Of Acid-Induced Hyperexcitability
Of The Thyroarytenoid Muscle In The
Anesthetized Canine By Median Nerve Stimulation That Mimics PC Meridian
Shengguang Yin, MD
Fred J. Stucker, MD
Background Traditionally, acupuncture has been used to reverse
laryngospasm in China. The underlying physiological mechanism is unknown.
Objective To test whether median nerve stimulation (MNS), which
mimics PC meridian stimulation in acupuncture, can reverse acid-induced
hyperexcitability of the thyroarytenoid muscle.
Intervention and Subjects Electromyography (EMG) and videolaryngoscope
were used on 3 anesthetized canines.
Main Outcome Measures Glottic movements were monitored with the
thyroarytenoid muscle and diaphragm EMG. Once hyperexcitability of the
thyroarytenoid muscle was established with application of an acidic
solution, the effect of MNS was compared during normal breathing and
hyperexcitability of the thyroarytenoid muscle.
Results The pattern of thyroarytenoid muscle EMG in response
to acid solution (pH 2.0) indicated consistent contraction, lasting
1100-1500 milliseconds with maximum amplitudes of 800-1000 mV, but no
changes in response to control solution pH 7.0, in which both vocal
folds maintained more adduction than seen in the laryngospasm. During
normal breathing, MNS did not change thyroarytenoid muscle EMG, but
increased duration of inspiratory firing in the diaphragm EMG. After
5 minutes of MNS, the thyroarytenoid muscle activity to acidic solution
was absent or significantly inhibited, but with inspiratory burst in
Conclusions MNS relaxes the thyroarytenoid muscle and activates
the diaphragm, completely releasing acid-induced hyperexcitability of
Laryngospasm, Median Nerve Stimulation, Acupuncture, Glottic Movement,
Laryngospasm is a critical condition, with an incidence of 8.7/1000
for all age groups, and 95.8/1000 for children with an upper respiratory
tract infection.1 It is often misdiagnosed as asthma.2 If not diagnosed
correctly and treated quickly, laryngospasm makes lung ventilation difficult
and can lead to hypercarbia, hypoxia, cardiac collapse, and even death.3-20
Clinical studies show that in some cases, severe complications (e.g.,
pulmonary edema) are possible and are often unrecognized or misdiagnosed.11,17,19,21,28,31-34
Investigators have suggested that the underlying mechanism of laryngospasm
initially involves a laryngeal reflex action. The glottic adduction
reflex can be elicited by pharyngeal stimulation,22 laryngeal stimulation,23
and cranial and peripheral nerve stimulation.24,25 Glottal adduction
reflex is phylogenetically a protective mechanism against
anterograde aand retrograde aspiration. However, laryngospasm is distinct
from the glottic adduction reflex under normal conditions.24 It is characterized
by hypopharyngeal spasm, sudden onset, and paradoxical, profound adduction
glottic movement triggered by superior laryngeal nerve (SLN) stimulation.2,3,24,26
|Table 1. Response Differences Between
Thyroarytenoideus and Diaphragm Muscles*
|Control solution (pH 7.0)
|Acidic solution (pH 2.5)
|MNS + acidic solution (pH 2.5)
||Absent or attenuation
|* MNS indicates median nerve stimulation.
Response: None, no change from baseline; small, 300-700 mV; and
large, more than 1000 mV.
Studies of possible treatments have focused on interfering with the
laryngeal reflex arc. Examples include reducing afferent input from
the supraglottic area with lidocaine,8,27 and eliciting a response from
the antagonistic muscle.28 However, while such methods generally block
the pathophysiological loop and consequently relieve symptoms, they
also interfere with normal physiological functioning. In addition, studies
show that bilateral SLN section did not affect laryngeal resistance
and ventilation during chemostimulation in cats29 and rabbits.30,31
It is possible that chemoreflex may be involved in laryngospasm, which
explains why lidocaine does not effectively control laryngospasm.
The pathophysiological changes in laryngospasm may involve the vagal
reflex, which is essential for cardiovascular control and shortterm
blood pressure regulation. Reflex afferents can come from baroreceptors
via the sinus nerve; mechanical and chemical stimulation reach the nucleus
of the solitary tract in the lower brainstem via SLN. The second-order
nucleus of the solitary tract neurons influence motor neurons, which
in turn control glottic movement, heart rate, total peripheral
resistance, and blood pressure. In laryngospasm episodes, therefore,
cardiopulmonary changes may be a result of vagal reflex and prolonged
glottic adduction, which itself can cause upper respiratory tract collapse.
