The Laryngoscope

Lippincott Williams & Wilkins, Inc., Philadelphia

2002 The American Laryngological,
Rhinological and Otological Society, Inc.

Swallowing Disorders in the Elderly

Joshua S. Schindler, MD; James H. Kelly, MD

Changes that occur as a natural part of senescence

in the complex action of deglutition predispose us to
dysphagia and aspiration. As the baby-boomers begin
to age, the onset of swallowing difficulties will begin to
manifest in a greater number of our population. Recent
advances in the evaluation of normal and abnormal
swallowing make possible more precise anatomical and
physiological diagnoses. Coupled with an understanding of swallowing physiology, such detailed evaluation
allows greater opportunity to safely manage dysphagia
with directed therapy and appropriate surgical intervention. The current study is a discussion of the
changes that occur in deglutition with normal aging, contemporary evaluation of swallowing function,
and some of the common causes of dysphagia in
elderly patients. Key Words: Dysphagia and swallowing, elderly, geriatric, videofluoroscopy, flexible fiberoptic evaluation of swallowing, stroke,
Parkinsons disease, drug, pill-induced esophageal injury, amyotrophic lateral sclerosis, cricopharyngeus, Zenkers diverticulum.
Laryngoscope, 112:589 602, 2002

INTRODUCTION
Dysphagia becomes an increasingly common problem
as we age. By the year 2020, it is estimated that 16.4% of
the population will be over the age of 65.1 With 6 to 10
million Americans currently reporting some degree of
swallowing difficulty,2 one might expect that the diagnosis
of dysphagia is as straightforward as it is common. However, despite a greater understanding of swallowing physiology and advances in dysphagia evaluation, disorders of
swallowing and feeding remain underappreciated by both
the general public and physicians.3
The difficulty in diagnosing dysphagia in the elderly
population is multifactorial. The causes or origins are
diverse, and their management spans numerous medical
and surgical specialties. Depression, cognitive dysfunc-

From the Departments of OtolaryngologyHead and Neck Surgery,

Johns Hopkins Medical Institution (J.S.S., J.H.K.) and Greater Baltimore
Medical Center (J.H.K.), Baltimore, Maryland, U.S.A.
Supported in part by resident training grants of the Johns Hopkins
Medical Institution and Greater Baltimore Medical Center.
Editors Note: This Manuscript was accepted for publication November 19, 2001.
Send Correspondence to James H. Kelly, MD, Department of
OtolaryngologyHead and Neck Surgery, Greater Baltimore Medical Center,
6701 North Charles Street, Suite 4202, Baltimore, MD 21204, U.S.A.

Laryngoscope 112: April 2002

tion, and behavioral changes may delay the recognition of

dysphagia in elderly patients by their providers. In addition, swallowing disorders are often insidious in their
onset and may not manifest clinically for years to decades.
Over such time periods, self-learned compensatory strategies mask the normal physiological changes that weaken
the integrity of deglutition as we age. Although these
changes have previously been described as presbypharynges and considered a natural part of senescence, the
ability to adapt gradually to changes in eating and swallowing renders the diagnosis of dysphagia abnormal at
any age. As such, the identification of swallowing disorders in elderly patients requires a comprehensive evaluation to determine the cause or origin and direct therapy.
Recent advances in the evaluation of dysphagia allow
for identification of specific anatomical and physiological
abnormalities during deglutition. Although such information is useful to demonstrate the site of dysfunction, the
origin or cause of a patients dysphagia may remain obscure without a basic understanding of the complex physiology of deglutition and the changes that occur with normal aging.

DISCUSSION
Anatomy and Physiology of Swallowing
Oral phase. Traditionally, deglutition has been divided into three neuroanatomical phases: oral, pharyngeal, and esophageal. Although arbitrary, this division
facilitates evaluation and communication among professionals. The oral phase begins with the entry of food into
the oral cavity and can be subdivided into the voluntary
oral preparatory and oral transport phases. The oral preparatory phase primarily involves bolus manipulation and
reduction in particle size. Facial musculature, especially
the orbicularis oris, and buccinator muscles help hold the
bolus within the oral cavity and positioned under the teeth
for mastication. Reduction of particle size occurs through
the coordinated action of the temporalis, masseter, and
medial and lateral pterygoid muscles creating a grinding
action of the teeth. The intrinsic musculature of the
tongue, innervated by the hypoglossal nerve, also helps to
manipulate the bolus and facilitate mastication through a
lateral rolling motion. During the oral preparatory stage
the soft palate bulges forward, effectively maintaining the
bolus in range of the tongues mobile tip and opening the
Schindler and Kelly: Swallowing Disorders

589

nasopharynx for breathing (Fig. 1). Sensory information is

provided through mechanoreceptive cells concentrated on
the tip of the tongue and along the center of the palate.
These cells provide information regarding bolus position
and size through trigeminal nerve afferent fibers. Modulation of oral peristaltic amplitude also depends on mechanoreceptor determination of bolus viscosity.4 Chemoreceptors and thermoreceptors also line the oral cavity and
provide information essential to bolus identification. Afferent stimulation from the oral cavity passes to the brainstem, where in turn it triggers the salivary nuclei. Parasympathetic secretomotor fibers from the glossopharyngeal and facial nerve innervate the parotid, submandibular, and sublingual glands. Saliva production occurs
throughout the oral preparatory phase and aids in bolus
formation and digestion.
After sufficient mastication and creation of a suitable
bolus, the oral transport phase begins with voluntary
movement of the bolus posteriorly by pressing the anterior
tongue against the hard palate (Fig. 2). Dynamic stimulation of hard palate mechanoreceptors initiates peristaltic movement of the tongue. As the bolus moves into the
oropharynx, the leading edge passes posterior to the faucial arch and triggers the involuntary pharyngeal swallow
through free nerve endings of the glossopharyngeal and
vagal nerves.4 The normal duration of posterior oral transit ranges from 1 to 1.25 seconds, regardless of viscosity.5
Pharyngeal phase. Electromyographic recordings
demonstrate that either the genioglossus or mylohyoid
muscle is the first to fire during the involuntary pharyngeal swallow.6 This initial segment of pharyngeal muscle

Fig. 2. The oral transport phase. Peristaltic anteriorposterior

tongue movement drives the bolus into the pharynx. Palatal musculature seals the nasopharynx. (Adapted with permission from
Rubin JS, Bradshaw CR. The physiological anatomy of swallowing.
In: Rubin JS, Broniatowski M, Kelly JH, eds. The Swallowing Manual. San Diego: Singular Publishing, 2000:120.)

