an in vivo canine model The effect of laryngeal …...investigation was designed to examine, by use of an in viva canine model of phonation, the effect of change in vocal fold mass

The effect of laryngeal nerve stimulation on phonation: A glottographic study usingan in vivo canine modelDennis M. MooreGerald S. Berke

Citation: The Journal of the Acoustical Society of America 83, 705 (1988); doi: 10.1121/1.396113View online: http://dx.doi.org/10.1121/1.396113View Table of Contents: http://asa.scitation.org/toc/jas/83/2Published by the Acoustical Society of America

http://asa.scitation.org/author/Moore%2C+Dennis+M

http://asa.scitation.org/author/Berke%2C+Gerald+S

/loi/jas

http://dx.doi.org/10.1121/1.396113

http://asa.scitation.org/toc/jas/83/2

http://asa.scitation.org/publisher/

The effect of laryngeal nerve stimulation on phonation: A giottographic study using an in vivo canine model

Dennis M. Moore

UCL•4 Division of Head and Neck Surgery, UCLA School of Medicine, Los Angeles, California 90024

Gerald S. Berke

UCL•4 Division of Head and Neck Surgery, UCL•4 School of Medicine, Los •4ngeles, California 90024 and Laryngeal Physiology Laboratory, West Los Angeles Y. A. Medical Center, Los Angeles, California 90073

(Received 5 January 1987; accepted for publication 14 October 1987)

The present investigation was designed to examine the effect of change in vocal fold mass and stiffness on vocal fold vibration. To do this, the effect of variation in superior laryngeal nerve stimulation (SLNS) and recurrent laryngeal nerve stimulation (RLNS) was studied. Photoglottography (PGG), electroglottography (EGG), and subglottic pressure (Psub) were measured in seven mongrel dogs using an in viva canine model of phonation. The PGG, EGG, and Psub signals were examined at three frequencies ( 100, 130, and 160 Hz) for SLNS and RLNS, using a constant rate of air flow. Increasing SLNS, which caused a contraction of the cricothyroid muscle, produced a marked increase in Fo, little change in P•u•, an increase in open quotient (OQ), and a decrease in the closed quotient (CQ) of the glotta! cycle. Increasing RLNS, which caused activation of the intrinsic laryngeal muscles, produced a modest increase in Fo, a marked increase in Psu•, no change in the OQ, and an increase in CQ. Phase quotient (Qp), which describes the interval between opening of the lower and upper fold margins, decreased with increasing RLNS and did not change significantly with increasing $LNS. Based upon changes in Fo, P•u•, OQ, CQ, and Qp, $LNS provides a physiologic correlate of the tension parameter Q, and RLNS provides a physiologic correlate of the parameter P•u• in the Ishizaka and Flanagan two-mass model.

PACS numbers: 43.70.Aj

INTRODUCTION

Knowledge of phonatory control mechanisms has increased tremendously during the past three decades. While clinicians and physiologists have seen the vocal cords as physiologic vibrators, engineers and speech scientists have tended to view the vocal cords as mechanical oscillators.

Based on physiologic observations using human and canine larynges, van den Berg (1958) advanced the myoelastic- aerodynamic theory of phonation. Ishizaka and Flanagan (1972) proposed a two-mass model of vocal fold vibration for synthesis of voiced sounds. Subsequent investigations have studied phonation in animal and computer assisted models. Although theoretical models have been indispensa- ble in consolidating known data and guiding the path toward future experimentation, verification of current theories will require the use of physiological preparations. The present investigation was designed to examine, by use of an in viva canine model of phonation, the effect of change in vocal fold mass and stiffness on vocal fold vibration. To do this, the effect of variation in superior and recurrent laryngeal nerve stimulation (SLNS and RLNS), under conditions of constant air flow, was studied photoglottographically and elec- troglottographically while measuring subglottic pressure.

The myoelastic-aerodynamic theory of phonation pos- tulated that the driving force for vocal fold vibration is the stream of air from the lungs. The fundamental frequency (Fo) of phonation depends on the effective mass and stiffness

of the vocal folds interacting with transglottal pressure. The mass and stiffness of the folds are determined by the action of the internal and external !aryngeal muscles. According to this theory, control of the Fo of the vibrating folds is in- fluenced by a number of independent physiologic parameters: ( 1 ) the effective mass of the vibrating part of the vocal folds; (2) the effective tension in the vibrating part of the vocal folds; (3) the effective area of the glottis during the vibratory cycle; (4) subglottic pressure; and (5) the damping of the vocal folds (van den Berg, 1958 ). Titze (1980), in his tutorial on the myoelastic-aerodynamic theory, stated that under large amplitude conditions Fo appears to be controlled entirely by static and amplitude tissue stiffness rather than explicitly by aerodynamics. Titze concludes that Fo control is primarily elastic with marked intonation patterns being programmed centrally and being implemented by major muscular contraction. Additional reflex intonation patterns appear to be controlled by peripheral feedback implemented by lesser, but significantly faster, contractions. Since control of fundamental frequency is myoelastic, this places limits on control of Fo by subglottal pressure alone and forces such control to be inseparably connected with vibra- tional amplitude or less directly with vocal intensity.

In 1972, Ishizaka and Flanagan published their experi- ence with synthesis of voiced sounds using a two-mass model of the vocal cords. They approximated the cords by a self- oscillating source composed of two stiffness-coupled masses, the upper and lower margins of the folds. Glottal waveforms

705 J. Acoust. Sec. Am. 83 (2), February 1988 0001-4966/88/020705-11500.80 (D 1988 Acoustical Society of America 705

of volume velocity, glottal area, and mouth-output sound pressure were simulated. They investigated the relationship between F o, subglottic pressure (P sub ), vocal cord tension, glottic area, and duty ratio. According to the two-mass model, Fo depends on the following independent control parameters: ( 1 ) the mass of upper and lower margins; (2) a dimen- sionless tension parameter (Q); (3) a phonation-neutral area (or rest area) of the glottis; (4) subglottic pressure (P sub ); and (5) a damping coefficient for the vocal cord oscillators. Using this model, computer simulations have produced highly realistic results with regard to quality of glottal area, glottal flow, and acoustic waveforms when compared to measures of human phonation. However, few experimentally confirmed physiologic correlates of the above- mentioned control parameters have been investigated.

