Professional Documents
Culture Documents
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-
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
590
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.)
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.
592
593
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
595
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
Laryngoscope 112: April 2002
596
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
TABLE I.
Commonly Prescribed Medications Associated With Dysphagia in the Elderly.
Effect on Swallowing
Xerostomia
Drug Category
Anticholinergic
Antihistamine
Antidepressant (tricyclic)
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
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
597
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
599
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.
BIBLIOGRAPHY
1. US Census Bureau. Current Population Reports: Population
Projections of the United States by Age, Sex, Race, and
Hispanic Origin1995 to 2050. US Census Bureau, 1996.
Publication P251130.
2. Erlichman M. The role of speechlanguage pathologists in
the management of dysphagia. Health Technol Assess
Reports 1989.
3. Gustafsson B, Tibbling L. Dysphagia: an unrecognized
handicap. Dysphagia 1991;6:193199.
4. Miller A, Biegler D, Conklin JL. Functional controls of deglutition. In: Perlman AL, Schulze-Delrieu K, eds. Deglutition and Its Disorders. San Diego: Singular Publishing
Group, 1997:4398.
5. Tracey JF, Logemann JA, Kahrilas PJ, Jacob P, Kobara M,
Krugler C. Preliminary observations on the effects of age
on oropharyngeal deglutition. Dysphagia 1989;4:90 94.
6. Plant RP. Anatomy and physiology of swallowing in adults and
geriatrics. Otolaryngol Clin North Am 1998;31:477 488.
7. Cook IJ, Dodds W, Dantas R, et al. Opening mechanisms of
the human UES. Am J Physiol Gastrointest Liver Physiol
1989;257:G748 G759.
8. Kelly JH, Kuncl RW. Myology of the pharyngoesophageal
segment: gross anatomic and histologic characteristics.
Laryngoscope 1996;106:713720.
9. Goyal RK, Martin SB, Shapiro J, et al. The role of the
cricopharyngeus muscle in pharyngoesophageal disorders.
Dysphagia 1993;8:252258.
10. Dantas R, Cook I, Dodds W, Kern M, Lang I, Brasseur
J. Biomechanics of cricopharyngeal bars. Gastroenterology
1990;99:1269 1274.
11. Martin RE, Sessle MDS. The role of cerebral cortex in swallowing. Dysphagia 1993;8:195202.
12. Miller AJ. The search for the central swallowing pathway:
the quest for clarity. Dysphagia 1993;8:195202.
13. Dray TG, Hillel AD, Miller RM. Dysphagia caused by neurologic deficits. Otolaryngol Clin North Am 1998;31:
507524.
14. Miller AJ. Neurophysiological basis of swallowing. Dysphagia 1986;1:91100.
15. Doty RW, Bosma JF. An electromyographic analysis of reflex deglutition. J Neurophysiol 1956;19:44 60.
16. Fucile S, Wright PM, Chan I, Yee S, Langlais M-E, Gisel EG.
Functional oral-motor skills: do they change with age?
Dysphagia 1998;13:195201.
17. Jaradeh S. Neurophysiology of swallowing in the aged.
Dysphagia 1994;9:218 220.
18. Nicosia MA, Hind JA, Roecker EB, et al. Age effects on the
temporal evolution of isometric and swallowing pressure.
J Gastroenterol 2000;55(Suppl A):M634 M640.
19. Ekberg O, Feinberg MJ. Altered swallowing function in
elderly patients without dysphagia. AJR Am J Roentgenol
1991;156:11811184.
20. Shaker R, Ren J, Zamir Z, et al. Effect of aging, position and
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
temperature on the threshold volume triggering pharyngeal swallows. Gastroenterology 1994;107:396 402.
Robbins J, Hamilton JW, Lof GL, Kempster GB. Oropharyngeal swallowing in normal adults of different ages. Gastroenterology 1992;103:823 829.
