Version May 2024
INTRODUCTION — Oropharyngeal dysphagia, also called transfer dysphagia, arises from disease of the upper esophagus and pharynx, or from upper esophageal sphincter (UES) dysfunction (table 1).
This topic will review the physiology of normal swallowing and the etiology and pathogenesis of oropharyngeal dysphagia. An overview of dysphagia; the etiology and evaluation of patients with esophageal dysphagia; the clinical features, diagnosis, and management of oropharyngeal dysphagia; the etiology, assessment, and management of swallowing disorders in palliative care populations are discussed separately. (See "Oropharyngeal dysphagia: Clinical features, diagnosis, and management" and "Approach to the evaluation of dysphagia in adults" and "Swallowing disorders and aspiration in palliative care: Definition, pathophysiology, etiology, and consequences" and "Swallowing disorders and aspiration in palliative care: Assessment and strategies for management".)
DEFINITIONS
●Dysphagia is defined as a subjective sensation of difficulty or abnormality of swallowing.
Dysphagia can be classified as follows:
●Oropharyngeal or transfer dysphagia is characterized by difficulty initiating a swallow. Swallowing may be accompanied by nasopharyngeal regurgitation, aspiration, and a sensation of residual food remaining in the pharynx.
●Esophageal dysphagia is characterized by difficulty swallowing several seconds after initiating a swallow and a sensation of food getting stuck.
PHYSIOLOGY OF SWALLOWING — Normal swallowing consists of three phases (oral preparatory, pharyngeal, and esophageal) that are usually performed effortlessly up to 600 times a day. Once swallowing has been initiated, it takes less than one second for a bolus to reach the esophagus (figure 1), and an additional 10 to 15 seconds to complete the swallow. This process involves more than 30 muscles. Therefore, precise timing and coordination during the oropharyngeal phase are crucial for normal swallowing.
The swallowing centers within the brainstem are interdependent and receive bilateral, though asymmetric, projections from the motor and premotor cortex. The degree of input from each hemisphere may be critical for determining recovery of swallowing after a stroke [1].
Oral preparatory phase — In the oral preparatory phase, the bolus is processed by mastication to an appropriate size, shape, and consistency to pass through the pharynx and esophagus. The oral phase is largely voluntary.
The tongue is a critical part of this phase, both for controlling the food so that proper chewing can occur and for directing the bolus to its proper position for swallowing. After chewing, the bolus is moved to the back of the tongue. The anterior portion of the tongue lifts up to the hard palate and retracts posteriorly forcing the bolus into the upper pharynx. Elevation of the posterior portion of the tongue by the mylohyoid muscles elevates the soft palate, thereby sealing the nasopharynx and preventing nasal regurgitation.
The oral preparatory phase is under voluntary control and involves use of cranial nerves V (trigeminal), VII (facial), and XII (hypoglossal) (table 2).
Pharyngeal phase — During the pharyngeal phase of swallowing, the bolus is advanced through the pharynx and into the esophagus by pharyngeal peristalsis. This occurs by approximation of the soft palate to the posterior nasopharyngeal wall, which seals off the nasopharyngeal inlet and by contraction of the superior constrictor muscles. Simultaneously, the larynx and hyoid are pulled upward and forward allowing the bolus to pass over the larynx without aspiration and causing relaxation of the cricopharyngeus muscle, which makes up much of the upper esophageal sphincter (UES) (figure 1).
The pharyngeal phase, unlike the oral phase, is controlled reflexively and is referred to as the swallow response. It involves cranial nerves V (trigeminal), IX (glossopharyngeus), X (vagus), and XII (hypoglossal). During swallowing, respiration is inhibited centrally.
Esophageal phase — In the esophageal phase of swallowing, peristaltic contractions in the body of the esophagus combined with simultaneous relaxation of the lower esophageal sphincter propel the bolus into the stomach.
EPIDEMIOLOGY — The estimated prevalence of oropharyngeal dysphagia in studies involving the general population has ranged from 2 to 16 percent [2]. Among patients with predisposing conditions (eg, dementia), the estimated prevalence of oropharyngeal dysphagia was 72 percent [3,4]. In a study of 200 patients admitted to a geriatric hospital (average age 84 years), the prevalence of oropharyngeal dysphagia was 29 percent, and rates were higher in males and in nursing home residents. Other risk factors included diabetes mellitus, chronic obstructive pulmonary disease, central nervous system disease, and use of selected medications (eg, antipsychotics, benzodiazepines, and antidepressants) [5].
ETIOLOGY AND PATHOGENESIS — Oropharyngeal dysphagia can arise from disorders that affect the oral preparatory and/or the pharyngeal phase of swallowing (table 1).
Disorders of the oral preparatory phase — A normal oral preparatory phase requires food to be adequately chewed and presented for swallowing. Proper mastication, adequate salivary production for softening the consistency of the bolus, intact mucosa within the oropharynx, and neuromuscular coordination are all necessary features for the initial phase of swallowing to occur.
Several disorders can disrupt normal completion of the oral preparatory phase by the following mechanisms:
●Poor dentition may lead to inadequate mastication of the bolus [6].
●A decrease in salivary flow may occur in diseases such as Sjögren's disease, following radiation to the head and neck, or from medications that reduce salivary flow (eg, anticholinergics, antihistamines, and antihypertensive agents). (See "Clinical manifestations of Sjögren's disease: Exocrine gland disease", section on 'Dry mouth'.)
●Following a cerebrovascular accident, patients may have dysphagia due to reduced lingual control in addition to an absent/delayed swallowing reflex, and weakened laryngopharyngeal musculature. (See "Complications of stroke: An overview", section on 'Dysphagia'.)