A. Laryngeal control parameters

A unifying assumption of one-, two-, and multimass models of the vocal folds is that the vibrating folds approximate simple mechanical vibrators. The natural vibrating frequency of a simple mechanical oscillator varies with the square root of the effective stiffness (k) to mass (m) ratio as follows:

/Fo• ( 1/2•r) ( k /m ) •/2 ( 1 ) (Titze, 1980; Tanabe et al., 1979 ). Determinants of the stiffness and mass of the vocal folds are the state of activation of

the extrinsic and intrinsic laryngeal muscles, which include the following: Cricothyroid muscle (CT), vocalis muscle (VOC), lateral cricoaryetenoid muscle (LCA), interarye- tenoid muscle (IA), posterior cricoaryetenoid muscle (PCA), and cervical strap muscles.

The CT muscle has been termed "the external tensor" of

the vocal cord. Through action potentials carried in the external branch of the superior laryngeal nerve (SLN), cricothyroid activation produces a lengthening and thinning of the cords. Studies of high-speed laryngeal photography during phonation in humans have associated a lengthening and thinning of the cords with rising Fo (Hollien and Moore, 1960). An increase in EMG activity of the CT muscle accompanied increases in Fo in humans (Arnold, 1961; Faa- borg-Anderson, 1957; Hirano et al., 1969; Shipp and McGlone, 1971 ). In dogs, Rubin (1963) showed that stimulation of the SLN produced F o increases from 135 to 540 Hz. Mechanistically, lengthening and thinning the vocal folds affect Fo by decreasing the effective vibrating mass [Eq. ( 1 ) ]. This is also supported by morphologic studies of Hir- ano (1974), whereby stimulation of the CT muscle produced a thinner, more convergent vocal fold. In addition, lengthening the vocal cord causes elongation of the vocalis muscle. Hast ( 1961 ) showed that passive and active tension in the VOC were greatly augmented by external stretching. By lengthening the VOC, CT activation elevates Fo by increasing vocal fold stiffness [Eq. ( 1 ) ].

Function of the vocalis muscle (VOC) is considered a contributor to Fo elevation in human and canine phonation, although the effect of the VOC on laryngeal adjustment has not been fully delineated. Electromyographic studies in humans have indicated that VOC activity increases with in-

creasing F0 (Faaborg-Anderson, 1957; Hirano et al., 1969; Shipp and McGlone, 1971 ). The vocalis has been shown to be an antagonist to external lengthening applied by the CT muscle (Arnold, 1961 ). Isometric contraction of the VOC increased its tension (Hast, 1961 ), thus elevating Fo by increasing vocal cord stiffness [Eq. ( 1 ) ]. Koike et al. (1974) noted that stimulation of the VOC uniquely causes a medial bulging at the midportion of the vocal cord. Hirano (1974; Hirano et al., 1983) also studied stimulation of the VOC and found that it produced a more rounded, thickened vocal cord. Stimulation of the recurrent laryngeal nerve (RLN) in the dog produces Fo elevation (Rubin, 1963 ), although to a much lesser degree than that produced by activation of the CT muscle. Also, RLN stimulation (RLNS) activates the VOC, LCA, IA, and PCA muscles so that, from a practical standpoint, isolated VOC stimulation in Rubin's in vivo canine preparation was not possible.

The degree to which the laryngeal adductors control Fo has not been determined. Hirano et al. (1969) showed an increase in LCA activity in humans with rising Fo. Shipp and McGlone ( 1971 ), however, failed to show a change in either LCA or IA activity with increasing Fo. Stimulation of the RLN in the dog (Rubin, 1963) caused a mass contraction of the VOC, LCA, IA, and the PCA with a modest rise in Fo, but the relationship of Fo increase to LCA and IA activity was not examined. Lofquist and Yoshioka (1980) have shown a reciprocal pattern of EMG activity in the IA and PCA muscles in voiceless obstruent production. The authors suggest that, based upon a number of studies, LCA be functionally grouped with vocalis, especially in control of glottal opening for voiceless sounds. That IA and LCA muscles bring the vocal cords to the midline and hold them there may be their major function in phonation, although an increase in their activity could lead to an increase in "medial compression" of the vocal fold tissues.

The PCA has been shown to be a powerful abductor of the vocal cords and functions primarily to dilate the glottal orifice during respiration. Its function during phonation has not been clearly defined. Dedo (1970), Gay et al. (1972), and Baer et al. (1976) reported increasing PCA activity at high Fo. Wyke ( 1981 ) reported that during the prephona- tory tuning phase of phonation, spontaneous PCA activity ceased only to resume once phonation ensued, especially at high Fo. Lofquist and Yoshioka (1980) described a reciprocal relationship between PCA and IA activity in voiceless obstruent production. Electromyographic measurement of PCA activity during voiceless consonant production and breathy phonation (Hirose, 1976) suggests that PCA activity is directly responsible for the size and temporal course of glottal opening during phonation. In addition, the activity of the PCA in phonation has been thought to brace the aryeten- oids against the anterior pull of the vocal folds during phonation (Harris, 1981 ).

Most studies of phonation cite a direct relationship between P•b and Fo. Using a canine preparation, Rubin (1963) showed that P• is the result of an interplay between tracheal air flow and glottic resistance. With isolated increases in air flow, he found a modest rise in Ps• without significant increase in Fo. Increased glottal resistance (by

706 J. Acoust. Soc. Am., Vol. 83, No. 2, February 1988 D.M. Moore and G. S. Berke: Effect of laryngeal nerve stimulation 706

stimulation of the RLNs), however, led to a concurrent increase in Psub and F o. The finding that Fo did not increase with increased air flow in Rubin's study is at variance with the phenomenon of "sudden abdominal thrust" in humans, whereby a sudden increase in air flow imparted by an abdominal thrust is associated with a transient rise in Fo (van den Berg, 1958; Baer, 1979). In a tutorial on the myoelastic- aerodynamic theory of phonation, Titze (1980) observed that Fo dependence on Psub stems from a myoelastic amplitude effect. Under large amplitude conditions (e.g., modal register), Fo is controlled by static and amplitude-dependent tissue stiffnesses, rather than by aerodynamic factors. He suggested that while alteration in tracheal air flow by abdominal effort can account for slow and deliberate Fo control, it does not explain rapid changes in Fo seen in normal speech and singing. It is likely that Fo is controlled in the modal register predominantly by laryngeal muscular activity, and that the relationship of Psub to Fo stems from increased glottal resistance as a result of increased adductor muscle activity.

