“Dysphagia” is an impaired ability to swallow. Dysphagia can result from anatomic variation or neuromuscular impairment anywhere from the lips to the stomach. Although some investigators choose to consider the voluntary oral preparatory stage of deglutition as a separate stage, swallowing is traditionally described as a three-stage event (oral, pharyngeal, and esophageal). Historically, research as well as evaluation and treatment of dysphagia were directed primarily toward the esophageal stage, which is generally treated by a gastroenterologist. However, over the past few decades, speech-language pathologists have become increasingly responsible for the research in, as well as the diagnosis and treatment of, the oral and pharyngeal aspects of deglutition.

The neuroanatomical substrate of dysphagia reflects lower motor neuron innervation by cranial nerves V, VII, IX, X, and XII. Dysphagia can result from unilateral or bilateral cortical insult. Within the cortex, primary sites that contribute to deglution include the premotor cortex, primary motor cortex, primary somatosensory cortex, insula, and the ventroposterior medial nucleus of the thalamus (Alberts et al., 1992; Daniels, Foundas, Iglesia, et al., 1996; Daniels and Foundas, 1997). Other portions of the cortical system have also been found to be active during swallowing (Hamdy et al., 1999, 2001; Martin et al., 2001).

Dysphagia is associated with an increased risk of developing malnutrition and respiratory complications such as aspiration pneumonia. In a study by Schmidt et al. (1994), the odds ratio that pneumonia would develop was 7.6 times greater for stroke patients who were identified as aspirators than for stroke patients who did not aspirate. Furthermore, the odds ratio of dying was 9.2 times greater for patients who aspirated thickened viscosities than for those who did not aspirate or who aspirated only thin fluids. Davalos et al. (1996) studied the effects of dysphagia on nutritional status in stroke patients who had similar nutritional status at the time of hospital admission. One week after the stroke, 48.3% of patients who developed dysphagia while in the hospital were malnourished, while only 13.6% of patients without dysphagia were malnourished. In a study of the nutritional status of patients admitted to a rehabilitation service, 65% of patients admitted with stroke and dysphagia were malnourished (Finestone et al., 1995).

Inadequate nutrition negatively affects the ability of the immune system to fight disease and contributes to the development of respiratory and cardiac insufficiency, the formation of decubitus ulcers, and impaired gastrointestinal function. The already comprised patient can become increasingly comprised, which prolongs the hospital length of stay and increases medical costs.

Certain clinical signs help to alert health care providers to the likely presence of dysphagia. Table 1 lists commonly observed clinical signs that are suggestive of dysphagia in the adult population. The absence of any or all of these signs does not indicate that a patient has a safe swallow or that the patient is able to ingest an adequate number of calories by mouth to remain properly nourished. For example, a diminished or absent gag has not been found to distinguish aspirators from nonaspirators (Horner and Massey, 1988). Many of these signs can be indicative of a serious medical illness. Therefore, patients who exhibit these signs and who have not been seen by a physician should be referred for medical examination.

Although clinical indicators have been found to have a relationship to laryngeal penetration, a significant number of patients who aspirate do so with no clinical indication. The incidence of silent aspiration is very high, and the difficulty of detecting it is suggested by the following: (1) Discriminant analysis of 11 clinical indicators resulted in identification of the presence of aspiration in only 66% of patients (Linden, Kuhlemeier, and Patterson, 1993). (2) In a heterogeneous group of 1101 patients with dysphagia, 276 (59%) of the 469 patients who aspirated were found to have silent aspiration (Smith et al., 1999). (3) When 47 stroke patients with mixed sites of lesions were examined, 24 (51%) of the patients were found to aspirate; of those 24 patients, 11 (46%) were silent aspirators (Horner and Massey, 1988). (4) In a study of 107 patients in a rehabilitation facility, 43 (40%) were found to aspirate on videofluoroscopic examination; however, clinical evaluation identified only 18 (42%) of the aspirators (Splaingard et al., 1988). Because of the additional expense encountered in caring for patients with respiratory or nutritional complications, studies such as these support the argument that money, as well as life, can be saved when patients are properly evaluated.

Dysphagia can occur at any age across the life span. Among young adults, traumatic brain injury is a not uncommon cause of acquired dysphagia, whereas elderly individuals are more likely to acquire dysphagia as a result of illness. However, young adults are also susceptible to the same causes of dysphagia as the elderly. Neurological disorders take a particular toll: it has been estimated that 300,000–600,000 persons per year experience dysphagia secondary to neurological disorders, and the greatest percentage of these experience dysphagia secondary to stroke (Doggett et al., 2001). After stroke and neurological disease, the most frequent causes of dysphagia in adults include muscle disease, head and neck surgery, radiation to the head and neck, dementia, motor end-plate disease, traumatic brain injury, systemic disease, cervical spine disease, medication effects, and senescent changes in the sensorimotor system.