Nilsson H, Ekberg O, Olsson R, et al. Quantitative aspects of
swallowing in an elderly nondysphagic population.
Dysphagia 1996;11:180 184.
Calhoun KH, Gibson B, Hartley L, Minton J, Hokanson JA.
Age-related changes in oral sensation. Laryngoscope 1992;
102:109 116.
Aviv JE, Martin JH, Jones ME, et al. Age-related changes in
pharyngeal and supraglottic sensation. Ann Otol Rhinol
Laryngol 1994;103:749 752.
Smith CH, Logemann JA, Colangelo L, Rademaker AW,
Pauloski BR. Incidence and patient characteristics associated with silent aspiration in the acute care setting.
Dysphagia 1999;14:17.
Ren J, Shaker R, Kusano M, et al. Effect of aging on the
secondary esophageal peristalsis: presbyesophagus revised. Am J Physiol Gastrointest Liver Physiol 1995;268:
G772G779.
Young EC, Durant-Jones L. Gradual onset of dysphagia: a
study of patients with oculopharyngeal muscular dystrophy. Dysphagia 1997;12:196 201.
Tibbling L, Gustafsson B. Dysphagia and its consequences
in the elderly. Dysphagia 1991;6:200 202.
Linden P, Siebens AA. Dysphagia: predicting laryngeal penetration. Arch Phys Med Rehabil 1983;64:281284.
Jordan PH. Dysphagia and esophageal diverticula. Postgrad
Med 1977;61:155161.
Miller RM. Evaluation of swallowing disorders. In: Groher
ME, ed. Dysphagia: Diagnosis and Management. Stoneham, MA: Butterworth, 1984:85110.
Schulze-Delrieu KS, Miller RM. Clinical assessment of dysphagia. In: Perlman AL, Schulze-Delrieu KS, eds. Deglutition and Its Disorders. San Diego: Singular Publishing
Group, 1997:125152.
Horner J, Massey EW, Riski JE, Lathrop DL, Chase KN.
Aspiration following acute stroke: clinical correlates and
outcome. Neurology 1988;38:1359 1362.
Horner J, Massey EM, Brazer SR. Aspiration in bilateral
stroke patients. Neurology 1990;40:1686 1688.
Warms T, Richards J. Wet voice as a predictor of penetration and aspiration in oropharyngeal dysphagia. Dysphagia 2000;15:84 88.
Priefer BA, Robbins J. Eating changes in mild-stage Alzheimers disease: a pilot study. Dysphagia 1997;12:212221.
Volicer L, Seltzer B, Rheaume Y, et al. Eating difficulties of
patients with probable dementia of the Alzheimers type.
J Geriatr Psychiatry Neurol 1989;2:188 195.
Martino R, Pron G, Diamant N. Screening for oropharyngeal
dysphagia in stroke: insufficient evidence for guidelines.
Dysphagia 2000;15:19 30.
Leder SB. Videofluoroscopic evaluation of aspiration with
visual examination of the gag reflex and velar movement.
Dysphagia 1997;12:2123.
Leder SB. Gag reflex and dysphagia. Head Neck 1996;18:
138 141.
Davies AE, Kidd D, Stone SP, MacMahaon J. Pharyngeal
sensation and gag reflex in healthy subjects. Lancet 1995;
345:487 488.
Splaingard ML, Hutchins B, Sulton LD, Chauduri G. Aspiration in rehabilitation patients: videofluoroscopy versus
bedside clinical assessment. Arch Phys Med Rehabil 1988;
69:637 640.
Smithard DG, ONeill PA, England RE, et al. The natural
history of dysphagia following a stroke. Dysphagia 1997;
12:188 193.
Linden P, Kuhlemeier KV, Patterson C. The probability of
correctly predicting subglottic penetration from clinical observations. Dysphagia 1993;8:170 179.
Aviv JE, Martin JH, Keen MS, Debell M, Blitzer A. Air pulse
quantification of supraglottic and pharyngeal sensation: a
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
601
602