It may be possible to control a series of pathophysiological changes
by interfering with central input processing instead of blocking peripheral
|Figure 1. Schematic
representation of identifying acupuncture points for laryngospasm.
A, LI 4 (Hegu). B, PC 8 (Laogong). C, Technique for acupuncture
pressure on both LI 4 and PC 8.
of laryngospasm have been reported in cats3 and dogs.3,26,35-39 The
methods proposed for triggering laryngospasm include electrical stimulation
of SLN and recurrent laryngeal nerve,26,37,38 chemical stimulation with
ammonia37 and with acidic solution,39 and physical stimulation with
continuous positive airway pressure.26,36 Although recurrentlaryngeal
nerve stimulation causes a contraction of the thyroarytenoid muscle,
resulting in complete and consistent closure of the glottis, clinical
observation indicates that laryngospasm is more related to the laryngeal
reflex triggered by SLN stimulation24 and gastroesophageal reflux.39
Loughlin and colleagues39 demonstrated that acid-sensitive supraglottic
chemoreceptors initiate laryngospasm at pH of 2.5 or less. In their
dog model, however, appearances of glottis, subglottic pressure, and
laryngeal EMG during laryngospasm were not normalized. Moreover, their
surgical approach remains to be improved, such as laryngofissure for
opening the larynx and carotid artery for monitoring blood pressure.
In our study, the acid-induced laryngospasm method was modified.
In Traditional Chinese Medicine (TCM), acupuncture often has been used
to reduce myocardial ischemia, arrhythmias, hypertension, and termination
of laryngospasm,40-48 but the basis of the therapeutic effects awaits
investigation. In acupuncture, stimulating LI 4 (Hegu) to reach PC 8
(Laogong) is effective in reversing laryngospasm with acupuncture needles.
Although LI 4 and PC 8, belong to different meridians, it is impossible
to stimulate only 1 meridian. Practically, acupoint pressure at these
2 acupoints is also effective. The technique is to apply pressure with
the thumb to LI 4, and with the index finger to PC 8 simultaneously
(Figure 1). The section of the PC in the forearm overlies the trunk
of the median nerve. Clinical trials and animal experiments have demonstrated
that transcutaneous electrical nerve stimulation and acupuncture with
manual or electrical stimulation are similarly effective in initiating
nerve impulses.48-50 Wang et al50 compared the effects of electroacupuncture
with transcutaneous nerve stimulation without needles. At all frequencies
tested, the results were similar.
Li et al51 reported that low-current electrical stimulation of PC 6,
or the median nerve, had the same effects of inhibition in a rabbit
model. Therefore, median nerve stimulation (MNS) appears to mimic stimulation
of the pericardium meridian from PC 6 and PC 8 in traditional acupuncture.
MNS does not change the baseline of physiological indices such as heart
rate, blood pressure, or coronary blood velocity in cats49 and dogs.52
The major advantage of this method of relieving laryngospasm is to achieve
the desired results without interrupting the normal reflex loop, thus
avoiding complications such as pulmonary edema.17 We hypothesized that
MNS (mimicking acupuncture-induced reversal of laryngospasm) may initiate
a mechanism that switches from a defensive pattern into a modulatory
pattern through the laryngeal center.53
|Figure 2. Schematic
diagram of the experimental arrangement. A, Syringes for instillation
of acid solution (pH 2.5) and phosphate-buffered saline solution
(pH 7.4) . B, Videolaryngoscopic recording. C, Suction device. D,
The study described herein represents an initial step toward assessing
the fundamental properties of MNS at acupuncture point PC 6. The responsive
pattern changes provide a general theoretical framework to connect MNS
and excitability of the glottis. If, as hypothesized, MNS can cause
a switch of the vagal reflex from a hyper-defensive pattern to a regulatory/modulatory
pattern in an animal model, possibly a similar mechanism exists in humans.
Although the characteristics of acupoint Neiguan (PC 6) have yet to
be fully elucidated, MNS probably plays an important role in effects
of PC 6. With this normalized canine model, extensive and systematic
investigation can be carried out to address crucial issues in neurolaryngology
Three 15-20 kg adult dogs (2 males and 1 female) were used. Animals
were anesthetized with intravenous Nembutal (25 mg/kg), and supplemental
anesthesia was administered with Nembutal (15 mg/kg) intravenously at
approximately 90-minute intervals to maintain the anesthetic level.
