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Journalof Voice

Vol. I0, No. 1, pp. 78-92


1996Lippincott-RavenPublishers, Philadelphia

External Laryngeal Frame Function in Voice Production


Revisited: A Review
E . V i l k m a n , *A. S o n n i n e n , *P. H u r m e , a n d t P . K 6 r k k 6
Department of Otolaryngology and Phoniatrics, University of Oulu, Oulu, *Department of Communication,
University of Jyviiskylgi, Jyviiskylii, and tDepartment of Logopedics and Phonetics, University of Oulu, Oulu, Finland

Summary: Reserch indicates significant contribution of extrinsic laryngeal


mechanisms to voice production. This article reviews the major theories of the
role of the external laryngeal factors in voice production and relevant experimental data. The review suggests that partly neglected external factors and
possibly even misinterpretation of some of the recently documented individual
variation in physiological data may have unnecessarily complicated the issues
pertaining to the interplay between the physiological mechanisms of the larynx. The implications of contemporary findings and documentation in the modeling of the extrinsic factors are discussed and a synthesis of empirical data into
two simple models of the extrinsic forces of pitch control is presented. Also
suggested by the review, a basic principle, probably underlying the laryngeal
control of phonation, is put forward. Key Words: Fundamental frequency-Pitch control--Laryngeal forces--Muscle activity--Vocal folds, length
adjustment.

There is little doubt that the contribution of the


external laryngeal muscles to voice production is
not insignificant. In the course of more than 100
years of research in this area, a number of theoretical explanations and accounts of the role of the
extrinsic muscles and of other external mechanisms
in the function of the phonatory system have
emerged. Kenyon's work (1), based on a systems
physiological approach, still remains a valid starting
point of analysis: "Particularly, the larynx, hyoid
and base of the tongue cannot but be considered as
a physiologic entity. The larynx is suspended from
the hyoid bone, the hyoid from the base of the
tongue, the tongue from the lower jaw and the skull.
All three are intimately involved in a complicated
musculature whose action alters their relationship
to each other and to the fixed bony structure of

sternum, spinal column and skull. They constitute


definite factors in vocal cord physiology and all
must be considered as belonging to the physiologic
larynx."
As pointed out by a number of authors, e.g., Brodie (2) and Fink and Demarest (3), the hyoid and
laryngeal structures are connected to each other
and to other adjacent structures with spring-like attachments (ligaments, muscles) within which a state
of equilibrium appears to exist. From a biomechanical point of view, the external mechanisms include
not only a great number of muscles but also the
often overlooked tracheal pull. Tracheal pull, i.e.,
the inferior force produced by the mass and tension
of the trachea, is mediated to the larynx through the
cricoid cartilage and adjacent soft tissues (4). The
external muscles considered to be capable of contributing to voice production include the strap muscles, i.e., the sternothyroid (ST), the hyothyroid
(HT) and the sternohyoid (SH) muscles, of which
ST and HT, together with the inferior pharyngeal
muscles, i.e., the cricopharyngeal (CP) and the thy-

Accepted September 13, 1995.


Address correspondence and reprint requests to Professor
E. Vilkman at Department of Otolaryngology and Phoniatrics,
Helsinki University Central Hospital, FIN-00290 Helsinki, Finland.

78

EXTERNAL LARYNGEAL FRAME FUNCTION

ropharyngeal (TP) muscles, are directly connected


to the larynx. The suprahyoid muscles, i.e., the digastric, the mylohyoid, the geniohyoid (GH), the
hyoglossus and the genioglossus muscles as well as
the infrahyoid muscles (SH, omohyoid) have an indirect effect on the larynx. Other indirect muscular
forces include those produced by the palatal, esophageal, and nuchal musculature, of which the palatopharyngeal muscle also has a partly direct connection to the larynx. As regards vocal fold biomechanics, it is important to notice that with the exception
of the CP muscle, the forces produced by the extrinsic laryngeal muscles act directly on the thyroid
cartilage. A more detailed description of the anatomy of the laryngeal region is not within the scope
of this article; for that information the reader is referred to established sources and textbooks (e.g.,
ref. 5).
It is obvious that the very complexity of the laryngeal biomechanics is responsible for the far from
conclusive and sometimes even contrasting views
presented in current discussions of the physiology
of the voice. The aims of the present article are (a)
to review the development of research in this special area of voice science with special emphasis on
singing voice and vowel articulation; (b) to review
and discuss research data and results relevant to
theories and models of the external laryngeal factors; and (c) in an attempt to relate the anatomicalphysiological framework to practical issues in voice
production, to put forward constructive, and perhaps also novel, ideas on the external laryngeal control of phonation.
MODELS OF EXTERNAL FACTORS IN THE
LENGTH ADJUSTMENT OF THE
VOCAL FOLDS
The Merkel and Kenyon models
Among the earliest and still valid comprehensive
models of the extrinsic mechanisms are those presented by Merkel (6) and Kenyon (1,7). The models
are based on reviews of literature and on palpatory
examination of the laryngeal structures. According
to both Merkel and Kenyon, the finer adjustments
of the vocal folds are controlled by intrinsic laryngeal muscles, whereas the gross relations between
the thyroid and cricoid cartilages are determined by
the extrinsic muscles. Changes in the relationship
between the thyroid and cricoid cartilages call for
new adjustments of the neighboring muscles; the
suspended mechanism must also be stabilized

79

within the whole framework of the physiological


larynx and, finally, fixed to bony structures. Kenyon's main conclusions include a reminder on the
close relationship between articulatory events
and voice production. As to the control of pitch,
Kenyon (7) showed that the view presented by
some earlier investigators, according to which the
lengthening of the vocal folds was caused by the ST
muscle contraction, was erroneous. His main argument against the ST theory was the observation that
the thyroid cartilage moves upward and probably
also slightly forward with rising pitch--a finding
that already had been reported by Merkel (6). Naturally, this laryngeal movement could not be explained in terms of ST activity, which had been assumed to be responsible for the lengthening of the
vocal folds in pitch control. Kenyon (7) also points
out that conclusions drawn from studies on the activity of individual muscles may lead to more or less
erroneous views on vocal function.
Schilling and the ST muscle
Schilling (8,9), who based his views on an anatomical and biomechanical study, proposed a model
of the control of the longitudinal tension of the vocal folds. His research was mainly concerned with
the function of the ST muscle as a tensor of the
vocal folds. In his study, the ST muscles of 20 cadavers were dissected free and pulled interiorly.
The resulting mutual movements of the thyroid and
cricoid cartilages were measured by monitoring the
displacement of needles attached to the respective
cartilages. In the majority of cases, the thyroid and
cricoid cartilages were observed to move apart, i.e.,
the cricothyroid (CT) distance increased. According to Schilling (8,9), the reason for this was that the
torque of the contraction of ST, which is attached to
the linea obliqua of the thyroid cartilage, is greater
on the posterior side than on the anterior side of the
rotational axis of the CT articulation. This finding
was interpreted by Schilling as evidence of the function of ST as a main shortener of the vocal folds.
Schilling also claimed that the ST acted as an antagonist to the CT muscle and emphasized the significance of ST in maintaining the low position of
the larynx in chest and middle register phonation in
singing.
The Zenker model
On the basis of extensive anatomic, biomechanical, and electromyographic studies, Zenker and
Zenker (10) proposed a relatively comprehensive
Journal of Voice, Vol. 10, No. 1, 1996

