Laryngeal and Pharyngeal Function

Applied Anatomy

In the illustrations of many textbooks, the membranous vocal folds are depicted as moving solely in the axial plane, with rotational motion similar to that of a windshield wiper. Details of motion of the posterior, cartilaginous portions of the larynx have been largely ignored. The reason is that early concepts of motion were based on observing laryngeal motion with a mirror and recording the observations with two-dimensional (2D) freehand drawings. However, with the advent of flexible endoscopy, stroboscopy, video recording, and computerized imaging, it has become clear that laryngeal motion is more complex than previously recognized. Vocal folds move in three dimensions and undergo conformational changes in length, shape, and volume ( Fig. 53.2 ). The terms cadaveric and paramedian have been commonly used to describe the position of paralyzed vocal folds. These terms are inadequate to describe the three-dimensional (3D) changes in configuration of the glottis in paralysis. Motion of the larynx is best understood as the net result of the interaction of its component parts.

The laryngeal skeleton consists of the hyoid bone and a series of cartilages. The hyoid bone is a U -shaped structure that opens posteriorly and is suspended from the base of the skull and mandible by muscles and ligaments. The thyroid cartilage, the largest cartilage in the larynx, is suspended from the hyoid bone. The word thyroid means “shield”—an appropriate name, because the structure is not only shaped like a shield but also provides support and protection for the vocal folds. In the axial plane, the thyroid cartilage looks like the letter V with two wings that project posteriorly. Like the hyoid bone, the thyroid cartilage is open posteriorly; the vocal folds attach to the anterior inner surface of the thyroid cartilage; and the posterior ends of the vocal folds are anchored to the arytenoid cartilages, the chief moving parts of the larynx. The arytenoid cartilages sit atop the posterior rim of the cricoid cartilage and articulate via shallow ball-and-socket joints. The cricoid cartilage is the only complete rigid ring within the airway. It is shaped like a signet ring and is broadest posteriorly. Inferiorly and just lateral to the cricoid joints, the inferior cornua of the thyroid cartilage articulates with the cricoid in two hinge-like joints that create a visor-like or “bucket handle” structure, with motion that controls the space between the anterior rims of the thyroid and cricoid cartilages.

The epiglottic cartilage is a leaf-shaped structure attached inferiorly to the anterior–interior surface of the thyroid cartilage. The upper margin is free and projects into the hypopharynx above the glottic opening. The mucosa that covers the epiglottis spreads laterally on both sides and is continuous with the mucosa over the arytenoid to create the aryepiglottic folds, the lateral borders of the supraglottis. Muscle fibers within each aryepiglottic fold contribute to constriction of the supraglottis; in addition, two small sesamoid cartilages, the corniculate and cuneiform cartilages, sit just above each arytenoid within the aryepiglottic fold.

The membranous vocal folds are suspended between the thyroid cartilage and the arytenoid cartilages. Abduction and adduction of the vocal folds are accomplished by the actions of the intrinsic laryngeal muscles that connect the arytenoid cartilages to either the cricoid or thyroid cartilages. These include the thyroarytenoid muscle (TA), lateral cricothyroid muscle (LCA), interarytenoid muscle (IA), and the posterior cricoarytenoid (PCA) muscle. Our understanding of the individual and combined actions of laryngeal muscles has been greatly advanced by 3D modeling of laryngeal motion.

The arytenoid rotates inwardly to close the glottis, and upward and outward to open it. The LCA is the primary adductor of the vocal fold, primarily via a rocking motion of the arytenoid in the coronal plane about the cricoid facet, with very horizontal sliding or rotation about a vertical axis. The LCA pulls the muscular process of the arytenoid anteriorly and caudally, which moves the vocal process medially. While it is the strongest adductor, the LCA alone does not completely close the anterior glottis. Complete glottic closure requires simultaneous action of all the adductors. There are two functional subunits of the TA muscle, with distinct actions on motion of the vocal fold. The lateral, muscularis portion (TAm) adducts the vocal fold, and its action is necessary for complete closure of the anterior glottis. The medial portion, also known as the vocalis muscle (TAv), shortens and thickens the vocal fold. Because IA connects the arytenoid cartilages, it is logically implicated in adduction, although 3D modeling suggests that isolated contraction of the IA actually abducts the vocal folds.

