Swallowing has become a major component of many speechlanguage pathologists' (SLPs') caseloads, even though it has nothing to do with communication. It does take advantage of the same anatomy as speech, though, so SLPs are capable professionals in the assessment and treatment of swallowing disorders. Like speech, swallowing is a complex process involving a number of muscles, nerves, and even glands. We will be surveying central control of swallowing in this chapter.
IN THIS CHAPTER
In this chapter, we will . . .
■ Review the steps and events in the normal swallow
■ Analyze the central swallowing system
■ Briefly discuss neurogenic swallowing disorders
1. The learner will briefly describe each stage of the normal swallow.
2. The learner will correctly identify the cranial nerves involved in each step of the normal swallow.
3. The learner will describe the main components of the central swallowing system.
4. The learner will list neurological disorders that cause dysphagia and note the specific nature of the swallowing problem for each disorder.
■ The Normal Swallow
• The Oral Preparatory Stage
• The Oral Stage
• The Pharyngeal Stage
• The Esophageal Stage
■ The Central Swallowing System
• Brainstem Involvement
• Subcortical and Cortical Controls
• Neurology of the Cough Response
• Neurology of Silent Aspiration
■ Neurological Swallowing Disorders
• The General Nature of Neurogenic Dysphagia
• Specific Neurological Conditions Involving Dysphagia
■ Summary of Learning Objectives
■ Key Terms
■ Draw It to Know It
■ Questions for Deeper Reflection
■ Case Study
■ Suggested Projects
When not eating, the average person swallows approximately two times per minute while awake and once a minute when sleeping. This adds up to 2,400 swallows every day not associated with eating. If the number of swallows when eating were factored in, human beings swallow many thousands of times during an average day. It is a process that we take for granted until something happens to it. In this chapter, both the peripheral and central swallowing systems will be surveyed.
► The Normal Swallow
The normal swallow can be thought of as occurring in four dynamic stages: the oral preparatory, oral, pharyngeal, and esophageal stages (FIGURE 13-1). Each of these stages will be briefly discussed along with the type of neural control associated with each stage (voluntary versus involuntary), the time it takes to complete each stage, and the muscles involved (TABLE 13-1). Of the 12 pairs of cranial nerves, half of them are involved in normal swallowing: V, VII, IX, X, XI, and XII. (As in Chapter 5, cranial nerve numbers are noted in parentheses throughout this chapter.) These nerves and their relationship to swallowing are also surveyed in this section.
The Oral Preparatory Stage
The oral preparatory stage is voluntary and variable in length, depending on the substance being eaten. In this stage, food is placed in the mouth and is prepared for swallowing. Essentially, solid and semisolid foods are masticated and mixed with saliva, forming a puree consistency, which makes swallowing safer and more efficient. Oral breathing ceases and nasal breathing takes over due to a labial seal being established and maintained in order to keep food in the oral cavity.
The trigeminal nerve’s (V) mandibular branch innervates the muscles for mastication (chewing). The main chewing muscles include the following mandibular elevators: masseters, temporalis, and pterygoid muscles. The masseter closes the mandible, which facilitates cutting food using the central and lateral incisors. The temporalis and the medial and lateral pterygoids are the prime muscles for grinding food via the molars. The trigeminal nerve also innervates muscles that depress or open the mandible. These muscles include the mylohyoid and the anterior belly of the digastric muscle.
Saliva is an important component in the process of breaking foods down for swallowing. It consists mostly of water, with the remaining portion being enzymes that break down foods. Three major salivary glands secrete saliva and mix it into the bolus (i.e., a food or liquid ball) during chewing (FIGURE 13-2). The parotid gland is stimulated by the general visceral efferent fibers of the glossopharyngeal nerve (IX), and the submandibular and sublingual glands are innervated by the general visceral efferent fibers of the facial nerve (VII).
FIGURE 13-1 The stages of the normal swallow. (Note: The oral preparatory stage is not pictured.) 1. The oral stage. 2. The pharyngeal stage. 3. The esophageal stage.
© Alila Sao Mai/Shutterstock.
TABLE 13-1 Summary of the Normal Swallow Stages
Type of Neural Control
Timing (in secs)
Cranial Nerve Involvement
Variable (depends on bolus type)
V—chewing IX—gland VII—gland
Mandibular elevators and depressors
VII—labial seal; taste
XII—anterior-to-posterior bolus movement
Face muscles (e.g., orbicularis oris) Intrinsic and extrinsic tongue muscles
V—soft palate closure; laryngeal elevation VII—laryngeal elevation
X— laryngeal, velar closure; pharyngeal constriction
XI— soft palate closure; pharyngeal constriction
XII— laryngeal elevation
Soft palate elevators and depressors
Intrinsic laryngeal muscles
Supra- and infrahyoid muscles
Variable (depends on bolus type)
X— upper esophageal sphincter control; esophageal peristalsis
Cricopharyngeus muscle Esophageal muscles
* It is possible to exercise voluntary control in the pharyngeal stage, but this is not typical behavior. However, the fact that you can exercise voluntary control is used in some swallowing therapy maneuvers.