80

E. V I L K M A N E T AL.

model to explain the significance and role of the


external mechanisms in the length adjustments of
the vocal folds. In their model, vocal fold lengthening can be brought about not only by the CT muscles but also by esophageal musculature, ligamentum conicum, and the TP muscle, which approximates the thyroid laminae and thus moves the
anterior fixation point of the vocal folds forward.
According to the Zenker model, the vocal folds, can
be shortened by the CP muscle, which rotates the
cricoid cartilage around the horizontal axis of the
CTjoint, as well as by tracheal pull, which tends to
lower the cricoid cartilage. In addition, the forces
shortening the vocal folds, i.e., opening the cricothyroid visor, include those produced by the muscles and connective tissues between the hyoid bone
and the thyroid cartilage, the hyomandibular musculature, and the functional chain. The functional
chain (1 I) in this model is supposed to be formed by
the arytenoid cartilages, aryepiglottal muscle, the
epiglottis and tongue, and/or hyoid bone and mandible. In the Zenker model, the role of the ST muscle as a pitch-lowering mechanism is seriously
doubted.
Sonninen and the external frame
On the basis of anatomic, radiographic, and stimulation studies, Sonninen (12,13) presented a model
that he called the external frame. According to the
external frame model, the function of the ST muscle
is dual. In normal head position, ST activity lengthens the vocal folds. This finding is at odds with
Schilling's observations (8,9). In Sonninen's model,
ST also is assumed to be responsible, in addition to
the pars obliqua of the CT, for the ventrodorsal
gliding in the CT articulation, which is suggested to
contribute significantly to vocal fold lengthening.
The most important function in this respect is the
forward movement of the thyroid cartilage, to
which muscles other than the ST, e.g., the muscles
of the bottom of the mouth, also can contribute.
According to Sonninen, the forward motion of the
thyroid cartilage lengthens the vocal folds, provided
that the cricoid cartilage is simultaneously fixed by
the contraction of the cricopharyngeal muscle.

THE MODELS IN LIGHT OF


RELEVANT RESEARCH
Anatoraieal and biomechanieal aspects
The structural and biomechanical features of the
CT articulation have been studied by several invesJournal of Voice, Vol. 10, No. 1, 1996

tigators during the past decades (e.g., refs. 14--16).


At least two of these studies suggest that ventrodorsal gliding in this joint may occur. In both of
these investigations, the amount of gliding was
found to depend on the amount of simultaneous rotation in the joint. When the CT visor was either
maximally opened or closed, the ceratocricoid ligaments were able to lock the joint stable and no
gliding occurred (14,16). However, the extremes of
rotation can obviously be considered unphysiological, because several studies using living subjects
(3,12,17) and a study in which excised human larynges were employed (18) suggest that moderate rotation is sufficient for producing the physiological
F0 range (see later herein).
In one of the quantitative studies on ventrodorsal
gliding it was found that, on the average (n = 10), a
ventral/dorsal force of ---1 N results in a glide of - 1
mm, depending on the degree of rotation (16). The
amount of gliding was estimated to be significant for
the control of vocal fold length; however, a considerable amount of interindividual variation also was
found. Two alternative explanations for such variation were considered possible. First, variation in
the stage of development of the articulatory facet of
the cricoid cartilage and, second, variation in the
collagen contents of the lateral ceratocricoid ligament, which was found to be the most important
ligament structure of the cricothyroid articulation
(16). The articulatory facet on the cricoid cartilage
of this joint has been found to vary. It appears to be
totally lacking in 20% of subjects and it is more or
less poorly defined in 50% of cases (15). This finding can be interpreted to indicate that the CT articulation is a pure hinge joint in only - 3 0 % of cases.
The significance of the articulatory facet in causing
limited movability of the joint has also been suggested in a qualitative study (19).
From a structural point of view, it seems reasonable to assume that in most cases ventrodorsal gliding is possible and that the horizontal axis of the CT
articulation cannot be considered a fixed point as
suggested by Zenker and Zenker (10). It is also to be
remembered that in young people, all the cartilaginous structures of the larynx are so elastic that not
only gliding in the CT joint, but also the bending of
the inferior cornua of the thyroid cartilage may contribute to vocal fold lengthening. Thus, the horizontal components of muscular forces such as produced by the oblique parts of the CT, the ST, and
HT muscles may cause anterior displacement of the
thyroid cartilage, provided there is a posteriorly

EXTERNAL LARYNGEAL FRAME FUNCTION

81

cording to their descriptions, CP consists of circular


and ascending fibers. The fibers circling the esophagus are attached to the cricoid cartilage; the ascending fibers run from the cricoid cartilage cranially and are attached to the "centrum tendineum"
of the posterior pharyngeal wall running to the base
of the skull. Considering the anatomy of the CP
muscle (11,23), it seems possible that the circular
fibers may contract the esophageal sphincter and
that the cranially running fibers attached to centrum
tendineum may expand the lumen of the esophagus
as well as pull the cricoid cartilage posteriorly and
cranially.

acting force on the cricoid cartilage. An age-related


ossification process that starts in the 3rd decade of
life in men (20,21) has a stiffening effect on the thyroid cartilage. Because of this process, the possibility of bending of the thyroid cartilage obviously diminishes with advancing age.
On the basis of an anatomical analysis, Maue (15)
claimed that ventrodorsal gliding in the CT articulation would be unphysiological because the articulatory facets on the cricoid cartilage are situated on
its posterolateral surface. This would indeed prevent sliding, if the inferior cornua of the thyroid
cartilage were nonelastic, which they obviously are
not. In experiments with intact excised larynges, it
has also been documented that gliding caused by
physiological forces is possible even when allowing
for these structural aspects of the cartilages. Interestingly, in the experimental arrangements used,
the laminae of the thyroid cartilage were found to
approximate as the inferior cornua glided anteriorly
and slightly laterally on the cricoid cartilage (see
ref. 22). This, again, may affect the length of the
vocal folds.
The CP muscle has been given a significant role in
the length adjustment of the vocal folds in both the
Zenker and Zenker model (10) and in Sonninen's
(13) model. The anatomy of CP has been studied in
detail by Zenker (11) and by Minnigerode (23). Ac-

