Gut, 1990, 31, 259-265

Oesophageal and gastric motor activity in patientswith bulimia nervosa

A Kiss, H Bergmann, Th-A Abatzi, C Schneider, S Wiesnagrotzki, J Hobart,G Steiner-Mittelbach, G Gaupmann, A Kugi, G Stacher-Janotta, H Steinringer, G Stacher

AbstractPrevious studies showed that symptoms ofoesophageal motor disorders can be misinter-preted as indicating anorexia nervosa and thatin primary anorexia nervosa gastric motility isfrequently impaired. We investigated in 32women with bulimia nervosa whether symp-toms of oesophageal motor disorders could beobscured by or be mistaken as forming part ofbulimic behaviour, and whether impaired gas-tric motility was frequent as well. Oesophagealmotility was normal in 18 of26 patients studied,another four had incomplete lower eosopha-geal sphincter relaxation. Two patients hadvigorous achalasia and each one achalasia anddiffuse oesophageal spasm, all ofwhom exper-ienced two types of vomiting: one selfinducedand one involuntary, in which the vomit wasnon-acidic and tasted as the preceding meal.Gastric emptying of a semisolid meal wasstudied in all patients except of the eight withoesophageal motor abnormalities. Emptyingwas significantly slower than in healthy con-trols and grossly delayed in nine of24 patients.Antral contraction amplitudes were lower andincreased less postcibally than in controls. Inconclusion (i) bulimic behaviour can obscuresymptoms of oesophageal motor disorders and(ii) gastric emptying is frequently delayed inbulimia nervosa.

Psychophysiology Unit atthe Departments ofPsychiatry and Surgery I,Division ofPsychosomatic Medicineof the Department ofPsychiatry, Division ofNuclear Medicine at theDepartment of MedicineII, Department ofMedicine I, University ofVienna; and LudwigBoltzmann Institute ofNuclear Medicine;Vienna, Austria.A KissH BergmannTh-A AbatziC SchneiderS WiesnagrotzkiJ HobartG Steiner-MittelbachG GaupmannA KugiG Stacher-JanottaH SteinringerG StacherCorrespondence to: ProfessorDr Georg Stacher,PsychophysiologischesLaboratorium, PsychiatrischeUniversitatsklinik, WahringerGurtel 18-20, A- 1090 Wien,Austria.

Accepted for publication12 June 1989

Bulimia nervosa is an eating disorder related toprimary anorexia nervosa, typically beginning inadolescence or early adult life. The disorder isdiagnosed increasingly frequent, and bulimicbehaviour has been reported to be increasinglyprevalent especially on college campuses.'2Clinically significant bulimia, however, seems tobe rare.34 Bulimia is characterised by recurrentepisodes of binge eating - that is, the rapidconsumption of a large amount of food in a

discrete period of time, a feeling of lack ofcontrol over eating behaviour during the eatingbinges, and, in order to prevent weight gain, theengagement of the affected individual in eitherselfinduced vomiting, use of laxatives or

diuretics, strict dieting or fasting, or vigorousex&rcise. Induced vomiting decreases the painof abdominal distension and allows either con-

tinued eating or termination of the binge, butmay lead to electrolyte imbalance and dehydra-tion. The recently revised diagnostic criteriarequire a minimum average of two binge eatingepisodes a week for at least three months and a

persistent over-concern with body shape andweight.5 In contrast with primary anorexianervosa, the concern with weight does not lead toa fall below a minimal normal weight, although

