13 Neurogenic Dysphagia

Impaired 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 on neuromuscular and neurogenic causes of dysphagia because processes in these categories are what 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 et al. 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 SWALLOWING Swallowing comprise a mixture of 1. voluntary 2. and reflex or automatic actions that are engineered and carried out by a combination of 26 pairs of pharyngeal and laryngeal muscles (not counting muscles used for chewing) and 5 cranial nerves that in turn receive directions from centers within the central nervous system. Reflex swallowing is coordinated and carried out at the brainstem level, where centers act directly on information received from sensory structures within the oropharynx and esophagus. Volitional swallowing is not surprisingly accompanied by additional activity that originates not only in motor and sensory cortices, but also in other cerebral structures.
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 into what have been termed the horizontal and vertical subsystems,

reflecting the direction of bolus flow in each component (when the individual is upright when swallowing). 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-like action, 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 the cricopharyngeal muscle, which functions as the upper esophageal sphincter (UES), relaxes and allows the bolus to enter the pharynx. As an example of the intricacy of movements during this phase of swallowing, the UES, prompted in part by traction produced by elevation of the larynx, actually relaxes just before arrival of the food bolus, creating suction that assists in guiding the bolus into the pharynx. The bolus then enters the esophagus where peristaltic contractions usher it distally and, upon relaxation of the lower esophageal sphincter, into the stomach.

NEUROPHYSIOLOGY OF SWALLOWING
Central control of swallowing has traditionally been ascribed to brainstem structures, with cortical supervision and modulation emanating from the inferior precentral 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 lateral motor cortex. 2. The SMA supplementary motor area may play a role in preparation for volitional swallowing 3. 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, and sequencing 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

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 medulla 2. 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 proximal esophagus.

MECHANICAL DYSPHAGIA
Structural abnormalities, both within and adjacent to the mouth, pharynx, and esophagus, can interfere with swallowing on a strictly mechanical basis, despite fully intact and functioning nervous and 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 mechanical dysphagia. 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 subclavian artery, 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 oropharyngeal and esophageal musculature and produce dysphagia as part of their broader neuromuscular clinical picture (Table 13.2). Certain muscular dystrophies, inflammatory myopathies, and mitochondrial myopathies all can display dysphagia, as can disease processes affecting the myoneural junction, such as myasthenia gravis.

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

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

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

Oculopharyngeal muscular dystrophy (OPMD) is a rare autosomal dominant disorder that is most frequently encountered in individuals with a French Canadian ethnic background. It is the consequence 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). OPMD is unique among the muscular dystrophies because of its appearance in older individuals, with symptoms 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 of the ptosis, patients with OPMD may assume an unusual posture characterized by raised eyebrows and extended neck. Dysphagia in OPMD is due to impaired function of the oropharyngeal musculature. Although it evolves slowly over many years, OPMD can eventually result not only in difficulty or discomfort with swallowing, but also in weight loss, malnutrition, and aspiration (Christopher et al. 2001). No specific treatment for the muscular dystrophy itself is available, but cricopharyngeal myotomy affords 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 at two 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 on chromosome 3 (Ranum and Day 2002).
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Gastrointestinal (GI) symptoms develop in more than 50% of individuals with the clinical phenotype of myotonic dystrophy and may be the most disabling component of the disorder in 25%. GI symptoms may actually antedate the appearance of other neuromuscular features. Subjective dysphagia 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). In one study, 75% of patients asymptomatic for dysphagia were still noted to have abnormalities on objective testing. A variety of abnormalities in objective measures of swallowing have been documented in myotonic dystrophy. Abnormal cricopharyngeal muscle activity is present in 40% of patients during electromyographic (EMG) testing (Ertekin et al. 2001). Impaired esophageal peristalsis has also been noted in affected individuals studied with esophageal manometry. In videofluoroscopic testing, incomplete relaxation of the UES and esophageal hypotonia are the most frequently noted abnormalities. Both muscle weakness and myotonia are felt to play a role in the development of dysphagia in persons with myotonic dystrophy, and in at least one study, a correlation was noted between the size of the CTG repeat expansion and the number of radiologic abnormalities in myotonic 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 with Duchenne's muscular dystrophy. Dysphagia has also been documented in patients with limb-girdle dystrophy and facioscapulohumeral muscular dystrophy