The optimal level of anesthesia was controlled using the following criteria:
(1) absence of voluntary movements, (2) presence of the corneal reflex,
(3) inspiratory movement of both vocal folds, and (4) absence of diaphragmatic
EMG activity. A midline incision in the anterior part of the neck was
made and the strap muscles were retracted to expose the trachea and
tracheoesophageal grooves. A tracheostomy was
performed at the 4th-5th tracheal ring. A cuffed T-shape tracheotomy
tube was inserted. The valve of the T-shape tube was allowed to continue
and separate above and below the tracheotomy airway. A balloon-tipped
catheter was then inserted into the rostral part of the "T"
tube to lie just caudal to the cricoid cartilage. Hooked wire electrodes
with Teflon-coated stainless steel were placed into the thyroarytenoid
muscle for laryngeal EMG recording. Hooked-wire electrodes for diaphragm
EMG were placed via midline laparotomy.39 The dogs were inserted transorally
with a 3-channel device for the application of: (1) instillation of
acid solution, (2) observation of the glottis with a flexible videolaryngoscope,
and (3) suction secretion (Figure 2). To mimic PC 6 acupuncture stimulation,
2 needle electrodes 10 mm apart were inserted at the 1/6 of right forearm
distally, serving as MNS and adjusted to produce a slight twitch in
the extremities at a frequency of 2 Hz. The intensity of stimulation
was at 2x threshold for the first detectable muscle twitch. The average
value of 2x threshold was 1.3 mA. Responses in the thyroarytenoid muscle
and the diaphragm was recorded in baseline activity of load-airway,
acid-solution (pH 2.0), and control solution (pH 7.0). Each time hyperexcitabilities
of thyroarytenoid muscle were recorded following acid application, the
supraglottic area was suctioned and the endolarynx rinsed 3 times with
phosphate-buffered saline solution (pH 7.4).
The response of thyroarytenoid muscle in EMG to the acid solution was
consistent contraction, lasting 1100-1500 milliseconds with maximum
amplitudes of 800-1000 mV (Figure 3). No changes occurred in response
to the control solution (pH 7.0) [Figure 4]. However, there were responses
with inspiratory 5-7 bursts per second to control solution
(pH 7.0) in the diaphragm EMG (Figure 4). During hyperexcitability episodes,
both vocal folds maintained more adduction than during the pre-installation
position with high tension and respiration arrest, obvious signs seen
in the laryngospasm (Figure 5). There were increased activities in diaphragm
EMG in response to acid, which consisted of enhanced inspiratory phase
(300-700 mV, 400 milliseconds and 0.75 Hz).
When the left median nerve was stimulated at 1.3 mA, duration of 0.2
milliseconds and a consistent rate of 2 Hz, there was no change in thyroarytenoid
muscle EMG activity. However, it did significantly increase the duration
of inspiratory firing in the diaphragm EMG recording from 350 to 600
milliseconds. Five minutes after MNS, acid was reapplied to the supraglottic
area in all 3 canines; the amplitude of thyroarytenoid muscle activity
was absent in 2 and significantly inhibited in 1, but with inspiratory
burst in the diaphragm EMG activity (Figure 6). The response differences
between thyroarytenoideus and diaphragm are shown in Table 1, and were
not treated statistically due to limited samples.
This study modified the acid-induced laryngospasm in a canine model
performed by Loughlin et al.39 The hyperexcitability of the thyroarytenoid
muscle, decrease of the glottic area due to consistent vocal fold adduction,
laryngeal apnea, and inactivation of the diaphragm serve as an experimental
laryngospasm condition. The results from exposure to acidic solution
also have been demonstrated in an impairment of the upper airway potency-maintaining
mechanisms in dogs.54 Under experimental laryngospasm condition, appearance
of the canine larynx is similar to that of human laryngospasm.
|Figure 3. The
responses to solution with pH 2.5 in the right (upper trace) and
left (lower trace) thyroarytenoid muscle.
||Figure 4. Electromyographic
activity of the right thyroarytenoid muscle (upper trace) and diaphragm
(lower trace) during instillation of solution with pH 7.0. Dark
marker indicates the onset of solution with pH 7.0.