Monsen et al. (1978) used the Ishizaka and Flanagan model to assess the contribution of Psu• and vocal fold tension (Q) to changes in Fo and simulated glottal waveforms. They described two types of change in the glottal waveform over time, depending on whether Fo was changed primarily by Psa• or by Q. By increasing the tension parameter Q, which increased Fo markedly, the waveforms showed a rise in OQ. Conversely, by increasing Psu•, the Fo increased only modestly with very little effect on the OQ discernible from the waveforms. A number of primarily theoretical studies (Monsen et al., 1978; Titze, 1984; Childers etal., 1986) have varied mechanical control parameters to demonstrate significant changes in simulated giottographic waveforms. How- ever, few studies to date have attempted to relate changes in physiologic control parameters to changes in measured temporal events.

As mechanical models of vocal fold vibration become

refined, their relationship to physiologic mechanismsf should be investigated. In the present study, techniques for generating giottographic waveforms and measuring Ps• were applied to an in viva canine preparation to determine the effect of superior and recurrent laryngeal nerve stimulation on temporal events of vocal cord vibration.

the canine (Galen's nerve) that are believed to be sensory. Longitudinal elasticity curves for the epithelium, ligament, and muscle of the canine larynx have different tension- length slopes than in humans, but their overall shape is similar. The cricoid and thyroid cartilages are more angulated and of less height than in humans. The ventricles are consid- erably larger and there is no well-defined vocal ligament. In spite of these differences, much of the information on the mechanics of vocal fold vibration has emerged from the study of excised canine larynges. Baer ( 1983, 1984) used excised canine larynges to describe the vertical and horizon- tal movements of vocal fold mucosa during vibration. Berke et al. (1987), using an in viva canine model, observed that phase differences exist between upper and lower margin vibration in the canine vocal fold, and that there is a smaller open quotient and higher speed quotient in the dog compared to man. Berke related the differences in open quotient and speed quotient to the greater vertical dimension of the canine vocal fold, which produces a greater distance between the upper and lower margins. The increased vertical distance leads to a greater time delay between the opening of the lower to upper margins, with a resulting decrease in the open quotient. The larger speed quotient in dogs may be due to the increased vocal fold vertical dimension, which may permit the lower margin to close rapidly due to its lack of anatomic coupling with the opening of the upper margin. A number of studies have suggested that excised larynges do not accurate- ly reproduc•e physiologic conditions of vocal fold tension and mass during vibration (Mueller, 1938; Perlman and Titze, 1983; Fukuda et al., 1983). In viva canine models, by main- taining blood flow and intrinsic laryngeal muscular tension while preventing postmortem deterioration of the tissue, appear to be more physiologic preparations for studying vocal fold vibration than excised larynges.

I. METHODS

A. Subjects

Seven adult male mongrel dogs, each weighing 25-30 kg, were used in the study. Each dog was screened to assess its suitability as a subject for the experiment. Dogs with long necks were preferred for ease of preparation.

B. In vivo canine model

The use of animals to study laryngeal function provides a setting in which new concepts can be tested, while at the same time allowing manipulation of variables not easily controlled in humans. Traditionally, investigators have used the canine as their principal animal model on which laryngeal studies have been based. The canine larynx is similar to the human larynx in terms of size and vocal fold histology. How- ever, the upper portion of the vocal fold has a thicker and a looser lamina propria than seen in humans, accounting for the increased thickness of the canine vocal fold (Hirano, 1981). The canine larynx has a posterior V-shaped chink behind the arytenoids, and there is a post glottic space in some animals during phonation. There are anastomotic fi- bers between the superior and recurrent laryngeal nerves in

B. Giottographic techniques

Giottographic techniques have shown potential as tools for studying the temporal events that occur during a vocal fold cycle. Photoglottography (PGG), introduced by Sonesson in 1959, is a technique that employs a photoelectric transducer to describe time-varying changes in the glottal area. Electroglottography (EGG) is a technique measuring impedance of a small electric current across the neck. Changes in impedance are modulated by changes in lateral vocal fold contact area (Childers and Krishnamurthy, 1985). They have shown that the differentiated EGG signal (dEGG) can provide temporal information on points of upper margin opening and lower margin closing. Baer et al. (1983) have demonstrated that combined analysis of PGG and EGG signals gives essentially the same information for


peak glottal opening and glottal closure as high-speed laryngeal photography. Application of giottographic techniques to physiologic laryngeal preparations should provide information about the micromechanics of vibration to assist in

verification and refinement of current theories.

C. Experimental preparation

The experimental setup was the same as described pre- viously by the authors, and was similar to prior in vivo canine studies (Berke et al., 1986; Rubin, 1963). Dogs were anes- thetized with 2 cc ketamine by intramuscular injection fol- lowed by intravenous pentobarbital until loss of the corneal reflex was achieved. The animals were then placed supine on an operating table (Fig. 1 ) and direct laryngoscopy was performed to confirm normal laryngeal anatomy. A 7-mm oral endotracheal tube was inserted, through which the animal breathed spontaneously. A vertical midline incision was made from the mandible to the sternum. The strap muscles and sternocleidomastoid muscles were retracted laterally to expose the larynx and trachea. The external branch of the superior laryngeal nerves were isolated at their entrance into the CT muscle. A gauze/silver electrode was applied to the nerves and insulated from the surrounding tissue. The recurrent laryngeal nerves were isolated at 5 cm inferior to the larynx. Electrodes were applied in the same fashion. Ground electrodes were sutured to the trachea and connected to the

anode Of the nerve stimulator. Electrical isolation between

recurrent laryngeal nerve and superior laryngeal nerve stimulation was verified by direct observation. Maximal stimulation of the recurrent laryngeal nerves to the point at which

the strap muscles were also noted to contract (approximately 9 V) was not observed to produce contraction of the cricothyroid muscle. In addition, no lengthening or thinning of the vocal cords occurred during maximal recurrent laryngeal nerve stimulation. Isolated maximal stimulation of the superior laryngeal nerves to the point at which the strap muscles were observed to contract did not demonstrate tens-

ing or bulging of the vocalis muscle on direct laryngoscopic observation. No arytenoid adduction or phonation could be illicited by maximal superior laryngeal nerve stimulation. Electroglottographic electrodes (Synchrovoice) were placed in direct contact with the thyroid cartilage while the ground electrode was sutured to the skin. A 1.0-cm button was placed to suspend the epiglottis anteriorly through the thyro-hyoid membrane to improve visualization of the vocal folds. A distal tracheotomy was performed and an endotracheal tube passed to permit the animal to breathe spontaneously. A more proximal tracheotomy was performed, through which a cuffed tracheotomy tube was placed with its tip resting 10 cm below the glottis. The catheter-tipped pressure transducer was inserted through this upper tracheotomy. The cuff on the superiorly directed tube was inflated to just seal the trachea. Air flow, obtained from the UCLA physical plant, was passed through the cephalad tracheotomy tube. The rate of air flow was measured with a flow- meter (Gilmont Inst. model F 1500), and kept at a constant rate of 375 cc/s throughout the study. Unlike human phonation that can be induced with subglottic pressure in the range of 6-10 cm of water, canine phonation requires at least 20 cm of water pressure for sustained oscillation. Because of the

