Comments on Selected Recent Dysphagia Literature

David W. Buchholz, MD and Stefanie Neumann, MA

Use of Tube Feeding to PreventAspiration PneumoniaFinucane TE, Bynum JPWThe Lancet 348:1421–1424, 1996

Finucane and Bynum point out that in 1991 more than75,000 percutaneous endoscopic gastrostomy tubes wereplaced in U.S. Medicare patients alone, many of thempatients with neurogenic dysphagia due to dementia orstroke for whom gastrostomy is, at least in part, intendedto reduce the risk of aspiration or pneumonia. Yet, as theauthors state, ‘‘[t]ube feeding has not been shown toreduce the risk of aspiration or pneumonia. No ran-domised trials of the intervention have been done, andsome data suggest ineffectiveness. Feeding tubes do notprevent aspiration of contaminated oral secretions or re-gurgitated gastric contents—both well-documentedcauses of aspiration pneumonia. Although enteral feed-ing tubes are often placed to prevent aspiration pneumo-nia, they have long been cited as risk factors for aspira-tion pneumonia’’ [1].

Finucane and Bynum performed a literaturesearch for articles published from 1991 to 1995 that in-cluded patients with neurogenic dysphagia and reportedaspiration pneumonia or mortality as outcomes in enter-ally fed patients. They found no perspective, randomizedtrial of oral vs. enteral feeding. The data vary widely, butmany studies revealed that one-third to two-thirds oftube-fed patients developed aspiration pneumonia.

The authors address the problem of defining as-piration and aspiration pneumonia. They state, ‘‘Abouthalf of normal adults and 70% of patients with depressedconsciousness aspirate oral contents into the lungs duringsleep’’ [2]. In terms of the definition of aspiration pneu-monia, Finucane and Bynum note, ‘‘What is most com-monly meant by aspiration pneumonia is pneumonia dueto normally non-pathogenic flora that cause infection be-

cause of high inoculum, impaired host defences, andother factors. To complicate matters further, many pa-tients who aspirate large volumes of acid gastric contentsdevelop areas of necrosis that become secondarily in-fected. In none of the studies was chemical pneumonitisdistinguished from pulmonary infection.’’

Finucane and Bynum also point out that ‘‘a pa-tient whose dysphagia is apparent during feeding willprobably continue to aspirate when nutrition is delivereddirectly to the stomach or beyond.’’ They refer to aspi-ration of not only contaminated oral secretions, fromwhich feeding tubes offer no protection, but also gastriccontents, reflux of which may be promoted by feedingtubes.

The authors mention other potential means ofpreventing aspiration pneumonia including parenteralnutrition and surgical procedures such as laryngotrachealseparation and others, but the role of these measuresremains undefined. The authors also advise, ‘‘Medica-tions that can worsen cognition, cause movement disor-ders, or otherwise interfere with swallowing should bestopped if possible. Anticholinergics, sedatives, andhigh-dose major tranquillisers are theoretically risky’’[3].

The authors conclude, ‘‘Although the use of feed-ing tubes is widespread, no data show that they reducethe risk of aspiration pneumonia in neurogenic dyspha-gia. There are data to the contrary, and the burdens offeeding tube placement can be severe. For almost allconscious patients we suggest a dedicated attempt atfeeding by hand. We would generally reserve the offer ofenteral tube feeding, as prophylaxis against aspirationand pneumonia, to those who have developed recurrentpneumonia despite our best efforts, those whose cough-ing during meals is extremely uncomfortable, and thosewho are acutely ill with impaired consciousness.’’

CommentsThis thoughtful review by Finucane and Bynum remindsus of how much we caregivers function in the dark with

Correspondence to:David W. Buchholz, M.D., 10753 Falls Road,Suite 315, Lutherville, MD 21093, USA

Dysphagia 12:226–231 (1997)

© Springer-Verlag New York Inc. 1997

one of our most fundamental interventions in patientswith neurogenic dysphagia, namely, placement of feed-ing tubes. Are we fooling ourselves and increasing therisk to our patients when we recommend gastrostomy forthe ostensible purpose of preventing aspiration pneumo-nia? The only way we will find out is by conducting acontrolled, randomized trial. Finucane and Bynum dis-cuss some of the difficult issues involved in designingsuch a trial including (1) ‘‘consent to randomisationwhen tube feeding is so commonly accepted,’’ (2) theneed to study patients with different neurologic diseasesseparately, (3) the role of risk factors such as smoking,immobility, and dental hygiene [4], (4) the definition ofaspiration pneumonia, (5) the wide variety of approachesto tube feeding (continuous vs. bolus feeding, fine-borevs. wide-bore tubes, and gastrostomy vs. jejunostomy),and (6) the definition of the control group.