The results showed enhancement of diaphragm activity and no recruitment
of RTA after instillation of water with pH 7.0 (Figure 4). Thus, MNS
not only reversed hyperexcitability of the thyroarytenoid muscle, but
also enhanced diaphragm activity (Figure 6). If this effect is due to
the same mechanism as PCA,56 there appears to be top-down regulation
thyroarytenoid muscle, PCA, and diaphragm activities. A peripheral mechanism
can be ruled out since it is innervated by different nerves.55 The observation
of PCA in experimental laryngospasm condition is compelling, and the
role of airway surface liquid on reflex responses also deserves attention.
Stimulation parameters demonstrated the effects of MNS on reversal of
glottic hyperexcitability. It successfully mimics acupuncture stimulation
at PC, which reverses the course of laryngospasm in humans. Although
it is too early to equate the effects of direct nerve stimulation and
manual needle stimulation, it appears that MNS has many of the same
effects as PC stimulation.57 During quiet respiration, there were no
changes in thyroarytenoid muscle to MNS, which abolished hyperexcitability
of thyroarytenoid muscle to acidic stimulation. These findings offer
some support for our hypothesis that MNS results in a switch from a
defensive pattern into a modulatory pattern, possibly via a central
The canine model of acid-induced laryngospasm is a promising preparation
for the study of the physiological basis of acupuncture, as well as
the study of laryngeal motor control. Although our preliminary study
yielded promising data, extensive work remains to be done, including:
(1) multi-channel, simultaneously recording the diaphragm, thyroarytenoid
muscle, cricothyroid muscle, and posterior cricoarytenoid muscle EMG
activity along with physiological index observation (heart rate, blood
pressure, and respiratory rate); (2) precise measurement of the glottic
area; (3) measurement of the pressure between supraglottic and subglottic
space during spontaneous breathing and episodes of hyperexcitability
of thyroarytenoid muscle with rectified signals; (4) signal analysis;
and (5) comparison among different acupoints and meridians reported
in literature46,47 for laryngospasm.
Hyperexcitability of the thyroarytenoid muscle triggered by acid solution
(pH 2.0) can be prevented or attenuated by MNS without interfering with
normal reflexive responses. Our data suggests that the mechanism of
acupuncture involves switching from a defensive to a modulatory pattern
in reversal of laryngospasm, without blocking the normal reflex arc.
|Figure 5. Hyperexcitability
of the right thyroarytenoid muscle (upper trace) EMG tracing during
the application of solution with pH 2.5: no significant change in
diaphragm (lower trace). The figure shows the glottic appearance
during pre-hyperexcitability phase of the thyroarytenoid muscle
(A), hyperexcitability of the thyroarytenoid muscle (B), and post-hyperexcitability
phase of the thyroarytenoid muscle (C). Dark marks indicate the
onset and offset of hyperexcitability of the thyroarytenoid muscle.
|Figure 6. Appearance
of the glottis (upper trace) and EMG activity (lower trace) of the
thyroarytenoid muscle (top line) and diaphragm (bottom line): (A)
during application of acidic solution (pH 2.5) and (B) when median
nerve stimulation on, hyperexcitability of the right thyroarytenoid
muscle was significantly attenuated and the diaphragm showed facilitation,
with duration 250 milliseconds and 0.15-Hz frequencies.
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Dr Shengguang Yin is Associate Professor and Director of Laryngeal Motor
Control Laboratory in the Department of Otolaryngology Head and Neck
Surgery at Louisiana State University Health Science Center in Shreveport,
Louisiana. Dr Yin's specialty is Neurolaryngology.
Shengguang Yin, MD*
1501 Kings Hwy
Shreveport, LA 71130-3359
Phone: 318-675-6262 Fax: 318-675-6260 E-mail: firstname.lastname@example.org
Dr Fred J. Stucker is Professor and Chairman of the Department of Otolaryngology
Head and Neck Surgery at Louisiana State University Health Science Center
in Shreveport, Louisiana. Dr. Stucker's specialty is Otolaryngology-HNS
and Plastic Surgery (Facial).
Fred J. Stucker, MD, FACS
1501 Kings Hwy
Shreveport, LA 71130-3359
Phone: 318-675-6262 Fax: 318-675-6260 E-mail: email@example.com
*Address all correspondence to Dr Shengguang Yin, Department of Otolaryngology
Head and Neck Surgery, Louisiana State University Health Science Center
at the address above.