Observations on the function of extrinsic


laryngeal muscles
The results of relevant biomechanical and stimulation studies on the function of extrinsic laryngeal
muscles are summarized in Table 1.
Schilling's results obtained in cadaver experiments (8) suggest that ST is an antagonist to the CT
muscle in the length adjustments of the vocal folds.
Sonninen (12), again, found that pulling the ST muscles always lowered the position of the larynx in
relation to the spine but expanded the CT space
only if the head was bent backward. In other circumstances, the CT space was observed to narrow.
Therefore, Schilling's (8) evidence for ST function-

T A B L E 1. A summary o f the results o f pull and stimulation studies on external muscles in relation to vocal f o l d

length adjustment
Study
Dreyfuss (30)
Schilling (8)
Sonninen (12)

Minnigerode (23)
U e d a et al. (27)

Sapir et al. (26)


Shin et ai. (28)

Martin and
Klingholz (32)

Material

Method

Muscle

Phonation

Pitch
range

Pitch
lowering

Pitch
raising

Dog
Human
Cadaver
Human
Cadaver
Several
humans
Ape
Dog

Myotomy
Manual
Pull
Manual
Pull
Stimulation

CP
ST

Phonation
n/a

n/a

+
-

ST

n/a

n/a

+b

+b

ST

Sustained

Stimulation
Stimulation

Phonation
Phonation

Rhesus
macaque
Dog

Stimulation

2 Males

Sphincter
pressure

CP
SH
ST
IPC
GH
ST
GH
TH
ST
TP
CP
CP

+
+
+
+
+
+
+

+
+
+
+
+
+
+
+

Stimulation

Phonation

Singing

Extremes

IPC, inferior pharyngeal constrictor; G H , geniohyoid muscle; CP, cricopharyngeal muscle; TP, thyropharyngeal m u s c l e ; ST, sternothyroid muscle; SH, s t e r n o h y o i d m u s c l e ; T H , thyrohyoid muscle. + , effect; - , no effect; n/a, not applicable.
a Widening o f the C T space.
b Widening or narrowing o f the C T space d e p e n d e n t on head position.

Journal of Voice, Vol. 10, No. 1, 1996

82

E. V I L K M A N E T A L .

hag as a vocal fold shortener seems to depend also


on other external factors, such as head position. It
also has to be taken into account that for obvious
reasons, the movement of the cricoid cartilage was
not constrained by tracheal pull in these cadaver
experiments.
Electrical stimulation experiments of human ST
muscles during surgical operations indicate that ST
contraction always results in the downward movement of the thyroid cartilage in relation to the spine.
However, this appears not to be accompanied with
noticeable pitch changes. Besides, there is also evidence that as the head is bent backward, the pitch
drops (12). In another stimulation study of human
subjects (24), the downward movement of the larynx has been reported to be accompanied by a widening of the laryngeal inlet and the abduction of the
vocal folds. This is apparently due to the increased
distance of the hyoid bone and the thyroid cartilage
and consequently diminished folding of the laryngeal tissues (cf. ref. 25). There are some findings
obtained with entirely different research methods
also implying that the ST and SH muscles contribute to producing the highest range of tones, i.e.,
tend to lengthen the vocal folds. ST and SH are
often severed during thyroid surgery and many
studies report postoperative loss of the highest
pitches (12,17).
Sapir et al. (26) studied the pitch control of rhesus
macaque by stimulating the GH, CT, and ST muscles in different combinations. As could be expected, the single effect of the CT muscle on F 0 was
the greatest, but also the stimulation of the GH and
ST muscles caused a rise in F0. The combinations of
either CT and GH or CT and ST stimulation, however, had the greatest overall effects. It is also noteworthy that in anesthetized dogs, stimulation of the
hypoglossal nerve seems to cause a contraction of
the suprahyoidal muscles. As a result, the length of
the vocal folds increases and so do glottal resistance
and subglottal pressure (27). Shin et al. (28) used
mongrel dogs in a stimulation study of 11 external
muscles. Thyrohyoid (TH) and ST stimulation elongated the vocal folds slightly, whereas the stimulation of GH and CP had a shortening effect. However, it is not entirely clear how the possible retrograde stimulation effects were excluded from the
response observed in these stimulation studies.
Namely, Murakami and Kirchner (29), when stimulating the internal (sensory) branch of the superior
laryngeal nerve, observed reflex responses in the
nerves innervating the extrinsic laryngeal muscles.
Journal of Voice, Vol. 10, No. 1, 1996

They also studied the effects of nerve stimulation


on vocal fold length and on subglottal pressure. Reflex response discharges were observed in the
nerves innervating CT, ST, GH, and CP, as well as
the stylopharyngeal, pterygopharyngeal, and palatopharyngeal muscles. The movements of the hyoid-laryngeal structures connected with these reflex responses showed an upward displacement of
the hyoid-laryngeal column. After denervation of
the CT muscle, the ascent of the thyroid cartilage
increased markedly and the cricothyroid distance
increased, which shortened the vocal folds. This
would be, at least in part, in agreement with the
findings by Shin et al. (28). It seems, thus, that the
muscles moving the larynx upward and forward
contribute to pitch lowering rather than to pitch
raising, if the reflexory CT muscle contraction is
blocked.
As regards the function of the inferior pharyngeal
constrictor in voice production, Dreyfuss found in
his experiments with dogs (30) that cutting these
muscle fibers disables barking and whimpering.
However, soon after the operation, the dog was still
able to grunt and, 5 days later, even bark in a hoarse
voice. On the basis of anatomical and experimental
studies on the function of the CT and CP muscles in
apes, Minnigerode (23,31) claimed that the functions of these muscles were synergistic. The function of the CP muscle in F 0 regulation has been
measured indirectly by Martin and Klingholz (32).
They observed the intraluminal esophageal pressure in human subjects at the level of the CP muscle
at varying pitch levels. They found increases in
pressure with rising Fo in the higher F 0 range and a
decrease in pressure values below rest level in low
pitch range due to CP activity (active expansion of
the sphincter; cf. ref. 32).
Studies on the movements of laryngeal structures in
singing and speech
Radiographic x-ray studies on the mutual movements of the cricoid and thyroid cartilages have
shown that in rest position the cricothyroid space is
open. The distance diminishes as pitch is raised
with about - 5 0 % shortening at the highest pitch
level (3,12,17). In addition to this rotatory approximation of the two cartilages, vocal fold length has
also been found to be increased by ventrodorsal
gliding in the CT articulation with rising pitch (3,12,
13).
As to the changes in the laryngeal structures
caused by an increased hyoid-to-thyroid distance,