I CAMERA I V•deo or 35 mm SLR

CONTINUOUS I XENON • • STROBOSCOPE LIGHT SOURCE

--3 CHANNEL FIBEROPTIC TELESCOPE

(strobe trigger)

Sup. Iorynge n

NERVoE STIMULATOR (bilateral)

iiii

iiii

EGG PROCESSOR

• (dEGG)-

•(EGG)--

NERVE ST IMUL ATOR • (PGG) m (bilateral) SENSOR

HUMIDIFIED _ PRESSURE •(press.)-- WARM TRANSDUCER

AIR SOURCE •x

Subsequent Data

Analyiis 4 CHANNEL FM TAPE RECORDER

MULTICHANNEL STORAGE OSCILLOSCOPE

SPONTANEOUS Recurrent n. I RESPIRATIONS

X-Y PLOTTER

FIG. 1. Diagramatic representation of experimental preparation.


canine's posterior glottic chink, which allows a significant dc escape of air flow during phonation, an air flow of approximately 375 cc/s is required to develop a subglottic pressure of at least 20 cm H20. It was also observed that in order to match target frequencies from 80-160 Hz, 375 cc/s of air flow was required. The air was bubbled through 5 cm H20 for warming and humidification. The temperature in the animals trachea was measured at 15-min intervals to assure a

constant air flow temperature of 37 øC. The photoglottogra- phic light sensor (Centronics OSD 50-2) was placed on the animals' trachea approximately 3 cm below the larynx. A xenon light source and fiberoptic cable provided supraglottic illumination for the PGG. A microphone (Sennheiser) was placed 15 cm from the vocal folds and connected to a Storz model 8000 laryngostroboscope for frequency analysis of the phonatory sound. In addition, stroboscopic video imaging was obtained using the Storz stroboscoby unit connected to a Storz 0 ø telescope via a fluid filled light cable. The Xenon light source for the PGG was connected to the other light port of the telescope. The image from the 0 ø scope was recorded by a Circon CCD video camera and a SONY •-in. video tape recorder. Although a low level of constant xenon light source was present during stroboscopic video recording, excellent stroboscopic video imaging was obtained (Berke et al., 1987 ). The system was not used for calculated measures; however, it was useful for interpretation of vibratory events recorded simultaneously with the PGG and EGG signals. A catheter-tipped pressure transducer (Gad- tee DCE-1 ) was calibrated at 37 øC by submerging it in a water bath at 37 øC to a depth just covering the sensor (0.5 cm). The catheter was then calibrated against a Hg manom- eter from 0-170-cm H20 pressure.

D. Stimulus parameters

Two nerve stimulators were used. A Grass (model 54H) nerve stimulator was used to provide variable voltage stimulation while a WPI (30 l-T) nerve stimulator was used to provide a low level of constant current stimulus. Voltages ranged from 0.5-0.9 V for the Grass stimulator. Currents ranged from 0.1-0.15 mA for the WPI stimulator. Frequen- cy of stimulus was 80 Hz, with a pulse duration of 1.5 ms for both the Grass and WPI units.

E. Data acquisition

The PGG, EGG, and P• signals were simultaneously recorded on a four-channel Tannberg FM tape recorder (model 115D). The signals were also monitored on two os- cilloscopes ( Textronix 5116, Hitachi V 1050-F) to assess the adequacy of the giottographic signals.

F. Experimental design

Seven animals were stimulated to phonate at "target frequencies" of 80, 100, 130, 160, and 180 Hz, while holding air flow constant at 375 cc/s. First, while delivering a low level of constant current stimulus to the recurrent laryngeal nerves (0.10 mA), voltage stimuli to the SLNs were varied to produce phonation at the target frequencies. This was done to examine the effect on vocal fold vibration of activa-

tion of the CT muscle to increasing Fo. Second, while delivering a low level of constant current stimulus to the SLNs (0.10 mA), voltage stimuli to the RLNs were varied to produce the target frequencies. This was done to demonstrate the effect on vocal cord vibration of activation of the intrin-

sic laryngeal muscles to increasing Fo. Two trials were performed of variable SLN stimulation (SLNS) and variable RLN stimulation (RLNS) to produce the five targed Fo's. The target frequencies were obtained in a random order for all subjects. The PGG, EGG, and subglottic pressure signals were recorded for each trial at each target frequency. Phona- tion at 80 and 180 Hz could not be achieved in some animals, so statistical analysis was limited to the middle target frequencies of 100, 130, and 160 Hz.

G. Data analysis

The recorded PGG, EGG, and Ps,b waveforms were low-pass filtered at 1500 Hz, digitized at a rate of 20 kHz with an LSI 11-73 computer, and stored on disk. A 0.5-s sample of stable phonation was used. A multipurpose computer software program was used for data analysis and gra- phic display. Figure 2 shows a representative glottic cycle obtained. Specific points in the glottic cycle were then picked

(5

Ai B i C i D i

I I 1 I

I

' I

• 5 10 I MS

'• DURATION OF VIBRATORY CYCLE

.ow.. MARGIN / CLOSED OPENING

UPPER LOWER

MARGIN MARGIN OPENING CLOSING

FIG. 2. The PGG, EGG, dEGG, and P,,,•, signals recorded from a canine preparation phonating in the modal register.


for determination of temporal events of the cycle. Moments ofglottal opening and closing were the same as those reported by Childers and Krishnamurthy (1985), Baer et al. (1983), and Berke et al. (1986). Point Ai was the point of initial separation of the lower fold margins, determined by the initial rise in the EGG impedance from its minimum. Point Bi was the moment of upper margin opening as determined by the positive deflection of the differentiated EGG waveform (dEGG). Point Ci was the moment of maximal glottal area as determined by the peak of the PGG waveform. Point Di identified lower margin closure, as determined by the nadir in the dEGG waveform. Point Ai +, was the lower margin opening of the next cycle. Points B i,Ci, and Di could be reliably determined, however, point Ai during high SLNS occurred on a gradual upslope in the EGG and was difficult to discern interactively. By marking the waveforms in this manner, periods of glottal events were divided

by the period of the vibratory cycle to determine the quotients of vocal fold vibration as follows: Qp is the time delay between opening of lower and upper margins/period, OQ is the duration of open glottis/period, CQ is the duration of complete glottal closure/period, Qog is the duration of glottal opening/period, Qcg is the duration of glottal closing/ period, and SQ is the duration ofglottal opening/duration of glottal closing.

