Brain Stem Control of the Phases of Swallowing

The phases of swallowing are controlled by central pattern-generating circuitry of the brain stem and peripheral reflexes. The oral, pharyngeal, and esophageal phases of swallowing are independent of each other. Although central pattern generators of the brain stem control the timing of these phases, the peripheral manifestation of these phases depends on sensory feedback through reflexes of the pharynx and esophagus. The dependence of the esophageal phase of swallowing on peripheral feedback explains its absence during failed swallows. Reflexes that initiate the pharyngeal phase of swallowing also inhibit the esophageal phase which ensures the appropriate timing of its occurrence to provide efficient bolus transport and which prevents the occurrence of multiple esophageal peristaltic events. These inhibitory reflexes are probably partly responsible for deglutitive inhibition. Three separate sets of brain stem nuclei mediate the oral, pharyngeal, and esophageal phases of swallowing. The trigeminal nucleus and reticular formation probably contain the oral phase pattern-generating neural circuitry. The nucleus tractus solitarius (NTS) probably contains the second-order sensory neurons as well as the pattern-generating circuitry of both the pharyngeal and esophageal phases of swallowing, whereas the nucleus ambiguus and dorsal motor nucleus contain the motor neurons of the pharyngeal and esophageal phases of swallowing. The ventromedial nucleus of the NTS may govern the coupling of the pharyngeal phase to the esophageal phase of swallowing.

The Digastric Muscle is Less Involved in Pharyngeal Swallowing in Rabbits

The swallowing reflex is centrally programmed by the lower brain stem, the so-called swallowing central pattern generator (CPG), and once the reflex is initiated, many muscles in the oral, pharyngeal, laryngeal, and esophageal regions are systematically activated. The mylohyoid (MH) muscle has been considered to be a "leading muscle" according to previous studies, but the functional role of the digastric (DIG) muscle in the swallowing reflex remains unclear. In the present study, therefore, the activities of single units of MH and DIG neurons were recorded extracellularly, and the functional involvement of these neurons in the swallowing reflex was investigated. The experiments were carried out on eight adult male Japanese white rabbits anesthetized with urethane. To identify DIG and MH neurons, the peripheral nerve (either DIG or MH) was stimulated to evoke action potentials of single motoneurons. Motoneurons were identified as such if they either (1) responded to antidromic nerve stimulation of DIG or MH in an all-or-none manner at threshold intensities and (2) followed stimulation frequencies of up to 0.5?kHz. As a result, all 11 MH neurons recorded were synchronously activated during the swallowing reflex, while there was no activity in any of the 7 DIG neurons recorded during the swallowing reflex. All neurons were anatomically localized ventromedially at the level of the caudal portion of the trigeminal motor nucleus, and there were no differences between the MH and DIG neuron sites. The present results strongly suggest that at least in the rabbit, DIG motoneurons are not tightly controlled by the swallowing CPG and, hence, the DIG muscle is less involved in the swallowing reflex.     

Objective Measures of Swallowing Function Applied to the Dysphagia Population: A One Year Experience

Quantitative, reliable measures of swallowing physiology can be made from an modified barium swallowing study. These quantitative measures have not been previously employed to study large dysphagic patient populations. The present retrospective study of 139 consecutive patients with dysphagia seen in a university tertiary voice and swallowing clinic sought to use objective measures of swallowing physiology to (1) quantify the most prevalent deficits seen in the patient population, (2) identify commonly associated diagnoses and describe the most prevalent swallowing deficits, and (3) determine any correlation between objective deficits and Eating Assessment Tool (EAT-10) scores and body mass index. Poor pharyngeal constriction (34.5 %) and airway protection deficits (65.5 %) were the most common swallowing abnormalities. Reflux-related dysphagia (36 %), nonspecific pharyngeal dysphagia (24 %), Parkinson disease (16 %), esophageal abnormality (13 %), and brain insult (10 %) were the most common diagnoses. Poor pharyngeal constriction was significantly associated with an esophageal motility abnormality (p < 0.001) and central neurologic insult. In general, dysphagia symptoms as determined by the EAT-10 did not correlate with swallowing function abnormalities. This preliminary study indicates that reflux disease is common in patients with dysphagia and that associated esophageal abnormalities are common in dysphagic populations and may be associated with specific pharyngeal swallowing abnormalities. However, symptom scores from the EAT-10 did not correspond to swallowing pathophysiology.     

