13 dysphagia

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13 Neurogenic DysphagiaImpaired swallowing, or dysphagia, can originate from disturbances in the

1. mouth,2. pharynx,3. or esophagus

and can involve

1. mechanical,2. musculoskeletal,3. or neurogenic mechanisms.

Although mechanical dysphagia is an important topic, this chapter primarily focuses onneuromuscular and neurogenic causes of dysphagia because processes in these categories arewhat the neurologist is most likely to encounter.

neurogenic dysphagia develops in approximately 400,000-800,000/year(Robbins 1999)

and that dysphagia is present in roughly 50% of inhabitants of long-term care units (Lin etal. 2002).

Moreover, dysphagia can lead to superimposed problems such as inadequate nutrition,dehydration, recurrent upper respiratory tract infections, and frank aspiration with

consequent pneumonia and even asphyxia. It thus constitutes a formidable and common problem confronting the neurologist in

everyday practice.

NORMAL SWALLOWINGSwallowing comprise a mixture of

1. voluntary2. and reflex or automatic actions that are engineered

and carried out by a combination of

26 pairs of pharyngeal and laryngeal muscles (not countingmuscles used for chewing)

and 5 cranial nerves that in turn receive directions from centerswithin the central nervous system.

Reflex swallowing

is coordinated and carried out at the brainstem level,

where centers act directly on information received from sensory structureswithin the oropharynx and esophagus.

Volitional swallowing is not surprisingly accompanied by additional activity thatoriginates not only in motor and sensory cortices, but also in other cerebralstructures.

The process of swallowing can conveniently be broken down into three distinct stages or phases:1. oral,2. pharyngeal,3. and esophageal.

when the individual is upright when swallowingThese components have also been distilled intowhat have been termed the

horizontal

and vertical subsystems,
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reflecting the direction of bolus flow in each component (when the individual is upright whenswallowing).

The oral phase of swallowing comprises

the horizontal subsystem

and is largely volitional in character,

whereas the pharyngeal and esophageal phases comprise

the vertical subsystem

and are primarily under reflex control.

In the oral, or swallow preparatory, phase

food is taken into the mouth and if needed is chewed;

saliva is secreted to provide both lubrication and the initial "dose" of digestive enzymes,

and the food bolus is formed and shaped by the tongue.

The tongue then propels the bolus backward to the pharyngeal inlet where, in a piston-likeaction, it delivers the bolus into the pharynx.

This in turn initiates the pharyngeal phase in which a cascade of intricate, extremely rapid, and

exquisitely coordinated movements seal off the nasal passages and protect the trachea while thecricopharyngeal muscle, which functions as the upper esophageal sphincter (UES), relaxes andallows the bolus to enter the pharynx.

As an example of the intricacy of movements during this phase of swallowing, the UES, promptedin part by traction produced by elevation of the larynx, actually relaxes just before arrival of the foodbolus, creating suction that assists in guiding the bolus into the pharynx. The bolus then enters theesophagus where peristaltic contractions usher it distally and, upon relaxation of the loweresophageal sphincter, into the stomach.

NEUROPHYSIOLOGY OF SWALLOWING

Central control of swallowing has traditionally been ascribed to brainstem structures, with corticalsupervision and modulation emanating from the inferiorprecentral gyrus.

PET studies of volitional swallowing does occur in

1. the lateral motor cortex within the inferior precentral gyrus, wherein lie the cortical

representations of tongue and face could be bilaterally symmetrical activation of the lateralmotor cortex.

2. The SMA supplementary motor area may play a role in preparation for volitional swallowing3. and the anterior cingulate cortex may be involved with monitoring autonomic and

vegetative functions.

4. Another area of activation during volitional swallowing is the anterior insula, particularly on

the right.

5. PET studies also consistently demonstrate distinctly asymmetrical, left-sided activation of

the cerebellum during swallowing.This activation may reflect cerebellar input concerning coordination, timing, andsequencing of swallowing.6. Activation of putamen has also been noted during volitional swallowing, but it has not been

possible to differentiate this activation from that seen with tongue movement alone.

Within the brainstem, swallowing appears to be regulated by central pattern generators that contain


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the programs directing the sequential movements of the various muscles involved with swallowing.

These pattern generators reside in the

1. medial reticular formation of the rostral medulla2. and the reticulum adjacent to the nucleus tractus solitarius .

