GI Motility Online

Review

PART 1 Oral cavity, pharynx and esophagus

GI Motility online (2006) doi:10.1038/gimo25
Published 16 May 2006

Radiographic evaluation of motility of mouth and pharynx

Bronwyn Jones, M.B., B.S., F.R.A.C.P., F.R.C.R.

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Key Points

  • Dysphagia can result from many diverse conditions.

  • Attention to detail is necessary in the radiographic evaluation of the dysphagic patient.

  • To evaluate the swallow, it is necessary to understand its anatomy and physiology.

  • The physiology of the oral and pharyngeal swallow can be subdivided into several phases.

  • Analysis of these six phases results in diagnosis of the normal and abnormal findings in a patient with dysphagia.

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Introduction

Dysphagia can result from many diverse conditions, including structural and motility disorders. This review focuses on normal and abnormal motility of the organs involved in the oral and pharyngeal phases of deglutition, but does not discuss the structural causes of dysphagia or esophageal motility.

Motility disorders can result from many neuromuscular conditions affecting any level of the neural system: cortex brainstem, cerebellum, basal ganglia, cranial nerves, peripheral nerves, myoneuronal junction, and even the muscles of deglutition themselves.1, 2, 3 Thus, dysphagia can be one of the principal symptoms in brain tumors,4 CVA,5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20 amyotrophic lateral sclerosis (ALS),21, 22, 23, 24 Parkinson's,25, 26, 27, 28, 29, 30, 31, 32, 33 multiple sclerosis,34, 35, 36 myasthenia gravis,37, 38, 39 muscular dystrophy,40, 41, 42 and myopathies or myositis.43, 44, 45 Other neurologic diseases such as Alzheimer's46 and Huntington's disease47, 48 can also produce dysphagia.

Systemic diseases such as dermatomyositis can affect swallowing, as the muscles of swallowing are striated muscles43; scleroderma, a disease of smooth muscle, usually spares the pharynx but can affect the oral phase of swallowing owing to a decrease in salivary flow associated with accompanying Sjögren's syndrome.49, 50 Medications can exacerbate swallowing difficulties by causing local effects such as oral or pharyngeal inflammation51 or by affecting the neuromuscular transmission of peristalsis.52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64

Although it is an artificial separation, I have taken the liberty of discussing this topic under two categories: doing the study and analyzing the study. Naturally this is such a dynamic process that "doing" and "analyzing" are integrally intertwined and interwoven during the actual study. Flexibility and continuous diagnosis of abnormalities or decompensations is essential; there is no real "cookbook" approach, but constant consultation and discussion among the team are necessary.

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Principles of Examination: Doing the Study

Tailoring the Examination to Each Patient65, 66

A brief relevant history should be taken prior to the examination; the history then guides the study. The basic routine can be modified in an attempt to reproduce symptoms and detect an abnormal swallow by provocative tests. The clinical condition of the patient is also important: the sicker the patient, the less routine and more tailored the examination. The examination is also varied depending on whether it is the initial diagnostic procedure or a therapeutic study directed at gauging the effect of various bolus consistencies or maneuvers on aspiration or other decompensations. Under these circumstances the study is performed jointly by the radiologist and an allied health professional trained in dysphagia management such as a speech-language pathologist (SLP) who will have evaluated the patient clinically prior to the study.

The Initial Swallow

Centering

The fluoroscope should be centered so that the entire mouth, pharynx, and larynx can be clearly seen; thus, decompensations such as drooling, premature leakage, nasopharyngeal regurgitation, and laryngeal penetration or aspiration can be appreciated.

Consistency

In general, it is best to begin with what is thought to be safest (this information may be volunteered by the patient or may be decided on by the SLP following the clinical evaluation). For example, if the clinical evaluation suggests that the patient chokes on liquids, it may be wise to begin with a small volume of purée, for example, 1/4 to 1/2 teaspoon, and "work down" through honey-thick to nectar-thick to thin liquid, whereas if there is a high suspicion of pharyngeal weakness, purée may be too thick to be handled safely and a thinner bolus may be better. If there is a suspicion of obstruction, a small volume of thin liquid may be better—again tailor the consistency to the patient.

Continuing On with the Study

Depending on what is observed during that first swallow, the next decision is whether to stay in that position or move on to the frontal position. For example, if aspiration is seen, one may decide to try different consistencies perhaps with compensatory maneuvers to try to decrease or abolish the aspiration. Such maneuvers might include "chin-tuck" (head flexion to the chest), which may abolish aspiration, as may the "supraglottic swallow" (in which the patient breathes in through the nose, holds the breath, swallows hard, and exhales with or without cough). Unilateral pharyngeal paresis and unilateral vocal fold immobility that may be difficult to appreciate in the lateral position but can easily be diagnosed in the frontal position may be treated by turning the patient's head toward the abnormal side, thus forcing the bolus to go down the normal side.

The frontal position is especially useful for assessing vocal fold movement (ask the patient to say "eee", "cookie-cookie-cookie"; and tell the patient to "sniff like you are smelling a flower"), as well as symmetry of pharyngeal contraction and bolus passage.

Positioning

The mouth and pharynx are best evaluated in the upright lateral and frontal positions with the patient either standing or sitting. Special chairs are available that are narrow enough to be wheeled in front of the fluoroscopic table for examining incapacitated patients in the position in which they normally eat or are fed. Smaller adult patients and pediatric patients can sit on the footrest of the fluoroscopic table if necessary.

Some fluoroscopic units have cross-table capability that allows rotation of the fluoroscopic tube rather than the patient. In such units, supine or semi-supine studies can be performed if the patient is unable to sit or stand. The patient may be strapped onto the fluoroscopic table for safety.

