▪ Laryngeal Skeleton

The larynx is composed of three pairs of small cartilages (arytenoid, corniculate, cuneiform) and three large unpaired cartilages (thyroid, cricoid, epiglottis). Figure 10.2 illustrates these structures and their interconnecting membranes and ligaments. The trachea directly links the larynx with the lungs. There are two synovial articulations or laryngeal joints: cricothyroid and cricoarytenoid. Hinge-like action of the former paired joints increases the anteroposterior length of the vocal folds. This adjustment results in increased tension and reduced cross-sectional mass of these structures; most notably influential during pitch variations in speech and song. The primary action of the latter joints is rocking motion of the arytenoids; anteromedial action is of paramount importance for vocal fold adduction, and posterolateral action is essential for vocal fold abduction. There is little evidence in the scientific literature to support classic textbook descriptions of rotary and gliding motions of the arytenoid cartilages during voice production or other valving activities.

Figure 10.2 Cartilaginous framework of the larynx, with associated ligaments and membranes.

▪ Laryngeal Muscles

Figures 10.3 and 10.4 illustrate the various intrinsic and extrinsic muscles of the larynx, respectively. Suffice it to say that the true vocal folds arise from or are components of the thyroarytenoid muscle bundles. The intrinsic group of muscles work harmoniously to open, close, tense, and relax the vocal folds during breathing, swallowing, and speaking. Although this entire group probably works in a coordinated and collective manner to achieve these movements; for ease of review, specific functions can be attributed to individual components. That is, contractions of the thyroarytenoid, lateral cricoarytenoid, and interarytenoid muscles generally contribute to vocal fold adduction. As noted earlier, the cricothyroid muscles chiefly lengthen and tense the vocal folds, which decreases their cross-sectional mass. Posterior cricoarytenoid muscle contractions are critical for vocal fold abduction, associated with deep breaths and cessation of vibrations during running speech to accommodate the demands of voiceless consonant production and to terminate voicing at the completion of an utterance.

Figure 10.3 Intrinsic laryngeal muscles.

Figure 10.4 Extrinsic laryngeal muscles.

The extrinsic muscles can be divided into two subgroups: suprahyoids and infrahyoids. In general, these elongated, strap-like muscles help to stabilize and alter the position of the larynx in the neck through anatomic linkages with neighboring head, neck, and chest structures. Contractions of the former group tend to pull the larynx anterosuperiorly, especially during swallowing and upward pitch adjustments during singing. Conversely, contractions of the infrahyoid muscles act to lower the larynx, such as during descending pitch production. It is important to note that anatomic or physiological alterations involving these extrinsic muscles, as may occur with head and neck cancer surgery, can contribute to substantial swallowing difficulties, and, to a lesser extent, limited pitch range during singing.

▪ The Vocal Folds

Figure 10.5 demonstrates the normally white and glistening appearances of the true vocal folds within the framework of the thyroid cartilage. The space between the vocal folds is called the glottis, and it varies in its anterior and posterior dimensions during various biological and phonatory behaviors. The vocal folds consist: of (1) an outermost layer of mucosa and stratified, nonkeratinizing squamous epithelium, known as the cover, and (2) deeper layers, which contain the aforementioned thyroarytenoid muscle fibers, as well as high density fibroblasts and elastic and collagenous tissues. Immediately deep to the cover there exists a potential space known as Reinke’s area, which consists mainly of amorphous material with few fibroblasts or elastic tissue. Later in the chapter, we will discuss the biomolecular make-up of the endolarynx and true vocal folds, particularly as it pertains to the presence or absence of mast cells and eosinophils, which normally mediate allergic inflammation in other components of the respiratory subsystem.

Figure 10.5 Videostroboscopic image of the right (R) and left (L) vocal folds.

Hirano described the cover-body concept of vocal fold vibration.¹² His elaborate explanations more than 30 years ago have been instrumental in the development of modern phonosurgical procedures for benign vocal fold pathologies. Because Reinke’s space possesses a gelatinous consistency, it enables fluid vibratory motion of the cover over the vocal fold body (thyroarytenoid muscle fibers) during phonation. Detailed appraisal of such activity can be achieved in the clinical setting using laryngovideostroboscopy. This quasi-slow motion imaging technique reveals traveling waves of mucosa from the inferior to superior surface of the vocal folds. Scarred or fibrotic vocal folds, as a result of invasive benign or malignant pathologies, do not produce normal mucosal waves.