the weight loss may be substantial. Mostresearch on bulimia has dealt with psychosocialand therapeutic aspects of the disorder, whereasrelatively few work has been done in the field ofbodily functions. In particular, the functioningof organs likely to be affected by the bulimicbehaviour, that is, the stomach and theoesophagus, has received little attention. This issurprising all the more, as symptoms indicativeof disordered gastrointestinal function, such aspostprandial fullness, early satiety, bloating andepigastric pain, are encountered in a substantialproportion of patients.67 That such symptoms infact often reflect grossly disordered gastric motoractivity is suggested by studies on patients withprimary anorexia nervosa, which revealed thatdelayed gastric emptying'-' and motor activity'3-'5 are frequent features in that disorder. Inpatients categorised as having primary anorexianervosa it was found that on primary evaluation,symptoms of vomiting and weight loss weremistaken in several instances as indicatingprimary anorexia nervosa, whereas the reevalua-tion of the patients' history and subsequentfluoroscopic, manometric, and pH-metricstudies revealed that they in fact suffered fromoesophageal motor disorders such as achalasia,diffuse oesophageal spasm and gastro-oesopha-geal reflux."1'2 Studies of gastric motor functionin patients with bulimia yielded contradictoryresults: gastric emptying was found to be delayedin part of the patients"' or to be within the normalrange,'617 and the motor activity of the gastricantrum was reported to be normal. 16 The presentstudy was aimed at investigating, in consecutivepatients diagnosed as having bulimia nervosa,whether symptoms of disordered oesophagealmotor function, such as vomiting and weightloss, were misinterpreted at primary evaluationas forming part of the bulimic behaviour or evenled to a misdiagnosis of bulimia, and, whethergastric emptying and antral motor activity weresimilarly affected in bulimia as in primaryanorexia nervosa.

Methods

SUBJECTS AND PROCEDUREThirty two female patients diagnosed as suffer-ing from bulimia nervosa and presenting con-secutively to the Division of PsychosomaticMedicine for hospitalisation and treatment parti-cipated in this study. The age of the patientsranged from 17 to 40 years (x=24 6 yr (0-9)SEM) and their percentage of desirable weightfrom 77 to 113% (R=90 8% (1-6) SEM). None ofthe patients had any evidence of diabetes mel-litus, connective tissue disease or neuropathy,

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and none had undergone gastric surgery orvagotomy. The diagnosis of bulimia nervosa wasmade according to the specific criteria outlined inthe DSM-III'9 and DSM-III R,5 respectively.Treatment included hospitalisation of six toeight weeks and psychotherapy according toaccepted psychiatric practice as well as goaloriented weight programmes. Thirteen patientshad a history of primary anorexia nervosa, ofwhom, however, none had fulfilled diagnosticcriteria for that disease during the precedingthree years. None of the patients was on anypsychotropic medication or on drugs, whichcould have affected autonomous nervous systemor smooth muscle function. Within the first weekafter admission to the hospital, oesophagealmotor activity could be recorded manometricallyin 26 patients. Subsequently, gastric emptyingand antral motor activity were studied in allpatients except of eight, in whom disorderedoesophageal motor function was revealed atmanometry. Gastric motility data of the patientswere compared with those of a group of 24healthy female volunteers studied earlier.'3 Thevolunteers ranged in age from 20 to 39 years (x=24-8 yr (0 9) SEM) and in their percentage ofdesirable weight from 82 to 120% (x=96 2%(2 2) SEM). None ofthe healthy control subjectstook any drugs at the time of investigation,except for oral contraceptives in the case of eightvolunteers. All studies were carried out between0800 and 1100 h. The subjects were instructed tohave their usual meal on the evening precedingthe studies but to refrain from eating after 2200 hand to eat and drink nothing before coming tothe laboratory on the study day. Informed con-sent was obtained from all patients and controlsubjects. The investigation was approved by theInstitutional Committee on Studies InvolvingHuman Beings.

