Reflex Inhibition Audiometry: A New Objective Technique

1978 ◽  
Vol 85 (1-6) ◽  
pp. 336-341 ◽  
Author(s):  
R. R. Marsh ◽  
H. S. Hoffman ◽  
C. L. Stitt
Keyword(s):  
2017 ◽  
Vol 595 (13) ◽  
pp. 4493-4506 ◽  
Author(s):  
Brian C. Horslen ◽  
J. Timothy Inglis ◽  
Jean-Sébastien Blouin ◽  
Mark G. Carpenter

2007 ◽  
Vol 98 (3) ◽  
pp. 1102-1107 ◽  
Author(s):  
Serajul I. Khan ◽  
John A. Burne

Muscle cramp was induced in one head of the gastrocnemius muscle (GA) in eight of thirteen subjects using maximum voluntary contraction when the muscle was in the shortened position. Cramp in GA was painful, involuntary, and localized. Induction of cramp was indicated by the presence of electromyographic (EMG) activity in one head of GA while the other head remained silent. In all cramping subjects, reflex inhibition of cramp electrical activity was observed following Achilles tendon electrical stimulation and they all reported subjective relief of cramp. Thus muscle cramp can be inhibited by stimulation of tendon afferents in the cramped muscle. When the inhibition of cramp-generated EMG and voluntary EMG was compared at similar mean EMG levels, the area and timing of the two phases of inhibition (I1, I2) did not differ significantly. This strongly suggests that the same reflex pathway was the source of the inhibition in both cases. Thus the cramp-generated EMG is also likely to be driven by spinal synaptic input to the motorneurons. We have found that the muscle conditions that appear necessary to facilitate cramp, a near to maximal contraction of the shortened muscle, are also the conditions that render the inhibition generated by tendon afferents ineffective. When the strength of tendon inhibition in cramping subjects was compared with that in subjects that failed to cramp, it was found to be significantly weaker under the same experimental conditions. It is likely that reduced inhibitory feedback from tendon afferents has an important role in generating cramp.


1965 ◽  
Vol 43 (2) ◽  
pp. 229-246
Author(s):  
DONALD KENNEDY ◽  
KIMIHISA TAKEDA

1. Fibres from the tonic, superficial abdominal flexor muscles in the crayfish receive a complex, highly polyneuronal innervation from among five motor axons and one inhibitor. All efferent nerve fibres show some degree of ‘spontaneous’ activity. 2. The muscle fibres therefore exhibit a constant flux of membrane potential, and hence of tension, in intact preparations. Depolarization is the result of facilitation and/or summation of junctional potentials of various amplitudes, and in some fibres of superimposed electrogenic responses. Neighbouring fibres tend to show similar innervation patterns, more distant ones dissimilar ones. 3. No useful distinction may be made between ‘fast’ and ‘slow’ motor axons. A given axon may produce junctional potentials of very different amplitudes (and some what different rise-times) in neighbouring muscle fibres while another exhibits a precisely reciprocal relationship. The largest axon produces facilitating junctional potentials in all the muscle fibres it innervates, but others may exhibit facilitation in one muscle fibre and antifacilitation in another. 4. Most muscle fibres are innervated by two or three excitatory axons; fibres with single, quadruple or quintuple motor innervation are relatively rare. There is a pronounced tendency for fibres with a rich excitatory innervation to receive the inhibitor as well. The innervation is not shared equally among motor axons: one serves over 90% of the muscle fibres, and two others 20% or less. Statistical analysis of the combinations of motor axons serving muscle fibres reveals that these are apparently random, with all variations from randomness accountable on the grounds of broad regional differences in distribution. 5. The motor axons are selectively activated by specific reflex inputs. Since muscle fibres receive, on the average, only a restricted sample of the available motor supply, it follows that they participate differentially in different reflex actions. Evidence is presented that the firing pattern of motor nerves is appropriate for the temporal properties of their neuromuscular junctions. 6. Reflex inhibition is accomplished by central inhibition of all excitatory motor outflow, accompanied by reciprocal firing in the inhibitor axon. This and the fact that less than half the muscle fibres receive inhibitory innervation demonstrate that, in contrast to the one other crustacean system analysed, reflex inhibition is primarily a central event. Peripheral inhibition in the slow flexor system must serve mainly as a device to achieve repolarization and thus terminate contractions. Such action necessarily depends upon post-synaptic rather than presynaptic mechanisms.


1984 ◽  
Vol 247 (6) ◽  
pp. E827-E832 ◽  
Author(s):  
D. L. Curry

The in situ brain-pancreas experimental model was used to investigate the influence of the vagus nerve during tonic direct central nervous system (CNS) inhibition of insulin secretion. Tonic CNS inhibition of insulin secretion was partially and transiently reversed following bilateral cervical vagotomy, suggesting that this inhibition includes a vagally mediated component. However, a substantial CNS inhibition of insulin secretion still occurred in the vagotomized preparations. This demonstrates that a major component producing tonic CNS inhibition of insulin secretion is independent of the vagus nerve and, furthermore, that it must be via direct sympathetic efferent pathways to the pancreas (because these preparations are functionally parasympathectomized via vagotomy). Further investigation into the vagus nerve involvement was carried out by stimulating either the afferent (central) or efferent (pancreatic) cut end of the vagus nerve of bilaterally vagotomized brain-pancreas preparations. Stimulation of the efferent vagus did not appreciably alter the effect of vagotomy on insulin secretion. However, when the central cut vagus was stimulated, the early transient reversal of tonic inhibition, which occurred in the vagotomized preparations, was totally reversed. This suggests that the vagally mediated early transient component of tonic CNS inhibition of insulin secretion is via afferent (central) neurons in the vagus nerve. These data demonstrate a reflex pathway for inhibition of insulin secretion that is comprised of vagal afferent neurons, the CNS, and sympathetic efferent neurons ending directly on the islets of Langerhans. It is tempting to speculate that gastrointestinal receptors exist that are capable of initiating this reflex inhibition of insulin secretion.


Sign in / Sign up

Export Citation Format

Share Document