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Clinical Anatomy and Physiologyof the Voice

Robert T. Satalo ff , MD, DMA *,Yolanda D. Heman-Ackah, MD,

Mary J. Hawkshaw, BSN, RN, CORLNDepartment of Otolaryngology–Head and Neck Surgery, Drexel University

College of Medicine, 1721 Pine Street, Philadelphia, PA 19103, USA

Anatomy

The anatomy of the voice is not limited to the region between the supra-sternal notch (top of the breast bone) and the hyoid bone. Practically all

body systems a ff ect the voice. The larynx receives the greatest attention be-cause it is the most sensitive and expressive component of the vocal mech-anism, but anatomic interactions throughout the patient’s body must beconsidered in treating the professional voice user. It is helpful to think of the larynx as composed of four anatomic units: skeleton, mucosa, intrinsicmuscles, and extrinsic muscles. The glottis is the space between the vocalfolds [1]. The portions of the larynx above the vocal folds are referred toas the supraglottis. The area below the vocal folds is referred to as the sub-glottis. The vocal tract includes those portions of the aerodigestive tract in-

volved in vocal production.

Larynx: skeleton

The most important parts of the laryngeal skeleton are the thyroid carti-lage, cricoid cartilage, and the two arytenoid cartilages ( Fig. 1 ). Intrinsicmuscles of the larynx are connected to these cartilages. One of the intrinsicmuscles, the thyroarytenoid, extends on each side from the arytenoid carti-lage to the inside of the thyroid cartilage just below and behind the thyroidprominence. The medial belly of the thyroarytenoid is also known as the

This article is modified from: Sataloff RT. Professional voice: the science and art of clinicalcare. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 143–77; with permission.

* Corresponding author.E-mail address: [email protected] (R.T. Sataloff).

0030-6665/07/$ - see front matter 2007 Elsevier Inc. All rights reserved.doi:10.1016/j.otc.2007.05.002 oto.theclinics.com

Otolaryngol Clin N Am

40 (2007) 909–929

mailto:[email protected]:[email protected]


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vocalis muscle, and it forms the body of the vocal fold. The laryngeal carti-

lages are connected by soft attachments that allow changes in their relativeangles and distances, thereby permitting alterations in the shape and tensionof the tissues extended between them. The arytenoids are capable of com-plex motion. It used to be said that the arytenoids rock, glide, and rotate.More accurately, with adduction of the vocal folds the cartilages arebrought together in the midline and revolve over the cricoid, moving inferi-orly and anteriorly. It seems that people use di ff erent strategies for

Fig. 1. Cartilages of the larynx. ( From Satalo ff RT. Professional voice: the science and art of clin-ical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 143–77; with permission.)

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approximating the arytenoids and that such strategies may inuence a per-son’s susceptibility to laryngeal trauma that can cause vocal process ulcers

and laryngeal granulomas.

Larynx: mucosa

The vibratory margin of the vocal fold is much more complicated than sim-ply mucosa applied to muscle or ligament. It consists of ve layers ( Fig. 2 ) [2].The thin, lubricated epithelium covering the vocal folds forms the area of con-tact between the vibrating vocal folds and acts somewhat like a capsule, help-ing to maintain vocal fold shape. The epithelium lining most of the vocal tract

is pseudo-stratied, ciliated, columnar epithelium, typical respiratory epithe-lium involved in handling mucous secretions. The vibratory margin of the vo-cal fold is covered with stratied squamous epithelium, better suited towithstand the trauma of vocal fold contact. The supercial layer of the laminapropria, also known as Reinke’s space, is composed of loose brous compo-nents and matrix. It contains few broblasts. The intermediate layer of lam-ina propria consists primarily of elastic bers and does contain broblasts.The deep layer of the lamina propria is composed primarily of collagenousbers and is rich in broblasts. The thyroarytenoid or vocalis muscle makes

up the body of the vocal fold and is one of the intrinsic laryngeal muscles. Theintermediate and deep layers of the lamina propria constitute the vocal liga-ment and lie immediately below the Reinke’s space.

Although variations along the length of the membranous vocal fold areimportant in only a few situations, the surgeon, in particular, should beaware that they exist. Particularly striking variations occur at the anteriorand posterior portion of the membranous vocal fold. Anteriorly, the inter-mediate layer of the lamina propria becomes thick, forming an oval masscalled the anterior macula ava. This structure is composed of stroma, bro-

blasts, and elastic bers. Anteriorly, it inserts into the anterior commissuretendon, a mass of collagenous bers that is connected to the thyroid carti-lage anteriorly, the anterior macula ava posteriorly, and the deep layerof the lamina propria laterally. As Hirano has pointed out, this arrangementallows the sti ff ness to change gradually from the pliable membranous vocalfold to the sti ff ness of the thyroid cartilage [3].

A similar gradual change in sti ff ness occurs posteriorly where the inter-mediate layer of the lamina propria also thickens to form the posterior mac-ula ava, another oval mass. It is structurally similar to the anterior macula

ava. The posterior macula ava attaches to the vocal process of the aryte-noid cartilage through a transitional structure that consists of chondrocytes,broblasts, and intermediate cells [4]. The sti ff ness thus progresses from themembranous vocal fold to the slightly sti ff er macula ava, to the sti ff er tran-sitional structure, to the elastic cartilage of the vocal process, to the hyalinecartilage of the arytenoid body. It is believed that this gradual change instiff ness serves as a cushion that may protect the ends of the vocal folds

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Fig. 2. An overview of the larynx and vocal tract showing the vocal folds and the region fromwhich the vocal fold was sampled to obtain the cross section showing the layered structure. ( Re- printed from : Satalo ff RT. The human voice. Sci Am 1992;267:108–15; with permission.)