Fig. 1. The oral preparatory phase. Voluntary action of the tongue

musculature holds bolus anteriorly while palatal and posterior
tongue musculature prevents premature pharyngeal seepage and
allows uninterrupted nasal breathing. (Adapted with permission
from Rubin JS, Bradshaw CR. The physiological anatomy of swallowing. In: Rubin JS, Broniatowski M, Kelly JH, eds. The Swallowing
Manual. San Diego: Singular Publishing, 2000:120.)

activity is called the leading complex. The styloglossus

pulls the tongue posteriorly while the palatoglossus raises
the posterior portion of the tongue and lowers the sides of
the soft palate. The remainder of the suprahyoid muscles
contract, drawing the hyoid bone superiorly, thereby elevating the larynx, and anteriorly while depressing the jaw
(Fig. 3). The velopharyngeal muscles (levator veli palatini,
tensor veli palatini, palatopharyngeus, and muscularis
uvula) act in unison to seal the nasopharynx in preparation for passage of the bolus to the muscular pharynx.
Through the coordinated actions of the suprahyoid musculature, laryngeal elevation and anterior repositioning
provide the fulcrum for inversion of the epiglottis by the
bolus. As the epiglottis folds posteriorly and inferiorly, the
bolus is directed laterally through the piriform sinuses.
Seepage into the airway is prevented by laryngeal elevation, inversion of the epiglottis, and closure of both the
true and false vocal folds (Fig. 4). Respiration momentarily ceases during this period. Once the bolus enters the
posterior pharynx, powerful contractions from the pharyngeal constrictor muscles (superior, middle, and inferior)
act to strip the bolus from the oropharynx and hypopharynx. The stylopharyngeus and salpingopharyngeus pull
the pharynx superiorly and medially to ensure thorough
removal of the bolus from the pharynx. Mechanoreceptors
present in the tonsillar pillar continually sense static
pressure in the oropharynx and continue pharyngeal
stripping until the entire bolus is cleared.4

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590

Schindler and Kelly: Swallowing Disorders

Fig. 3. The pharyngeal phase. The bolus is directed into the vallecula. Suprahyoid musculature pulls the larynx superiorly and anteriorly. (Adapted with permission from Rubin JS, Bradshaw CR. The
physiological anatomy of swallowing. In: Rubin JS, Broniatowski M,
Kelly JH, eds. The Swallowing Manual. San Diego: Singular Publishing, 2000:120.)

Completion of the pharyngeal phase requires passage

through the upper esophageal sphincter (UES). This is a
manometrically defined region of approximately 3 to 4 cm
in length, which functions to prevent aerophagia and limit
esophageal reflux. Anatomically, the UES incorporates
the cricopharyngeus (CP) muscle, as well as some of the
some of the lower fibers of the inferior pharyngeal constrictor and superior fibers of the circular muscle of the
esophagus.7,8 The CP muscle, which is composed of horizontal fibers (pars fundiformis) and oblique fibers (pars
obliqua),9 appears tonically active at rest. Inhibitory stimulation allows relaxation of the CP and opening of the
sphincter during maximal anteriorsuperior hyoid elevation. The inhibitory trigger for UES relaxation remains
unclear, but the degree of relaxation depends on the size of
the bolus.10
Esophageal phase. The esophageal phase begins
after bolus passage through the UES. The esophagus is a
muscular tube that begins at the cricoid cartilage and
terminates in the fundus of the stomach. The elastic layer
of the pharynx becomes the muscularis mucosae of the
esophagus. This layer joins the inner (circumferential)
and outer (longitudinal) layers of muscularis externa.
Completely under involuntary control, the muscularis externa is composed of striated muscle fibers for the proximal 5% of the esophagus, which then blend with smooth
muscle fibers throughout the mid portion of the esophagus. The distal esophagus is composed almost entirely of
smooth muscle and contains another manometrically defined sphincter. Specialized smooth muscle fibers with
intrinsic tonic myogenic activity create a high-pressure
Laryngoscope 112: April 2002

Fig. 4. Pharyngoesophageal transition. Epiglottic retroversion and

intrinsic laryngeal muscle contraction completely seal the airway as
bolus passes posteriorly through the relaxed upper esophageal
sphincter. (Adapted with permission from Rubin JS, Bradshaw CR.
The physiological anatomy of swallowing. In: Rubin JS, Broniatowski M, Kelly JH, eds. The Swallowing Manual. San Diego: Singular Publishing, 2000:120.)

sphincter near the gastroesophageal junction.6 The vagus

nerve mediates inhibition of this lower esophageal sphincter (LES) in response to bolus stimulation, as well as
gastric distention. Passage of the bolus through the LES
completes the act of deglutition.

Neuroanatomy of Swallowing
Because the most common cause of dysphagia in elderly patients is stroke, a basic understanding of the neuroanatomy of deglutition is essential to diagnosis and
therapy. Although coordination of most of the more than
40 paired muscles involved in deglutition comes from the
brainstem, the cerebral cortex is essential to the voluntary
oral and portions of the pharyngeal phase. Bilateral cortical input maintains facial tone and prevents spillage of
oral content. Patterned responses, modulated by the cerebral cortex, govern mastication and bolus control during
the oral preparatory phase. In animals, lesions of precentral and inferior frontal gyrus produce significant impairment in facial, tongue, and masticatory coordination, as
well as pharyngeal-phase activities such as hyoid elevation and vocal fold closure. Conversely, stimulation of
these regions evokes a functional swallow coupled with
masticatory activity.6,11 Other regions adjacent to the sylvian fissure and lateral precentral cortex have been shown
to evoke swallowing responses associated with orofacial
movement and salivation in humans during awake craniotomy for epilepsy focus ablation.6,12 Although cortical
brain centers can initiate a voluntary swallow, these acSchindler and Kelly: Swallowing Disorders

591

tivities appear to be primarily modulatory because observations in stroke patients have demonstrated that removal of all cortical and subcortical stimulation above the
level of the brainstem still allows a functional swallow
with appropriate pharyngeal stimuli.13
The brainstem houses the motor nuclei of nearly all
the muscles involved in deglutition, as well as the pattern
generators necessary to evoke a complete swallowing reflex. The two brainstem regions most directly related to
swallowing are the nucleus tractus solitarius and the nucleus ambiguus. The nucleus tractus solitarius, or master
nucleus, lies within the dorsal medulla and receives both
cortical and subcortical input, as well as peripheral sensory input through free nerve endings of glossopharyngeal
and vagal afferent fibers within the oropharynx.14 Simulation from these sources passes to short-latency interneurons within the nucleus and projects to specific cranial
nuclei, causing sequential muscle firing, which results in
a coordinated swallow.4,6,12 The nucleus ambiguus, or
switching nucleus, houses the vagal motor nuclei and is
responsible for the esophageal phase of swallowing. Pharyngeal afferent fibers trigger motor nuclei with projections directly onto striated muscle of the distal pharynx
and proximal esophagus. These neurons have longer latencies than the nucleus tractus solitarius interneurons
and produce sequential excitatory activity.4,6
Propagation of esophageal contraction occurs within
the body of the esophagus itself. Between the longitudinal
and circular muscle layers lies the myenteric plexus of
Auerbach. Although the trigger for primary peristalsis is
the vagal nucleus, the intrinsic nerves of the esophagus
propagate secondary, or autonomous, peristalsis from the
junction between striated and smooth muscle fibers. Thus,
central control of swallowing is maintained from the oral
cavity to the midportion of the esophagus.

