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Neural mechanisms underlying the clasp-knife reflex in the cat. II. Stretch-sensitive muscular-free nerve endings.

1. The goal of this study was to determine the contribution of muscular free nerve endings to the clasp-knife reflex by comparing their response properties and reflex actions to the clasp-knife reflex. 2. The responses of single muscle afferents were examined in anesthetized cats using stretch and isometric contraction of ankle extensor muscles identical to those that evoked clasp-knife inhibition in decerebrated and dorsal spinal-hemisectioned cats. 3. Fifty-three stretch-sensitive mechanoreceptor afferents were identified as free nerve ending afferents based on their conduction velocities, location within the muscle, uniformity of response, and dissimilarity to other muscle proprioceptors. The afferent conduction velocities were in both the group III (56%) and group II (44%) range, including five fast-conducting group II afferents (greater than 55 m/s). 4. The stretch response of stretch-sensitive, free nerve endings (SSFNEs) showed several characteristic features: 1) afferents were excited only by large stretches that produced significant passive force; 2) afferent activity began after a brief delay and exhibited segmentation of discharge during ramp stretch, a maximum at the end of ramp stretch, and rapid and complete decay during static stretch, and 3) afferent response adapted to repeated stretches. These properties match those of clasp-knife inhibition described in the companion paper, except that the SSFNE segmentation and maximum were more pronounced and their decay during maintained stretch was more rapid. 5. Isometric contraction produced by electrical stimulation of the muscle nerve, which induced force-evoked inhibition in decerebrated and dorsal hemisectioned cats, also consistently excited SSFNEs. Stretch evoked greater excitation than contraction, indicating that both length and force contribute to SSFNE activity. 6. Stimulation of free nerve endings by squeezing the achilles tendon in cats exhibiting the clasp-knife reflex evoked powerful, homonymous inhibition and a flexion-withdrawal pattern of reflex action--that is, inhibition of extensor and excitation of flexor muscles throughout the hindlimb, which parallels the spatial divergence of the clasp-knife reflex. 7. Intrathecal application of capsaicin, which preferentially blocks the reflex actions of small afferent fibers, blocked clasp-knife inhibition in decerebrated, dorsal hemisectioned cats. 8. The similarities between the reflex actions and response properties of SSFNEs and the properties of the clasp-knife reflex suggest that SSFNEs mediate clasp-knife inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

Inhibition and facilitation of different nocifensor reflexes by spatially remote noxious stimuli.

1. Noxious stimuli have been shown to produce a diffuse inhibition of nociresponsive neurons in the spinal and trigeminal dorsal horns. The present study sought to extend these electrophysiological studies of diffuse noxious inhibitory controls (DNIC) by determining the effect of a spatially remote noxious stimulus on behavioral measures of nociception. Changes in latency for hindpaw withdrawal and tail flick reflexes were measured in lightly halothane-anesthetized or awake, spinally transected rats before, during, and after application of a spatially remote noxious stimulus. 2. Surprisingly, in no case did application of a spatially remote noxious stimulus inhibit the hindpaw withdrawal reflex. The latency for this reflex was either reduced or did not change when the tail or contralateral hindpaw was placed in hot water (50 degrees C) or when a noxious pinch was applied to the ear. In contrast, the latency for the tail flick reflex was consistently increased when the hindpaw was placed in hot water. Both the hindpaw reflex facilitation and the tail flick reflex inhibition produced by a noxious conditioning stimulus were attenuated in spinally transected rats indicating supraspinal modulation of both reflexes. 3. In addition, and consistent with the work of others, placing the tail in hot water reduced the evoked activity of convergent neurons in both the trigeminal and lumbar spinal dorsal horns. Thus inhibition of the activity of nociresponsive neurons in the dorsal horn is consistent with inhibition of the tail flick reflex, but not with facilitation of the hindpaw withdrawal reflex.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

Loop gain of reflexes controlling human standing measured with the use of postural and vestibular disturbances.