Ten contiguous glottal cycles from a recording of stable phonation were analyzed. For each subject, this procedure yielded mean data on glottal quotients (see above) at target frequencies of 100, 130, and 160 Hz for two random trials (trials 1 and 2) and for two stimulation effects (SLNS and RLNS). Measured frequency Fo was also compared to targed Fo. Measurement of Psub maximum, minimum, and rms mean were obtained for each glottic cycle analyzed.

The six glottal quotients, which represent the mean of

5 10 15 20

MS

30 O• 25 'r

20 E• 15

5 10 15 20

MS

65 0 55 -r

E 45 •

5 10 15 20

30% 25 'r

20

5 10 15 20

MS MS

85 -r E

75

5 t0 15 20

40 O• m 35 3: : 3oE o a_• 25

(f) '•

5 10 15 20

MS MS

100 0

90 -r

80

FIG. 3. Typical recordings from a subject for three levels of target frequency (TFo). (a)-( c ) are TFo of 100, 130, and 160 Hz for SLNS. (d)-(f) are TFo of 100, 130, and 160 Hz for RLNS.


two random trials for ten contiguous cycles for the seven subjects, were analyzed within an analysis of variance (AN- OVA) framework. Separate analyses of variance were applied for the type of stimulation on each quotient, with target frequency and trial as repeated measures. No difference was shown between trials 1 and 2 for any of the quotients.

II. RESULTS

Electrical stimulation produced Fo's of 54-340 Hz, spanning the low-modal, modal, and falsetto registers per- ceptually. Figure 3 shows representative waveforms plotted for one subject at three target frequencies for the effects of SLNS and RLNS. As the frequency increased due to an increasing level of SLNS [Fig. 3 (a)-(c) ], the width (Bi to Di in Fig. 2) of the EGG waveform remained nearly constant despite a diminishing period. This was reflected qualitatively in an increasing open portion and a decreasing closed portion of the cycle. In contrast, as frequency increased by increasing RLNS [ Fig. 3 (d)-(f) ], a narrowing of the EGG waveform occurred. This was associated with a decreasing open portion and a markedly increasing closed portion of the cycle. For this particular subject, mean subglottic pressure rose from 22 cm H20 at 100 Hz to 32 cm H20 at 160 Hz for SLNS [ Fig. 3 (a)-(c) ]. For increasing RLNS, mean Psub rose from 57 cm H20 at 100 Hz to 90 cm H20 at 160 Hz [Fig. 3(d)-(f)].

Examination of giottographic waveforms in Figs. 2 and 3 reveals several findings with regard to subglottic pressure. Here, Psub rises throughout the vocal fold vibratory cycle until upper margin opening is reached (Fig. 2, Bi ), at which point it drops rapidly. Upon lower margin closure (Fig. 2, Di ), the P•u• abruptly increases, and then increases steadily until the upper margin opening of the next glottic cycle. As Fo increases (Fig. 3 ), high-frequency components appear in the P•u• waveform superimposed on the mean P•u•.

Table I displays mean Fo measured for SLNS and RLNS versus the target frequencies desired for the seven subjects. The experimentally measured Fo's closely approximated the desired target frequencies. Figure 4 displays temporal events in the glottal cycle as glottal quotients versus target frequency for SLNS. The Qog increased steadily with increasing Fo [F(2,12) = 4.74, p<0.05], in parallel with OQ. The Qcg was not shown to change significantly as Fo increased in this study. The CQ decreased markedly [F(2,12) = 4.50, p < 0.05] as Fo increased, most notably at low frequency.

0.6

0.5

0.4

0.3

0.2

0.1

--J CQ

5 •; '•; Qcg

I I I I I I I

100 130 160

FREQUENCY(Hz)

FIG. 4. Mean values ( + S.E.M.) for Qp, OQ, Qog, CQ, and Qcg for seven subjects for SLNS at 3 TFo ( 100, 130, and 160 Hz).

The Qp was not shown to change significantly over the frequency range examined.

Figure 5 shows the effect of RLNS on temporal events of the glottal cycle for frequencies 100, 130, and 160 Hz. The Qog and Qcq were not shown to change significantly as frequency increased. Because OQ is the sum of Qog and Qcg, it also did not change. The CQ increased markedly [F(2,12) = 11.06, p <0.01 ], while Qp decreased steadily as frequency increased [F(2,12) = 10.94, p <0.01 ].

Figure 6(a)-(f) displays plots ofOQ, Q•, CQ, Qog, Qcg, and SQ for levels of target Fo for the effects of SLNS vs RLNS. The data represent the means of two trials pooled for the seven subjects. The OQ, which increased with Fo for SLNS, was not affected by increasing RLNS. The Q• decreased for RLNS as Fo increased, but was unaffected by SLNS. The CQ changed as Fo increased for both effects, but in opposing direction. The Qog increased with Fo for SLNS but was unaffected by Fo increases due to RLNS. The Qcg was not shown to significantly change as Fo increased in this study. No significant change in SQ was observed as the target Fo was increased by either effect.

Figure 7 displays mean Psub for five target Fo's for one subject. Here, P•u• ranged from 22-116 cm H20. Whereas Psub rose minimally for SLNS as Fo increased, it rose markedly for RLNS. The alternating component of the pressure

0.6

TABLE I. Target frequency (TFo) versus measured frequency (Fo) for seven subjects. Value is the mean of two trials for seven subjects over ten contiguous glottal cycles (standard deviation in parentheses).

Measured Fo (Hz)

Target F o (Hz) SLNS RLNS

80 80.2(1.1) 79.7(3.8) 100 101.8(1.7) 99.5(2.6) 130 130.1 (4.3) 131.8(4.1 ) 160 157.1 (3.7) 162.5(4.2) 180 178.8(4.2) 184.5(5.5)

0.5

0.4

0.3

0.2

0.1

100 130 160

FREQUENCY(Hz)

FIG. 5. Mean values ( + S.E.M.) for Qp, OQ, Qog, CQ, and Qcg for seven subjects for RLNS at 3 TFo ( 100, 130, and 160 Hz).


0.36

0.32

0.28

('a) 0.28

ß [] S 0.24 • 0.20 []J --ß R , , , • , , •' ,0.16

1 O0 130 160

(d) s

i i i i i i i t

100 130 160

0.52

z

uJ 0 44 _ ,

o

o

0.36

o o.12

•ß•ß O.lO 0.09-

R

i i t i - ; ;

100 130 160

(e) ß

[]•a s

i i i i i i

100 130 160

FIG. 6. Mean values for SLNS(S) vs

RLNS(R). (a) -- OQ; (b) -- Qp; (c) = CQ; (d) = Qog; (e) = Qcg; (f) = SQ.

