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Evaluation of expiratory effort on dysphonic patients on increasing vocal intensity
Evaluation of expiratory effort on dysphonic patients on increasing vocal intensity KIYOSHI MAKIYAMA, MD, AKINORI KIDA, MD, and MASAYUKI SAWASHIMA, MD, Tokyo and Yokohama, Japan
It is conceivable that the subjects who have phonatory disorders, in comparison with normal individuals, exert a greater expiratory effort when phonating loudly. Furthermore, we presume that the extent and pattern of the changes in the expiratory effort for increasing vocal intensity may vary according to the types of laryngeal lesions. To prove these hypotheses, we investigated the changes in expiratory effort for increments of the vocal intensity by measuring the expiratory lung pressure. The subjects included 10 each of normal controls, patients with Reinke’s edema, and those with recurrent laryngeal nerve paralysis. For the normal controls, the increase in vocal intensity was achieved by slightly increasing the expiratory lung pressure. The patients with Reinke’s edema showed a greater increase in expiratory lung pressure, as compared with the normal group. The patients with recurrent laryngeal nerve paralysis exhibited greater expiratory effort with extreme increases in airflow than normal group for louder phonation. It was concluded that the subjects who have phonatory disorders, in comparison with normal individuals, require a greater expiratory effort. This phonatory function test with an increase in voice intensity made the aerodynamic pathologic condition clearer. (Otolaryngol Head Neck Surg 1998;118:723-7.)
Aerodynamic conditions of the glottis and glottal efficiency in phonation can be evaluated to some extent by an aerodynamic phonatory function test. We have evaluated results of an aerodynamic phonatory function test and laryngeal findings. In patients with vocal cord nodules, the mean flow rate (MFR) was higher with a larger nodule. In patients with Reinke’s edema, the expiratory lung pressure was higher with more marked edema. However, in patients with mild vocal cord nodules or Reinke’s edema, phonatory function test results were in the normal range. With vocal cord polyps, no definite association was observed between the size of the polyp and results of the phonatory function test. This was because there were individual differences in the site of polyps and the size of the glottal gap during phonation and a difference in weight between the right and left vocal cords. Thus, in disorders such as vocal nodules, recurrent laryngeal nerve paralysis (RNP), and Reinke’s edema in which the physical properties of the vocal cord
is relatively uniform, phonatory function test results appear to reflect the pathologic condition of the larynx relatively well. One purpose of a phonatory function test is evaluation of glottal efficiency. We speculated that the expiratory lung power required for phonation is greater in patients with voice disorders than in normal persons, and therefore the glottal efficiency and laryngeal adjustment ability are low. To prove this hypothesis, we evaluated the changes in expiratory efforts and glottal efficiency when the voice intensity was increased by determining the expiratory lung pressure, a parameter in the phonatory function test that reflects the expiratory effort. We also investigated whether there are differences in expiratory efforts according to the types of laryngeal lesions when the voice intensity is raised during phonation. This phonatory function test with an increase in the voice intensity can make the aerodynamic condition at the glottis clearer. SUBJECTS
From the Department of Otolaryngology (Drs. Makiyama and Kida), Nihon University, School of Medicine; and Yokohama Seamen’s Insurance Hospital (Dr. Sawashima). Presented at the Annual Meeting of the American Academy of Otolaryngology–Head and Neck Surgery, Washington, D.C., Sept. 29–Oct. 2, 1996. Kiyoshi Makiyama, MD, Department of Otolaryngology, Nihon University Surugadai Hospital, 1-8-13, Kanda-surugadai, Chiyodaku, Tokyo, 101-8309, Japan. Copyright © 1998 by the American Academy of Otolaryngology– Head and Neck Surgery Foundation, Inc. 0194-5998/98/$5.00 + 0 23/77/87899
The subjects were 30 men who visited the Voice Clinic of the Department of Otolaryngology, Nihon University Surugadai Hospital, Tokyo. Ten men who showed no abnormalities in voice quality or in the larynx were used as normal controls. Ten men had Reinke’s edema, and 10 had unilateral RNP. Our previous studies have shown a high airway resistance in patients with Reinke’s edema and a low airway resistance in those with RNP. Therefore these two contrasting disorders were selected for evaluation. The age of 723
724
Otolaryngology– Head and Neck Surgery May 1998
MAKIYAMA et al.