1. In this study we measured the loop gain of postural reflexes in standing human subjects. Reflex activity is conventionally described in terms of the muscle activation arising from a perturbation, but in this study the ability of the evoked muscle activity to correct the perturbation was also measured, and the behavior of the entire feedback loop is described. 2. A weak continuous random perturbation was applied at waist level to standing subjects. The effects of the perturbation on body sway and soleus electromyogram (EMG) were identified by cross-correlation, and spectral analysis was used to estimate the open-loop reflex transmission characteristics (i.e., sway to EMG). Under the same conditions, activity in the leg muscles was evoked by galvanic vestibular stimulation with the use of a continuous randomly varying current. The effects on soleus EMG and the subsequent body sway were identified by cross-correlation. This allowed calculation of the open-loop muscle and load behavior (i.e., EMG to sway). From these open-loop reflex and muscle and load transfer functions, the loop gain and phase were calculated. 3. In addition to the gain of the feedback loop, the study describes the transmission characteristics of reflex responses in the leg muscles associated with body sway and the effects of excluding visual and proprioceptive contributions to the response; the transfer function of human soleus with a stimulus that preserves the normal recruitment of motoneurons, including the effects of different load conditions on the muscle; and the transmission characteristics of vestibular pathways that evoke responses in the leg muscles during standing in situations that might modify the reflexes. 4. When standing, the loop gain of reflex feedback is approximately unity and is unchanged by eye closure and stability of support. Reflex transmission introduced a marked phase advance, and this served to offset most of the phase lag introduced by muscle and load. The residual phase lag could explain the frequency of tremor observed during standing (6-8 Hz). 5. The gain of the feedback loop (approximately 1) is higher than suggested by both previous estimates and theoretical considerations, but is still insufficient to explain the stability of normal human standing. This implies that, although sensory information is used to control posture, it does not do so exclusively through a negative feedback control process. The experimental findings are consistent with a reflex response based on a feed-forward process, and this would result in prediction of the response necessary to counteract a postural disturbance.

Adult↗

Central modifications of reflex parameters may underlie the fastest arm movements.

Descending and reflex pathways usually converge on common interneurons and motoneurons. This implies that active movements may result from changes in reflex parameters produced by control signals conveyed by descending systems. Specifically, according to the lambda-model, a fast change in limb position is produced by a rapid change in the threshold of the stretch reflex. Consequently, external perturbations may be ineffective in eliciting additional reflex modifications of electromyographic (EMG) patterns unless the perturbations are relatively strong. In this way, the model accounts for the relatively weak effects of perturbations on the initial agonist EMG burst (Ag1) usually observed in fast movements. On the other hand, the same model permits robust reflex modifications of the timing and shape of the Ag1 in response to strong perturbations even in the fastest movements. To test the model, we verified the suggestion that the onset time of the Ag1, even in the fastest movements, depends on proprioceptive feedback in a manner consistent with a stretch reflex. In control trials, subjects (n = 6) made fast unopposed elbow flexion movements of approximately 60 degrees (peak velocity 500-700 degrees/s) in response to an auditory signal. In random test trials, a brief (50 ms) torque of 8-15 Nm either assisting or opposing the movement was applied 50 ms after this signal. Subjects had no visual feedback and were instructed not to correct arm deflections in case of perturbations. In all subjects, the onset time of the Ag1 depended on the direction of perturbation: it was 25-60 ms less in opposing compared with assisting load conditions. Assisting torques caused, at a short latency of 37 ms, an additional antagonist EMG burst preceding the Ag1. The direction-dependent effects of the perturbation persisted when cutaneous feedback was suppressed. It was concluded that the direction-dependent changes in the onset time and duration of the Ag1 as well as the antagonist activation preceding the Ag1 resulted from stretch reflex activity elicited by the perturbations rather than from a change in the control strategy or cutaneous reflexes. The results support the hypothesis on the hierarchical scheme of sensorimotor integration in which EMG patterns and movement emerge from the modification of the thresholds and other parameters of proprioceptive reflexes by control systems.

Adult↗

Aging effects of sympathetic reflex activities on skin nerves.