MEASUREMENT OF OESOPHAGEAL MOTORACTIVITYOesophageal pressures were recorded by meansof a Konigsberg model 31 probe (KonigsbergInstruments Inc, Pasadena, CA) fitted with threestrain gauge force transducers spaced at 5 cmintervals and oriented radially 120° apart. Thesignals were processed by Beckman 9853Acouplers and recorded by a R-411 Dynograph(Sensormedics, Anaheim, CA). The probe waspassed into the stomach through the nose andslowly withdrawn at 5 mm steps and one minuteintervals. During each one minute period, thepatients were requested to take one wet swallow.The resting pressure within the lower oesopha-geal sphincter and the pressure level obtainedduring swallow induced relaxation weremeasured, in millimeters of mercury (mmHg),using end-expiratory pressure with the meanfundic pressure as the zero reference. Loweroesophageal sphincter resting pressures wereexpressed as the mean value of the recordingsfrom each of the three transducers as obtainedbefore a swallow from the zone of maximalpressure. For each swallow induced sphincterrelaxation, the difference between the restingpressure and the pressure level during relaxationwas calculated and expressed as percent relaxa-

tion from resting pressure. At each transducersite, at least three sphincter relaxations uponswallowing were recorded. Amplitude of con-tractions within the oesophageal body wasmeasured from the oesophageal base linepressure to the peak of the complex. Duration ofcontractions was measured, in seconds (s), fromthe intersection of lines for mean resting intra-oesophageal pressure and the upstroke of thecomplex to its return to mean resting pressure.Propagation velocity was measured as the timeelapsing from the onset of a swallow contractionat the oral transducer to the onset of contractionat the intermediate and from the intermediate tothe aboral transducer. Mean values were deter-mined from at least 10 swallow induced contrac-tions in the lower, middle, and upper third of theoesophageal body, respectively. The restingpressure of the upper oesophageal sphincter aswell as its relaxation upon swallowing weredetermined from at least three swallows at eachtransducer site and expressed as mean values. Allrecordings were scored independently andblindly by two investigators. The initiation ofswallowing was recorded by a surface electro-myogram of the submental muscles. Two Beck-man biopotential electrodes were attached 1 cmfrom the right and left mandibular bow, respec-tively. The signal was integrated by a Beckman9852A coupler.

MEASUREMENT OF GASTRIC EMPTYINGAND ANTRAL CONTRACTILE ACTIVITYGastric emptying and antral motor activity wererecorded by means of an isotope technique. 12 13 20A semisolid test meal labelled with a dose of 74MBq (2 mCi) 99m-Technetium sulphur colloiddiluted in isotonic saline (0- 15 M) was used. Themeal was prepared from 250 ml whole milk (8-75g protein, 8 75 g fat, 12 5 g carbohydrates), 15 gsugar, 14 g maize starch (MaizenaR, Knorr,Wels, Austria; 11-9 g carbohydrates) and, forflavouring, cinnamon. It had a caloric content of1150 kJ. The meal was cooked slowly undercontinuous stirring until a homogenous, ratherstiff, semisolid consistency was reached. Aftercooling to a temperature at which it could beingested, it was mixed thoroughly with theradioisotope. Thirty minutes after drug adminis-tration, the subjects ate the test meal with aspoon (six patients with bulimia) or sucked itthrough a wide lumen polyethylene tube (18patients and all controls). During the latterprocedure, no air swallowing was noted andbelching after meal ingestion was very rare inboth patients and control subjects. Recordingwas started with the beginning ofmeal ingestion.A dual-headed gamma scintillation camera(ROTA-CAMERA, Siemens AG, Erlangen,West Germany) coupled to a computer system(Digital Equipments Corporation, SystemGAMMA- 1i1) with one camera in an anterior andthe other in a posterior position recorded theradioactivity over the stomach and over theremaining abdomen for 50 minutes. In minutesseven to 10, 27 to 30 and 47 to 50 after the start ofrecording, data were acquired in frame modewith 80 serial images over three seconds each andin the remaining time with serial images of one

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Oesophageal andgastric motor activity in patients with bulimia nervosa

minute frame time. To avoid possible overpro-jection of the stomach and the small intestine,the patients were seated in an armchair tilted atan angle of 30 degree backwards.

