We studied stretch reflexes of soleus muscles of intercollicularly decerebrated cats using a new technique for estimating the component of a stretch reflex that results from the purely mechanical properties of the active muscle (mechanical response). The difference between a net stretch reflex and its underlying mechanical response provided a direct measure of reflex action. 1. The relative contributions of reflex action and the mechanical response are different for stretch and release. With stretch, reflex action is generally large and the mechanical response small. The opposite is true with release. The property that remains relatively constant, when stretch and release are compared, is the net stiffness in opposition to length change. We concluded that reflex action compensates for variations in the inherent stiffness of the muscle. 2. Compensation is effective over a range of intermediate values of initial force, but it fails whenever the reflex force approaches zero or the maximal force at that length. 3. Reflex action is capable of modifying muscular force within 22 ms of the onset of length change. This indicates that even during a fast gallop, there is sufficient time for reflex action. 4. The mechanical properties of the active soleus muscle are highly nonlinear; e.g., muscular stiffness becomes negative transiently during stretch. In stable decerebrate preparations we found that reflex action resulted in a considerable improvement in linearity. 5. Our results support two complementary hypotheses: a) stiffness may be the regulated property of the stretch reflex, and b) the main function of autogenetic reflexes may be to conpensate for variations in the properties of skeletal muscle rather than to oppose changes in load.
The overall scheme for control is as follows: central command sets basic patterns of cardiovascular effector activity, which is modulated via muscle chemo- and mechanoreflexes and arterial mechanoreflexes (baroreflexes) as appropriate error signals develop. A key question is whether the primary error corrected is a mismatch between blood flow and metabolism (a flow error that accumulates muscle metabolites that activate group III and IV chemosensitive muscle afferents) or a mismatch between cardiac output (CO) and vascular conductance [a blood pressure (BP) error] that activates the arterial baroreflex and raises BP. Reduction in muscle blood flow to a threshold for the muscle chemoreflex raises muscle metabolite concentration and reflexly raises BP by activating chemosensitive muscle afferents. In isometric exercise, sympathetic nervous activity (SNA) is increased mainly by muscle chemoreflex whereas central command raises heart rate (HR) and CO by vagal withdrawal. Cardiovascular control changes for dynamic exercise with large muscles. At exercise onset, central command increases HR by vagal withdrawal and "resets" the baroreflex to a higher BP. As long as vagal withdrawal can raise HR and CO rapidly so that BP rises quickly to its higher operating point, there is no mismatch between CO and vascular conductance (no BP error) and SNA does not increase. Increased SNA occurs at whatever HR (depending on species) exceeds the range of vagal withdrawal; the additional sympathetically mediated rise in CO needed to raise BP to its new operating point is slower and leads to a BP error. Sympathetic vasoconstriction is needed to complete the rise in BP. The baroreflex is essential for BP elevation at onset of exercise and for BP stabilization during mild exercise (subthreshold for chemoreflex), and it can oppose or magnify the chemoreflex when it is activated at higher work rates. Ultimately, when vascular conductance exceeds cardiac pumping capacity in the most severe exercise both chemoreflex and baroreflex must maintain BP by vasoconstricting active muscle.
