healthy subjects while standing or lying during varied knee flexion angles may establish a reference for comparison for patients with ACL injury. Vastus medialis and soleus H-reflexes were recorded from 14 healthy subjects while lying and standing during 0, 30, 45, and 60 degrees knee flexion. EMG unit was used to electrically stimulate the tibial and femoral nerves (using 0.5 ms pulses at 0.2 pps of H-maximum amplitude) and to record four traces of the soleus and vastus medialis H-wave and one trace of the M-wave peak-to-peak amplitudes. Repeated measures three-way ANOVAs were calculated with the global alpha=0.05. Results showed that (1) the average soleus H-reflex amplitude was significantly less during standing than lying across all knee flexion conditions, (2) the average vastus medialis H-reflex amplitudes showed no measurable significant differences between neutral standing compared with lying, (3) the average vastus medialis H-reflex amplitudes were significantly greater during standing knee flexion conditions (30, 45, and 60 degrees ) than lying or neutral standing, and (4) there were no differences between soleus and vastus medialis H-reflex amplitudes during lying across all knee flexion conditions. Data from H/M ratio follow the same pattern of H-amplitude. Recording the vastus medialis H-reflex amplitude during standing and knee flexion may be a reflective of the knee function. It is more specific than the soleus H-reflex because it reflects the changes in the excitability of the quadriceps motoneurons acting directly around the knee joint.

Action Potentials↗

Laryngeal inputs in defensive airway reflexes in humans.

Stimulation of laryngeal receptors is the natural starting point of defensive airway reflexes including the cough reflex, expiration reflex, spasmodic panting, and apnoea with laryngospasm. Although several different types of laryngeal receptors have been reported, the laryngeal irritant receptors are considered to play the most essential role in elicitation of defensive airway reflexes. Based on the knowledge that the laryngeal irritant receptors are stimulated by water solutions lacking chloride anions, we have developed an experimental method to elicit defensive airway reflexes with a direct instillation of distilled water onto the laryngeal mucosa in humans. Using this experimental method, we studied the characteristics of defensive airway reflexes in lightly anaesthetized patients with multiple system atrophy (MSA). The reflex responses to water stimulation observed in these patients were characterized by apnoea with laryngospasm while the cough reflex was never elicited. Endoscopic images of the larynx in these patients were also characterized by laryngeal oedema. Considering the pathological changes occurring in the central nervous system and the laryngeal mucosa, it is possible that the defensive airway reflexes may be modified by central and/or peripheral mechanisms in patients with MSA.

Apnea↗

The cough reflex and its relation to gastroesophageal reflux.

Each cough involves a complex reflex arc beginning with the stimulation of sensory nerves that function as cough receptors. There is evidence, primarily clinical, that the sensory limb of the reflex exists in and outside of the lower respiratory tract. Although myelinated, rapidly adapting pulmonary stretch receptors (RARs), also known as irritant receptors, are the most likely type of sensory nerve that stimulates the cough center in the brain, afferent C-fibers and slowly adapting pulmonary stretch receptors (SARs) also may modulate cough. RARS, C-fibers, and SARs have been identified in the distal esophageal mucosa; however, studies have not been performed to determine whether they can participate in the cough reflex. Although gastroesophageal reflux disease can potentially stimulate the afferent limb of the cough reflex by irritating the upper respiratory tract without aspiration and by irritating the lower respiratory tract by micro- or macroaspiration, there is evidence that strongly suggests that reflux commonly provokes cough by stimulating an esophageal-bronchial reflex. Theoretically, the pathways of this reflex may be modeled in a variety of ways, and these are speculated upon in this article. The predominant role of acid in triggering cough by means of this reflex is unclear because of conflicting results from provocative challenge studies. It is interesting to speculate that a distal esophageal-bronchial reflex evolved as an early warning defense so that coughing could be started, just in case the refluxate were to reach the inlet of the lower respiratory tract. That is, thinking teleologically, it is possible that an esophageal-bronchial reflex evolved as one of several mechanisms designed to protect the lungs from aspiration of gastric contents.