FIGURE 13-2 A lateral view of the internal oral cavity illustrating the parotid, sublingual, and submandibular glands.
The Oral Stage
The oral stage is also a voluntary stage lasting approximately 1 second. It begins once mastication ceases. A bolus is formed and placed on the tongue. The anterior tip of the tongue rises and its posterior portion drops, forming a ramp. The bolus is then squeezed posteriorly through the oral cavity by the tongue’s rolling contact against the palate. During this activity, the labial seal is maintained and nasal breathing continues.
The facial nerve (VII) controls motor and sensory function in swallowing. It innervates the muscles of the face via special visceral efferent fibers, especially the lip muscles (e.g., orbicularis oris, buccinator) responsible for compressing and sealing the lips to keep the bolus in the oral cavity. Its special visceral afferent fibers convey taste information to the brain from the anterior two-thirds of the tongue; its general visceral efferent fibers stimulate the production of saliva used to keep the mouth moist and to help in the breakdown of food during mastication.
In addition to playing an important role in innervating the chewing muscles, the trigeminal nerve is responsible for tongue retraction via innervation of the digastric and mylohyoid muscles. This action is important in the oral stage of the swallow when the tongue forms a ramp to move the bolus from the anterior portion of the mouth to the posterior. The trigeminal’s general somatic afferent fibers carry information regarding temperature, pressure, and touch from the oral cavity to the brain.
Anterior-to-Posterior Bolus Movement
The hypoglossal nerve (XII) is a motor nerve. It controls all the intrinsic and most of the extrinsic tongue muscles. The tongue is obviously crucial to the oral stage of the swallow in gathering up the bolus and moving it posteriorly to the pharynx. The intrinsic and extrinsic tongue muscles control the shape of the tongue and are responsible for not only forming the ramp the bolus will travel down but also squeezing the bolus through the oral cavity.
The Pharyngeal Stage
The pharyngeal stage is essentially involuntary, though one could exert conscious control over it. Like the oral stage, it lasts approximately 1 second. As the bolus contacts the faucial arches, the soft palate elevates, the vocal cords adduct, and respiration pauses. The larynx elevates and moves forward and the epiglottis lowers, directing the bolus toward the esophageal segment. Simultaneously, the cricopharyngeus muscle at the top of the esophagus relaxes, allowing the bolus to enter the esophagus.
Soft Palate Closure
Soft palate elevation is crucial in keeping liquids and solids out of the nasal cavity during swallowing. Five muscles control the soft palate during swallowing. The levator veli palatini and palatoglossal muscles, innervated by the vagus (X) and accessory (XI) nerves, raise the soft palate and seal off the nasal cavity. The tensor veli palatini muscle assists these muscles by tensing the soft palate. It is innervated by the trigeminal nerve (V). The musculus uvulae muscle, innervated by the vagus and accessory nerves, also assists these muscles by shortening and raising the uvula. The pal- atopharyngeus muscles pull the pharynx up and constrict it. They also help to open the soft palate once the bolus has passed. They are innervated by the vagus and accessory nerves.
During the pharyngeal stage of the swallow, the larynx closes three valves to prevent food and liquid from penetrating the airway, which could lead to aspiration. First, the cartilaginous epiglottis closes over the top of the larynx and, thus, guards the airway. The aryepiglot- tic and thyroepiglottic muscles, when contracted, lower the epiglottis. Both of these muscles are controlled by the recurrent laryngeal branch of the vagus nerve.
The second valve is the false vocal folds, or the ventricular folds. These thick folds of mucous membrane are brought toward midline as the true vocal folds contract. They do not contain muscle.
The third and final valve is the true vocal folds. There are a number of intrinsic laryngeal muscles that control the vocal folds. The intrinsic adductor muscles are the most relevant in swallowing because these adduct the vocal folds during swallowing. There are three adductor muscles, the lateral thyroarytenoid and the oblique arytenoids, which are paired, and the transverse arytenoid. All three of these muscles are innervated by the recurrent laryngeal nerve of the vagus.
During the pharyngeal stage of swallowing, the larynx elevates under the epiglottis. This is achieved through several extrinsic suprahyoid muscles, which include the digastricus, stylohyoid, mylohyoid, geniohyoid, hyoglossus, and genioglossus. The digas- tricus muscle has an anterior belly innervated by the mandibular branch of the trigeminal nerve (V) and a posterior belly controlled by the facial nerve (VII). The mylohyoid also has its nerve supply from the mandibular branch of the trigeminal nerve. The stylohyoid receives stimulation from the facial nerve (VII). The hypoglossal nerve (XII) innervates the hyoglossus and genioglossus. The geniohyoid is controlled by cervical spinal nerve 1 through the hypoglossal nerve.
The vagus (X) and accessory (XI) nerves innervate the superior, middle, and inferior pharyngeal constrictor muscles. These muscles form a muscular tube that, when contracted, squeezes the bolus through the pharynx to the esophagus. This squeezing action is initiated when the bolus meets sensory receptors near the faucial pillars, tonsils, and soft palate. Sensation is then sent through cranial nerves VII, IX, and X to the medulla, which then sends motor commands through cranial nerves X and XI.