Fig. 1. Relationship between the expiratory lung pressure and MFR.
the subjects ranged from 44 to 66 years (mean, 51.8 years) for the normal group, from 30 to 65 years (mean, 53.4 years) for the Reinke’s edema group, and from 55 to 88 years (mean, 67.8 years) for the RNP group. METHODS
The expiratory lung pressure was determined simultaneously with the fundamental frequency (F0), sound pressure level (SPL), and MFR, by use of a Nagashima PS77E phonatory function analyzer,1 into which an air way interruption shutter was incorporated. The subjects were instructed first to phonate a sustained vowel /a/ at the pitch and loudness that were easiest for them (moderate phonation). Next, they were instructed to phonate the same sustained vowel at the loudest and softest possible levels without changes in the vocal pitch (F0). After a practice session, the measurement was conducted twice, and the mean value was entered as the final
Fig. 2. Relationship between SPL and expiratory lung power. The product of MFR and the expiratory lung pressure was defined as the expiratory lung power and expressed by use of a logarithmic scale.
data. Those patients who were unable to control the voice intensity without changing the pitch were excluded from this study. The SPL was determined 20 cm anterior to the oral cavity and expressed in decibels (i.e., 0.0002 dyne/cm2). The expiratory lung pressure was expressed in millimeters of water, and MFR was expressed in milliliters per second. RESULTS
In the normal group the mean SPL for the moderate voice was 74 dB, that for the high-intensity voice was 80 dB, and that for the low-intensity voice was 69 dB. In the group with Reinke’s edema, the mean SPL for the moderate voice was 75 dB, that for the high-intensity voice was 82 dB, and that for the low-intensity voice
Otolaryngology– Head and Neck Surgery Volume 118 Number 5
MAKIYAMA et al.
725
Table 1. Means and ranges of expiratory lung pressure and MFR in each group Expiratory lung pressure (mm H2O) Subjects
Normal High intensity Moderate intensity Low intensity Reinke’s edema High intensity Moderate intensity Low intensity RNP High intensity Moderate intensity Low intensity
MFR (ml/sec)
Mean
Range
Mean
78 56 39
53-95 38-71 21-64
189 166 149
152-290 122-265 96-260
138 81 54
47-195 42-125 24-92
270 207 168
177-349 142-275 114-237
183 104 66
92-289 49-263 36-123
902 555 411
476-1166 237-1131 237-662
was 70 dB. In the RNP group, the mean SPL for the moderate voice was 72 dB, that for the high-intensity voice was 80 dB, and that for the low-intensity voice was 66 dB. The SPL for the moderate voice and that for the low-intensity voice in the RNP group were 3 to 4 dB lower than those in the other two groups. The means and ranges of expiratory lung pressure and MFR in each group are shown in Table 1. Both the expiratory lung pressure and MFR were high in the RNP group. The Reinke’s edema group also showed higher expiratory lung pressure and MFR than the normal group. The relationship between the expiratory lung pressure and MFR in each group is shown in Fig. 1. In the normal group the degree of changes in the expiratory lung pressure and MFR, especially that in MFR, with an increase in the voice intensity was small. The Reinke’s edema group showed a marked increase in the expiratory lung pressure and a slight increase in MFR with an increase in the voice intensity. In the RNP group, the increase in both the expiratory lung pressure and MFR with an increase in the voice intensity was far greater than in the other two groups, and the degree of the increase in MFR was more marked. The product of the expiratory lung pressure and MFR is the aerodynamic power of the expiratory airflow for phonation. The relationship between the aerodynamic power and SPL in each group is shown in Fig. 2, where the aerodynamic power was expressed by a logarithmic scale. In the normal group the aerodynamic power slightly increased with an increase in the voice intensity. In the Reinke’s edema group, the aerodynamic power was higher than that in the normal group and markedly increased with an increase in the voice intensity from the moderate- to high-intensity voice. In the RNP group, the aerodynamic power was higher than
Range
that in the other two groups and more markedly increased with an increase in the voice intensity. DISCUSSION