References

1. Wynne JW, Modell JH: Respiratory aspiration of stomach con-tents.Ann Intern Med 87:466–474, 1977

2. Huxley EJ, Viroslav J, Gray WR, Pierce AK: Pharyngeal aspi-ration in normal adults and patients with depressed conscious-ness.Am J Med 64:564–568, 1978

3. Buchholz DW: Oropharyngeal dysphagia due to iatrogenic neu-rological dysfunction.Dysphagia 10:248–254, 1995

4. Langmore S, Loesche W, Schork T, Terpening M, Lopatin D,Murray J: Swallowing, functional, and dental/oral status as pre-dictors of pneumonia (Abstract).Dysphagia 12:110, 1997

Does Empiric Esophageal Dilation Benefit DysphagiaWhen Endoscopy is Normal?Marshall JB, Chowdhury TADig Dis Sci 41:1099–1101, 1996

Over a 5-year period Marshall performed esophageal di-latation on 40 consecutive patients with ‘‘symptoms ofesophageal dysphagia’’ (these symptoms are undefined)and with normal endoscopic findings. Less than half ofthe patients had undergone barium studies of the esopha-gus, and these were normal. Esophageal dilatation wasperformed up to 54-Fr using a bougie technique. Thirty-seven of the 40 patients were available for follow-up.

Response to dilatation was categorized as com-plete resolution, partial improvement, or no improve-ment. The patients were divided into two groups: (1)patients with solid food dysphagia only (n4 20) and (2)patients with solid and liquid dysphagia (n4 17).

There was complete resolution of dysphagia in 19of 20 patients (95%) in the solid dysphagia group. Only2 of 17 patients (12%) in the solid and liquid dysphagiagroup had complete resolution of dysphagia followingdilatation, although another 6 (35%) had partial improve-

ment. The difference between the two groups was highlysignificant (p < 0.0001). There was no complication ofdilatation.

Of the 19 patients with solid dysphagia who hadcomplete resolution of symptoms postdilatation, 13 re-ported no recurrence of dysphagia at the time of lastfollow-up at a median of 20 months postdilatation(range: 1–60 months). The other 6 patients in this groupexperienced recurrence of dysphagia at a median periodof 18 months postdilatation (range: 8–60 months). Twoof these patients were redilated and again experiencedresolution of dysphagia.

In reference to the patients with solid food dys-phagia who had complete resolution after dilatation,Marshall and Chowdhury ‘‘speculate that these patientshad benign mechanical narrowing of the esophagus, pos-sibly from a mild Schatzki ring or other mild benignstricture, that was not appreciated at the time of endos-copy.’’ They add, ‘‘We believe that the practice of omit-ting radiography and proceeding immediately with en-doscopy is justifiable and cost-effective in patients withsolid-food-only dysphagia. . . . In patients with solid-food-only dysphagia in whom endoscopy is negative, theresults of our study showed empiric dilation is justifiedand that the vast majority of patients improve.’’

With regard to the patients with both solid andliquid dysphagia, the authors suggest, ‘‘This group ofpatients most likely had esophageal motor dysfunction asthe cause of their dysphagia.’’ Three patients in thisgroup underwent subsequent esophageal manometry, andall had ‘‘nonspecific esophageal body motor abnormali-ties, manifested by an increased incidence of nonperi-staltic activity.’’ They conclude that in ‘‘the patient withdysphagia to both solids and liquids and a normal en-doscopy. . . , obtaining a radiographic study prior to en-doscopy may be indicated.’’

CommentsMarshall and Chowdhury are not the first to suggest thatempiric esophageal dilatation may be helpful in reducing‘‘esophageal dysphagia’’ despite normal endoscopy and/or barium studies [1]. This may in fact be a relativelycommon practice, despite lack of published evidence tosupport its efficacy.

The evidence provided by the authors is intrigu-ing but not convincing. The patients’ ‘‘symptoms ofesophageal dysphagia’’ are undefined. Moreover, lessthan half of patients were studied with barium swallows.Without more rigorous, systematic evaluation of the di-agnostic and therapeutic impact of barium studies, it ispresumptuous for Marshall and Chowdhury to assert that‘‘the practice of omitting radiography and proceedingimmediately with endoscopy is justifiable and cost-effective in patients with solid-food-only dysphagia.’’