Inflammatory Myopathies

Dermatomyositis and polymyositis are the most commonly occurring of the inflammatory myopathic disorders. Both are characterized by progressive, usually symmetrical, weakness affecting proximal muscles more prominently than distal. Fatigue and myalgia may also occur. Malignant disease is associated with the disorder in 10-15% of patients with dermatomyositis and 5-10% of those with polymyositis. 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 present more severe, in dermatomyositis. Dysphagia is present in 20-55% of individuals with dermatomyositis, but in only 18% with polymyositis (Parodi et al. 2002). It is the consequence of involvement of striated muscle in the pharynx and proximal esophagus. Involvement of pharyngeal and esophageal musculature in polymyositis and dermatomyositis is an indicator of poor prognosis and can be the source of significant morbidity (Marie et al. 1999). The resulting dysphagia can be severe enough to require enteral feeding. Acute total obstruction by the cricopharyngeal muscle has been reported in dermatomyositis, necessitating cricopharyngeal myotomy. Dysphagia in both conditions may respond to corticosteroids, and intravenous immune globulin (IVIG) therapy has produced 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 group of individuals in whom inclusion body myositis mimicked and was confused with motor neuron disease, dysphagia was present in 44%. A focal inflammatory myopathy involving the pharyngeal muscles and producing isolated pharyngeal dysphagia has also been described in elderly individuals older than 69 years. It has been suggested that this is a distinct clinical entity characterized by cricopharyngeal hypertrophy, although polymyositis localized to the pharyngeal musculature has also been reported.

Mitochondrial Disorders
The mitochondrial disorders are a family of diseases that develop as a consequence of dysfunction in the mitochondrial respiratory chain. Most are the result of mutations in mitochondrial deoxyribonucleic acid (DNA) genes, but nuclear DNA mutations may be responsible in some. Mitochondrial disorders are by nature multisystemic, but myopathic and neurological features often predominate and symptoms may vary widely, even between individuals within the same family. In addition to the classic constellation of symptoms that include progressive external ophthalmoplegia, retinitis pigmentosa, cardiac conduction defects, and ataxia, individuals with Kearns-Sayre syndrome may also develop dysphagia (Katsanos et al. 2001, 2002; Kornblum et al. 2001). Severe abnormalities of pharyngeal and upper esophageal peristalsis have been documented in this disorder. Cricopharyngeal dysfunction is common, but impaired deglutitive coordination may also develop (Kornblum et al. 2001). Dysphagia has also been described in other mitochondrial disorders, but descriptions are only anecdotal and formal study has not been undertaken.

Myasthenia Gravis
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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 the neuromuscular junction, with destruction of the receptors and reduction in their number. The clinical consequence of this process is the development of fatigable muscle weakness that progressively increases with repetitive muscle action and improves with rest. MG occurs more often in women than men, and although symptoms can develop at any age, the reported mean age at onset in women is 28-35 years and in men 42-49 years (Kalb et al. 2002). Although myasthenic symptoms remain confined to the extraocular muscles in about 20% of patients, in most individuals more widespread muscle weakness becomes evident (Kalb et al. 2002; Wirtz et al. 2002).

Involvement of bulbar musculature, with resultant dysphagia, is relatively common in MG. In approximately 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 as the disease progresses. Dysphagia in MG can be due to dysfunction at oral, pharyngeal, or even esophageal levels. Oral phase involvement can be due to fatigue and weakness of the tongue or masticatory muscles. In patients with MG who have bulbar symptoms, repetitive nerve stimulation studies of the hypoglossal nerve have demonstrated abnormalities (Lo et al. 2002), whereas studies using EMG of the masticatory muscles recorded while chewing have also revealed impaired performance (Weijnen et al. 2002). Pharyngeal dysfunction is also common in patients with MG who have dysphagia, as demonstrated with videofluoroscopy. Aspiration, often silent, may be present in 35% or more of these individuals (Colton-Hudson et al. 2002); in elderly patients, the frequency of aspiration may be considerably higher. Motor dysfunction involving the striated muscle of the proximal esophagus has also been documented in MG. In one study, 96% of patients with MG demonstrated abnormalities, such as decreased amplitude and prolongation of the peristaltic wave, in this region on testing with esophageal manometry. Cricopharyngeal sphincter pressure was also noted to be reduced.

