All of these muscular contractions are effected largely by cranial nerve X (vagus). The palatopharyngeal muscles pull the pharynx up over the bolus and the stylopharyngeal muscles draw the sides of the pharynx outward (nerve IX). At the same time, the upward movement of the larynx opens the cricopharyngeal sphincter. A wave of peristalsis then begins in the pharynx, pushing the bolus through the sphincter into the esophagus. These muscles relax as soon as the bolus reaches the esophagus. The entire swallowing ensemble can be elicited by stimulation of the superior laryngeal nerve (this route is used in experimental studies.)
Reflex swallowing requires only medullary functioning and is retained in the vegetative and locked-in states as well as in normal and anencephalic neonates. The integrated sequence of muscle activity for swallowing is organized in a region of brainstem that roughly comprises a swallowing center, located in the region of the NTS, close to the respiratory centers. This juxtaposition ostensibly allows the refined coordination of swallowing with the cycle of breathing. Besides a programmed period of apnea, there is a slight forced exhalation after each swallow that further prevents aspiration. The studies of Jean, Kessler, and others (cited by Blessing), using microinjections of excitatory neurotransmitters, have localized the swallowing center in animals to a region adjacent to the termination of the superior laryngeal nerve. Unlike the generators of respiratory rhythm, the entire reflex apparatus for swallowing may be located in the NTS. There is, however, no direct connection between the NTS and the cranial nerve motor nuclei. Thus it is presumed that control must be exerted through premotor neurons located in adjacent reticular brainstem regions. There have been few comparable anatomic studies of the structures responsible for swallowing in humans. As to the cortical regions that are involved in swallowing, it appears from PET studies that the inferior precentral gyrus and the posterior inferior frontal gyrus are activated, and lesions in these parts of the brain give rise to the most profound cases of dysphagia.
Weakness or incoordination of the swallowing apparatus is manifest as dysphagia and, at times, aspiration. The patient himself is often able to discriminate one of several types of defects: (1) difficulty initiating swallowing, which leaves solids stuck in the oropharynx; (2) nasal regurgitation of liquids; (3) frequent coughing and choking immediately after swallowing and a hoarse, “wet cough” following the ingestion of fluids; or (4) some combination of these. Extrapyramidal diseases, notably Parkinson disease, reduce the frequency of swallowing and cause an incoordination of breathing and swallowing, as noted later.
It is surprising how often the tongue and the muscles that cause palatal elevation appear on direct examination to act normally despite an obvious failure of coordinated swallowing. Similarly, the use of the gag reflex as a neurologic sign is quite limited, being most helpful when there is a medullary lesion or the lower cranial nerves are damaged. In our experience, palatal elevation in response to touching the posterior pharynx only demonstrates that cranial nerves IX and X and the local musculature are not entirely dysfunctional; in other words, the presence of the reflex does not ensure the smooth coordination of the swallowing mechanism and, more importantly, does not obviate aspiration. Difficulties with swallowing may begin subtly and express themselves as weight loss or as a noticeable increase in the time required to eat a meal. Nodding or sideways head movements to assist the propulsion of the bolus, or the need to repeatedly wash food down with water, are other clues to the presence of dysphagia. Often, recurrent minor pneumonias are the only manifestation of intermittent (“silent”) aspiration.