Central organizing center
The medulla oblongata houses paired swallowing centers responsible for processing afferent sensory signals and programming the motor swallowing sequences [46–48]. These centers are poorly defined areas and comprise the NTS, ventromedial reticular formation (VMRF), and nucleus ambiguus (NA) [49]. There is increasing evidence that cortical structures have a significant influence on the brainstem swallowing centers [50]. Cortical areas in the preorbital gyrus and lateral precentral gyrus have been implicated in modulation of deglutition. Cortical projections have been found connecting the cortical and medullary swallowing centers. Although poorly understood, experimental evidence suggests the presence of a close functional, structural, and physiologic interaction between deglutitive and respiratory centers and their afferent and efferent inputs.
Figure 3.2 Sequence of events during primary swallows. (A–D) The primary swallow resulted in bolus transport from the mouth into the pharynx and esophagus. Straight arrows indicate pharyngeal lumen. (A, E) Bolus of 5 mL of barium is held in the oral cavity immediately before the onset of swallowing. Tongue base and soft palate are in contact (curved arrow), segregating the oral bolus from the pharyngeal cavity. (B, F) Tongue base is depressed and soft palate has elevated and is in contact with the posterior pharyngeal wall. This resulted in closing off the nasopharynx and allowing the bolus to enter the pharynx. (C, G). Bolus transferring to the pharynx while the nasopharynx and oral cavity are sealed off by approximation of the soft palate and posterior pharyngeal wall, and apposition of the tongue base and soft palate, respectively. The hyoid bone has moved upward and forward. (D, H) The barium bolus has cleared the pharynx, the oral cavity and nasopharynx are open, and the larynx and hyoid bone have returned to the resting position. B, barium bolus; H, hyoid bone.
Source: Shaker et al. [37] with permission of Elsevier.
Motor efferent pathways
Motor output to the muscular apparatus of the oropharynx for swallowing is transmitted by axons, whose cell bodies are located in the brainstem swallowing centers. These include motor nuclei of the trigeminal (V), facial (VII), and hypoglossal (XII) nerves [44]. It also includes the NA, which not only consists of the premotor commanding neuron, but also houses large motor neurons that are distributed to striated muscles innervated by the glossopharyngeal (IX) and vagus (X) nerves [45].
Musculature
The muscular apparatus of oropharyngeal swallowing consists of a total of 30 paired striated muscles [7]. Cranial nerve XII and the ansa cervicalis (C1‐C2) control the tongue, while the vagus nerve exerts predominant control over the muscles of the palate, pharynx, and larynx, as well as the cricopharyngeus muscle. Deglutitive orad movement of the hyoid bone, larynx, and UES, and active opening of the UES following its relaxation, are induced by the supra‐ and infra‐hyoid muscles that are innervated by the ansa cervicalis (C1‐C2), cranial nerve V3, and cranial nerve VII [51].
Figure 3.3 Relationship of deglutitive vocal cord kinetics to other events of the oropharyngeal phase of swallowing during 5 mL barium swallows. Bolus transit through the pharynx and across the upper esophageal sphincter (UES) begins and ends with the vocal cords at maximal adduction. TB‐O, onset of tongue base movement; SH‐O, onset of superior hyoid movement; SM‐O, onset of submental myoelectrical activity; UESO, UES opening; OT‐O, onset of bolus movement from the mouth; PT‐O, arrival of bolus into pharynx.
Presentation
Most patients with OPD seek help because of symptoms, although a subset are silent aspirators who may present with recurrent pneumonia. Dysphagia symptoms reflect a breakdown in the transport or protective functions of oropharyngeal swallowing (Table 3.1). These symptoms are highly specific and should not be simply dismissed as functional or psychogenic. Every effort should be exerted to arrive at a specific diagnosis, although subtle abnormalities often escape detection.
A sensation of “food sticking in my throat” is often reported and reflects inadequate clearance of the bolus from the pharynx. Although this sensation may be caused by the presence of a large amount of residue in the pyriform sinus or vallecula, an obstructive lesion of the proximal or distal esophagus may lead to the very same complaint. Thus, patients with complaints of cervical dysphagia should undergo a thorough evaluation of the esophagus. Of course, careful direct visualization of the hypopharyngeal area must also rule out inflammation, abrasion, or tumors in this area.
Misdirection of the bolus into the airway leading to swallow‐related coughing or choking is another common complaint. Invasion of the upper airway by the bolus may occur before initiation of, during, or after completion of oropharyngeal swallowing, and results in a coughing or choking sensation [52]. Aspiration into the airway may occur prior to deglutition because of the premature loss of the bolus into the hypopharynx from the mouth while the path to the airway is still open, a condition commonly encountered in post‐stroke dysphagic patients. An inability to segregate the oral bolus from the pharynx by apposition of the tongue base and soft palate results in this premature spillage, called pre‐deglutitive aspiration. If pharyngeal sensation is deranged, and swallowing is not initiated by entry of the prematurely passed bolus into the pharynx, pre‐deglutitive aspiration and its concomitant complications follow. Deglutitive aspiration occurs either because of an incompetent glottis or one that does not close properly during the swallowing sequence, which leads to invasion of the airway by the bolus while it is being transported through the hypopharynx. Finally, post‐deglutitive aspiration develops when the bolus transport is incomplete and a large residue remains in the pyriform sinus or vallecula, a condition encountered in parkinsonism, post stroke, myasthenia gravis, and multiple sclerosis. When the glottis opens and respiration is resumed, the large residue is either inhaled or overflows into the trachea.
The history is helpful to distinguish OPD from globus sensation. Globus is a sensation of a lump or tightness in the throat. Globus is purely sensory and occurs between meals without impairment in bolus transfer [53–56]. It should not be diagnosed in the presence of dysphagia. Patients occasionally have associated psychiatric disorders, such as anxiety, depression, panic disorder, etc. Evaluation often involves otolaryngology.
Similar to esophageal dysphagia, the history can be helpful in narrowing the differential diagnosis in OPD. Solid food dysphagia is often indicative of a structural abnormality. Progressive symptoms associated with weight loss raise the concern for malignancy. Sudden onset of symptoms associated with a neurologic deficit suggests stroke. Foul breath and delayed regurgitation may be indicative of a Zenker’s diverticulum. Myopathies often present as slowly progressive dysphagia. Other systemic symptoms such as features of Parkinson’s or memory loss may be helpful in determining a diagnosis.
A history of aspiration pneumonia is an important clue to oropharyngeal dysphagia [57]. Langmore et al. found that dysphagia is an important risk factor in elderly patients but is generally insufficient to cause pneumonia unless other risk factors are present. Risk factors include feeding and oral care dependence, decayed teeth, tube feeding, medications, and smoking [58, 59].
In the preparatory phase of swallowing, several protective reflexes are present,