0.40' 2.8

(C) ß•ß R ('0 2.6 032

'

2.4

0.24

ß •[] 2.2 2,0 0.16 S

;o ' '1;o' ' 1; ' ' 1 o lOO

[] s

i i i i i

130 160

FREQUENCY(Hz) FREQUENCY(Hz)

wave for this subject varied between 14-24 cm H20 for all levels of Fo achieved, and did not increase as Ps,b increased. The Ps,b trends for RLNS and SLNS were similar in all seven subjects.

III. DISCUSSION

The present investigation was designed to study the effect of SLNS and RLNS on temporal events of the vocal fold vibratory cycle over a frequency range of 80-180 Hz, under conditions of constant air flow. This range was chosen to represent frequencies within the canine modal register. Data regarding frequency ranges for canine phonation do not exist. However, it appears that dogs develop both modal and falsetto registers in their normal phonation, as evidenced by the growl, the bark, and the shrill cry that dogs commonly exhibit. Hollien and Michel (1968) investigated the register frequencies of 12 adult human males. They found a range of 94-287 Hz for the modal register. As the canine larynges are somewhat thicker and more massive than human larynges (Hirano, 1974), the dog likely has a lower range of frequency for the modal register.

The profound effect of SLNS to increase F o was confirmed by this study. Frequencies as high as 340 Hz were obtained with activation of the CT muscle. The Fo elevation by increasing SLNS was not accompanied by a significant

increase in P•.b (Fig. 7), which parallels normal human phonation in speech. The effect of SLNS on increasing OQ for increased Fo agrees with studies of increased Fo in human speech (Hildebrand, 1976). This may be explained in the two-mass model by increased coupling between the lower and upper margins brought about by a thinning of the vocal cords, so that there is less vertical distance between the lower and upper margins, which produces a more convergent glottis. Conversely, the CQ decreased markedly as Fo was in-

lOO

6O

2O

ß s

I I I - - ' ; ; ; i ; ;

80 100 130 160 180

FREQUENCY (Hz)

FIG. 7. P.•ub in cm H20 for SLNS(S) vs RLNS(R) for one subject.


creased by SLNS. This may similarly be explained by increased coupling between the lower and upper margins. The initial rise in Qp for SLNS was offset by a decline at 160 Hz [Fig. 6(b) ], so that no net change in Qp was observed. The difficulty in determining the point Ai for increasing SLNS may have contributed to an error in the calculation Q•, thus leading to the observation of no net change.

The results of this study for increasing SLNS are in close agreement with values extracted from Ishizaka and Flana- gan simulations (1972). For increasing Fo from 133-222 Hz by increasing the tension parameter Q from 0.8-1.5, OQ increased from 0.6 to 0.72, CQ decreased from 0.2 to 0.11, and Q• showed no change. The trend for increased OQ with increased Fo also agrees with computer simulations of Monson et al. (1978) for the effect of increased Q.

Of interest is the close association of Qog to OQ for SLNS (Fig. 4). Most of the change in OQ was due to upper margin opening, rather than by lower margin closing [Qcg, Fig. 3 (e) ]. In other words, as Fo increases by increased CT activity, the opening phase of the vibratory cycle increases, while the closing phase remains unchanged. This substan- tiates the concept that as CT activity is increased in the modal register, a more convergent glottis is produced such that the upper margin governs changes in the open portion of the cycle.

Stroboscopic video imaging during increasing superior laryngeal nerve stimulation showed that there was a diminu- tion in the excursion of the vocal cords laterally, but this was associated with what appeared to be a decrease in the amplitude of the traveling wave. As superior laryngeal nerve stimulation was increased beyond modal voice, it was observed that the two-margin system was replaced by a one-margin system, or the lower and upper margins were observed to fuse into a one-mass vibration.

As shown in Fig. 7, SLNS produced very little increase in Psub as Fo increased. Apparently, CT activation has little effect on glottal resistance. According to the Ishizaka and Flanagan model, an increase in the tension parameter Q leads to a marked increase in Fo with an increase in OQ, a decrease in CQ, and no change in Q• (Ishizaka and Flana- gan, 1972; Monson et al., 1978). Thus CT muscle activation may be a physiologic correlate of the tension parameter Q in the two-mass model. It is of interest to note that Flanagan et al. (1976) stated that Q could be derived from EMG cricothyroid energy based upon the observation that CT acts as a vernier pitch control, superposed on the modal pitch value through extra tension of the vocal cords.

A modest increase in Fo affected by an increase in RLNS was confirmed in the present investigation. All subjects developed Fo elevation to 160 Hz with increasing RLNS. How- ever, no animals developed phonation at greater than 190 Hz by this method. The OQ did not change significantly for increasing Fo by RLNS, although it tended to decrease. This is in agreement with the Ishizaka and Flanagan prediction of a decreasing OQ with rising Psub from 2-8 cm H20 and a small downward trend in OQ beyond 10 cm H20 (Ishizaka and Flanagan, 1972).

Supraglottic stroboscopic imaging showed that increasing RLNS produced an increase in the amplitude of the trav-

cling wave, but appeared to decrease the effective anterior to posterior vibratory fold length and lateral excursion. Both RLN and SLN stimulation demonstrated the CT muscles

ability to thin and lengthen the folds for any given level of RLNS.

Stimulation of the recurrent laryngeal nerve activates the VOC, LCA, IA, and PCA muscles. Activation of the VOC muscle increases the stiffness of the vocal cord, leading to an increased Fo [Eq. ( 1 ) ]. In addition, VOC activation leads to a slackening of the mucosal cover of the vocal cord (Stevens, 1977). This "slackening" may have produced a relative uncoupling of the upper and lower margins, which prevented the increased OQ, as observed when Fo was increased due to increased SLNS. Vocalis activation uniquely caused a medial bulging of the vocal fold, which contributed to an increased medial compression of the folds, a decreased phonation-neutral area, and thus an increased CQ. Recruit- ment of intrinsic adductor muscles may also have produced increased medial compression. That Q• decreased significantly for increased Fo by RLNS may reflect this increased "medial compression." One explanation for the decreased Qp is that when the lower margin finally began to open during a cycle, the folds were rapidly parted by the resultant high P•,•. Neither Qos or Qcs was shown to change significantly as Fo increased by RLNS.

