As noted earlier in this chapter, the act of swallowing requires multiple muscles in the mouth, throat, and esophagus to produce a precisely controlled and coordinated cascade of movement. This, perhaps not surprisingly, turns out to be difficult for the individual with PD. Survey studies reveal a rather broad range of positive responses when PD patients are asked whether they perceive difficulty swallowing. While the two large survey studies67 each catalogued a subjective sense of dysphagia in approximately 50% of participants with PD, other studies have suggested that anywhere from 30 to 82% of PD patients may be aware of difficulty swallowing.76-79 The reason for this broad range is uncertain but may simply reflect the degree of detail in the questionnaire.79 While most attention regarding dysphagia in PD has centered on oropha-ryngeal abnormalities, it is clear that esophageal dysfunction may also play a role in the generation of dysphagia in some individuals.
Objective studies of swallowing generally have demonstrated an even higher frequency of swallowing abnormalities than the subjective survey studies. The most frequently employed test has been the modified barium swallow (MBS) test, and various investigators have reported abnormalities on MBS in 75 to 97% of PD subjects tested.80-83 An array of abnormalities in both the oral and pharyngeal phases of swallowing have been identified during MBS testing. Within the oral phase, alterations in lingual control and oral mobility, presumably due to rigidity and bradykinesia, result in abnormal bolus formation, delayed initiation of swallowing, repeated tongue pumping to accomplish the swallow, piecemeal deglutition, and the presence of residual material on the tongue or in the lateral or anterior sulci following swallowing.84-89 An equally impressive roster of abnormalities have been identified in the pharyngeal phase, including pharyngeal dys-motility, misdirected swallows, pharyngeal and vallecular stasis, vallecular residue, and reflux of material from the vallecular and pyriform sinuses into the mouth.81,84,85 With MBS testing, it has become abundantly clear that dysphagia can be present in individuals with PD, even if they have no symptoms to alert either patient or physician to its presence.
An important and potentially serious ramification of dysphagia in PD is the development of aspiration. Studies suggest that aspiration occurs in a significant proportion of PD patients, with the range of reported frequencies extending from 15 to 56%.81,84,86,87,90,91 As is true with dys-phagia itself, it has also become quite clear that symptoms alone are not sufficient predictors of the presence of aspiration in persons with PD. Entirely asymptomatic aspiration has been documented in 15 to 33% of PD patients.81,86,92 Even this surprising figure may underestimate the potential problem. Bird and colleagues noted the presence of vallecular residue, an abnormality indicative of increased aspiration risk, in 88% of 16 PD patients they studied, all of whom were without any symptomatic dys-phagia.92 The high frequency of dysphagia and aspiration, both symptomatic and asymptomatic, in individuals with PD, and the recognition that the development of these abnormalities may be independent of disease severity, has led at least one investigator to suggest that screening videofluoroscopy be performed early in the course of PD to identify those patients with subclinical dysphagia and institute appropriate treatment measures.91
In the large survey studies, the presence of symptomatic dysphagia seemed to correlate with disease progres-sion.7 However, this correlation is not clearly evident when objective testing of swallowing is employed. Bushman and colleagues noted the presence of MBS abnormalities in approximately 50% of patients with early (Hoehn and Yahr stages 1 and 2) PD,81 and other investigators have emphatically confirmed that the development of both dysphagia and aspiration is independent of both disease duration and severity.90,91
Cricopharyngeal muscle dysfunction is yet another source of swallowing impairment in PD. The cricopha-ryngeal muscle, serving as the UES, is tonically contracted, opening in response to the piston-like propulsive force of the tongue as it drives the food bolus into the pharynx. In individuals with PD those propulsive forces may be inadequate to trigger adequate cricopharyngeal relaxation, resulting in difficulty swallowing.90 In some individuals, however, the cricopharyngeal muscle itself may be the source of the problem, with failure to relax resulting in oropharyngeal bar formation.90 In one study, 22% of PD patients referred for evaluation of dysphagia were found to have cricopharyngeal bars or Zenker's diverticula.93 Zenker's diverticula, which form in Killian's triangle and are felt to be the consequence of incomplete cricopharyngeal relaxation, are another structural source of dysphagia that, in addition to causing a sense of food hanging up in the throat, can also produce delayed regurgitation of undigested food that had been trapped in the diverticulum and halitosis. Perforation, especially during instrumentation such as nasogastric tube placement, with consequent mediastinitis, is a potentially life-threatening complication.
Esophageal dysfunction and its role in parkinsonian dys-phagia has not been as extensively studied and thoroughly delineated as its oropharyngeal counterpart. However, videofluoroscopic abnormalities have been described in 5 to 86% of patients studied with PD 10,82,87,89,94,95 and disordered function during esophageal manometry in 61 to 73%.96,97 An array of abnormalities have been observed, including slowed esophageal transit, segmental esoph-ageal spasm, repetitive spontaneous contractions of the proximal esophagus, multiple simultaneous contractions producing diffuse esophageal spasm, ineffective or tertiary contractions with air trapping, aperistalsis, esophageal dilatation, and reduced pressure at the LES.89 94-99 LES dysfunction has also been observed in PD, where advanced reflux disease with consequent esophagitis may produce dysphagia, in addition to the more typical gas-troesophageal symptoms.93
Behavioral, pharmacological, and surgical treatment methods have all been employed in the treatment of dys-phagia in PD. Behavioral management approaches may include compensatory techniques, such as postural strategies and swallowing maneuvers, and are useful for some individuals.
In contrast to the very predictable improvement in the conventional motor features of PD that occurs with levodopa treatment, there is conflicting evidence regarding the response of oropharyngeal dysphagia to standard antiparkinson medications. Improvement in dysphagia, sometimes striking, has been noted by some investigators, including Cotzias and colleagues in their pioneering studies.100-103 However, more formal studies employing MBS have demonstrated objective improvement in only 33 to 50% of patients following levodopa or apomorphine administration.81 83 104 Formal studies evaluating other dopamine agonists in this regard have not been published. The basis for this inconsistent response to dopaminergic medication is uncertain but may simply reflect the intricacy of movement necessary for normal swallowing and the difficulty reconstructing this with systemic drug administration, like trying to do calligraphy with a paint roller. Anticholinergic drugs have been reported to both improve98 and exacerbate105 dysphagia in PD patients.
Cricopharyngeal dysfunction may be amenable to more specific treatment maneuvers. Percutaneous injection with BTX has been successfully employed,106 as has cricopharyngeal myotomy.107 However, cricopharyngeal myotomy (and probably BTX injection also) should not be performed if the concomitant presence of esophageal dysmotility might leave the individual at greater risk for aspiration following myotomy.107
Improvement in esophageal dysphagia has been reported with apomorphine administration,108,109 although extensive testing has not been undertaken. It has been suggested that sildenafil might be of benefit in the treatment of spastic esophageal motor disorders110 because of its effect on nitric oxide, but there have been no published reports of its use for this purpose in PD. It is worth noting that transient esophageal obstruction has been attributed to levodopa, with resolution following drug discontinua-tion.111
It is very unusual for dysphagia in idiopathic PD to become sufficiently severe to require percutaneous endo-scopic gastrostomy placement, but this procedure can be employed as a final step in patients in whom other treatment approaches have failed and both adequate nutritional support and medication administration have become impossible.12,112
Was this article helpful?