Dysphagia,reflux and related sequelae due to altered physiology in scleroderma

Systemic sclerosis is a connective tissue disease that presents with significant gastrointestinal involvement, commonly in the esophagus. Dysphagia is a common clinical manifestation of systemic sclerosis and is strongly related to esophageal dysmotility. However, there are multiple other contributing factors in each step in the physiology of swallowing that may contribute to development of severe dysphagia. The oral phase of swallowing may be disrupted by poor mastication due to microstomia and poor dentition, as well as by xerostomia. In the pharyngeal phase of swallowing, pharyngeal muscle weakness due to concurrent myositis or cricopharyngeal muscle tightening due to acid reflux can cause disturbance. The esophageal phase of swallowing is most commonly disturbed by decreased peristalsis and esophageal dysmotility. However, it can also be affected by obstruction from chronic reflux changes, pill-induced esophagitis, or Candida esophagitis. Other contributing factors to dysphagia include difficulties in food preparation and gastroparesis. Understanding the anatomy and physiology of swallowing and evaluating systemic sclerosis patients presenting with dysphagia for disturbances in each step can allow for development of better treatment plans to improve dysphagia and overall quality of life.     

The search for the central swallowing pathway: The quest for clarity

As the work of Dr. Martin Donner has brought a clarity to understanding swallowing, so has the work of various neuroscientists, including that of a Nobel Laureate, in providing us with a better comprehension of this complex motor pattern. Understanding the neural control of swallowing has been a process that has occurred during this century in which several investigators, primarily from Europe, Japan, Canada, and the United States, have brought their perspectives in applying particular techniques to decipher how the central and peripheral nervous system control swallowing. Swallowing represents a complex muscular response of the oral, pharyngeal, and esophageal regions which are integrated to provide an effective functional pattern that prepares and transports food while simultaneously protecting the airway. This adaptation of the upper gastrointestinal tract in mammals has been extensively studied peripherally by two methods: recording from the peripheral nerves and muscles, and stimulating peripheral nerves and their receptive fields that can induce the pharyngeal and esophageal phases of swallowing. The study of the peripheral nervous system has provided insight into the sensory receptive fields that evoke or facilitate swallowing, and has established the first serious evidence of the all-or-none sequential contraction pattern of the oropharyngeal and esophageal muscles. It has been these electromyographic studies of the muscles that has established much of the criteria for evaluating the central swallowing pathway. Five techniques have been applied to the central nervous system to study swallowing and include lesioning or destroying discrete regions to determine how swallowing is impaired or modified, electrically stimulating the central neural tissue to determine the type of effects on swallowing, recording from the central neural tissue with macro- and microelectrodes to ascertain when neurons respond in timing to the peripheral muscle activity during swallowing, applying pharmacological agents through micropipettes which could mimic or inhibit potential transmitters, and using immunochemical techniques to tag specific chemicals that could be transmitters used by the neurons in the central swallowing pathway. These various techniques have provided insight into how the central swallowing pathway is organized but the details of the central control are still in the process of being defined and will require as much effort this next century as has been previously developed over the past 90 years.Presented in part at the Fourth Multidisciplinary Symposium on Dysphagia, Baltimore, MD, April 22–24, 1992.     

Oropharyngeal and esophageal interrelationships in patients with nonobstructive dysphagia

Normal swallowing requires the close functional coordination of the mouth, pharynx, and esophagus, and if one of these components becomes functionally impaired, it is likely that the others may be affected. Using videofluoroscopy and manometry in this study, we examined the esophageal phase of swallowing in 12 patients with oropharyngeal dysphagia (group A) and the oropharyngeal components of swallowing in 29 patients with esophageal motor dysfunction and nonobstructive dysphagia (group B). A wide range of esophageal function abnormalities was seen in the first group, including delayed esophageal body peristalsis, spontaneous or simultaneous (tertiary) contractions, esophageal body dilation, proximal bolus redirection, and poor lower esophageal sphincter relaxation. Manometrically, 92% of group A patients were classified as having nonspecific esophageal motility disorder (NSEMD). In a similar fashion, group B patients exhibited many oropharyngeal function abnormalities on videofluorography including disturbed lingual peristalsis, slowed pharyngeal transit time with poor constriction of pharyngeal muscles, and laryngeal vestibular and tracheal bolus penetration. Manometrically, group B patients were classified as having NSEMD, achalasia, diffuse esophageal spasm, nutcracker esophagus, scleroderma, and chronic intestinal pseudoobstruction. In conclusion, oropharyngeal function is significantly altered in patients with esophageal motility disorders and dysphagia, and esophageal motor dysfunction occurs in patients with oropharyngeal dysphagia. These changes may represent either a compensatory mechanism or concomitant involvement of the oropharynx or the esophagus by the underlying neuromotor disorder. We suggest that assessment by esophageal motility and videofluoroscopy of both the oropharyngeal and esophageal phases of swallowing may improve diagnosis and therapy in patients with nonobstructive dysphagia.     