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from mechanical damage caused by contact or vibrations [4]. It may also actas a controlled damper that smoothes mechanical changes in vocal fold ad-

justment. This arrangement seems particularly well suited to vibration, asare other aspects of the vocal fold architecture. For example, blood vesselsin the vibratory margin come from posterior and anterior origins and runparallel to the vibratory margin, with few vessels entering the mucosa per-pendicularly or from underlying muscle. The vibratory margin containsno glands, whose presence would likely interfere with the smoothness of vi-bratory waves. Even the elastic and collagenous bers of the lamina propriarun approximately parallel to the vibratory margin. The more one studiesthe vocal fold, the more one appreciates the beauty of its engineering.

Functionally, the ve layers have di ff erent mechanical properties andmay be thought of as somewhat like ball bearings of di ff erent sizes that al-low the smooth shearing action necessary for proper vocal fold vibration.The posterior two fths (approximately) of the vocal folds are cartilaginous,and the anterior three fths are membranous (from the vocal process for-ward) in adults. Under normal circumstances, most of the vibratory func-tion critical to sound quality occurs in the membranous portion.

Mechanically, the vocal fold structures act more like three layers consist-ing of the cover (epithelium and Reinke’s space), transition (intermediate

and deep layers of the lamina propria), and the body (the vocalis muscles).Understanding this anatomy is important because di ff erent pathologic enti-ties occur in di ff erent layers and require di ff erent approaches to treatment.For example, broblasts are responsible for scar formation. Lesions that oc-cur supercially in the vocal folds (such as nodules, cysts, and most polyps)should therefore permit treatment without disturbance of the intermediateand deep layers, broblast proliferation, or scar formation.

In addition to the ve layers discussed above, recent research has shownthat there is a complex basement membrane connecting the epithelium to

the supercial layer of the lamina propria [5]. The basement membrane isa multilayered, chemically complex structure. It gives rise to Type VII col-lagen loops that surround Type III collagen bers in the supercial layerof the lamina propria. Knowledge of the basement membrane has alreadybeen important in changing surgical technique. Additional research is likelyto show its great importance in other matters, such as the ability to heal fol-lowing trauma, possibly the development of certain kinds of vocal fold pa-thology, and probably in histopathologic di ff erential diagnosis.

The vocal folds may be thought of as the oscillators of the vocal mechanism

[6]. Above the true vocal folds are tissues known as false vocal folds. Unlikethe true vocal folds, they do not make contact during normal speaking or sing-ing. They may produce voice during certain abnormal circumstances, how-ever. This phenomenon is called ‘‘dysphonia plica ventricularis.’’ Untilrecently, the importance of the false vocal folds during normal phonationwas not appreciated. In general, they are considered to be used primarilyfor forceful laryngeal closure and they may be used excessively during



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pathologic conditions. Contrary to popular practice, however, surgeonsshould recognize that they cannot simply be removed without phonatory ef-

fects. The physics of airow through the larynx are complex, involving vortexshedding and sophisticated turbulence patterns that are essential to phona-tion. The false vocal folds provide a downstream resistance that is importantin this process, and they probably play a role in vocal tract resonance also.

Larynx: the intrinsic muscles

Intrinsic muscles are responsible for abduction, adduction, and tension of the vocal folds ( Figs. 3 and 4 ). All but one of the muscles on each side of thelarynx are innervated by one of the two recurrent laryngeal nerves. Becausethis nerve runs a long course from the neck down into the chest and back upto the larynx (hence the name ‘‘recurrent’’), it is easily injured by trauma,neck surgery, and chest surgery. Such injuries may result in abductor andadductor paralysis of the vocal fold. The remaining muscle, the cricothyroidmuscle, is innervated by the superior laryngeal nerve on each side, which isespecially susceptible to viral and traumatic injury. The recurrent and supe-rior laryngeal nerves are branches of the 10th cranial nerve, or vagus nerve.The superior laryngeal nerve branches o ff the vagus high in the neck at theinferior end of the nodose ganglion. It divides into an internal and external

Fig. 3. The intrinsic muscles of the larynx. ( From Satalo ff RT. Professional voice: the scienceand art of clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 143–77;with permission.)

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Fig. 4. Action of the intrinsic muscles. In the bottom four gures the directional arrows suggestmuscle actions but may give a misleading impression of arytenoid motion. These drawingsshould not be misinterpreted as indicating that the arytenoid cartilage rotates around a verticalaxis. The angle of the long axis of the cricoid facets does not permit some of the motion impliedin this gure. The drawing still provides a useful conceptualization of the e ff ect of individualintrinsic muscles, however, so long as the limitations are recognized. ( From Satalo ff RT. Profes-sional voice: the science and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing,Inc.; 2006. p. 143–77; with permission.)


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branch. The external branch supplies the cricothyroid muscle. An extensionof this nerve may also supply motor and sensory innervation to the vocal

fold. The internal branch is primarily responsible for sensation in the mu-cosa above the level of the vocal fold, but it may also be responsible forsome motor innervations of laryngeal muscles. The recurrent laryngealnerves branch o ff the vagus in the chest. On the left, the nerve usually loopsaround the aortic arch. On the right, it usually loops around the brachioce-phalic artery. This anatomic relationship is usually, but not always, present,and nonrecurrent recurrent nerves have been reported particularly on theright side, where they are more likely to be injured during neck surgery.There are interconnections between the superior and recurrent laryngeal

nerves, particularly in the region of the interarytenoid muscle.For some purposes, including electromyography, voice therapy, and sur-

gery, it is important to understand the function of individual laryngeal mus-cles in greater detail. The muscles of primary functional importance arethose innervated by the recurrent laryngeal nerve (thyroarytenoid, posteriorcricoarytenoid, lateral cricoarytenoid, and interarytenoid or arytenoideus)and the superior laryngeal nerve (cricothyroid) (see Figs. 3 and 4 ; Fig. 5 ).