Experiments were done to determine the amplitude of the monosynaptically mediated H-reflex of the soleus muscle at various phases of the step cycle, using a computer-based analysis procedure. In all subjects tested the amplitude of the H-reflex was strongly modulated in amplitude during the walking cycle and was highest during the stance phase. In many subjects the peak reflex amplitude occurred at about the same time as the peak soleus electromyographic (EMG) activity, but in others it occurred earlier. The form of the reflex variation (i.e., envelope of H-reflex amplitude versus phase in cycle) during the step cycle could also be quite different from that of the EMG produced during stepping. At an equal stimulus strength and EMG level, the H-reflex was always much larger, up to 3.5 X, during steadily maintained contractions while standing than during walking. The large reflexes when subjects were standing are consistent with the control of position required to maintain a stable posture in this task. Similarly, the reflexes during walking are greatest during the stance phase, when they will assist in maintaining the upright position of the body against gravity. The reflexes are smallest during the swing phase when they would oppose ankle flexion. However, since the reflex amplitude is task-dependent (i.e., greater during standing than during walking at the same EMG and stimulus levels) and is not always closely related to the EMG produced during a given task such as walking, the strong modulation of H-reflex during walking is not simply a passive consequence of the alpha-motoneuron excitation level.(ABSTRACT TRUNCATED AT 250 WORDS)
1. The Hoffman reflex, or H reflex, was strongly modulated in the human soleus muscle during both walking (4 km/h) and running (8 km/h). It was relatively low at the time of heel contact, increased progressively during the stance phase, and reached its maximum amplitude late in the stance phase. During ankle dorsiflexion the H reflex was absent. 2. During running the peak e.m.g. level of the soleus was on average 2.4 times higher than during walking but the maximum amplitude of the H reflex was never larger than during walking. In fact, the H reflex was on average significantly (P less than 0.05 for one-tailed t test) smaller during running than during walking. Furthermore, the slope of the least-squares line fitted to the relation between the H reflex amplitude and the background e.m.g. was always steeper for the walking data than for the running data. 3. The difference in the H reflex in the two tasks is evidence that the size of the H reflex is not simply a passive consequence of the alpha-motoneurone excitation level, as indicated by the e.m.g., but is also influenced by other central neural mechanisms. We suggest that presynaptic inhibition is the most likely mechanism accounting for the change in the slope. 4. The modulation of the reflexes during walking and running can be interpreted in terms of the idea of automatic gain compensation. The decreased gain during running may be appropriate to reduce saturation of motor output and potential instability of the stretch reflex feed-back loop.
1. The stretch reflex in the elbow flexor musculature was studied in 23 human subjects. The subjects were required to establish an initial force equivalent to 10% maximum at a prescribed initial length; mechanical disturbances delivered at random times increased load force to 15% or reduced it to 5%. We measured arm force, displacement, and EMG (usually biceps); acceleration was calculated from displacement, and average responses from sets of 10 like trials. 2. Modification of the stretch reflex was studied by comparing average responses obtained with different instructions, but with the same disturbance. The usual introductions were "compensate for arm deflection" and "do not intervene voluntarily". The initial response did not depend on instruction; changes in response that depended on instruction began abruptly after a latent period which ranged from 70 to 320 ms (measured from force and acceleration), depending on conditions and subject. The latency became longer (10-50 ms) and more variable when the subject did not know the direction of disturbance in advance. This and other observations indicate that modifications of the stretch reflex are not produced by servo actions. They are produced by triggered reactions, which occur at both short and long latencies and which have properties resembling the movements produced in a reaction-time task. 3. We confirmed that most subjects can suppress triggered reactions when the instruction calls for no intervention, leaving an unmodified reflex response. This response consists of a compliant deflection of the arm in the direction of the disturbance. 4. The compensatory actions associated with unmodified stretch (and unloading) reflexes were assessed from EMG responses of biceps. During a 300-ms transient phase, EMG changes were notably asymmetric when responses to symmetric disturbances were compared. Increased force stretched biceps and produced a prominent increase in EMG, whereas decreased force allowed biceps to shorten and produced either an EMG decrease of smaller magnitude or an actual increase. These asymmetric reflex actions produced quite symmetric mechanical responses (arm displacements and forces), which implies the existence of and compensation for nonlinear muscle mechanical properties. This result is discussed in relation to the hypothesis that the function of the stretch reflex is to compensate for variations in muscle properties, thus maintaining stiffness. 5. Effective control of muscle length or joint position does not result from servo action by the stretch reflex. Errors in position are corrected only when triggered reactions are superimposed on the reflex response.