3. These centers then project to the nucleus ambiguus and the dorsal motor nucleus of

the vagus, which directly control motor output to the pharyngeal musculature and proximalesophagus.

MECHANICAL DYSPHAGIA

Structural abnormalities, both within and adjacent to the mouth, pharynx, and esophagus, caninterfere with swallowing on a strictly mechanical basis, despite fully intact and functioning nervousand musculoskeletal systems (Table 13.1).

1. Within the mouth

macroglossia,

temporomandibular joint dislocation,

certain congenital anomalies,

and intraoral tumors can impede effective swallowing and produce mechanicaldysphagia.

2. Pharyngeal function can be compromised by processes such as retropharyngeal tumor

or abscess,

cervical anterior osteophyte formation,

Zenker's diverticulum,

or thyroid gland enlargement.3. Esophageal function, including

malignant or benign esophageal tumors,

metastatic carcinoma,

esophageal stricture from numerous causes,

vascular abnormalities such as aortic aneurysm or aberrant origin of the subclavianartery, or even primary gastric abnormalities such as hiatal hernia.

Gastroesophageal reflux can also produce dysphagia.

NEUROMUSCULAR DYSPHAGIA

A variety of neuromuscular disease processes of diverse etiology can involve the oropharyngealand esophageal musculature and produce dysphagia as part of their broader neuromuscularclinical picture (Table 13.2). Certain muscular dystrophies, inflammatory myopathies, andmitochondrial myopathies all can display dysphagia, as can disease processes affecting themyoneural junction, such as myasthenia gravis.
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Table 13-1. Mechanical dysphagia

Oral

Amyloidosis

Congenital abnormalities

1. Intraoral tumors

2. Lip injuries

Burns

Trauma

3. Macroglossia

4. Scleroderma

5. Temporomandibular joint dysfunction

6. Xerostomia

Sjgren's syndrome

Pharyngeal

1. Cervical anterior osteophytes

2. Infection

Diphtheria

3. Thyromegaly

4. Retropharyngeal abscess

5. Retropharyngeal tumor

6. Zenker's diverticulum

Esophageal


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1. Aberrant origin of right subclavian artery

2. Caustic injury

3. Esophageal carcinoma

4. Esophageal diverticulum

5. Esophageal infection

Candida albicans

Herpes simplex virus

Cytomegalovirus

Varicella-zoster virus

6. Esophageal intramural pseudodiverticula

7. Esophageal stricture

8. Esophageal ulceration

9. Esophageal webs or rings

10. Gastroesophageal reflux disease

11. Hiatal hernia

12. Metastatic carcinoma

13. Posterior mediastinal mass

14. Thoracic aortic aneurysm

Table 13-2. Neuromuscular dysphagia

Oropharyngeal

Inflammatory myopathies

Dermatomyositis

Inclusion body myositis

Polymyositis

Mitochondrial myopathies


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Kearns-Sayre syndrome

Mitochondrial neurogastrointestinal encephalomyopathy

Muscular dystrophies

1. Duchenne's

2. Facioscapulohumeral

3. Limb-girdle

4. Myotonic

5. Oculopharyngeal

Neuromuscular junction disorders

Botulism

Lambert-Eaton syndrome

Myasthenia gravis

Tetanus

Scleroderma

Stiff-man syndrome

Esophageal

1. Amyloidosis

2. Inflammatory myopathies

Dermatomyositis

Polymyositis

3. Scleroderma

Oculopharyngeal Muscular Dystrophy


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Oculopharyngeal muscular dystrophy (OPMD) is a rare autosomal dominant disorder that is mostfrequently encountered in individuals with a French Canadian ethnic background. It is theconsequence of a GCG trinucleotide repeat expansion in the poly(A)-binding protein nuclear 1 gene(also called poly[A]-binding protein 2, or PABP2, gene) on chromosome 14 (Hill et al. 2001). OPMDis unique among the muscular dystrophies because of its appearance in older individuals, withsymptoms typically first appearing between ages 40 and 60 years (Brais et al. 1999). It is

characterized by slowly progressive ptosis, dysphagia, and proximal limb weakness. Because ofthe ptosis, patients with OPMD may assume an unusual posture characterized by raised eyebrowsand extended neck.