The Esophageal Stage
The esophageal stage is an involuntary stage; like the oral preparatory stage it is variable in length (8-20 seconds), depending on the substance eaten. After the bolus enters the esophagus, peristaltic waves (i.e., involuntary wavelike contractions) move the bolus to the stomach in conjunction with gravity. When not swallowing, the cricopharyngeus muscle contracts to prevent reflux, and respiration resumes.
The esophagus lies posterior to the trachea. At its superior end is a muscular valve called the upper esophageal sphincter. The cricopharyngeus muscle, which powers this valve, is normally contracted but relaxes as the bolus reaches the posterior pharyngeal wall. This muscle is innervated by the pharyngeal branch of the vagus nerve.
The esophagus is an 18- to 25-centimeter (cm)-long tube that is collapsed when not containing food or liquids. It can be divided into three segments: the cervical, thoracic, and abdominal esophagus.
The cervical esophagus is approximately 4 to 5 cm long and is made up of striated muscle. The thoracic esophagus is approximately 18.5 to 20.5 cm long; the upper half consists of a mix of striated and smooth muscle, and the inferior portion is smooth muscle only. Striated muscle is voluntary in nature, whereas smooth muscle is involuntary. The abdominal esophagus is 0.5 to 2.5 cm long and made of smooth muscle. It meets the stomach at the lower esophageal sphincter (Corbin-Lewis, Liss, & Sciortino, 2005).
Sequential, wavelike muscle contractions, referred to as peristalsis, move food through the esophagus. These contractions are coordinated by the medulla, with the proximal end of the esophagus contracting while the distal end is relaxed. The striated muscle in the cervical segment is controlled by parasympathetic fibers of the vagus nerve, and the thoracic and abdominal portions are controlled by the enteric nervous system. The vagus nerve is the prime controller of esophageal peristalsis.
The process of swallowing is a complicated, dynamic process, and staging it is a helpful but artificial way of conceptualizing it. FIGURE 13-3 illustrates these stages’ interdependent and highly coordinated nature and summarizes the main events we have discussed so far.
► The Central Swallowing System
Like the cochlear nucleus in the central auditory system, the swallowing system has specialized nuclei in the brainstem as well (FIGURE 13-4). The first of these is the nucleus tractus solitarius (NTS), which is Latin for “nucleus of the solitary tract.” The NTS is located in the medulla. It acts as a swallowing sensory center by receiving afferent information, such as touch and taste, from cranial nerves V, VII, IX, and X, as well as sensory input from the respiratory and cardiovascular brainstem nuclei. This sensory information is then transferred to the second brainstem nucleus, the nucleus ambiguus (NA) or “ambiguous nucleus” also located in the medulla. The NA is the motor swallowing center that innervates the swallowing muscles via cranial nerves in the peripheral swallowing system. These cranial nerves include IX, X, and XII. Because of the tight functional integration between the NTS and NA, these are sometimes referred to as the swallowing center of the medulla.
FIGURE 13-3 The normal swallow involves four separate stages that are interdependent and highly coordinated: the oral preparatory stage, the oral stage, the pharyngeal stage, and the esophageal stage. This series of illustrations demonstrates a lateral view of bolus propulsion during the swallow: A. The oral stage uses the tongue to voluntarily move the bolus toward the back of the mouth; the soft palate raises to prevent nasal regurgitation. B. The pharyngeal stage is initiated and the larynx raises, causing the epiglottis to drop down to cover the larynx and prevent penetration of food or liquid. Both the true and false vocal folds close to prevent material from falling into the trachea. C. The epiglottis descends completely and the bolus reaches the upper esophageal valve. D. The upper esophageal valve opens, allowing the bolus to enter the esophagus. E. The upper esophageal valve closes once the bolus has completely passed. F. The larynx descends, causing the epiglottis to rise to its normal position, and the true and false vocal folds open. The base of the tongue and soft palate move to their resting positions. Esophageal peristalsis helps propel the bolus to the lower esophageal valve, which opens and allows the bolus to enter the stomach.
Subcortical and Cortical Controls
The NTS ascends to the pons, hypothalamus, and thalamus and terminates in the primary sensory cortex (Brodmann areas [BAs] 1-3) of the parietal lobe (FIGURE 13-5). The hypothalamus regulates hunger and thirst, so it is connected to the eating and swallowing process. The thalamus relays the NTS’s fibers to the primary sensory cortex for processing.
Motor fibers leading to the NA begin in the inferior primary motor cortex (IPMC) and descend to the substantia nigra and then to the reticular formation of the pons. The fibers then course down to the medulla where they terminate in the NA. In addition to these fibers, there are fibers from the hypothalamus and cerebellum that may influence swallowing.