Bronchi↗

Age-dependent effects of muscle vibration and the Jendrassik maneuver on the patellar tendon reflex response.

OBJECTIVE: To explore possible effects of aging on the excitability of spinal reflexes. DESIGN: Using a cross-sectional design, the influences of muscle vibration and the Jendrassik maneuver on patellar tendon reflex function were compared between 30 young adults and 15 older adults. SETTING: Motor control research laboratory. SUBJECTS: The young adults were volunteers of college age. The older adults (74.5 +/- 4.14 yr) were volunteers from the local community. All subjects were free of medications and neurological conditions that would affect normal neuromuscular responses. MAIN OUTCOME MEASURES: A force-time curve analysis of the patellar tendon reflex response was used to assess the inhibition and facilitation of spinal reflexes. In the experimental protocol to assess spinal reflex inhibition, 100 Hz vibration was applied to the right quadriceps muscle. In another experimental protocol, spinal reflex facilitation was assessed using the Jendrassik maneuver. To perform the Jendrassik maneuver, subjects were instructed to grasp their hands together and to pull as hard as possible while breathing normally. After a 2-second count, the tendon tap was delivered to the right leg and the subject was instructed to relax. In both experimental protocols, control patellar tendon reflexes were collected. RESULTS: Analysis of variance for reflex peak force revealed a significant 30% reduction in the amount of vibration-induced reflex inhibition with increasing age, and a similar 33% reduction in the amount of Jendrassik maneuver facilitation observed for the older adults as compared with the younger adults. CONCLUSION: These results support the hypothesis that inhibitory and excitatory influences acting on the alpha motoneuron pool are different in young and older adults.

Adult↗

Spinal NK1 receptors contribute to the increased excitability of the nociceptive flexor reflex during persistent peripheral inflammation.

Hyperalgesia is a characteristic of inflammation and is mediated, in part, by an increase in the excitability of spinal neurons. Although substance P does not appear to mediate fast synaptic events that underlie nociception in the spinal cord, it may contribute to the hyperalgesia and increased excitability of spinal neurons during inflammation induced by complete Freund's adjuvant. We examined the role of endogenous substance P in changes in the excitability of spinal neurons during adjuvant-induced, peripheral inflammation by determining the effect of a selective NK1 receptor antagonist (RP67580) on the nociceptive flexor reflex in adult rats. Experiments were conducted 2 or 3 days after injection of adjuvant. Animals exhibited moderate thermal hyperalgesia at this time. The flexor reflex was evoked by electrical stimulation of the sural nerve and was recorded in the ipsilateral hamstring muscles. The flexor reflex ipsilateral to the inflamed hindpaw was enhanced approximately two-fold compared to the flexor reflex evoked in untreated animals as determined by the number of potentials and the duration of the reflex. The enhanced reflex in adjuvant-treated animals was most likely due to an increase in the excitability of spinal interneurons because short-latency activity in the hamstring muscles did not differ between untreated animals and adjuvant-treated animals following electrical stimulation of the L5 dorsal root or the nerve innervating the muscle with a stimulus that was 1.3-1.5 times the threshold for excitation of A-fibers. Intrathecal administration of RP67580 (2.3 and 6.8 nmol) attenuated the flexor reflex evoked in adjuvant-treated animals, but had no effect in untreated animals. Intravenous or intraplantar injection of RP67580 (6.8 nmol) did not affect the flexor reflex in adjuvant-treated animals indicating a spinal action of the drug following intrathecal administration. RP68651, the enantiomer of RP67580, was without effect at doses up to 6.8 nmol, indicating that the effects of comparable doses of RP67580 were due to an action of the drug at NK1 receptors. However, intrathecal administration of 23 nmol of both drugs attenuated the reflex in adjuvant-treated and control animals indicating that effects of RP67580 at this dose were not mediated entirely by its action at NK1 receptors. Overall, these data suggest that endogenous substance P has a role in the increased excitability of spinal interneurons observed during persistent inflammation and support the hypothesis that substance P released in the spinal cord contributes to the hyperalgesia that accompanies adjuvant-induced persistent, peripheral inflammation.