Equipment

Dynamic recording allows the frame-by-frame analysis necessary to evaluate the normal and abnormal swallow. This is easily accomplished by hooking up a link between the fluoroscopic foot pedal or hand switch and an S-VHS recorder (VHS does not have adequate resolution) such that when the fluoroscope is on, the VCR automatically records the fluoroscopic image. The 30-frames-per-second rate allows assessment of individual structures in real time, slow motion, backup mode, and frame-by-frame analysis.

Unfortunately, the 100- or 105-mm spot-film camera with maximum frame rates of 6 to 8 frames per second is inadequate in the evaluation of swallowing because subtle but important laryngeal penetration or even aspiration may be visible on only one or two frames out of the 30/second sequence. The six to eight frames per second rate also does not allow perception of the dynamic movement of the individual structures.

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Analyzing (Interpreting) the Study

It is necessary to understand the anatomy of the mouth, larynx, and pharynx in order to be able to evaluate the physiology of the swallow67, 68, 69, 70, 71, 72, 73, 74 (Figures 1 and 2).

Figure 1: Lateral sagittal views of the pharynx comparing line drawings with contrast radiographs at rest and during phonation.
Figure 1 : Lateral sagittal views of the pharynx comparing line drawings with contrast radiographs at rest and during phonation. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

a: Line drawing indicates the constrictor and suspensory musculature of the pharynx viewed from the side. The constrictor muscles overlap, the inferior constrictor being the most external, and the superior the most internal.The middle constrictor is seen between the superior and inferior constrictor muscles. The inferior constrictor is continuous with the proximal circular muscle fibers of the esophagus. The fascicles of the cricopharyngeal portion of the inferior constrictor merge with the fascicles of the circular muscle of the esophagus. b: Sagittal line drawing showing structures in the sagittal plane including the tongue, soft palate, epiglottis, vestibule, false and true cords, arytenoid mass, cricoid cartilage, and trachea. (a,b: Source: Netter images, with permission from Elsevier Science.) c: Lateral view of the pharynx, which has now been coated by high-density barium. Structures can be seen including the soft palate (u), the dorsum of the tongue (T), the valleculae (V), the epiglottis (arrow), and the piriform sinuses (P). There is minimal retention of contrast in the valleculae and piriform sinuses. d: Lateral view during phonation, with the structures outlined by contrast. The soft palate (u) has elevated to a right angle, revealing the tonsillar fossa (arrows), expanding the valleculae (V) and piriform sinuses (P). T, tongue. (c,d: Source: Levine MS, ed. Radiology of the Esophagus. Philadelphia, WB Saunders, 1989, with permission from Elsevier Science.)


Figure 2: Comparisons between line drawings and radiographs in the coronal (frontal) plane.
Figure 2 : Comparisons between line drawings and radiographs in the coronal (frontal) plane. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

a: The constrictor and lateral suspensory muscles of the pharynx viewed from the posterior aspect, showing: the pharyngeal raphe, and the superior, middle and inferior pharyngeal constrictor muscles, the thyropharyngeus muscle and the cricopharyngeus muscle. Note again that the constrictor muscles overlap, the inferior being the more external and the superior the more internal. Note also that the fibers of the cricopharyngeus or horizontal fibers of the inferior constrictor muscle merge with the fascicles of the proximal circular muscle of the esophagus. b: The structures in the anterior wall of the pharynx as viewed from the posterior aspect. Note the uvula, epiglottis, piriform sinus and tongue. The mucosa remains intact. This drawing shows the contours of the valleculae and piriform sinuses and demonstrates the relationship of the valleculae to the base of the tongue and epiglottis. (a, b: Source: Netter images, with permission from Elsevier Science.) c: The pharynx has now been coated with high-density barium outlining the valleculae (v) and piriform sinuses (p). In this patient the epiglottis is not clearly visualized on this view at rest. d: The patient demonstrates "blowing up a balloon." The pharynx is now expanded especially in the region of the proximal portions of the piriform sinus. There is more symmetric distention proximally than distally because the superior portion lacks the support of the thyroid cartilage. (c,d: Source: Jones B, Donner MW. Examination of the patient with dysphagia. Radiology 1988;167:319–326, with permission from the Radiological Society of North America.)


Individual structures are analyzed in the radiographic study (such as tongue thrust, epiglottic tilt, hyoid elevation, etc.). Therefore, each individual structure needs to be analyzed, first in isolation and then in combination with others. Individual structures that should be analyzed include the tongue, palate, pharyngeal constrictor wave, epiglottis, hyoid elevation, and cricopharyngeal opening and closing.

One should also be looking for signs of decompensation, such as drooling or premature leakage, nasopharyngeal regurgitation, retention in the oral cavity, laryngeal penetration or aspiration, to name some of the decompensations that indicate a compromised swallow.

In other words, sometimes information is gained by analyzing the structures themselves. At other times the shape or position of the bolus indicates abnormality: Does the bolus fragment? Does it pool in abnormal places such as the floor of the mouth or cheek? Is it misdirected such as into the nasopharynx or larynx?

Functional Evaluation of the Normal and Abnormal Swallow

(Figures 3 and 4)

Figure 3: Line drawing of the normal swallow.
Figure 3 : Line drawing of the normal swallow. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

a: The bolus is held in the oral cavity by apposition of the soft palate and tongue with the surrounding laryngeal structures and airway at rest. b: The bolus is conveyed into the oropharynx by the tongue and the soft palate has elevated. The airway and surrounding larynx have elevated in preparation for swallow. c: The bolus is descending into the hypopharynx on either side of the cricoid prominence. The epiglottis has tilted down to cover the closed laryngeal aditus. The larynx has reached its maximum elevation. d: The bolus continues through the hypopharynx, through the open cricopharyngeal segment, and into the esophagus, with the peristaltic wave descending behind it. The nasopharynx begins to open and opening progresses in a descending sequence. e: The wave of pharyngeal contraction has obliterated the oropharyngeal cavity and moved into the hypopharynx, with the bolus descending further through the open cricopharyngeal segment into the esophagus. The nasopharyngeal airway continues to open in a cephalocaudal fashion. f: The bolus has disappeared into the esophagus. All structures have returned to the open position: the normal contours of the airway are again visible, although the larynx has not yet completed its descent to its original resting position. Barium is coating the valleculae and piriform sinuses.(Source: Netter images, with permission from Elsevier Science.)