Changes in Geriatric Swallow

Despite numerous studies demonstrating physiological changes in swallowing with advancing age, there remains strong disagreement regarding what constitutes
normal swallowing in elderly patients and whether these
changes represent dysphagia. Doty and Bosma15 were
among the first to note swallowing changes in the elderly
when they studied electromyographic responses during
deglutition in young and old patients. They posited that
swallowing, like locomotion, was subject to different levels
of arousal and pharyngeal stimulation, which diminishes
as the subject ages.15 Recent advances in videoendoscopy
and fluoroscopy have allowed more focused studies of
swallowing and have pinpointed a number of discrete
physiological changes in normal deglutition as we age.
Overall, few clinically significant abnormalities arise
during the oral phase, and feeding performance does not
significantly worsen with age in otherwise healthy patients.16 Most difficulties are the result of generalized
age-related changes in skeletal muscle strength and include reduced facial muscle strength causing poor cup
drinking16 and decreased masticatory strength.17 More
substantial changes occur in the tongue because elderly
patients have diminished lingual pressure reserve necessary to drive pharyngeal swallowing.18 In addition, inLaryngoscope 112: April 2002

592

creased connective tissue within the body of the tongue

restricts bolus control, requiring multiple tongue movements that hold the bolus more posteriorly and allow the
bolus to enter the vallecula prematurely.5,17 Although
feeding performance does not seem to be significantly
affected by changes in oromotor skills,16 oral-phase problems are common because difficulty ingesting, controlling,
or delivering the bolus relative to swallowing initiation is
noted in 63% of healthy elderly subjects.19 These abnormalities frequently lie clinically silent because the patient
effectively compensates by changing diet consistency and
feeding duration.
Pharyngeal-phase abnormalities are of greater clinical significance because they reduce the swallowing reserve, a measure of strength and coordination in excess of
that needed to prevent aspiration. These abnormalities
are the least common,19 and aspiration is usually secondary to other conditions present in the subject.20 Manometric studies have demonstrated that the amplitude of pharyngeal pressures, duration of pressures, and rate of
propagation are preserved in elderly patients.21 Despite
the preservation of muscular activity, pharyngeal swallowing is delayed in healthy elderly subjects relative to
younger subjects,5,21 and elderly subjects frequently require multiple swallows to effectively clear a bolus from
the pharynx.22 During this time, these subjects are three
times more likely to have inspiration rather than expiration after swallowing and have more laryngeal penetration as evidenced by coughing and polyphasic laryngeal
movements.22 Coupled with deficits in pharyngolaryngeal
sensory discrimination that occur with age,23,24 this reduction in pharyngeal reserve may lead to silent aspiration in the otherwise healthy subject, as demonstrated by
Smith et al.25 in patients greater than 90 years of age.
Despite somewhat contradictory studies regarding
normal changes in UES function as we age, decreased
pharyngeal clearance may also be the result of CP and
proximal esophageal abnormalities. Although Ekberg and
Feinberg19 reported defective opening of the CP in 39% of
elderly patients, subsequent manometric studies have
demonstrated either no change or decreased resting tone
in the UES of elderly patients.20 Delayed egress of material from the pharynx may still occur, despite normal CP
tone, as a result of increased connective tissue in the UES
and decreased cross-sectional area of the esophageal inlet.
This supposition is supported by the identification of
higher hypopharyngeal wave amplitudes in elderly subjects.20 Once through the cricopharyngeal segment, primary esophageal peristalsis is preserved, but secondary
peristalsis, which serves to strip esophageal residue following the leading complex, is less frequent or entirely
absent in elderly patients.26 Together, these abnormalities in the pharyngoesophageal transport may lead to
longer feeding times, increased pharyngeal residue, and
aspiration in some elderly patients.

Evaluation of Dysphagia in Elderly Patients

Evaluation of swallowing disorders in elderly patients begins with a comprehensive history and physical
examination. The first important determination to be
made is whether the patient has a feeding or a swallowing
Schindler and Kelly: Swallowing Disorders

disorder or both. Although such a distinction may seem

simple, in practice, it can be difficult to elucidate. Careful
questioning regarding eating habits, duration of feeding,
diet, frequency of meals, and weight changes is essential.
Patients with feeding problems secondary to cognitive difficulties may eat sporadically for short periods. Meal times
are often irregular, and many of these patients progressively lose weight. Patients with primary dysphagia often
require longer feeding periods as they gradually adapt
through strategies such as multiple swallows, smaller
bites, and prolonged chewing.27 They may become selfconscious and even embarrassed by their slow feeding or
fear of choking or coughing on certain foods or liquids. As
a result, elderly patients frequently avoid social meals
with family members, allowing dysphagia to go unrecognized for years.3,28 Unlike patients with primary eating
disorders, patients with mild oropharyngeal dysphagia
may actually gain weight as they turn to more processed
foods, such as milkshakes and dietary supplements, with
higher calorie content.3 As a result, physicians must initiate discussions regarding eating habits to detect early
signs and symptoms of dysphagia.
Once the diagnosis of dysphagia is suspected, it is not
uncommon for physicians to turn their attention to physical examination and testing. However, careful questioning focused on many of the common characteristics of
dysphagia can lead to a diagnosis in many cases. The
presence of solid, semisolid, or liquid dysphagia can help
direct the discussion immediately. Linden and Siebens29
demonstrated that, in general, patients with fixed obstructions such as webs or strictures complain of solid
rather than liquid dysphagia. Other symptoms associated
with fixed esophageal lesions (especially, CP dysfunction
and Zenkers diverticulum) include globus pharyngeus,
halitosis, wet vocal quality, and history of gastroesophageal reflux.30,31 Odynophagia may also be related to fixed
obstructions or reflux; however, it is more commonly associated with neoplasms in elderly patients. Recurrent
pneumonia may be seen in patients with both fixed obstructions and neuromuscular weakness.
Patients who complain of difficulties with liquids are
more likely to have neurological conditions that weaken
the pharyngeal musculature or result in discoordination of
the swallowing reflex.29 Associated symptoms including
nasopharyngeal regurgitation and dysarthria may point
to the level of the lesion. Breathy hoarseness may represent glottic incompetence, which places the patient at risk
for aspiration in the setting of other neurological abnormalities (e.g., decreased sensation or poor cough). Although wet vocal quality is commonly thought to be a
symptom of swallowing incompetence,32 controversy exists over its importance.3335 Whereas dysphonia has been
associated with aspiration following acute stroke,34,35 wet
vocal quality alone failed to demonstrate significant association with aspiration on videofluoroscopy.35 Thus, voice
changes may be useful correlates during bedside examination to evaluate swallowing function and response to
therapy but are insufficient to predict aspiration in the
absence of more objective studies. Completion of the dysphagia history includes a comprehensive review of systems and discussion of current medications. This informaLaryngoscope 112: April 2002