D.W. Buchholz and S. Neumann: Recent Dysphagia Literature 227

Of further concern is the group of patients withsolid and liquid dysphagia who did not generally respondwell to dilatation. These patients were considered to have‘‘symptoms of esophageal dysphagia,’’ even though thepossibility of pharyngeal dysphagia is suggested to us by(1) the presence of liquid dysphagia, (2) normal endos-copy, and (3) generally poor response to dilatation.Rather than pursuing the possibility of pharyngeal dys-phagia by means of videofluorography, the authors at-tributed these patients’ problems to ‘‘esophageal motordysfunction,’’ despite minimal supporting evidence. Weare reminded that the tendency to assume that dysphagiahas an esophageal basis and to overlook the possibility ofa pharyngeal (and usually neurogenic) problem remainsstrong among physicians, including gastroenterologistswith an interest in dysphagia such as Marshall andChowdhury.

References

1. Graham DY: Treatment of benign and malignant strictures of theesophagus. In: Silvis SE (ed.):Therapeutic Gastrointestinal En-doscopy,2nd ed. New York: Igaku-Shoin, 1990, 1–41

Complications and Outcome after Acute Stroke: DoesDysphagia Matter?Smithard DG, O’Neill PA, Park C, Morris J, Wyatt R,England R, Martin DFStroke 27:1200–1204, 1996

Smithard et al. ‘‘conducted a perspective study to deter-mine whether dysphagia is related to the development ofcomplications after acute stroke and whether it is anindependent predictor of final outcome.’’ They enrolled149 consecutive patients, 28 of whom could not be as-sessed because of ‘‘significantly reduced level of con-sciousness during the first week.’’ The remaining 121patients were evaluated with a standardized bedside as-sessment performed by a physician. (This assessment,which is appended to this article, was validated in 1994according to the authors, but these data have not beenpublished.) Patients also underwent videofluorographywithin 3 days of stroke onset.

Based on the standardized bedside assessment ofswallowing, patients were categorized as having dyspha-gia or not. The videofluorographic findings were definedas aspiration (barium below the true vocal cords) or noaspiration. Intermediate outcomes were dehydration, nu-trition, or occurrence of chest infection. These interme-diate outcomes were carefully defined and were wellstudied. Outcome measures were survival, functionaloutcome according to Barthel activities of daily livingscores, length of stay, and residence at discharge and at6 months.

Sixty (50%) of the 121 patients were consideredto have an unsafe swallow based on bedside assessment.Of the 94 patients who underwent videofluorography(which was not medically feasible in the other 27 pa-tients) 20 patients aspirated and 74 did not.

Chest infections during the first week were morefrequent in patients with an unsafe swallow according tobedside assessment (p < 0.05). However, aspiration dem-onstrated by videofluorography was not associated withan increased incidence of chest infection (p > 0.05).Twenty-two patients were withdrawn from the study af-ter 1 week because of various complications includingfurther stroke in 14 patients. These 22 patients were notanalyzed with regard to longer-term outcome measures.

Mortality was higher in patients with dysphagia,as determined by bedside assessment (p < 0.001), butaspiration on videofluorography was not associated withincreased mortality (p > 0.1). Dysphagia by bedside as-sessment was associated with a lower median BarthelIndex score at 6 months after stroke (15 vs. 18,p 40.02), but aspiration according to videofluorography wasnot associated with a statistically significant lower Bar-thel Index score (13 vs. 18,p > 0.1).

Patients with dysphagia by bedside assessmentwere more likely to be discharged to institutionalizedcare (45% vs. 21%,p < 0.05), and their mean length ofstay was prolonged (44.8 days vs. 24.5 days for thosewith normal bedside assessment,p < 0.01). Aspiration onvideofluorography was not associated with increasedlength of stay. Nutritional indices deteriorated over thefirst month in patients with both dysphagia by bedsideassessment and aspiration on videofluorography.Changes in hydration status were not found, regardless ofability to swallow, although patients with dysphagia bybedside assessment were more likely to use parenteralfluids (p < 0.001) and for longer times (p < 0.0001).