E X T E R N A L LAR YNGEAL F R A M E FUNCTION

there is documentation that as the epiglottis tilts


forward, the vestibule of the larynx expands and the
ventricular folds and the vocal folds abduct due to a
reduction in the folding of these structures with increasing vertical tension (3,11,24,33). This vertical
change is caused by either the elevation of hyoid
bone or the lowering of the larynx to an extent that
exceeds the movement of the larynx or the hyoid,
respectively.
In singing, the entire laryngeal column moves
vertically more or less in correlation with pitch. The
elevation of the larynx for high pitches and lowering
for low pitches, especially in untrained singers, is a
well-known phenomenon. In trained singers, however, laryngeal displacement is significantly smaller
and can even be reversed (34-36). This difference
has been explained as depending on the need to
maintain stable acoustical circumstances in the vocal tract in good quality singing (25,37). On the
other hand, in a radiographic study of a professional
singer with an ability to deliberately use the unfavorable " o p e n " quality of singing, the thyroid cartilage was observed to approach the hyoid bone as
the upper limit of the pitch range was reached (13).
Furthermore, the vestibular space of the larynx has
also been observed to decline with pitch when the
so-called open quality is used in voice production
(38). Obviously, these findings refer to a hyperkinetic or effort-type of closure of the glottis (cf. refs.
3 and 39).
Differences between nonsingers and singers in
their use of the movement of laryngeal structures
for vocal fold length-adjustment are evident. This
view is supported by a recent radiographic study of
vocal-fold length control, in which differences between nonsingers and singers are clear. While nonsingers and singers both appear to increase vocal
fold length with pitch, singers do so only up to a
certain point, after which no elongation occurs.
Also, compared with singers, nonsingers increase
vocal fold length with pitch more for a given pitch
range. These findings imply that to raise Fo in the
high pitch range, singers prefer to use a mechanism
that presumably reduces the vibrating mass of the
vocal folds instead of a mechanism that increases
the longitudinal tension in the folds (40).
In a recent study, Sonninen et al. (41) report of
radiographic findings and indirect observations on
CP function in covered and open voice singing. On
the basis of the movements of the cricoid cartilage,
they conclude that CP may participate in raising F0
at high pitches by tensing the vocal folds. Accord-

83

ing to Sonninen et al. (41), the finding that the


cricoid-to-cervical-spine distance is shortened when
pitch is raised, especially in open voice, can only be
explained by the external force produced by CP
contraction. The data in Sonninen et al. also indicate that in the production of extremely low
pitches, the cricoid cartilage again approaches the
cervical spine or spinal column. As also suggested
by, for instance, Martin and Klingholz (32), this is a
mechanism contributing to the shortening of the vocal folds.
To improve the view of the larynx during indirect
examination, the techniques of opening the laryngeal vestibule with the production of the relatively
high-pitched v o w e l s / i / a n d / e / a r e employed in everyday clinical practice. On the other hand, in low
pitch ranges, the downward tilt of the epiglottis and
the overall narrowing of the laryngeal vestibule may
prevent visual inspection of the vocal folds (e.g.,
ref. 42). In addition to the purely passive biomechanical events connected with changes in laryngeal height, the downward tilt of the epiglottis can
be brought about even by the active contraction of
the aryepigiottal musculature (cf. refs. 10, 43). In
the so-called hyperkinetic dysphonia, the position
of the larynx is high and the space of the laryngeal
vestibule declines (e.g., ref. 39). This positional
change can be explained as occurring, at least in
part, due to an approximation of the thyroid cartilage to the hyoid bone (e.g., ref. 44) and increased
folding as observed during swallowing and effort
closure, for instance (cf. refs. 3, 1l, 25).
Studies of the intrinsic F 0 of vowels indicate that
in comparable environments, the high vowels/i/and
/u/tend to be associated with higher Fo--and lower
larynx position--than the low vowels /a,m/ (see
refs. 45 and 46 for reviews). The relationship between vowel F0 and larynx height has been observed to be inverted in speech as compared with
singing (e.g., ref. 47). In other words, in speech high
intrinsic F 0 is accompanied by a low larynx position, whereas in singing low notes tend to be produced with low larynx and high notes with high larynx position. Several hypotheses have been presented to explain the variation in the intrinsic F0 of
vowels. One of these is the so-called vertical pull
hypothesis, according to which vertical changes in
the pharyngeal-laryngeal tissues cause a thinning of
the mucosa of the vocal folds; thus, F0 is raised in
high vowels as the result of the vertical tension
caused by a raised tongue and a lowered position of
the larynx (48). In a recent study in which excised
Journal of Voice, Vol. 10, No. 1, 1996

84

E. V I L K M A N E T AL.

larynges were used, the vertical changes observed


in the vocal folds were found to support the vertical
pull hypothesis. However, the changes were too
small to explain conclusively the in vivo measured
F0 variation in vowels. In the study, the vertical
changes were brought about by pulling the hyoid
bone cranially while the thyroid and cricoid cartilages were fixed (25). Obviously, other vertical factors, such as the height of the hyoid-larynx column
and the position of the tongue as well as tracheal
pull and even the position of the soft palate, are
relevant in this respect.
Radiographic studies of speech production have
shown that the size of the laryngeal ventricles varies in vowel articulations. The ventricles have been
found to be larger for the high v o w e l / u / a s compared with the low vowel/a/(49). This phenomenon
can be explained in terms of the vertical changes
in the hyoid-laryngeal column. In several radiographic studies, the larynx has been found to be in
a lower position for the high v o w e l s / u / a n d / i / i n
comparison with the low vowels, especially the
vowel/a/. However, considerable amounts of interindividual variation can be found in the studies
(47,50-52). The hyoid bone and the thyroid cartilage
are generally assumed to move as one block, even if
a certain amount of freedom were permitted by the
ligamentous structures. However, according to
SOderberg's (52) measurements, the independent
movement of the corpus of the hyoid bone and the
thyroid cartilage in vowel production is - 3 - 4 mm.
This mutual movement is likely to be related to the
vowel specific features of laryngeal articulation.
In addition to vertical movements in the laryngeal
region, the horizontal movement of the hyoid bone
in relation to vowel production has also been investigated. In these studies, the hyoid bone has been
found to hold the most anterior position for the
vowel/i/, followed by / u / a n d /a/in the posterior
direction (47,51-53). Overlap in the horizontal positions of the hyoid bone in different vowels has
also been documented (e.g., ref. 47). However, statistical analyses reveal that vowels tend to have
their own identity, i.e., a characteristic horizontal
position of the hyoid bone (51).
Eleetromyographic activity of external
laryngeal muscles
Results of a number of electromyographic (EMG)
studies relevant to the discussion are presented in
Table 2. Most EMG studies on muscle activity in
various voice production tasks, unfortunately, in.Journal of Voice, Vol. 10, No. 1, 1996