The thyroarytenoid muscle adducts, lowers, shortens, and thickens thevocal fold, rounding the vocal fold edge. The cover and transition are e ff ec-

tively made more slack, whereas the body is sti ff ened. Adduction from

Fig. 5. The superior and recurrent laryngeal nerves branch from the vagus nerve and enter thelarynx.

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vocalis contraction is active, particularly in the membranous segment of thevocal folds. It tends to lower vocal pitch. The thyroarytenoid originates an-

teriorly from the posterior (interior) surface of the thyroid cartilage and in-serts into the lateral base of the arytenoid cartilage from the vocal process tothe muscular process. More specically, the superior bundles of the muscleinsert into the lateral and inferior aspects of the vocal process and run pri-marily in a horizontal direction. The anteroinferior bundles insert into theanterolateral aspect of the arytenoid cartilage from its tip to an area lateralto the vocal process. The most medial bers run parallel to the vocal liga-ment. There are also cranial bers that extend into the aryepiglottic fold.Anteriorly, the vertical organization of the muscle results in a twisted con-

guration of muscle bers when the vocal fold is adducted. The thyroaryte-noid muscle is divided into two compartments. The medial compartment isalso known as the vocalis muscle. It contains a high percentage of slowtwitch muscle bers. The lateral compartment has predominantly fast twitchmuscle bers. One may infer that the medial compartment (vocalis) is spe-cialized for phonation, whereas the lateral compartment (muscularis) is spe-cialized for vocal fold adduction, but these suppositions are unproven.

The lateral cricoarytenoid muscle is a small muscle that adducts, lowers,elongates, and thins the vocal fold. All layers are sti ff ened and the vocal fold

edge takes on a more angular or sharp contour. It originates on the upperlateral border of the cricoid cartilage and inserts into the anterior lateralsurface of the muscular process of the arytenoid. The interarytenoid muscle(arytenoideus, a medium-sized intrinsic muscle) primarily adducts the carti-laginous portion of the vocal folds. It is particularly important in providingmedial compression to close the posterior glottis. It has little e ff ect on thestiff ness of the membranous portion. The interarytenoid muscle consistsof transverse and oblique bers. The transverse bers originate from the lat-eral margin of one arytenoid and insert into the lateral margin of the oppo-

site arytenoid. The oblique bers originate from the base of one arytenoidinto the apex of the contralateral arytenoid.The posterior cricoarytenoid muscle abducts, elevates, elongates, and

thins the vocal fold by rocking the arytenoid cartilage posterolaterally. Alllayers are sti ff ened, and the edge of the vocal fold is rounded. It is the secondlargest intrinsic muscle. It originates over a broad area of the posterolateralportion of the cricoid lamina and inserts on the posterior surface of the mus-cular process of the arytenoid cartilage, forming a short tendon that coversthe cranial aspect of the muscular process.

When the superior laryngeal nerves are stimulated, the cricothyroid mus-cle moves the vocal folds into the paramedian position. It also lowers,stretches, elongates, and thins the vocal fold, sti ff ening all layers and sharp-ening the vocal fold’s contour. It is the largest intrinsic laryngeal muscle.The cricothyroid muscle is largely responsible for longitudinal tension, animportant factor in control of pitch. Contraction tends to increase vocalpitch. The cricothyroid muscle originates from the anterior and lateral



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portions of the arch of the cricoid cartilage. It has two bellies. The obliquebelly inserts into the posterior half of the thyroid lamina and the anterior

portion of the inferior cornu of the thyroid cartilage. The vertical (erect)belly inserts into the inferior border of the anterior aspect of the thyroidcartilage.

Intrinsic laryngeal muscles are skeletal muscles. All skeletal muscles arecomposed primarily of three types of bers. Type I bers are highly resistantto fatigue, contract slowly, anduse aerobic (oxidative) metabolism. They havelow glycogen levels, high levels of oxidative enzymes, and they are relativelysmaller in diameter. Type IIA bers use principally oxidative metabolismbut contain high levels of oxidative enzymes and glycogen. They contract rap-

idly but are also fatigue resistant. Type IIB bers are the largest in diameter.They use aerobic glycolysis primarily, containing much glycogen but rela-tively few oxidative enzymes. They contract quickly, but fatigue easily.

The ber composition of laryngeal muscles di ff ers from that of mostlarger skeletal muscles. Elsewhere, muscle ber diameters are fairly con-stant, ranging between 60 to 80 mm. In laryngeal muscles there is consider-ably more variability [7,8], and ber diameters vary between 10 and 100 mm,with an average of 40 to 50 mm. Laryngeal muscles have a higher proportionof Type IIA bers than most other muscles. The thyroarytenoid and lateral

cricothyroid muscles are particularly specialized for rapid contraction. Thelaryngeal muscles in general seem to have ber distributions and variationsthat make them particularly well suited to rapid contraction with fatigue re-sistance [9]. In addition, many laryngeal motor units have multiple neuralinnervation. There seem to be approximately 20 to 30 muscle bers per mo-tor unit in a human cricothyroid muscle [10], suggesting that the motor unitsize of this laryngeal muscle is similar to that of extraocular and facial mus-cles [11]. In the human thyroarytenoid muscle, 70% to 80% of muscle bershave two or more nerve endplates [12]. Some bers have as many as ve

nerve endplates. Only 50% of cricothyroid and lateral cricoarytenoid musclebers have multiple endplates, and multiple innervation is even less commonin the posterior cricoarytenoid (5%). It is still not known whether one mus-cle ber can be part of more than one motor unit (receive endplates fromdiff erent motor neurons) [9].