Multivariate logistical regression analysis wasperformed to determine whether the association betweendysphagia or aspiration with poor outcome remained af-ter other accepted indicators of poor prognosis had beentaken into account. Unsafe swallowing diagnosed bybedside assessment remained a significant predictor ofmortality (p 4 0.01) after adjusting for confoundingvariables (e.g., age, weakness, incontinence). On theother hand, ‘‘The presence of aspiration as demonstratedon videofluorography was not an independent predictorof mortality or the presence of chest infection.’’

Smithard et al. conclude that ‘‘dysphagia, as de-tected at the bedside, was an independent predictor ofmortality and occurrence of chest infection and served toidentify patients at risk for inadequate nutrition.’’ Theyalso note, ‘‘Detection of aspiration by videofluorographydid not appear to add greatly to this risk profile.’’ On theother hand, the authors comment, ‘‘Because of the small

228 D.W. Buchholz and S. Neumann: Recent Dysphagia Literature

number of patients shown to be aspirating on videofluo-rography and the number of patients withdrawn from thestudy, a real effect [of aspiration by videofluorography]may have been missed. Nevertheless, the data obtainedsuggest that the usefulness of videofluorography in iden-tifying aspiration during the acute phase of stroke may belimited.’’ The authors conclude, ‘‘A controlled interven-tion trial examining the management of dysphagia andaspiration in relation to complications and outcome isneeded.’’

CommentsThis study is well done and well reported. The readershould be cautious about the evidence suggesting thatvideofluorography is unhelpful in predicting the risk ofdysphagia complications following stroke, because thenumber of patients found to have aspiration on video-fluorography and followed long-term was small. It isimperative that there be further study of whether or notthere is a role for videofluorography in establishing rela-tive risks of dysphagia complications not only in acutestroke patients but also in patients with other forms ofneurogenic oral/pharyngeal dysphagia.

With regard to the standardized bedside assess-ment of swallowing that is appended to this article, theauthors have apparently not previously published eitherthis assessment or its validation. The assessment in-volves a scoring system, but the article does not indicatethe scoring level at which a patient is considered to havedysphagia and/or be unsafe for swallowing.

The article does not mention swallowing therapyor any other specific dysphagia treatment. Smithard et al.correctly note that ‘‘A controlled intervention trial ex-amining the management of dysphagia and aspiration inrelation to complications and outcome is needed.’’ Al-though the authors ask a good question (‘‘Does dyspha-gia matter?’’), an even better question is ‘‘Does knowingabout dysphagia matter?’’ If the findings of bedside as-sessment, videofluorography, or other diagnostic toolsdo not guide specific treatment interventions that lead toimproved clinical outcomes, then in a very real sense theanswer is ‘‘no.’’

Delayed Radiation-Induced Bulbar PalsyShapiro BE, Rordorf G, Schwamm L, Preston DCNeurology 46:1604–1606, 1996

Shapiro et al. ‘‘report an unusual case of severe delayedradiation-induced bulbar palsy in a patient 14 years afterreceiving treatment for a nasopharyngeal carcinoma.’’This 41-year-old man had gradually progressive dyspha-gia and dysarthria over 2 years, ultimately resulting in

recurrent aspiration pneumonia and 40-pound weightloss. He was initially diagnosed as having ‘‘bulbar palsyvariant of amyotrophic lateral sclerosis (ALS).’’

Physical examination revealed fibrotic skinchanges around his neck, dysarthric speech, decreasedpalatal elevation and gag reflex, diffuse atrophy andweakness of the anterior cervical musculature, and weak-ness and ‘‘continuous undulating movements of thetongue at rest.’’ His neurologic examination was other-wise unremarkable.

Modified barium swallow examination ‘‘revealedvery poor pharyngeal movement.’’ Contrast magneticresonance imaging (MRI) of the brain and cervicomed-ullary junction was normal. Extensive blood and spinalfluid tests were normal. Electromyography (EMG)showed ‘‘a combination of complex repetitive dis-charges, neuromyotonia, and myokymic discharges’’ inmuscles supplied by the lower cranial nerves.

Shapiro et al. note that these EMG findings havebeen associated with radiation-induced nerve damage inother parts of the body and are not found in ALS. Theauthors comment, ‘‘Delayed radiation-induced nervedamage is thought to be due to either direct damage tothe nerve cells themselves or damage to the vascularendothelium, which results in ischemia to adjacent tis-sues, connective tissue fibrosis, and secondary compro-mise of neural tissue.’’