There have been many studies on breath control to increase the voice intensity. Some studies have shown an increase in the voice intensity with an increase in MFR.2-4 Studies in which both MFR and the subglottic pressure were measured have shown a more marked increase in the subglottic pressure than in MFR with an increase in the voice intensity.5-9 Therefore to increase the voice intensity, the subglottic power should be increased by increasing the subglottic pressure. The source of the subglottic power is the power of the expiratory air. There have also been studies on expiratory effort for an increase in the voice intensity. Timcke et al.10 and Okamura11 increased the expiratory lung pressure by pressing the abdomen during phonation or by acutely changing the pressure in the body plethysmograph and observed a slight increase in the sound pressure. Thus expiratory effort as a source of the subglottic aerodynamic power appears to play an important role in the control of the voice intensity. In these studies normal volunteers were used because measurement of the subglottic pressure or the body plethysmograph method is a burden to the subjects. We measured the expiratory lung pressure simultaneously with SPL and MFR instead of the subglottic pressure. The expiratory lung pressure was measured with the airway interruption method. This method is noninvasive and appropriate for clinical examination on patients.12-18 Sawashima et al.15 measured the expiratory lung pressure and subglottic pressure simultaneously and reported their correspondence in a certain MFR range, demonstrating that the degree of changes in the expiratory lung pres-
726
Otolaryngology– Head and Neck Surgery May 1998
MAKIYAMA et al.
sure reliably reflects that of changes in the subglottic pressure. In the normal group the expiratory lung pressure and the aerodynamic power slightly increased with an increase in the voice intensity. These findings suggest a slight increase in the subglottic pressure with an increase in the voice intensity in normal subjects and were similar to the findings reported by Curry,5 van den Berg,6 Isshiki7,8 and Tanaka.9 In the Reinke’s edema group, MFR in moderate phonation was similar to that in the normal group, but the expiratory lung pressure was higher. With an increase in the voice intensity, both MFR and the expiratory lung pressure increased, whereas the degree of increase was much more marked in the expiratory lung pressure than in the MFR. In patients with Reinke’s edema, the glottic resistance may be higher than in normal people, and the expiratory lung pressure may show a greater increase with an increase in the voice intensity. The aerodynamic power was also higher than that in the normal group. These results suggest that more marked expiratory effort is required in patients with Reinke’s edema than in normal subjects when the voice intensity is increased. In the RNP group both the expiratory lung pressure and MFR (but especially MFR) were high even with low voice intensity. With an increase in voice intensity, both MFR and the expiratory lung pressure (but especially MFR) increased. In patients with RNP, the glottic resistance may be very low. Because it is impossible to increase the glottal resistance for phonation of a highintensity voice, the expiratory flow volume may be increased, and a resulting increase in the turbulent noise component that is generated at the glottis may increase SPL. The aerodynamic power in this group was much higher than that in the normal group and the Reinke’s edema group. Figure 2 compares the aerodynamic power as an energy source and the SPL. In this figure, the aerodynamic efficiency in phonation can be evaluated. In the normal group, when the voice intensity was increased from the moderate- to the high-intensity voice, the aerodynamic power only slightly increased. This finding suggests that the normal group increased the efficiency by laryngeal control for the increase in intensity, as already reported by Sawashima et al.18 The Reinke’s edema group increased the voice intensity by increasing the aerodynamic power, suggesting that efficiency control in the larynx was less than that in the normal group. In the RNP group the aerodynamic power was already high in both low and moderate phonation, and the efficiency was very low. A higher aerodynamic power was necessary for phonation of a high-intensity voice