Larynx: extrinsic muscles

Extrinsic laryngeal musculature maintains the position of the larynx in

the neck. This group of muscles includes primarily the strap muscles. Be-cause raising or lowering the larynx may alter the tension or angle betweenlaryngeal cartilages, thereby changing the resting lengths of the intrinsicmuscles, the extrinsic muscles are critical in maintaining a stable laryngealskeleton so that the delicate intrinsic musculature can work e ff ectively. Inthe Western classically trained singer, the extrinsic muscles maintain the lar-ynx in a relatively constant vertical position throughout the pitch range.

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Training of the intrinsic musculature results in vibratory symmetry of thevocal folds, producing regular periodicity. This phenomenon contributes

to what the listener perceives as a ‘‘trained’’ sound.The extrinsic muscles may be divided into those below the hyoid bone (in-

frahyoid muscles) and those above the hyoid bone (suprahyoid muscles).The infrahyoid muscles include the thyrohyoid, sternothyroid, sterno-

hyoid, and omohyoid. The thyrohyoid originates obliquely on the thyroidlamina of the hyoid bone. Contraction brings the thyroid and hyoid bonecloser together, especially anteriorly. The sternothyroid muscle originatesfrom the rst costal cartilage and posterior aspect of the manubrium of the sternum, and it inserts obliquely on the thyroid cartilage. Contraction

of the sternothyroid muscle lowers the larynx. The sternohyoid muscle orig-inates from the clavicle and posterior surface of the manubrium of the ster-num, inserting into the lower edge of the body of the hyoid bone.Contraction of the sternohyoid muscle lowers the hyoid bone. The inferiorbelly of the omohyoid originates from the upper surface of the scapula andinserts into the intermediate tendon of the omohyoid muscle. The superiorbelly originates from the intermediate tendon and inserts into the greatercornu of the hyoid bone. The omohyoid muscle pulls down on the hyoidbone, lowering it.

The suprahyoid muscles include the digastric, mylohyoid, geniohyoid,and stylohyoid muscles. The posterior belly of the digastric muscle origi-nates from the mastoid process of the temporal bone and inserts into the in-termediate tendon, which connects to the hyoid bone. The anterior bellyoriginates from the inferior aspect of the mandible near the symphysisand inserts into the intermediate tendon. The anterior belly pulls the hyoidbone anteriorly and raises it. The mylohyoid muscle originates from the in-ner aspect of the body of the mandible (mylohyoid line) and inserts intoa midline raphe with bers from the opposite side. It raises the hyoid

bone and pulls it anteriorly. The geniohyoid muscle originates from themental spine at the mental symphysis of the mandible and inserts on the an-terior surface of the body of the hyoid bone. It raises the hyoid bone andpulls it anteriorly. The stylohyoid muscle originates from the styloid processand inserts into the body of the hyoid bone. It raises the hyoid bone andpulls it posteriorly. Coordinated interaction among the extrinsic laryngealmuscles is needed to control the vertical position of the larynx and other po-sitions, such as laryngeal tilt.

The supraglottic vocal tract

The supraglottic larynx, tongue, lips, palate, pharynx, nasal cavity (seeFig. 2 ), and possibly the sinuses shape the sound quality produced at thelevel of the vocal folds by acting as resonators. Minor alterations in the con-guration of these structures may produce substantial changes in voice qual-ity. The hypernasal speech typically associated with a cleft palate or the



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hyponasal speech characteristic of severe adenoid hypertrophy is obvious.Mild edema from an upper respiratory tract infection, pharyngeal scarring,

or muscle tension changes produce less obvious sound alterations. These areimmediately recognizable to a trained vocalist or astute critic, but they oftenelude the common listener.

The tracheobronchial tree, lungs, and thorax

The lungs supply a constant stream of air that passes between the vocalfolds and provides power for voice production. Singers often are thought of as having ‘‘big chests.’’ Actually, the primary respiratory di ff erence betweentrained and untrained singers is not increased total lung capacity, as is pop-ularly assumed. Rather, the trained singer learns to use a higher proportionof the air in his or her lungs, thereby decreasing his or her residual volumeand increasing respiratory e ffi ciency [13].

The abdomen

The abdominal musculature is the so-called ‘‘support’’ of the singingvoice, although singers generally refer to their support mechanism as theirdiaphragm. The function of the diaphragm muscle in singing is complex

and somewhat variable from singer to singer (or actor to actor). The dia-phragm primarily generates inspiratory force. Although the abdomen canalso perform this function in some situations [14], it is primarily an expira-tory-force generator. The diaphragm is co-activated by some performersduring singing and seems to play an important part in the ne regulationof singing [15]. Actually, the anatomy of support for phonation is compli-cated and not completely understood. The lungs and rib cage generatepassive expiratory forces under many common circumstances. Passive inspi-ratory forces also occur. Active respiratory muscles working in consort with

passive forces include the intercostal, abdominal wall, back, and diaphragmmuscles. The principle muscles of inspiration are the diaphragm, the exter-nal intercostal muscles that connect the bony ribs, and the interchondralportions of the internal intercostal muscles that connect the cartilaginousribs. Accessory muscles of inspiration include the pectoralis major; pector-alis minor; serratus anterior; subclavius; sternocleidomastoid; anterior, me-dial, and posterior scalenus; serratus posterior and superior; latissimusdorsi; and levatores costarum. During quiet respiration, expiration is largelypassive. Many of the muscles used for active expiration (forcing air out of

the lungs) are also used in support for singing and acting. Muscles of activeexpiration either raise the intra-abdominal pressure, forcing the diaphragmupward, or lower the ribs or sternum to decrease the dimension of the tho-rax, or both. They include the internal intercostals that connect the bonyribs, sti ff en the rib interspaces, and pull the ribs down; transversus thoracis,subcostal muscles, and serratus posterior inferior, all of which pull the ribsdown; and the quadratus lumborum, which depresses the lowest rib. In