Shapiro et al. also mention that ‘‘abnormal move-ment secondary to myokymia and neuromyotonia can beabolished with the use of anticonvulsants.’’ Their patientwas unable to tolerate phenytoin or carbamazepine, andneither had an effect on speech or swallowing. Theirpatient ‘‘underwent placement of a J-tube, gained 20pounds over the course of 2 months, and was referred fora possible pharyngeal narrowing procedure and crico-pharyngeal myotomy.’’ The authors also note that‘‘Glantz et al recently reported the successful use ofanticoagulation in a small group of patients with radia-tion-induced nervous system injury, including patientswith myelopathy and brachial plexopathy. Whether suchtreatment would be useful in delayed radiation-inducedbulbar syndromes remains unknown’’ [1].

CommentsDelayed radiation-induced bulbar palsy may be morecommon than is recognized. Another recent report inNeurologydescribed two similar patients with delayedradiation-induced bulbar dysfunction and tongue myoky-mia [2]. Within recent months we have seen 2 such casesat The Johns Hopkins Swallowing Center. Both thesepatients were similar to the patient described by Shapiroet al. One had a latency of 15 years following radiationtherapy before progressive dysphagia first appeared.Both patients had myokymia on EMG.

D.W. Buchholz and S. Neumann: Recent Dysphagia Literature 229

One reason why delayed radiation-induced bul-bar palsy may go unrecognized is the remarkably longlatency between radiation therapy and the onset of dys-phagia and dysarthria. Similar lengthy delay in the clini-cal appearance of radiation-induced neurologic damagehas been described in other parts of the nervous system.

Another reason that radiation-induced nervedamage may go unrecognized is that these patients’problems tend to be attributed to fibrosis resulting infixation of structures such as the larynx. This may be apart of the problem, but it is clear from the EMG findingsthat in at least some cases, such as this case reported byShapiro et al. and those seen recently by us, nerve dam-age is a major factor.

Unfortunately, at the present time it is unlikelythat making the diagnosis of delayed radiation-inducedbulbar palsy will directly benefit a patient, since there isno generally effective treatment. It is nonetheless impor-tant to consider this diagnosis so as to avoid mislabelingpatients as having, for example, ALS. In patients withotherwise unexplained neurogenic oral/pharyngeal dys-phagia, a history of prior radiation therapy around theneck should be sought, and, if the history is positive,EMG should be performed to look for myokymia andneuromyotonia.

References

1. Glantz MJ, Burger PC, Friedman AH, et al.: Treatment of ra-diation-induced nervous system injury with heparin and warfa-rin. Neurology 44:2020–2027, 1994

2. Poncelet AN, Auger RG, Silber MH: Myokymic discharges ofthe tongue after radiation to the head and neck.Neurology46:259–260, 1996

Cricopharyngeal Dysfunction in Parkinson’s Disease:Role in Dysphagia and Response to MyotomyBorn LJ, Harned RH, Rikkers LF, Pfeiffer RF, QuigleyEMMMovement Disorders 11:53–58, 1996

In their summary, Born et al. state: ‘‘We report fivepatients with Parkinson’s disease (PD) and dysphagiawho were found, by radiological and manometric evalu-ation, to have evidence of cricopharyngeal (CP) dysfunc-tion, which included the presence of a Zenker’s diver-ticulum in two. CP myotomy was performed in four pa-tients with excellent and sustained improvement inswallowing. We conclude that CP function should becarefully evaluated in patients with Parkinson’s diseaseand dysphagia and that surgical treatment should be con-sidered in appropriate cases.’’

Cases 1 and 2 were similar. Both patients hadZenker’s diverticula but no radiographic evidence of CP

dysfunction. Manometry of the CP region was normal.Both patients underwent Zenker’s diverticulectomy andmyotomy and had sustained symptomatic improvement.

In case 3, videofluorography ‘‘showed normaldeglutition but moderate prominence of the cricopharyn-geus with barium pooling above it.’’ There was no di-verticulum, and manometry of the CP region was nor-mal. A CP myotomy was performed, and there was nosymptomatic improvement, even though repeat video-fluorography ‘‘now revealed no evidence of obstructionor prominence at the level of the cricopharyngeus.’’ De-spite a 10-year history of Parkinson’s disease, this patienthad never been treated with medication for PD. Oneweek after starting levodopa/carbidopa ‘‘symptoms ofchoking resolved (and) the patient . . . remained free ofchoking and dysphagia at follow-up 13 months later.’’