Solitarial premotor neuron projections to the rat esophagus and pharynx: Implications for control of swallowing

Background & Aims: The buccopharyngeal and esophageal phases of swallowing are controlled by distinct networks of premotor neurons localized in the nucleus tractus solitarius. The neuronal circuitry coordinating the two phases was investigated using a combination of central and peripheral tracing techniques. Methods: Using pseudorabies virus, a transsynaptic tracer, in anesthetized rats, third-order esophageal neurons (neurons projecting to premotor neurons) were identified. In a separate protocol that combined transsynaptic and retrograde fluorescent tracing, third-order esophageal neurons projecting to pharyngeal motoneurons (buccopharyngeal premotor neurons) were then identified. Results: Third-order esophageal neurons were identified in the interstitial and intermediate subnuclei of the nucleus tractus solitarius and in other medullary, pontine, midbrain, and forebrain nuclei. A subpopulation of these neurons (double labeled) in the interstitial and intermediate subnuclei were found to project to pharyngeal motoneurons (buccopharyngeal premotor neurons) and to be linked synaptically to esophageal premotor neurons. Conclusions: The synaptic link between buccopharyngeal and esophageal premotor neurons provides an anatomic pathway for the central initiation of esophageal peristalsis and its coordination with the pharyngeal phase of swallowing. This neural circuitry within the nucleus tractus solitarius is consistent with a complex central control mechanism for the swallowing motor sequence that can function independently of afferent feedback.GASTROENTEROLOGY 1998;114:1268-1275     

Videofluorographic Study of Swallowing in Parkinson's Disease

We studied 16 patients with Parkinson's disease (PD) with dysphagia and 8 young and 7 elderly normal controls videofluorographically to evaluate the nature of swallowing disorders in PD patients. In 13 patients, abnormal findings in the oral phase were residue on the tongue or residue in the anterior and lateral sulci, repeated pumping tongue motion, uncontrolled bolus or premature loss of liquid, and piecemeal deglutition. Thirteen patients showed abnormal findings in the pharyngeal phase, including vallecular residue after swallow, residue in pyriform sinuses, and delayed onset of laryngeal elevation. Ten of these patients also showed abnormal findings in both the oral and pharyngeal phases. Aspiration was seen in 9 patients. The oral transit duration was significantly longer in the patients with and without aspiration than in the control subjects. The stage transition duration, pharyngeal transit duration, duration of the upper esophageal sphincter (UES) opening, and total swallow duration were significantly longer in the patients with and without aspiration than in the young controls, but were not longer than in the elderly controls. These durational changes in the pharyngeal phase of swallowing were similar to those in the elderly controls. The findings suggest that the disturbed motility in the oral phase of swallowing may be due to bradykinesia. Although PD patients with dysphagia evince a variety of swallowing abnormalities, the duration of pharyngeal swallowing may remain within the age-related range until the symptoms worsen.     

Pharyngoesophageal (Zenker's) diverticulum: a reappraisal

Manometric evaluation of pharyngeal contraction and upper esophageal sphincter relaxation was performed in a group of patients with Zenker's diverticulum using a specially designed low compliance manometric recording system. The results were compared with those in normal controls. In all cases, the upper esophageal sphincter showed complete relaxation during swallowing and no incoordination between pharyngeal contraction and upper esophageal sphincter relaxation could be demonstrated compared to time intervals found in the control group. Resting upper esophageal sphincter pressures were significantly lower in diverticulum patients than in controls. It is concluded that symptomatic patients with Zenker's diverticulum have normal pharyngeal-upper esophageal sphincter coordination, exhibit complete upper esophageal sphincter relaxation on swallowing, and have low resting upper esophageal sphincter pressures. These results seriously question the previous concept of abnormalities of pharyngeal-upper esophageal sphincter coordination in patients with Zenker's diverticulum.     