because of the marked decrease in the efficiency of phonation. Because capacity of the laryngeal control is very poor, the voice intensity may be controlled by expiratory effort only. Marked differences were observed in the aerodynamic power, especially during phonation of a high-intensity voice, as compared with the groups of normal subjects and those with Reinke’s edema. Thus, aerodynamic abnormalities were clarified by examination with an increase in the voice intensity. The results in this study confirmed our hypothesis that the degree and pattern of changes in expiratory effort differ among the types of lesions (aerodynamically different pathologic conditions). CONCLUSIONS
We evaluated changes in the SPL, expiratory lung pressure, and MFR for an increase in the voice intensity without changes in the voice pitch in normal subjects, patients with Reinke’s edema, and those with RNP. 1. The normal group changed the voice intensity by slightly increasing the expiratory lung pressure. The degree of the increase in the aerodynamic power was slight, and the phonation efficiency could be increased by laryngeal control. 2. In the Reinke’s edema group the degree of the increase in the expiratory lung pressure was more marked than that in the normal group. The aerodynamic power in moderate phonation was higher, and the degree of the increase in the power for an increase in the voice intensity was more marked than that in the normal group. Laryngeal control in this group was less than that in the normal group, and the voice intensity was more dependent on expiratory effort. 3. In the RNP group both the expiratory lung pressure and MFR (but especially MFR) were high. A larger amount of expiratory flow volume was necessary when the voice intensity was increased. The phonation efficiency was very low, and laryngeal control ability was very poor. Therefore a very marked increase in the expiratory effort was needed. 4. A phonatory function test with an increase in the voice intensity made aerodynamic abnormalities clearer. REFERENCES 1. Sawashima M, Honda K, Aoki S. Use of the airway interruption method for evaluating aerodynamic conditions in phonation. Jpn J Logop Phoniatr 1987;28:257-64. 2. Negus V. The mechanism of the larynx. St. Louis: CV Mosby; 1929. 3. van den Berg JW, Tan TS. Results of experiments with human larynxes. Practica Oto-Rhino-Laryngologica 1959;21:425-50. 4. Vogelsanger GJ. Experimentelle Prufung der Stimmleistung beim Singen. Folia Phoniatrica 1954;6:193-227.
Otolaryngology– Head and Neck Surgery Volume 118 Number 5
5. Curry R. The mechanism of the human voice. New York: Longmans Greene; 1940. 6. van den Berg JW. Direct and indirect determination of the mean subglottic pressure. Folia Phoniatr 1956;8:1-21. 7. Isshiki N. Regulatory mechanism of the pitch and volume of voice. Oto-rhino-laryngol Clin (Kyoto) 1959:52:1065-94. 8. Isshiki N. Regulatory mechanism of voice intensity variation. J Speech Hear Res 1964;7:17-29. 9. Tanaka S. Intensity and efficiency of the voice, Practica Otologica (Kyoto) 1987;80(Suppl 12):1-27. 10. Timcke R, von Leden H, Moore P. Laryngeal vibrations: measurements of the glottic waves. Part I. The normal vibratory cycle. Arch Otolaryngol 1958;68:1-19. 11. Okamura H. The effect of the respiratory muscles upon voice. Practica Otologica (Kyoto) 1975;68:919-35. 12. Nishida Y, Suwoya H. Indirect measuring method of the subglottic pressure in the voice production—intraesophageal method and interruption method. Otologica Fukuoka 1964;10:264-70. 13. Nishida Y. Aerodynamic studies on voice regulation. Otologica Fukuoka 1967;13(Suppl 1):44-66.
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14. Sawashima M, Kiritani S, Sekimoto S, et al. The airway interruption technique for measuring expiratory air pressure during phonation. Annual Bulletin Research Institute Logopedics and Phoniatrics 1983;17:23-32. 15. Sawashima M, Honda K, Kiritani S, et al. Further works on the airway interruption method of measuring expiratory air pressure during phonation. Annual Bulletin Research Institute Logopedics and Phoniatrics 1984;18:19-26. 16. Sawashima M, Honda K, Niimi S, et al. Some clinical data on aerodynamic examination using the airway interruption method. Annual Bulletin Research Institute Logopedics and Phoniatrics 1986;20:217-24. 17. Sawashima M, Honda K. An airway interruption method for estimating expiratory air pressure during phonation. In: Baer T, Sasaki C, Harris KS, editors. Laryngeal function in phonation and respiration. Boston: College-Hill; 1987. p. 439-47. 18. Sawashima M, Niimi S, Horiguchi S, et al. Expiratory lung pressure, airflow rate, and vocal intensity: data on normal subjects. In: Fujimura O, editor. Vocal physiology, voice production, mechanisms and functions. New York: Raven Press; 1988. p. 415-22.