BACKGROUND: Muscle sympathetic nerve activity (MSNA) at rest is widely known to increase with aging, but changes in skin sympathetic nerve activity (SSNA) with aging are less well defined. We examined the aging effects of reflex activities on SSNA, sympathetic skin response (SSR), and sympathetic flow response (SFR). OBJECTIVE: We studied the aging effect of reflex activities on SSNA, SSR and SFR. METHODS: SSNA, SSR and SFR were simultaneously recorded during randomly administered electrical stimuli. RESULTS: The mean SSNA reflex latency was 763.1 +/- 39.8 ms, mean SSNA amplitude was 12.6 +/- 6.3 microV, mean SSR reflex latency was 1,809.0 +/- 90.6 ms, mean SSR reflex amplitude was 0.519 +/- 0.449 mV, mean SFR reflex latency was 4,398.9 +/- 761.7 ms, and mean SFR reflex amplitude was 8.21 +/- 5.14 ml/min/100 g. None of these parameters were significantly affected by aging. The reflex bursts on SSNA could be recorded in all subjects studied. While the frequencies of SSR and SFR were recorded in more than 80% of young subjects under age 40 years, the frequencies of SSR were recorded in less than 25% of subjects over age 80 years, and the frequencies of SFR were recorded in less than 5%. CONCLUSION: There were no differences in electrical stimuli-induced reflex SSNA between young and older subjects, but effector organ responses such as SSR and SFR were diminished in older subjects.

Adult↗

The oto-respiratory reflex.

The oto-respiratory (O-R) reflex consists of the cough reflex produced by direct mechanical stimulation of the deep portion of the posterior wall of the external auditory meatus. Because the efferent pathways are different for coughing and bronchoconstriction, some subjects can have an O-R reflex (coughing) without the oto-bronchial (O-B) reflex (bronchoconstriction). This study also states that on stimulation of the mechanoreceptors in the external ear, 20 out of 125 normal subjects (16%) presented with the O-R reflex; in 7 of the 20 subjects, bronchoconstriction ('responders') was also documented (O-B reflex). The O-B reflex was particularly evident in 3 of the 7 responders. These normal subjects referred a family history of atopy. Only through animal experimentation can the exact nervous pathway of the O-R reflex be defined. From the physiological point of view, it is difficult to imagine how this 'irritative' reflex could have a protective function against auditory aggression.

Acoustic Stimulation↗

[Experimental studies on the suppression of the stapedius reflex in comparison with EMG-results in idiopathic facial paresis].

The recording of intra-aural muscle reflexes elicited by acoustic stimulation is a routine method in clinical audiology. The most important quantitative examinations of the reflex dynamic, i.e. Metz recruitment and reflex decay in low frequencies, allow the judgement of function of the afferent pathway in the stimulated inner ear and acoustic nerve. Quantitative determinations of the efferent branch were carried out by several authors in a few normal subjects and in several patients with multiple sclerosis or facial palsy. Absolute acoustic impedance - a method yielding wide scattering - was used in order to determine changes in reflex activity in pathological conditions. In the first part of our investigations we tried to find a parameter or reflex dynamic allowing to characterize the functional capacity in the efferent part of the reflex arch in the facial nerve. We examined particularly the steepness of the onset of recorded reflex. Statistical analysis showed an extraordinary stability of this parameter in normal and pathological conditions. Measurements in normal subjects yielded very small intra- and inter-individual variability. In the second part of our experiments we studied normal-hearing patients with unilateral Bells palsy. In the early phase of the lesion we found a significant decrease of the onset steepness in the reflex diagram recorded on the paralyzed side. The greatest reduction of this parameter was seen with a 1,000-Hz stimulus. The time course of the alteration of the onset steepness also seems to have a characteristis pattern. In a further investigation we compared the variations of this reflex parameter with findings in stimultaneously recorded electroneuronograms.

Adult↗

Vagal cardiopulmonary reflexes after left ventricular deafferentation.