Cortical control of swallowing most likely includes additional areas besides the IPMC because cortical and subcortical lesions outside this area lead to dysphagia (i.e., swallowing trouble). Zald and Pardo (1999) used positron emission tomography (PET) scans to measure cerebral blood flow in eight patients during swallowing. In addition to the activity in the inferior primary motor cortex, there was substantial activity in the claustrum (a sheetlike membrane of neurons under the cortex), cerebellum, basal ganglia, thalamus, and right temporal lobe. Hamdy et al. (1999) used functional magnetic resonance imaging and detected cortical activity during swallowing in the sensorimotor cortex, anterior insula, premotor cortex, frontal operculum, anterior cingulate and prefrontal cortex, anterolateral and posterior parietal cortex, precuneus, and superiomedial temporal cortex. Less consistent activations were also observed in the posterior cingulate cortex and the basal ganglia. Martin,
FIGURE 13-4 Cranial nerve nuclei (NTS and NA) and their relationship to cranial nerves involved in swallowing.
Goodyear, Gati, and Menon (2001) observed activation within the lateral precentral gyrus, lateral postcentral gyrus, right insula, superior temporal gyrus, middle and inferior frontal gyri, and frontal operculum. Daniels and Foundas (1997) also found activation in the anterior insula. Cola et al. (2010) reported that subcortical stroke in the left periventricular white matter caused dysphagia involving oral control and transfer. These studies suggest that there is a large cortical and subcortical network responsible for swallowing in addition to the IPMC and the swallowing center (NTS + NA) in the medulla. How do these cortical and subcortical structures function in swallowing?
The primary motor cortex (BA 4) is probably the easiest to explain given that it activates muscles via the pyramidal system. Thus, the primary motor cortex activates the oral, pharyngeal, and cervical esophageal muscles for swallowing. Across the central fissure, the primary sensory cortex (BAs 1-3) likely processes sensation from the oral cavity as a person manipulates food in the oral preparatory and oral stages of the swallow. The insula is thought to mediate motor and sensory information in the oral and pharyngeal cavities as well as the esophagus. It may also play some role in the control of the swallow. The frontal operculum (BA 44) may play a role in some of the motor and sensory functions in the oral cavity. The anterior cingulate cortex may provide the attention necessary for swallowing. The premotor cortex (BA 6) plays a role in motor planning, so it would be logical to assume it plays a role in swallowing motor planning. Activations in the posterior part of the brain (parietal and temporal lobes) most likely relate to sensorimotor integration. The thalamus and basal ganglia may incorporate sensory information from food and liquid as the bolus passes through the swallowing structures into the actual movements of swallowing (Daniels, Brailey, & Foundas, 1999; Daniels & Foundas, 1997, 1999; Kern, Jaradeh, Arndorfer, & Shaker, 2001; Malandraki, Perlman, Karampinos, & Sutton, 2011; Martin et al., 2001; Mosier & Bereznaya, 2001).
Neurology of the Cough Response
Coughing is an important defensive reflex in swallowing. It clears not only secretions from the airway but also any food or drink that has penetrated the laryngeal defenses and made it to the vocal folds.
There are three main components in the cough reflex arc (FIGURE 13-6). First, the afferent fibers from the vagus nerve convey signals from cough receptors located in the pharynx, larynx, and trachea. These cough receptors are sensitive to chemical stimulation. Second, these signals go to a cough center located in the upper brainstem and the pons. Third, efferent signals are sent from the cough center via the vagus, phrenic, and spinal nerves to the respiratory muscles and via the vagus nerve to the larynx. Inhalation of air occurs that is needed to generate the cough’s power, and the larynx closes. Pressure is thus built up. The glottis suddenly opens and releases the built-up air, which results in the coughing behavior (Polverino et al., 2012).
FIGURE 13-5 Neuroregulation of swallowing.
FIGURE 13-6 Neural pathways for the cough. Cough receptors are shown in red.
Neurology of Silent Aspiration
Aspiration occurs when food or liquid penetrates below the vocal cords and then has a clear path to the lungs. Typically, the cough reflex arc is stimulated when material penetrates the larynx; however, neurological damage can suppress this reflex arc, and patients can experience silent aspiration, which is aspiration without any apparent signs of it (i.e., no cough or throat clearing). Silent aspiration is estimated to occur in one-third of dysphagic patients (Corbin-Lewis, Liss, & Sciortino, 2005). Daniels, Ballo, Mahoney, and Foundas (2000) attempted to compile a list of clinical indicators of aspiration broader than just cough.
In addition to watching for cough after swallow, they suggested looking for dysphonia, dysarthria, abnormal gag reflex, abnormal volitional cough, and any voice changes after swallow (TABLE 13-2). A patient demonstrating two or more of these indicators should be labeled an aspiration risk and have further evaluation with a videofluoroscopic swallow study or a fiberoptic endoscopic evaluation of swallowing (BOX 13-1).
TABLE 13-2 Six Clinical Indicators of Aspiration Risk
A voice disturbance in the parameters of vocal quality, pitch, or intensity
A speech disorder resulting from disturbances in muscular control affecting the areas of respiration, articulation, phonation, resonance, or prosody
Abnormal gag reflex
Either absent or weakened velar or pharyngeal wall contraction, unilaterally or bilaterally, in response to tactile stimulation of the posterior pharyngeal wall
Abnormal volitional cough
A weak response, verbalized response, or no response when given the command to cough
Cough after swallow
Cough immediate or within 1 minute of ingestion of calibrated volumes of water (5, 10, and 20 mL presented in duplicate)
Voice change after swallow
Alteration in vocal quality following ingestion of calibrated volumes of water
Data from Daniels, S. K., Ballo, L. A., Mahoney, M. C., & Foundas, A. L. (2000). Clinical predictors of dysphagia and aspiration risk: Outcome measures in acute stroke patients. Archives of Physical Medicine and Rehabilitation, 81(8), 1030-1033.