Afferent Pathways↗

Effects of food consistency on the modulatory mode of the digastric reflex during chewing in freely behaving rabbits.

Effects of food consistency on the mode of the phase-linked modulation in the digastric reflex amplitude were examined in naturally chewing rabbits. Two test foods with different textures (bread as a soft food, pellet as a hard food) were used. The digastric reflex was elicited by electrical stimulation (10 train pulses at 2 kHz) of the inferior alveolar nerve. The amplitude of the digastric reflex measured was divided into three categories depending on the chewing phases in which the stimulus was delivered and each value was compared with the control response obtained when the animal was resting. The reflex was strongly inhibited in the jaw-opening phase and no difference was observed in the inhibitory effect between the foods. In the jaw-closing phase, larger digastric reflexes than those in the opening phase were elicited with both foods. This was the case in both the fast-closing and slow-closing phases. Reflex amplitude was significantly larger during chewing of the hard food than the soft food and, thereafter, inhibition of the reflex was observed only during chewing of the soft food in the closing phase. The results suggest the following: (1) food consistency may affect the central mechanism which regulates the digastric reflex and (2) the reflex may contribute to the regulation of masticatory force during chewing particularly hard food.

Animal Feed↗

Movement-induced modulation of soleus H reflexes with altered length of biarticular muscles.

Passive pedaling movements of the leg results in the phasic modulation of the soleus H reflex of that leg. In contrast, the H reflex of the contralateral leg is attenuated tonically. The phasic modulation of the reflex ipsilaterally can be attributed to the afferent discharge associated with the cyclic lengthening of the extensor muscles. We hypothesized that the tonic attenuation of the contralateral reflex could be explained if the afferent feedback arising from the lengthening of the biarticular muscles had an increased importance in regulating the amplitude of the contralateral reflex. To test this, the passive pedaling movements were reduced to those about either the knee or hip alone. Despite the alteration in the pattern of stretching of the biarticular muscles, the contralateral soleus H reflex was tonically attenuated during both forms of single joint movements. We suggest that the same phasic afferent discharge responsible for the modulation of the ipsilateral soleus H reflex initiates the tonic attenuation contralaterally, but that the signal undergoes a complex transformation in crossing the cord. These results do not rule out the possibility that the stretching of the biarticular muscles contributes to the attenuation of the ipsilateral soleus H reflex, which is subsequently masked by a powerful influence from the stretching of the uniarticular extensor muscles. To test this possibility, a second experiment manipulated the lengths of the muscles of the leg by altering the positions of the static joints during isolated rotation of either the knee or hip and measuring the amplitude of the ipsilateral soleus H reflex. From the results, it was clear that stretching the uniarticular extensor muscles produced the most dramatic effects. However, the stretch of the biarticular muscles yielded mild inhibitory influences if these muscles were near their maximal lengths.

Adult↗

Differential effects of (R)- and (S)-8-hydroxy-2-(di-n-propylamino)tetralin on the monosynaptic spinal reflex in rats.

