Maximal Reflex Research Articles

Movement modulation of a short latency reflex linking the lower leg and the knee extensor muscles in humans

Movement modulation of a heteronymous short latency spinal reflex was investigated with transcutaneous, low threshold, stimuli to the common peroneal nerve, during leg pedalling in humans. Electromyographic (EMG) electrodes on the skin over the quadriceps muscles revealed an excitatory response at a minimum latency of 22.8 msec. Samples were obtained at 5 phases in the cycle of pedal crank rotation, and for stimulus intensities to evoke both maximal, and submaximal, reflexes in quadriceps. Over the pedal cycle, the peak-to-peak magnitude of the reflex, in the 3 quadriceps muscles studied, was deeply modulated, including an areflexive phase. The reflex magnitude was linearly dependent on the ongoing EMG activity in quadriceps. It could be fully re-initiated if contractions were produced out of phase in pedalling. The slopes of the regression lines of reflex magnitude (as % maximum reflex) on contraction level (% maximum voluntary contraction) when pedalling (1.05 ( r = 0.86, P < 0.01)), and with isometric contractions in the same subjects seated (1.03 ( r = 0.69, P < 0.01)), were very similar, with similar thresholds. This contrasts with the inhibition of soleus H reflexes during human gait. The present heteronymous reflex, acting between limb segments, is modulated coincident with ongoing contraction level in the target muscle.

Excitotoxin-induced degeneration of rat vagal afferent neurons

The inferior vagal or nodose ganglion contains the perikarya of vagal afferent neurons that function as cardiopulmonary and abdominal visceral receptors as well as aortic arch baroreceptors. In this study we have sought to utilize the axon-sparing properties of the excitotoxins kainic acid,N-methyl- d-aspartic acid and α-amino-3-hydroxy-4-isoxazolepropionic acid to destroy the perikarya of these sensory neurons and thus selectively de-afferent the vagus in the rat. Kainic acid (0.5 nmol/μl, 2 × 2μl) was applied topically to both nodose ganglia and the rats were allowed to recover for 7–8 days. Baroreceptor heart rate reflex activity was assessed in these conscious rats. Baroreceptor heart rate reflex gain was reduced (−51%) in kainic acid-treated rats, as was the maximal reflex bradycardia induced by the pressor agent, phenylephrine. Kainic acid treatment did not alter resting mean arterial pressure or heart rate. Vagal efferent neurons were spared by kainic acid treatment since bradycardic responses to electrical stimulation of the peripheral end of a cut vagus were not impaired. Histological studies showed marked destruction of perikarya within the nodose ganglia of kainic acid-treated rats: inflammatory and degenerative changes were evident at 2 days, and at 10 days there was considerable loss of neuronal cell bodies, but sparing of axons. Topical application to the nodose ganglion of α-methyl- dl-aspartic acid (6.8 nmol/μl, 2 × 2μl), a non-excitotoxic dicar☐ylic acid, failed to alter baroreflex sensitivity or produce perikaryal degeneration in nodose ganglia. In other studies, kainic acid (0.5 nmol/μl, 2 × 2 μl),N-methyl- d-aspartic acid (6.8 nmol/μl, 2 × 2μ1) or α-amino-3-hydroxy-4-isoxazolepropionic acid (0.54 nmol/μl, 2 × μl), when applied unilaterally to the nodose ganglion, produced after 7–8 days significant reductions in the 5-hydroxytryptamine-induced Bezold-Jarisch reflex after contralateral vagotomy and appreciable losses of neuronal cell bodies. These findings suggest that the excitotoxins may be useful as selective agents for inducing chemical deafferentation of mixed peripheral nerves and, in particular, for studying the role of vagal afferent neurons in cardiovascular reflexes.