QUANTIFICATION OF GASTRIC EMPTYINGThe one-minute frames were used for the genera-tion of gastric emptying curves. Backgroundactivity was calculated and subtracted from thecounts of the anterior and posterior camera,respectively. Thereafter, the arithmetic mean ofthe counts obtained from the two cameras wascalculated, so that a falling count rate wasrepresentative of the marker remaining in thestomach. By using a dual-headed camera, arte-facts caused by movement and absorption, asoccurring in measurements with one cameraonly, could be avoided. The percent emptyingrates for the first 10 minutes and for the entire 50minutes after the start of meal ingestion werecalculated from the emptying curves. In addi-tion, the half emnptying time (t½/) was calculatedfrom the regression line of the count rate plottedon a logarithmic scale against time on a linearscale.2'

QUANTIFICATION OF ANTRAL MOTORACTIVITYThe serial images with three seconds frame timerecorded in the three periods seven to 10, 27-30and 47-50 min after the start of meal ingestionwere used for measuring antral motor activity.The stomach was displayed on an oscilloscopeand three small regions of interest were posi-tioned at right angles to the axis of the antrum.To control for movements of the subject or herstomach, these regions were adjusted for everyperiod of measurement. By using a dual headedcamera, again, artefacts arising from variationsin depth of radioactivity could be avoided. Theamplitude of antral contractions was calculatedfrom the more or less sinusoidal variations ofradioactivity in each of the regions positionedacross the antrum. These curves were high passfiltered by transforming them into the Fourierspace, applying a filter with a lower frequencycut-off at 1 5 Hz, and back transformation. Thealgorithm of the fast Fourier transform was usedfor these computations. The modulation depthof the oscillations of the curve was calculated as ameasure of the amplitude of antral contractions

TABLE I Gastrointestinal symptoms in bulimia patients with and without demonstratedoesophageal motor disorders

Vigorous Normal motorAchalasia achalasia DOS 'Hypochalasia' activity

n 1 2 1 4 18

Dysphagia for solids 1 2 - - -

Dysphagia for solids and liquids - - 1Vomiting spontaneous non-acidic 1 2 1Vomiting selfinduced non-acidic 1 2 1Vomiting selfinduced acidic 1 2 1 4 18Excessive saliva regurgitation 1 1Chest pain 1 1 1Heart burn - - - 1Postprandial fullness and bloating 1 1 1 4 14Epigastric pain 1 - - 2 8Belching - 1 3 11Constipation 1 2 1 2 13

DOS, diffuse oesophageal spasm; 'hypochalasia', incomplete relaxation of lower oesophagealsphincter but propulsive swallow induced contractions in the oesophageal body.

and expressed as mean modulation depth overeach recording period.'320 After this procedure,the curve was low pass filtered with an upper cut-off frequency of 5 5 Hz using the methoddescribed above. Then the autocorrelation func-tion of the curve was computed and used todetermine the frequency of antral contractions.Based on this frequency, a 'gated' study22 wasgenerated by adding all images of the threesecond frames belonging to the same state ofcontraction of the antral wall. An amplitude aswell as a phase image were obtained by applyinga Fourier analysis ofthe first component - that is,by fitting only the first sinusoid of the Fourierexpansion to the time activity curve for eachpixel of the gated study. Since in the phase imageregions ofequal phase appear in the same colour,the distances between points ofequal contractionstate could be calculated. These distances wereused, together with the contraction period, tocompute the propagation velocity of antralcontractions. '3

STATISTICAL ANALYSISThe percentage of marker remaining in thestomach and the data on antral motor activitywere subjected to analyses of variance forrepeated measures23 accounting for the fixedfactors 'group' (patients, controls) and 'time'(periods of measurement), and of the randomfactor 'subjects'. To evaluate differencesbetween mean values in each period of time, asequentially rejective multiple test procedurewas used.24 In this procedure, which was basedon the analysis of variance, directional tests werecarried out and an overall significance level ofoc= 005 was adopted. The t½/2 values wereanalysed by a nonparametric test - that is, theMann-Whitney U-test for differences betweenindependent samples.25