We examined the effects of (R)- and (S)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT) on the monosynaptic spinal reflex in rats. In intact rats, (R)-8-OH-DPAT (10 microg/kg, i.v.) enhanced the amplitude of the monosynaptic reflex, whereas at 100 microg/kg, it reduced the amplitude. (S)-8-OH-DPAT enhanced the monosynaptic reflex dose-dependently. In spinalized rats, (R)-8-OH-DPAT produced dose-dependent inhibition, but the (S)-enantiomer did not affect the monosynaptic reflex. Pretreatment with spiroxatrine or 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]-piperazine (NAN-190) inhibited (R)-8-OH-DPAT-induced monosynaptic reflex enhancement in intact rats, as did 5-hydroxytryptamine (5-HT) depletion. Ketanserin reduced the effect of (R)-8-OH-DPAT. These pretreatment regimens had no effect on the monosynaptic reflex depression produced by the (R)-enantiomer in intact and spinalized rats. Pretreatment with prazosin inhibited (S)-8-OH-DPAT-induced monosynaptic reflex enhancement in intact rats, as did noradrenaline and 5-HT depletion. These results suggest that supraspinal 5-HT1A receptors and the descending serotonergic system are involved in the stimulatory effect of (R)-8-OH-DPAT on the monosynaptic reflex, while both the descending serotonergic and noradrenergic systems, the latter acting via alpha1-adrenoceptors, are involved in the effect of the (S)-enantiomer on this reflex.

5,6-Dihydroxytryptamine↗

Paraspinal muscle reflex dynamics.

Neuromuscular control of spinal stability may be represented as a control system wherein the paraspinal muscle reflex acts as feedback response to kinetic and kinematic disturbances of the trunk. The influence of preparatory muscle recruitment for the control of spinal stability has been previously examined, but there are few reported studies that characterize paraspinal reflex gain as feedback response. In the current study, the input-output dynamics of paraspinal reflexes were quantified by means of the impulse response function (IRF), with trunk perturbation force representing the input signal and EMG the output signal. Surface EMGs were collected from the trunk muscles in response to a brief anteriorly directed impact force applied to the trunk of healthy participants. Reflex behavior was measured in response to three levels of force impulse, 6.1, 9.2 and 12.0 Ns, and two different levels of external trunk flexion preload, 0 and 110 N anterior force. Reflex EMG was quantifiable in response to 91% of the perturbations. Mean reflex onset latency was 30.7+/-21.3 ms and reflex amplitude increased with perturbation amplitude. Impulse response function gain, G(IRF), was defined as the peak amplitude of the measured IRF and provided a consistent measure of response behavior. EMG reflex amplitude and G(IRF) increased with force impulse. Mean G(IRF) was 2.27+/-1.31% MVC/Ns and demonstrated declining trend with flexion preload. Results agree with a simple systems model of the neuromechanical feedback behavior. The relative contribution of the reflex dynamics to spinal stability must be investigated in future research.

Adaptation, Biological↗

Neurochemical plasticity and the role of neurotrophic factors in bladder reflex pathways after spinal cord injury.

Transection of the spinal cord that interrupts the spinobulbospinal micturition reflex pathway, abolishes voluntary voiding and initially produces an areflexic bladder with complete urinary retention. However, depending upon the species, reflex bladder activity slowly recovers over the course of weeks or months. In chronic spinal animals, reflex mechanisms in the lumbosacral spinal cord are capable of duplicating many of the functions performed by reflex pathways in animals with an intact spinal cord and can induce bladder hyperreflexia. However, the bladder does not empty efficiently due to a loss of bladder-sphincter coordination (bladder-sphincter dyssynergia). In contrast to normal animals in which the sphincter relaxes during voiding, animals with a spinal cord injury exhibit sphincter contractions during voiding, an increase in urethral outlet resistance, urinary retention, bladder hyperreflexia, bladder overdistension, and an increase in bladder afferent cell size. Changes in electrophysiological or neurochemical properties of bladder afferent cells in the dorsal root ganglia and of spinal pathways could contribute to the emergence of the spinal micturition reflex, bladder hyperreflexia and changes in the pharmacologic responses of reflex pathways in the lumbosacral spinal cord after spinal cord injury. Urinary bladder hyperreflexia after spinal cord injury may reflect a change in the balance of neuroactive compounds in bladder reflex pathways. This review will detail: (1) changes in the neurochemical phenotype of bladder afferent neurons and of spinal neurons mediating micturition reflexes after spinal cord injury, with an emphasis on three neuroactive compounds, neuronal nitric oxide synthase (nNOS), galanin, and pituitary adenylate cyclase activating polypeptide (PACAP); (2) possible functional consequences on bladder reflexes of changes in spinal cord neurochemistry after spinal cord injury, and (3) the potential role of neurotrophic factors expressed in the urinary bladder or spinal cord after spinal cord injury in mediating these neurochemical changes.