▪ Peripheral Laryngeal Innervation

Volitional voice production depends upon a complex loop of neural interactions between the central nervous system, peripheral nervous system, and various respiratory and speech musculature. Kotby et al¹³ described a six-level hierarchy of laryngeal neuromuscular integration. Of these interrelated segments, the higher levels generally function to activate, inhibit, and modulate output of the lower levels for purposeful voice production. Some of the lower level activities are organized into reflex pathways. Based on a top-down model of control, conceptual programming of speech and voice occurs at the highest level. At the cerebellar level below, movement adjustments are coordinated, and errors are detected and corrected for accurate performance. The pyramidal or upper motor neuron system serves the next level of function as the primary initiator of all muscular contractions through synapses with motor nuclei of all cranial and spinal nerves normally involved in speech production. The extrapyramidal level functions as an ongoing, automatic and subconscious regulator of all sensorimotor outputs and underlying muscle tone, via complex loop circuitry between the central and peripheral nervous system. The vestibular–reticular level helps to activate and regulate motor inputs to and sensory outputs from the cranial and spinal nerves (lower motor neurons) and the muscles responsible for speech and voice production. The lower motor neurons represent the lowest level of this integrated system. They form motor units within the muscle tissues they innervate to stimulate muscle contractions for volitional movement purposes.

The vagus or Xth cranial nerve pair arise from the medulla on the brain stem. They descend into the neck through the jugular foramen, and distribute three primary branches that help control and regulate voice and speech activities: (1) pharyngeal nerve, (2) superior laryngeal nerve, and (3) recurrent laryngeal nerve. The first of these branches provides nerve fibers to the pharynx and most of the soft palate. The second branch contains an internal and external laryngeal nerve component. The former one enters the larynx and divides into two additional branches, both of which contain sensory fibers from the mucous membranes that line the endolarynx above the vocal folds, and from neighboring muscles’ spindles and stretch receptors. The external branch is the chief motor nerve supply of the cricothyroid (pitch changing) muscle and inferior constrictor muscles of the pharynx. The recurrent laryngeal nerve or third primary branch of the vagus nerve, descends past the larynx and then loops back up to provide motor innervation to all of the other intrinsic laryngeal muscles. Whereas the right recurrent nerve loops under the ipsilateral subclavian artery en route to the larynx, the left one descends more inferiorly in the chest, deep to and winding under the arch of the aorta, before it ascends in the tracheoesophageal groove to enter the larynx behind the cricothyroid joint on either side. In addition to its widespread motor inputs, it supplies sensory filaments to the mucous membranes within the lining of the subglottis, immediately below the vocal folds. These fibers transmit afferent output from these tissues as well as stretch receptors in the surrounding musculature.

Mechanoreceptors mediated by the recurrent and superior laryngeal nerves are abundantly located within the mucosal lining, muscles, and joints of the larynx. These sensory elements influence respiratory and vegetative reflexes, and they contribute to what may be termed the intrinsic laryngeal monitoring system, as they relay oscillating discharges to the lower brain stem in response to air pressure fluctuations that occur during voice production. Polysynaptic loops are then formed with the motor neuron pools of the vagus nerve at this level to establish the so-called tonic servo-reflex system of the larynx.¹⁴ Figure 10.6 offers a schematic representation of these hierarchical neurologic pathways associated with voice production. For more detailed reviews of the neurologic substrates of phonation, the reader is referred to other sources.^15,16

Figure 10.6 Central and peripheral nervous system interactive substrates of voice production.