Figure 4: Selected stop-frame prints from a cinepharyngogram demonstrate several stages of a normal swallow.
Figure 4 : Selected stop-frame prints from a cinepharyngogram demonstrate several stages of a normal swallow. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

a: The bolus (B) is retained in the mouth by apposition of the posterior aspect of the tongue and the relaxed soft palate (U). A small amount of contrast has been introduced through the nose and is coating the posterior nasopharyngeal wall and the superior portion of the soft palate. b: As the bolus is propelled into the oropharynx, the soft palate elevates to a right angle and apposes to the converging posterior pharyngeal wall, Passavant's cushion (pc). c: The soft palate (U), posterior pharyngeal wall, and dorsum of the tongue (T) remain closely in contact until the bolus has cleared from the oropharynx. The proximal stripping wave (sw) has begun. d: The posterior stripping wave (sw) has become more pronounced and is proceeding distally. The epiglottis has completely inverted and the vestibule is closed as the bolus passes through the hypopharynx. Note the closed larynx with the appearance of the conus (arrow) and the tracheal air column (T). The cricopharyngeus is completely open to allow easy passage of the bolus. There is a tiny amount of contrast in the entry to the vestibule, which is extruded as swallowing proceeds. e: The stripping wave (sw) has proceeded further. There is a small amount of bolus (B) still trapped in the hypopharynx. The larynx is still closed. (a-d: Source: Jones B, Kramer SS, Donner MW. Dynamic imaging of the pharynx. Gastrointest Radiol 1985;10:213–224, with permission of the authors.)


Each swallow may be divided into several phases:

  1. Oral phase
  2. Tongue/palate seal
  3. Nasopharyngeal (soft palate/superior constrictor) seal
  4. Compression and propulsion of bolus
  5. Hyoid/larynx/epiglottic tilt (laryngeal complex)
  6. Cricopharyngeal opening
  7. Esophageal peristalsis

Phases 1 to 6 are discussed here.

Oral Phase

The normal oral phase (Figures 3a and 4a)  The lips engulf the bolus, which is held at rest toward the front of the mouth in a midline groove. With a larger bolus, the bolus sits further toward the back of the oral cavity. The average normal bolus size for thin liquids is 21 mL [standard deviation (SD) plusminus 5 mL).75 Boluses commonly used in clinical practice are 5 and 10 mL.67

There are two types of normal oral phase, based on where the bolus is held at the beginning of swallow: the "tipper" and the "dipper."76 In the more common "tipper swallow" (95%), the bolus is held above the tongue in a central groove and is then transferred into the pharynx by a progressive upward and posterior movement of the tongue blade, a movement that completely obliterates the oral cavity behind the bolus, the tongue progressively abutting the hard palate.

In the less common "dipper swallow" (5%), the bolus is held under the tongue in the floor of the mouth at rest; a downward scooping movement of the tongue blade transfers the bolus into the oral cavity and on into the pharynx in the same way as a tipper swallow. An individual's swallow is always either a "tipper" or a "dipper" type.

Occasionally one will see a "chipmunk swallow," when a large bolus is partially held in the cheeks and the patient then swallows several times to clear the oral cavity, each swallow decreasing the amount held in the cheeks. However, pooling in one or both cheeks after completion of a swallow indicates weakness, for example, after a stroke.

The abnormal oral phase  Weakness of the lip seal results in drooling. Both bolus and tongue movements can suggest tongue weakness. Malpositioning or fragmenting of the bolus, difficulty propelling the bolus, multiple tongue blade movements to gradually propel the bolus, tremor or myoclonus, undulations of tongue blade, failure to obliterate the oral cavity, atrophy of the tongue, and low hyoid position can all be signs of tongue weakness. In the frontal view, asymmetry of the tongue or asymmetry of bolus position and preservation of air in the apex of the mouth during bolus transfer are also signs of weakness.

Also, failure to maintain the bolus in the central tongue groove with loss of bolus in the floor of the mouth is a sign of tongue weakness (Figure 5a). The bolus has now fragmented and may be left behind in the floor of the mouth after the swallow. Do not confuse this with a "dipper" swallow.

Figure 5: Oral decompensations with abnormal retained bolus.
Figure 5 : Oral decompensations with abnormal retained bolus. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

Two different patients demonstrate pooling in the floor of the mouth (a) (arrows) and in the cheek (b) (arrow). (Source: Jones B, ed. Normal and Abnormal Swallowing: Imaging in Diagnosis and Therapy. New York: Springer-Verlag, 2003, with permission.)


Pooling in the cheek after the swallow is abnormal, indicating weakness, as is ballooning of the cheek (Figure 5b).

Tongue/Palate Seal

Normal (Figure 3a, b)  Normally a bolus can be maintained in the mouth and does not leak out anteriorly, owing to the competence of the lip seal and tongue to the soft palate seal posteriorly. Normally, at rest the soft palate apposes the posterior tongue blade.

Abnormal  A kink in the palate in the erect position is abnormal and a sign of soft palate weakness or an indication of palatal compensation for a weak tongue (Figure 6). In the supine position, however, the palatoglossus muscle contracts to maintain the bolus within the mouth, producing a kink in the soft palate.

