Is its origin related to disruption of the fixed sequences of contraction of the pharyngeal and parapharyngeal muscles ?
J. Christensen (Iowa City)
Oropharyngeal dysphagia must be carefully distinguished from esophageal dysphagia because the two have quite different causes. The perception of the difficulty at the suprasternal notch is common in esophageal dysphagia, and this can lead it to be confused with Oropharyngeal dysphagia. When the dysphagia is accompanied by prominent or frequent aspiration of swallowed material or by nasopharyngeal reflux of swallowed material, that signifies that the problem is really arising in the oropharynx.
Oropharyngeal dysphagia represents disordered motions of the oropharynx and/or upper esophageal sphincter in swallowing. Disordered motion can have two sources. First, the sequence of excitation of the striated musculature can be disrupted. Second, the excitation of the striated muscle may be proceeding normally, but its normal motion in contracting may be impaired by a mass lesion of a mechanical obstruction.
The possibility of a mechanical problem must not be overlooked. Many sorts of mechanical problems can produce oropharyngeal dysphagia, but mechanical problems usually produce a milder degree of dysphagia than do physiological problems. Any of the several kinds of tumors that can arise in the neck produce oropharyngeal dysphagia. Those that lie in the wall of the oropharynx simply impede normal pharyngeal motion. Those that arise outside the oropharynx probably cause the symptom partly by impinging on the oropharynx or by altering the motions of the parapharyngeal muscles.
Tumors are not only mechanical causes of oropharyngeal dysphagia. Radiation-induced fibrosis of parapharyngeal tissues or of the oropharyngeal wall itself cause mild oropharyngeal dysphagia.
As for the physiological causes, it is clear that disruption of the normal excitation of the striated musculature causes oropharyngeal dysphagia. The striated musculature is normally excited in a fixed sequence. This is possible because of the way this striated muscle is innervated. One somatic motor nerve from the responsible cranial nerve enters the muscle and supplies a small, discrete and fixed population of muscle cells. This number is probably only 5-10 muscle cells per motor nerve fiber.
One such set of muscle fibers is called a motor unit. Thus, probably only about one hundred or so motor nerves supply all the motor units that make up the whole oropharynx. These nerves arise in the brain-stem nuclei, which are paired, right and left in the brainstem. There is very little or no crossover of those fibers in the oropharynx. That is, the right-sided nuclei in the brainstem supply the right side of the oropharynx and the left-sided nuclei supply the left side of the oropharynx.
In order for a peristaltic contraction to be produced, the motor units must be excited in a fixed sequence that corresponds to their craniocaudad positions. This means that each nerve cell in the nuclei of the brainstem must be excited separately in the correct sequence. Since there are two sets of such nuclei, right and left the corresponding nerve cells, right and left, must be excited simultaneously in order that a symmetrical contraction of the orapharynx will be produced.
Obviously, this requires a very intricate and highly-organized set of interconnections in the brain-stem. It seems to be a very rugged system, for it does not seem to become dysfunctional very often except in the case of brain-stem infarction. Brain-stem infarctions most commonly are unilateral, due to the occlusion on one side of the arterial blood supply to the cerebellum and adjacent brain-stem. The syndrome that results thus includes signs of cerebellar dysfunction and other signs of brain-stem dysfunction in addition to oropharyngeal dysphagia. The dysphagia in such cases represents the loss of function of the motor nuclei that supply the oropharynx only on the affected side. As a result, the oropharynx contracts
asymmetrically rather than being wholly paralyzed. This is probably the explanation for the fact that patients who have had brain-stem strokes may sometimes have rather mild oropharyngeal dysphagia, though of course it can still be life-threatening because of the risk of aspiration pneumonia.
Bilateral or complete dysfunction of oropharyngeal motor function occurs in myasthenia gravis and other primary disorders of striated muscle. Here, the problem lies in the muscle itself rather than in the neurological programming of its excitation. The severity of the problem varies according to the severity of the muscle disease.
Of course, there still remain rare patients whose oropharyngeal dysphagia cannot be found to be attributable to any of the above causes. It is possible in such cases that the problem may in fact be a disordered sequence in the excitation of motor units in the oropharyngeal musculature. There is presently no way to determine if that is so. This could, for example, be the problem that underlies and leads to the formation of a Zenker's diverticulum. It seems a reasonable idea, at least.