Afferent Pathways↗

Distension-evoked ascending and descending reflexes in the isolated guinea-pig stomach.

Distension-evoked gastric reflexes were studied by intracellular recording from circular muscle cells in the gastric fundus, corpus and antrum in the isolated guinea-pig stomach. Localised electrical stimulation, 2 mm circumferential to the recording electrode, evoked inhibitory junctions potentials in all three gastric regions, sometimes followed by depolarisations in the antrum. In the mid corpus, the inhibitory responses were substantially reduced by Nw-nitro-L-arginine (100 microM), unmasking excitatory junction potentials. Residual hyperpolarisations were blocked by apamin (0.5 microM) which also enhanced the amplitude of excitatory junction potentials. These excitatory junction potentials were abolished by hyoscine (1 microM). Thus transmission from inhibitory motor neurons is mediated by both nitric oxide and an apamin-sensitive mechanism. Transmission from excitatory motor neurons to the circular muscle is mediated by acetylcholine via muscarinic receptors. Balloon distension of 10 s duration of the fundus or antrum elicited inhibitory junction potentials in circular muscle cells of the mid corpus. These inhibitory junction potentials were blocked by tetrodotoxin (0.6 microM) and were greatly reduced by Nw-nitro-L-arginine (100 microM). The residual hyperpolarisations were blocked by apamin (0.5 microM). This indicates the presence of ascending and descending inhibitory reflex pathways in the stomach. In 3 out of 7 experiments, following blockade of inhibitory transmission, small nerve-mediated excitatory junction potentials were evoked by antral distension indicating the presence of an additional ascending excitatory reflex pathway. Distension of the corpus elicited prominent inhibitory junction potentials, sometimes followed by large depolarisations, in circular muscle cells in the fundus, but not in the antrum. This suggests that there is also an ascending inhibitory reflex pathway from the corpus to the fundus but no distension-sensitive descending reflex pathway from the corpus to the antrum. These results demonstrate that within the stomach there are reflex pathways which can be activated by localised distension and project at some distance orally and aborally within the gastric wall. It is likely that the inhibitory reflex pathways are involved in gastric adaptive relaxation which occurs when the intact, isolated stomach is distended. The excitatory reflex pathways from the antrum to the corpus are likely to be involved in the intrinsic excitatory reflex responses observed in the isolated intact stomach to distension and thus be involved in the mixing and emptying of gastric contents.

Animals↗

Spinal neurokin3 receptors facilitate the nociceptive flexor reflex via a pathway involving nitric oxide.

The present study examined the effects of intrathecal administration of neurokinin3 receptor agonists on the electrically-evoked nociceptive flexor reflex in decerebrate and spinalized adult rats. The reflex was evoked by stimulating the isolated sural nerve at an intensity that activates C fibers and was measured by recording the number of compound potentials in the ipsilateral hamstring muscles. Intrathecal senktide (1-30 nmol), a neurokinin3 receptor agonist, dose-dependently facilitated the reflex reaching a maximum effect of 230% of the baseline reflex at 10 nmol. SR 142801 (60 nmol), a non-peptide neurokinin3 receptor antagonist, blocked facilitation of the reflex induced by 10 nmol senktide, providing further support that the effect of senktide is mediated by neurokinin3 receptors. The intrathecal administration of senktide (10 nmol) did not alter the monosynaptic reflex elicited by stimulating the L5 dorsal root at an intensity that was at the threshold for activating A fibers. This indicates that the senktide-induced facilitation of the nociceptive flexor reflex was not at the level of the motor neuron. Pretreatment with N(G)-nitro-L-arginine methyl ester (30 nmol), a nitric oxide synthase inhibitor, attenuated the effect of senktide, indicating that facilitation of the reflex by senktide is also mediated by the production of nitric oxide. Data from the present work have shown that spinal neurokinin3 receptors facilitate the nociceptive flexor reflex through a pathway that involves interneurons and the production of NO. Therefore, neurokinin3 receptors are likely to be involved in enhancing nociceptive neurotransmission at the level of the spinal cord.