In case 4 videofluorography ‘‘showed normaltransfer of barium from the oral cavity to the hypophar-ynx and normal contraction of pharyngeal constrictors,but only partial and occasional relaxation of the crico-pharyngeus.’’ Manometry revealed normal CP functionbut low amplitude pharyngeal contraction. A percutane-ous endoscopic gastrostomy (PEG) was placed. ‘‘Speechtherapy’’ was unhelpful. After CP myotomy the patient‘‘began taking liquids and solids without difficulty (and)experienced an increase in weight; the PEG tube wasremoved.’’

In case 5 videofluorography ‘‘showed mild slow-ing of transfer of barium from tongue to oropharynx,reduced hypopharyngeal peristalsis with incompleteclearing, a prominent cricopharyngeal bar and discoor-dination between pharyngeal peristalsis and cricopharyn-geus relaxation.’’ Manometry of the CP region was nor-mal but ‘‘esophageal manometry showed a hypotensivelower esophageal sphincter, esophageal dysmotility withsimultaneous waves, and decreased amplitude of peri-stalsis.’’ Born et al. state, ‘‘It was felt that the patient’smarked esophageal dysmotility precluded the possibilityof a cricopharyngeal myotomy, and, also, possibly ac-counted for his symptoms.’’

CommentsAt first glance this article appears to support the hypoth-esis that CP myotomy may be effective for selected pa-tients with neurogenic pharyngeal dysphagia [1]. Acloser look reveals otherwise.

Cases 1 and 2 were complicated by Zenker’s di-verticula, and the positive outcomes of surgery may beattributable to diverticulectomy, not CP myotomy. It isnot clear that these two patients had any CP dysfunction.Though it has long been suspected that Zenker’s diver-ticula may arise because of CP dysfunction leading toincreased pressure above the CP segment, the radio-graphic and manometric evidence in these cases indi-

230 D.W. Buchholz and S. Neumann: Recent Dysphagia Literature

cates that they had normal CP function. Consequently, itis unreasonable to generalize their apparent benefit fromsurgery, including not only CP myotomy but also diver-ticulectomy, to other patients with neurogenic pharyn-geal dysphagia who do have radiographic and/or mano-metric evidence of CP dysfunction (but not Zenker’sdiverticulum) and for whom myotomy alone might beconsidered.

Case 3 argues against myotomy and in favor ofdopaminergic medication for relief of pharyngeal dys-phagia symptoms in patients with PD. Case 4 is the 1case of the 5 reported that supports the hypothesis thatselected patients with neurogenic pharyngeal dysphagiaand videofluorographic evidence of CP dysfunction maybenefit from CP myotomy. Case 5 does not belong withthe other 4 cases in that no surgery was performed. Bornet al.’s discussion of this case raises the unresolved issueof to what extent esophageal dysfunction, particularlygastroesophageal reflux (which was not demonstrated inthis case), represents a contraindication for CP myotomy.

There are two take-home messages from this ar-ticle. First, a busy reader may be tempted to rely on anabstract or summary of an article rather than reading thearticle, but abstracts or summaries can be misleading.Second, the only way to ever settle the issue of whether

or not CP myotomy is indicated for selected patients withneurogenic oral/pharyngeal dysphagia and to determinewhat selection criteria are appropriate is to conduct arandomized multicenter trial. In designing any such trialit would be important to consider alternative approachesto the problem of resistance to pharyngeal outflow at theCP level, including dilatation [2], local injection of botu-linum toxin [3], and exercise [4,5].

References

1. Buchholz DW: Cricopharyngeal myotomy may be effectivetreatment for selected patients with neurogenic dysphagia.Dys-phagia 10:255–258, 1995

2. Ravich W, Buchholz D, Neumann S, Jones B: Dilatation ofpharyngoesophageal (PE) segment narrowing for treatment ofneurogenic pharyngeal dysphagia (NPD): report of 5 cases.Dys-phagia 11:159, 1996

3. Crary MA, Glowasky AL, Antonelli P: Transcutaneous injectionof botulinum toxin A to facilitate opening of the pharyngo-esophageal segment.Dysphagia 11:160, 1996

4. Shaker R, Kern M, Arndorfer RC, Hofmann C, Easterling C:Effect of exercise on deglutitive UES opening in the elderly.Dysphagia 11:160, 1996

5. Shaker R, Kern M, Bardan E, Arndorfer RC, Hofmann C, East-erling C: Effect of isotonic/isometric head lift exercise on hy-popharyngeal intrabolus pressure.Dysphagia 12:107, 1997

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