Swallowing disorders occur in up to 90% of individuals with PD (69) and may be among the first, though subtle or covert, signs of the disease (9). Identification of swallowing disorders is extremely important in this population, given the ramifications on nutrition and the ability to take oral medication appropriately. Silent aspiration may be observed and pneumonia can be a cause of death in advanced PD.
Swallowing abnormalities have been reported in all stages of PD (79) and many individuals with PD have more than one type of swallowing dysfunction (7). Disorders in both oral and pharyngeal stages of swallowing have been observed (7,79). Sharkawi et al. (8) found abnormalities in the oral phase of swallowing in PD, the most predominant being reduced tongue control and strength and reduced oral transit times. Others have reported a rocking-like motion of the tongue during the oral phase (9). This motion seemed to occur when the patients were unable to lower the posterior portion of the tongue to propel the bolus into the pharynx. Inability or delayed ability to trigger the swallowing reflex has also been observed in this population (9). These disorders may limit the ability of the individual with PD to control the food or liquid bolus while in the oral cavity. These problems may lead to choking, penetration, or aspiration of the food or liquid. Reduced nutritional intake, lack of enjoyment in eating, and difficulty taking medications appropriately can result from oral-phase swallowing dysfunction. The specific neurophysiologic mechanisms underlying such dysphagic abnormalities in PD are not clear. Sensory gating and cueing deficits, which have been implicated in the hypokinetic dysarthria of individuals with PD, may also be etiologic factors in dysphagia during the oral phase.
Pharyngeal stage dysfunction includes residue in the valleculae due to reduced tongue base retraction. Sharkawi et al. (8) reported this problem to be the most common disorder in the pharyngeal stage of swallowing. Blumin et al. (44) reported that 15 (100%) patients with severe PD had some degree of pharyngeal residue of solids on videostroboscopy and fiberoptic endoscopic evaluation of swallowing. Aspiration may occur in these patients as a result of the residue left in the pharynx after the swallow is complete (9). Leopold and Kagel (7) found several disorders of laryngeal movement during swallowing in PD. These included slow closure, incomplete closure, absent closure, and slowed or delayed laryngeal excursion (7). Increased pha-ryngeal transit time was also reported.
Silent aspiration has been observed in the later stages of PD and can be a contributory cause of death (10). Dysfunction in the pharyngeal stage of swallowing may also lead to choking, penetration, aspiration, reduced nutritional intake, or reduced ability to take medication orally. Again, sensory and internal cueing deficits may underlie these swallowing problems. It is unlikely that muscle rigidity is responsible for the dysphagia, since swallowing dysfunction occurs even when individuals with PD are considered optimally medicated. Referral for swallowing evaluation is extremely important at the first sign of problems even if this is early in the disease.
Dysphagia is not merely a sensorimotor disorder. As suggested by Leopold and Kagel (7), swallowing involves a five-stage process of ingestion: preoral (anticipatory), preparatory, lingual, pharyngeal, and esophageal. The first stage involves an interaction of preoral motor, cognitive, psychosocial, and somataesthetic elements engendered by the meal. If deficits in internal cueing, sensorimotor gating, scaling of movement amplitude, and self-regulation of effort affect swallowing, especially during the preoral, preparatory, and lingual stages, and if mealtime is a social event, swallowing and conversation may be performed simultaneously or alternatively and might be especially problematic for individuals with PD creating a greater risk for dysphagia and aspiration.
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