Analysis of Video Fluoroscopic Swallowing Study in Patients with Vocal Cord Paralysis

We reviewed the findings of a video fluoroscopic swallowing study (VFSS) of 28 patients with vocal cord paralysis (VCP) who complained of swallowing difficulties. VFSSs were performed with thick and thin liquid using modified Logemann methods. The patients were grouped according to whether their VCP was of central or peripheral origin, and the VFSS findings of the groups were compared. The patients showed oral phase dysfunction and pharyngeal dysfunction, especially when the cause was of central origin. Oral phase abnormalities were found in 13 patients and pharyngeal phase abnormalities were found in all patients, including penetration in 20 patients and aspiration in 14 patients. Improper lip closure (LC) and bolus formation (BF) and a delay in triggering pharyngeal swallow (TPS) and upper esophageal sphincter release (UESR) were significantly more frequent in patients with central VCP. With thin-liquid swallowing, pharyngeal transit time (PTT) and pharyngeal delay time (PDT) were significantly more prolonged in central VCP. The results suggest that the delay in triggering and poor coordination of swallowing were profound in patients with central VCP, but dysfunction in peripheral VCP may originate from poor pharyngeal movement.     

Sequence Variability During Hypopharyngeal Bolus Transit

The pharyngeal phase of deglutition is considered to occur in a reflexive, preprogrammed fashion. Previous studies have determined a general sequence of events based on the mean timing of bolus transit and swallowing gestures. Individual variability has not been studied, however. The purpose of this study was to determine the amount of sequence variability that normally occurs during the hypopharyngeal phase of deglutition. Dynamic swallow studies from 60 normal volunteers were evaluated and event sequence variability was determined for 12 two-event sequences during swallowing of three bolus sizes. There was found to be some variability in event sequences for almost all events evaluated except for the following : (1) arytenoid cartilage elevation always began prior to opening of the upper esophageal sphincter, (2) the sphincter always opened prior to the arrival of the bolus at the sphincter, (3) larynx-to-hyoid approximation always occurred after the onset of upper esophageal sphincter opening, and (4) maximum pharyngeal constriction always occurred after maximal distension of the upper esophageal sphincter. Variability was more common during swallowing of the smallest bolus size. This information may be helpful in evaluating event coordination in patients with dysphagia.     

Facioscapulohumeral Muscular Dystrophy: A Radiologic and Manometric Study of the Pharynx and Esophagus

Facioscapulohumeral muscular dystrophy (FSHD) is not a recognized neuromuscular cause of dysphagia. However, a study of pharyngoesophageal function in FSHD has not been performed or reported. The aim of this study was to ascertain by relatively noninvasive techniques whether the dystrophic muscle disease that underlies FSHD involves the pharyngeal and/or the esophageal striated and smooth muscles. We used conventional cineradiography and intraluminal esophageal manometry on separate occasions to study pharyngeal and esophageal function in 20 patients with FSHD at various stages of disease, with or without complaints of deglutition. Age- and sex-matched control data were used for comparison of the manometric component of the study. Twelve men and eight women with FSHD were studied. The mean patient age was 38.1 years (41.9 years for controls), and the age range was 19-61 years (22-55 years for controls). The mean disease duration was 16.7 years (range = 4-39 years).Five patients admitted to having intermittent oropharyngeal dysphagia (difficulty to initiate swallowing, cough after swallowing, sensation of food stuck in throat, or nasal regurgitation), and three patients admitted to intermittent esophageal dysphagia (difficulty swallowing both liquids and solids). Chest roentgengrams showed a hiatal hernia in four patients, but no active cardiopulmonary disease. Abnormal instrumental results were documented in eight patients: Cineradiography detected ineffectual pharyngeal contractions (2 patients), pharyngeal diverticula but normal pharyngeal motility (2 patients), and decreased cricopharyngeal and upper esophageal relaxation (2 patients). The mean manometric pressure of the patient group was not significantly different from the control data. However, manometry detected motility abnormalities that were not reflected in the mean data and included increased lower esophageal sphincter resting pressure with normal or abnormal relaxation (2 patients) and inconsistent, high-amplitude, long-duration, primary peristaltic contractions (1 patient). Patients with FSHD did not spontaneously volunteer intermittent complaints of deglutition. This study did not definitely establish that the cause of abnormal pharyngeal and cervical esophageal function was related to the dystrophic process that underlies FSHD. Any esophageal dysmotility was nonspecific and insignificant and was caused by an undetermined, probably neuropathic, process unrelated to the muscular dystrophy.     