Figure 6: Weakness of the soft palate.
Figure 6 : Weakness of the soft palate. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

Kinking of the soft palate as a sign of weakness. Note that the superior surface of the soft palate has been coated by instillation of barium through the nose. There is a kink partway down the uvula (arrow), which in the erect position is a sign of weakness. (Source: Jones B, ed. Normal and Abnormal Swallowing: Imaging in Diagnosis and Therapy. New York: Springer-Verlag, 2003, with permission.)


Incompetence of the seal between the tongue and the palate results in premature leakage from the mouth into the pharynx before initiation of swallowing, with the potential for aspiration into the open, unprotected larynx (Figure 7). In the frontal position, unilateral premature leakage versus central leakage points to the side of the weakness (Figure 7b).

Figure 7: Premature leakage.
Figure 7 : Premature leakage. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

Films from two separate patients reveal the appearance of premature leakage from the mouth. a: This still frame from a cinepharyngogram in the lateral projection demonstrates contrast leaking over the dorsum of the tongue into the valleculae (black arrows). Note that the soft palate (u) is incompletely apposed to the posterior portion of the tongue. There is the potential for aspiration into the open vestibule of the larynx (white arrows). b: In the frontal projection there is unilateral leakage over the back of the left side of the tongue into the left vallecula (v) with overflow into the left piriform sinus (ps). (Source: Jones B, ed. Normal and Abnormal Swallowing: Imaging in Diagnosis and Therapy. New York: Springer-Verlag, 2003, with permission.)


Soft Palate/Superior Constrictor

Normal soft palate/Passavant cushion seal (Figures 3b, 4b)  As the bolus is propelled into the pharynx, the soft palate elevates to a right angle, apposing Passavant's cushion, a forward moving bulge, produced by focal contraction of the upper fibers of the superior constrictor muscle.

Abnormal palate/constrictor seal  Weakness of the soft palate or superior constrictor muscle can result in nasopharyngeal regurgitation (Figures 8 and 9).

Figure 8: Nasopharyngeal regurgitation.
Figure 8 : Nasopharyngeal regurgitation. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

Contrast is seen in the nasopharynx (black arrows) posterior to the uvula. Contrast is retained in the valleculae and along the back of the tongue. Contrast is seen along the posterior surface of the epiglottis (white arrows) indicating that laryngeal penetration has occurred. Note also squaring of the valleculae and prevertebral soft tissue atrophy, signs of pharyngeal paresis. (Source: Jones B, Kramer SS, Donner MW. Dynamic imaging of the pharynx. Gastrointest Radiol 1985;10:213–224, with permission from the authors.)


Figure 9: Multiple abnormalities.
Figure 9 : Multiple abnormalities. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

There is nasal regurgitation (straight arrow). The epiglottis has remained upright during bolus passage (curved arrow), but there is no laryngeal penetration as there is normal laryngeal elevation and closure. (Source: Jones B, Donner MW. The Pharynx In: Taveras JM, Ferrucci JT, eds. Rad-Diag-Imaging-Intervention. Philadelphia: Lippincott Williams & Wilkins, 1986, with permission.)


Compression and Propulsion of Bolus

Normal (Figures 3c, d and 4c-e)  Bolus is propelled and compressed by a combination of pharyngeal contraction and tongue base retraction. The tongue base and constrictors should tightly appose, obliterating the pharyngeal cavity. The constrictor stripping wave can be observed in the lateral position as a progressive forward movement of the posterior pharyngeal wall and in the frontal position as the movement of the lateral walls of the pharynx completely to the midline.

Tongue base retraction should be completely backward to appose the converging pharyngeal wall.

(Figure 10)

Figure 10: Pharyngeal paresis.
Figure 10 : Pharyngeal paresis. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

Frontal view shows asymmetry of distention, with the left piriform sinus (ps) bulging much more than the right piriform sinus because of weakness of the constrictor muscles. A small amount of contrast medium is present in the laryngeal vestibule (arrow), and a moderate flow defect (arrowheads) can be seen. (Source: Gore RM, Levine MS, Laufer I, eds. Textbook of Gastrointestinal Radiology. Philadelphia: WB Saunders, 1994, with permission from Elsevier Science.)


Pharyngeal paresis/paralysis  No movement of the posterior pharyngeal wall indicates paralysis; poor movement indicates paresis or weakness. Failure of the lateral pharyngeal walls to come to the midline indicates pharyngeal paresis. No movement toward the midline or bulging during swallow indicates paralysis.

Unilateral weakness results in asymmetry in the frontal view. The contracting normal side can push the bolus across the midline to the atonic side so the bolus passes down the paralyzed side. Without dynamic imaging, the contacting normal side may be misinterpreted as a mass, whereas the abnormality is actually on the noncontracting, bulging side.

It is not uncommon in neurologic diseases affecting the pharynx to see weakness of the superior and middle constrictor muscles with some residual constriction of the inferior constrictor muscles.77

Hyoid/Larynx/Epiglottic Tilt (Laryngeal Complex)

Normal (Figures 3c-f and 4c, d)  This phase is discussed under two categories: hyoid elevation and epiglottic tilt.

Normal: Hyoid and laryngeal movement  As the bolus enters the pharynx, the hyoid begins to elevate, moving upward and forward, apposing to the angle of the mandible. There is a correlation between the excursion of the hyoid bone and the volume of the bolus.78 A 2-mL bolus results in a mean elevation of 13.0 mm (females) and 13.5 mm (males), whereas a 10-mL bolus produces a 14.8-mm elevation (females) and 16.7 mm (males). The hyoid bone can elevate in one or two steps.79 Descent to the resting position occurs in a one-step fashion simultaneously with the upward tilting of the epiglottis to its resting position.