BOX 13-1 Evaluation for Dysphagia
SLPs are the main health care professionals for assessing swallowing mechanism, diagnosing dysphagia, and providing treatment. The evaluation process begins at the bedside with what is called the bedside swallowing evaluation. An SLP performs an oral motor examination and small trials of swallowing water or ice chips, watching for the clinical indicators listed in Table 13-2. If the patient is identified as an aspiration risk, further evaluation takes place with either a videofluoroscopic swallow study (VSS; also known as a modified barium swallow study [MBSS], FIGURE 13-7) in the radiology department or a fiberoptic endoscopic evaluation of swallowing (FEES) at the bedside. There are benefits and drawbacks to each procedure. For example, FEES does not expose patients to radiation and can be done at the bedside without the use of barium (i.e., a radiopaque substance used in MBSS that patients do not enjoy swallowing); however, FEES cannot be used to assess the oral preparatory, oral, or esophageal stages of the swallow. It is focused on what happens just before and after the pharyngeal stage. The clinician can observe all stages of the swallow with VSS. The FEES procedure is more sensitive to detecting aspiration, while the VSS procedure is better at seeing the whole of the swallowing process (Gerek, Atalay, ^ekin, Ciyiltepe, & Ozkaptan, 2005).
FIGURE 13-7 A videofluoroscopic swallow study. Note: the dark substance in the pharynx and esophagus is the bolus mixed with barium.
Neurological Swallowing Disorders
Deglutition (Latin for “to swallow down”) is the medical term for the process of swallowing, and dysphagia is the formal term for a swallowing disorder. Dysphagia literally means “impaired eating.” It can be caused by a variety of conditions, so it is a common occurrence in the medical field. Prior to the 1970s, there were few articles published on dysphagia, and, thus, little medical expertise was available in assessment or treatment (Massey & Shaker, 2003). Patients with swallowing trouble typically receive a gastric tube and may never eat by mouth again. With the explosion of imaging technology in the 1970s and 1980s, research attention shifted to swallowing and swallowing disorders. In fact, in 1986 the journal Dysphagia was established, which greatly advanced knowledge in this important area.
There are numerous neurological disorders in which dysphagia is a symptom. Cerebrovascular accident is one of the most common reasons people experience dysphagia. Swallowing problems will vary in these patients, depending on the location and site of lesion. Traumatic brain injury, which causes diffuse brain injury, can also lead to disorders of swallowing. Other neurological conditions include neoplasms (cancerous or benign tumors), infections (e.g., meningitis, encephalitis), toxin exposure (BOX 13-2), degenerative diseases (e.g., amyotrophic lateral sclerosis), metabolic disorders, and spinal cord injury.
The General Nature of Neurogenic Dysphagia
The neurological conditions outlined in the previous section can lead to a variety of sensorimotor problems in swallowing. At this point, we will look at common issues in each stage of the swallow.
Oral Preparatory Stage
In this stage, neurological injury can lead to weakness or impairment in the muscles of mastication, leading to chewing problems and prolonged oral preparation time. Chewing problems can put patients at risk for choking due to being unable to break down foods properly. People may also have difficulty controlling the bolus well enough during mastication, resulting in food or liquid spilling out of the mouth.
BOX 13-2 Toxin Exposure and Dysphagia: The Woman Who Drank Bleach
I received a request to complete a swallow evaluation on a 23-year-old woman who had attempted suicide. At first I was confused, wondering how a suicide attempt could impair swallowing. My mind raced through possibilities. Maybe she tried to hang herself and had injured her larynx or pharynx? Or perhaps she had attempted carbon monoxide poisoning and had an anoxic episode. As I perused her medical chart, I discovered the nature of her attempt and the cause of her swallowing problems: She had attempted suicide by drinking bleach FIGURE 13-8. The bleach had badly burned her oral, pharyngeal, laryngeal, and esophageal regions, resulting in severe edema.
She was able to generate some evidence of a swallow at bedside, so we took her to radiology and performed a VSS. The burns and edema were so significant that they greatly impaired her sensorimotor abilities in the oral and pharyngeal phases of the swallow, putting her at risk for aspiration. The patient was put on a nasogastric tube in order to receive nutrition and hydration. She would need to heal before she could safely swallow again.
FIGURE 13-8 Bottle of Bleach.