Un examen de l'histoire du réflexe indique que la définition historique n'a jamais été tout à fait justifiée et qu'elle comporte des interprétations occasionnelles (décrivant le réflexe comme inconscient, involontaire, non appris et ainsi de suite) lesquelles remontent à des présuppositions non scientifiques concernant le comportement des organismes. On offre une définition alternative, basée sur les seules évidences positives fournies par les données, où le réflexe est défini comme une corrélation observée de deux événements, un stimulus et une response. L'emploi phyisologique du mot et la méthode physiologique sont examinés et l'on trouve qu'ils ne nuisent pas à cette interprétation. Ensuite on discute certains aspects du rapport entre le réflexe et la description du comportement. On considère que l'analyse est nécessaire à cette description, et on examine les méthodes de l'analyse. On considère certaines questions actuelles remontant à l'emploi de l'analyse et les trouve sans signification. On décrit brièvement le rapport entre son processus expérimental et le réflexe comme ici défini, et on définit le concept “force du réflexe” et appuie sur son importance. On considère que la description du comportement se compose de la détermination de lois fonctionnelles comme celles ici présentées et ainsi qu'elle est incluse presque entièrement dans le principe du réflexe Referat Ein Ueberblick über die Geschichte des Reflexes weist darauf hin, dass die traditionelle Definition nie vollkommen berechtigt worden ist, und dass damit beiläufige Deutungen verbunden worden sind, (Beschreibung des Reflexes als unbewusst, unwillkürlich, ungelehrt, usw.), welche ihren Ursprung haben in unwissenschaftlichen Voraussetzungen über das Verhalten der Organismen. Es wird eine alternative Definition dargeboten, worin der Reflex als eine beobachtete Korrelation zwischen zwei Begebenheiten,— namentlich zwischen Reiz und Reaktion,—erklärt wird. Der Gebrauch des Wortes 'Reflex' in physiologischem Sinne und die physiologische Methode werden untersucht, und man findet, dass sie diese Deutung nicht entkräften. Es werden dann gewisse Seiten der Beziehung des Reflexes zu der Beschreibung des Verhaltens (behavior) besprochen. Die Analyse wird als zu dieser Beschreibung nötig betrachtet, und es werden analytische Methoden besprochen. Gewisse herrschende Fragen, welche im Gebrauch der Analyse ihren Ursprung haben, werden erwägt und als ohne Bedeutung betrachtet. Die Beziehung unseres experimentellen Verfahrens zu dem Reflex wie er hier definiert worden ist, wird kurz erörtert. Der Begriff der 'Reflexenstärke' (reflex strength) wird erörtert, und die Wichtigkeit dieses Begriffes wird betont. Es wird behauptet, dass die Beschreibung des Verhaltens aus der Bestimmung funktioneller Gesetze von der Art des hier dargebotenen bestehe, und dass sie also fast vollständig in dem Prinzip des Reflexes eingeschlossen sei.
The purpose of this study was to compare the amplitude of the flexion reflex of the biceps femoris muscle (BF) with the intensity of the painful sensation elicited by a nociceptive stimulation resulting from application of constant-current either on the sural nerve or on the skin in its distal receptive field. Experiments were carried out on 15 normal volunteers. It was observed that: (1) Stimulation of the sural nerve (either on or through the skin) elicits two different reflex responses in the BF: the first (RII) is of short latency, low threshold and corresponds to a tactile reflex. The second (RIII) is of longer latency and higher threshold, and corresponds to a nociceptive reflex. The threshold of RIII was found to be the threshold of a pain sensation. (2) Stimulation of the skin elicits only a late nociceptive (RIII) response in the BF. The threshold of this response was also found to be that of pain. (3) The threshold of both pain and RIII were found to be higher for sural nerve stimulation (10 mA) than for cutaneous stimulation (5 mA). It was suggested that the large diameter cutaneous fibers could have an inhibitory effect of both pain and the nociceptive reflex. This was supported by the results obtained during a selective ischemic block of the largest diameter fibers in the sural nerve, when a 10 mA stimulation was applied to the nerve. In this case, a decrease of the RII reflex was observed in BF, together with an increase of both RIII and pain sensation. Functional implications of these results are discussed.
The control of arterial pressure during sleep was studied in 13 untreated, unsedated subjects aged 20 to 46, including 7 with hypertension. Arterial pressure was measured directly. A transient rise of arterial pressure up to 30 mm Hg was produced by the sudden intravenous injection of 0.25 to 2 µg of angiotensin. Linear plots were obtained in 10 of 13 subjects when the systolic pressures of successive pulses during the pressure rise were plotted against the pulse intervals which began the next beat. The relationship was disturbed by movement or arousal, and was better when pulse intervals falling in inspiration were discarded. The slope of the line (milliseconds of cardiac slowing per millimeter rise in systolic pressure) in the awake subject ranged from 2 to 15.5 msec/mm Hg, and from 4.5 to 28.9 during sleep. Reflex sensitivity was highest in dreaming sleep. In 7 of 10 subjects, baroreflex sensitivity increased significantly during sleep; in 6, the prevailing arterial pressure was inversely correlated with the baroreflex sensitivity. The pressure appeared to be the dependent variable. It is concluded that the baroreceptor reflex are can be rapidly reset, particularly during sleep. The lower arterial pressures during sleep may be actively maintained in some subjects by increased baroreflex sensitivity.