Results

OESOPHAGEAL MOTOR ACTIVITYOesophageal manometry revealed that 18 of the26 patients studied had an entirely normaloesophageal motor activity. In four patients, thelower oesophageal sphincter relaxed incom-pletely upon swallowing (64%, 47%, 46% and33%, respectively), the swallow induced contrac-tions in their oesophageal body, however, werepropulsive. Two of these patients with loweroesophageal sphincter 'hypochalasia' had highamplitude (>200 mmHg), long duration (>8 s)contractions in the lower third of their oesopha-geal body. None of the four patients showed anincreased incidence of nonpropulsive, tertiarycontractions or of nonpropulsive reactions toswallows, and none of them had presented anysymptoms prior to the manometric investiga-tion, which could have been indicative fora disordered oesophageal motor function(Table I).

In four patients, distinct disorders of oesopha-geal motility were found to be present in mano-metric and fluoroscopic studies: one had anachalasia of the lower oesophageal sphincter andnon-propulsive contractions of low amplitude in

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Kiss, Bergmann, Abatzi, Schneider, Wiesnagrotzki, Hobart, Steiner-Mittelbach, Gaupmann, Kugi, Stacher-Janotta, Steinringer, Stacher

0-

40

60-

i . . . . . .5 10 20 30 40 50

Time (min)Figure 1: Mean percent rate ofgastric emptying (SEM) ofthetest meal in the 24 patients with bulimia nervosa()and in the 24 healthy control subjects (--).

the oesophageal body, two had a vigorousachalasia and non-propulsive, repetitive contrac-tions in the lower third of the oesophageal body,and the fourth patient had diffuse oesophagealspasm as defined by the manometric criteriaproposed by Richter and Castell.26 Subsequentfluoroscopic studies yielded results compatiblewith the manometric diagnoses. At investigationbefore manometry, all of these four patients hadindicated to experience two different types ofvomiting: one selfinduced, in which the vomitedmaterial tasted either acidic or non-acidic andlike the preceding meal, and one involuntary, inwhich the vomited material always was nonacidicand of the same taste as the preceding meal(Table I). The patients with achalasia andvigorous achalasia also had dysphagia for solidfood and two of them reported chest pain and aseries of events, in which food stuck behind thesternum and could not be swallowed down. Thepatient with diffuse spasm had dysphagia forsolid and liquid food as well as chest pain. Thesecond, involuntary type of vomiting dis-appeared after mechanic dilatation in the patientwith achalasia, and under nifedipine (Adalat-retardR, Bayer, Leverkusen, West Germany)medication in the three patients with vigorousachalasia and diffuse spasm, respectively. Thesetherapeutic measures, however, had no influenceon the bulimic behaviour of the patients, who allcontinued their binge eating and selfinducedvomiting. One of the patients was concernedbefore the initiation of nifedipine medicationthat this drug could interfere with her ability tovomit selfinduced. The presence or absence ofdisordered oesophageal motor activity was in nodiscernible relationship with the frequency of

TABLE II Emptying rate in thefirst 10 minutes and during the50 minutes after the start ofmeal ingestion in healthy controlsubjects and in patients with bulimia nervosa

Emptying rate (%/min)n First 10 min Entire 50 min

Control subjects 24 0-61 (0 10) 0-98 (0-05)Bulimia patients 24 0 51 (0 08) 0-67 (006)*

Values are means (SEM). *Significantly different (t-test for pairedobservations) from values of control group.

300

200

EC

EE

100-

n

.

0

v 0-S~~~~~~~~-

- A- I_ __ _ _ _ _S

0 00*w~~~~~~*owlm-X__ _ ____

I-

Bulimia ControlsFigure 2: Gastric half-emptying time, in minutes, oftheisotopically labelled test meal in the 24 patients with bulimianervosa and in the 24 healthy control subjects.median times. Area between ---: mean halfemptying time±2 standard deviations in the 24 health control subjects.

self-induced vomiting and the duration of thehistory of bulimia.