volve a single subject only. However, a summary


with some general observations seems both justified
and worthwhile because the results of most of these
studies, especially those on strap muscles, agree
with each other. A summary of the information presented in Tables I and 2 is given in Table 3.
It appears that both in speech and in singing, the
activity of the ST and the SH muscles increases in
the low pitch range with pitch lowering and in the
high pitch range with pitch raising (17,58--70).
As regards other extrinsic laryngeal muscles,
research and studies are relatively sparse. There
is documentation, however, that the genioglossal
muscle shows a positive phase relationship with
pitch (10,53,71) and that the activity of the geniohyoid muscle correlates with F0 rise (53,66). Further, the digastric muscle has been reported to activate during difficulties in phonatory tasks, in register transitions, for instance (60), and in some
studies increases in the EMG activity of the CP
muscle in the extreme low and high pitch ranges
(10,64) have also been found. Honda and Fujimura
also have recently studied the EMG activity of the
CP muscle (72). They found CP activity in one subject to coincide with the final drop of F 0 in sentences, i.e., with F 0 declination (72). They also report CP activity to be inversely correlated with Fo in
word productions. However, because the inverse
correlation of CP activity and Fo in words produced
by one subject reported in the study is on the order
of -0.60, as computed from the graphic data presented in the articles, the alleged relationship obviously needs further substantiation.
Finally, the function of the levator veli palatini
muscle, which raises the soft palate, has been found
to be related to the production of high vowels. The
activity of the muscle is higher for high than for low
vowels (73) and its role in pitch control has been
reported to be negligible (60). On the other hand,
the palatopharyngeal muscle, which lowers the soft
palate for nasal sounds (73), shows increased activity with pitch (60).
Tracheal pull
Tracheal pull is the force that pulls the cricoid
cartilage and consequently, the larynx, downward;
the pull is generated by the activity of the diaphragm as well as by passive forces. The magnitude
of tracheal pull has been measured by Zenker and
Glaninger (4). In the three cases reported, the minimal values ranged from 20 to 30 g. When the
cricoid cartilage was moved 2 cm cranially, the

EXTERNAL LARYNGEAL

FRAME FUNCTION

85

TABLE 2. A summary o f the results o f electromyographic studies on external muscles in relation to vocal fold
length adjustment
Study
Faaborg-Andersen,
and Sonninen (58)
Zenker and Zenker
(10)
Hirano et al. (59)
Minnigerode (23)
Ohala and Hirose
(54)
Vennard et al. (60)

Shipp (62)
Baer et al. (64)

Estiil et al. (55)

Niimi et al. (70)


Simada and Hirose
(56)
Collier (57)

Material
7 Males,
7 females
Human
3 Males
25 Humans
3 Males
1 Female,
2 males

6 Males
Human,
several

I Male

2 Males
Human
1 Male

Erickson (57)

I Male

Atkinson and
Erickson (65)
Atkinson (67)

I Male
1 Male

Muscle

Phonation

Pitch
range

Pitch
lowering

Pitch
raising

+
+
+
+
+

(+)
(+)
+
+
+
+
+
+

+
+
(+)
+
+
+
+
o
o
o
o
o
o
o
o
o
o
o
o

+
+
(+)
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
(+)

(+ )
(+)
o
o
o
o
+

(+ )
(+)
+
o
o
o
-

+
(+ )

(+ )

ST
MH
TH
TP
CP
SH
CP
SH

Singing,
sustained

Extremes

Singing

Extremes

Singing
Phonation
Sustained

Extremes

TH
SH
DG
LP
pp
ST
TH
TH
SH
CP
LP
MH
GG
SC
LP
PP
GH
MC
GGP
TH
ST
ST
SH

Singing

Extremes

Singing

Extremes

Singing

Extremes,
arpeggio

Singing

Two
octaves

Singing
Speech, stress

Vibrato
Speech

SH
ST
TH
GH
SH
ST
TH
SH

Speech,
intonation

Speech

Speech, stress
and
intonation

Speech

Speech,
intonation
Speech,
intonation

Speech

SH
ST

Extremes

Speech

IPC, inferior pharyngeal constrictor; DG, digastric muscle; GGP, geniogiossus, posterior part; LP, ievator palatini; MC, middle
constriction; GH, geniohyoid muscle; MH, myohyoid muscle; SC, superior constrictor; CP, cricopharyngeal muscle; TP, thyropharyngeal muscle; SH, sternohyoid muscle; ST, sternothyroid muscle; TH, thyrohyoid muscle; GG, genioglossal muscle; PP, palatopharyngeal muscle. +, effect; - , no effect; o, not studied; (+), inconsistent.
m a x i m a l f o r c e s d u r i n g i n s p i r a t i o n v a r i e d f r o m 430
to 1,480 g (n = 3) a n d d u r i n g e x p i r a t i o n f r o m 320 to
1,300 g. It c a n b e s p e c u l a t e d that a c o n s i d e r a b l e
e x t r a load is i m p o s e d o n the C T m u s c l e b y s i n g i n g
high p i t c h e s w i t h a high l a r y n x p o s i t i o n . A c c o r d i n g
to Z e n k e r a n d G l a n i n g e r , t r a c h e a l pull is p r e s e n t
e v e n w h e n t h e s u b j e c t is in s u p i n e p o s i t i o n a n d in a
state o f artificial a p n e a d u e to a n e s t h e s i a .
A s c a n b e e x p e c t e d , t r a c h e a l pull f o r c e s also affect the f u n c t i o n o f the C T m u s c l e . S u n d b e r g et al.

(74) r e c o r d e d the E M G a c t i v i t y o f t h e C T m u s c l e in
t h r e e s i n g e r s f o r d i f f e r e n t t r a c h e a l t e n s i o n s . All
t h r e e s u b j e c t s s h o w e d a n i n c r e a s e d C T m u s c l e activity for a d e s c e n t o f the d i a p h r a g m d u r i n g sust a i n e d p h o n a t i o n . T r a c h e a l pull w a s c h a n g e d e i t h e r
b y high l u n g v o l u m e s o r c o n s c i o u s d e s c e n t o f the
d i a p h r a g m , o r b o t h . A c l e a r i n d i c a t i o n o f t h e effect
o f t r a c h e a l pull is t h a t as t h e l a r y n x d e s c e n d s d u e to
strap m u s c l e a c t i v i t y d u r i n g i n s p i r a t i o n , t h e C T dist a n c e still r e m a i n s c o n s t a n t (3). I n o t h e r w o r d s , tra-

Journal of Voice, Vol. 10, No. 1, 1996

86

E. V I L K M A N ET AL.

TABLE 3. A summary o f the effects o f the major


extrinsic muscles in pitch control as documented in
reviewed research (number o f i's indicates the number

of observations of the effect in question)

Muscle
CP
ST
IPC
GH
TH
TP
SH

Pitch
lowering

Pitch
raising

Pitch
raising

iii
ii

iii
iiiiii
i
i
ii
ii
iiiiiii

i
ii
i
i
i
i
ii

iiiiii
iiiiiii

(-)

i
iiii

(+)

(-)

iii1

HM

Pitch
lowering

(+)

ii
iiiiii
i
iiiii

CP, cricopharyngeal muscle; TP, thyropharyngeal muscle;


IPC, inferior pharyngeal constrictor; ST, sternothyroid muscle;
GH, geniohyoid muscle; TH, thyrohyoid muscle; SH, sternohyoid muscle. (+), effect; ( - ) , no effect.

