Laryngeal Spasm: A Neurophysiologic Redefinition

1977 ◽  
Vol 86 (2) ◽  
pp. 150-157 ◽  
Author(s):  
Masafumi Suzuki ◽  
Clarence T. Sasaki
Keyword(s):  
Sensory Input ◽  
Superior Laryngeal Nerve ◽  
Spatial Summation ◽  
Laryngeal Nerve ◽  
Glottic Closure ◽  
Laryngeal Spasm ◽  
Afferent Nerves ◽  
Temporal And Spatial ◽  
Glottic Closure Reflex ◽  
Stimulation Of

Within the limits of standard neurophysiologic techniques, we have attempted to redefine laryngeal spasm as distinct from the glottic closure reflex. This distinction is based upon the observation that laryngeal spasm is solely mediated by the superior laryngeal nerve. Stimulation of other afferent nerves, capable of eliciting the glottic closure reflex, produces little adductor after-discharge activity that is characteristic of laryngeal spasm. In this regard, modification of output function from the adductor motoneuron aggregate by means of temporal and spatial summation of sensory input data has been described, and its characteristics further defined in response to varying ventilatory states and barbiturate levels.

Cross-Innervation of the Thyroarytenoid Muscle by a Branch from the External Division of the Superior Laryngeal Nerve

1997 ◽  
Vol 106 (7) ◽  
pp. 594-598 ◽  
Author(s):  
Sina Nasri ◽  
Joel A. Sercarz ◽  
Pouneh Beizai ◽  
Young-Mo Kim ◽  
Ming Ye ◽  
...  
Keyword(s):  
Vocal Fold ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Spasmodic Dysphonia ◽  
Clinical Implications ◽  
Motor Innervation ◽  
Vocal Fold Vibration ◽  
Adductor Spasmodic Dysphonia ◽  
Thyroarytenoid Muscle ◽  
Stimulation Of

The neuroanatomy of the larynx was explored in seven dogs to assess whether there is motor innervation to the thyroarytenoid (TA) muscle from the external division of the superior laryngeal nerve (ExSLN). In 3 animals, such innervation was identified. Electrical stimulation of microelectrodes applied to the ExSLN resulted in contraction of the TA muscle, indicating that this nerve is motor in function. This was confirmed by electromyographic recordings from the TA muscle. Videolaryngostroboscopy revealed improvement in vocal fold vibration following stimulation of the ExSLN compared to without it. Previously, the TA muscle was thought to be innervated solely by the recurrent laryngeal nerve. This additional pathway from the ExSLN to the TA muscle may have important clinical implications in the treatment of neurologic laryngeal disorders such as adductor spasmodic dysphonia.

Nucleus tractus solitarius and excitatory amino acids in afferent-evoked inspiratory termination

1994 ◽  
Vol 76 (3) ◽  
pp. 1293-1301 ◽  
Author(s):  
D. R. Karius ◽  
L. Ling ◽  
D. F. Speck
Keyword(s):  
Nmda Receptors ◽  
Nucleus Tractus Solitarius ◽  
Excitatory Amino Acid ◽  
Superior Laryngeal Nerve ◽  
Nmda Antagonist ◽  
Intercostal Nerve ◽  
Laryngeal Nerve ◽  
Receptor Antagonists ◽  
Adult Cats ◽  
Stimulation Of

This study tested the hypothesis that excitatory amino acid (EAA) neurotransmission at non-N-methyl-D-aspartate (non-NMDA), but not NMDA, receptors within medial regions of the nucleus tractus solitarius (NTS) is required in the inspiratory termination elicited by vagal or intercostal nerve (ICN) stimulation. Adult cats were anesthetized, decerebrated, vagotomized, and ventilated. After control responses to stimulation of the superior laryngeal nerve (SLN), vagus, and ICN were obtained, EAA receptor antagonists were injected into the medial aspects of the NTS. Injections of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) or 6,7-dinitro-quinoxaline-2,3-dione (DNQX), EAA receptor antagonists; (+/-)-2-amino-5-phosphonopentanoic acid (AP5), an NMDA antagonist; or 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline (NBQX), a non-NMDA antagonist, ipsilateral to the vagus abolished the termination response. The SLN-elicited response persisted after AP5 injection but was abolished by NBQX injections. The ICN-elicited response persisted after bilateral injections of CNQX/DNQX or procaine. We conclude that the inspiratory termination elicited by ICN stimulation is independent of the regions medial to the NTS. Inspiratory termination elicited by vagal or SLN stimulation requires non-NMDA-mediated EAA neurotransmission within medial aspects of the NTS, but the vagally elicited response also requires NMDA receptors.