BACKGROUND: Cardiac transplantation and chronic myocardial infarction interrupt vagal afferent nerve fibers, which originate mainly from the ventricles. Marked abnormalities of reflexes mediated by cardiopulmonary receptors with vagal afferent fibers have been demonstrated after both cardiac transplantation and chronic myocardial infarction. The relation between these reflex abnormalities and ventricular deafferentation is not known. METHODS AND RESULTS: To further assess this relation, we investigated the effects of left ventricular (LV) deafferentation on the control of renal sympathetic nerve activity (RSNA) by the vagal cardiopulmonary reflex in chloralose-anesthetized, mechanically ventilated dogs with sinoaortic denervation. Responses of left atrial pressure (LAP) and RSNA to hemorrhage and volume expansion were measured before and after application of 88% phenol to either the inferoposterior LV (n = 12) or the entire LV (n = 14). In control experiments, measurements were made before and after application of saline to the LV (n = 12). Reflex sensitivity (percent change in RSNA per mm Hg change in LAP) measured during volume expansion was mildly attenuated after both total (prephenol, -9.1 +/- 0.7; postphenol, -6.6 +/- 0.7; P < .05) and inferoposterior (pre, -12.5 +/- 1.8; post, -8.1 +/- 0.6; P = .055) LV deafferentation. Reflex sensitivity measured during hemorrhage was not significantly altered by inferoposterior or total LV deafferentation. Epicardial saline had no significant effect on reflex sensitivity values measured during either volume expansion or hemorrhage. Reflex inhibition of RSNA in response to intracoronary nicotine was abolished after phenol application, indicating adequate ventricular deafferentation. Phenol application had no significant effect on LAP-myocardial segment length relations measured by sonomicrometry (n = 6). CONCLUSIONS: Interruption of vagal afferent input from the LV has only modest effects on the control of RSNA by the vagal cardiopulmonary reflex. These data indicate that there is considerable redundancy in the vagal cardiopulmonary reflex such that receptors from the lungs and other cardiac chambers can largely compensate for the loss of afferent input from the LV.

Animals↗

Role of prostaglandins and kinins in the renal pressor reflex.

In previous studies we identified an afferent renal nerve-dependent pressor reflex elicited by acute unilateral renal artery stenosis (50% decrease in renal blood flow) in conscious, instrumented rats with reduced responsiveness of arterial baroreceptor reflexes and the renin-angiotensin system. The pressor reflex involves a neurogenic increase in peripheral resistance. The present study examined the nature of the intrarenal stimulus underlying this renal pressor reflex. Rats were subjected to sinoaortic denervation and, 7 to 10 days later, were chronically instrumented with Doppler flow probes on the right renal artery, superior mesenteric artery, and abdominal aorta and with an occluder on the right renal artery. Following surgical recovery and inhibition of the renin-angiotensin system (captopril), animals received intravenous isotonic saline, 6% of body weight over 60 minutes. Saline infusion did not alter baseline hemodynamics, vascular neurogenic tone, or responsiveness to tyramine, but it attenuated the reflex by 70%. A second series of experiments examined a possible role for intrarenal prostaglandins, kinins, or adenosine in the activation of renal sensory receptors during renal stenosis. Prostaglandin inhibition with intravenous administration of indomethacin and meclofenamate virtually abolished the reflex in the face of enhanced tyramine responsiveness, whereas kallikrein inhibition (aprotinin) attenuated the reflex pressor response by 33%. Adenosine inhibition with aminophylline or adenosine deaminase had no effect on the reflex; these agents and aprotinin did not affect vascular neuroeffector responsiveness (tyramine). The data suggest that the renal pressor reflex may be mediated by renal sensory nerves, possibly chemoreceptors, whose activation could depend on renal excretory function and synthesis of prostaglandins and kinins.

Adenosine↗

Baroreceptor reflex modulation by vasopressin microinjected into the nucleus tractus solitarii of conscious rats.

To determine whether the central vasopressinergic system at the level of nucleus tractus solitarii (NTS) modulates the reflex control of heart rate, we employed a new method for microinjection into the brainstem of conscious, freely moving rats. Baroreceptor reflex function was assessed during pressure changes induced by intravenous administration of phenylephrine (0.25-8 micrograms/kg) and sodium nitroprusside (0.5-16 micrograms/kg) in rats microinjected, through a permanent cannula into the brainstem, with saline, arginine vasopressin (AVP), or an AVP blocker. Baseline levels of pressure and heart rate were not changed by either peptide pretreatment. Restricted injection of AVP (20 ng-0.2 microliter) into the NTS attenuated the reflex bradycardia during pressure increases, with an upward displacement of the baroreceptor reflex function line (p less than 0.01) without change in the sensitivity. Local blockade of endogenous AVP, d(CH2)5Tyr(Me)AVP (1 microgram-0.2 microliter), depressed baroreceptor reflex sensitivity with intense bradycardia to either small or large pressure increases. Baroreceptor reflex control of heart rate in response to decreases in pressure was preserved during pretreatment with AVP, whereas endogenous blockade of AVP increased baroreceptor reflex sensitivity. These effects were specific to the NTS, since in another four rats there were no effects when the injections were made 1 mm above, into the cerebellum. The changes in baroreceptor reflex control of heart rate in conscious, unrestrained rats caused by administration of AVP and its endogenous blockade provide evidence that central vasopressinergic synapses at the NTS are important physiological modulators of baroreceptor reflex function.