Facilitation and inhibition of synaptic transmission in the spinal cord: an electroneurographic study in humans

The neurographic activity evoked either by stimulation of the tibial nerve at the popliteal fossa or by percussion of the Achilles tendon has been recorded at lumbar and thigh levels, in order to find out whether conduction time, temporal dispersion and central delay of the neural volleys underlying the monosynaptic reflex (H or T) may change as a function of stimulus intensity; under facilitatory or inhibitory experimental conditions; "spontaneously", i.e. during the steady state. The reflexly evoked ventral root discharge (VRD) decreases in latency with increasing stimulus intensity up to the maximum reflex response in the absence of changes in afferent (thigh to spine) or efferent (spine to thigh) conduction times. Reduction of the central delay was greater with mechanical than electrical stimulation, probably due to the combined effect of spatial and temporal summation under the former experimental condition. The latency of the VRD related to the maximal H response was not further modified by supramaximal stimulus strengths. The Jendrassik manoeuvre caused a significant decrease in latency of the VRD, the opposite effect being observed during calf muscle vibration. A significant relationship between amplitude and latency of single VRDs could be demonstrated during the "steady state". Our data point to the existence of a positive correlation between the size of the motoneuronal pool activated by an afferent volley and speed of transmission in the reflex pathway, both during the "steady state" and under either facilitatory or inhibitory experimental conditions, provided that the test stimulus strength does not exceed the maximum reflex response (H or T). No detectable signs of peripheral dispersion of the VRD could be demonstrated, irrespective of the stimulus employed: this suggests that the axon diameters of the motoneurones contributing to the monosynaptic reflex fall within a fairly narrow distribution.

Phasic stretch reflex of the abdominal muscles

This analysis of the abdominal stretch reflex (ASR) evoked by a tap to the abdomen was designed to explore how abdominal motoneurons process signals from respiratory and nonrespiratory sources. We recorded surface EMGs from the external and internal oblique muscles in standing subjects. Amplitudes of the abdominal stretch reflex varied despite constant tap forces, but strong taps evoked a larger reflex than weak taps. Trunk rotation toward the recording side, or voluntary contraction of the external and internal oblique muscles increased the reflex amplitudes, whereas contralateral rotation reduced their occurrence. An abdominal stretch reflex during a voluntary contraction was followed by a silent period of 40 to 80 ms. Often a late wave followed a reflex by 20 to 40 ms. Amplitudes during breathholds at residual lung volume were larger than those evoked during a breathhold at functional residual capacity, suggesting that abdominal stretch reflex amplitudes are inversely proportional to static lung volume. During quiet breathing the reflex amplitude reached a maximum slightly before end-expiration and decreased progressively to a minimum close to end-inspiration. During rebreathing, background abdominal activity was augmented with highest activity in late expiration. Abdominal stretch reflex amplitudes continued to wax and wane in phase with respiration, and the maximal reflex occurred progressively earlier in expiration. In summary, the abdominal stretch reflex reflects strong control from abdominal muscle spindles, lung proprioceptors, and chemoreceptors. The relative contributions of these inputs need to be determined.

Reflex cardiovascular responses caused by stimulation of pulmonary C-fibers with capsaicin in dogs.

The purpose of these studies was to determine quantitatively the reflex cardiovascular responses to stimulation of the pulmonary C-fibers in dogs. We used a preparation in which the airway, pulmonary artery, and the pulmonary veins to the left lung were cannulated in situ. Ventilation and perfusion of the right lung maintained the animal in relatively normal homeostasis. Capsaicin, a decylenic acid amide of vanillylamine that selectively stimulates nerve endings of unmyelinated fibers (C-fibers), was injected into the left pulmonary artery in 5-ml boluses. Maximal reflex responses were obtained with concentrations as low as 0.8-1.6 X micrograms-1 X kg-1. Heart rate, hindlimb resistance, and left ventricular contractility were lowered transiently (the maximal responses showing declines of 40, 13, and 15.2%, respectively). As a result of these changes, combined with vasodilation in other resistance vessels, cardiac output fell 28% and blood pressure fell 35%. Interrupting the afferent neural pathway by severing the ipsilateral cervical vagus nerve eliminated these responses, confirming the distribution of their reflex origin. Although the role of these reflexes in homeostasis has not been decided, the results of this study suggest that the lungs of dogs, if appropriately stimulated, potentially can exert a major inhibitory influence on the neural regulation of cardiovascular function.

Vascular capacitance: its control and importance.

