Stimulation of the phrenic nerve as a complication of vagus nerve pacing in a patient with epilepsy

Neurology ◽  
1998 ◽  
Vol 51 (4) ◽  
pp. 1224-1225 ◽  
Author(s):  
F. S.S. Leijten ◽  
P. C. Van Rijen
1985 ◽  
Vol 58 (3) ◽  
pp. 911-920 ◽  
Author(s):  
R. A. Mitchell ◽  
D. A. Herbert ◽  
D. G. Baker

In anesthetized paralyzed open-chested cats ventilated with low tidal volumes at high frequency, we recorded phrenic nerve activity, transpulmonary pressure (TPP), and either the tension in an upper tracheal segment or the impulse activity in a pulmonary branch of the vagus nerve. The TPP and upper tracheal segment tension fluctuated with respiration, with peak pressure and tension paralleling phrenic nerve activity. Increased end-tidal CO2 or stimulation of the carotid chemoreceptors with sodium cyanide increased both TPP and tracheal segment tension during the increased activity of the phrenic nerve. Lowering end-tidal CO2 or hyperinflating the lungs to achieve neural apnea (lack of phrenic activity) caused a decrease in TPP and tracheal segment tension and abolished the inspiratory fluctuations. During neural apnea produced by lowering end-tidal CO2, lung inflation caused no further decrease in tracheal segment tension and TPP. Likewise, stimulation of the cervical sympathetics, which caused a reduction in TPP and tracheal segment tension during normal breathing, caused no further reduction in these parameters when the stimulation occurred during neural apnea. During neural apnea the tracheal segment tension and TPP were the same as those following the transection of the vagi or the administration of atropine (0.5 mg/kg). Numerous fibers in the pulmonary branch of the vagus nerve fired in synchrony with the phrenic nerve. Only these fibers had activity which paralleled changes in TPP and tracheal tension. We propose that the major excitatory input to airway smooth muscle arises from cholinergic nerves that fire during inspiration, which have preganglionic cell bodies in the ventral respiratory group in the region of the nucleus ambiguus and are driven by the same pattern generators that drive the phrenic and inspiratory intercostal motoneurons.


1959 ◽  
Vol 197 (3) ◽  
pp. 511-514 ◽  
Author(s):  
N. C. Jefferson ◽  
T. Ogawa ◽  
J. Toman ◽  
W. Scruggs ◽  
H. Necheles

In dogs, the central end of the cut phrenic or vagus nerve was anastomosed to the distal end of the phrenic nerve. After phreno-phrenic anastomosis, slight atrophy of the muscle and nerve elements of the diaphragm occurred up to 7–8 weeks, followed by regeneration. At that time, electric stimulation of the nerve above the anastomosis produced contraction of the diaphragm, although respiratory function was absent. Ten to eleven weeks after anastomosis, spontaneous respiration recurred. In the case of vagophrenic anastomosis, spontaneous respiration did not reappear within 58 weeks, but stimulation of the vagus above the anastomosis produced contraction of the diaphragm, and histologic study showed regeneration of muscle and nerve elements. It is concluded, that trophic maintenance of the diaphragm depends on the presence of functionable innervation, not necessarily on functioning innervation.


1964 ◽  
Vol 206 (4) ◽  
pp. 815-817
Author(s):  
N. C. Jefferson ◽  
T. Ogawa ◽  
Y. Kuroyanagi ◽  
T. Geisel ◽  
J. Toman ◽  
...  

It has been shown that if the proximal end of a cut vagus nerve is anastomosed to the distal end of a cut phrenic nerve, the musculature of the hemidiaphragm is preserved, although inactive; it contracts upon direct stimulation and, also, upon stimulation of the vagus nerve above its anastomosis. These observations lasted for 22.7–31.5 months and confirm previous work which was of shorter duration. Thus, it is demonstrated that preservation of structure of muscle by innervation by a "foreign" nerve may last, perhaps indefinitely, in the absence of the normal respiratory motion of the hemidiaphragm.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jonathan A. Shulgach ◽  
Dylan W. Beam ◽  
Ameya C. Nanivadekar ◽  
Derek M. Miller ◽  
Stephanie Fulton ◽  
...  