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addition, the latissimus dorsi, which may also act as a muscle of inspiration,is capable of compressing the lower portion of the rib cage and can act as

a muscle of expiration and a muscle of inspiration. The above muscles allparticipate in active expiration (and support). The primary muscles of activeexpiration are the abdominal muscles, however. They include the externaloblique abdominus, internal oblique abdominus, rectus abdominus, andtransversus abdominus. The external oblique is a at broad muscle locatedon the side and front of the lower chest and abdomen. On contraction, it pullsthe lower ribs down and raises the abdominal pressure by displacing abdom-inal contents inward. It is an important muscle for support of singing andacting voice tasks. It should be noted that this muscle is strengthened by ab-

dominal exercises that involve the combination of rotation and contraction,and other exercises, but is not developed e ff ectively by traditional trunk curlsit-ups. Appropriate strengthening exercises of the external oblique musclesare often inappropriately neglected in voice training. The internal oblique isa at muscle in the side and front wall of the abdomen. It lies deep to the ex-ternal oblique. When contracted, the internal oblique drives the abdominalwall inward and lowers the lower ribs. The rectus abdominus runs parallelto the midline of the abdomen originating from the xiphoid process of thesternum and the fth, sixth, and seventh costal cartilages. It inserts into

the pubic bone. It is encased in the brous abdominal aponeurosis. Contrac-tion of the rectus abdominus lowers the sternum and ribs and stabilizes theabdominal wall. The transversus abdominus is a broad muscle located underthe internal oblique on the side and front of the abdomen. Its bers run hor-izontally around the abdomen. Contraction of the transverse abdominuscompresses the abdominal contents, elevating abdominal pressure.

The abdominal musculature receives considerable attention in vocaltraining. The purpose of abdominal support is to maintain an e ffi cient, con-stant power source and inspiratory–expiratory mechanism. There is dis-

agreement among voice teachers as to the best model for teaching supporttechnique. Some experts describe positioning the abdominal musculatureunder the rib cage; others advocate distension of the abdomen. Eithermethod may result in vocal problems if used incorrectly, but distendingthe abdomen (the inverse pressure approach) is especially dangerous, be-cause it tends to focus the singer’s muscular e ff ort in a downward and out-ward direction, which is ine ff ective. The singer thus may exert considerableeff ort, believing he or she is practicing good support technique, without ob-taining the desired e ff ect. Proper abdominal muscle training is essential to

good singing and speaking, and the physician must consider abdominalfunction when evaluating vocal disabilities.

The musculoskeletal system

Musculoskeletal condition and position a ff ect the vocal mechanism andmay produce tension or impair abdominal muscle function, resulting in



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voice dysfunction. Stance deviation, such as from standing to supine, pro-duces obvious changes in respiratory function. Lesser changes, such as dis-

tributing one’s weight over the calcaneus rather than forward over themetatarsal heads (a more athletic position), alter the conguration of theabdominal and back musculature enough to adversely inuence the voice.Tensing arm and shoulder muscles promotes cervical muscle strain, whichcan adversely a ff ect laryngeal function. Careful control of muscle tensionis fundamental to good vocal technique. In fact, some teaching methodsuse musculoskeletal conditioning as the primary focus of voice training.

The psychoneurologic system

The psychologic constitution of the singer impacts directly on the vocalmechanism. Psychologic phenomena are reected through the autonomicnervous system, which controls mucosal secretions and other functions crit-ical to voice production. The nervous system is also important for its medi-ation of ne muscle control. This fact is worthy of emphasis, becauseminimal voice disturbances may occasionally be the rst sign of serious neu-rologic disease.

Physiology

The physiology of voice production is exceedingly complex and is sum-marized only briey in this article. Greater detail may be found elsewhere[1,16–21] .

Overview of phonatory physiology

Volitional voice production begins in the cerebral cortex. Complex inter-

actions among centers for speech, musical expression, and artistic expressionestablish the commands for vocalization. The idea of the planned vocaliza-tion is conveyed to the precentral gyrus in the motor cortex, which transmitsanother set of instructions to motor nuclei in the brainstem and spinal cord.These areas transmit the complicated messages necessary for coordinatedactivity of the larynx, thoracic, and abdominal musculature and of the vocaltract articulators and resonators. Additional renement of motor activity isprovided by the extrapyramidal (cerebral cortex, cerebellum, and basal gan-glion) and autonomic nervous systems. These impulses combine to produce

a sound that is transmitted not only to the ears of listeners but also to thoseof the speaker or singer. Auditory feedback is transmitted from the ear tothe cerebral cortex by way of the brainstem, and adjustments are made topermit the vocalist to match the sound produced with the intended sound.There is also tactile feedback from the throat and other muscles involvedin phonation that undoubtedly help in ne-tuning vocal output, althoughthe mechanism and role of tactile feedback are not fully understood. In

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many trained singers, the ability to use tactile feedback e ff ectively is culti-vated as a result of frequent interference with auditory feedback by ancillary

noise in the concert environment (eg, an orchestra or band).The voice requires interactions among the power source (the lungs, ab-

dominal and back muscles, and the vocal folds), the oscillator, and the res-onator. The power source compresses air and forces it toward the larynx.The mucosal cover of the vocal folds opens and closes when the vocal foldsare in the adducted state, permitting small bursts of air to escape betweenthem. Numerous factors a ff ect the sound produced at the glottal level, in-cluding the pressure that builds below the vocal folds (subglottal pressure),the amount of resistance to opening the glottis (glottal impedance), volume

velocity of air ow at the glottis, and supraglottal pressure. The vocal foldsdo not vibrate like the strings on a violin. Rather, they separate and collidesomewhat like buzzing lips. The number of times they do so in any givensecond (ie, their frequency) determines the number of air pu ff s that escapeand, thus, the pitch of the voice. The frequency of glottal closing and open-ing is one factor in determining vocal quality. Other factors a ff ect loudness,such as subglottal pressure, glottal resistance, and amplitude of vocal folddisplacement from the midline during each vibratory cycle. The sound cre-ated at the vocal fold level is a buzz, similar to the sound produced when

blowing between two blades of grass. This sound contains a complete setof harmonic partials and is responsible in part for the acoustic characteris-tics of the voice. Complex and sophisticated interactions in the supraglotticvocal tract may accentuate or attenuate harmonic partials, acting as a reso-nator. This portion of the vocal tract is largely responsible for the beautyand variety of the sound produced.

