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2.5 Mechanical Stress in Phonation
2.5 Mechanical Stress in Phonation
Ingo R. Titze
Department of Speech Pathology and Audiology, National Center for Voice and Speech, University of Iowa, Iowa
City, Iowa, and Recording and Research Center, Denver Center for the Performing Arts, Denver, Colorado, U.S.A.
This article was motivated by the lifelong inves- amount? We also believe that persistent "pressing"
tigations of voice disorders by Moore (1). Moore together of the arytenoid cartilages is a cause of
convinced this author, and many others in the field, contact ulcers, and rubbing vocal fold tissue with
that voice disorders and voice physiology are one foreign objects (such as an endotracheal tube) is
and the same topic. One cannot understand normal known to cause granulomas, but, again, we have
vocal fold vibration with a disregard for abnormal no criteria for how much mechanical stress is abu-
vibration patterns. This is becoming increasingly sive.
more evident in light of modern views of nonlinear Benign lesions are apparently a reaction to, and
dynamics. Chaotic behavior is part of a normal self- ultimately a fortification against, mechanical insult
oscillating vocal fold system, and "normal" vibra- to vocal fold tissues. Little is known, however,
tion patterns can be seen when the vocal folds are about the kind of stress that routinely occurs during
visually impaired. vocal fold vibration, and how that stress is distrib-
Nowhere is this gray boundary between normal uted within the tissues. If the stress fields were
function and dysfunction more evident than in the known for various phonation types, perhaps some
assessment of mechanical stress in phonation. It is strategies for healthy, nonabusive voice production
generally assumed that excessive mechanical stress would become clearer. Specifically, it would be de-
can lead to organic disorders. But how much is ex- sirable to weigh phonation type and increases in
cessive? Although repeated collision of the vocal vocal loudness against increases in tissue stress to
folds is likely to be the primary cause of vocal nod- obtain a cost/benefit ratio for certain vocal produc-
ules, we cannot produce much sound without col- tions.
liding the vocal folds. So what is a tolerable The present study is an extension of the summary
article on vocal strain written by Sonninen et al. (2),
Accepted March 31, 1993. who summarized the types of mechanical loads and
Address correspondence and reprint requests to Dr. I. R. deformations found in the vocal folds. Twenty
Titze at Department of Speech Pathology and Audiology, Na-
tional Center for Voice and Speech, University of Iowa, Iowa years later, we can shed only a little additional light
City, IA 52242, U.S.A. on these critical questions: (a) What types of
99
100 I . R . TITZE
................................
..... Maximum active
pars obliqua
F = 207rAF2pAxAyAz (8)
Pars recta passive stress
~ = ~ O ~ p a esrtss s~~i~. v e If A y A z is taken to be the impact surface and Ax the
depth of the vibrating tissue, then the collision
o stress is
o t'o 2'0 3'0 40
Strain (%)
F
FIG. 3. Maximum active contractile stress of two components of ~r - AyA~ - 20"rrAFZpAx (9)
the CT muscle of canine larynges, The passive stress is also
shown (after ref. 4).
For an amplitude of vibration of 10 -3 m, a depth
second law, the average collision force over an im- of vibration of 10 -3 m, and an Fo of 200 Hz, this
pact interval At is stress is 2.6 kPa. Peak impact stresses on the order
of 0.5-5.0 kPa were measured by Jiang and Titze (5)
F = mAv/At (4) and are shown in Fig. 5 as a function of subglottal
pressure. Similar increases in contact stress were
where Av is the change in velocity during impact. obtained by Reed et al. (6) with a piezoelectric
Jiang and Titze (5) estimated the impact interval to transducer placed between the vocal folds of a hu-
be on the order of man subject.
Values of Fo in Fig. 5 were <200 Hz. For fre-
r0 quencies approaching 1,000 Hz, one would expect
At- 10 (5)
much higher impact stresses if the amplitude and
depth of vibration were to remain constant. Typi-
where To is the fundamental period. cally, however, both amplitude and depth of vibra-
The velocity change in Eq. 4 can be estimated by tion decrease with F0, making the exact stress un-
assuming sinusoidal motion with amplitude A and certain. One would expect that the impact stress
radian frequency o~ = 2¢rFo. The maximum veloc- could increase an order of magnitude, to - 5 0 kPa,
ity, which occurs near impact, is then for high F 0 and high subglottal pressure.
v = oJA = 2 w F o A (6)
5.0"
Collision
boundary Tissue element of 4.0
mass pAxAyAz &
3.0,
"5
2.0,
Q.