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It is conceivable that the subjects who have phonatory disorders, in comparison with normal individuals, exert a greater expiratory effort when phonating loudly. Furthermore, we presume that the extent and pattern of the changes in the expiratory effort for increasing vocal intensity may vary according to the types of laryngeal lesions. To prove these hypotheses, we investigated the changes in expiratory effort for increments of the vocal intensity by measuring the expiratory lung pressure. The subjects included 10 each of normal controls, patients with Reinke’s edema, and those with recurrent laryngeal nerve paralysis. For the normal controls, the increase in vocal intensity was achieved by slightly increasing the expiratory lung pressure. The patients with Reinke’s edema showed a greater increase in expiratory lung pressure, as compared with the normal group. The patients with recurrent laryngeal nerve paralysis exhibited greater expiratory effort with extreme increases in airflow than normal group for louder phonation. It was concluded that the subjects who have phonatory disorders, in comparison with normal individuals, require a greater expiratory effort. This phonatory function test with an increase in voice intensity made the aerodynamic pathologic condition clearer. (Otolaryngol Head Neck Surg 1998;118:723-7.)
Aerodynamic conditions of the glottis and glottal efficiency in phonation can be evaluated to some extent by an aerodynamic phonatory function test. We have evaluated results of an aerodynamic phonatory function test and laryngeal findings. In patients with vocal cord nodules, the mean flow rate (MFR) was higher with a larger nodule. In patients with Reinke’s edema, the expiratory lung pressure was higher with more marked edema. However, in patients with mild vocal cord nodules or Reinke’s edema, phonatory function test results were in the normal range. With vocal cord polyps, no definite association was observed between the size of the polyp and results of the phonatory function test. This was because there were individual differences in the site of polyps and the size of the glottal gap during phonation and a difference in weight between the right and left vocal cords. Thus, in disorders such as vocal nodules, recurrent laryngeal nerve paralysis (RNP), and Reinke’s edema in which the physical properties of the vocal cord
is relatively uniform, phonatory function test results appear to reflect the pathologic condition of the larynx relatively well. One purpose of a phonatory function test is evaluation of glottal efficiency. We speculated that the expiratory lung power required for phonation is greater in patients with voice disorders than in normal persons, and therefore the glottal efficiency and laryngeal adjustment ability are low. To prove this hypothesis, we evaluated the changes in expiratory efforts and glottal efficiency when the voice intensity was increased by determining the expiratory lung pressure, a parameter in the phonatory function test that reflects the expiratory effort. We also investigated whether there are differences in expiratory efforts according to the types of laryngeal lesions when the voice intensity is raised during phonation. This phonatory function test with an increase in the voice intensity can make the aerodynamic condition at the glottis clearer. SUBJECTS
From the Department of Otolaryngology (Drs. Makiyama and Kida), Nihon University, School of Medicine; and Yokohama Seamen’s Insurance Hospital (Dr. Sawashima). Presented at the Annual Meeting of the American Academy of Otolaryngology–Head and Neck Surgery, Washington, D.C., Sept. 29–Oct. 2, 1996. Kiyoshi Makiyama, MD, Department of Otolaryngology, Nihon University Surugadai Hospital, 1-8-13, Kanda-surugadai, Chiyodaku, Tokyo, 101-8309, Japan. Copyright © 1998 by the American Academy of Otolaryngology– Head and Neck Surgery Foundation, Inc. 0194-5998/98/$5.00 + 0 23/77/87899
The subjects were 30 men who visited the Voice Clinic of the Department of Otolaryngology, Nihon University Surugadai Hospital, Tokyo. Ten men who showed no abnormalities in voice quality or in the larynx were used as normal controls. Ten men had Reinke’s edema, and 10 had unilateral RNP. Our previous studies have shown a high airway resistance in patients with Reinke’s edema and a low airway resistance in those with RNP. Therefore these two contrasting disorders were selected for evaluation. The age of 723
724
Otolaryngology– Head and Neck Surgery May 1998
MAKIYAMA et al.