The P•,• increased with increasing Fo, due to RLNS, in all subjects. Increase in P•u• may be related to increased glottal resistance affected by RLNS. Giottographically, this is represented by an increase in the closed portion of the cycle (CQ). Subglottic pressure elevation with RLNS in this study substantiated the findings of Rubin (1963). The P•u• for human phonation is maintained between 3 and 10 cm H:O in normal conversational and declaratory speech, 10- 20 cm H:O when singing at moderate loudness, and reaches a peak of 50-70 cm H:O for singing at loudest intensities (Wyke, 1974). Proctor (1974) stated that the human phonatory system is capable of generating Ps•b as high as 100 cm H:O. That it does not do so may reflect feedback of subglottal mucosal mechanoreceptors. When these receptors are blocked by topical anesthesia, mean P• rises using similar pitch and intensity levels in both speech and singing (Gould and Okamura, 1974). During stimulation of the SLN and RLN in the present study, depolarization occurred in both prodromic and antidromic directions, thus effectively inter- rupting reflex pathways. Therefore, the high P• obtained with RLNS in both this study and that of Rubin (1963) may reflect supra-physiologic levels of stimulation. It is conceiv- able, however, that specialized functions of the canine phonatory systemrathe barkwnecessitates a high P• when abrupt, intense phonatory bursts are desirable.

The observation in the present study that the ac pressure waveform is close to its maximum before upper margin opening and then falls to reach a nadir at closure does not match with similar records from humans obtained with pressure-tip transducers passed through the glottis into the trachea (Kitzing and Lofquist, 1975; Cranen and Boves, 1985). In these records there is a sharp increase in subglottal pressure at the onset of glottal closure and a marked decrease at the onset of glottal opening. It is possible that the discrepan-

713 J. A½oust. So½. Am., Vol. 83, No. 2, February 1988 D.M. Moore and G. S. Berke: Effect of laryngeal nerve stimulation 713

cies observed may be related to the pressure transducer-am- plifier used in the present study distorting the ac waveform obtained, or that the experimental procedure used gave different waveforms from those recorded in humans, or that some tracheal acoustic factor in humans contributed to the

records that is not present in dogs due to the presence of an endotracheal tube, or another factor. However, phenomeno- logically, since the driving force for glottic opening is subglottic pressure, a pressure rise and peak prior to opening and a fall in pressure as flow ensues resulting in glottic closure does help to explain sustained oscillation.

Monsen et al. (1978), using the Ishizaka and Flanagan model to simulate giottographic waveforms, studied the effect of increasing Psub on Fo, intensity and quality of the waveforms. They noted a modest increase in Fo ( 151 to 174 Hz) and a slight decrease in the closing portion of the open phase of simulated giottographic waveforms as Psub was al- lowed to increase. In the present study, RLNS produced a moderate Fo increase as well as a marked increase in P•u•. Therefore, we believe that the primary physiologic correlate of P•u• (under conditions of constant airflow) in the Ishi- zaka and Flanagan model may be activation of the vocalis and adductor muscles by RLNS.

IV. CONCLUSIONS

Study of the effect of superior and recurrent laryngeal nerve stimulation on phonation in an in vivo canine model yields the following conclusions.

( 1 ) Increasing SLNS, which activates the cricothyroid muscle, caused a marked increase in Fo with an increase in OQ and little increase in P•u•. The opening segment of the open phase was most affected, as evidenced by increasing Qog. CQ decreased markedly with increasing $LNS. Qp was not shown to change significantly with increasing SLNS. This method of frequency elevation may provide a physiologic correlate for the tension parameter Q in the Ishizaka and Flanagan model.

(2) Increasing RLNS, which as a net effect activates the vocalis and intrinsic adductor muscles, produced a modest increase in Fo and a marked increase in P•u•. No change in OQ was observed. Increasing RLNS produced an increase in CQ and a decrease in Qp. This method of Fo elevation may provide a physiologic correlate of the parameter Psub in the Ishizaka and Flanagan model.

(3) Speed quotient was not shown to be significantly altered by Fo elevation in the present study.

ACKNOWLEDGMENTS

This research was supported by a Veterans Administra- tion National Merit Review Grant and a UCLA Academic

Senate Grant. The authors would like to thank Dr. David G.

Hanson, Dr. Vicente Honrubia, and Dr. Judy Dubno for the use of their technical support and laboratories. The authors are indebted to Dr. Ted Bell for his assistance with statistical

analysis and experimental design. Finally, the authors Wish to express their gratitude to Dr. Bruce Gerratt and Dr. Larry Hoffman for their expertise in speech science and neuro- physiology.

Arnold, G. E. (1961). "Physiology and pathology of the cricothyroid muscle," Laryngoscope 71, 687-753.

Baer, T., Gay, T., and Niimi, S. (1976). "Control of fundamental frequency, intensity and register in phonation," Haskins Lab. Stat. Rep. Speech Res. SR-45/46, 175-185.

Baer, T. (1979). "Reflex vibration of laryngeal muscles by sudden induced subglottal pressure changes," J. Acoust. Soc. Am. 65, 1271-1275.

Baer, T., Lofquist, A., and McGarr, N. (1983). "Laryngeal vibrations: A comparison between high-speed filming and giottographic techniques," J. Acoust. Soc. Am. 73, 1304-1308.

Baer, T. (1973). "Measurement of vibration patterns of excised larynges," J. Acoust. Soc. Am. 54, 318 (abs.).

Baer, T. (1974). "Vibration patterns of excised larynges," J. Acoust. Soc. Am. Suppl. 1 55, S79.

Berke, G. S., Hantke, D. R., Hanson, D. G., and Gerratt, B. (1986). "An experimental model to test the effect of change in tension and mass on laryngeal vibration," in Proceedings of the International Conference on Voice, edited by M. Hirano (Kurume U. P., Kurume, Japan), pp. 1-8.

Berke, G. S., Moore, D. M., Hanson, D. G., Hantke, D. R., Gerratt, B. R., and Burstein, F. (1987). "Laryngeal modeling: Theoretical, in vitro, in vivo," Laryngoscope 97, 871-881.

Childers, D. G., and Krishnamurthy, A. K. (1985). "A critical review of electroglottography," CRC Crit. Rev. Biomed. Eng. 12, 131-161.

Childers, D. G., Hicks, D. M., Moore, G. P., and Alsaka, Y. A. (1986). "A model for vocal fold vibratory motion, contact area, and the electroglot- togram," J. Acoust. Soc. Am. 80, 1309-1321.

Cranen, B., and Boves, L. (1985). "Pressure measurements during speech production using semiconductor miniature pressure transducers: Impact on models for speech production," J. Acoust. Soc. Am. 77, 1543-1551.

