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Sallowing Disorder
Sallowing Disorder
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Content
Background
Swallowing
Anatomical structure
Neural coordination of swallowing
Normal physiology of swallowing
Swallowing disorder
Pathophysiology of swallowing along with various diseases
References
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Objective
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There is evidence that swallowing begins to develop in utero as
early as 15 weeks gestation to regulate amniotic fluid volume.
The suck, swallow, and breathing sequence continues to evolve
in the early stages of life as infants are introduced to new foods
and begin to control their swallowing consciously.
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Multiple organ systems are involved in this process, including the
musculoskeletal, neuromuscular, and respiratory systems.
Normal swallowing requires a coordinated effort of over thirty
muscles, the central nervous system, and five cranial nerves.
Additionally, the nose, the nasal cavity, the oral cavity, and the
pharynx are key anatomical structures involved in this process.
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Anatomical structure
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Oral Phase
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2. Airway Protection
The pharyngeal phase protects the airway via swallowing apnea,
a well-coordinated physiologic response where respiration ceases
during swallowing. This apneic period tends to interrupt the
expiratory phase of breathing, lasting approximately 0.5 to 1.5
seconds, preventing aspiration during inspiration.
The primary mechanism of airway protection is the closure of the
vocal folds. The posterior cricoarytenoid, contracted at rest, is
inhibited, and the lateral cricoarytenoids are stimulated to adduct
the cords. The oblique and transverse arytenoid muscles bring the
arytenoid cartilage together, aiding in glottic closure.
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Concurrently, the arytenoids are tilted forward to contact the
epiglottis and assist in opening the passage towards the
esophagus. While not directly involved in airway protection,
retroversion of the epiglottis by the tongue helps direct the food
bolus towards the piriform fossa and into the esophagus.
3.) Elevation of the hyoid-laryngeal complex
The pharynx becomes elevated and pulled anteriorly by contraction
of the suprahyoid muscles, which helps to open the pharyngeal-
esophageal transition.
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4.) Bolus transport
The bolus is moved inferiorly by a peristaltic-like sequential
contraction of the superior, middle, and inferior pharyngeal
constrictor muscles in a top-to-bottom fashion. A pattern of rapid
stimulation and inhibition in the pharyngeal muscles creates a
cranial-caudal wave of pressure that directs the food bolus towards
the UES. The speed is remarkably fast, occurring at rates of 20 to
40cm/s. Once initiated, the pharyngeal phase behaves in an ‘all or
none’ fashion, much like a reflex, hence why this phase is
considered irreversible.
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5.) Transit through UES
The end of the pharyngeal phase involves the food bolus descending
through a patent UES into the esophagus. The sphincter remains in
tonic contraction at rest to prevent air from entering the esophagus
but is opened by three sequential mechanisms: 1) contraction of the
thyrohyoid to move the larynx and hyoid superiorly and anteriorly,
thereby initiating the opening of the sphincter, 2) manometric
relaxation of the cricopharyngeus, and 3) Pressure-dependent
distension of the UES by the bolus.
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Esophageal Phase
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Swallowing disorder
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Pathophysiology
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Another cause of food retention in the pharynx after swallowing
is impaired opening of the UES. This can be caused by increased
stiffness of the UES, as in fibrosis or inflammation, or failure to
relax the closing muscle of the sphincter (primarily the
cricopharyngeus muscle). Because UES opening is an active
process, failure of opening can also be caused by weakness of the
muscles of sphincter opening, particularly the anterior suprahyoid
musculature. Dyscoordination of the swallow can also lead to
failure of UES opening. Because the UES is ordinarily closed
between swallows, its opening is obligatory for swallowing to
occur. This means that failure of UES relaxation and opening can
produce obstruction of the food pathway.
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Airway protection is a critical function of swallowing; however,
airway protection mechanisms are not always effective. Failure of
laryngeal protective mechanisms can reflect reduced laryngeal
elevation, incomplete closure of the laryngeal vestibule, or
inadequate vocal fold closure caused by weakness, paralysis, or
anatomic fixation.