Normal epiglottic tilt  Epiglottic tilt is a two-step movement in most people.

The initial movement, to the horizontal position is probably passive and related to hyoid elevation and tongue thrust. The second movement, to the completely inverted position, is an active one and is probably the result of contraction of the thyroepiglottic muscle.80

The completely inverted epiglottis looks like a seagull on the frontal view. A flow defect can occur quite commonly below the inverted epiglottis (Figure 11).

Figure 11: Normal epiglottic tilt.
Figure 11 : Normal epiglottic tilt. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

The epiglottis itself can be seen as a "seagull" or inverted flat V (arrows). The tilted epiglottis has deflected the bolus into the lateral food channels, creating a filling defect or "pseudomass." (Source: Jones B, ed. Normal and Abnormal Swallowing: Imaging in Diagnosis and Therapy. New York: Springer-Verlag, 2003, with permission.)


Abnormal hyoid motion  The hyoid may elevate incompletely or move not at all. It may elevate momentarily and not be sustained.

Aspiration can occur if there is failure of laryngeal protective mechanisms, which include laryngeal elevation, laryngeal closure, and epiglottic tilt. Laryngeal closure has at least three levels of defense: closure of arytenoids, closure of true vocal folds, and closure of the false vocal folds.

Laryngeal penetration is entry of the bolus into the laryngeal vestibule or lower in the larynx but not through the vocal folds (Figure 12). Aspiration occurs when contrast goes below the vocal folds (Figure 13).

Figure 12: Laryngeal penetration.
Figure 12 : Laryngeal penetration. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

Curved collection of contrast is seen entering the incompletely closed vestibule of the larynx (arrow). Faint contrast is seen in the larynx and on the tracheal anterior wall caused by previous aspiration (arrowheads).


Figure 13: Aspiration.
Figure 13 : Aspiration. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

a: Frontal view of the pharynx demonstrates aspiration of retained bolus. Note that there is retention of contrast in the valleculae (v) and piriform sinuses (ps). No swallow is taking place, yet there is entry of contrast into the laryngeal vestibule (ve) and between the vocal folds and in the ventricle (arrows). (Source: Jones B, ed. Normal and Abnormal Swallowing: Imaging in Diagnosis and Therapy. New York: Springer-Verlag, 2003, with permission.) b: A stop-frame print from a cinepharyngogram in the lateral position shows incomplete laryngeal closure during swallowing with laryngeal penetration (arrows) and aspiration (arrowheads) down into the trachea. The bolus is passing through the open cricopharyngeus into the cervical esophagus. Degenerative change is noted in the cervical spine. (Source: Jones B, ed. Normal and Abnormal Swallowing: Imaging in Diagnosis and Therapy. New York: Springer-Verlag, 1991, with permission.)


Both penetration and aspiration can result in a reflexive cough (normal) or not produce a cough (i.e., be silent). Silent aspirators do not know they are aspirating, and clinical prediction of aspiration, especially in silent aspirators, is notoriously inaccurate.81, 82, 83, 84

Aspiration can occur before a swallow; a classical cause is premature leakage from the mouth. Aspiration can also occur during a swallow or after a swallow (overflow of retained bolus, reflux or regurgitation).

Cricopharyngeus

Normal (Figures 3d, e and 4d, e)  The cricopharyngeus muscle is the horizontal lowermost portion of the inferior constrictor muscle and arises from the cricoid cartilage. There is a zone of sparse musculature immediately above (Killian's triangle) and below (area of Laimer) the cricopharyngeus, where there is the potential for the development of a diverticulum.

The upper esophageal sphincter (UES) is longer than the cricopharyngeus and consists of a zone of high pressure consisting of some fibers of the inferior constrictor muscle, the cricopharyngeal muscle, and some circular fibers of the proximal cervical esophagus.

Between swallows, the cricopharyngeus is closed, presumably to prevent overdistention of the esophagus during respiration. The cricopharyngeus must both relax and open completely to allow unimpeded passage of bolus from the pharynx into the cervical esophagus.

Several factors open the lumen at the level of the cricopharyngeus:

1. Cricopharyngeal relaxation

2. Anterior traction from superior and anterior movement of hyoid and larynx

3. A push from above from contraction of the pharyngeal constrictor muscles (and probably from tongue-base retraction also)

4. Pressures of the bolus itself

Thus, cricopharyngeal prominence can result from failure of relaxation (probably the least common cause), a frozen larynx, or pharyngeal weakness.

Radiographically the cricopharyngeus is located at the C5-6 disk level.

Abnormal85, 86, 87, 88, 89, 90  The cricopharyngeus should open completely to allow unimpaired passage of bolus into the cervical esophagus. The cricopharyngeus may open late or incompletely or close early, sometimes trapping fluid in the sphincter segment.

Radiographically, a posterior indentation at approximately the C5-6 or C6-7 level during bolus passage indicates the level of the cricopharyngeus (Figure 14).

Figure 14: Multiple abnormalities.
Figure 14 : Multiple abnormalities. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

Lateral radiograph demonstrates multiple abnormalities, including laryngeal penetration (black arrow), aspiration (white arrow), and cricopharyngeal prominence (arrowhead). Note the jet of contrast material below the prominent cricopharyngeus. (Source: Jones B, Kramer SS, Donner MW. Dynamic imaging of the pharynx. Gastrointest Radiol 1985;10:213–224, with permission from the authors.)


