Introduction

The true incidence of dysphagia in the general population remains unknown to date. The incidence has been described in select patient populations, and its prevalence in the general population can be inferred to be significant. A review of nursing home residents demonstrated that 30% to 40% have clinical evidence of dysphagia. Another well-studied population is those suffering stroke. Studies have shown that 30% to 40% of stroke patients will demonstrate symptoms of severe dysphagia, and as many as 20% will die from aspiration pneumonia in the first year (1). Given the number of new cerebrovascular events yearly, this is a significant number.

A single swallow consists of a series of complex neuromuscular events that must occur in a coordinated fashion. This complexity lends itself to dysfunction. The central control processors for swallowing are located in the brainstem, adjacent to the areas controlling such basic functions as respiration, core body temperature, and blood pressure. They are located dorsally in the brainstem, within and adjacent to the nucleus of the tractus solitarius as well as in the ventral region near the nucleus ambiguous (2). They lie adjacent to both sensory and motor nuclei of the vagus nerve, underlying this nerve's importance in swallowing physiology. The swallow reflex does not function in isolation, however, as Sasaki and Suzuki described, alterations in these reflex activities by a host of physiologic changes, including hypercapnia, hypoxia, and sedation, can dramatically alter it.

Dysphagia can be broadly divided into two distinct entities, oropharyngeal dysphagia and esophageal dysphagia. These will be treated separately in this chapter.

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