Motor problems can lead to paresis or paralysis in the orbicularis oris muscle, resulting in drooling. People may experience pocketing of food in the cheek due to impaired buccinator and risorius muscles. This pocketing (what I call “chipmunking” to patients) is dangerous, especially when there is sensory loss in the cheek. A person may not realize there is food in the cheek and may lie down to sleep, causing food to dislodge and be aspirated. In the oral stage, weak tongue muscles lead to impaired bolus control in the oral cavity. There can be great difficulty in forming the bolus, placing it on the tongue, forming the ramp, and then moving the bolus from the front of the mouth to the back of the mouth (i.e., anterior-to-posterior transport). Because of these problems, tongue pumping is often seen in the oral stage of swallow. This is a compensatory strategy (though often very inefficient) for moving the bolus to the pharynx. A sensory issue that may occur is a hyperactive gag response that triggers when utensils (e.g., fork, spoon) are used. Food itself may trigger the gag, making oral nutrition and hydration challenging.
The pharyngeal stage of the swallow can be either delayed, weak, or completely absent, which can put a patient at risk for aspiration. These issues can result from oral, pharyngeal, laryngeal, and/or esophageal dysfunction of the musculature. Damage to the brainstem NTS and/or NA can result in the swallow response being absent. Weak pharyngeal constrictors lead to a lack of pharyngeal squeezing, causing food and liquids to pool in the valleculae and/or pyriform sinus. In addition to the issues with the swallow response, a lack of laryngeal elevation and closure can also result in aspiration. Laryngeal elevation may be impaired because of suprahyoid muscle weakness. Impairment to the intrinsic laryngeal adductors results in a lack of glottal closure. Weakness to the soft palate musculature results in incomplete velopharyngeal closure and nasal regurgitation of foods and liquids.
The upper esophageal sphincter may be dysfunctional, resulting in the bolus not efficiently entering into the esophagus and pooling in the pyriform sinuses. Damage to any of the nerves that innervate esophageal peristalsis can result in dismotility. With this kind of damage, spasms may also occur in the esophagus that can be painful. Achalasia is a condition in which smooth esophageal muscle fails to relax, resulting in pain and regurgitation.
Specific Neurological Conditions Involving Dysphagia
Stroke and Traumatic Brain Injury
Stroke is the main cause of dysphagia. It can result in oral transit problems, delayed triggering of the pharyngeal swallow, pooling of material in the pharynx, penetration of the airway, and aspiration. The severity of the swallowing deficits will vary based on the extent of the stroke, the number of strokes, and the location of the lesion. Brainstem strokes often are the most debilitating due to the location of the swallowing centers in it. With brainstem strokes, the entire swallow response may be absent. The positive side is that most patients make significant recovery over time (Corbin-Lewis, Liss, & Sciortino 2005). Predictors for long-term dysphagia include dyspho- nia, dysarthria, abnormal gag reflex, abnormal volitional cough, cough after swallow, and voice change after swallow. Patients with four or more of these factors have a poor prognosis for oral intake (Schroeder, Daniels, McClain, Corey, & Foundas, 2006).
Although stroke damage is typically focal in nature, traumatic brain injury (TBI) is diffuse, involving large portions of the cerebral cortex and subcortical white matter. TBI patients may experience oral mobility issues, delayed pharyngeal swallow, and aspiration (Lazarus & Logemann, 1987). Poor prognostic factors for TBI patients include increased age, low score on the Rancho Levels of Cognitive Functioning scale, tracheostomy tube placement, and aphonia (Mandaville, Ray, Robertson, Foster, & Jesser, 2014).
Multiple sclerosis (MS) is a progressive, degenerative, demyelinating disease caused by an abnormal immune response. Dysphagia is a common symptom of MS, occurring in 33% to 43% of MS patients (Thomas & Wiles, 1999). Pharyngeal stage problems are the most common issue with MS patients, probably due to swallow delay and poor pharyngeal squeezing. These issues put MS patients at risk for aspiration (Abraham & Yun, 2002; Poorjavad et al., 2010).
Parkinson disease (PD) is another progressive, degenerative nervous system disease caused by degeneration of the midbrain’s substantia nigra and a loss of the neurotransmitter dopamine. The three main symptoms of PD are bradykinesia, rigidity, and tremor. Dysphagia is a common complication in PD, affecting an estimated 40% to 90% of PD patients (Leopold & Kagel, 1997; Muller et al., 2001; Rosenbek & Jones, 2006).
In terms of swallowing, PD patients have mastication problems due to muscle rigidity in the oral preparatory stage. It is common to see tongue pumping in the oral stage due to this same rigidity issue. This results in poor anterior-to-posterior movement of the bolus. Drooling is evident due to poor labial seal. In the pharyngeal stage, PD patients often have delayed swallow responses and rigidity in the pharynx. This rigidity leads to a poor pharyngeal squeeze and residue material being left in the pharynx. Laryngeal elevation is reduced and the cough response is often suppressed in PD (Tjaden, 2009).
Huntington disease (HD) is a progressive, degenerative, inherited disease of the basal ganglia. Patients with HD suffer from dyskinesias, especially chorea. They have balance issues, resulting in falls, as well as speech and emotional issues. Dementia is an inevitable consequence of the disease (Corbin-Lewis, Liss, & Sciortino, 2005).