Fig. 1. Relationship between the expiratory lung pressure and MFR.
the subjects ranged from 44 to 66 years (mean, 51.8 years) for the normal group, from 30 to 65 years (mean, 53.4 years) for the Reinke’s edema group, and from 55 to 88 years (mean, 67.8 years) for the RNP group. METHODS
The expiratory lung pressure was determined simultaneously with the fundamental frequency (F0), sound pressure level (SPL), and MFR, by use of a Nagashima PS77E phonatory function analyzer,1 into which an air way interruption shutter was incorporated. The subjects were instructed first to phonate a sustained vowel /a/ at the pitch and loudness that were easiest for them (moderate phonation). Next, they were instructed to phonate the same sustained vowel at the loudest and softest possible levels without changes in the vocal pitch (F0). After a practice session, the measurement was conducted twice, and the mean value was entered as the final
Fig. 2. Relationship between SPL and expiratory lung power. The product of MFR and the expiratory lung pressure was defined as the expiratory lung power and expressed by use of a logarithmic scale.
data. Those patients who were unable to control the voice intensity without changing the pitch were excluded from this study. The SPL was determined 20 cm anterior to the oral cavity and expressed in decibels (i.e., 0.0002 dyne/cm2). The expiratory lung pressure was expressed in millimeters of water, and MFR was expressed in milliliters per second. RESULTS
In the normal group the mean SPL for the moderate voice was 74 dB, that for the high-intensity voice was 80 dB, and that for the low-intensity voice was 69 dB. In the group with Reinke’s edema, the mean SPL for the moderate voice was 75 dB, that for the high-intensity voice was 82 dB, and that for the low-intensity voice
Otolaryngology– Head and Neck Surgery Volume 118 Number 5
MAKIYAMA et al.
725
Table 1. Means and ranges of expiratory lung pressure and MFR in each group Expiratory lung pressure (mm H2O) Subjects
Normal High intensity Moderate intensity Low intensity Reinke’s edema High intensity Moderate intensity Low intensity RNP High intensity Moderate intensity Low intensity
MFR (ml/sec)
Mean
Range
Mean
78 56 39
53-95 38-71 21-64
189 166 149
152-290 122-265 96-260
138 81 54
47-195 42-125 24-92
270 207 168
177-349 142-275 114-237
183 104 66
92-289 49-263 36-123
902 555 411
476-1166 237-1131 237-662
was 70 dB. In the RNP group, the mean SPL for the moderate voice was 72 dB, that for the high-intensity voice was 80 dB, and that for the low-intensity voice was 66 dB. The SPL for the moderate voice and that for the low-intensity voice in the RNP group were 3 to 4 dB lower than those in the other two groups. The means and ranges of expiratory lung pressure and MFR in each group are shown in Table 1. Both the expiratory lung pressure and MFR were high in the RNP group. The Reinke’s edema group also showed higher expiratory lung pressure and MFR than the normal group. The relationship between the expiratory lung pressure and MFR in each group is shown in Fig. 1. In the normal group the degree of changes in the expiratory lung pressure and MFR, especially that in MFR, with an increase in the voice intensity was small. The Reinke’s edema group showed a marked increase in the expiratory lung pressure and a slight increase in MFR with an increase in the voice intensity. In the RNP group, the increase in both the expiratory lung pressure and MFR with an increase in the voice intensity was far greater than in the other two groups, and the degree of the increase in MFR was more marked. The product of the expiratory lung pressure and MFR is the aerodynamic power of the expiratory airflow for phonation. The relationship between the aerodynamic power and SPL in each group is shown in Fig. 2, where the aerodynamic power was expressed by a logarithmic scale. In the normal group the aerodynamic power slightly increased with an increase in the voice intensity. In the Reinke’s edema group, the aerodynamic power was higher than that in the normal group and markedly increased with an increase in the voice intensity from the moderate- to high-intensity voice. In the RNP group, the aerodynamic power was higher than
Range
that in the other two groups and more markedly increased with an increase in the voice intensity. DISCUSSION