1.0,
J
11o 21o 31o 4.0
Av Subglottal pressure (kPa)
Impact stress = (pAx) ~ -
FIG. 5. Peak collision stress versus subglottal pressure in a ca-
FIG. 4. Illustration of impact stress. nine hemilarynx (after ref. 5).
cr = 47r2AF02pAx (1 1)
dx -rrA
- tan0 -~ sin0 (15)
This stress is approximately half of the impact dy y=O,L L
stress, on the order of 1-2 kPa for normal phona-
tion. For an amplitude of 0.2 mm and a length of 10 mm,
A e r o d y n a m i c stress sin 0 = 0.6.
The mean aerodynamic driving stress is the mean The shear modulus tx of the collagen fibers in the
intraglottal pressure, which has been estimated as macula flavae is not known to this author, which
makes it impossible to estimate the absolute value
of the shear stress. All one can say is that it in-
creases with amplitude of vibration and decreases
with vocal fold length. The A / L ratio is a key vari-
in the open phase (6). Here P,. is the input pressure able for dynamic shear stress.
to the vocal tract (supraglottal pressure), al is the
glottal entry area, a2 is the glottal exit area, and P= Summary of relative magnitudes of stresses
is the subglottal pressure. The greatest pressure oc- A summary chart of the relative magnitudes of
curs for a highly convergent glottis, where az/al "~ the various mechanical stresses is given in Fig. 7.
0, in which case Pg ~ P=" Estimates are made for conditions of normal pho-
In high-effort phonation, P~ can be as high as 5-6 nation (clear bars) and maximum stress (cross-
kPa, and occasionally reaches 10 kPa (8). This can hatched bars). Note the large maximum tensile
be taken as the upper limit on aerodynamic stress. stresses relative to all other stresses. Note also the
relatively small aerodynamic stresses. Active con-
A r y t e n o i d contact stress tractile, arytenoid contact, impact, and inertial
Maximum contact stress between the arytenoid stresses are intermediate in size.
cartilages has been estimated by Rethi (9) and
Kakeshita (10) to be on the order of 50-100 kPa in Anteriorboundary
animals who had the adductor muscles fully con-
tracted. This range would tend to agree with the
7///S,
maximum active stresses measured in the CT and
TA muscles of canines. Adduction stress for normal
I~O~ Vocalligament
phonation is much lower than that, however, even
for so-called "pressed voice." Values reported by
Scherer et al. (11) were on the order of 1-5 kPa. i
Shear stress at anterior and posterior macula flava
The shear stress in the ligament increases with
the amplitude of vibration. If the ligament is pinned
at the endpoints (anterior and posterior macula
flava), then the shear stress -r can be written as Shear stress =/.tsinO
"r = Ixsin0 (13) FIG. 6. Illustration of shear stress in the vocal ligament.
1000,
30 ¸ E
100-
UnbaccePt
ratiotunabl
vimagni e4A~~ep~le
des
&
20 ¸
10-
_/ vibration
8
10. 1
0
0 i , i , o 1'o 16o lC;OO 10000
lO 20 3'0 4'0 so
Frequency (Hz)
Strain (%) ;.
FIG. 11. 1SO standard for hand-transmitted vibration (after ref.
FIG. 10. S t r e s s - s t r a i n curve for the vocal fold cover of canines 14). Data point suggests that vocal fold vibration could exceed
during cyclic stretch and release. the m a x i m u m r e c o m m e n d e d dose.
destruction of surface microvillae, of squamous ep- that aerodynamic stresses of themselves do not
ithelial cells, and of the basement membrane zone. pose a damage risk.
Future investigations should quantify this type of
destruction in terms of measured impact stress. It Acknowledgment: This study was supported by grant
would also be extremely valuable to know the time no. P60 DC00976 from the National Institute on Deafness
and Other Communication Disorders. I thank Julie
course and degree of the healing process. Lemke for manuscript preparation and Mark Peters for
graphic support.
CONCLUSION
REFERENCES
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