Animals↗

Baroreceptor reflex impairment and mild hypertension in rats with dietary-induced obesity.

Cardiovascular dysfunction associated with obesity was assessed by comparing rats that had been maintained on a regular or high fat diet since weaning. Rats on the high fat diet not only gained weight faster than age-matched controls but also had higher systolic and mean pressures. Development of mild hypertension in obese rats was first detected by indirect tail-cuff measurement and confirmed later by recording intra-arterial pressures directly from indwelling femoral catheters. To assess baroreceptor reflex sensitivity, reflex heart rate responses were elicited by lowering blood pressure with sodium nitroprusside or elevating it with phenylephrine. Initial tests showed that, although reflex tachycardia during depressor responses to sodium nitroprusside did not differ between groups, reflex bradycardia during pressor responses to phenylephrine was weaker in obese than in control rats. Underlying autonomic mechanisms were then examined by repetition of baroreceptor reflex tests after cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Reflex tachycardia was equally inhibited in both groups by either antagonist. By contrast, reflex bradycardia was reduced more in obese than in control rats by beta-adrenergic blockade but was equally reduced by cholinergic blockade. Because residual responses after beta-adrenergic blockade would represent remaining parasympathetic mediation, these results indicate that reflex bradycardia was selectively impaired because of deficient parasympathetic mediation. Considered collectively, our results suggest that impaired parasympathetic mediation of reflex bradycardia could either result from or contribute to the blood pressure elevation in obese rats.

Adrenergic beta-Antagonists↗

Differential modulation of the baroreceptor reflex by brain and plasma vasopressin.

Plasma vasopressin sensitizes the baroreceptor reflex, whereas vasopressin given into the cerebral ventricle overrides the baroreceptor reflex by means of sympathetic stimulation. To test the hypothesis that arginine vasopressin stimulates two different receptor subtypes (V1 and V2) in the central nervous system, we measured the baroreceptor reflex (change in pulse interval vs change in blood pressure) after administering methoxamine (10-300 micrograms/kg i.v.) in conscious rats. Animals were pretreated either with a V1 vasopressin receptor antagonist administered intravenously or intracerebroventricularly, or with a V2 receptor antagonist administered intravenously. The central V1 antagonist caused sensitization of the baroreceptor reflex, whereas the intravenous V2 antagonist attenuated it. The intravenous V1 vasopressin antagonist had no effect on baroreceptor reflex sensitivity. When the experiments were repeated in rats with hereditary diabetes insipidus, neither antagonist influenced the baroreceptor reflex. Volume expansion lowered circulating vasopressin levels and also attenuated the baroreceptor reflex--effects similar to those observed with the intravenous V2 antagonist. We conclude that vasopressin sensitizes the baroreceptor reflex through V2 receptors accessible from the blood and inhibits the reflex through V1 receptors in the brain that cannot be reached from the blood. These observations suggest a direct interaction between hormonal and neuronal vasopressin in cardiovascular control.

Animals↗

Influence of carotid chemoreceptors on the vagal reflex-induced tracheal constriction.