GASTRIC EMPTYING

Percentage ofmarker remaining in the stomachThe emptying curves over time followed closelya mono-exponential pattern. No initial lag phaseas reported to occur after the ingestion of solidmeals was observed. In the patients withbulimia, gastric emptying was significantlyslower than in the 24 healthy control subjects(Fig 1). This difference was not present in thefirst 10 minutes after the start of meal ingestion(Table II).

Half emptying timeGastric half emptying time was grossly pro-longed - that is, longer than the mean t½/2 of thecontrol subjects plus two standard deviations(SD) in nine patients. The respective t½/2s ofthese patients ranged from 99 to 272 minutes(Fig 2). As a group, the patients had significantlylonger t½/2s (median: 74 minutes) than the controlsubjects (median: 47 minutes; Mann-Whitney UTest: p<0001), and only one patient had a t½/2shorter than the median t½/2 of the controlsubjects. Long t½/2s were associated with lowserum potassium levels (r (23)=0A427, p<0Q05).Long t½/2s tended also to be associated with a lowpercentage of desirable body weight and withlong illness duration, statistical significance,however, was not reached. There were norelationships between the length of t½/2 and thefrequency of vomiting per week, the abuse oflaxatives and the presence of a history of primaryanorexia nervosa, respectively.

ANTRAL MOTOR ACTIVITYIn all patients with bulimia as well as in all of thehealthy control subjects, phasic antral contrac-

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Oesophageal and gastric motor activity in patients with bulimia nervosa

TABLE III Antral contractile activity in healthy control subjects and in patients with bulimianervosa. Amplitude, frequency and propagation velocity ofcontractions at seven to 10, 27-30and 47-50 minutes after the start ofmeal ingestion

n 7-10 min 27-30 min 47-50 min

Amplitude (modulation depth in %)Control subjects 24 24-2 (1-9) 26 5 (1-7) 29 7 (2-2)Bulimia patients 19 20-8 (1-7) 20-4 (16)* 21-2 (1-7)*

Frequency (cycles/min)Control subjects 24 3-08 (0 05) 3 03 (0 03) 2 95 (0-03)Bulimia patients 19 3 06 (0-06) 3-01 (0 05) 3-01 (0 06)

Propagation velocity (mm/s)Control subjects 24 3-02 (0 29) 2 75 (0 23) 2-74 (0-21)Bulimia patients 19 3 04 (0-26) 3 04 (0 22) 3-17 (0-24)

Values are means (SEM) measured in the three regions of interest positioned across the antrum.*Significantly different (t-test for treatment means) from values of control group.

tions were present all the time and no 'silent'phases were observed in any individual.

Amplitude ofantral contractionsThe contraction amplitudes were lower in thepatients with bulimia than in the 24 healthycontrol subjects during all of the three recordingperiods - that is, seven to 10 minutes, 27-30minutes and 47-50 minutes after the start ofmealingestion (Table III). In the healthy subjects,contraction amplitudes increased steadily overthe postprandial 50 minutes of recording. In thebulimia patients no or only slight increasesoccurred and the contraction amplitudesremained more or less unchanged over the 50minutes of recording. In the periods 27-30minutes and 47-50 minutes after the start ofmealingestion, amplitudes were significantly lower inbulimia patients than in the healthy individuals(Table III).

Frequency ofantral contractionsIn the patients with bulimia having received nodrug or placebo, the frequency decreasedslightly less over the 50 minutes after mealingestion than in the healthy control subjects(Table III), in whom this decrease correlatedwith the simultaneous increase in contractionamplitude. The mean contraction frequencyaveraged over the three postprandial recordingperiods was within the range of the mean fre-quencies of the control subjects in all of thepatients.