Dysphagia in OPMD is due to impaired function of the oropharyngeal musculature. Although itevolves slowly over many years, OPMD can eventually result not only in difficulty or discomfort withswallowing, but also in weight loss, malnutrition, and aspiration (Christopher et al. 2001). Nospecific treatment for the muscular dystrophy itself is available, but cricopharyngeal myotomyaffords dysphagia relief in more than 80% of treated individuals (Fradet et al. 1997). More recently,botulinum toxin injections have been successfully used to treat dysphagia in OPMD (Restivo et al.2000).

Myotonic Dystrophy

Myotonic dystrophy is an autosomal dominant disorder whose phenotypic picture includes not only

skeletal muscle, but also cardiac, ophthalmological, and endocrinological involvement. Mutations attwo distinct locations have now been associated with the clinical picture of myotonic dystrophy.Type 1 myotonic dystrophy is due to a CTG expansion in the DMPK gene on chromosome 19,whereas type 2 is the consequence of a CCTG repeat expansion in the ZNF9 gene onchromosome 3 (Ranum and Day 2002).

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Gastrointestinal (GI) symptoms develop in more than 50% of individuals with the clinical phenotypeof myotonic dystrophy and may be the most disabling component of the disorder in 25%. GIsymptoms may actually antedate the appearance of other neuromuscular features. Subjectivedysphagia is one of the most prevalent GI features and has been reported to be present in 37-56%of patients (Ertekin et al. 2001). Coughing when eating, suggestive of aspiration, may occur in 33%.Objective measures paint a picture of even more pervasive impairment, demonstrating

disturbances in swallowing in 70-80% of persons with myotonic dystrophy (Ertekin et al. 2001). Inone study, 75% of patients asymptomatic for dysphagia were still noted to have abnormalities onobjective testing.

A variety of abnormalities in objective measures of swallowing have been documented in myotonicdystrophy. Abnormal cricopharyngeal muscle activity is present in 40% of patients duringelectromyographic (EMG) testing (Ertekin et al. 2001). Impaired esophageal peristalsis has alsobeen noted in affected individuals studied with esophageal manometry. In videofluoroscopic testing,incomplete relaxation of the UES and esophageal hypotonia are the most frequently notedabnormalities. Both muscle weakness and myotonia are felt to play a role in the development ofdysphagia in persons with myotonic dystrophy, and in at least one study, a correlation was notedbetween the size of the CTG repeat expansion and the number of radiologic abnormalities inmyotonic patients.

Other Muscular Dystrophies

Although less well characterized, dysphagia also occurs in other types of muscular dystrophy.Difficulty swallowing and choking while eating occur with increased frequency in children withDuchenne's muscular dystrophy. Dysphagia has also been documented in patients with limb-girdledystrophy and facioscapulohumeral muscular dystrophy

Inflammatory Myopathies
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Dermatomyositis and polymyositis are the most commonly occurring of the inflammatory myopathicdisorders. Both are characterized by progressive, usually symmetrical, weakness affecting proximalmuscles more prominently than distal. Fatigue and myalgia may also occur. Malignant disease isassociated with the disorder in 10-15% of patients with dermatomyositis and 5-10% of those withpolymyositis. In individuals older than 65 years, more than 50% are found to have cancer.

Although dysphagia can develop in both conditions, it more frequently is present, and when presentmore severe, in dermatomyositis. Dysphagia is present in 20-55% of individuals withdermatomyositis, but in only 18% with polymyositis (Parodi et al. 2002). It is the consequence ofinvolvement of striated muscle in the pharynx and proximal esophagus. Involvement of pharyngealand esophageal musculature in polymyositis and dermatomyositis is an indicator of poor prognosisand can be the source of significant morbidity (Marie et al. 1999). The resulting dysphagia can besevere enough to require enteral feeding. Acute total obstruction by the cricopharyngeal musclehas been reported in dermatomyositis, necessitating cricopharyngeal myotomy. Dysphagia in bothconditions may respond to corticosteroids, and intravenous immune globulin (IVIG) therapy hasproduced dramatic improvement in dysphagia in individuals who were unresponsive to steroids(Marie et al. 1999).

Although dysphagia develops less often in inclusion body myositis, it can occur. In fact, in a groupof individuals in whom inclusion body myositis mimicked and was confused with motor neurondisease, dysphagia was present in 44%. A focal inflammatory myopathy involving the pharyngealmuscles and producing isolated pharyngeal dysphagia has also been described in elderlyindividuals older than 69 years. It has been suggested that this is a distinct clinical entitycharacterized by cricopharyngeal hypertrophy, although polymyositis localized to the pharyngealmusculature has also been reported.