▪ Voice Production

As shown in Figure 10.1, vocal fold vibrations during speech efforts send a traveling wave of acoustic energy upstream through the vocal tract. This pathway, which includes the oral and nasal cavities, acts as a resonating chamber to enhance, absorb, and reflect the sounds generated into distinctive voice qualities. The infraglottal tract consists of the respiratory musculature, lungs, trachea, and immediate subglottis. These structures function as a collective power source for phonation by providing ongoing airflow dynamics required to drive vocal fold vibrations during speech efforts. The vibratory activity itself is largely a passive act. That is to say, at the start of a vibratory cycle the vocal folds are volitionally preset in an adducted position at the midline of the glottis. Assuming the lungs have been supplied with a sufficient amount of inspired air in preparation for speech, pressure increases within the trachea with expiratory effort to generate upstream airflow to induce vocal fold vibrations and voice. When subglottic pressure exceeds the level of resistance created by the adducted vocal folds, a puff of air is emitted into the vocal tract. This momentary break in the glottal seal initiates the vacuumous Bernoulli effect. This aerodynamic phenomenon results from increases in the velocity of air molecules passing through the narrow glottic inlet. As this occurs, air pressure between the vocal folds decreases, which, in turn, induces glottic closure to complete the vibratory cycle (closed–open–closed). This wave is assisted by intrinsic laryngeal myoelastic properties. Sustained phonation depends upon adequate intrinsic laryngeal muscle and elastic glottal closing forces, and sufficient and continuous infraglottal airflow support to initiate and drive vocal fold vibrations.

▪ Parameters of Voice

Quality, loudness, and pitch are the primary parameters of human voice. Quality represents the overall timbre or pleasantness of voice. The rhythm and symmetry of vocal fold vibrations, and the adequacy of glottal closure, significantly influences vocal quality. Irregular motion and glottal incompetence during the closed phases of vibration usually result in escapes of unphonated air, which distorts the voice signal. Hoarse, harsh, raspy, breathy, wet-gurgly, spasmodic, and tremorous, are common terms used to classify vocal quality disorders. The speech diagnostic terms hyponasality and hypernasality are sometimes used within this context of vocal quality disturbances. However, these disorders result from upstream velopharyngeal and nasal cavity disturbances.

Vocal loudness, also referred to as intensity, is measured in decibles (dB). This parameter largely depends on the degree of subglottal pressure, glottal resistance created by the adductory forces of the intrinsic laryngeal muscles, transglottal airflow rate, and amplitude or excursion of the vocal folds from the midline of the glottis during the open phases of vibration. Generally, increases in the degree of these variables produce perceptually louder voice, and vice versa. A voice that is habitually either too loud, too soft, limited in range (monoloud), or characterized by unusual volume outbursts represents abnormal loudness control.

Vocal pitch is measured in cycles per second or Hertz (Hz). It is directly related to the frequency of vocal fold vibrations; the faster the cyclic speed the higher the pitch, and vice versa. Intrinsic laryngeal muscle contractions that alter the length, tension, and cross-sectional mass of the vocal folds significantly influence pitch adjustments during speaking and singing. When the vocal folds are lengthened, they are concurrently under more tension and their cross-sectional mass is reduced. These biomechanical alterations promote faster vibratory speed, and thus higher pitched voice. Conversely, when the vocal folds are shortened, intrinsic tension is reduced and cross-sectional mass is increased. These biomechanical alterations retard the speed of vocal fold vibrations, and thus contribute to the production of lower pitched voice. These opposing physiological phenomena can be envisioned by stretching and relaxing a rubber band, and alternately plucking it to appreciate the differences in the speed of vibration and the perceived pitch under each associated condition. Adult females normally generate an habitual pitch of 256 Hz; equivalent to the middle “C” note on the piano keyboard. Male counterparts habitually vocalize at approximately one half this speed, one full octave below middle C. Abnormalities in pitch control are usually categorized as either too high or too low for the individual’s age and sex. Limited pitch range (monotone) and unusual pitch outbreaks (shrill) are also problems of concern.

It is important to note that in addition to the aforementioned biomechanical vocal fold and respiratory activities, voice output is also significantly influenced by the dynamic adjustments in the shape of the supraglottic larynx, pharynx, and oral and nasal cavities during speaking and singing. These vocal tract components variably enhance and attenuate sound energy levels at various frequencies of production. Because each of us possesses a unique anatomic configuration of this complex system, we accordingly exhibit voice attributes that are easy to identify perceptually and distinguish us from all other speakers.

