A 76-year-old woman with a history of stroke, diabetes mellitus, and hypertension is seen in the outpatient clinic for evaluation of recurrent pneumonia. Over the past 6 months, she has been hospitalized three times for pneumonia treated with broad-spectrum antibiotics. She admits to coughing during meals and intermittent nasal regurgitation while drinking fluids. On physical exam, she appears thin and is noted to have a residual left facial droop from her prior cerebrovascular accident (CVA). She is given a glass of water to drink and takes small sips and tucks her chin when swallowing. Her voice after drinking is wet sounding. She swallows a bite of pudding without noticeable difficulty.

There is limited published data regarding the incidence and prevalence of dysphagia in the population. Dysphagia becomes more common with aging and one study of patients in a primary care setting aged 62 years and older found that 7 % complained of solid food dysphagia. The incidence of dysphagia has been estimated to be as high as 33 % in acute care clinics and 30–40 % in nursing homes. The prevalence of achalasia, a primary motility disorder of the esophagus, has been estimated at 7.9–12.6 per 100,000 population with an incidence rate of 1 in 100,000 people.

The natural history of dysphagia differs based on the underlying etiology. For example, malignant causes of dysphagia will progress as will benign disorders such as achalasia and eosinophilic esophagitis. In contrast, anatomical disorders such as a Schatzki’s ring or a stricture due to gastroesophageal reflux may remain static for years until treatment is initiated.

Swallowing is a complex process of synchronized neuromuscular activity that is composed of two phases—the oropharyngeal phase and the esophageal phase. Dysphagia occurs when a mechanical (anatomic) or a motility (motor) disorder affects the coordinated swallowing mechanism required to transport a food bolus from the oral cavity to the stomach.

The oropharyngeal phase of swallowing consists of synchronized neuromuscular actions which move the food bolus from the oral cavity into the esophagus. The initial phase is voluntary and includes closure of the lips and elevation of the tongue against the palate to push the food bolus posteriorly into the pharynx. The soft palate then elevates to seal the nasopharynx, the hyoid moves anteriorly and forward, and the bolus passes from the oral cavity into the pharynx. This stimulates involuntary pharyngeal muscle peristalsis which causes elevation of the pharynx. As the pharynx elevates, the cricopharyngeus relaxes which results in the opening of the upper esophageal sphincter (UES), thus allowing passage of the food bolus into the esophagus. The cerebral cortex and cranial nerves V and IX–XII are vital in coordinating and controlling these actions both from a voluntary and involuntary level. It is also important to note that these same actions not only facilitate bolus passage through the oropharynx but also provide protective mechanisms against aspiration including epiglottic closure over the laryngeal vestibule and elevation of the larynx away from the bolus.

The esophageal phase is involuntary and commences after relaxation of the UES with passage of the bolus into the proximal esophagus. Peristalsis is initiated in the striated upper third of the proximal esophagus under brainstem control and sustained in the distal smooth muscle esophagus under the control of the myenteric plexus. The food bolus then passes through the lower esophageal sphincter (LES), which relaxes primarily via nitric oxide release from the myenteric neurons, and into the stomach.

The first step in the evaluation of dysphagia is to distinguish between oropharyngeal and esophageal dysphagia (see Table 2.2 and 2.3). A thorough history and physical exam will differentiate these two processes and help guide the selection of appropriate diagnostic testing. The Mayo Dysphagia Questionnaire has been shown to be useful in both clinical practice and research studies in this regard.