Interactions among the various components of the vocal tract ultimatelyare responsible for all the vocal characteristics produced. Many aspects of the voice still lack complete understanding and classication. Vocal range

is reasonably well understood, and broad categories of voice classicationsare generally accepted. Other characteristics, such as vocal register, are con-troversial. Registers are expressed as quality changes within an individualvoice. From low to high, they may include vocal fry, chest voice, middlevoice, head voice, falsetto, and whistle, although not everyone agrees thatall categories exist. The term modal register, used most frequently in speechterms, refers to the voice quality generally used by healthy speakers, as op-posed to a low, gravelly vocal fry or high falsetto.

Vibrato is a rhythmic variation in frequency and intensity. Its exact

source remains uncertain, and its desirable characteristics depend on voicerange and the type of music sung. It seems most likely that the frequencymodulations are controlled primarily by intrinsic laryngeal muscles, espe-cially the cricothyroid and adductor muscles. Extrinsic laryngeal musclesand muscles of the supraglottic vocal tract may also play a role. Intensityvariations may be caused by variations in subglottal pressure, glottal adjust-ments that a ff ect subglottal pressure, secondary e ff ects of the frequency



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variation because of changes in the distance between the fundamental fre-quency and closest formant, or rhythmic changes in vocal tract shape that

cause uctuations in formant frequencies. When evaluating vibrato, it ishelpful to consider the waveform of the vibrato signal, its regularity, extent,and rate. The waveform is usually fairly sinusoidal, but considerable varia-tion may occur. The regularity, or similarity, of each vibrato event to previ-ous and subsequent vibrato events is greater in trained singers than inuntrained voice users. This regularity seems to be one of the characteristicsperceived as a trained sound. Vibratory extent refers to deviation from thestandard frequency (not intensity variation) and is usually less than 0.1semitone in some styles of solo and choral singing, such as Renaissance mu-

sic. For most well-trained Western operatic singing, the usual vibrato extentat comfortable loudness is 0.5 to 1 semitone for singers in most voice clas-sications. Vibrato rate (the number of modulations per second) is generally5 to 7. Rate may also vary greatly from singer to singer, and in the samesinger. Vibrato rate can increase with increased emotional content of thematerial, and rate tends to decrease with older age (although the age atwhich this change occurs is highly variable). When variations from the cen-tral frequency become too wide, a wobble in the voice is perceived; this isgenerally referred to as tremolo. It is not generally considered a good musi-

cal sound, and it is unclear whether it is produced by the same mechanismsresponsible for normal vibrato. Ongoing research should answer many of the remaining questions.

Respiration

Basic functions of the nose, larynx, and elemental concepts of inspirationand expiration are discussed elsewhere [1]. A brief review of selected aspectsof pulmonary function is included here to assist readers in understanding the

processes that underlie support and in understanding pulmonary disordersand their assessment.Starting from the mouth, the respiratory system consists of progressively

smaller airway structures. The trachea branches at the carina into mainstembronchi, which then branch into progressively smaller bronchial passagesand terminate in alveoli. Gas exchange between the lungs and the blood-stream occurs at the alveolar level. Air moves in and out of the alveoli topermit this exchange of gases. Air is forced out of the alveoli also to createthe air stream through which phonation is produced. Ultimately, alveolar

pressure is the primary power source for phonation and is responsible forthe creation of the subglottal pressure involved in phonation. Alveolar pres-sure is actually greater than subglottal pressure during phonation and expi-ration because some pressure is lost because of the airway resistancebetween the alveoli and the larynx. As the air passes from the alveoli, it en-ters rst the bronchioles, which are small, collapsible airways surrounded bysmooth muscle but devoid of cartilage. From the bronchioles, air passes to

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progressively larger components of the bronchial tree and eventually to thetrachea. These structures are supported by cartilage and are not fully col-

lapsible, but they are compressible and respond to changes in external pres-sure during expiration and inspiration. During expiration, the pressure inthe respiratory system is greatest in the alveolus (alveolar pressure) and leastat the opening of the mouth where pressure is, theoretically, equal to atmo-spheric pressure. Theoretically, all pressure is dissipated between the alveo-lus and the mouth during expiration because of airway resistance betweenthese structures. Expiration pressure is the total of the elastic recoil com-bined with active forces created by muscular compression of the airway.The active pressure is distributed throughout all the components of the air-

way, although it may exert greater e ff ect on the alveoli and bronchioles be-cause they are fully collapsible. When the airway is opened, the air pressurein the alveoli (alveolar pressure) is equal to the atmospheric pressure in theroom. To ll the alveoli, the alveolar pressure must be decreased to less thanatmosphere pressure, creating a vacuum that sucks air into the lungs. Tobreathe out, alveolar pressure must be greater than atmospheric pressure.As discussed above, there are passive and active forces operative duringthe inspiratory–expiratory process.