tion may point to other comorbid conditions affecting

appetite, feeding behavior, or swallowing.
Physical examination of the oral cavity and upper
aerodigestive tract in conjunction with neurological evaluation focusing on mental status and cranial nerves can
be useful in diagnosis and management of patients with
dysphagia. Assessment should begin with assessment of
the oral cavity and integrity of the oral mucosa. Saliva
quantity and quality should be assessed because moisture
is essential, not only for bolus formation but also as a
trigger of the pharyngeal swallow through glossopharyngeal afferents. The presence of dental plates should be
noted because denture wearers demonstrate a significant
decrease in feeding performance that is independent of
age.16 Although the relationship between dental appliances and feeding is not clear, it is thought that dentures
may block palatal mechanoreceptors. Diminished palatal
sensation leads to poor bolus control and oral transit delays, which results in longer feeding times.
Neurological evaluation should include an assessment of the patients level of arousal, orientation, and
cognitive skills and thorough cranial nerve examination.
Swallowing competence depends on skeletal muscle and,
as such, is subject to weakness with diminished arousal
states.15 Brief examination of the patients mental status
may point to subtle cognitive difficulties that affect appetite, self-feeding, and dysphagia.36,37 Cranial nerve evaluation should focus on trigeminal (fifth), facial (seventh),
glossopharyngeal (ninth), vagus (tenth), and hypoglossal
(twelfth) cranial nerve function. Facial (seventh nerve) or
tongue (twelfth nerve) weakness may cause oral preparatory delays and become evident through anterior loss of
bolus, premature bolus leakage over the tongue base, and
increased oral residual. Similar findings may be noted in
patients with sensory loss within the oral cavity through
trigeminal nerve weakness or progressive loss of two-point
discrimination. Gag reflex testing is a common component
of the cranial nerve examination and assesses both glossopharyngeal sensation in the posterior pharyngeal wall
and soft palate and vagus nerve motor function with velar
movement, glottic closure, and hyoid elevation. Although
gag reflex testing provides information about numerous
components of deglutition, the significance of a poor gag
response with regard to swallowing competence is less
clear. Despite identification of poor gag response as the
only significant predictor of aspiration following acute
stroke,38 other studies of patients with normal and abnormal gag responses have failed to demonstrate any significant correlation with aspiration on videofluoroscopic
swallowing study (VFSS).39,40 It is important to note that
the gag reflex is not a part of normal deglutition and is
absent in more than one-third of healthy adults without
dysphagia.41 Brief peripheral neurological evaluation
with attention to pyramidal weakness, sensory deficits,
extrapyramidal movements, or clonus may also help identify systemic neurological disorders associated with dysphagia, such as multiple sclerosis or Parkinsons disease.
In the evaluation of the dysphagic patient, the most
important determination is the risk of aspiration; this
determines the patients feeding method (i.e., bolus unrestricted, bolus restricted, alternative to oral intake), comSchindler and Kelly: Swallowing Disorders

593

pensatory strategies, and need for swallowing therapy.

However, confounding problems, such as diminished laryngeal sensation and poor cough, render bedside swallowing evaluation inadequate to assess pharyngeal and
esophageal dysphagia or predict aspiration.29,42,43,44
Studies have demonstrated that bedside swallowing assessment fails to identify 33% to 50% of patients with
significant aspiration on VFSS.42,43 In an extensive metaanalysis of studies addressing dysphagia following stroke,
Martino et al.38 confirmed the difficulty in detecting patients at risk for aspiration by physical examination. Data
from 13 suitable studies identified only 2 of 49 bedside
findings that were capable of predicting aspiration by
videofluoroscopy: reduced unilateral pharyngeal sensation and coughing with 50-mL water swallow.38 Numerous noninvasive procedures, including respiratory pattern
monitoring, pulse oximetry, cough reflex, ultrasonography, and acoustic monitoring, have been developed to assist the physician in identifying patients with swallowing
incompetence. Although useful in following subsets of patients with dysphagia, the noninvasive procedures are not
widely used because of expense, limitations of technique,
and inferior sensitivity relative to more invasive
evaluations.35

Swallowing Studies
There are many studies available to aid clinicians in
their evaluation of the dysphagic patient. Because these
studies vary in diagnostic capability, invasiveness, inconvenience to the patient, and cost, it is important to use the
history and physical examination to choose the most appropriate evaluation. In addition, one must assess the
patients risk of aspiration and, if indicated, select a study
that addresses the patients swallowing safety.
The simplest evaluation of upper airway anatomy is
the barium swallow. During this study the patient swallows a suspension of barium with concurrent radiography
of the neck and thorax. Such imaging provides an inexpensive and relatively noninvasive means of diagnosing
anatomical lesions of the pharynx and esophagus. However, the true diagnostic power of barium swallow examinations comes through numerous modifications of the
basic technique. By varying the consistency of the barium
suspension, one can evaluate swallowing competence and
identify aspiration through laryngeal penetration of contrast agent. The addition of air-contrast granules may be
used to distend the pharyngeal and esophageal lumen,
providing visualization of subtle mucosal and submucosal
lesions.
The most important modification of the original barium swallow is the addition of videofluorography and presence of a speech-language pathologist or radiologist
trained in swallowing physiology. Defined as the gold
standard for swallowing evaluation and identification of
aspiration, the VFSS provides a dynamic view of deglutition from the oral cavity to the lower esophageal sphincter
and substantially extends the diagnostic capability of the
study. Furthermore, addition of a speech-language pathologist allows assessment of compensatory swallowing
strategies, which facilitates safe, effective swallowing and
provides the basis for swallowing rehabilitation. DrawLaryngoscope 112: April 2002

594

backs of this study include the radiation used during the

procedure (roughly equivalent to a chest radiograph); the
reliance on multiple personnel, including speech-language
pathologist, radiologist and technician, in its performance;
and its cost. Obviously, these factors must be weighed
against the significant morbidity and cost of aspiration
pneumonia in the elderly population.
A useful adjunct to VFSS is the fiberoptic endoscopic
evaluation of swallowing. This portable study incorporates the use of flexible fiberoptic laryngopharyngoscopy
to assess dynamic swallowing abnormalities and aspiration. Using liquids and solids of different consistencies
combined with blue dye, elements of pharyngeal swallowing may be observed directly for pathological changes.
With this technique, subtle abnormalities in laryngeal
elevation, epiglottis inversion, pooling, and late aspiration
can be detected without the use of radiation or fluoroscopy
suite. In addition to evaluating swallowing safety, this
study may be performed during rehabilitation to directly
assess the progress and effectiveness of different swallowing strategies and food consistencies. Fiberoptic endoscopic evaluation with sensory testing adds air pulsation
through the flexible scope to provide a comprehensive and
quantifiable assessment of pharyngeal sensation of
difficult-to-access regions such as the aryepiglottic and
false vocal folds.45 Although appropriate for patients who
are too sick to undergo VFSS, fiberoptic evaluation is
limited in its ability to detect aspiration during bolus
movement because the field is obscured by epiglottic excursion. As such, the study is most useful for assessing
swallowing ability and for patient teaching, rather than
for comprehensive evaluation of swallowing function.
Other swallowing studies are available to address
specific abnormalities noted by radiographic imaging. Abnormalities in the region of the UES or LES may be
studied using manometry.46 Esophageal manometric
probes use solid-state pressure sensors along the length of
the upper aerodigestive tract to the stomach and allow for
quantitative evaluation of the UES and LES physiology,
as well as esophageal waveforms. This study is useful to
identify neuromuscular abnormalities associated with
gastroesophageal reflux, cricopharyngeal dysfunction, or
achalasia but is uncomfortable for the patient and limited
by its inability to diagnose fixed lesions. A more comprehensive evaluation combines this technique with radiography in the form of manofluorography. Such studies may
provide useful physiological information to physicians
treating neuromuscular disorders of the UES because the
functional sphincter is anatomically ill-defined. Electromyography may also be useful in delineating the functional UES and has been described in the performance of
percutaneous chemical myotomy using botulinum toxin.47