In this review I have presented evidence that vascular capacitance can be controlled by a number of cardiovascular reflexes. In particular, changes in the stimulus to baroreceptors can result in near maximal responses of capacitance. The vessels in the abdomen are almost certainly the only ones which make a significant contribution to the overall response and these vessels are particularly sensitive to low frequencies of sympathetic discharge. The overall maximal reflex change in capacitance, particularly if the spleen is excluded, is quite small in relation to changes in volume which occur secondarily to changes in tissue blood flow or in venous pressure from other causes. There are likely to be few manoeuvres which would result in an active capacitance response in man greater than about 200 ml and the maximal response is unlikely to be much more than about 300 ml. It seems likely that most of the capacitance “reserve” would be taken up when man assumes an upright posture and it is unlikely that any large further mobilizable reserve is available. However, although the total response seems to be small, it may not be entirely unimportant. Standing reduces cardiac output by about one-third under normal circumstances and, presumably, despite constriction of the capacitance vessels. Without this constriction, it would probably be equivalent to a small haemorrhage, and following even quite small haemorrhage postural hypotension is much more common.

Epidural morphine strongly depresses nociceptive flexion reflexes in patients with postoperative pain.

The comparative effects of low doses (0.03-0.04 mg/kg) of epidural morphine on a nociceptive flexion reflex of the lower limb and on postoperative pain in volunteer patients were studied after orthopedic surgery on one knee. According to the stimulation parameters, it was found that 40-50 min after the injection, morphine produced an increase of 87% and 83% of the reflex threshold and of the threshold of maximal reflex response, respectively, as well as a 80-90% depression of the nociceptive responses when elicited by a constant level of stimulation. Onset of pain relief occurred by the 25th min and increased to a maximum stable level 40-50 min after the injection. These data support the hypothesis that the main site of the pain-relieving effect of epidural morphine is located directly at a spinal level.

Studies on pain. Effects of morphine on a spinal nociceptive flexion reflex and related pain sensation in man

The nociceptive flexion reflex and the corresponding subjective pain score elicited by sural nerve stimulation were studied in 6 healthy volunteers. A significant correlation was found between the respective recruitment curves of the reflex and of the pain score as a function of stimulus intensity. Consequently, the reflex (T r) and the pain (T p) thresholds were found to be almost identical (mean: 10.6 and 10.3 mA, respectively). Similarly, the threshold of the maximal reflex response (T mr) was very close to that of intolerable pain (T ip): 37.1 and 38.8 mA, respectively. These four parameters were studied before and after intravenous administration of morphine chlorhydrate (0.05, 0.1, 0.2 and 0.3 mg/kg) and subsequent administration of naloxone hydrochloride (0.02 mg/kg; i.v.). While 0.05 mg/kg morphine remained without any effect, higher doses produced an increase in the four thresholds (T r, T p, T mr, T ip). Furthermore, a very significant linear relationship was found between the importance of the increase and the dose of morphine. Morphine also depressed in a dose-dependent fashion, the nociceptive reflexes elicited by a constant stimulation intensity (1.2–1.3 T r). All these effects were immediately reversed by subsequent naloxone. During all the pharmacological situations, variations in T r and T p as well as in T mr and T ip were found to be very significantly linearly related, indicating a close relationship between the effects of morphine on the nociceptive reflex and on the related pain sensation. These results suggest that, in our model involving a brief ‘epicritic’ nociceptive stimulus, the mechanisms of morphine-induced analgesia in man can be explained by a depressive effect on the nociceptive transmission directly at a spinal level.

Forelimb responses to cutaneous nerve stimulation during locomotion in intact cats

The reflex responses of forelimb muscles to electrical stimulation of the cutaneous superficial radial nerve were recorded during treadmill locomotion in chronically implanted cats. In brachialis and cleidobrachialis (muscles which are active mainly during the swing phase) the responses were maximal during the swing phase and minimal or absent during the stance phase. In the long head of triceps which is active mainly during the stance phase, responses were also minimal during stance and maximal during swing. It is concluded that, for some muscles, the period of maximal reflex responsiveness can be out of phase with the period of the step cycle during which they are normally active.