AbstractDysfunction and diseases of the gastrointestinal (GI) tract are a major driver of medical care. The vagus nerve innervates and controls multiple organs of the GI tract and vagus nerve stimulation (VNS) could provide a means for affecting GI function and treating disease. However, the vagus nerve also innervates many other organs throughout the body, and off-target effects of VNS could cause major side effects such as changes in blood pressure. In this study, we aimed to achieve selective stimulation of populations of vagal afferents using a multi-contact cuff electrode wrapped around the abdominal trunks of the vagus nerve. Four-contact nerve cuff electrodes were implanted around the dorsal (N = 3) or ventral (N = 3) abdominal vagus nerve in six ferrets, and the response to stimulation was measured via a 32-channel microelectrode array (MEA) inserted into the left or right nodose ganglion. Selectivity was characterized by the ability to evoke responses in MEA channels through one bipolar pair of cuff contacts but not through the other bipolar pair. We demonstrated that it was possible to selectively activate subpopulations of vagal neurons using abdominal VNS. Additionally, we quantified the conduction velocity of evoked responses to determine what types of nerve fibers (i.e., Aδ vs. C) responded to stimulation. We also quantified the spatial organization of evoked responses in the nodose MEA to determine if there is somatotopic organization of the neurons in that ganglion. Finally, we demonstrated in a separate set of three ferrets that stimulation of the abdominal vagus via a four-contact cuff could selectively alter gastric myoelectric activity, suggesting that abdominal VNS can potentially be used to control GI function.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
K. Friedrich Kuhn ◽  
Julius J. Grunow ◽  
Pascal Leimer ◽  
Marco Lorenz ◽  
David Berger ◽  
...  

AbstractDiaphragm weakness affects up to 60% of ventilated patients leading to muscle atrophy, reduction of muscle fiber force via muscle fiber injuries and prolonged weaning from mechanical ventilation. Electromagnetic stimulation of the phrenic nerve can induce contractions of the diaphragm and potentially prevent and treat loss of muscular function. Recommended safety distance of electromagnetic coils is 1 m. The aim of this study was to investigate the magnetic flux density in a typical intensive care unit (ICU) setting. Simulation of magnetic flux density generated by a butterfly coil was performed in a Berlin ICU training center with testing of potential disturbance and heating of medical equipment. Approximate safety distances to surrounding medical ICU equipment were additionally measured in an ICU training center in Bern. Magnetic flux density declined exponentially with advancing distance from the stimulation coil. Above a coil distance of 300 mm with stimulation of 100% power the signal could not be distinguished from the surrounding magnetic background noise. Electromagnetic stimulation of the phrenic nerve for diaphragm contraction in an intensive care unit setting seems to be safe and feasible from a technical point of view with a distance above 300 mm to ICU equipment from the stimulation coil.


2017 ◽  
Vol 47 (3) ◽  
pp. 345-351
Author(s):  
S. Yu. Zhilyaev ◽  
A. N. Moskvin ◽  
T. F. Platonova ◽  
I. T. Demchenko

1911 ◽  
Vol 14 (3) ◽  
pp. 217-234 ◽  
Author(s):  
G. Canby Robinson ◽  
George Draper

In hearts showing auricular fibrillation mechanical stimulation of the right vagus nerve causes, as a rule, marked slowing or stoppage of ventricular rhythm, without producing any appreciable effect in the electrocardiographic record of the auricular fibrillation. The ventricular pauses are apparently due to the blocking of stimuli from the auricles. The force of ventricular systole is distinctly weakened for several beats after vagus stimulation, and ectopic ventricular systoles have been seen in several instances, apparently the result of the vagus action. There may, in some cases, be lowered excitability of the ventricles, while no constant change is seen in the size of the electrical complexes representing ventricular systole.


PEDIATRICS ◽  
1973 ◽  
Vol 51 (4) ◽  
pp. 755-755
Author(s):  
David S. Bachman

The article on prolonged apnea and the sudden infant death syndrome (SIDS) by Steinschneider1 is very exciting in that it suggests the possibility of identifying infants at risk from SIDS before the final event. Obviously, it is of great importance to learn the mechanism causing the preceding apneic episodes. Do they represent vagal overactivity? Stimulation of the intact vagus nerve in the unanesthetized monkey causes apnea, as well as bradycardia and even arrhythmias.2 In fact, we have seen myocardial myocytolysis secondary to vagal stimulation.3


Sign in / Sign up

Export Citation Format

Share Document