Common Causes and Management of Dysphagia

in Elderly Patients
Cerebrovascular disease. With as many as 200,000
patients who have cerebrovascular accidents in the United
States annually, stroke is by far the most common cause of
dysphagia in elderly patients. Of patients who have
strokes, 45% to 65% experience swallowing difficulties
within the first 6 months after the event.13,48,49 Although
Schindler and Kelly: Swallowing Disorders

many of these patients eventually recover competent

swallowing, the morbidity of stroke-related dysphagia is
high. Nearly half of all stroke patients aspirate early after
the event,50 and as many as 25% of all patients having
cerebrovascular accidents die of aspiration pneumonia
within the first year of rehabilitation.13,51 With such a
large number of cases annually and high associated mortality, it is important to understand the evolution of dysphagia following stroke and attempt to predict which patients are at greatest risk for complications during
rehabilitation.
Attempts to predict the likelihood of dysphagia and
prognosis for recovery following acute stroke by lesion
location have met with only limited success. Specific patterns of dysmotility are difficult to ascribe to specific neuroanatomical lesions because strokes are rarely isolated
and many of the pathways that facilitate lingual and
pharyngeal motility are not completely understood. Frequently, patients with single-hemisphere lesions identified by computed tomography following acute unilateral
stroke have one or more confounding lesions in the asymptomatic hemisphere on magnetic resonance imaging.13 As
one might expect, studies of cortical strokes suggest that
larger infarctions are associated with an increased likelihood of dysphagia and aspiration.50 This finding was confirmed and refined in a small study by Daniels et al.,52
who noted that subcortical and periventricular white matter lesions were significantly associated with poor lingual
coordination and oral-phase dysphagia. Such lesions may
interrupt cortex to basal ganglia connections resulting in
a disruption of motor planning and dysphagia.
Despite the difficulties associated with identifying
patients with discrete, unifocal lesions, many investigators have attempted to characterize the swallowing abnormalities associated with hemispheric lesions in an attempt to identify patients most at risk of aspiration
following cerebrovascular accident. To date, the evidence
is contradictory. Robbins et al.53 found the greatest abnormalities in swallowing function in 40 patients following
left-hemisphere strokes despite a greater frequency of aspiration with right-sided strokes. Left-sided cortical lesions were associated with oral and buccofacial apraxia
producing significant oral-phase delays.53 Contrary to
neurophysiological studies in primates suggesting bilateral cortical representation in lingual coordination,54 Robbins et al.53 proposed that lingual, labial, and mandibular
coordination is predominantly a left-hemisphere function.
This hypothesis remains in dispute because a subsequent
study of lingual coordination following acute stroke found
that nearly two-thirds of the patients with oral-phase
delays on VFSS had right-hemisphere lesions.52 Although
there is no agreement regarding the importance of lesion
side in dysphagia following acute stroke, both studies
suggested that anterior lesions of either hemisphere are
associated with significantly longer swallowing durations53 and greater difficulty with lingual coordination.52
Brainstem strokes are less common than cortical infarctions but carry a higher incidence of dysphagia and
aspiration.55,56 Unlike cortical infarctions, lesion localization in the brainstem is a critical determinant of swallowing dysfunction because swallowing function may be imLaryngoscope 112: April 2002

paired either through weakness of the corticobulbar

fibers, which control pharyngeal musculature, or injury to
the swallowing center pattern generators (the nucleus
tractus solitarius and the nucleus ambiguus) within the
medulla. Medial medullary lesions, characterized by flaccid hemiparesis, hemisensory deficits, and cranial nerve
palsies (including lingual hemiparesis), have a 5- to 10fold lower incidence of dysphagia when compared with
lateral brainstem lesions.57 Wallenberg syndrome of lateral medullary infarction results from occlusion of the
posterior inferior cerebellar artery and produces characteristic signs including ataxia, hemisensory deficits, nystagmus, Horner syndrome, and hiccup.58 Patients with
lesions in this distribution frequently note some degree of
dysphagia, and as many as 44% have aspiration on
VFSS.56 Lateral lesions of the mid portion of the medulla,
especially those with significant vertical extension, may
damage the trigeminal nucleus or solitary tract, producing
pharyngeal and laryngeal sensory deficits. Lesions of the
inferolateral medulla are associated with unilateral true
vocal fold paresis through injury to the vagal nucleus and
may impair the pharyngeal swallowing reflex through
injury of the nucleus ambiguus.56
Management of dysphagia following cerebrovascular
accident depends largely on the severity of neurological
damage and rate of recovery. During rehabilitation of
brainstem strokes, intensive swallowing therapy has been
shown to decrease the risk of aspiration and speed the
return to normal oral feeding.55 Such therapy, directed by
a speech-language pathologist, is directed toward increasing the sensory awareness of food and improving pharyngeal stripping by chin-tuck positioning and the doubleswallow technique. A dietitian may be helpful in altering
the consistency of foods and increasing the nutritional
value of meals to decrease feeding times. Medialization
thyroplasty is appropriate for patients with dysphagia
and dysphonia secondary to persistent weakness of vocal
fold adduction.59 Following surgical correction, patients
demonstrate improved management of secretions and thin
liquids, as well as decreased reliance on compensatory
strategies. In cases of severe stroke, early percutaneous
endogastric tube placement has been found to reduce the
incidence of aspiration during the poststroke period when
compared with nasogastric tube feeding.60 Although critical for ventilatory support in some patients with devastating neurological sequelae of stroke or pulmonary complications, tracheotomy alone does not prevent deglutitive
aspiration.61
Despite the tremendous morbidity associated with
dysphagia following cerebrovascular accident, most patients who survive return to their prestroke diet within
several weeks of the event. Studies of the natural history
of dysphagia following cerebrovascular accident demonstrate that half of the patients recover to premorbid status
within 1 week48,62 and up to 87% resume normal oral
intake by 6 months after the event.49 Interestingly, serial
examination of 95 patients by VFSS following acute stroke
suggests that recovery is not a linear process. Although
there was an overall decline in the number of patients
with incompetent swallowing following stroke, there was
a shift in the population of patients with dysphagia such
Schindler and Kelly: Swallowing Disorders

595

that two-thirds of patients with aspiration by VFSS at 1

month showed no evidence of aspiration 3 weeks earlier.43
Whether this late dysphagia represents the result of ongoing silent infarctions or stroke progression is unclear.
However, patients with competent swallows in the immediate poststroke period require careful surveillance for
several months following the event.