Acoustic-Reflex Adaptation

Acoustic-reflex adaptation was studied in 35 subjects with normal hearing using nine pure-tone activators (250-6000 Hz) and a broadband-noise activator. The individual subject data generated by the 31-s activators presented 10 dB above the reflex threshold were digitized, corrected for baseline drift and ear canal volume, and analyzed in terms of the acoustic-admittance change in acoustic mmhos and in terms of the percentage of maximum-reflex magnitude. Reflex adaptation increased as a function of frequency. The adaptation functions for the lower frequencies (less than or equal to 1500 Hz) were essentially linear over the 31-s activator period, whereas the functions for the higher frequencies (greater than or equal to 2000 Hz) were curvilinear over the activator period. The experimental half-life data are compared with a theoretical half-life function that was generated to estimate normal acoustic-reflex adaptation as a function of activator frequency. Finally, the means and standard deviations are reported and discussed for (a) the onset time of adaptation, (b) the half-life time, and (c) the percentage of maximum reflex magnitude at 5-s intervals from 5 to 30 s.

Baroreceptor heart rate reflex in rabbits after reversal of renal hypertension.

The baroreceptor heart rate reflex was studied in 26 renal hypertensive and 17 normotensive rabbits and in 13 rabbits after reversal of hypertension. Blood pressure and heart rate were varied by bolus injections of methoxamine or nitroglycerine in conscious rabbits, and a logistic sigmoid function was fitted to the pressure-heart rate data to estimate upper and lower heart rate plateaus, median blood pressure, and reflex sensitivity. In hypertensive rabbits, resetting of the blood pressure-heart rate curves to higher pressures was associated with reduced reflex sensitivity, increased lower heart rate plateau, and operating pressures significantly greater than the region of maximum reflex sensitivity, resulting in substantial attenuation of reflex bradycardia in response to hypertension. Reflex bradycardia after smoke inhalation was normal. Reversing the hypertension completely reversed the abnormalities in baroreflex control of heart rate. Renal hypertension in the rabbit produces functional changes that are completely reversible in the baroreceptor-heart rate reflex, probably in the afferent limb.

Psychophysical and electrophysiological approaches to the pain-relieving effects of heterotopic nociceptive stimuli.

The nociceptive flexion reflex (RIII reflex) and the concurrent subjective pain score elicited by right sural nerve stimulation at random intensities were studied in 10 healthy volunteers. A close relationship was found between the recruitment curves of the reflex and the pain score as a function of stimulus intensity. As a consequence, the threshold of the RIII reflex (Tr) and of pain sensation (Tp) were found to be almost identical (mean: 9.8 and 11.3 mA, respectively). Similarly, the threshold for obtaining a maximal reflex response (Tmr) was found to be very close to that for intolerable pain (Tip): 33.5 and 35.1 mA, respectively. These four parameters were studied before and during the immersion of the left hand into a heated thermoregulated waterbath at various temperatures (from 40 to 47.5 degrees C). While nonnociceptive temperatures (40 to 44 degrees C) were without effect, higher conditioning temperatures induced an increase in the four thresholds. In addition, a highly significant linear relationship was observed between the increase in these thresholds and the intensity of the conditioning stimulus in the 44 to 47.5 degrees C range. These four parameters were also studied before and during three other nociceptive conditioning stimuli: immersion of the left hand into a 6 degrees C waterbath, 10 watts muscular exercise of the left hand performed under ischaemia and a painful (5.5 kg/cm2) pinch applied on the nasal septum. These three conditioning situations induced a very significant increase of the four thresholds considered in this study with the greatest being observed during nociceptive cold applied to the left hand. During all the conditioning situations, variations in Tr and Tp as well as in Tmr and Tip were found to be linearly related. This indicates a close relationship between the effects of the conditioning nociceptive stimuli on the reflex and the related pain sensation. These results suggest that the modulation of pain by heterotopic nociceptive stimuli can be explained at least in part by a depression in the transmission of nociceptive messages at the spinal level. They are discussed with reference to the counterirritation phenomena and common features with 'diffuse noxious inhibitory controls' (DNIC) are underlined.

Neuroethological studies of reflex plasticity in intact Aplysia.