Mitochondrial Disorders

The mitochondrial disorders are a family of diseases that develop as a consequence of dysfunctionin the mitochondrial respiratory chain. Most are the result of mutations in mitochondrialdeoxyribonucleic acid (DNA) genes, but nuclear DNA mutations may be responsible in some.Mitochondrial disorders are by nature multisystemic, but myopathic and neurological features oftenpredominate and symptoms may vary widely, even between individuals within the same family.

In addition to the classic constellation of symptoms that include progressive externalophthalmoplegia, retinitis pigmentosa, cardiac conduction defects, and ataxia, individuals withKearns-Sayre syndrome may also develop dysphagia (Katsanos et al. 2001,2002; Kornblum et al.2001). Severe abnormalities of pharyngeal and upper esophageal peristalsis have beendocumented in this disorder. Cricopharyngeal dysfunction is common, but impaired deglutitivecoordination may also develop (Kornblum et al. 2001). Dysphagia has also been described in othermitochondrial disorders, but descriptions are only anecdotal and formal study has not beenundertaken.

Myasthenia Gravispage 168

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Myasthenia gravis (MG) is an autoimmune disorder characterized by the production of

autoantibodies directed against the postsynaptic 1 muscle nicotinic acetylcholine receptors at theneuromuscular junction, with destruction of the receptors and reduction in their number. The clinicalconsequence of this process is the development of fatigable muscle weakness that progressivelyincreases with repetitive muscle action and improves with rest. MG occurs more often in womenthan men, and although symptoms can develop at any age, the reported mean age at onset inwomen is 28-35 years and in men 42-49 years (Kalb et al. 2002). Although myasthenic symptomsremain confined to the extraocular muscles in about 20% of patients, in most individuals morewidespread muscle weakness becomes evident (Kalb et al. 2002;Wirtz et al. 2002).
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Involvement of bulbar musculature, with resultant dysphagia, is relatively common in MG. Inapproximately 6-30% of patients, bulbar involvement is evident from the beginning (Wirtz et al.2002), but most patients eventually develop bulbar symptoms such as dysphagia and dysarthria asthe disease progresses. Dysphagia in MG can be due to dysfunction at oral, pharyngeal, or evenesophageal levels. Oral phase involvement can be due to fatigue and weakness of the tongue ormasticatory muscles. In patients with MG who have bulbar symptoms, repetitive nerve stimulation

studies of the hypoglossal nerve have demonstrated abnormalities (Lo et al. 2002), whereasstudies using EMG of the masticatory muscles recorded while chewing have also revealed impairedperformance (Weijnen et al. 2002). Pharyngeal dysfunction is also common in patients with MGwho have dysphagia, as demonstrated with videofluoroscopy. Aspiration, often silent, may bepresent in 35% or more of these individuals (Colton-Hudson et al. 2002); in elderly patients, thefrequency of aspiration may be considerably higher. Motor dysfunction involving the striated muscleof the proximal esophagus has also been documented in MG. In one study, 96% of patients withMG demonstrated abnormalities, such as decreased amplitude and prolongation of the peristalticwave, in this region on testing with esophageal manometry. Cricopharyngeal sphincter pressurewas also noted to be reduced.

NEUROGENIC DYSPHAGIA

A variety of disease processes originating in the central and peripheral nervous systems can alsodisrupt swallowing mechanisms and produce dysphagia. Processes affecting cerebral cortex,subcortical white matter, subcortical gray matter, brainstem, spinal cord, and peripheral nerves canelicit dysphagia as a component of their clinical picture (Table 13.3).

Table 13-3. Neurogenic dysphagia

Oropharyngeal

Arnold-Chiari malformation

Basal ganglia disease

Body_ID: T013003.150

Biotin responsive

Body_ID: T013003.200

Corticobasal degeneration

Body_ID: T013003.250

Dementia with Lewy bodies

Body_ID: T013003.300

Huntington's disease

Body_ID: T013003.350

Multiple system atrophy

Body_ID: T013003.400

NeuroacanthocytosisBody_ID: T013003.450

Parkinson's disease

Body_ID: T013003.500

Progressive supranuclear palsy

Body_ID: T013003.550

Wilson's disease

Body_ID: T013003.600
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Central pontine myelinolysis