Neuromuscular Disease
Parkinsons disease. The most common neuromuscular disease seen in elderly patients that frequently results in dysphagia is Parkinsons disease (PD). Caused by
a deficiency in dopamine production within the substantia
nigra, PD is a slowly progressive disease of the basal
ganglia that results in the inability to execute learned
motor skills. There are 40,000 new cases of Parkinsons
disease annually in the United States, and as many as 1%
of individuals over 50 years of age show signs of basal
ganglion dysfunction.13 The classic signs include pillrolling tremor, bradykinesia, and cog-wheeling rigidity.
The disease primarily affects the ability to initiate and
coordinate complex motor tasks. As the disease
progresses, cranial nerve function may be affected and
difficulties with speech and swallowing are common. Indeed, studies demonstrate that 15% to 20% of patients
with PD without overt dysphagia have radiographic evidence of aspiration.62,63 Unlike in the less common atypical parkinsonian disorders (progressive supranuclear
palsy, corticobasal degeneration, dementia with Lewy
bodies, and multiple system atrophy), which often present
with dysphagia, in PD the latency to swallowing dysfunction is typically greater than 1 year after diagnosis.64
Although swallowing dysfunction is a rare presenting
symptom in PD, dysphagia latency correlates with survival time in all parkinsonian disorders.64
Dysphagia in patients with PD appears to be multifactorial. As with other complex coordinated muscle activities in patients with PD, swallowing is significantly affected by rigidity and bradykinesia producing delays in
the oral preparatory, oral transport, and esophageal
phases. Videofluoroscopic studies demonstrate characteristic increases in the oral-pharyngeal transit times, regardless of disease stage.65 67 Tongue movement is substantially reduced with impaired coordination of the
anterior and posterior tongue surfaces causing increased
oral residue on the tongue and sulci, piecemeal deglutition, and spillage. Patients with PD demonstrate impaired
movement of the epiglottis, hypokinetic laryngeal elevation, and incomplete vocal fold closure.68,69 Although pharyngeal transport is often preserved for the majority of the
bolus,67 some patients exhibit delayed triggering of pharyngeal swallowing and UES relaxation.67,70 Coupled
with hypokinesia of the pharyngeal musculature, the additive effect of the pharyngeal changes results in delayed
esophageal entry and increased residue within the pharynx predisposing the patient to aspiration.67,68
Evaluation and management of dysphagia in parkinsonian patients present a number of difficulties. As mentioned, although dysphagia is a common finding in PD, it
presents late in the disease and leaves the physician in the
difficult position of determining how and when to monitor
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596

for compromised swallowing in these patients. The onset

and severity of swallowing dysfunction in PD is independent of the degree of locomotor disturbance.65,71 Therefore, physical examination alone is not a reliable indicator
of dysphagia severity. Although there are promising noninvasive methods of evaluating subclinical dysphagia and
aspiration based on nasal airflow measurement, the
equipment is not yet widely available.72 Thus, physicians
must remain vigilant in their surveillance for symptoms of
dysphagia in patients with PD and should consider studying asymptomatic patients periodically.
The treatment of dysphagia in patients with PD presents further difficulties. Although motor function improves with the administration of the dopamine precursor
levodopa (L-DOPA), several studies have noted that dysphagia persists despite optimal treatment of locomotor
dysfunction62,65,73 and shows little relation to the welldescribed on off phenomenon of motor disturbance associated with declining blood levels of L-DOPA between
doses.74 These findings suggest that degeneration of systems other than the dopaminergic system may be the
cause of swallowing difficulty in PD. Cricopharyngeal dysfunction may be amenable to treatment by dilation, cricopharyngeal myotomy, or botulinum injection.75,76
Amyotrophic lateral sclerosis. Amyotrophic lateral sclerosis (ALS) is a rapidly progressive degenerative
disease of upper and lower motor neurons. Although substantially less common than PD, ALS typically presents in
the sixth decade of life and frequently causes dysphagia.
Subclinical swallowing abnormalities may be noted by
VFSS before the appearance of cranial nerve weakness,77
and almost all patients with ALS demonstrate linear progression of corticobulbar degeneration that ultimately
manifests as dysarthria and oral transport difficulties.78
Voluntary swallowing initiation is prolonged early in the
disease secondary to degeneration of both excitatory and
inhibitory corticobulbar pyramidal fibers that control the
swallowing center.79 Interestingly, despite abnormalities
in laryngeal elevation and coordinated opening of the cricopharyngeal segment, aspiration is rarely a problem in
ALS because laryngeal sensation and cough remain intact.13 Management is typically supportive because there
are no interventions that alter the relentless progression
of muscle weakness. Swallowing therapy is warranted
when patients begin having difficulty with solid foods.
Compensatory swallowing techniques such as chin-tuck
positioning and the double swallow may allow patients
with mild to moderate dysphagia to continue oral feeding.
When oral intake is insufficient to meet caloric needs,
dietary changes or enteral feeding may be instituted.

Medications
Medication use patterns change as we age. A recent
study of elderly patients in Denmark showed that more
than 65% of patients over 70 years of age take at least one
medication and nearly half take two or more medications
regularly.80 If nonprescription medications are added, the
number is much higher because more than 80% of individuals over 65 years of age have at least one chronic
health problem.81 The number of both prescription and
nonprescription medications that have the undesirable
Schindler and Kelly: Swallowing Disorders

effects on swallowing is large and spans several classes of

pharmacological agents (Table I).
The most common cause of medication-induced dysphagia is xerostomia. Dryness of the mouth impairs bolus
transport, resulting in increased residual in both the oral
cavity and oropharynx. Saliva also contains bicarbonate
that helps neutralize stomach acid and protect the esophagus and hypopharynx from chemical injury. Because saliva production is controlled by parasympathetic stimulation of muscarinic acetylcholine receptors, xerostomia
results from all medications with significant anticholinergic activity. These effects are dose-dependent and may
worsen with age despite stable dosing, because of agerelated changes in drug metabolism and clearance.82

Common classes of drugs with anticholinergic side effects

are antihistamines, tricyclic antidepressants, neuroleptics, antiemetics, atropine-containing antidiarrheal
agents and anti-parkinsonian medications. In addition to
direct cholinergic interference on saliva production, diuretics frequently worsen xerostomia indirectly through
dehydration.
Many medications that alter or depress central nervous system activity may cause dysphagia in elderly patients. As mentioned, an individuals level of arousal is
important to his or her overall muscular tone and coordination, which includes swallowing ability. Anxiolytics
such as benzodiazepines, commonly used for sleep disorders, are often metabolized slowly in elderly patients and

TABLE I.
Commonly Prescribed Medications Associated With Dysphagia in the Elderly.
Effect on Swallowing