There have been many studies on breath control to increase the voice intensity. Some studies have shown an increase in the voice intensity with an increase in MFR.2-4 Studies in which both MFR and the subglottic pressure were measured have shown a more marked increase in the subglottic pressure than in MFR with an increase in the voice intensity.5-9 Therefore to increase the voice intensity, the subglottic power should be increased by increasing the subglottic pressure. The source of the subglottic power is the power of the expiratory air. There have also been studies on expiratory effort for an increase in the voice intensity. Timcke et al.10 and Okamura11 increased the expiratory lung pressure by pressing the abdomen during phonation or by acutely changing the pressure in the body plethysmograph and observed a slight increase in the sound pressure. Thus expiratory effort as a source of the subglottic aerodynamic power appears to play an important role in the control of the voice intensity. In these studies normal volunteers were used because measurement of the subglottic pressure or the body plethysmograph method is a burden to the subjects. We measured the expiratory lung pressure simultaneously with SPL and MFR instead of the subglottic pressure. The expiratory lung pressure was measured with the airway interruption method. This method is noninvasive and appropriate for clinical examination on patients.12-18 Sawashima et al.15 measured the expiratory lung pressure and subglottic pressure simultaneously and reported their correspondence in a certain MFR range, demonstrating that the degree of changes in the expiratory lung pres-
726
Otolaryngology– Head and Neck Surgery May 1998
MAKIYAMA et al.
sure reliably reflects that of changes in the subglottic pressure. In the normal group the expiratory lung pressure and the aerodynamic power slightly increased with an increase in the voice intensity. These findings suggest a slight increase in the subglottic pressure with an increase in the voice intensity in normal subjects and were similar to the findings reported by Curry,5 van den Berg,6 Isshiki7,8 and Tanaka.9 In the Reinke’s edema group, MFR in moderate phonation was similar to that in the normal group, but the expiratory lung pressure was higher. With an increase in the voice intensity, both MFR and the expiratory lung pressure increased, whereas the degree of increase was much more marked in the expiratory lung pressure than in the MFR. In patients with Reinke’s edema, the glottic resistance may be higher than in normal people, and the expiratory lung pressure may show a greater increase with an increase in the voice intensity. The aerodynamic power was also higher than that in the normal group. These results suggest that more marked expiratory effort is required in patients with Reinke’s edema than in normal subjects when the voice intensity is increased. In the RNP group both the expiratory lung pressure and MFR (but especially MFR) were high even with low voice intensity. With an increase in voice intensity, both MFR and the expiratory lung pressure (but especially MFR) increased. In patients with RNP, the glottic resistance may be very low. Because it is impossible to increase the glottal resistance for phonation of a highintensity voice, the expiratory flow volume may be increased, and a resulting increase in the turbulent noise component that is generated at the glottis may increase SPL. The aerodynamic power in this group was much higher than that in the normal group and the Reinke’s edema group. Figure 2 compares the aerodynamic power as an energy source and the SPL. In this figure, the aerodynamic efficiency in phonation can be evaluated. In the normal group, when the voice intensity was increased from the moderate- to the high-intensity voice, the aerodynamic power only slightly increased. This finding suggests that the normal group increased the efficiency by laryngeal control for the increase in intensity, as already reported by Sawashima et al.18 The Reinke’s edema group increased the voice intensity by increasing the aerodynamic power, suggesting that efficiency control in the larynx was less than that in the normal group. In the RNP group the aerodynamic power was already high in both low and moderate phonation, and the efficiency was very low. A higher aerodynamic power was necessary for phonation of a high-intensity voice