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Dysphagia can result from a wide variety of disorders. A major
cause of dysphagia is stroke. Dysphagia is found in
approximately half of individuals with a recent stroke. Most
recover within the first 2 weeks, but dysphagia can be severe and
persistent. Brainstem lesions can result in particularly severe
dysphagia, given their proximity to the major swallow centers.
Reduced laryngeal elevation, insufficient UES opening, vocal
fold weakness, and severe weakness of oropharyngeal muscles
are common in patients with stroke.
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Cerebral lesions can result in dyscoordination of the swallow,
with impaired oropharyngeal bolus propulsion and airway
protection. Swallow dysfunction is typically more severe in
bilateral cerebral lesions because there is a bilateral cortical
representation for swallow function.
By contrast, the brainstem motor nuclei innervate only ipsilateral
muscles, so lesions of cranial nerves or their nuclei can result in
unilateral sensory or lower motor neuron dysfunction.
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In neurodegenerative disorder: Dysphagia can be the first
symptoms.
Oral-stage dysphagia is common in Parkinson disease,
characterized by tremor, dyskinesia, and bradykinesia in lips,
tongue, jaw, and larynx, which hamper oral and pharyngeal food
transport.
In motor neuron disease, progressive degeneration of motor neurons
in the brain and spinal cord results in weakness in the muscles of
mastication, respiration, and swallowing.
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Inflammatory muscle diseases, including dermatomyositis and
polymyositis, commonly affect striated muscles, resulting in
weakness of the pharynx. By contrast, progressive systemic
sclerosis affects smooth muscle and commonly produces
esophageal dysfunction, including reduced peristalsis, dilatation
of the lower esophagus, and gastroesophageal reflux disease
(GERD).
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Structural abnormalities whether congenital or acquired, can
impair swallow function. Birth defects, such as clefts of the lip
and palate often produce inadequate labial control for sucking
and bolus control, or velopharyngeal insufficiency with nasal
regurgitation. The resulting dysphagia can lead to malnutrition,
requiring surgical repair of the defect during infancy.
Structural abnormalities can impair pharyngeal transport and
airway protection.
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GERD can affect swallowing indirectly. In GERD, the LES has
insufficient tone, rendering it ineffective for preventing gastric
contents from passing back through the LES into the esophagus.
Because the esophageal lining is not resistant to acid (as is the
stomach lining), reflux of highly acidic stomach contents can
result in inflammation (esophagitis) or scarring (stricture) of the
esophagus. This can lead to pain or obstructive symptoms.
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Dysphagia is often iatrogenic. Several drugs can impair
swallowing, including anticholinergic drugs and benzodiazepines.
Neuroleptic agents, also called antipsychotic drugs, can cause
movement disorders affecting the face and mouth, such as tardive
dyskinesia, especially after long-term use. These can impair
eating and swallowing. Any medication that causes sedation can
have an adverse effect on swallowing and potentially impair
airway clearance (e.g., cough) in response to aspiration.
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Postoperative dysphagia is a common complication of anterior
cervical fusion, occurring in approximately half of patients.139
Individuals with multiple cervical surgical levels demonstrate a
higher risk of having dysphagia when compared with those
undergoing survey at one level.
The mechanism is unclear, but it might be related to injury of the
pharyngeal constrictor muscles or their innervation. Most patients
recover within the first 2 months.
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Compromised and altered respiratory function increases the risk
for dysphagia. Chronic obstructive pulmonary disease alters the
coordination of respiration and deglutition. Patients who have
undergone lung transplantation may demonstrate dysphagia, with
a high risk of silent aspiration.
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Evaluation of dysphasia
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2. Bedside/Clinical Swallow Assessments
Swallow Screenings.
Clinical Swallow Examination.
Blue Dye Clinical Swallow Examination.
Cervical Auscultation.
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References
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