To clarify the mechanisms involved, the alveoli may be thought of as tiny

balloons. If a balloon is lled with air, and the lling spout is opened, theelastic properties of the balloon allow most of the air to rush out. This pro-cess is analogous to passive expiration, which relies on the elastic propertiesof the alveoli themselves. Alternatively, we may wrap our hands around theballoon and squeeze the air out. This squeezing may allow us to get the airout faster and more forcefully, and it allows us to get more of the air out of the balloon than is expelled through the passive process alone. This processis analogous to active expiration, which involves the abdominal, chest, andback muscles. If we partially pinch the lling spout of the balloon, air comes

out more slowly because the outow tract is partially blocked. The air alsotends to whistle as it exits the balloon. This situation is analogous to ob-structive pulmonary disease, and its commonly associated wheeze. If wetry to blow up the balloon while our hands are wrapped around it, the bal-loon is more di ffi cult to inate and cannot be inated fully because it is re-stricted physically by our hands. This phenomenon is somewhat analogousto restrictive lung disease. Under these circumstances, it may also take morepressure to ll the balloon, because the lling process must overcome the re-stricting forces. Under any of these circumstances, the more we ll the alve-

olar ‘‘balloon,’’ the greater the pressure, as long as the balloon is notruptured. When the pressure is greater, the increased elastic recoil resultsin more rapid and forceful air escape when the air is released. The pressureinside the balloon can be increased even above its maximal elastic recoil levelsimply by squeezing the outside of the balloon. This analogy is helpful in un-derstanding the forces involved in breathing (especially expiration) and ingenerating support for phonation.



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Although inspiration is extremely important, this discussion concen-trates primarily on expiration, which is linked closely to support for speech

and singing. The elastic component of expiratory pressure (specically, al-veolar pressure) depends on lung volume and the elastic forces exerted bythe chest and the lungs. The lung is never totally deated. At rest the lungis inated to about 40% of total lung capacity (TLC). The amount of airin the lungs at rest is the functional residual capacity (FRC). At FRC, thethorax (chest cavity) is at a volume much less than its rest (or neutral) pos-ture, which is actually closer to 75% of TLC. At FRC the thorax hasa passive tendency to expand, as happens during inspiration. Conversely,at FRC, the lung would collapse if it were not acted on by other forces.

The collapsing elastic forces of the lung are balanced by the expandingelastic forces of the thorax. The lung and thorax interact closely, and theirrelative positions of contact vary constantly. This situation is facilitated bythe anatomy of their boundary zone. The inner surface of the thorax iscovered by the parietal pleura, and the lung is covered by the visceralpleura. A thin layer of pleural uid exists between them. Hydrostaticforces hold these surfaces together while allowing them to slide freely. Un-der pathologic circumstances (eg, following surgery or radiation) these sur-faces may stick together, impairing lung function and a ff ecting support for

phonation adversely.Thoracic and lung elastic behavior can be measured. The basic principlefor doing so involves applying pressure and noting the volume changescaused by the pressure. This change creates a pressure/volume (P/V) curve.The slope with the P/V curve for the thorax reects its compliance (C CW )and the slope of the P/V curve for the lung represents its compliance(C L ). When pressure is applied to the entire system a di ff erent P/V curveis created and its slope reects the compliance of the entire respiratory sys-tem (C RS ). Starting from FRC, if air is expelled such that the volume of the

system is dropped below FRC, an expanding (negative pressure) force is cre-ated. The magnitude of this expanding force is increased as the volume de-creases. Conversely, during inspiration greater than FRC, collapsing(positive pressure) forces increase with increasing volume.

When one inspires, volumes increase well above FRC. Passive expiration,such as occurs during quiet breathing, occurs when one relaxes the dia-phragm. The passive elastic recoil forces air out of the alveoli, because inat-ing them has created an alveolar pressure that is greater than atmosphericpressure (and is predictable using the P/V curve). The deeper the inspiration,

the greater the di ff erence between alveolar and atmospheric pressure, andthe elastic recoil and the expiratory air pressure are greater as a consequence.Inspiration from FRC is an active process, primarily. Thoracic muscles ele-vate the ribs and increase the diameter of the thorax. The external intercos-tal muscles are important to this process. Inspiration also involvescontraction of the diaphragm muscle, which attens and also increases in-trathoracic volume.

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Active expiration is created by forces that decrease thoracic volume. Ac-tive expiration is achieved by muscles that pull the ribs down or compress

the abdominal contents, pushing them upward and thus making the volumeof the thorax smaller. The principle muscles involved are the internal inter-costal muscles, abdominal, back, and other muscles, as reviewed earlier inthis chapter.

For projected phonations, such as singing or acting, airow is achievedthrough active expiration. After inspiration, elastic recoil and external forcescreated by expiratory muscles determine alveolar pressure, which is substan-tially greater than atmospheric pressure. The combination of passive (elas-tic) and active (muscular) forces pushes air out against airway resistance.

As the pressure decreases on the path from alveolar to atmospheric (atthe mouth) pressure, there is a point along that path at which the pressureinside the airway equals the active expiratory pressure (without the elasticrecoil component), which is called the equal pressure point (EPP). As expi-ration continues toward the mouth, pressure drops below the EPP. As air-way pressure diminishes below the EPP, the airway collapses. Thisphysiologic collapse of the airway increases airway resistance by decreasingthe diameter of the airway. The greater the active expiratory forces, thegreater the airway compression after the EPP has been passed. Expiratory

pressure and airway compression are important for control of expiratoryairow rate and are inuenced by EPP.Under normal circumstances, the EPP is reached in the cartilaginous por-

tion of the airway, which does not collapse completely ordinarily, even dur-ing forceful expiration This part of the physiologic mechanism allows one tocontinue to sing while running out of air. Under pathologic circumstances,however, the location of the EPP may have shifted. Asthma is the classic ex-ample. During bronchospasm or bronchoconstriction, the diameters of thebronchioles are narrowed by smooth muscle contraction and airway resis-

tance in the bronchioles is increased. As the air moves from the alveoliinto the bronchioles, airway pressure diminishes more quickly than normaland EPP may be reached closer to the alveoli and bronchioles, which col-lapse more easily and more completely. In severe circumstances, the distalairway may collapse fully, trapping air in the alveoli and causing hyperina-tion of the lungs. Expiratory airow rate is lowered substantially by the in-creased resistance in the distal airway, resulting in a lower-than-normalsubglottic pressure. This phenomenon can have profoundly adverse e ff ectson phonation.