Xerostomia

Drug Category

Anticholinergic
Antihistamine
Antidepressant (tricyclic)

Mental status changes

Neuroleptic
Antiemetic
Antidiarrheal
Antiparkinsonian
Antihypertensive
Alcohol
Sedative-hypnotic
Antihistamine
Antiemetic
Anticonvulsant

Dyskinesia
Gastroesophageal reflux

Antiparkinsonian
Neuroleptic
Steroid
Analgesic
Muscle Relaxant
Neuroleptic
Antiparkinsonian
Bronchodilators
Antiangina
Calcium-channel blocker

Esophagitis

Laryngoscope 112: April 2002

Alcohol
Anxiolytic
Bisphosphonate
Non-steroidal Anti-inflammatory
Steroid
Mineral

Common Examples

Oxybutinin
Diphenhydramine
Cetirizine
Nortriptyline
Doxepin
Thioridazine
Scopolamine
Diphenoxylate (with atropine)
Benztropine
Clonidine
Wine
Lorazepam
Chloral hydrate
Hydroxyzine
Prochlorperazine
Metocloperamide
Carbamazepine
Gabapentin
Levodopa
Haloperidol
Prednisone
Oxycodone
Cyclobenzaprine
Chlorpromazine
Levodopa
Theophylline
Isosorbide mononitrate
Nitroglycerin
Nifedipine
Diltiazem
Beer
Alprazolam
Alendronate
Ibuprofen
Methylprednisolone
Potassium chloride
Ferrous sulfate

Schindler and Kelly: Swallowing Disorders

597

may be associated with dysphagia. Alcohol, found in many

over-the-counter medication preparations, has an identical effect and predisposes to gastroesophageal reflux
through LES relaxation. Antihistamines, phenothiazinebased antiemetics, anticonvulsants, antipsychotics, opiates, and lithium also impair cognitive function and level
of alertness. Treatment of schizophrenia in the geriatric
population presents additional difficulties with swallowing dysfunction. In addition to variable anticholinergic
and central nervous system depressant activity, neuroleptic medications may cause extrapyramidal symptoms
manifest as hyperfunctional involuntary movements (dyskinesia) of the oral or pharyngeal musculature.83 Common
examples include repetitive tongue thrusting during swallowing and perioral hyperkinesia (rabbit syndrome). Rigidity and spasm of the pharyngeal musculature may also
result because these neuroleptics block dopamine receptors and may induce a drug-induced parkinsonism in 12%
to 45% of patients.84 Such side effects are more common in
elderly patients85 and may lead to aspiration through
bolus misdirection during oral and pharyngeal transport.
Most extrapyramidal symptoms depend on the dose of
neuroleptic medication, although some persist despite cessation of all antipsychotic medication. All neuroleptic
medications are considered equally effective in comparable doses, and many of the newer agents such as risperidone, olanzapine, and clozapine have a substantially reduced incidence of extrapyramidal side effects.
A number of frequently prescribed medications in
elderly patients cause esophageal dysfunction. The most
common esophageal side effect is diminished LES tone
with resultant gastroesophageal reflux (gastroesophageal
reflux disease [GERD]). Theophylline, nitrates, calcium
channel blockers, benzodiazepines, and alcohol are com-

Fig. 5. Anatomy of the upper esophageal sphincter. (Reprinted with

permission from Graney DO. Anatomy. In: Cummings CW, et al.
OtolaryngologyHead and Neck Surgery, 2nd ed. St. Louis:
MosbyYear Book, 1993:2209.)

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598

mon medications associated with GERD in elderly patients. Over time, dysphagia may result from chemical
injury of the mucosa of the upper aerodigestive tract
through sensory loss and mucosal edema. Older patients
are also prone to direct injury to the esophagus from
certain medications. Xerostomia, esophageal compression
secondary to cardiomegaly or thoracic surgery, and decreased stripping amplitude all contribute to localized ulceration because pills fail to transit the esophagus quickly
and dissolve within its lumen. A meta-analysis of 221
cases of pill-induced esophageal injury found antibiotics
(especially doxycycline) to be the most common causes of
drug-related esophageal injury worldwide.86 In the United
States, elderly patients developed esophageal injury while
taking potassium chloride, iron sulfate, quinidine, nonsteroidal anti-inflammatory drugs, and steroids.86 More recently, alendronate, a selective inhibitor of osteoclastmediated bone resorption used to treat osteoporosis in
elderly women, has been noted to cause a severe ulcerative
esophagitis if not taken with adequate fluid.87 Patients
who retain pills within the esophagus most commonly
report odynophagia and retrosternal chest pain, which
may occur hours to weeks after pill ingestion.86,87 Dysphagia is primarily reported in association with esophageal
strictures.86 The best treatment for drug-related esophageal dysfunction is prevention by implementing reflux
precautions, ingestion of medication with food in an upright position, and clearing medication from the upper
aerodigestive tract with sufficient fluid.

Anatomical Disorders
Cricopharyngeus dysfunction. One of the more
perplexing causes of dysphagia in elderly patients is CP
dysfunction. Although it is clear that some patients have
abnormalities of the UES and may improve after procedures directed at CP disruption, understanding and diagnosing abnormalities of the cricopharyngeal segment is
not easy. This difficulty begins with the discrepancy between the physiological sphincter and its muscular components. As discussed previously, the UES is a manometrically defined region at the level of the cricoid cartilage
that marks the junction between the hypopharynx and
esophagus (Fig. 5). Although distinct physiologically, the
UES is 3 to 4 cm in height and encompasses both the pars
fundiformis and pars obliqua of the CP muscle and portions of the inferior constrictor muscle and circular muscle
of the esophagus. The pars fundiformis, generally referred
to as the cricopharyngeus muscle by clinicians,9 consists
of horizontal muscular fibers that create a sling from
either side of the cricoid cartilage encircling the esophagus. This muscle is histologically distinct, with a large
proportion of elastic fibers and highly oxidative type I
fibers commonly seen in tonically active muscle.7 Manometric and electrophysiological studies indicate that the
region of greatest pressure, on average, is 1.0 cm in length
and appears to be immediately superior to these horizontal fibers.88 This region, between the pars fundiformis and
the pars obliqua, is called Killians dehiscence because it is
relatively devoid of muscle fibers.8 Understanding the
physiological and anatomical relationships of the UES is
critical to the diagnosis and treatment of CP dysfunction.
Schindler and Kelly: Swallowing Disorders