Significant luminal narrowing may produce severe dysphagia, especially with a "cricopharyngeal bar," a thumb-like indentation into the lumen from the posterior aspect (Figure 15). Cricopharyngeal bars may occur alone or in combination, for example, with Zenker's diverticulum. Cricopharyngeal prominence or bar may be seen in the elderly, as a secondary response to esophageal disease such as gastroesophageal reflux disease or spasm and, as discussed earlier, in association with pharyngeal paresis or a frozen larynx

Figure 15: Cricopharyngeal bar with jet phenomenon.
Figure 15 : Cricopharyngeal bar with jet phenomenon. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

There is a very prominent thumb-like indentation at the pharyngoesophageal junction (white arrow) representing a cricopharyngeal bar. A flow or "jet phenomenon" (black arrows) is seen below confirming luminal narrowing. (Source: Jones B, Kramer SS, Donner MW. Dynamic imaging of the pharynx. Gastrointest Radiol 1985;10:213–224, with permission from the authors.)


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Conclusion

Videofluoroscopy and radiography of the mouth and pharynx can be extremely useful in the evaluation of functional and structural abnormalities. Careful attention to radiographic technique and the movement of structures and bolus results in a diagnosis of the normal and abnormal swallow.

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References

  1. Kirshner S. Causes of neurogenic dysphagia. Dysphagia 1989;3:184–188. | Article | PubMed |
  2. Buchholz D. Neurologic causes of dysphagia. Dysphagia 1987;1:152–156. | Article |
  3. Silbiger ML, Pikheney R, Donner MW. Neuromuscular disorders affecting the pharynx: cineradiographic analysis. Invest Radiol 1967;2:442–448. | PubMed | ChemPort |
  4. Wesling M, Brady S, Jensen M, Nickell M, Statkus D, Escobar N. Dysphagia outcomes in patients with brain tumors undergoing inpatient rehabilitation. Dysphagia 2003;18(3):203–210.
  5. Paciaroni M, Mazzotta G, Corea F, et al. Dysphagia following stroke. Eur Neurol 2004;51(3):162–167.(Epub 2004 Apr 1.)
  6. Parker C, Power M, Hamdy S, Bowen A, Tyrrell P, Thompson DG. Awareness of dysphagia by patients following stroke predicts swallowing performance. Dysphagia 20040;19(1):28–35.
  7. Smithard DG. Swallowing and stroke. Neurological effects and recovery. Cerebrovasc Dis 2002;14(1):1–8.
  8. Martino R, Terrault N, Ezerzer F, Mikulis D, Diamant NE. Dysphagia in a patient with lateral medullary syndrome: insight into the central control of swallowing. Gastroenterology 2001;121(2):420–426.
  9. Mann G, Hankey GJ. Initial clinical and demographic predictors of swallowing impairment following acute stroke. Dysphagia 2001;16(3):208–215.
  10. Han TR, Paik NJ, Park JW. Quantifying swallowing function after stroke: a functional dysphagia scale based on videofluoroscopic studies. Arch Phys Med Rehabil 2001;82(5):677–682.
  11. Buchholz D, Neumann S. Aphagia due to pharyngeal constrictor paresis from acute lateral medullary infarction. Dysphagia 1999;14(3):187.
  12. Nilsson H, Ekberg O, Olsson R, Hindfelt B. Dysphagia in stroke: a prospective study of quantitative aspects of swallowing in dysphagic patients. Dysphagia 1998;13(1):32–38.
  13. Neumann S, Buchholz D, Jones B, Palmer J. Pharyngeal dysfunction after lateral medullary infarction is bilateral: review of 15 additional cases. Dysphagia 1995;10:136.
  14. Neumann S, Buchholz D, Wuttge-Hannig A, Hannig C, Prosiegel M, Schröter-Morasch H. Bilateral pharyngeal dysfunction after lateral medullary infarction (LMI). Dysphagia 1994;9:263.
  15. Buchholz DW. Clinically probable brainstem stroke presenting primarily as dysphagia and nonvisualized by MRI. Dysphagia 1993;8(3):235–238.
  16. Robbins JA, Levine RL, Maser A, Rosenbek JC, Kempster GB. Swallowing after unilateral stroke of the cerebral cortex. Arch Phys Med Rehabil 1993;74(12):1295–1300.
  17. Alberts MJ, Faulstich ME, Gray L. Stroke with negative brain magnetic resonance imaging. Stroke 1992;23(5):663–667.
  18. Robbins JA, Levine RL. Swallowing after unilateral stroke of the cerebral cortex: preliminary experience. Dysphagia 1988;3:11–17. | Article | PubMed | ChemPort |
  19. Gordon C, Hewer RL, Wade DT. Dysphagia in acute stroke. Br Med J 1987;295:411–414. | ISI | ChemPort |
  20. Veis SL, Logemann JA. Swallowing disorders in persons with cerebrovascular accident. Arch Phys Med Rehabil 1985;66:372–375. | PubMed | ChemPort |
  21. Kawai S, Tsukuda M, Mochimatsu I, et al. A study of the early stage of Dysphagia in amyotrophic lateral sclerosis. Dysphagia 2003;18(1):1–8.
  22. Higo R, Tayama N, Watanabe T, Nitou T. Videomanofluorometric study in amyotrophic lateral sclerosis. Laryngoscope 2002;112(5):911–917.
