Archives of Disease in Childhood 1993; 69: 564-568

Effects of a few food diet in attention deficitdisorder

C M Carter, M Urbanowicz, R Hemsley, L Mantilla, S Strobel, P J Graham, E Taylor

AbstractSeventy eight children, referred to a dietclinic because of hyperactive behaviour,were placed on a 'few foods' eliminationdiet. Fifty nine improved in behaviourduring this open trial. For 19 of thesechildren it was possible to disguise foodsor additives, or both, that reliably pro-

voked behavioural problems by mxng

them with other tolerated foods and to testtheir effect in a placebo controlled doubleblind challenge protocol. The results of acrossover trial on these 19 childrenshowed a significant effect for the provok-ing foods to worsen ratings of behaviourand to impair psychological test perfor-mance. This study shows that observa-tions of change in behaviour associatedwith diet made by parents and otherpeople with a role in the child's care can

be reproduced using double blindmethodology and objective assessments.Clinicians should give weight to theaccounts of parents and consider thistreatment in selected children with a

suggestive medical history.(Arch Dis Child 1993; 69: 564-568)

Institute of ChildHealth, London,Behavioural SciencesUnitC M CarterM UrbanowiczL MantillaP J Graham

Department ofImmunologyS Strobel

Institute ofPsychiatry,London, DepartmentofPsychologyR Hemsley

MRC Child PsychiatryUnitE Taylor

Correspondence to:Ms Christine Carter,Dietetics Department,Queen Elizabeth Hospital forChildren, Hackney Road,London E2 8PS.Accepted 23 July 1993

The effect offood and food additives on hyper-activity remains controversial. Initial sugges-

tions by Feingold1 implicating food additivesand natural salicylates were largely uncon-

firmed by controlled studies of hyperactivechildren,2 though single case control studiesshowed the effect of artificial colours inindividual children.3The occurrence of adverse skin, gut, and

other physical reactions to foods such as milkand wheat stimulated speculation that suchfoods could also produce adverse behaviouraleffects. A double blind controlled study4 con-

ducted by a team including two of the presentauthors (CMC, PJG), suggested that foodsand additives could be shown to affect hyper-active behaviour adversely. This was based on

ratings by parents, but not shown on objectivepsychological testing. Criticism of this studyrelated to (a) the correct diagnosis of hyper-activity, (b) the selected study population, and(c) the high tartrazine challenge dose. Sincethen three studies with limited scope lookingonly at food dyes have been published57 withcontradictory results. Kaplan et al, in a placebocontrolled study of a diet excluding additives,chocolate, caffeine, and any other foodssuspected by parents, found that more thanhalf their 24 preschool subjects showedan improvement.8 Egger et al found marked

effects of a few food diet in an open trial, butdid not proceed to test the response in a blindtrial as their design led them instead to use theopen response as a measure of the effectivenessof a hyposensitisation procedure.9

In the absence of clear confirmation orrefutation of the results of the earlier study andin an attempt to meet some of the criticisms,we undertook the current study using a similardesign, but with improved methodology andclearly defined outcome measures.

MethodsChildren were referred by general prac-titioners, paediatricians, and psychiatrists to aspecial diet and behaviour clinic set up at theHospital for Sick Children. All childrenaccepted for the study met DSM III criteria forattention deficit disorder with hyperactivity,10were between 3 and 12 years old, and had IQsabove 70. Where children were already ondiets their parents were asked to take them offthe diet for a week before the initial interview.This interview included a systematic medicaland social history, a standardised psychiatricinterview, a school report, Conners' parentand teacher scales, 1 a cognitive assessmentusing the standard Wechsler intelligence scalefor children - revised,12 or Wechsler preschooland primary scale of intelligence,13 a Nealereading test,14 and an assessment of familyrelationships. 15

Treatment proceduresFIRST PHASE: FEW FOOD DIETThe children were put on a restricted (or 'fewfoods') diet for a period of three to four weeks.The foods allowed were typically two meats(often lamb and turkey), two carbohydratesources (rice and potato), two fruits (oftenbanana and pear), a range of root and greenvegetables, bottled water, sunflower oil, andmilk free margarine.16 This diet was varied tosuit the child's preferences and to avoid foodsalready suspected, or foods for which the childhad a particular craving or dislike. If there wasno improvement by the end of the second weekthe diet was changed or further restricted forthe last week. Failure to improve by the end ofthis period meant that the child left the trial atthis point.