Body_ID: T013003.650

Cerebral palsy

Body_ID: T013003.700

Drug related

Body_ID: T013003.750

Cyclosporin

Body_ID: T013003.800

Tardive dyskinesia

Body_ID: T013003.850

Vincristine

Body_ID: T013003.900

Infectious

Body_ID: T013003.950

Brainstem encephalitis

Body_ID: T013003.1000

Listeria

Body_ID: T013003.1050

Epstein-Barr virus

Body_ID: T013003.1100

Diphtheria

Body_ID: T013003.1150

Poliomyelitis

Body_ID: T013003.1200

Progressive multifocal leukoencephalopathy

Body_ID: T013003.1250

Rabies

Body_ID: T013003.1300

Mass lesionsBody_ID: T013003.1350

Abscess

Body_ID: T013003.1400

Hemorrhage

Body_ID: T013003.1450

Metastatic tumor

Body_ID: T013003.1500

Primary tumor

Body_ID: T013003.1550

Motor neuron diseases

Body_ID: T013003.1600Amyotrophic lateral sclerosis

Body_ID: T013003.1650

Multiple sclerosis

Body_ID: T013003.1700

Peripheral neuropathic processes

Body_ID: T013003.1750

Charcot-Marie-Tooth disease


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Body_ID: T013003.1800

Guillain-Barr syndrome (Miller Fisher's variant)

Body_ID: T013003.1850

Spinocerebellar ataxias

Body_ID: T013003.1900

Stroke

Body_ID: T013003.1950

Syringobulbia

Body_ID: T013003.2000

Esophageal

Body_ID: T013003.2050

Achalasia

Body_ID: T013003.2100

Autonomic neuropathies

Body_ID: T013003.2150

Diabetes mellitus

Body_ID: T013003.2200

Familial dysautonomia

Body_ID: T013003.2250

Paraneoplastic syndromes

Body_ID: T013003.2300

Basal ganglia disorders

Body_ID: T013003.2350

Parkinson's disease

Body_ID: T013003.2400

Chagas' disease

Body_ID: T013003.2450

Esophageal motility disorders

Body_ID: T013003.2500Scleroderma

Lots missed

EVALUATION OF DYSPHAGIA.ext

EVALUATION OF DYSPHAGIA

Body_ID: HC0013019

Various diagnostic tests, ranging from simple bedside analysis to sophisticated radiologic andneurophysiologic procedures, have been developed to evaluate dysphagia (Logemann 1996).

Although most are actually performed by specialists other than neurologists, it is important forneurologists to have an awareness of them so they can be employed when clinical circumstances

are appropriate (Table 13.4).Body_ID: P013055

Body_ID: T013004

Table 13-4. Diagnostic tests

Body_ID: None

Oropharyngeal

Body_ID: T013004.50
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Clinical examination

Body_ID: T013004.100

Cervical auscultation

Body_ID: T013004.150

Timed swallowing tests

Body_ID: T013004.200

3-ounce water swallow test

Body_ID: T013004.250

Modified barium swallow test

Body_ID: T013004.300

Pharyngeal videoendoscopy

Body_ID: T013004.350

Pharyngeal manometry

Body_ID: T013004.400

Videomanofluorometry

Body_ID: T013004.450

Electromyographic recording

Body_ID: T013004.500

Esophageal

Body_ID: T013004.550

Endoscopy

Body_ID: T013004.600

Esophageal manometry

Body_ID: T013004.650

Videofluoroscopy

Body_ID: T013004.700

Body_ID: T013004Body_ID: None

Clinical examination is somewhat limited because of the inaccessibility of some structures involvedwith swallowing, but both history and examination results can provide useful clues to localizationand diagnosis (Table 13.5). Difficulty initiating swallowing or the need for repeated attempts tosucceed at swallowing suggests an oropharyngeal source for the dysphagia, whereas a sensationof food "hanging up" in a retrosternal location implicates esophageal dysfunction. Individuals whoreport dysphagia for solid food but not liquids are more likely to have a mechanical obstruction,whereas dysphagia for both solids and liquids equally is more typical for an esophageal motilitydisorder. Lip and tongue function can be easily assessed during routine neurological examination,and both palatal and gag reflexes can be evaluated.