Swallowing is impaired by the chorea. Patients will orally hold onto the bolus, a phenomenon known as squirreling. Bolus formation and transport are typically poor. In the pharyngeal stage, swallowing is often delayed, with pooling and laryngeal penetration and possible aspiration. The continuous movements of the head exacerbate these issues (Kagel & Leopold, 1992; Leopold & Kagel, 1985).
Amyotrophic Lateral Sclerosis
Amyotrophic lateral sclerosis (ALS) is a progressive, degenerative disease of both the upper and lower motor neurons. About 1 in 10 cases is genetic, but the remaining cases have an unknown etiology.
The oral stage is typically the first swallowing stage to be affected in ALS. Patients experience a loss of lip and tongue movement, making bolus formation and transport challenging. Early pharyngeal issues include delayed swallow response and poor pharyngeal squeeze. As the disease progresses, patients experience poor airway protection and subsequent aspiration. Eventually ALS patients will not be able to swallow safely and will require long-term means of nutrition and hydration. It is the SLP’s job to determine the timing of transition from oral feedings to nonoral options (Chapman, 2013).
Guillain-Barre syndrome (GBS) is a peripheral nerve disease of unknown origin. Patients experience a rapid onset of whole-body paralysis, including the muscles of respiration. With supportive care, patients will spontaneously recover over time. All stages of the swallow are affected as GBS progresses, with the patient eventually being unable to swallow. The SLP has to evaluate people with GBS on both ends of the disease—on the front end for when they no longer can eat by mouth and on the back end as they improve and can possible eat safely again.
Most of the neurological diseases surveyed so far have been progressive, with the exception of most stroke and TBI cases. Myasthenia gravis (MG) is also a progressive, degenerative neurological disease of the neuromuscular junction. Postsynaptic acetylcholine receptors are impaired by the body’s autoimmune system, leading to muscle fatigue and weakness. When muscles are rested, patients typically recover some level of strength. Swallowing is most at risk during periods of muscle use that lead to this fatigue and weakness. Symptoms of dysphagia include the logical result of weakness, including pharyngeal dismo- tility, pharyngeal pooling of material, aspiration, and poor esophageal motility in the cervical esophagus (Corbin-Lewis, Liss, & Sciortino, 2005).
Cervical Spinal Cord Injury
Spinal cord injury (SCI) is not typically associated with dysphagia, but SCI in the higher cervical regions can lead to impaired motor and sensory abilities in the neck. C1 innervates the geniohyoid, a laryngeal elevator. This function demonstrates that the cervical spinal cord is involved with normal swallowing.
Kirshblum, Johnston, Brown, O’Connor, and Jarosz (1999) found that 22.5% of the 187 patients with SCI studied had symptoms of dysphagia. Wolf and Meiners (2003) examined 51 patients with cervical spinal cord injury (CSCI) and found that 41% had severe dysphagia and 39% had mild dysphagia. Severe dysphagia was characterized by impairments in mastication, sensation, swallow reflex, and cough reflex. These problems led to massive aspiration of both saliva and food. Mild dysphagia was characterized by normal sensation, mastication, and swallow reflex, but mild aspiration of liquids was noted. The cough response was intact, and subjects were able to clear the aspirated materials. Both of these studies indicate that people with CSCI are at risk for dysphagia and should undergo routine evaluation for possible issues.
Like language, our ability to swallow is something we probably take for granted. Our ability to eat is intimately connected to our social life. Just think about how many conversations you have over a meal. Now imagine losing the ability to swallow. What impact would that have on your social interactions?
Eating is also important to religious communities. Jewish people celebrate a number of religious feasts, including the feasts of Passover, Trumpets, and Tabernacles. Consider the Christian tradition and the importance of the Lord’s Supper that reminds Christians of Christ’s death, but also the unity Christians are to have with one another. Many other religions attach great importance to food and sharing a meal. How devastating might a swallow disorder be to a person of faith?
SUMMARY OF LEARNING OBJECTIVES
The following were the main learning objectives of this chapter. The information that should have been learned is below each learning objective.
1. The learner will briefly describe each stage of the normal swallow.
• Oral preparatory stage: a voluntary swallowing stage that varies in length depending on the substance being eaten. Food is prepared for swallowing. Mastication occurs with solids.
• Oral stage: a voluntary stage lasting approximately 1 second. It begins once mastication ceases. It involves moving the bolus posterior to the pharynx.
• Pharyngeal stage: an essentially involuntary stage lasting approximately 1 second. The bolus is moved through the pharynx to the esophagus.
• Esophageal stage: an involuntary stage that is variable in length (8-20 seconds) depending of the substance eaten. The bolus is moved through the esophagus to the stomach.
2. The learner will correctly identify the cranial nerves involved in each step of the normal swallow.
• Oral preparatory stage: V, IX, VII
• Oral stage: V, XII
• Pharyngeal stage: V, VII, X, XI, XII
• Esophageal stage: X
3. The learner will describe the main components of the central swallowing system.
• Nucleus tractus solitarius (NTS): The NTS is located in the medulla and acts as a swallowing sensory center by receiving afferent information, such as touch and taste, from cranial nerves V, VII, IX, and X as well as sensory input from the respiratory and cardiovascular brainstem nuclei.