Propagation velocity ofantral contractionsThe propagation velocity was slightly higher inthe bulimia patients than in the healthy subjects(Table III). No retropulsive waves could bedetected in any patient with bulimia and in anycontrol subject.

DiscussionThe results of the present study show thatsymptoms of oesophageal motor disorders can beobscured by coexisting bulimic behaviour.Other than reported to have occurred in patientscategorised on primary evaluation as havingprimary anorexia nervosa however,'12 suchsymptoms in no instance gave rise to a misdiag-nosis of bulimia nervosa. That the symptoms ofoesophageal motor disorders were overlooked or

misinterpreted by the patients' physicians andpsychiatrists has to be attributed not so much toan inadequate history taking, but to the fact thatthe symptoms were misinterpreted by thepatients themselves. Directed questioning, how-ever, will yield information indicative of thepresence or absense of a swallowing disturbance.This was also the case in the present study inwhich, at the investigation before manometry,all of the four patients, in whom subsequentlythe presence of achalasia, vigorous achalasia anddiffuse oesophageal spasm, respectively, wasdocumented, reported to experience two dif-ferent types of vomiting: one selfinduced, inwhich the vomited material tasted either acidicor non-acidic and like the preceding meal, andthe other involuntary, in which the vomitedmaterial was always non-acidic and of the sametaste as the preceding meal. Although the in-voluntary emesis occurred also in situations inwhich the patients not at all intended to get rid ofthe ingested food, all of them thought that thistype of vomiting and the symptoms of dysphagiaand retrosternal pain, as well, were conse-quences of their selfinduced vomiting. Thisseemed the more plausible to them, as all had hadno such symptoms before the onset of theirbulimic behaviour. There is no reason to assume,however, that the oesophageal motor disordersdetected could have been induced or their onsetfacilitated by the vomiting behaviour. Self-induced emesis, however, may cause oesopha-geal perforation, which, with its frequently ensu-ing mediastinitis, is a life threatening event. Inpatients with primary anorexia nervosa, in-cidences of mediastinal emphysema as a conse-quence of selfinduced vomiting have been des-cribed.2728 In one paper29 it has been reportedthat a patient with bulimia and chronic alcoholabuse suffered from 'mechanical dysphagia' -that is, 'solids or large bolus-sized foods wouldget 'stuck' at an area under the xiphisternum'.Endoscopically, 'an area 4 cm above the gastro-esophageal junction' was found that 'contracted(and relaxed) like a second sphincter'. Onmanometry, however, no high pressure zoneabove the lower oesophageal sphincter was seenand the resting pressure of the sphincter was lowand acid infused into the mid-oesophagusresulted in 'lower retrosternal pain'. A fluoro-scopic investigation was not performed. Thus,the description yields no information as to thenature or even the mere presence of the pre-sumed 'mechanical dysphagia'. The highincidence of oesophageal motor disorders in ourgroup of patients with bulimia nervosa in rela-tion to the incidence to be expected in the generalpopulation certainly cannot be extrapolated toother patient groups. There seems also to be noreason to assume an underlying disorderaccounting for both bulimia and oesophagealcontraction abnormalities, although one groupof workers has reported an association betweencontraction abnormalities and criteria definedpsychiatric illness in diabetic30 and non-diabeticpatients.3' The results of the present study showthat the clinical evaluation of patients withbulimia nervosa should always include the takingof a thorough history regarding swallowing andvomiting and the nature as well as the taste