Evaluations of the UES by videofluoroscopy, manometry, and histological examination suggest at least two
distinct forms of CP dysfunction: functional and structural. Functional CP disorders result from partial or complete failure of UES relaxation. Commonly seen in association with neurological disorders affecting the upper
aerodigestive tract, functional UES disorders are characterized by delayed or incomplete opening of the cricopharyngeal segment with bolus stasis at the level of the hypopharynx. As expected, in the absence of UES relaxation,
the extent of sphincter opening primarily depends on pharyngeal propulsion.89 Although videofluoroscopy may be
useful to visualize the cricopharyngeal segment and to
determine the degree of swallowing dysfunction, manometry is essential to distinguish functional abnormalities
from structural or anatomical abnormalities of the UES.90
Functional CP disorders may be seen following brainstem
strokes with damage to the medullary swallow center
(Wallenberg syndrome),57,90 after head trauma, or in association with neurodegenerative diseases.
In contrast to the failed sphincter relaxation of functional CP disorders, patients with structural abnormalities of the UES demonstrate delayed or incomplete opening of the cricopharyngeal segment despite normal
relaxation of the muscular sphincter. Structural abnormalities in the region of the cricopharyngeal segment have
been noted in patients with pharyngeal cancers who have
been treated with radiotherapy or surgery.91,92 Manometric studies of otherwise healthy patients with radiographic
abnormalities of the cricopharyngeal segment have demonstrated regions of increased intrabolus pressure despite
normal UES relaxation and flow rates.10 Cook et al.93
have suggested that this segment of noncompliant pharyngoesophageal muscle is the cause of pharyngeal outpouching known as Zenkers diverticulum. Support for the
hypothesis of static pharyngoesophageal narrowing in the
pathogenesis of CP dysfunction comes from histological
analysis of the UES in patients with Zenkers diverticulum, which demonstrates muscle degeneration and replacement by fibroadipose tissue.94 Similar histopathological changes have been found in the absence of Zenkers
diverticulum95 and distinguish structural from functional
CP dysfunction.
The observed frequency of CP dysfunction varies
greatly depending on the diagnostic modality used and the
population studied. Since 1957, studies have reported a
radiographic incidence of 6% to 61% in patients with dysphagia.96,97 Determination of the true incidence of CP
dysfunction is complicated because of disagreement regarding the definition and significance of the cricopharyngeal bar seen on radiography (Fig. 6). This bar is the
radiographic impression of the UES on the pharyngoesophageal column of contrast at the lower portion of the
cricoid cartilage. Although patients with a cricopharyngeal bar have reduced dimensions of lumen in the cricopharyngeal segment,10 the impact of this narrowing is
unclear because there is no significant difference in reported dysphagia between patients with those without a
CP bar.98,99 It is possible that the 5% of nondysphagic
elderly patients with a visible CP98 are asymptomatic
because of compensatory increases in pharyngeal propulLaryngoscope 112: April 2002

Fig. 6. Cricopharyngeal bar. Prominent cricopharyngeal muscle

indentation of the cervical esophagus with the appearance of a
cricopharyngeal bar (long arrow). There is also an active stripping
wave evident above the advancing bolus (short arrows). (Reprinted
with permission from Jones B. Radiological techniques and findings
in patients with dysphagia. In: Rubin JS, Broniatowski M, Kelly JH,
eds. The Swallowing Manual. San Diego: Singular Publishing, 2000:
120.)

sion. This hypothesis is supported by the demonstration of

normal pharyngoesophageal flow rates despite increased
intrabolus pressure in asymptomatic patients with a CP
bar.10
Despite our enhanced understanding of the complex
pathophysiology and advances in videofluorography and
manometry, the diagnosis of CP dysfunction is primarily
clinical. Patients commonly localize their swallowing difficulties to the cervical region by noting regurgitation of
undigested food from this region or globus sensation, or
both. Many patients describe the need to perform multiple
swallows, particularly with thicker bolus consistencies, to
complete deglutition. Because CP dysfunction is often unmasked by the development of pharyngeal-phase abnormalities, careful attention must be paid to lower cranial
nerve function. In particular, deficiencies in tongue
strength, movement, or coordination and the degree of
laryngeal elevation should be noted. Neurological conditions, including cerebrovascular occlusive disease, ALS,
Schindler and Kelly: Swallowing Disorders

599

pseudobulbar palsy, and oculopharyngeal dystrophy, may

be associated with CP dysfunction; thus, a careful neurological examination may help direct further evaluation
and management. Radiographic demonstration of a CP
bar in the setting of dysphagia warrants manometric evaluation of the UES to distinguish structural from functional CP disorders. Although neither peak pharyngeal
pressure nor poor coordination of pharyngeal musculature
is a good predictor of response to surgical management,
elevated intrabolus hypopharyngeal pressure is associated with resolution of dysphagia after CP disruption.100
Dysphagia associated with CP dysfunction may be
managed in a variety of ways depending on the degree of
swallowing difficulty, type of dysfunction, and overall
health of the patient. Medical management of neurological
conditions that affect tongue motion and pharyngealphase swallowing, such as PD, should be optimal. Swallowing therapy with teaching of compensatory strategies
including chin-down and rotated-head positions during
swallowing may help overcome tongue weakness and diminish piriform sinus residue in the setting of CP dysfunction.101 Although no controlled studies of UES dilation
exist in elderly patients, stricture dilation is effective in
the lower esophagus102 and is used to treat disorders
pharyngeal dysphagia. When Zenkers diverticulum is
present, surgical management with extended cricopharyngeal myotomy and diverticulopexy or diverticulotomy is
necessary to alleviate dysphagia. In anatomically appropriate patients, similar results have been obtained with
endoscopic diverticulotomy allowing faster recovery and
shorter operative time.103 Operative management of cricopharyngeal dysfunction with Zenkers diverticulum is
effective in as many as 88% of patients and has a low
procedure-associated morbidity in carefully selected elderly patients.104 Although functional disorders of the
UES may also be managed surgically,105,106 recent studies
of CP injection with botulinum toxin type A show promise
in the management of incomplete UES relaxation.107,108
Further study of patients with neurogenic CP dysfunction,
as defined by manometry, is needed to determine the
efficacy of this noninvasive modality.

CONCLUSION
The basis for contemporary diagnosis and management of dysphagia in elderly patients is a thorough understanding of the complex anatomy and physiology of
deglutition. Numerous redundant mechanisms exist to
allow competent swallowing and prevention of aspiration.
With advancing age, diffuse changes in muscle strength,
mobility, and coordination, as well as diminished pharyngeal sensory discrimination, predispose individuals to dysphagia. In the absence of comorbid conditions, these
changes are well compensated and remain undetected by
both physicians and patients. However, in the setting of
acute or progressive illness, the patient may quickly lose
this ability to compensate for age-related changes in
deglutition.
The goal of dysphagia management is to maximize
the patients feeding ability and enjoyment, thereby increasing independence. Recent advances in the evaluation
of swallowing disorders, including VFSS and fiberoptic
Laryngoscope 112: April 2002

600

endoscopic evaluation of swallowing, allow detailed analysis of swallowing dysfunction and, when used appropriately, may help guide diagnosis and therapy to maximize
function. Although stroke is the most common cause of
dysphagia in elderly patients, any condition that affects
neurological function within the head and neck may result
in significant swallowing abnormalities. As specialists in
conditions pertaining to the head and neck, otolaryngologists must remain vigilant in their evaluation of elderly
patients for swallowing disorders.

Acknowledgments
The authors thank Donna C. Tippett, MPH, MA,
CCC-SLP, and Brian P. Dunham, MD, for their critical
reviews of the manuscript.

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