In this study, the effects of carotid chemoreceptors on reflex tracheal constriction were investigated in anesthetized, paralyzed, and artificially ventilated mongrel dogs. Reflex tracheal constriction was measured as changes in the intratracheal pressure of an air-filled balloon introduced into the rostral side of the transected trachea. A hypoxic condition was produced by ventilating the dog with 12% O2-88% N2. The reflex tracheal constriction induced by histamine inhalation to the bronchial side was reduced by section of the bilateral sinus nerves. The hypoxic condition significantly potentiated the reflex tracheal constriction induced by histamine inhalation. The potentiated reflex tracheal constriction during hypoxia was abolished by section of the bilateral sinus nerves. The afferent electrical stimulation to the central cut end of the vagus nerve caused a reflex tracheal constriction. The reflex tracheal constriction was significantly potentiated by hypoxia, and the potentiating response was abolished by section of the bilateral sinus nerves. The infusion of NaCN into the bilateral carotid arteries significantly potentiated the reflex tracheal constriction. The NaCN-induced potentiating effect was abolished by section of the bilateral sinus nerves. These results suggest that hypoxia potentiates the vagal reflex-induced tracheal constriction and that the hypoxia-induced potentiating effects may be mediated by carotid chemoreceptors.

Administration, Inhalation↗

Reflex inhibition of thigh muscles in knee injury. Causes and treatment.

There are several common findings and contradictions noted in the research related to thigh muscle reflex inhibition and sequelae that occur with knee joint injury. Reflex inhibition may be measured directly by electromyography, or the sequelae of reflex inhibition may be measured, as commonly occurs in the clinic setting. Electromyography is useful in determining the causes of reflex inhibition. The most frequently cited causes of thigh muscle reflex inhibition in knee injury are pain, joint effusion and knee immobilisation. The other measurement methods described vary from thigh circumference measurement to muscle biopsy. These methods are useful in determining the magnitude and duration of the deleterious sequelae that affect the thigh muscles after reflex inhibition. Finally, there is selectivity of reflex inhibition after knee joint injury: the quadriceps versus the hamstrings, the different components of the quadriceps muscle group, and the different types of muscle fibres. In light of these findings, several suggestions have been offered for prevention of reflex inhibition and for techniques that can be applied to rehabilitate the most affected muscle group: the quadriceps femoris. Techniques used to prevent or limit the amount of reflex inhibition include cryotherapy, transcutaneous electrical nerve stimulation, iontophoresis, phonophoresis, joint mobilisation, rest and proper positioning of the knee in rest and exercise. Electromyostimulation, electromyographic biofeedback and traditional exercise training are 3 methods used to rehabilitate the quadriceps.

Humans↗

The effects of circumferential air-splint pressure on flexor carpi radialis H-reflex in subjects without neurological deficits.

The purposes of this study were to investigate the effects of circumferential pressure on flexor carpi radialis (FCR) H-reflex in subjects without neuromuscular deficits and to evaluate the skin's contribution to this effect. FCR H-reflex was assessed in 43 subjects by measuring the peak-to-peak amplitude change before, during, and after circumferential pressure was applied to the forearm. Twelve H-reflexes (H/M ratio: M = 25%, SD = 14) were recorded before pressure application to obtain a baseline value (H(baseline)) to which all data were compared. A pneumatic 15 to 20-cm air splint inflated to 51-60 mmHg provided the pressure around the forearm. H-reflex recordings were taken at 1, 3, and 5 min. during (H(pressure)) and after pressure application. A second smaller study (placebo), in which the air splint was inflated to 0 mmHg, was conducted in 5 subjects to ensure that changes in reflex amplitudes were not a result of cutaneous effects. Two types of responses were observed in the FCR H-reflex following pressure application. One group of subjects significantly increased in H-reflex amplitude while another group decreased in H-reflex amplitude when compared to H(baseline). Regression analysis found that H(max) explained 37.2% of the variance when controlling for H(baseline). Subjects with larger H(max) showed an increase in H(pressure) while subjects with lower H(max) showed decreases in H(pressure) The placebo study revealed no differences in H-reflex amplitude from baseline values, implying that skin stimulation from the air splint has no role in the effects observed. The dichotomous result indicates that pressure influences the upper extremity differently than it does the lower extremity in certain individuals. Clinicians, using circumferential pressure as a therapeutic modality to lower muscle activity of the upper extremity, need to be cognizant that pressure may have contrasting effects on their patients.

Adult↗

The lateralization of the grasp reflex in human newborns.