SECOND PHASE: OPEN REINTRODUCTIONWhere behavioural improvement occurred,foods and additives were reintroduced at therate of one a week in normal amounts and

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Effects ofa few food diet in attention deficit disorder

incorporated into the diet if there was norelapse. If the parent was worried about thepossibility of a bad reaction, the amounts werestepped up to normal over a few days.Food additives (colours, flavours, and

preservatives) were usually introduced asmixtures in additive-containing foods such asham, bacon, sausages, coloured sweets, anddrinks with colour, preservatives, and flavours.In an effort to obtain a clearer idea of thecomponents of the foods responsible for anyadverse reaction, artificial colours were thengiven where possible using capsules containing6-5 mg mixed colours. These were usuallygiven in increasing amounts, starting with onecapsule on the first day and increasing rapidlyto no more than four capsules a day by the endof one week. If the children refused thecapsules, these colours were mixed withmelted chocolate or carob bars.

THIRD PHASE: DOUBLE BLIND OR EXPERIMEN-TAL PHASEWhere possible, children were asked to enter adouble blind, crossover, placebo controlledtrial of reintroduction of one or more incrimi-nated foods or additives. This stage was

offered to all children who were receiving an

acceptable and adequate diet, whose parentsagreed, and where a provoking item could begiven in sufficient amount and be adequatelydisguised in a food known to be tolerated (toact as excipient and placebo). The order inwhich incriminated foods and placebo weregiven was allocated randomly by CMC (by thetoss of a coin). Each was given for one weekwith a two week washout period betweenactive and placebo phases.

Material was prepared individually for eachchild and the amount of incriminated foodgiven was based on the amount which seemedto be needed to provoke problems on openreintroduction. For example, between 120 and200 ml of cows' milk was given daily disguisedin a milk substitute (for example soya milk) forprovocation, while milk substitute was given asplacebo. Artificial colours were given disguisedin capsules rendered opaque with iron oxide.Each capsule contained 6-5 mg mixed colours(1 mg tartrazine, 1 mg sunset yellow, 1 mgquinoline yellow, 0.5 mg carmoisine, 0 5 mgbrilliant blue, 0 5 mg erythrosine, 0 5 mg greenS, 0-5 mg indigocarmine, 0-5 mg amaranth,and 0 5 mg ponceau 4R with glucose as filler).The number of capsules given varied, but no

child received more than 26 mg colouringdaily, which is roughly equivalent to four tofive packs of children's sweets a day. Capsulescontaining glucose alone were given asplacebo. For children who would not swallowthe capsules, the colours were disguised incarob or chocolate as already described.Benzoic acid and sodium metabisulphite (25mg increasing to 50 mg during the week) were

given dissolved in a suitable non-provokingdrink. Drinks were prepared and immediatelyfrozen, to be thawed and consumed on a dailybasis by the child. Orange juice was disguisedin a mixture of pureed pears and pineapple

juice. Apple juice was disguised in pineappleand apricot juice. Chocolate was disguised incarob confectionery. Most of the childrenreceived more than one provoking item. Forexample, one child, who was receiving a veryrestricted diet, received food colours disguisedin vegetable soup as well as apple juice dis-guised in carrot juice.The preparations were made and coded by

CMC and given to the family by MU. At thistime CMC took no part in the managementand everyone else remained blind to the orderin which active and placebo foods were given.

