The journal of the American Academy of Medical Acupuncture with acupuncture research articles, reviews, abstracts and case studies.      
             
     

Medical Acupuncture
A Journal For Physicians By Physicians

Volume 13 / Number 2
"Aurum Nostrum Non Est Aurum Vulgi"

     
     
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Reversal Of Acid-Induced Hyperexcitability
Of The Thyroarytenoid Muscle In The
Anesthetized Canine By Median Nerve Stimulation That Mimics PC Meridian Stimulation
Shengguang Yin, MD
Fred J. Stucker, MD

ABSTRACT
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 the diaphragm.
Conclusions MNS relaxes the thyroarytenoid muscle and activates the diaphragm, completely releasing acid-induced hyperexcitability of thyroarytenoid muscle.

KEY WORDS
Laryngospasm, Median Nerve Stimulation, Acupuncture, Glottic Movement, Thyroarytenoid

INTRODUCTION
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*
  Thyroarytenoideus Diaphragm
Control solution (pH 7.0) None Small
Acidic solution (pH 2.5) Large Small
MNS None Small
MNS + acidic solution (pH 2.5) Absent or attenuation Inspiratory burst
* 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 pathophysiological loop.

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.

Animal models 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, Three-channel device.


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 and acupuncture.

METHODS
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).

RESULTS
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.

DISCUSSION
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 mechanism.

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.

CONCLUSION
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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AUTHORS' INFORMATION
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: syin@lsuhsc.edu

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: aray@lsuhsc.edu

*Address all correspondence to Dr Shengguang Yin, Department of Otolaryngology Head and Neck Surgery, Louisiana State University Health Science Center at the address above.

     
     

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