The strength of the grasp reflex from the right and left hands was estimated in male and female newborns within the second day after birth. In the total sample (N = 121), the mean strength of the grasp reflex from the right hand was found to be significantly higher than that from the left hand. There was a significant positive linear correlation between reflex strengths from the right and left hands. The mean right minus left (R - L) reflex strength was found to be significantly larger than zero. There was a positive linear relationship between the R-L reflex strength and the reflex strengths from the right and left hands. This was more pronounced for the right hand than the left hand. The reflex strengths from the right and left hands were found to be positively linearly correlated with the weight of the newborn babies. These results indicated a grasp reflex lateralization in newborns. The right-bias in the grasp-reflex asymmetry established in this work would create a basis for the development of the right-hand preference in adulthood.

Body Weight↗

There is a relatively left-biased grasp-reflex asymmetry in human newborns with familial sinistrality compared to those without familial sinistrality.

Grasp-reflex asymmetry was studied in human newborns with regard to familial sinistrality (FS). In the total sample, the following results were obtained. The mean grasp-reflex strength from the right hand was found to be significantly greater than that from the left hand in FS- subjects. There was no significant difference between these parameters in FS+ subjects. The mean right minus left (R-L) reflex strength was significantly greater than zero in FS- subjects. The mean R-L reflex did not significantly differ from zero in FS+ subjects. The mean reflex strength from the right hand was found to be significantly greater in FS- subjects than FS+ subjects. There was no significant difference between the mean reflex strengths from the left hands of the FS- and FS+ subjects. The mean R-L reflex in subjects FS- was found to be significantly greater than that in FS+ subjects. Similar results were obtained from the male and female subjects. It was concluded that FS is an important factor determining the degree of the grasp-reflex asymmetry in newborns. The relatively left-biased grasp-reflex asymmetry under the influence of FS indicates a genetic origin of the motor asymmetry in newborns. This, in turn, suggests that cerebral lateralization inducing manual asymmetry in humans may have been preprogrammed genetically.

Female↗

Effect of manual acupuncture and transcutaneous electrical nerve stimulation on the H-reflex.

Several studies find that manual acupuncture and transcutaneous electrical nerve stimulation (TENS) are via different mechanisms and generate different effect on the central nervous system, therefore, the aim of the present study was to compare the effect of manual acupuncture (MA) and TENS on the spinal cord using H-reflex recordings. A total of 13 healthy adult volunteers were studied. The electrical stimuli were delivered to the posterior tibial nerve transcutaneously at the left popliteal fossa to evoke the soleus H-reflex. MA, 2Hz TENS, 100 Hz TENS, respectively, was applied to the surface of the right first dorsal interosseous muscle exactly at the Hegu acupoint (LI.4). Four assessments were performed randomly, separated by an interval of at least three days in all the subjects as follows: 1) Control assessment: a pair of electrodes placed on the surface of the right Hegu acupoint (LI.4), but no electrical stimulation was delivered throughout the test; 2) MA assessment: MA was done at the right Hegu acupoint (LI.4) for 15 minutes; 3) TENS assessment at 2Hz: electrical stimulation (40 mA in intensity) at 2Hz was applied to the surface of the right Hegu acupoint (LI.4) for 15 minutes; 4) TENS assessment at 100 Hz: electrical stimulation (20 mA in intensity) at 100 Hz was applied to the surface of the right Hegu acupoint (LI.4) for 15 minutes. Each assessment was divided into three periods as follows: 1) Baseline period: H-reflexes recorded prior to MA or TENS; 2) TENS period: six H-reflex recordings after MA or TENS for a duration of 4-5 min, 9-10 min and 14-15 min, respectively; 3) Post TENS period: H-reflex recordings of 6 after TENS period 4-5 min and 9-10 min, respectively. Our results indicate that both 2Hz TENS and 100 Hz TENS increased the amplitude of the H-reflex, and that these increases may be retained longer with 100 Hz TENS than with 2 Hz TENS, whereas MA could not increase the amplitude of the H-reflex. MA, TENS at 2 Hz or 100 Hz didn't change the latencies of the H-reflexes. We conclude that both 2Hz and 100 Hz TENS increased the amplitude of the H-reflex, suggesting that TENS enhances the excitability of the motoneuron pool in the spinal cord, and 100 Hz TENS has a greater effect than 2Hz TENS, whereas MA was not similar effect to TENS on spinal cord.

Acupuncture Therapy↗