• Nucleus ambiguus (NA): The NA is a motor swallowing center found in the medulla that innervates the swallowing muscles via cranial nerves in the peripheral swallowing system.
• The NTS and NA together are sometimes referred to as the swallowing center of the medulla.
• Subcortical controls: The hypothalamus regulates hunger and thirst, so it is connected to the eating and swallowing process. The thalamus relays the NTS’s fibers to the primary sensory cortex for processing.
• Cortical controls: the inferior primary motor cortex, claustrum, and others.
4. The learner will list neurological disorders that cause dysphagia and note the specific nature of the swallowing problem for each disorder.
• Stroke: oral transit problems, delayed triggering of the pharyngeal swallow, pooling of material in the pharynx, penetration of the airway, and aspiration
• Traumatic brain injury: oral mobility issues, delayed pharyngeal swallow, and aspiration
• Multiple sclerosis: swallow delay, poor pharyngeal squeezing, aspiration risk
• Parkinson disease: tongue pumping, poor anterior-to-posterior bolus movement, drooling, delayed swallow, poor pharyngeal squeeze, pooling of bolus in pharynx, reduced laryngeal elevation, and suppressed cough response
• Huntington disease: squirreling, poor bolus formation and transport, swallow delay, pharyngeal pooling, laryngeal penetration, and aspiration
• Amyotrophic lateral sclerosis: poor bolus formation and transport, delayed swallow, poor pharyngeal squeeze, eventual severe aspiration due to absent swallow response
• Guillain-Barre syndrome: Devastates all stages of the swallow, but swallow improves as patient recovers from the condition
• Myasthenia gravis: pharyngeal dismotility, pharyngeal pooling of material, aspiration, and poor esophageal motility in the cervical esophagus
• Cervical spinal cord injury: impairments in mastication, sensation, swallow reflex, and cough reflex; possible aspiration
Achalasia Aspiration Bolus Claustrum Cricopharyngeus
Nucleus ambiguus (NA)
Nucleus tractus solitarius (NTS)
Oral preparatory stage
DRAW IT TO KNOW IT
1. Draw sagittal sections of the head and illustrate the oral, pharyngeal, and esophageal stages of the swallow.
QUESTIONS FOR DEEPER REFLECTION
1. List and describe the four stages of the normal swallow, including their timing and major events.
2. List and describe the function(s) of central swallow control structures.
3. How does neurological dysfunction affect the four stages of swallowing in general?
Les is a 54-year-old man who was referred to speechlanguage pathology due to gradual onset of swallowing and speech difficulty. In terms of swallowing, Les has begun to cough when drinking thin liquids as well as sometimes on his own saliva. In terms of speech, he reports that his tongue feels “thick and slow” and that his voice has become hoarse. Overall, Les demonstrates both upper motor neuron (UMN) and lower motor neuron (LMN) symptoms. His neurologist just diagnosed him with amyotrophic lateral sclerosis (ALS).
1. Given what you know about ALS, what stages of the swallow will be affected by this condition as it progresses?
2. What is the long-term prognosis for Les in terms of eating safely by mouth?
1. Obtain something to eat and drink. As you eat and drink, compare and contrast what your oral and pharyngeal cavities do as you swallow.
2. Choose one of the neurological conditions mentioned in this chapter and write a two- to three-page paper detailing the condition’s effect on swallowing.
3. Survey a recent issue of the journal Dysphagia, choose an article of interest, read it carefully, and present the article in class.
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Chapman, B. (2013, April). Dysphagia and communication management of the ALS patient. Presentation at the 2013 annual meeting of the Indiana Speech-Language-Hearing
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Corbin-Lewis, K. M., Liss, J. M., & Sciortino, K. F. (2005). Clinical anatomy and physiology of the swallow mechanism. Clifton Park, NY: Thompson-Delmar Learning.
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Kagel, M. C., & Leopold, N. A. (1992). Dysphagia in Huntington’s disease: A 16-year retrospective. Dysphagia, 7(2), 106-114.
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Leopold, N. A., & Kagel, M. C. (1985). Dysphagia in Huntington’s disease. Archives of Neurology, 42(1), 57.
Leopold, N. A., & Kagel, M. C. (1997). Pharyngo-esophageal dysphagia in Parkinson’s disease. Dysphagia, 12(1), 11-18.
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Muller, J., Wenning, G. K., Verny, M., McKee, A., Chaudhuri, K., & Jellinger, K., . . . Litvan, I. (2001). Progression of dysarthria and dysphagia in postmortem-confirmed parkinsonian disorders. Archives of Neurology, 58(2), 259.
Polverino, M., Polverino, F., Fasolino, M., Ando, F., Alfieri, A., & De Blasio, F. (2012). Anatomy and neuro-pathophysiology of the cough reflex arc. Multidisciplinary Respiratory Medicine, 7(1), 1-5.
Poorjavad, M., Derakhshandeh, F., Etemadifar, M., Soleymani, B., Minagar, A., & Maghzi, A. (2010). Oropharyngeal dysphagia in multiple sclerosis. Multiple Sclerosis, 16(3), 362-365.
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