TP
CP

'\ \\\ /
4

_1

ST

cheal pull apparently contributes to the descent of


the larynx by tensing the CT ligaments. Another
indication of this can be found in Sonninen's (12)
study in which, in spite of the fact that the ST
muscle stimulation caused a downward movement
of the thyroid cartilage, the pitch remained unchanged. Furthermore, in the study by Murakami
and Kirchner (29, see earlier herein), it was found
that the denervation of the CT muscle not only
opened the CT visor but also the ascent of the thyroid cartilage increased with neural stimulation.

(A)

EXTERNAL LARYNGEAL FACTORS AND


CHANGES IN FUNDAMENTAL FREQUENCY:
A SYNTHESIS OF DATA INTO MODELS
An attempt to synthesize the reviewed data on
the external laryngeal forces in the form of two
models is presented in Fig. 1. Included in these
models are only those of the external mechanisms
that affect the length adjustment of the vocal folds.
The models are based on those presented earlier by
Merkel (6), Kenyon (7), Zenker and Zenker (10),
Sonninen (13), and Martin and Klingholz (32), with
important modifications suggested by more recent
findings in the studies reviewed above earlier
herein.
In the light of available scientific evidence, it
seems justified to interpret the contribution of the
extrinsic mechanisms to pitch rising as follows (Fig.
1A). Pitch may be raised by a forward movement of
the thyroid cartilage that is caused by the activity of
the strap muscles and the musculature of the bottom of the mouth, in case the CP muscle pulls the
cricoid cartilage posteriorly. Because this maneuJournal of Voice, Vol. 10, No. 1, 1996

SH / /
I
ST
tracheal pull

(B)
FIG. 1. Schematic representation of external laryngeal forces.
A: Forces lengthening the vocal folds and raising Fo. B: Forces
shortening the vocal folds and lowering F o. CP, cricopharyngeal
muscle; ST, sternothyroid muscle; TP, thyropharyngeai muscle;
AE, aryepiglottic muscle; HM, hyomandibular muscles; HT,
hyothyroid muscle; SH, sternohyoid muscle.

EXTERNAL LARYNGEAL FRAME FUNCTION

ver usually involves a rise in the position of the


larynx, the increase in tracheal pull has to be overcome by CT activity. There are also theoretical calculations and some indirect evidence that in the extreme high pitch range, the direction of the force
vector of the CP muscle becomes unfavorable if the
larynx is allowed to rise too much (13,75). The report that the distance between the cervical spine
and the larynx increases rapidly as pitch reaches its
ultimate upper extreme, which implies a failure of
the CP muscle (13,41), provides further evidence in
support of this view. In addition, Fig. 1A also illustrates that the TP may contribute to the lengthening
of the vocal folds by approximating the thyroid laminae (10). Due to changes concomitant with aging
(20,21), this mechanism is probably possible in
young persons only.
On the basis of the reviewed data, we interpret
the optional contribution of the extrinsic mechanisms to pitch lowering as follows (Fig. IB). The
lowering of the thyroid cartilage caused by ST and
SH activity creates circumstances in which the contraction of the CP muscle, by opposing the cranial
displacement of the larynx, rotates the cricoid cartilage around the axis of the CTjoint, and; thus the
vocal folds are shortened (Fig. 1). Simultaneous CT
relaxation, or, at least CT deactivation, is also necessary. In addition, tracheal pull, although diminished due to a lowered larynx position, may contribute to the opening of the CT visor (cf. refs. l0
and 13). Assisted by contractions of the SH and TH
muscles, these events pull the hyoid bone toward
the thyroid cartilage, which leads to changes in the
laryngeal column, to increased folding in particular,
as often seen in laryngoscopic examinations. In addition to the effects brought about by the hyoid-tothyroid approximation, the function of the aryepiglottal muscles may also contribute to F 0 change by
lowering the epiglottis or by rotating the cricoid cartilage.
DISCUSSION
The analysis of the net effects of a combination of
external laryngeal forces is not a simple task. The
structural components in question are used in voice
production and also for vegetative functions, especially swallowing and respiration as well as for effort stabilization of the torso. These nonphonatory
functions are, to a great extent, based on reflex interplay between the structures. It is possible, phylogenetically, that in the relatively new use of these
organs for speech and voice there are acts that have

87

little significance in voice production as such, i.e.,


they occur simply because the reflex arcs exist.
These potential reflex functions are not disturbing
enough for voice and speech production to necessitate special damping or inhibition mechanisms. It
is also obvious that in some voice disorders, the
phylogenetically young phonatory mechanism is
more or less replaced by the archaic mechanism. In
hyperfunctional dysphonia, for instance, effort-type
glottal closures are often observed (e.g., ref. 39).
All this is to say that distinguishing between essential and secondary biomechanical events and muscular activities in phonation may sometimes be difficult if not impossible. This difficulty is not in the
least alleviated by the fact that the data on the external functions are from such a diverse collection
of sources and research approaches in general. Differences in data resulting from variation in sample
size or in speech and singing tasks, among other
things, can easily confuse otherwise straightforward relationships.
Considering the significant role of the intrinsic
muscles and factors in voice production, welldocumented in Titze's work (e.g., ref. 76), a logical
and timely starting point for discussion is the general role and scope of the external laryngeal forces
in F 0 control.
External laryngeal factors and Fo change
One of the most important means of pitch control
is adjusting the length of the vocal folds, in which
intrinsic muscles, notably the CT, have an important role. As far as vocal fold elongation is concerned, CT does not necessarily need assistance
from the external laryngeal muscles. The contractile force of the CT muscle is known to exceed
clearly that of its biomechanical antagonist, the thyroarytenoid muscle (77)--not necessarily an antagonist to CT in voice physiology--even if tracheal
pull were taken into account. Besides, there are no
external muscles capable of assisting the CT to resist possible increases in tracheal pull and in maintaining a stable CT distance and, consequently, stable pitch. Furthermore, from the point of view of
vocal fold lengthening, it is well known that the
vocal folds are longest during deep inspiration (e.g.,
ref. 78) and the production of the upper limits of the
chest register phonation does not require maximal
lengthening of the vocal folds. It seems reasonable
to conclude, then, that the vocal folds can be elongated by external mechanisms mediated by certain
articulatory maneuvers of speech production and
Journal of Voice. Vol. 10, No. 1, 1996

88

E. V I L K M A N E T AL.

also by physiological arrangements other than those


directly connected with F0 control in high-quality
singing. However, as stated already, the active
shortening of the vocal folds for pitch lowering is
not so well understood.
The role of external mechanisms in articulatory
and resonatory functions as well as in the general
suspension of the larynx seems fairly straightforward. Vertical displacement studies in professional
singers, however, indicate that the rise of the hyoid-larynx column with F 0 rise is not necessary
(36,62). Moreover, in some singing techniques, it
has been a long-standing pedagogical principle to
teach the students to maintain a low larynx position
even for high tones (e.g., ref. 37).