NEUROGENIC DYSPHAGIA
A variety of disease processes originating in the central and peripheral nervous systems can also disrupt swallowing mechanisms and produce dysphagia. Processes affecting cerebral cortex, subcortical white matter, subcortical gray matter, brainstem, spinal cord, and peripheral nerves can elicit 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 Neuroacanthocytosis Body_ID: T013003.450 Parkinson's disease Body_ID: T013003.500 Progressive supranuclear palsy Body_ID: T013003.550 Wilson's disease Body_ID: T013003.600

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 lesions Body_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: T013003.1600 Amyotrophic lateral sclerosis Body_ID: T013003.1650 Multiple sclerosis Body_ID: T013003.1700 Peripheral neuropathic processes Body_ID: T013003.1750 Charcot-Marie-Tooth disease

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: T013003.2500 Scleroderma

Lots missed EVALUATION OF DYSPHAGIA.ext EVALUATION OF DYSPHAGIA

Body_ID: HC0013019 Various diagnostic tests, ranging from simple bedside analysis to sophisticated radiologic and neurophysiologic procedures, have been developed to evaluate dysphagia (Logemann 1996). Although most are actually performed by specialists other than neurologists, it is important for neurologists 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

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: T013004 Body_ID: None Clinical examination is somewhat limited because of the inaccessibility of some structures involved with swallowing, but both history and examination results can provide useful clues to localization and diagnosis (Table 13.5). Difficulty initiating swallowing or the need for repeated attempts to succeed at swallowing suggests an oropharyngeal source for the dysphagia, whereas a sensation of food "hanging up" in a retrosternal location implicates esophageal dysfunction. Individuals who report 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 motility disorder. 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

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 Body_ID: T013005 Body_ID: None Cervical auscultation is not widely used to evaluate swallowing but may be useful to assess coordination between respiration and swallowing (Table 13.6 and Figure 13.1) (Logemann 1996). In the normal situation, swallowing occurs during exhalation, which reduces the risk of aspiration. Dyscoordinated swallowing in the midst of inhalation, conversely, increases the possibility that food might be drawn into the respiratory tract. Body_ID: P013057 Body_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 Clinical examination Body_ID: T013006.150 Cervical auscultation Body_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 Clinical examination Body_ID: T013006.500 3-ounce water swallow Body_ID: T013006.550 Timed swallowing Body_ID: T013006.600 Primary test: Body_ID: T013006.650

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 Body_ID: T013006 Body_ID: None 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 display a number of abnormalities, including slower swallowing speed (<10 mL per second) and coughing, which may indicate the presence of dysphagia or aspiration (Logemann 1996). Some concern has been voiced, however, that the relatively large amounts of fluid used in these timed tests could present a significant risk for pulmonary complications as a consequence of aspiration, even if it is water that is used (Logemann 1996). Body_ID: P013059 A standardized 3-ounce water swallow test has been advocated as a simple bedside evaluation of oropharyngeal dysphagia. The presence of cough on swallowing during this test has been reported to provide a positive predictive value with regard to the presence of aspiration of 84% and a negative predictive value of 78% (Mari et al. 1997). The test, however, does not provide any information regarding the specific mechanism of dysphagia in the patient. Body_ID: P013060
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Body_ID: P0174 Body_ID: P013058

Add to lightbox

Body_ID: F013001
Figure 13.1 Dysphagia assessment.

The MBS test has become a standard method for assessing oropharyngeal dysphagia (Logemann 1996). Patients are observed via videofluoroscopy swallowing barium-impregnated food of differing consistencies (thin liquid, pudding, cookie). Both oral and pharyngeal function can be characterized, the presence of aspiration can be accurately documented, and the response to corrective measures, such as positioning techniques, can also be evaluated. Body_ID: P013061 Videoendoscopy of the pharynx, via the nasal passageway, allows direct visualization of the pharyngeal component of swallowing before and after passage of the food bolus. Its primary value is to demonstrate the presence of residual material in the pharynx after a swallow, indicative of increased risk of aspiration. Body_ID: P013062 Pharyngeal manometry provides physiologic information regarding function of both the pharynx and the UES (Hila, Castell, and Castell 2001). The information derived is complementary to that obtained by videofluoroscopy and a combined procedure, termed videomanofluorometry, in which both 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, and videofluoroscopy. Scintigraphic procedures can also be employed to evaluate oral, pharyngeal, and esophageal function but are not widely used (Galli et al. 2000). Body_ID: P013064 More sophisticated electrodiagnostic procedures have also been developed to study dysphagia.

EMG recording of cricopharyngeal function and integrated submental activity has been useful in a research setting to characterize aspects of swallowing, but this procedure has not yet come into general use. Body_ID: P013065