Multi-unit recording of siphon nerve activity in intact Aplysia california with chronically implanted cuff electrodes provided a monitor of activity in a central pattern generator, the Interneuron II (Int II) network, which produces large siphon and gill contractions both spontaneously and after tactile stimulation of the siphon. The phase-response curve of the Int II oscillator for single stimuli at different phases of the cycle showed a "refractory" period early in the cycle after which most stimuli phase advanced the oscillator and caused a short-latency Int II burst and a large contraction. The amplitude of gill withdrawal and the duration of siphon withdrawal in response to different stimulus intensities depended on whether an Int II burst was triggered. Activation of the Int II oscillator transformed the reflex from one that was graded smoothly with stimulus intensity to one in which nearly maximal responses were elicited even by weak stimuli. Entrainment and habituation training both involved monotonous repetition of a stimulus at specific intervals. With repeated siphon stimuli, nearly maximal reflex responses were maintained in intact animals as long as the Int II oscillator was entrained, whereas habituation was associated primarily with failure to entrain the oscillator. Long-term sensitization of the reflex was characterized by large and prolonged withdrawal responses. Sensitized animals showed significantly more triggered Int II bursts than did controls. In addition, digital spike-train analysis indicated that individual siphon motoneurons showed significantly increased background activity which often persisted for several minutes.

Reactivated response of blink reflex in the cat.

Three reflex responses in the orbicularis oculi muscles were observed by electrical stimulation of the trigeminal nerve in lightly anesthetized or conscious cats. The third response, following the first and second responses, was concluded as being a "reactivated response" of the blink reflex as it was set up by the trigeminal afferent input evoked by the palpebral movement of the preceding blink. The reasons for this were as follows: 1) the third response disappeared on administration of muscle relaxants and 2) was enhanced by touching the palpebral hair; 3) the palpebral movement activated the afferent discharges of the trigeminal exteroceptors which were strong enough to yield the reflex responses and 4) the latency of the first reflex response by the palpebral movement corresponded to the time lag between the preceding large reflex response and the third response; 5) the third response was hardly suppressed at all until the first response disappeared over a period of maximum reflex suppression following the conditioned stimulation of the trigeminal nerve.

Role of bulbar serotonergic neurotransmission in the initiation of swallowing in the rat

In rats anaesthetized with urethane and subjected to pharyngolaryngeal deafferentation, activation of central serotonin receptors was shown to evoke repetitive swallowing. Dose-response relationships were examined for the deglutitory effects of l-tryptophan, l-5-hydroxytryptophan ( l-5-HTP), quipazine (QPZ), chloro-piperazinyl-pyrazine (CPP), 5-methoxydimethyltryptamine (5-MeODMT) and tryptamine. Agonists could be grouped according to their efficacy in increasing either repetitive swallowing rate or buccopharyngeal deglutitory pressure. With respect to the former, the efficacy increased in the following order: 5-MeODMT, l-tryptophan < tryptamine, l-5-HTP < QPZ < CPP; with respect to the latter, it decreased in the order: 5-MeODMT, QPZ > l-5-HTP, l-tryptophan > tryptamine, CPP. The stimulatory effects on the swallowing rate were inhibited by methysergide, metergoline and d-lysergic acid diethylamide (LSD). The persistence of these effects after decerebration and their elicitation, upon close-arterial and topical drug administration to the fourth ventricle, implicate the rhombencephalon as the major locus of action. Serotonin agonists enhanced reflex deglutition elicited by electrical stimulation of the superior laryngeal nerve or the solitary tract. Antagonists blocked the facilitation of reflex swallowing at the same dose levels at which they abolished agonist-evoked swallowing; however, they failed to diminish maximal reflex responses. The data support the hypothesis that the neural substrate of serotonergically-evoked, “automatic” swallowing is organized within the rhombencephalon and operates to set a facilitatory bias for deglutitory internuncial neurones as well as effector motoneurones.