Additional aspects of extrinsic muscles and


F o change
As mentioned already, Honda and Fujimura (72)
report CP activity to be inversely correlated with
F 0. Claiming that the mechanism of F 0 lowering has
not yet been accounted for physiologically and that
CT relaxation is not effective in Fo lowering in low
pitch ranges, which typically occur in phrase final
positions, they also propose a new mechanism of
pitch lowering. According to their new hypothesis,
the bulging of the belly of the CP muscle moves the
cricoid cartilage forward, which leads to the shortening of the vocal folds and the lowering of/7o.
When assessing the validity and feasibility of the
bulging theory, the structural anatomy of the CP
muscle is of crucial importance. In light of the anatomical descriptions presented by Minnigerode
(23) and Zenker (11), the pitch-lowering mechanism
based on the concept of CP bulging seems highly
implausible. Moreover, there is recent evidence
that the production of extremely low pitches is accompanied by a diminished distance between the
cricoid cartilage and the cervical spine (41). Quite
possibly, the new bulging hypothesis is based on the
misconception that the structural features of the inferior constrictor are similar to those of the superior
constrictor in which a part of the palatopharyngeal
muscle is known to cause a so-called Passavant's
pad (5).
On the other hand, a contraction of the aryepiglottal musculature (see ref. 43 for a review) might
be one of the other mechanisms contributing to F 0
lowering in connection with the production of low
vowels such as /a/. However, to the best of our
knowledge, there are no EMG studies of the aryepJournal of Voice, Vol. I0, No. I, 1996

iglottai muscle activity in connection with vowel


production or F 0 changes in general.
The positive correlation between EMG activity of
the ST and F0 found in a study on singers' vibrato
has been interpreted to be caused by a downward
movement of the thyroid cartilage towards the
cricoid cartilage, which results in the lengthening of
the vocal folds (70). However, as pointed out elsewhere in this article, the cricoid cartilage should not
be considered a fixed structure that permits thyroid
cartilage movements to be mediated directly to vocal fold length changes. Furthermore, as mentioned
earlier (13,36), the larynx usually goes up with ris-'
ing pitch even in good quality singing which, again,
cannot be explained by ST activity. The findings
by Niimi et al. (70) might be explained simply by
the inertia of the cricoid cartilage and the trachea
during these short increases in ST activity, if the
thyroid cartilage really (this has not been studied)
moves downward during a pitch rise in a vibrato
cycle.
The role of the hyoid bone and suprahyoid
dynamics in Fo change
In the past decades, the puzzle of the intrinsic Fo
of vowels has produced numerous theories (see
refs. 45 and 46 for reviews). One of the foremost
explanations is that the anterior component of the
hyoid bone displacement in vowel articulation pulls
the superior cornua of the thyroid cartilage forward,
thus causing rotation in the CT articulation (46,53,
72). There are, however, some problems inherent to
this model. First, it is assumed that the "mutual
movement of the hyoid bone and the thyroid cartilage is most restricted at the lateral thyrohyoid ligament" (53). According to Zenker's (11) qualitative
study and the quantitative studies by Vilkman and
Karma (25), this is not the state of affairs. Namely,
there is evidence that the middle hyothyroid ligament connecting the corpus of the hyoid bone to the
anterior-superior part of the thyroid cartilage in fact
restricts the mutual movements of the anterior part
of the hyoid bone significantly more than the
amount to which the lateral ligaments are able to
restrict the movements of the greater cornua of the
hyoid bone (25). Moreover, the lateral ligaments are
in an almost vertical position, and, naturally, they
do not constitute a beam structure. This means that
the forward movement of the hyoid bone really
ought to pull the ligament first in a more horizontal
direction. In addition, the hyoid-laryngeal column
descends in the production of high vowels (47,50-

EXTERNAL LARYNGEAL FRAME FUNCTION

52). Second, perhaps the greatest problem in the


"hyoid forward movement" model is that it also
fails to explain the fixed position of the cricoid cartilage. The model implies that the cricoid cartilage is
firmly fixed, yet there is substantial evidence of a
constant tension or pull by the trachea being applied
on the cricoid cartilage (see earlier). As already
pointed out, the external forces that act on the
cricoid cartilage include tracheal pull (diaphragm)
and also forces produced by esophageal tissues and
musculature as well as contraction of the CP muscle.
The anterior movement of the hyoid bone as a
vocal fold tensor mechanism seems to need further
investigation before a full account of all relevant
factors can be given. One possible solution toward
this end originates from Sonninen's (12,13) model,
according to which the forward movement of the
hyoid bone and the thyroid cartilage (TH and suprahyoidal muscles and ST contraction) might
cause an Fo rise provided that the CP muscle pulls
the cricoid cartilage dorsally by gliding in the CT
joint (12,13). On the other hand, the Zenker (10)
model of the effects of external laryngeal forces
states that the suprahyoidal muscles--other forces
kept constant--would contribute to F 0 lowering by
pulling the anterior tip of the thyroid cartilage in an
anterior-superior direction.
Nevertheless, the hyoid horizontal movement hypothesis of intrinsic F o is supported by experiments
with animals in which the stimulation of the suprahyoid muscles raised F0 in sustained phonation
(26,79). These findings are simultaneously at great
odds with some of the other stimulation experiments (28,29) which, again, are in agreement with
the Zenker model. However, it is not clear how the
possible reflex-like activation of the primary Fo control system, the CT muscle, was inhibited or monitored in the stimulus studies by Amenomori (79)
and Sapir et al. (26). Besides, as reported by Bothorel et al. (47), in singing (or sustained phonation),
the correlation of F 0 and larynx height is the inverse
of that found in vowel production (cf. ref. 50). Thus,
in addition to the general limitations of animal experiments, it is difficult to draw conclusions about
intrinsic F 0 variation from these stimulation experiments. The controversy can possibly be resolved
by the fact that vowel-specific CT muscle activation
(to be discussed later herein) overcomes the effects
of the external mechanisms connected with vowel
articulation.
In discussions of the horizontal displacement of

89

the hyoid bone, the functional chain that connects


the arytenoid cartilage via aryepiglottic folds and
finally to the mandible also is relevant. According
to the Zenker model (10), this mechanism is capable
of pulling the arytenoids in an anterior direction,
thereby causing rotation in the CT joint, which
leads to the opening of the CT space and to the
lowering of F o. In an experiment with vibrating excised human larynges (25), this chain of events was
observed to lower F0; the effect was caused by an
anterior movement of the arytenoid cartilages even
when the cricoid cartilage was fixed. Because the
genioglossal muscle is partly connected to the epiglottis and there are also ligamental structures connecting the hyoid bone to the epiglottis, this mechanism can also be considered relevant to pitch control. However, because it is likely that it tends to
lower F 0, the intrinsic F0 of vowels cannot be explained by this mechanism, simply because the epiglottis is in its highest position for the high vowel/i/.
Reflex mechanisms and F o change