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264 Kiss, Bergmann, Abatzi, Schneider, Wiesnagrotzki, Hobart, Steiner-Mittelbach, Gaupmann, Kugi, Stacher-Janotta, Steinringer, Stacher

of the vomited materials. In cases in whomsymptoms are suggestive of an oesophagealmotor disorder, radiographic and manometricstudies should be performed. Gastric emptyingof the semisolid test meal was grossly delayed inmore than one third of the studied patients, andantral contraction amplitudes were markedlylower than in the healthy control subjects and thenormally occurring postprandial increase in con-traction amplitude was not present. This showsthat gastric motor function is impaired not onlyin a high proportion of patients with primaryanorexia nervosa as reported previously,8-'7 butalso in many patients with bulimia. Our resultsconfirm those of a recent study,8 in which gastricemptying of cream of wheat was found to bedelayed in 12 of 20 bulimia patients. Theobservation made in that study that the remain-ing eight patients, by contrast, had rapid empty-ing, does, however, not correspond with theresults ofthe present investigation, in which onlyone patient had a shorter t/2 than the median t½/2of the healthy controls. Other authors foundgastric emptying of a solid meal to be delayed inonly one of 10 patients with bulimia'7 or to benormal.'6 In the latter study,'6 however, empty-ing data of the bulimic patients were comparedwith those of a very heterogenous control groupof 16 premenopausal women, which includedpatients with morbid obesity and inflammatorybowel disease and whose t½/2s for solid mealcomponents were highly scattered. In the samestudy it was reported that, in three patients withbulimia, antral motor activity as recordedmanometrically was normal and even higherthan in the controls. 16 The latter findings have tobe viewed with caution regarding the very smallnumber of patients studied and the recordingtechnique used, which is prone to detect no morethan 50% of actually occurring contractions.32 Asthere is no information available on the rate ofgastric emptying in patients hospitalised forpsychiatric diseases without eating disorders, thequestion of how emptying in such patientsrelates to that in patients hospitalised for bulimiacannot be answered.The mechanisms underlying the impaired

gastric motor function in patients with bulimiaare unknown. As revealed in the present study,the absence or presence of a history of primaryanorexia nervosa, the absence or presence oflaxative abuse and the frequency ofvomiting perweek bore no relationship to the rate of gastricemptying. There was, however, a significantinverse relationship between t½/2s and serumpotassium concentrations, which were below thenormal range in four of the 24 patients studiedand near the lower borderline of normal inanother eight. There was also a tendency of lowpercentages of desirable weight being associatedwith long t½/2s, which, however, did not attainstatistical significance. Incidences of dilatation,infarction and rupture of the stomach upon theingestion of large quantities of food, which wereobserved not only in depleted patients withprimary anorexia nervosa33-37 but also in patientswith bulimia,36 39 suggest that weakness andatrophy of gastric smooth muscle, caused bymalnutrition and/or electrolyte depletion result-ing from the repetitive self-induced vomiting,

might play a crucial role. This also could havebeen the case in a number of our patients, whowere substantially underweight by up to 23%,although the average weight of the patients wasonly about 10% below their calculated desirableweight. Disordered gastric motor function mayalso be the result of abnormal autonomic func-tion'5 or of peripheral neurophathy as found toimpair skeletal muscle function in patients withprimary anorexia nervosa and bulimia.4'4I Therewas no evidence of such changes, however, inany of our patients.

It is concluded that bulimic behaviour canobscure symptoms of oesophageal motor dis-orders and that delayed gastric emptying, lowantral contraction amplitudes and an impairedcontractile response of the antrum to the inges-tion of a meal are frequent not only in primaryanorexia nervosa but also in bulimia nervosa.

Presented at Digestive Disease Week, New Orleans, May 14-20,1988, and published in Abstract form in Gastroenterology 1988; 94:A228.

1 Halmi KA, Falk JR, Schwarz E. Binge eating and vomiting: asurvey of a college population. Psychol Med 1981; 11:697-706.

2 Pyle RL, Halvorson PA, Neuman PA, Mitchell JE. Theincreasing prevalence of bulimia in freshman collegestudents. IntjEatingDisord 1986; 5: 631-47.

3 Schotte DE, Stunkard AJ. Bulimia vs bulimic behaviors on acollege campus. JAMA 1987; 258: 1213-5.

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