Videofluoroscopic evaluation of patients with Guillain-Barré syndrome

We reviewed 14 patients with clinically confirmed Guillain-Barré syndrome for swallowing dysfunction. All had swallowing dysfunction varying from mild to severe. Six patients (43%) had equivalent impairment during oral and pharyngeal phases. Seven patients (50%) had more severe functional abnormalities during the pharyngeal phase than during the oral phase. One patient (7%) had moderate disorder during the oral phase and mild disorder during the pharyngeal phase. Thirty-six percent of the patients had moderate-to-severe dysfunction during the oral phase, and 71% had moderate-to-severe dysfunction during the pharyngeal phase. In 5 patients who had multiple sequential examinations, moderate or severe swallowing disorders improved to mildto-moderate disorders within 4–8 weeks after the onset of the symptoms. Residual swallowing disorders may be seen in those who had severe swallowing dysfunction during the later phases of their disease. Further investigations are needed to determine if swallowing abnormalities persist after complete recovery from Guillain-Barré syndrome.     

Dysphagia in a patient with lateral medullary syndrome: insight into the central control of swallowing

BACKGROUND & AIMS: Central control of swallowing is regulated by a central pattern generator (CPG) positioned dorsally in the solitary tract nucleus and neighboring medullary reticular formation. The CPG serially activates the cranial nerve motor neurons, including the nucleus ambiguus and vagal dorsal motor nucleus, which then innervate the muscles of deglutition. This case provides insight into the central control of swallowing. METHODS: A 65-year-old man with a right superior lateral medullary syndrome presented with a constellation of symptoms, including dysphagia. The swallow was characterized using videofluoroscopy and esophageal motility and the results were compared with magnetic resonance imaging (MRI) findings. RESULTS: Videofluoroscopy showed intact lingual propulsion and volitional movements of the larynx. Distal pharyngeal peristalsis was absent, and the bolus did not pass the upper esophageal sphincter. Manometry showed proximal pharyngeal contraction and normal peristaltic activity in the lower esophagus (smooth muscle), but motor activity of the upper esophageal sphincter and proximal esophagus (striated muscle) was absent. MRI showed a lesion of the dorsal medulla. CONCLUSIONS: These findings are compatible with a specific lesion of the connections from a programming CPG in the solitary tract nucleus to nucleus ambiguus neurons, which supply the distal pharynx, upper esophageal sphincter, and proximal esophagus. There is functional preservation of the CPG control center in the solitary tract nucleus and of the vagal dorsal motor nucleus neurons innervating the smooth muscle esophagus.     

Dysphagia following Anterior Cervical Spine Surgery

Although previous reports have identified dysphagia as a potential complication of anterior cervical spine surgery (ACSS), current understanding of the nature and etiologies of ACSS-related dysphagia remains limited. The present study was undertaken to describe the patterns of dysphagia that may occur following ACSS. Thirteen patients who exhibited new-onset dysphagia following ACSS were studied retrospectively by means of chart review and videofluoroscopic swallow study analysis. Results indicated that a variety of swallowing impairments occurred following ACSS. In 2 patients, prevertebral soft tissue swelling near the surgical site, deficient posterior pharyngeal wall movement, and impaired upper esophageal sphincter opening were the most salient videofluoroscopic findings. In another 5 patients, the pharyngeal phase of swallowing was absent or very weak, with resulting aspiration in 3 cases. In contrast, an additional 4 patients exhibited deficits primarily of the oral preparatory and oral stages of swallowing including deficient bolus formation and reduced tongue propulsive action. Finally, 2 patients exhibited impaired oral preparatory and oral phases, a weak pharyngeal swallow, as well as prevertebral swelling. Thus, a variety of swallowing deficits, due possibly to neurological and/or soft tissue injuries, may occur following ACSS.     