Other lung dysfunction can also impair subglottal pressure, even if air-way resistance is normal. The classic example is emphysema, which occurscommonly in smokers. This condition results from damage to the alveoliin which the alveolar walls are destroyed and elasticity is lost. Destructionof the alveolar walls e ff ectually causes coalescence of multiple alveoli intoone large alveolar structure, with collagen deposition and scarring in areaswhere elastic bers were once deposited. Consequently, because elastic recoil



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pressures are lower and the alveolar volume is greater, alveolar pressure isdecreased compared with normal. Even if the active expiratory forces are

normal, the diminished alveolar pressure results in a lower pressure gradientbetween alveolar and atmospheric pressure over the same airway distance,shifting the location of the EPP distally toward or into collapsable airways.Even when active expiratory e ff orts are increased under these circumstancesthey do not help because they collapse the distal airways, trapping air in thealveoli and diminishing subglottal pressure.

Summary

This overview highlights only some of the more important components of lower respiratory physiology. Laryngologists should bear these principles inmind in understanding the importance of diagnosis and treatment of respi-ratory dysfunction in voice professionals. In patients who have ‘‘Olympicvoice demands,’’ even slight changes from optimal physiology may haveprofound consequences on phonatory function that are responsible com-monly for hyperfunctional compensatory e ff orts. If one treats voice hyper-function as if it were the primary problem, failing to recognize that it maybe secondary to an underlying organic or pulmonary disorder, then treat-ment will not be successful in the long term and preventable voice dysfunc-tion and vocal fold injury may ensue.

References

[1] Satalo ff RT. Clinical anatomy and physiology of the voice. In: Satalo ff RT, editor. Profes-sional voice: the science and art of clinical care. 3rd edition. San Diego (CA): Plural Publish-ing, Inc.; 2005. p. 143–78.

[2] Hirano M. Structure and vibratory pattern of the vocal folds. In: Sawashima N, Cooper FS,editors. Dynamic aspects of the speech production. Tokyo: University of Tokyo Press; 1977.p. 13–27.

[3] Hirano M. Surgical anatomy and physiology of the vocal folds. In: Gould WJ, Satalo ff RT,Spiegel JR, editors. Voice surgery. St. Louis (MO): Mosby-Year Book; 1993. p. 135–58.

[4] Hirano M, Yoshida T, Kurita S, et al. Anatomy and behavior of the vocal process. In: BaerT, Sasaki C, Harris K, editors. Laryngeal function in phonation and respiration. Boston:College-Hill Press; 1987. p. 1–13.

[5] Gray S. Basement membrane zone injury in vocal nodules. In: Gau ffin J, Hammarberg B,editors. Vocal fold physiology: acoustic,perceptual andphysiologic aspects of voice mechan-ics. San Diego (CA): Singular Publishing Group; 1991. p. 21–7.

[6] Sundberg J. The acoustics of the singing voice. Sci Am 1977;236(3):82–91.[7] Brooke MH, Engle WK. The histographic analysis of human muscle biopsies with regard to

bre types. 1. Adult male and female. Neurology 1969;19:221–33.[8] Sadeh M, Kronenberg J, Gaton E. Histochemistry of human laryngeal muscles. Cell Mol

Biol 1981;27:643–8.[9] Lindestad P. Electromyographic and laryngoscopic studies of normal and disturbed vocal

function. Stockholm: Suddinge University; 1994. 1–12.

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[10] English ET, Blevins CE. Motor units of laryngeal muscles. Arch Otolaryngol 1969;89:778–84.

[11] Faaborg-Andersen K. Electromyographic investigation of intrinsic laryngeal muscles inhumans. Acta Physiol Scand 1957;41(Suppl 140):1–149.

[12] Rossi G, Cortesina G. Morphological study of the laryngeal muscles in man: insertions andcourses of the muscle bers, motor end-plates and proprioceptors. Acta Otolaryngol(Stockh) 1965;59:575–92.

[13] Gould WJ, Kamura H. Static lung volumes in singers. Ann Otol Rhinol Laryngol 1973;82:89–95.

[14] Hixon TJ, Ho ff man C. Chest wall shape during singing. In: Lawrence V, editor. Transcriptsof the seventh annual symposium, care of the professional voice. New York: The VoiceFoundation; 1978;1:9–10.

[15] Sundberg J, Leanderson R, von Euler C. Activity relationship between diaphragm andcricothyroid muscles. J Voice 1989;3(3):225–32.

[16] Letson JA, Tatchell R. Arytenoid movement. In: Satalo ff RT, editor. Professional voice: thescience and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006.p. 179–94.

[17] Baken RJ. An overview of laryngeal function for voice production. In: Satalo ff RT, editor.Professional voice: the science and art of clinical care. 3rd edition. San Diego (CA): PluralPublishing, Inc.; 2006. p. 237–56.

[18] Scherer RC. Laryngeal function during phonation. In: Satalo ff RT, editor. Professionalvoice: the science and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing,Inc.; 2006. p. 257–74.

[19] Sundberg J. Vocal tract resonance. In: Satalo ff RT, editor. Professional voice: the science

and art of clinical care. 3rd edition. San Diego (CA): Plural Publishing, Inc.; 2006. p. 275–92.[20] Bhatia R, Hawkshaw MJ, Satalo ff RT. Chaos in voice research. In: Satalo ff RT, editor.Professional voice: the science and art of clinical care. 3rd edition. San Diego (CA): PluralPublishing, Inc.; 2006. p. 293–302.

[21] Baken RJ. Dynamical disorders of voice: a chaotic perspective on vocal irregularities. In:Satalo ff RT, editor. Professional voice: the science and art of clinical care. 3rd edition.San Diego (CA): Plural Publishing, Inc.; 2006. p. 303–20.


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