▪ Team Approach

A team approach to the evaluation and treatment of patients with suspected laryngeal allergic sequelae is usually most successful. Members in this effort should minimally include an allergy physician with a background in otolaryngology or immunology, a speech-language pathologist with expertise in the area of vocal pathologies, and a nurse practitioner. The diagnosis of chronic allergic laryngitis should be considered for patients who present with histories of upper respiratory allergies and co-occurring phonation subsystem disturbances, such as globus sensations, excessive laryngeal mucus and reactive throat clearing and coughing behaviors, dry-itchy throat, and voice difficulties. With this clinical population, the history component of the examination usually produces the most indispensable diagnostic data. In this vein, the exploration of antecedent events or triggers of allergy symptoms almost always proves to be of paramount importance to accurate diagnoses, as does the time course or seasonality of such complaints. Whether the patient suffers from any co-occurring diseases, such as asthma, otitis media, sinusitis, and chronic acid reflux, should be evaluated because these conditions can exacerbate the underlying allergy. Prior or current use of medical or complementary therapies to treat these problems should be factored into the differential diagnostic and subsequent management equations.

After a thorough review of the patient’s background history, the physician should conduct a comprehensive physical examination, with special attention paid to the tympanic membranes and middle ears for signs of effusion. Next, the nose should be examined to determine the presence of edema, mucosal paleness or hyperemia, mucoid or mucopurulent rhinorrhea, or nasal polyps. Such findings may be sequelae to allergic rhinitis. The status of the pharynx should be evaluated next for signs of lymphoid hypertrophy or prominent lateral pharyngeal bands. The head and neck exam is usually completed with mirror or fiberoptic examination of the larynx to rule out significant laryngeal pathology, which may require closer analysis via videolaryngostroboscopy. The latter instrumentation technique is often performed by a speech-language pathologist, in consultation with the referring physician. During this examination, vocal fold biomechanics and glottal, supraglottal, and perilaryngeal tissue appearances are appraised for significant variations from normal characteristics. Oftentimes, for patients with notable dysphonia at presentation, additional voice laboratory studies are indicated, including acoustic and speech aerodynamic analyses, and voice sampling using a high quality (e.g., digital) audiotape format. If allergy is suspected following analyses by team members of all examination results, serum (in vitro) or skin testing should be conducted to confirm the presence and types of allergies.

In general, dysphonia can develop acutely or gradually. In some cases, voice difficulties are intermittent. In others, the problem is more persistent. The severity of the disturbance is not necessarily correlated with the frequency of symptoms. Patients with transient dysphonia may present with severely abnormal voice characteristics; those with more chronic conditions may exhibit only mild difficulty, and vice versa. In all cases, the degree of dysphonia may worsen, improve, or remain stable over the course of the problem. The underlying causes, coupled to any ongoing treatments, usually dictate these potentially variable clinical presentations.

In the following segment of the chapter commonly employed qualitative and quantitative phonation subsystem evaluation techniques are described in detail. Most of the procedures discussed are not routinely performed by physicians, unless they have undergone training in the area of otolaryngology, or they have worked closely with medical colleagues or speech-language pathologists with such expertise. Notwithstanding this limitation, it is not unfeasible to suggest that virtually all of the techniques below can be easily learned by the inquiring and determined physician, regardless of his or her medical subspecialty background. Those clinicians who prefer to send the dysphonic patient to a laryngologist should, at the very least, achieve a working knowledge of the rationale for and diagnostic benefits of all of these testing procedures. Acquiring this understanding will foster communication with the practitioners to whom the patient is referred, and such information will facilitate comprehensive diagnostic and treatment discussions.

▪ History of the Dysphonia and Initial Examiner Impressions

The origin and course of abnormal voice signs and symptoms are of vital importance to differential diagnosis and management. Initially, the examiner should render a perceptual impression of the overall severity of dysphonia that the patient exhibits during the history-taking process. The types of underlying disturbances in vocal quality, pitch, and loudness should be noted, and each perceived difficulty should be behaviorally defined and rated with respect to degree of impairment. Box 10.1 provides a rating form that may prove helpful for such purposes.