Animals↗

Primitive reflex profiles in infants: differences based on categories of neurological abnormality.

In order to clarify reflex profiles in the first year of life in connection with categories of neurological abnormality, six primitive reflexes, i.e., the crossed extensor reflex, suprapubic extensor reflex, heel reflex, Galant response, asymmetric tonic neck reflex and plantar grasp response, were examined in 458 normal infants, 78 infants with cerebral palsy (CP) and 81 infants with mental retardation (MR), whose diagnoses were confirmed at a later follow-up examination. The change in the mean score for each of these reflexes with age was characteristic for each category or type of neurological abnormality. This implies that a presumptive diagnosis can be made in neurologically high-risk infants by examination of the primitive reflexes. Such reflexes are therefore of specific significance, among other neurological criteria, in infants within the first year of life.

Ataxia↗

Relationship between the degree of inhibited stretch reflex activities of the wrist flexor and reaction time during quick extension movements.

It has been reported that stretch reflex responses, including the long latency component, are modulated by motor preparation for the direction and type of movement. In the present study, human subjects were required to make a reaction movement in the direction of the wrist extension following a muscle stretch to the wrist flexor, and we investigated the relationship between the modulation of reflex activities of the wrist flexor and the length of reaction time (premotor time) of the wrist extensor. Twenty-five healthy males, ranging in age from 20 to 28, participated in the experiments. A DC torque motor was used to evoke the reflex EMG responses on the flexor. Averaging the rectified EMG, recorded with the surface electrodes over the flexor, showed short and long latency reflexes (M1 and M2 components) in response to the muscle stretch. For all subjects, the amplitudes of the reflex components during the extension reaction movement decreased, compared to those amplitudes in the non-reaction tasks. The decrease in the M2 component, which is considered a transcortical reflex, was significantly larger than the decrease in the M1 component, which is a spinal reflex. Moreover, there were correlations between reaction time to muscle stretch and the degree of decrease in reflex activities with the extension reaction (r = 0.652 for M1, r = 0.813 for M2, P < 0.01). It became clear that the subjects with shorter reaction times inhibited their reflex activities of the flexor, particularly the M2 component which prevents the extension movement, to a greater degree than the subjects with longer reaction times. Therefore, our results suggest that the degree of M2 modulation directly reflects the individual motor control required to perform quick movements.

Adult↗

H-reflexes of different sizes exhibit differential sensitivity to low frequency depression.

The amplitude of the H-reflex declines when activated repetitively. The magnitude of decline is greater when the amplitude of the H-reflex is small. To explore whether pre- or postsynaptic factors contribute to the differences observed in H-reflexes of different sizes, changes in the amplitude of H-reflexes of different sizes were measured during a train of stimulation in 10 normal subjects. Amplitudes of different sizes were obtained using differing stimulus intensities or during superimposed contraction, two manipulations which differently affect the number of active afferents and the excitation of the motoneuron pool. Small amplitude H-reflexes depressed to a lower plateau than larger H-reflexes and superimposed contraction did not alleviate the depression during each train. Nearly all the decline in larger amplitude H-reflexes occurred in a component that was in common with smaller amplitude H-reflexes. This suggests that the depressibility of the earliest activated units is greater than later activated units in H-reflexes and that the magnitude of decline is affected by prior activity as well as size.

Adult↗