  23. Strand EA, Miller RM, Yorkston KM, Hillel AD. Management of oral-pharyngeal dysphagia symptoms in amyotrophic lateral sclerosis. Dysphagia 1996;11(2):129–139.
  24. Leighton SE, Burton MJ, Lund WS, Cochrane GM. Swallowing in motor neuron disease. J R Soc Med 1994;87(12):801–805.
  25. Nagaya M, Kachi T, Yamada T, Sumi Y. Videofluorographic observations on swallowing in patients with dysphagia due to neurogenerative diseases. Nagoya J Med Sci 2004;67(1–2):17–23.
  26. Pfeiffer RF. Gastrointestinal dysfunction in Parkinson's disease. Clin Neurosci 1998;5(2):136–146.
  27. Nagaya M, Kachi T, Yamada T, Igata A. Videofluorographic study of swallowing in Parkinson's disease. Dysphagia 1998;13(2):95–100.
  28. Leopold NA, Kagel MC. Pharyngo-esophageal dysphagia in Parkinson's disease. Dysphagia 1997;12(1):11–18.
  29. Leopold NA, Kagel MC. Laryngeal deglutition movement in Parkinson's disease. Neurology 1997;48(2):373–376.
  30. Leopold NA, Kagel MC. Dysphagia in progressive supranuclear palsy: radiologic features. Dysphagia 1997;12(3):140–143.
  31. Johnston BT, Castell JA, Stumacher S, et al. Comparison of swallowing function in Parkinson's disease and progressive supranuclear palsy. Mov Disord 1997;12(3):322–327.
  32. Neumann S, Reich S, Buchholz D, Purcell L, Jones B. Progressive supranuclear palsy (PSP): characteristics of dysphagia in 14 patients. Dysphagia 1996;11:164.
  33. Born LJ, Harned RH, Rikkers LF, Pfeiffer RF, Quigley EM. Cricopharyngeal dysfunction in Parkinson's disease: role of dysphagia and response to myotomy. Mov Disord 1996;11(1):53–58.
  34. Prosiegel M, Schelling A, Wagner-Sonntag E. Dysphagia and multiple sclerosis. Int MS J 2004;11(1):22–31.
  35. Wiesner W, Wetzel SG, Kappos L, et al. Swallowing abnormalities in multiple sclerosis: correlation between videofluoroscopy and subjective symptoms. Eur Radiol 2002:12(4):789–792.(Epub 2001 Sep 5.)
  36. Daly DD, Code CF, Anderson HA. Disturbances of swallowing and esophageal motility in patients with multiple sclerosis. Neurology 1962;59:250–256.
  37. Llabres M, Molina-Martinez FJ, Miralles F. Dysphagia as the sole manifestation of myasthenia gravis. Neurol Neurosurg Psychiatry 2005;76(9):1297–1300.
  38. Murray JP. Deglutition in myasthenia gravis. Br J Radiol 1962;35:43–52. | PubMed | ChemPort |
  39. Eaton LM, Lambert EH. Electromyography and electric stimulation of nerves and diseases of motor unit: observations on myasthenia syndrome associated with malignant tumors. JAMA 1957;163:1117. | ChemPort |
  40. Leonard RJ, Kendall KA, Johnson R, McKenzie S. Swallowing in myotonic muscular dystrophy: a videofluoroscopic study. Arch Phys Med Rehabil 2001;82(7):979–985.
  41. Perie S, Eymard B, Laccourreye L, et al. Dysphagia in oculopharyngeal muscular dystrophy: a series of 22 French cases. Neuromuscul Disord 1997;7(1):S96–S99.
  42. Castell JA, Castell DO, Duranceau CA, Topart P. Manometric characteristics of the pharynx, upper esophageal sphincter, esophagus, and lower esophageal sphincter in patients with oculopharyngeal muscular dystrophy. Dysphagia 1995;10(1):22–26.
  43. Ertekin C, Secil Y, Yuceyar N, Avdogdu I. Oropharyngeal dysphagia in polymyositis/dermatomyositis. Clin Neurol Neurosurg 2004;107:32–37. | Article | PubMed |
  44. Buchholz DW, Neumann S, Ravich W, O'Brien R, Jones B. Inclusion body myositis presenting as dysphagia: report of 3 cases. Dysphagia 1997;12:110.
  45. Rimington DS, Chambers ST, Parkin PJ, Pollock M, Donaldson IM. Inclusion body myositis presenting solely as dysphagia. Neurology 1993;43(6):1241–1243.
  46. Horner J, Alberts MJ, Dawson DV, Cook GM. Swallowing in Alzheimer's disease. Alzheimer Dis Assoc Disord 1994;8(3):177–189.
  47. Kagel MC, Leopold NA. Dysphagia in Huntington's disease: 16-year retrospective. Dysphagia 1992;7:106–114. | PubMed | ChemPort |
  48. Leopold NA, Kagel MC. Dysphagia in Huntington's disease. Neurology 1985;42:57–60. | ChemPort |
  49. Montesi A, Pesaresi A, Cavalli ML, Ripa G, Candela M, Gabrielli A. Oropharyngeal and esophageal function in scleroderma. Dysphagia 1991;6(4):219–223.
  50. Weisman RA, Calcaterra TC. Head and neck manifestations of scleroderma. Ann Otol Rhinol Laryngol 1978;87(3 pt 1):332–339.
  51. Kikendall JW. Pill esophagitis. J Clin Gastroenterol 1999;28(4):298–305.
  52. Stewart JT. Reversible dysphagia associated with neuroleptic treatment. J Am Geriatr Soc 2001;49(9):1260.
  53. Hhayashi T, Nishikawa T, Koga I, Uchida Y, Yamawaki S. Life-threatening dysphagia following prolonged neuroleptic therapy. Clin Neuropharmacol 1997;20(1):77–81.
  54. Sokoloff LG, Pavlakovic R. Neuroleptic-induced dysphagia. Dysphagia 1997;12(4):177–179.
  55. Dantas RO, Nobre Souza MA. Dysphagia induced by chronic ingestion of benzodiazepine. Am J Gastroenterol 1997;92(7):1194–1196.