Influences of superior laryngeal afferent stimulation on expiratory activity in cats

1988 ◽  
Vol 65 (1) ◽  
pp. 385-392 ◽  
Author(s):  
F. Bongianni ◽  
M. Corda ◽  
G. Fontana ◽  
T. Pantaleo
Keyword(s):  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Tetanic Stimulation ◽  
Bötzinger Complex ◽  
Dependent Activity ◽  
Inspiratory Activity ◽  
Polysynaptic Reflex ◽  
Expiratory Muscles ◽  
Excitatory Responses ◽  
Stimulation Of

The effects of superior laryngeal nerve (SLN) stimulation on the activity of the expiratory muscles and medullary expiration-related (ER) neurons were investigated in 24 pentobarbital-anesthetized cats. In some experiments the animals were also paralyzed and artificially ventilated. Sustained tetanic stimulation of SLN consistently caused an apneic response associated with the appearance of tonic CO2-dependent activity in the expiratory muscles and in ER neurons located in the caudal ventral respiratory group (VRG) and the Botzinger complex. Single shocks or brief tetani at the same stimulation intensities failed to evoke excitatory responses in the expiratory muscles and in the vast majority of ER neurons tested. At higher stimulation strengths, single shocks or short tetani elicited excitatory responses in the expiratory muscles (20- to 35-ms latency) and in the majority of ER neurons of the caudal VRG (7.5- to 15.5-ms latency). These responses were obtained only during the expiratory phase and proved to be CO2 independent. On the contrary, only inhibitory responses were evoked in the activity of Botzinger complex neurons. The observed tonic expiratory activity most likely represents a disinhibition phenomenon due to the suppression of inspiratory activity; activation of expiratory muscles at higher stimulation intensities appears to be a polysynaptic reflex mediated by ER neurons of the caudal VRG but not by Botzinger complex neurons.

Reflex Vocal Fold Adduction in the Porcine Model: The Effects of Stimuli Delivered to Various Sensory Nerves

2008 ◽  
Vol 117 (10) ◽  
pp. 749-752 ◽  
Author(s):  
Jeong-Soo Woo ◽  
Jagdeep S. Hundal ◽  
Clarence T. Sasaki ◽  
Mikhail W. Abdelmessih ◽  
Stephen P. Kelleher
Keyword(s):  
Vocal Fold ◽  
Porcine Model ◽  
Superior Laryngeal Nerve ◽  
Sensory Nerves ◽  
Internal Branch ◽  
Pharyngeal Plexus ◽  
Closing Force ◽  
Intercostal Nerves ◽  
Glottic Closure Reflex ◽  
Stimulation Of

Objectives: The aim of this study was to identify a panel of sensory nerves capable of eliciting an evoked glottic closure reflex (GCR) and to quantify the glottic closing force (GCF) of these responses in a porcine model. Methods: In 5 pigs, the internal branch of the superior laryngeal nerve (iSLN) and the trigeminal, pharyngeal plexus, glossopharyngeal, radial, and intercostal nerves were surgically isolated and electrically stimulated. During stimulation of each nerve, the GCR was detected by laryngeal electromyography and the GCF was measured with a pressure transducer. Results: The only nerve that elicited the GCR in the 5 pigs was the iSLN. The average GCF was 288.9 mm Hg. Conclusions: This study demonstrates that the only afferent nerve that elicits the GCR in pigs is the iSLN, and that it should remain the focus of research for the rehabilitation of patients with absent or defective reflex vocal fold adduction.

scholarly journals Chronic Electrical Stimulation of the Superior Laryngeal Nerve in the Rat: A Potential Therapeutic Approach for Postmenopausal Osteoporosis

Biomedicines ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 369
Author(s):  
Kaori Iimura ◽  
Nobuhiro Watanabe ◽  
Philip Milliken ◽  
Yee-Hsee Hsieh ◽  
Stephen J. Lewis ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Thyroid Gland ◽  
Venous Blood ◽  
Disease Model ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Mineral Density ◽  
Ovx Rats ◽  
Chronic Electrical Stimulation ◽  
Stimulation Of