Dedo, H. H. (1970). "The paralyzed larynx: An electromyographic study in dogs and humans," Laryngoscope 80, 1455-1517.

Faaborg-Anderson, K. (1957). "Electromyographic investigation of intrinsic laryngeal muscles in humans," Acta Physiol. Scand. Suppl. 41, 140.

Flanagan, J. L., Rabiner, L. R., Christopher, D., and Bock, D. E. (1976). "Digital analysis of laryngeal control in speech production," J. Acoust. Soc. Am. 60, 446-456.

Fukuda, H., Saito, S., Kitihara, S., Isogai, Y., Makino, K., Tsuzuki, T., Kogawa, N., and Ono, H. (1983). "Vocal fold vibration in excised larynges view with an x-ray stroboscope and an ultra-high-speed camera," in Vocal FoM Physiology, edited by D. M. Bless and J. H. Abbs (College- Hill, San Diego), pp. 238-252.

Gay, T., Hiroso, H., Strome, M., and Sawashima, M., (1972). "Electro- myography of the intrinsic laryngeal muscles during phonation," Ann. Otol. Rhinol. Laryngol. 81, 401-409.

Gould, W. J., and Okamura, H. (1974). "Interrelationship between voice and laryngeal muscles reflexes," in Ventilatory and Phonatory Control Systems, edited by B. D. Wyke (Oxford U. P., London), pp. 347-369.

Harris, K. S. (1981). "Electromyography as a technique for laryngeal investigation," ASHA Rep. 11, 70-87.

Hast, M. H. (1961). "Physiological mechanisms of phonation; tension of the vocal fold muscle," Acta Oto-laryng.62, 309-310.

Hildebrand, B. H. (1976). "Vibratory patterns of the human vocal cords during variations in frequency and intensity," Ph.D. dissertation, Univ. of Florida, Gainesville, Fl.

Hirano, M., Ohala, J., and Vennard, W. (1969). "The function oflaryngeal muscles in regulating fundamental frequency and intensity of phonation," J. Speech Hear. Res. 12, 616-628.

Hirano, M. (1974). "Morphological structure of the vocal cord as a vibra- tor and its variations," Folia Phoniatr. 26, 89-94.

Hirano, M. (1981). "Structure of the vocal fold in normal and disease states. Anatomical and physical studies," ASHA Rep. 11, 11-30.

Hirano, M., Matsuo, K., Kakita, Y., Kawasaki, H., and Kurita, S. (1983). "Vibratory behavior versus the structure of the vocal fold," in VocalFoM Physiology.' Current Research and Contemporary Issues, edited by D. M. Bless and J. H. Abbs (College-Hill, San Diego), pp. 26-40.

Hirose, H. (1976). "Posterior cricoaryetenoid as a speech muscle," Ann. Otol. Rhinol. Laryngol. 85, 334-342.

Hollien, H., and Moore, G. P. (1960). "Measurements of the vocal folds during changes in pitch," J. Speech Hear. Res. 3, 157.

Hollien, H., and Michel, J. F. (1968). "Vocal fry as a phonational register," J. Speech Hear. Res. 11, 600-604.

Ishizaka, K., and Flanagan, J. L. (1972). "Synthesis of voiced sounds from a two mass model of the vocal cords," Bell Sys. Tech. J. 51, 1233-1268.

Kitzing, P., and Lofquist, A. (1975). "Subglottal and oral pressure during


phonation--Preliminary investigation using a miniature transducer system," Med. Biol. Eng. 13, 644-648.

Koike, Y., Hirano, M., and Morio, M. (1974). "Function of the laryngeal muscles on the position and shape of the vocal cord," in Proceedings of the 16th International Congress of Logopedics and Phoniatrics, edited by E. Loebell (Karger, Basel), pp. 257-263.

Lofquist, A., and Yoshioka, H. (1980). "Laryngeal activity in Swedish obstruent clusters," J. Acoust. Soc. Am. 63, 792-801.

Monsen, R. B., Engebretson, A.M., and Vemula, N. R. (1978). "Indirect assessment of the contribution of subglottal air pressure and vocal fold tension to changes of fundamental frequency in English," J. Acoust. Soc. Am. 64, 65-78.

Mueller, E. (1938). "Stimmphysiologische Untersuchungen an einem Kehlkopfmodell," Arch. Sprach. Stimmphysiol. 2, 197-214.

Perlman, A. L., and Titze, I. (1983). "Measurement of viscoelastic proper- ties in live tissue," in VocalFold Physiology, edited by I. R. Titze and R. C. Scherer (Denver Center for the Performing Arts, Denver), pp. 271-281.

Proctor, D. F. (1974). "Breathing mechanics during phonation and singing," in Ventilatory and Phonatory ControlSystems, edited by B. D. Wyke (Oxford U. P., London), pp. 39-57.

Rubin, H. J. (1963). "Experimental studies on vocal pitch and intensity in

phonation," Laryngoscope 73, 973-1015. Shipp, T., and McGlone, R. E. (1971). "Laryngeal dynamics associated

with voice frequency change," J. Speech Hear. Res. 14, 761-768. Sonesson, B. (1959). "A method for studying the vibratory movements of

the vocal cords. A preliminary report," J. Laryngol. Otol. 73, 732-737. Stevens, K. N. (1977). "Physics of laryngeal behavior and larynx modes,"

Phonetica 34, 264-279. Tanabe, M., Isshiki, N., and Sawada, M. (1979). "Damping ratio of the

vocal cord," Folia Phoniatr. 31, 27-34. Titze, I. R. (1980). "Tutorial. Comments on the myoelastic-aerodynamic

theory of phonation," J. Speech Hear. Res. 23, 495-510. Titze, I. R. (1984). "Parameterization of the glottal area, glottal flow, and

vocal fold contact area," J. Acoust. Soc. Am. 75, 570-580. van den Berg, J. W. (1958). "Myoelastic-aerodynamic theory of voice pro-

duction," J. Speech Hear. Res. 1, 227-244. Wyke, B. D. (1974). "Laryngeal neuromuscular control systems in sing-

ing," Folio Phoniatr. 26, 295-306. Wyke, B. D. (1981). "Neuromuscular control systems in voice produc-

tion," in Vocal Fold Physiology, edited by K. N. Stevens and M. Hirano (Univ. of Tokyo, Tokyo), pp. 71-76.


Documents

an in vivo canine model The effect of laryngeal …...investigation was designed to examine, by use of an in viva canine model of phonation, the effect of change in vocal fold mass