●Patients with Parkinson disease may complain of oropharyngeal dysphagia during late stages of the disease [7]. Dysphagia results from lingual pumping, a nonpropulsive back-and-forth movement of the tongue that prevents the food bolus from leaving the oral cavity. (See "Clinical manifestations of Parkinson disease", section on 'Cardinal features'.)
●Disruption of the oropharyngeal mucosa from mucositis, aphthous ulcers, herpetic lesions, or trauma may inhibit normal processing of the bolus. (See "Oral toxicity associated with systemic anticancer therapy", section on 'Mucositis' and "Oral lesions", section on 'Erosive, ulcerative, and bullous lesions'.)
Disorders of the pharyngeal phase — A normal pharyngeal phase requires neuromuscular coordination for propulsion of the bolus, an unobstructed lumen, and normal relaxation of the upper esophageal sphincter (UES). During this phase, the larynx elevates and closes at the level of the epiglottis, mainly by closure of the aryepiglottic folds and vocal cords, to prevent laryngeal penetration and aspiration.
Several structural and functional disorders can result in dysphagia by affecting the pharyngeal phase of swallowing (table 1):
●Neurologic disorders that involve the central nervous system (eg, stroke and motor neuron disease [amyotrophic lateral sclerosis]), or the peripheral nervous system (eg, myasthenia gravis) can cause oropharyngeal dysphagia by disrupting the neuromuscular coordination required during the pharyngeal phase of swallowing [8,9]. Muscular dystrophies such as oculopharyngeal muscular dystrophy can result in oropharyngeal dysphagia in addition to palpebral ptosis due to progressive muscle weakness. In patients with Parkinson disease, a delayed swallow response and weak pharyngeal contraction result in pooling of food residue in the vallecular and pyriform sinuses following a swallow. (See "Oculopharyngeal, distal, and congenital muscular dystrophies", section on 'Clinical features' and "Bell's palsy: Pathogenesis, clinical features, and diagnosis in adults", section on 'Clinical features' and "Clinical manifestations of myasthenia gravis" and "Clinical manifestations of Parkinson disease", section on 'Cardinal features'.)
●Poor compliance of the UES causes incomplete relaxation during swallowing, resulting in dysphagia.
•Patients with Parkinson disease frequently have incomplete relaxation of the UES and reduced UES opening [10].
•Patients with primary cricopharyngeal dysfunction, a rare functional disorder, have inadequate pharyngeal contraction, lack of coordination between the pharynx and the UES, and/or inadequate UES relaxation/reduced muscular compliance.
●In patients with a cricopharyngeal bar and hypopharyngeal diverticulum, both functional and structural abnormalities in the pharynx can result in dysphagia. A cricopharyngeal bar is a radiographic finding of posterior indentation of barium caused by impaired opening of the UES due to decreased muscular compliance [11,12]. Although it is a common radiographic finding in patients undergoing videofluoroscopy (5 to 19 percent) and is frequently asymptomatic, it may be associated with dysphagia [13,14]. Over time, decreased UES compliance results in a rise in hypopharyngeal pressure and development of a pharyngoesophageal (Zenker's) diverticulum due to protrusion of hypopharyngeal mucosa between the inferior pharyngeal constrictor and the cricopharyngeus. The diverticulum, when enlarged sufficiently to contain food or liquid, can then produce symptoms of dysphagia due to extrinsic compression on the esophageal lumen (image 1) [15-18]. (See "Zenker's diverticulum", section on 'Clinical manifestations'.)
In contrast with Zenker's diverticulum, a Killian-Jamieson diverticulum is less common, and it protrudes through a muscular gap in the anterolateral wall of the proximal cervical esophagus [19,20].
●Obstructions within the oropharynx are most commonly due to malignancies. Benign lesions that cause oropharyngeal dysphagia due to obstruction include cervical rings or webs. Cervical osteophytes can also cause obstructive dysphagia by displacing the hypopharynx anteriorly and impeding the transit of a food bolus. Similarly, masses of the parapharyngeal and retropharyngeal space can cause a similar mass effect. (See "Esophageal rings and webs", section on 'Clinical presentation'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Dysphagia".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Dysphagia (The Basics)")
SUMMARY
●Definitions – Dysphagia is defined as a subjective sensation of difficulty or abnormality of swallowing. (See 'Definitions' above.)
Oropharyngeal or transfer dysphagia is characterized by difficulty initiating a swallow. Swallowing may be accompanied by nasopharyngeal regurgitation, aspiration, and a sensation of residual food remaining in the pharynx. Esophageal dysphagia is characterized by difficulty swallowing several seconds after initiating a swallow and a sensation of food getting stuck.
●Physiology of swallowing – Normal swallowing consists of an oral preparatory, pharyngeal, and esophageal phase. In the oral preparatory phase, the bolus is processed by mastication to an appropriate size, shape, and consistency to pass through the pharynx and esophagus. During the pharyngeal phase of swallowing, the bolus is advanced through the pharynx and into the esophagus by pharyngeal peristalsis. In the esophageal phase of swallowing, peristaltic contractions in the body of the esophagus combined with simultaneous relaxation of the lower esophageal sphincter propel the bolus into the stomach. (See 'Physiology of swallowing' above.)
●Etiology and pathogenesis – Oropharyngeal dysphagia arises from structural or functional diseases of the upper esophagus and pharynx, or upper esophageal sphincter (UES) that affect the oral preparatory or pharyngeal phase of swallowing (table 1). (See 'Etiology and pathogenesis' above.)
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