1. The gain of the vestibuloocular reflex (slow-phase eye velocity/head velocity) was measured in 17 adult cats. 2. The gain of the reflex, in the dark, was 0.90 (+/-0.15 SD) over the frequency range 0.03-1.2 Hz. 3. In the range 0.01-0.15 Hz, the phase behaved as though the overall reflex time constant were 12 s or greater. The cupula time constant is 4 s. Therefore, the central part of the reflex must manipulate the canal signal to improve its low-frequency response by a factor of at least three. 4. When the cats wore left-right reversing prisms chronically and were also rotated for 2 h every day, the reflex underwent large, plastic changes. The gain, tested in the dark, decreased by 93% at 0.05 Hz and 55% at 1.2 Hz. In effect, the low-frequency response was abolished. The process took about 8 days. 5. In the light, with reversed vision, the gain decreased further and, at low frequencies, the eye movements did reverse in direction. 6. When the vestibulocerebellum was removed, the gain, in the dark, rose to about 1.17 and the plastic changes caused by reversing prisms were completely abolished. 7. Reversing prisms create vestibuloocular dysmetria. The change in gain they produce is considered to be an adaptive response designed to reduce image motion on the retina during head movements. The vestibulocerebellum is necessary for this adaptive process. It is proposed that detecting and repairing dysmetria (of natural origin) is an important cerebellar function.
The vestibulo-ocular reflex (VOR) is an elementary reflex, which attracted the attention of a number of classical neurophysiologists who studied, in particular, the reflexive compensatory eye movements induced by head movements (cfMagnus 1924, Lorente de No 1931). The major pathway for this reflex is the well-defined trineuronal are, composed of primary vestibu lar neurons, secondary vestibular neurons, and oculomotor neurons (Ra mon y Cajal 1909, Lorente de N6 1931, 1933, Szentagothai 1943, 1950, 1964, Brodal & Pompeiano 1957). The pioneering electrophysiological work by Lorente de N6 (1939) and by subsequent investigators recognized that the vestibulo-ocular reflex involves both excitation and inhibition (Szentllgothai 1950, Cohen et al 1964). More recent data about the VOR have been reviewed by Brodal (1974), Cohen (1974), Precht (1978), and Wilson & Melvill Jones (1979). In recent years, the vestibulo-ocular refiex has been reexamined in detail because of its close relationship with the cerebellum. Supported by remark able advances in cerebellar physiology and eye movement studies, the VOR has become an interesting and important subject of neurophysiology, espe cially for investigation of cerebellar control mechanisms. This article re views the efforts made in the past decade toward understanding the
No better description of the purpose of this book can be made than that given by the authors in the preface: "This small book attempts on behalf of the student of medicine— indeed, on behalf of any student interested in the physiology of the nervous system—a concise account of elementary features of reflex mechanism, as illustrated particularly by the mammalian spinal cord.... To that end the plan here followed is to introduce and describe seriatim a number of reflexes typically obtainable from the mammalian preparation. These in every instance are reflexes which take expression in the skeletal musculature, predominantly in that of the limbs. The description and discussion given of them in each case are directed mainly toward analysis of the working of the reflex mechanism. In that connection an object of study kept in view throughout is the individual motor unit as a basal element of the reflex response.