Reflex cardiovascular responses induced by electrical stimulation of glossopharyngeal nerves in the rat

Reflex cardiovascular responses to electrical stimulation of glossopharyngeal nerves (GPN) were studied in Dial-Urethane anesthetized rats. GPN stimulation at 3 V, 0.3 msec and 50 Hz produced maximal reflex depressor (34 ± 2 mmHg) and bradycardia (21 ± 2 beats min ) responses that were altered as follows: pentolinium (0.25 mg kg , i.a.) blocked approximately 72% and 89% of control values of depressor and bradycardia responses, respectively; tripelennamine (5 mg kg , i.a.) significantly reduced depressor responses (76%); whereas atropine (0.4 mg kg , i.a.) blocked only bradycardia (85%). Regional blood flow studies showed that GPN stimulation reduced systemic arterial pressure (approximately 25%), and increased iliac artery blood flow (5%), and decreased blood flow through the renal (14%) and superior mesenteric (13%) arteries. Hence, decreases in vascular resistance during GPN stimulation were greater in the hindlimb vascular bed (28%) than in the renal (14%) or the mesenteric vasculatures. In addition, the magnitude of decreases in hindlimb vascular resistance by GPN stimulation was reduced (80%) by pretreatment with tripelennamine, but not by atropine. The results suggest that reductions in arterial blood pressure and hindlimb vascular resistance of the rat in response to GPN stimulation may be mediated via a histaminergic vasodilator mechanism, and that there may be a differential pattern of reflex vascular adjustments of blood flow and vascular resistance among regional vasculatures of the rate.

Unaltered maximum reflex vasodilatory capacity of the perfused hindquarters of spontaneously hypertensive rats.

Hindquarter reflex vasodilation (RVD delta mmHg decrease in perfusion pressure) in response to arterial pressure elevations by intravenous norepinephrine (NE) was examined in young (2 1/2-3 months) and mature (8-10 months) spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) normotensive rats to ascertain whether maximum reflex vasodilatory capacity is altered in the developmental and/or established stages of spontaneous hypertension. The maximal RVD was not significantly different in young or mature SHR (young 26.2 +/- 1.9 and mature 36.2 +/- 3.2) compared to age-matched WKY controls (young 23.9 +/- 1.8 and mature 29.6 +/- 2.3) (P greater than 0.05 between SHR vs. WKY at both ages). However, the rise in mean systemic arterial pressure by NE which produced maximal RVD was greater in mature SHR (116.0 +/- 7.4 mmHg) than in WKY controls (78.3 +/- 6.2 mmHg) (P less than 0.01), whereas no such differences were found between young SHR (85.1 +/- 6.5 mmHg) and its WKY controls (87.5 +/- 2.3 mmHg). There was no difference in the dose of NE that required maximal responses of reflex vasodilation in young or mature SHR compared to WKY controls. In each age group of SHR or WKY rats, RVD was linearly related to the arterial pressure increments. The slope (a +/- SEM) of the regression line for the correlation between the pressure rises and resultant RVD was similar in young SHR (a = 0.424 +/- 0.061) and WKY controls of (a = 0.458 +/- 0.013). In contrast, the slope of the regression line for these two parameters in mature SHR (a = 0.250 +/- 0.004) was significantly smaller than that of either WKY controls (a = 0.364 +/- 0.010) or young SHR (P less than 0.01). The direct hindquarter vasodilation of mature SHR in response to intra-arterial administration of histamine or nitroglycerin was not different compared to that of WKY controls. The results indicate an unaltered maximum hindquarter reflex vasodilatory capacity during the developmental and established stages of genetic hypertension in SHR. An additional finding in the present study was the abnormal responsiveness of the baroreceptor reflex vasodilator system of mature SHR to a wide range of arterial pressure elevations. This abnormal responsiveness may contribute to the maintenance of high blood pressure in the established stage of hypertension.

Regional flow patterns during the serotonin-induced cardiogenic hypertensive chemoreflex.