because of the marked decrease in the efficiency of phonation. Because capacity of the laryngeal control is very poor, the voice intensity may be controlled by expiratory effort only. Marked differences were observed in the aerodynamic power, especially during phonation of a high-intensity voice, as compared with the groups of normal subjects and those with Reinke’s edema. Thus, aerodynamic abnormalities were clarified by examination with an increase in the voice intensity. The results in this study confirmed our hypothesis that the degree and pattern of changes in expiratory effort differ among the types of lesions (aerodynamically different pathologic conditions). CONCLUSIONS
We evaluated changes in the SPL, expiratory lung pressure, and MFR for an increase in the voice intensity without changes in the voice pitch in normal subjects, patients with Reinke’s edema, and those with RNP. 1. The normal group changed the voice intensity by slightly increasing the expiratory lung pressure. The degree of the increase in the aerodynamic power was slight, and the phonation efficiency could be increased by laryngeal control. 2. In the Reinke’s edema group the degree of the increase in the expiratory lung pressure was more marked than that in the normal group. The aerodynamic power in moderate phonation was higher, and the degree of the increase in the power for an increase in the voice intensity was more marked than that in the normal group. Laryngeal control in this group was less than that in the normal group, and the voice intensity was more dependent on expiratory effort. 3. In the RNP group both the expiratory lung pressure and MFR (but especially MFR) were high. A larger amount of expiratory flow volume was necessary when the voice intensity was increased. The phonation efficiency was very low, and laryngeal control ability was very poor. Therefore a very marked increase in the expiratory effort was needed. 4. A phonatory function test with an increase in the voice intensity made aerodynamic abnormalities clearer. REFERENCES 1. Sawashima M, Honda K, Aoki S. Use of the airway interruption method for evaluating aerodynamic conditions in phonation. Jpn J Logop Phoniatr 1987;28:257-64. 2. Negus V. The mechanism of the larynx. St. Louis: CV Mosby; 1929. 3. van den Berg JW, Tan TS. Results of experiments with human larynxes. Practica Oto-Rhino-Laryngologica 1959;21:425-50. 4. Vogelsanger GJ. Experimentelle Prufung der Stimmleistung beim Singen. Folia Phoniatrica 1954;6:193-227.
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5. Curry R. The mechanism of the human voice. New York: Longmans Greene; 1940. 6. van den Berg JW. Direct and indirect determination of the mean subglottic pressure. Folia Phoniatr 1956;8:1-21. 7. Isshiki N. Regulatory mechanism of the pitch and volume of voice. Oto-rhino-laryngol Clin (Kyoto) 1959:52:1065-94. 8. Isshiki N. Regulatory mechanism of voice intensity variation. J Speech Hear Res 1964;7:17-29. 9. Tanaka S. Intensity and efficiency of the voice, Practica Otologica (Kyoto) 1987;80(Suppl 12):1-27. 10. Timcke R, von Leden H, Moore P. Laryngeal vibrations: measurements of the glottic waves. Part I. The normal vibratory cycle. Arch Otolaryngol 1958;68:1-19. 11. Okamura H. The effect of the respiratory muscles upon voice. Practica Otologica (Kyoto) 1975;68:919-35. 12. Nishida Y, Suwoya H. Indirect measuring method of the subglottic pressure in the voice production—intraesophageal method and interruption method. Otologica Fukuoka 1964;10:264-70. 13. Nishida Y. Aerodynamic studies on voice regulation. Otologica Fukuoka 1967;13(Suppl 1):44-66.
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14. Sawashima M, Kiritani S, Sekimoto S, et al. The airway interruption technique for measuring expiratory air pressure during phonation. Annual Bulletin Research Institute Logopedics and Phoniatrics 1983;17:23-32. 15. Sawashima M, Honda K, Kiritani S, et al. Further works on the airway interruption method of measuring expiratory air pressure during phonation. Annual Bulletin Research Institute Logopedics and Phoniatrics 1984;18:19-26. 16. Sawashima M, Honda K, Niimi S, et al. Some clinical data on aerodynamic examination using the airway interruption method. Annual Bulletin Research Institute Logopedics and Phoniatrics 1986;20:217-24. 17. Sawashima M, Honda K. An airway interruption method for estimating expiratory air pressure during phonation. In: Baer T, Sasaki C, Harris KS, editors. Laryngeal function in phonation and respiration. Boston: College-Hill; 1987. p. 439-47. 18. Sawashima M, Niimi S, Horiguchi S, et al. Expiratory lung pressure, airflow rate, and vocal intensity: data on normal subjects. In: Fujimura O, editor. Vocal physiology, voice production, mechanisms and functions. New York: Raven Press; 1988. p. 415-22.
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