Abstract In a recent paper (cited henceforth as I) I have shown that the phenomena concerning the emission or reflexion of electrons by metals can be treated by calculating the emission or reflexion coefficient for the electrons at the surface of the metal and integrating over all incident electrons according to the electron theory of conductivity of Sommerfeld. In a further paper (cited henceforth as II), R. H. Fowler and the present author have treated the cold emission in intense electric fields on the same principle. The surface of the metal is characterised thereby as a region with a very sudden variation of the potential, that, according to the wave mechanics causes a reflexion. The emission coefficient is, of course, the ratio of the number of electrons going through to the number of incident electrons, and the relation R + D = 1 (1) (R = reflexion coefficient, D = emission coefficent) is therefore always valid.
The reasoning that neural reflexes maintain homeostasis in other body organs, and that the immune system is innervated, prompted a search for neural circuits that regulate innate and adaptive immunity. This elucidated the inflammatory reflex, a prototypical reflex circuit that maintains immunological homeostasis. Molecular products of infection or injury activate sensory neurons traveling to the brainstem in the vagus nerve. The arrival of these incoming signals generates action potentials that travel from the brainstem to the spleen and other organs. This culminates in T cell release of acetylcholine, which interacts with α7 nicotinic acetylcholine receptors (α7 nAChR) on immunocompetent cells to inhibit cytokine release in macrophages. Herein is reviewed the neurophysiological basis of reflexes that provide stability to the immune system, the neural- and receptor-dependent mechanisms, and the potential opportunities for developing novel therapeutic devices and drugs that target neural pathways to treat inflammatory diseases.
This theoretical model of emotion is based on research using the startle-probe methodology. It explains inconsistencies in probe studies of attention and fear conditioning and provides a new approach to emotional perception, imagery, and memory. Emotions are organized biphasically, as appetitive or aversive (defensive). Reflexes with the same valence as an ongoing emotional state are augmented; mismatched reflexes are inhibited. Thus, the startle response (an aversive reflex) is enhanced during a fear state and is diminished in a pleasant emotional context. This affect-startle effect is not determined by general arousal, simple attention, or probe modality. The effect is found when affects are prompted by pictures or memory images, changes appropriately with aversive conditioning, and may be dependent on right-hemisphere processing. Implications for clinical, neurophysiological, and basic research in emotion are outlined.
ABSTRACT Graham (1975) demonstrated that a weak prestimulus could effectively inhibit or facilitate the eyeblink component of the startle reflex in humans, depending on the temporal duration of the prestimulus. This study had three goals: 1) to replicate the findings of Graham, 2) to establish the reliability of this phenomenon by a test‐retest comparison, and 3) to compare the eyeblink reflex response of normal subjects with schizophrenic subjects. Seven prestimulus durations of continuous tone (from 0 to 2000 msec) were presented to 20 normal subjects and the results confirmed that maximal inhibition of eyeblink amplitude occurred in the 120 msec prestimulus condition. Increased amplitude occurred nonsignificantly when the prestimulus lasted for 2000 msec. On retest, 14 normal subjects showed a significant degree of reliability. When 20 normal subjects were compared to 12 schizophrenic subjects, significant differences in eyeblink response were found for blink amplitude and latency in the 60 msec prestimulus condition. This change is consistent with information processing “overload” theories of sensory overstimulation in schizophrenia. The blink reflex is a rather stable phenomenon and is probably altered in schizophrenia and/or by antipsychotic medication.
BACKGROUND: Chronic reflex sympathetic dystrophy (also called the complex regional pain syndrome) is a painful, disabling disorder for which there is no proven treatment. In observational studies, spinal cord stimulation has reduced the pain associated with the disorder. METHODS: We performed a randomized trial involving patients who had had reflex sympathetic dystrophy for at least six months. Thirty-six patients were assigned to receive treatment with spinal cord stimulation plus physical therapy, and 18 were assigned to receive physical therapy alone. The spinal cord stimulator was implanted only if a test stimulation was successful. We assessed the intensity of pain (on a visual-analogue scale from 0 cm [no pain] to 10 cm [very severe pain]), the global perceived effect (on a scale from 1 [worst ever] to 7 [best ever]), functional status, and the health-related quality of life. RESULTS: The test stimulation of the spinal cord was successful in 24 patients; the other 12 patients did not receive implanted stimulators. In an intention-to-treat analysis, the group assigned to receive spinal cord stimulation plus physical therapy had a mean reduction of 2.4 cm in the intensity of pain at six months, as compared with an increase of 0.2 cm in the group assigned to receive physical therapy alone (P<0.001 for the comparison between the two groups). In addition, the proportion of patients with a score of 6 ("much improved") for the global perceived effect was much higher in the spinal cord stimulation group than in the control group (39 percent vs. 6 percent, P=0.01). There was no clinically important improvement in functional status. The health-related quality of life improved only in the 24 patients who actually underwent implantation of a spinal cord stimulator. Six of the 24 patients had complications that required additional procedures, including removal of the device in 1 patient. CONCLUSIONS: In carefully selected patients with chronic reflex sympathetic dystrophy, electrical stimulation of the spinal cord can reduce pain and improve the health-related quality of life.