Small amounts of serotonin injected into the left atrium produce a hypertensive cardiogenic chemoreflex. The afferent pathway is through the vagus, while both the sympathetic and the vagus nerves participate in the efferent response. In 44 anaesthetised dogs, using flow probes, we studied the direction, extent and time sequence of the changes in aortic and regional blood flow during this hypertensive chemoreflex. After serotonin mean aortic pressure rose from 14.1 to 25.9 kPa. Coinciding with the early phase of hypertension, mean cardiac output decreased from 1.95 to 1.60 litre·min−1 which resulted in a significant increase in calculated systemic resistance (+49%). After the transient initial decline there was a rapid increase in cardiac output that virtually doubled in the following 10 s. Three types of organ system dependent flow patterns are readily distinguishable. Whereas no reflex vasoconstriction is detectable in the coronary arteries, both the renal and the mesenteric vascular circuits undergo profound reduction in blood flow. At rest flow in the left anterior descending coronary artery averaged 30 cm3·min−1 and peak flow achieved during the reflex increased to 164 cm3·min−1. Control renal and mesenteric flow averaged 170 and 195 cm3·min−1 respectively. At the time of maximal reflex vasoconstriction flow was reduced to 20 and 15 cm3·min−1 respectively resulting in a 13 and 18 fold increase in calculated resistance. Between the extremes represented by the non-responding coronary circulation and marked response in renal and mesenteric circulations, an immediate but minor vasoconstriction was also observed in the regional circuits of the carotid and femoral arteries. The observed reflexly mediated adjustments of flow resemble the response patterns that characterise flight or fight reaction and may represent an important type of survival reflex.

Tremor in the tension developed isometrically by soleus during the tonic vibration reflex in the decerebrate cat.

1. Irregularities in the development of tension during the tonic vibration reflex of the soleus muscle of the decerebrate cat have been analysed into their frequency components. The reflex was recorded isometrically and elicited by longitudinal vibration, normally at 150 Hz. The amplitude of vibration was set so as to elicit a maximal reflex response, suggesting 1:1 driving of the majority of the Ia afferents at the frequency of vibration. 2. The resulting power spectrum regularly showed a well marked tremor peak separated by a trough from any slow irregularities. The predominant frequency of this tremor varied from 4 to 11 Hz in different preparations, with a mean of 7.4 Hz; on average, frequencies within 1.7 Hz on either side contained over half the power of the predominant frequency. Altering the frequency of vibration did not alter the distribution of tremor frequencies. 3. The root mean square value of the tension irregularities, over the range 4-14 Hz, varied from 12 to 110 mN in different preparations (median value, 23 mN); this was superimposed on mean active reflex tensions varying from 2 to 10 N. 4. The 'tremor' due to a single motor unit was estimated from spectral analysis of tetanic contractions of the whole muscle and decreased with increasing frequency of activation. Comparison of the single unit values with the tremor seen during vibration in the same preparations showed that equivalent amounts of tremor to the latter could typically have been produced by the continued synchronous contraction of about five 'average' motor units firing at the predominant tremor frequency. 5. When a tonic stretch reflex was present its tremor frequencies did not differ consistently from those of the tonic vibration reflex. On average, the tremor was smaller for the stretch reflex than for the tonic vibration reflex; the difference was usually slight and might have been related to the stretch refex tension being smaller. 6. Evidence was obtained that the tremor was not due to any insecurity of 1:1 driving of the Ia afferents by the vibration. First, the tremor did not increase when the amplitude of vibration was decreased sufficiently to ensure that the degree of 1:1 driving must have been reduced. Secondly, the introduction of a comparable 'artificial tremor' by sinusoidally oscillating the muscle at low frequency did not produce the e.m.g. response that would have been expected if the applied 'tremor' had been modulating the firing of the Ia or any other group of afferents. 7. It is concluded that the observed tremor cannot be attributed to 'oscillation in the stretch reflex arc', though without prejudice to the role of this mechanism under other conditions and especially when the recording is not isometric. However, the genesis of the tremor has not been established and much of it might result simply from the chance synchronization of motor units that are firing below their tetanic fusion frequency.

Clinical features of the Guillain-Barré syndrome

In a country-wide search for patients with Guillain-Barré syndrome (GBS) in Israel, 89 patients were found between 1969 and 1972 who met standardized diagnostic criteria. These cases, derived from a well defined population, were analyzed to provide a more accurate picture of the full range of clinical signs than is available from selected case series in the literature. Preceding illnesses, presenting symptoms, maximal neurological deficit, reflex changes, sensory deficit, cranial nerve, sphincter, respiratory, autonomic disturbances and spinal fluid changes were determined. Mortality was 5.6% which is lower than in many series. Alternatives to account for the apparent benignity of GBS in Israel were offered.