Electrical stimulation of myelinated afferent fibers of the superior laryngeal nerve (SLN) facilitates calcitonin secretion from the thyroid gland in anesthetized rats. In this study, we aimed to quantify the electrical SLN stimulation-induced systemic calcitonin release in conscious rats and to then clarify effects of chronic SLN stimulation on bone mineral density (BMD) in a rat ovariectomized disease model of osteoporosis. Cuff electrodes were implanted bilaterally on SLNs and after two weeks recovery were stimulated (0.5 ms, 90 microampere) repetitively at 40 Hz for 8 min. Immunoreactive calcitonin release was initially measured and quantified in systemic venous blood plasma samples from conscious healthy rats. For chronic SLN stimulation, stimuli were applied intermittently for 3–4 weeks, starting at five weeks after ovariectomy (OVX). After the end of the stimulation period, BMD of the femur and tibia was measured. SLN stimulation increased plasma immunoreactive calcitonin concentration by 13.3 ± 17.3 pg/mL (mean ± SD). BMD in proximal metaphysis of tibia (p = 0.0324) and in distal metaphysis of femur (p = 0.0510) in chronically SLN-stimulated rats was 4–5% higher than that in sham rats. Our findings demonstrate chronic electrical stimulation of the SLNs produced enhanced calcitonin release from the thyroid gland and partially improved bone loss in OVX rats.

Sympatholytic response to stimulation of superior laryngeal nerve in rats

1991 ◽  
Vol 260 (2) ◽  
pp. R290-R297 ◽  
Author(s):  
D. H. Huangfu ◽  
P. G. Guyenet
Keyword(s):  
Receptor Antagonist ◽  
Superior Laryngeal Nerve ◽  
Single Pulse ◽  
Laryngeal Nerve ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Onset Latency ◽  
Medullary Reticular Formation ◽  
Pulse Stimulation ◽  
Stimulation Of

The central pathway mediating a sympatholytic response to stimulation of the superior laryngeal nerve (SLN) was studied in halothane-anesthetized, paralyzed rats. Single-pulse stimulation of SLN inhibited lumbar sympathetic nerve discharge (LSND) with onset latency of 113 +/- 1.7 ms. LSND inhibition was markedly attenuated by bilateral microinjection of kynurenic acid (Kyn, glutamate receptor antagonist, 4.5 nmol/side) into the caudal ventrolateral medulla (CVL) or by bilateral administration of bicuculline methiodide (Bic; gamma-aminobutyric acid-receptor antagonist, 225 pmol/side) into the rostral ventrolateral medulla (RVL). In 13 of 14 cases, the baroreceptor reflex was also severely reduced. Injections of Bic or Kyn elsewhere in the medullary reticular formation were ineffective. Single-pulse stimulation of SLN inhibited 19 of 26 RVL reticulospinal barosensitive cells (onset latency 46 +/- 1.4 ms). This inhibition was attenuated (from 92 +/- 6 to 14 +/- 12%) by iontophoretic application of Bic (n = 7), which also reduced the cells' inhibitory response to aortic coarctation. The remaining seven barosensitive neurons were unaffected by SLN stimulation. In conclusion, the sympathetic baroreflex and the sympathoinhibitory response to SLN stimulation appear to be mediated by similar medullary pathways.

Effects of respiratory afferent stimulation on phrenic neurogram during hypoxic gasping in the cat

1993 ◽  
Vol 75 (5) ◽  
pp. 2091-2098 ◽  
Author(s):  
J. E. Melton ◽  
L. O. Chae ◽  
N. H. Edelman
Keyword(s):  
Pattern Formation ◽  
Carotid Sinus ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Carotid Sinus Nerve ◽  
Burst Frequency ◽  
Burst Pattern ◽  
Progressive Hypoxia ◽  
Stimulation Period ◽  
Stimulation Of

Previous studies suggested that phrenic motor output is largely refractory to afferent stimuli during gasping. We tested this concept by electrically stimulating the carotid sinus nerve (CSN) or the superior laryngeal nerve (SLN) of anesthetized peripherally chemodenervated vagotomized ventilated cats during eupnea or gasping induced by hypoxia. During eupnea, phrenic neurogram amplitude (PNA) increased by 110% during 30 s of supramaximal CSN stimulation, but burst frequency did not change. Progressive hypoxia caused gasping after arterial O2 content was reduced by 75%. During gasping, CSN stimulation caused premature onset of gasp in 12 of 13 trials, shortened intergasp interval [6.3 +/- 0.9 vs. 14.8 +/- 2.5 (SE) s], and resulted in a small (20%) but significant increase in PNA. Intensity of SLN stimulation was adjusted to abolish phrenic activity during the 30-s eupneic stimulation period. During gasping, SLN stimulation of the same intensity tended to delay onset of the next gasp, increased intergasp interval (16.9 +/- 1.9 vs. 13.3 +/- 1.2 s), and reduced PNA by 32%. Thus the respiratory burst pattern formation circuitry responds to afferent stimuli during gasping, albeit in a manner different from the eupneic response. These observations suggest that gasping is the output of a modified eupneic burst pattern formation circuit.