  56. Leopold NA. Dysphagia in drug-induced parkinsonism: a case report. Dysphagia 1996;11(2):151–153.
  57. Buchholz D, Jones B, Neumann S, Ravich W. Benzodiazepine-induced pharyngeal dysphagia: report of two probable cases. Dysphagia 1995;10:142.
  58. Buchholz DW. Oropharyngeal dysphagia due to iatrogenic neurological dysfunction. Dysphagia 1995;10(4):248–254.
  59. Hughes TA, Shone G, Lindsay G, Wiles CM. Sever dysphagia associated with major tranquilizer treatment. Postgrad Med J 1994;70(826):581–583.
  60. Bazemore PH, Tonkonogy J, Ananth R. Dysphagia in psychiatric patients: clinical and videofloroscopic study. Dysphagia 1991;6(1):2–5.
  61. Miller CD, Oleshansky MA, Gibson KF, Cantilena LR. Procainamide-induced myasthenia-like weakness and dysphagia. Ther Drug Monit 1993;15(3):251–254.
  62. Swift TR. Disorders of neuromuscular transmission other than myasthenia gravis. Muscle Nerve 1981;4:334. | Article | PubMed | ChemPort |
  63. Pittinger CB, Eryase Y, Adamson R. Antibiotic induced paralysis. Anesth Analg 1970;49:487. | PubMed | ChemPort |
  64. McQuillen MP, Cantor HE, O'Rourke JRJr. Myasthenic syndrome associated with antibiotics. Arch Neurol 1968;18:402–415. | PubMed | ChemPort |
  65. Jones B. The tailored examination of the dysphagic patient. Appl Radiol February 1995;27–32.
  66. Jones B, Donner MW. How I do it: Examination of the patient with dysphagia. Dysphagia 1989;3(4):209–266.
  67. Dodds WJ, Stewart ET, Logemann JA. Physiology and radiology of the normal oral and pharyngeal phases of swallowing. AJR 1990;154:953–963. | PubMed | ChemPort |
  68. Rubesin SE, Jessurun J, Robertson D, Jones B, Bosma JF, Donner MW. Lines of the pharynx. RadioGraphics 1987;7(2):217–237.
  69. Miller AJ. Neurophysiological basis of swallowing. Dysphagia 1986;1:91–100. | Article |
  70. Bosma JF, Donner MW, Tanaka E, Robertson D. Anatomy of the pharynx, pertinent to swallowing. Dysphagia 1986;1:23–33. | Article |
  71. Curtis DJ. Radiographic anatomy of the pharynx. Dysphagia 1986;1:51–62. | Article |
  72. Donner MW, Bosma JF, Robertson DL. Anatomy and physiology of the pharynx. Gastrointest Radiol 1985;10:196–212. | PubMed | ChemPort |
  73. Miller AJ. Deglutition. Physiol Rev 1982;62:129–184. | PubMed | ISI | ChemPort |
  74. Bosma JF. Deglutition: pharyngeal stage. Physiol Rev 1957;37:275–300. | PubMed | ChemPort |
  75. Adnerhill I, Ekberg O, Groher ME. Determining normal bolus size for thin liquids. Dysphagia 1989;4(1):1–3.
  76. Dodds WJ, Taylor AJ, Stewart ET, Kern MK, Logemann JA, Cook IJ. Tipper and dipper types of oral swallows. AJR 1989;153:1197–1199. | PubMed | ChemPort |
  77. Jones B, Buchholz DW, Ravich WJ, Donner MW. Swallowing dysfunction in the post-polio syndrome: a cinefluorographic study. AJR 1992;158:283–286. | PubMed | ChemPort |
  78. Dodds WJ, Man KM, Cook IJ, Kahrilas PJ, Stewart ET, Kern MK. Influence of bolus volume on swallow-induced hyoid movement in normal subjects. AJR 1988;150:1307–1309. | PubMed | ChemPort |
  79. Ekberg O. The normal movements of the hyoid bone during swallow. Invest Radiol 1986;5:408–441.
  80. Ekberg O, Sigurjonsson S. Movements of the epiglottis during deglutition: a cineradiographic study. Gastrointest Radiol 1982;7:101–107. | Article | PubMed | ChemPort |
  81. Ryu JS, Park SR, Choi KH. Prediction of laryngeal aspiration using voice analysis. Am J Phys Med Rehabil 2004;83(10):753–757.
  82. McCullough GH, Wertz RT, Rosenbek JC. Sensitivity and specificity of clinical/bedside examination signs for detecting aspiration in adults subsequent to stroke. J Commun Disord 2001;34(1–2):55–72.
  83. Linden P, Kuhlemeier KV, Patterson C. The probability of correctly predicting subglottic penetration from clinical observations. Dysphagia 1993;8(3):170–179.
  84. Linden P, Siebens AA. Dysphagia: predicting laryngeal penetration. Arch Phys Med Rehabil 1983;64(6):281–284.
  85. Halum SL, Merati AL, Kulpa JI, Danielson SK. Jaradeh SS, Toohill RJ. Videofluoroscopic swallow studies in unilateral cricopharyngeal dysfunction. Laryngoscope 2003;113(6):981–984.
  86. Olsson R, Ekberg O. Videomanometry of the pharynx in dysphagic patients with a posterior cricopharyngeal indentation. Acad Radiol 1995;2(7):597–601.
  87. Brady AP, Stevenson GW, Somers S, Hough DM, Di Giandomenico E. Premature contraction of the cricopharyngeus: a new sign of gastroesophageal reflux disease. Abdom Imaging 1995;20(3):225–229.
  88. Ekberg O. Cricopharyngeal bar: myth and reality. Abdom Imaging 1995;20(2):179–180.
  89. Curtis DJ, Cruess DF, Berg T. The cricopharyngeal muscle: a videorecording review. AJR 1984;142:497–500. | PubMed | ChemPort |
  90. Ekberg O, Nylander B. Dysfunction of the cricopharyngeal muscle. Radiology 1982;143:481–486. | PubMed | ChemPort |