Body_ID: P013056

Body_ID: T013005

Table 13-5. Dysphagia clues

Body_ID: None

Difficulty initiating swallowing Oropharyngeal dysfunction

Body_ID: T013005.50

Repetitive swallowing Oropharyngeal dysfunction

Body_ID: T013005.100

Retrosternal "hanging up" sensation Esophageal dysfunction
http://www.nicp.com/passthru/linktopage.cfm?showtab=toc&xrefID=T013005http://www.nicp.com/passthru/linktopage.cfm?showtab=toc&xrefID=T013005


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Body_ID: T013005.150

Difficulty with solids, but not liquids Mechanical obstruction

Body_ID: T013005.200

Difficulty with both solids and liquids Esophageal dysmotility

Body_ID: T013005.250

Regurgitation of undigested food Zenker's diverticulum

Body_ID: T013005.300

Halitosis Zenker's diverticulum

Body_ID: T013005.350


Cervical auscultation is not widely used to evaluate swallowing but may be useful to assesscoordination between respiration and swallowing (Table 13.6 and Figure 13.1) (Logemann 1996). Inthe normal situation, swallowing occurs during exhalation, which reduces the risk of aspiration. Dys-coordinated swallowing in the midst of inhalation, conversely, increases the possibility that foodmight be drawn into the respiratory tract.

Body_ID: P013057Body_ID: T013006

Table 13-6. Dysphagia testing

Body_ID: None

If oral phase dysfunction suspected:

Body_ID: T013006.50

Screening tests:

Body_ID: T013006.100


Body_ID: T013006.150

Cervical auscultationBody_ID: T013006.200

3-ounce water swallow

Body_ID: T013006.250

Primary test:

Body_ID: T013006.300

Modified barium swallow

Body_ID: T013006.350

If pharyngeal phase dysfunction suspected:

Body_ID: T013006.400

Screening tests:

Body_ID: T013006.450


Body_ID: T013006.500

3-ounce water swallow

Body_ID: T013006.550

Timed swallowing

Body_ID: T013006.600

Primary test:

Body_ID: T013006.650
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Modified barium swallow

Body_ID: T013006.700

Complementary tests:

Body_ID: T013006.750

Pharyngeal videoendoscopy

Body_ID: T013006.800

Pharyngeal manometry

Body_ID: T013006.850

Electromyography

Body_ID: T013006.900

Videomanofluorometry

Body_ID: T013006.950

If esophageal dysfunction suspected:

Body_ID: T013006.1000

Primary test:

Body_ID: T013006.1050

Videofluoroscopy

Body_ID: T013006.1100

Endoscopy

Body_ID: T013006.1150

Complementary test:

Body_ID: T013006.1200

Esophageal manometry

Body_ID: T013006.1250


Timed swallowing tests, which require repetitive swallowing of specific amounts of water, have also

been employed in the evaluation of dysphagia. Individuals with swallowing impairment may displaya number of abnormalities, including slower swallowing speed (


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Add to lightbox

Body_ID: F013001 Figure 13.1 Dysphagia assessment.

The MBS test has become a standard method for assessing oropharyngeal dysphagia (Logemann1996). Patients are observed via videofluoroscopy swallowing barium-impregnated food of differingconsistencies (thin liquid, pudding, cookie). Both oral and pharyngeal function can becharacterized, the presence of aspiration can be accurately documented, and the response tocorrective measures, such as positioning techniques, can also be evaluated.

Body_ID: P013061

Videoendoscopy of the pharynx, via the nasal passageway, allows direct visualization of thepharyngeal component of swallowing before and after passage of the food bolus. Its primary valueis to demonstrate the presence of residual material in the pharynx after a swallow, indicative ofincreased risk of aspiration.

Body_ID: P013062

Pharyngeal manometry provides physiologic information regarding function of both the pharynx andthe UES (Hila, Castell, and Castell 2001). The information derived is complementary to thatobtained by videofluoroscopy and a combined procedure, termed videomanofluorometry, in whichboth videofluoroscopy and manometry are performed simultaneously, can also be used (Higo et al.

2002). Though very useful, this procedure is not always readily available.Body_ID: P013063

Evaluation of esophageal function can be assessed by endoscopy, esophageal manometry, andvideofluoroscopy. Scintigraphic procedures can also be employed to evaluate oral, pharyngeal, andesophageal function but are not widely used (Galli et al. 2000).

Body_ID: P013064

More sophisticated electrodiagnostic procedures have also been developed to study dysphagia.
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EMG recording of cricopharyngeal function and integrated submental activity has been useful in aresearch setting to characterize aspects of swallowing, but this procedure has not yet come intogeneral use.

Body_ID: P013065

13 dysphagia

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