Figure 6.4 Relationship of larynx to pharynx in a patient who has aspirated. (A) Frontal view of the pharynx during inspiration. The larynx is related to the lower hypopharynx, causing an extrinsic mass impression on the pharynx anteriorly. The true and false vocal cords are widely separated (the right true [t] and right false [f] vocal cords are identified). The laryngeal ventricle (arrow) is identified. The muscular processes of the arytenoids (arrowheads) are separated. (B) Frontal view of the pharynx during a modified Valsalva maneuver demonstrates that the true vocal cords (right cord – t) are now apposed. The muscular processes of the arytenoids (arrowheads) are close together. The space between them is the interarytenoid notch (small arrow). The pharynx is markedly distended in its posterior portion (large arrow), ballooning posterior to the confines of the thyroid cartilage (arrow – T). The pharynx also bulges at the thyrohyoid membrane (open arrow).
Source: Reproduced from Rubesin and Glick [23], with permission.
A bolus is selected and brought to the lips by volitional activity. A liquid is sucked or poured into the mouth. A solid is placed on top of the tongue. Liquids do not require much oral manipulation and are therefore easily transferred to the oropharynx. Solids must be chewed and mixed with saliva to achieve a satisfactory consistency for swallowing. During bolus preparation, the bolus is contained in the oral cavity in young adults. Older “normal” adults frequently spill the bolus prematurely into the oropharynx before swallowing [12].
Once the bolus is prepared, the tongue collects and sizes the bolus and transfers it into the oropharynx. The tongue tip rises to appose the hard palate, and the mid tongue forms an inclined plane directing the bolus into the oropharynx [10] (Figure 6.6). The velopharyngeal portal is closed as the soft palate rises to appose the posterior pharyngeal wall and the superior constrictor muscle contracts to appose the soft palate [9].
The pharynx and larynx are elevated by the suprahyoid muscles and intrinsic elevators of the pharynx. Pharyngeal‐laryngeal elevation participates in closure of the laryngeal aditus and laryngeal vestibule, epiglottic tilt, and opening of the pharyngoesophageal segment [8].
Epiglottic tilt is accomplished by contraction of the suprahyoid muscles, the thyrohyoid muscle, and the intrinsic epiglottic muscles. Elevation of the hyoid bone by the suprahyoid muscle group pulls on the hyoepiglottic ligament attached to the petiole (lower portion) of the epiglottic cartilage. Hyoid elevation pulls the petiole superiorly, tilting the upper epiglottis towards the horizontal in a fulcrum‐like motion. Contraction of the aryepiglottic and oblique arytenoid muscles and the thyroepiglottic muscles then inverts the epiglottis.
Figure 6.5 Postcricoid squamous mucosa. Just posterior to the cricoid cartilage, the anterior wall of the pharyngoesophageal segment has redundant mucosa that changes size and shape during swallowing. Note how the mucosa has a wavy appearance (arrows). When identified, this mucosa identifies the level of the cricoid cartilage and the level of the cricopharyngeus during pharyngography.
Source: Reproduced from Rubesin [6], with permission.
The epiglottis acts as a stream diverter, directing the bolus into the lateral swallowing channels. The tilting epiglottis also helps cover the laryngeal vestibule. The larynx closes in a retrograde fashion. The true vocal cords close at the beginning of the swallow, followed by the false vocal cords and the remainder of the laryngeal vestibule. If a portion of the bolus has penetrated the laryngeal vestibule, it is pushed back into the hypopharynx by retrograde laryngeal closure. The bolus flows through the pharynx by a combination of gravity, elevation of the pharynx over the bolus, tongue push, and sequential contraction of the constrictor muscles. Although the upper esophageal sphincter relaxes at the beginning of a swallow, the pharyngoesophageal segment does not open until the bolus reaches the lower hypopharynx. Elevation of the larynx and pharynx pulls the anterior wall of the pharyngoesophageal segment anteriorly. Tongue base retraction, constrictor contraction, and gravity increase bolus pressure to open the pharyngoesophageal segment.
Neuromuscular disorders
Most patients with swallowing dysfunction have neural or muscular disorders that alter timing of events or muscular contraction rather than causing oral or pharyngeal structural damage. Some diseases affect a patient’s ability to self‐feed despite normal swallowing. Other diseases affect both the ability to feed and to swallow. For example, patients with Parkinson’s disease often have difficulty sitting and manipulating food as well as having abnormal bolus transfer [14].
About one‐fourth of cerebrovascular accidents cause dysphagia [14, 15]. In general, left‐sided strokes alter the oral phase of swallowing, whereas right‐sided strokes alter the pharyngeal phase [15, 16]. The corticobulbar pathways in the internal capsule can be damaged by large hemispheric strokes or small‐vessel disease. Acute strokes or small‐vessel disease resulting from hypertension, diabetes, or other causes can also affect the swallowing center in the pons and medulla [17].
Diseases that directly damage motor neurons in the swallowing center or cranial nerves in the skull base may result in bulbar palsy with oral and pharyngeal swallowing difficulties [18–22]. Lower motor neural destruction occurs in amyotrophic lateral sclerosis and 10–15% of patients with acute poliomyelitis [19, 20]. Some patients with a history of poliomyelitis have progressive disintegration of axon terminals in surviving but overworked residual motor neurons, resulting in pharyngeal muscle weakness caused by “post‐polio muscular atrophy” [21]. Meningeal carcinomatosis may also result in dysphagia. Unilateral pharyngeal paresis is often caused by destruction of motor nerves at the skull base or in the neck as a result of tumor, trauma, or surgery [10]. Abnormal transmission at the myoneural junction in myasthenia gravis may result in dysphagia that is initiated or exacerbated by prolonged swallowing.
Dysphagia resulting from inflammatory or endocrine‐related myopathies is potentially treatable [14]. Dermatomyositis and polymyositis directly damage the intrinsic or extrinsic muscles of the pharynx. Pharyngeal muscle myopathy may be caused by a variety of endocrine disorders, including hyperthyroidism, hypothyroidism, and Cushing’s syndrome [22].
The end result of these various neuromuscular disorders is poor timing of oral and pharyngeal events, or abnormal movement of oral and pharyngeal structures. A bolus may be directed in a normal fashion, but because of poor timing, the bolus may enter the laryngeal vestibule or nasopharynx. Laryngeal penetration is defined as passage of the bolus into the laryngeal vestibule either just before the swallow or during swallowing [23, 24]. Abnormal tongue motion, pharyngeal contraction, or epiglottic tilt may also lead to laryngeal penetration (Figures 6.7 and 6.8). Abnormal oral or pharyngeal movement may result from a structural abnormality or neuromuscular disorder. Abnormal epiglottic tilt or pharyngeal muscular contraction may also lead to stasis in either the valleculae or piriform sinuses, respectively. Marked stasis in the piriform sinuses may cause the bolus to overflow into the larynx through the interarytenoid notch when the patient breathes or subsequently swallows for a second time. Thus, overflow aspiration is defined as barium entering the laryngeal vestibule while the patient is breathing normally [23, 24] (Figure 6.9), or as barium entering the laryngeal vestibule as a result of poor timing when the patient swallows for a second time, and there is moderate stasis in the valleculae and piriform sinuses. Aspiration may also result from regurgitation of esophageal contents into the pharynx.