The PCA muscle abducts the vocal fold and provides posterior support during phonation. PCA contraction pulls the muscular process of the arytenoid posteriorly and caudally. The structure of the cricoarytenoid joint prevents the entire arytenoid from being pulled along this vector. Instead, the arytenoid rotates, which displaces the vocal process upward and laterally and, hence, abducts the vocal fold ( Fig. 53.3 ). The human PCA has two compartments supplied by separate nerve branches; they differ in fiber type and insert on opposite sides of the muscular process ( Fig. 53.4 ). The functional significance of this compartmentalization is unknown.

The most recently recognized intrinsic muscle is a small bundle of fibers in the aryepiglottic fold that can constrict the supraglottis. This muscle is implicated in Valsalva and swallowing and is likely active in patients with vocal hyperfunction.

The cricothyroid muscles connect the anterior edges of the thyroid and cricoid cartilages. CT contraction pulls the thyroid and cricoid cartilages closer together, which increases the distance between the anterior commissure and the cricoid. The result is a stretching of the vocal fold and an increase in its length and tension ( Fig. 53.5 ). Because both vocal folds insert on the anterior commissure, contraction of either CT muscle affects both ipsilateral and contralateral vocal folds—that is, unilateral CT contraction does not result in rotation of the glottis. In contrast to other intrinsic laryngeal muscles, the CT muscle does not insert on the arytenoid cartilage and, therefore, does not adduct or abduct the vocal fold. Aerodynamic studies, cadaveric anatomic studies, and computational models of motion have indicated that CT contraction does not increase glottic area or reduce translaryngeal resistance during inspiration.

Extrinsic laryngeal muscles connect the larynx to other structures and exert traction on the laryngeal cartilages. The sternohyoid, thyrohyoid, and omohyoid muscles pull the larynx caudally. Muscles that exert a cephalad force include the geniohyoid, anterior belly of the digastric, mylohyoid, and stylohyoid muscles. In patients with hyperfunctional dysphonia, excess activity can usually be palpated in the extrinsic laryngeal muscles.

The nerve supply to the larynx is via the superior and recurrent laryngeal nerves, both of which are branches of the vagus nerves. The superior laryngeal nerve leaves the vagus nerve high in the neck at the nodose ganglion; its internal branch exits the lateral thyrohyoid membrane and carries sensory afferent fibers from the supraglottis and vocal folds, whereas the external branch of the superior laryngeal nerve supplies motor fibers to the CT muscle. All other intrinsic laryngeal muscles are supplied by the recurrent laryngeal nerve, which leaves the vagus nerve in the chest and then travels back up to enter the larynx near the cricothyroid joint. The course of the recurrent laryngeal nerve is much longer on the left side, because it runs under the ligamentum arteriosum, a vestigial remnant of embryonic connection between the aorta and pulmonary artery. On the right side, the recurrent nerve travels only as far caudally as the subclavian artery before returning cephalad.

The laryngeal mucosa is richly supplied with sensory receptors. In fact, there are many more sensory receptors in the larynx than in the lungs, which have a vastly larger area of surface mucosa. Laryngeal sensory receptors respond to a variety of stimuli, including mechanical, thermal, chemical, and taste. These receptors provide important input for protection of the larynx and information on the movement of air in and out of the lungs. The receptors provide the afferent limbs of a variety of reflexes.

Protection

When the larynx is mechanically stimulated, it closes abruptly and respiration ceases. Apnea can also occur in response to such diverse chemical agents as ammonia, phenyl diguanide, and cigarette smoke. These are appropriate and beneficial responses that prevent the entry of foreign matter into the lower airway, although strong laryngeal stimulation may result in responses that appear to be maladaptive, such as laryngospasm and prolonged bronchoconstriction. These reflexes may be produced in experimental animals by electrical stimulation of the superior laryngeal nerve and probably represent an oversaturation of pathways that serve a useful function at lower levels of input.

The larynx occupies a protected position in the body, and it is rarely subject to direct stimulation. Therefore, laryngospasm and apnea are not everyday occurrences. Severe laryngeal reflexes are most often encountered in patients in the operating room in response to direct stimulation during intubation, endoscopy, or extubation. These reflexes most likely occur in patients during light anesthesia and in those who are well oxygenated.