Chemical specificity of a laryngeal apneic reflex in puppies

1982 ◽  
Vol 53 (2) ◽  
pp. 455-462 ◽  
Author(s):  
D. F. Boggs ◽  
D. Bartlett
Keyword(s):  
Phosphate Buffer ◽  
Superior Laryngeal Nerve ◽  
Critical Factor ◽  
Laryngeal Nerve ◽  
Sodium Salts ◽  
Single Fibers ◽  
Buffer Solutions ◽  
Chloride Salts ◽  
Cation Substitutions ◽  
Stimulation Of

In neonatal mammals the introduction of water and some other fluids into the larynx causes prolonged reflex apnea by stimulation of afferents in the superior laryngeal nerve (SLN). We have studied the chemical specificity of this reflex in 1- to 9-day-old anesthetized puppies. The laryngeal lumen was perfused with a variety of substances while ventilation through a tracheal cannula was recorded. Water consistently elicited apnea, which was terminated by 150 mM NaCl. Sucrose and urea solutions (100–500 mM) also elicited apnea, suggesting that osmolarity is not a critical factor. Phosphate buffer solutions containing NaCl and ranging in pH from 4.5 to 8.7 did not elicit apnea nor did cation substitutions in 150 mM chloride salts, with the exception of K+. Anion substitutions in 150 mM sodium salts indicated that anions of relatively large hydrated size (F-, acetate, formate, gluconate, tartrate, SO2–4, diatrizoate, IO-3, BrO-3, H2PO-4, HCO-3, borate, CO2–3) do induce apnea, whereas small anions (NO-3, ClO-3, SCN-, I-, Br-) similar to Cl- in size do not. Large anion salts and the nonelectrolytes sucrose, urea, and milk ceased to be effective stimuli in the presence of Cl- in concentrations of 80 or more meq/l. The principal stimulus for this apneic reflex is thus the absence or reduced concentration of Cl- (or small anions that can functionally replace Cl-) in the laryngeal fluid. Single fibers in the SLN were responsive to all the substances found capable of eliciting apnea and unresponsive to those not capable of doing so.

Central GABAergic mechanisms are involved in apnea induced by SLN stimulation in piglets

2001 ◽  
Vol 90 (4) ◽  
pp. 1570-1576 ◽  
Author(s):  
Jalal M. Abu-Shaweesh ◽  
Ismail A. Dreshaj ◽  
Musa A. Haxhiu ◽  
Richard J. Martin
Keyword(s):  
Electrical Stimulation ◽  
Phrenic Nerve ◽  
Superior Laryngeal Nerve ◽  
Laryngeal Nerve ◽  
Receptor Blocker ◽  
Inspiratory Time ◽  
Before And After ◽  
Four Levels ◽  
Stimulation Of

Stimulation of the superior laryngeal nerve (SLN) results in apnea in animals of different species, the mechanism of which is not known. We studied the effect of the GABAA receptor blocker bicuculline, given intravenously and intracisternally, on apnea induced by SLN stimulation. Eighteen 5- to 10-day-old piglets were studied: bicuculline was administered intravenously to nine animals and intracisternally to nine animals. The animals were anesthetized and then decerebrated, vagotomized, ventilated, and paralyzed. The phrenic nerve responses to four levels of electrical SLN stimulation were measured before and after bicuculline. SLN stimulation caused a significant decrease in phrenic nerve amplitude, phrenic nerve frequency, minute phrenic activity, and inspiratory time ( P < 0.01) that was proportional to the level of electrical stimulation. Increased levels of stimulation were more likely to induce apnea during stimulation that often persisted beyond cessation of the stimulus. Bicuculline, administered intravenously or intracisternally, decreased the SLN stimulation-induced decrease in phrenic nerve amplitude, minute phrenic activity, and phrenic nerve frequency ( P < 0.05). Bicuculline also reduced SLN-induced apnea and duration of poststimulation apnea ( P < 0.05). We conclude that centrally mediated GABAergic pathways are involved in laryngeal stimulation-induced apnea.

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