Recent findings of the vowel specificity of the CT


muscle activity (72,80,81) allow for yet another line
of speculation. There is some evidence suggesting
that the vertical as well as the horizontal articulatory movements of the vocal tract structures, which
lead to a reflex-like contraction of the CT muscle,
are partly responsible for the variation in the vowelintrinsic F 0 (80,82). The contraction of CT would be
entirely logical because it would resist vertical
stretch and consequent overextension in this vital
laryngeal region. This kind of reflex arrangement
might be based on the phylogeny of the laryngeal
structures. In reptiles the cricoid and thyroid cartilage are not separate but form one single block (cf.
ref. 83); in mammals the development of CT articulation for the control of pitch apparently necessitates an automatic mechanism to protect the CT
space from overstretching. Such reflex connections
have been shown to exist in cats (29).
Thus, the articulatory movement as such would
not necessarily affect the longitudinal tension of the
vocal folds; the change would simply occur as a
reflex-like compensation to vertical changes such as
tongue and palate heightening, and lowering of the
larynx. However, such findings and events could
also be explained on the basis of a central control of
the intrinsic F 0 (72). The finding that vowel quality
affects pitch perception (84) certainly supports the
view but seems to call for further elucidation. However, the conclusion that the control of intrinsic F0
Journal of Voice, Vol. 10, No. 1, 1996

90

E. V I L K M A N ET AL.

is not directly based on the external frame function


seems justified.
Vertical changes in the laryngeal folds and

voice production
External forces together with CT activity may, as
some cadaver studies suggest, also contribute to the
transsectional shape of the vocal folds. This is important from the point of view of controlling registers and modes of phonation. Rotation seems to increase adduction through an increase in the folding
of the vocal folds, whereas gliding mainly affects
the longitudinal tension of the vocal folds and is
more likely to cause abduction (13,85). Thus, rotation in the CT articulation seems to produce a setting for the control of phonation different from the
one produced by gliding in this joint. This conclusion is supported by observations in a radiograph
study in which singers were found to use a greater
amount of ventrodorsai gliding for length adjustments of the vocal folds compared with nonsingers,
who preferred rotation, i.e., increased folding of the
vocal fold s (3); the untrained singers also used a higher
laryngeal position (13,36).
Vertical changes in the laryngeal column may, in
addition to slight Fo changes and abductory-adductory influence, also affect the register control of
phonation (25,86), as suggested by Schilling as early
as 1940. These findings in experiments with cadaver
material imply that the state of tension of the vocal
fold mucosa and the supporting connective tissue
structure of the vocal folds, conus elasticus, may be
important from the point of view of vocal physiology. The high larynx position in high-pitched singing probably makes delicate adjustments, such as
the so-called covering of the voice (e.g., ref. 40)
with rising pitch in classical singing, difficult or
even impossible, because of the circumstances created in the vocal fold tissues.
Changes in vocal fold stiffness and shape may
affect the wave mechanics of the vocal fold mucosa,
which is known to be of central importance in sustaining vocal fold vibrations (87--89). The effects of
these external adjustments on the transsectional
shape of the vocal folds, however, have neither
been studied thoroughly with living subjects nor
simulated with computer models.
In both speech therapy and singing pedagogy,
maintaining a low position of the larynx has traditionally been considered favorable for good quality
voice production. Clinical and pedagogical experience suggests that the physiological basis of this
Journal of Voice, Vol. 10, No. I, 1996

concept is related not only to resonatory and muscular tension aspects in general, but probably also
to an intentional avoidance of excessive vocal fold
folding, such as observed in an effort type of glottal
closure in connection with a TH approximation.
Considering the external factors and changes in the
laryngeal column, there seem to be some grounds
for a tentative formulation of a basic principle probably underlying the laryngeal control of voice production as follows: In good quality voice production, the intrinsic laryngeal muscles have to be allowed maximum independence in the delicate
control of the stiffness and transsectional shape of
the vocal folds. In this framework, increased folding, due to either articular rotation in the CTjoint or
a hyoid-thyroid approximation, would be a violation of an important laryngeal setting.
The deformation of the laryngeal tract, i.e., folding, associated with pitch lowering and the activity
of ST and SH that pull the hyoid bone downward,
has sometimes been interpreted as a sphincter constriction of the larynx typical of the low pitch area
(90). However, anatomical and physiological facts
clearly indicate that the change should really be
considered a result of the folding of the laryngeal
structures due to vertical changes in the structures
rather than a true sphincter action (3,25).
CONCLUDING REMARKS
To summarize, it would seem that in modeling the
contribution of the external laryngeal mechanisms
to voice production, Kenyon's reminder (7) to the
effect that the physiological larynx has to be considered a complex interactive system is still modern
and important. Significant factors in this interactive
system that have often been neglected, both in studies of the external frame and in the interpretation of
physiological data on external laryngeal forces, include tracheal pull and its interaction with CT activity, the gross vertical movements of the larynx,
the interplay between thyroid cartilage biomechanics and CP muscle function, and finally, the sparse
muscular connections to the cricoid cartilage. The
models presented herein, into which we have tried
to synthesize the salient external factors relevant to
pitch control, cannot be considered comprehensive.
However, formulating a more strict and a more
comprehensive model of external frame function in
pitch control on the basis of data as diverse as the
one reviewed may turn out to be impossible. The
major problems that still need to be resolved arise

EXTERNAL LARYNGEAL FRAME FUNCTION

from the interindividual variations observed in the


use of the external factors and also from the variation found in different voice production tasks, especially speech and singing.
REFERENCES
I. Kenyon EL. Significance of the extrinsic musculature of the
larynx. JAMA 1922;79:428-31.
2. Brodie AG. Anatomy and physiology of head and neck musculature. Am J Orthodont 1950;36:831--44.
3. Fink B, Demarest R. Laryngeal biomechanics. Cambridge:
Harvard University Press, 1978.
4. Zenker W, Glaninger J. Die St~irke des Trachealzuges beim
lebenden Menschen und seine Bedeutung fiir die Kehlkopfmechanik. Ztschr Biol 1959;I 11:155--64.
5. Zemlin WR. Speech and hearing science, 3rd ed. Englewood
Cliffs: Prentice-Hall, 1988.
6. Merkel CL. Anatomie und Physiologie des Menschliche
Stimm- und Sprach-Organs. Leipzig: Abel, 1863.
7. Kenyon EL. Relation of oral articulative movements of
speech and of extrinsic laryngeal musculature in general to
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