Recurrent paroxysmal laryngospasm is occasionally encountered in clinical practice. In some patients, it is caused by gastroesophageal reflux, which responds to acid-suppressing medication. In other patients, the pathophysiology appears to be a hypersensitive laryngeal closure reflex, because such patients report some triggering event, such as eating or inhaling steam or odors. The onset frequently occurs during an upper respiratory infection, but it can also occur after surgical trauma to the recurrent laryngeal nerve. Most often the condition resolves spontaneously within a few months, but it may become a permanent and debilitating problem. The laryngeal closure reflex is particularly sensitive in infants and can be elicited by a stimulus as weak as water. During early infancy, the strength of this reflex increases and then decreases, and it does so along a time course similar to that of the incidence of sudden infant death syndrome, which suggests that laryngeal reflexes may play a role in its cause.

Cough

Another important protective reflex that involves the larynx is the cough, which ejects mucus and foreign material from the lungs. Cough can be a voluntary action or a reflexive response to stimulation of the larynx or receptors in the lungs. The cough reflex is suppressed during sleep, so that a greater stimulus is required with progressive stages of sleep. During deep sleep, a cough cannot be elicited unless the stimulus first results in arousal to a lighter level of sleep.

The first phase of a cough is inspiratory. The larynx opens widely to permit rapid and deep inhalation. In voluntary cough, the extent of inspiratory effort is varied according to the intended strength of the cough. The second phase is compressive and involves tight closure of the glottis and strong activation of expiratory muscles; thus, the effectiveness of the cough is impaired by glottic incompetence. Finally, the larynx suddenly opens widely, which results in a sudden and rapid outflow of air at speeds of as high as 10 L/s. Cough plays an important role in cleaning the tracheobronchial tree and in maintaining patency of the lower airways. Abnormal cough can be a serious clinical problem that interferes with normal daily function and impairs quality of life.

Control of Ventilation

The role of the larynx as an active organ of respiration is not widely recognized. The larynx is located at the entrance into the trachea; not only is it capable of opening and closing rapidly, it can also create sudden alterations in resistance. Hence, the larynx is better adapted than any other portion of the respiratory tract to regulate airflow. Abduction and adduction of the larynx in phase with respiration plays an important role in regulating respiration. The resistance changes that result from laryngeal responses to respiratory stimuli, such as negative airway pressure and blood gas changes, have a beneficial effect on ventilation.

Widening of the glottis during inspiration is a primary action of ventilation that ceases only during deep anesthesia or sleep. The PCA muscle, the only active dilator of the larynx, begins to contract with each inspiration before activation of the diaphragm. The level of PCA activity, and, hence, laryngeal movement with breathing varies. Laryngeal motion may be imperceptible during unlabored, quiet breathing; however, with increasing respiratory drive, peak inspiratory PCA activity increases proportionately with diaphragmatic activity. Important differences have been noted between PCA activity and diaphragmatic behavior ( Fig. 53.6 ). When the upper airway is partially occluded, inspiration generates negative airway pressure, which is a potent stimulus to the PCA and several other muscles that dilate the upper airway. In contrast, the diaphragm responds by actually decreasing inspiratory force and by increasing the duration of inspiration. This response occurs because during partial airway obstruction, the PCA and the diaphragm have opposing effects on patency of the lumen. Increasing PCA contraction dilates the airway. However, increasing the strength of diaphragmatic contraction increases negative intrathoracic pressure, which tends to collapse the intrathoracic airway. During strong respiratory demand, the PCA continues to contract during expiration after the diaphragm has relaxed; this delays expiratory adduction and facilitates the outflow of air. During panting, the glottis sustains an abducted posture to ensure maximal airflow. Because of these physiologic differences, the phrenic nerve is not an ideal choice for reinnervation of the PCA in patients with laryngeal paralysis.

Closure of the larynx during expiration during sleep is passive due to relaxation of abductor muscles. But during wakefulness, adductor muscles are variably activated to prolong the duration of exhalation. Expiratory duration is also modulated by diaphragmatic activity. Simultaneous recordings of TA electromyography (EMG), upper airway pressure, and airflow have documented that expiratory airflow is inversely proportional to the level of laryngeal adductor activity, while transglottal airflow resistance and duration of expiration are increased by laryngeal adduction (see Fig. 53.7 ).

Laryngeal regulation of breathing is not essential for life, as evidenced by the fact that patients ventilate satisfactorily through a tracheotomy, although the inability to breathe and speak normally through natural orifices has a devastating impact on quality of life. Optimal function of the upper aerodigestive tract requires normal laryngeal function.