In the mammalian retina, a small subset of retinal ganglion cells (RGCs) are intrinsically photosensitive, express the opsin-like protein melanopsin, and project to brain nuclei involved in non-image-forming visual functions such as pupillary light reflex and circadian photoentrainment. We report that in mice with the melanopsin gene ablated, RGCs retrograde-labeled from the suprachiasmatic nuclei were no longer intrinsically photosensitive, although their number, morphology, and projections were unchanged. These animals showed a pupillary light reflex indistinguishable from that of the wild type at low irradiances, but at high irradiances the reflex was incomplete, a pattern that suggests that the melanopsin-associated system and the classical rod/cone system are complementary in function.
The vestibulo-ocular reflex functions to prevent head movements from disturbing retinal images by generating compensatory eye movements to offset the head movements. In the monkey--the species mainly under consideration here--this reflex is machine-like and very effective. In the short-term, the VOR operates as an open-loop control system without the benefit of feedback and its performance is fixed and immutable: No matter what pattern of eye-head coordination the animal uses to view external objects, there is a continuing need for the VOR and it continues to operate; however, should the VOR consistently fail to stabilize the retinal images during head turns, it will gradually undergo long-term adaptive gain changes that restore, that stability. This adaptive capability is ultimately dependent upon vision, and a variety of optical devices that disturb the visual input normally associated with lead turns have been used to induce large changes in the reflex. Insofar as the monkey is concerned, all of the available evidence suggests to us that the modifiable elements underlying these long-term adjustments are located in the brainstem vestibular pathways and not, as previously suggested by others, in the floccular lobes of the cerebellum. However, the flocculus does appear to have an important, inductive role in the adaptive process providing at least part of the error signal guiding the long-term adjustments in the brainstem. In our view, the VOR is a particularly well-defined example of a plastic system and promises to be a most useful model for studying the cellular mechanisms underlying memory and learning the central nervous system.
<h3>THE PROBLEM</h3> The actual anatomic foundations of the concept of the reflex arc were laid by Ramón y Cajal between 1887 and 1892, when he carried out a systematic study of the spinal cord with the method of Golgi. Cajal's findings were soon confirmed by the best neuro-anatomists (van Gehuchten, von Lenhossek, Held, Retzius, von Kölliker and others).<sup>1</sup>A short time later, when Cajal and van Gehuchten developed the concept of axonal polarization, the elementary reflex arc acquired a more general significance; it became the expression of the fundamental plan of structure and function of the nervous system. Figure 1 reproduces the original diagram of Cajal, showing the reflex arc composed of the afferent sensory neuron, the efferent motoneuron and a connecting link that may either be only a collateral from the posterior root or also include one or more intercalated (internuncial) neurons. When the internuncial neurons lie outside
The time constant of the decay of slow-phase eye velocity of postrotatory nystagmus or optokinetic after-nystagmus is reduced during exposure to a stationary visual surround (visual suppression). It is also reduced after tilting the head (tilt suppression). A "dump" mechanism in the vestibulo-ocular reflex has been proposed to rapidly discharge activity from the central vestibular system during both types of suppression. Monkeys lost this mechanism after lesions of the nodulus and uvula. They also lost the ability to habituate the time constant of nystagmus on repeated exposure to optokinetic and vestibular stimuli. Periodic alternating nystagmus, which is believed to represent an instability in the vestibulo-ocular reflex, was observed in two of three monkeys. These data indicate that the nodulus and uvula play an important role in suppressing, habituating, and stabilizing the vestibulo-ocular reflex.