The Effects of Aspiration Status, Liquid Type, and Bolus Volume on Pharyngeal Peak Pressure in Healthy Older Adults

The reasons for aspiration in healthy adults remain unknown. Given that the pharyngeal phase of swallowing is a key component of the safe swallow, it was hypothesized that healthy older adults who aspirate are likely to generate less pharyngeal peak pressures when swallowing. Accordingly, pharyngeal and upper esophageal sphincter pressures were examined as a function of aspiration status (i.e., nonaspirator vs. aspirator), sensor location (upper vs. lower pharynx), liquid type (i.e., water vs. milk), and volume (i.e., 5 vs. 10?ml) in healthy older adults. Manometric measurements were acquired with a 2.1-mm catheter during flexible endoscopic evaluation. Participants (N?=?19, mean age?=?79.2?years) contributed 28 swallows; during 8 swallows, simultaneous manometric measurements of upper and lower pharyngeal and upper esophageal pressures were obtained. Pharyngeal manometric peak pressure was significantly less for aspirators (mean?=?82, SD?=?31?mmHg) than for nonaspirators (mean?=?112, SD?=?20?mmHg), and upper pharyngeal pressures (mean = 85, SD = 32?mmHg) generated less pressure than lower pharyngeal pressures (mean?=?116, SD?=?38?mmHg). Manometric measurements vary with respect to aspiration status and sensor location. Lower pharyngeal pressures in healthy older adults may predispose them to aspiration.     

High resolution impedance manometric findings in dysphagia of Huntington's disease

Conventional manometry presents significant challenges, especially in assessment of pharyngeal swallowing, because of the asymmetry and deglutitive movements of oropharyngeal structures. It only provides information about intraluminal pressure and thus it is difficult to study functional details of esophageal motility disorders. New technology of solid high resolution impedance manometry (HRIM), with 32 pressure sensors and 6 impedance sensors, is likely to provide better assessment of pharyngeal swallowing as well as more information about esophageal motility disorders. However, the clinical usefulness of application of HRIM in patients with oropharyngeal dysphagia or esophageal dysphagia is not known. We experienced a case of Huntington's disease presenting with both oropharyngeal and esophageal dysphagia, in which HRIM revealed the mechanism of oropharyngeal dysphagia and provided comprehensive information about esophageal dysphagia.     

Effects of stroke‐induced damage to swallow‐related areas in the brain on swallowing mechanics of elderly patients

Aim: Our objective was to determine the relationship between defective swallowing mechanics and the location of brain lesions in stroke patients. Methods: We evaluated swallowing mechanics in 37 stroke patients and 10 age‐matched control subjects by videofluoroscopy. Subjects were asked to swallow 10 successive 1.0‐mL and three successive 2.5‐mL boluses of barium suspension at intervals of approximately 15–30 s. We measured oral transit time, pharyngeal delay time and pharyngeal transit time. Results: Patients could be divided into two groups based on the pharyngeal delay time for a 1.0‐mL bolus swallow. One group showed little variation during successive swallowing tests, similar to the control group. In the other group pharyngeal delay times varied during successive trials often tending to increase with successive swallows. Magnetic resonance imaging studies of the brain revealed infarcts or hemorrhages in swallow‐related areas in the latter group, while in the former group lesions were localized to areas unrelated to swallowing. Conclusion: Damage to swallow‐related areas may reduce their sensitivity to incoming signals from the oral cavity thereby impairing preparations to generate motor command signals and compromising their ability to send sufficient voluntary descending command signals to activate the swallowing central pattern generator located in the medulla. This deficiency becomes more evident with successive swallows and manifests as impaired swallowing mechanics.     

Pharyngeal dysmotility in a patient with wilson’s disease

Wilson’s disease (WD) is an inherited inborn error of copper metabolism. Patients develop tremor, rigidity, dysarthria, sialorrhea, dysphagia, intracorneal pigmentation, and psychiatric and hepatic disease. Dysphagia may progress to such a degree that the patient is unable to eat. Few reports have detailed the nature of the swallowing dysfunction in patients with WD. Previous reports have shown upper esophageal dysmotility, but none has analyzed pharyngeal motility. We performed a videofluoroscopic swallowing evaluation on a 49-year-old woman with WD who had a history of progressive dysphagia. Videofluoroscopy showed significant pooling of swallowed material in the valleculae and pyriform sinuses, suggesting a reduction in pharyngeal peristalsis. Pooled material in the valleculae was cleared only after repeated swallowing of liquid. These findings suggest that dysphagia in WD may involve pharyngeal as well as esophageal dysmotility. Pharyngeal dysmotility is important to identify, since this places the patient at risk for aspiration pneumonia. Documentation of this finding in these patients is also important for the therapeutic management of their swallowing. Such findings could prove to be of diagnostic value in identifying the disease and monitoring its progression.