PSYCHOLOGICAL ASSESSMENTSystematic assessment of behaviour wasundertaken using a battery of outcome mea-sures at three points in time: at entry to theexperimental phase, at the end of the firstexperimental period (one week later), and atthe end of the second period (a further threeweeks later). These measures had shown dif-ferences between hyperactive and non-hyper-active children and between stimulant drugand placebo in previous research.17

Behaviour was assessed with Conners'behavioural rating scale for parents 11 and witha global rating of severity of behaviour prob-lems made by the parent with most contactwith the child. (It was not possible to gatherteacher ratings on a satisfactory number ofchildren mainly because of the parents' wish tocarry out the trial during the school holidays.)

Behaviour during testing was directlyobserved by the psychologist and rated ondimensions of fidgetiness, restlessness (involv-ing movements of the whole body), and inat-tentiveness. These observations were summedinto a single scale of hyperactive behaviour. Apaired associate learning test'8 was used tomeasure new learning: the score is the numberof errors during learning of a list to criterion.Impulsiveness versus reflectiveness wasassessed using the revised form of the matchingfamiliar figures test.'9 For children under 6years of age we used a simplified form of thetest developed by Cohen and Minde.20 Themeasures taken from each child are the meanlatency to first response and the number oferrors made for each stimulus.

AnalysisThe analysis followed from the study's designas a two period crossover trial in which eachchild acted as his or her own control.2'Continuous measures were tested for differ-ences of means with t tests. Square root trans-formations were carried out before significancetesting because of some skew in the measures;the means, differences, and standard errorsreported in table 3 are based on untransformeddata. Order effects (that is, first v secondadministration) and treatment effects (that is,active food v placebo) were tested with paired ttests; interactive effects were tested with com-parisons of the two order groups (active first vplacebo first) on the difference between activeand placebo. If a measure was unavailable for

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Carter, Urbanowicz, Hemsley, Mantifla, Strobel, Graham, Taylor

an individual child (for example, if theConners' scale had been incompletely filled inby parents), then the child was excluded fromthe analysis for that measure only.The one categorical measure - the global

ratings made by the parents - was tested (inview of small numbers) by Fisher's exact prob-ability test with a one tailed level of significanceset at 0 05. One tailed significance testing wasjustified because of the study's position as areplication of previous work, so that therecould be no doubt of its having set out to testthe specific hypothesis of foods worsening thechild's behaviour.

SubjectsEighty four of the 130 children referred tothe clinic were judged to meet the admissioncriteria and their parents agreed to participatein the trial. Of these, 78 children (69 boys andnine girls) completed the initial period on a fewfood diet; the remaining families were unableto tolerate the regimen.The 78 children who completed the first

phase of the trial ranged in age from 3 to 12years. The range ofIQ was between 72 and 135(average 104). Forty seven were referreddirectly by their general practitioners, 10 bypsychiatrists, three by neurologists, 14 bypaediatricians, and four by psychologists. Theparents of 23 children reported asthma (whichwas under control with drugs) or hay fever, orboth; the parents of 38 children reportedeczema or skin rashes; the parents of 12children reported headaches; the parents of 30children reported gastrointestinal symptoms;and the parents oftwo reported fits. Fourteen ofthe children had no physical symptoms. Manyof these symptoms were mild and managed bythe general practitioner. Twenty four of the 78children who completed the first phase hadbeen seen by specialists for physical symptoms:12 for asthma, five for gastrointestinal prob-lems, one for diabetes, two for fits, three foreczema, six for 'allergies', and one for enuresis.Of the 78 children, 24 were exposed to

adverse psychosocial situations such as dis-cordant intrafamilial relations, inconsistent

Completed few food diet

Becameworse

Became worse

Reintroduction, no ri

Improved591

Failed to improveS7

Reintroduction with relapses, 'responders'elapses

4 Unable to c

I i

(Considered for double blind phase)

continue

Entered double blind Entered study too late

No suitable foods for double blind Refused double blind mE3 10m

Table 1 Foods most commonly implicatedfor the 47responders duing open reintroduction

No No %tested reacting Reacting

One or more additive-containing foods

ChocolateCows' milkOrangeCows'cheeseWheatOther fruitsTomatoEgg

323745353147473538

2228262014211787

706464574545362218

The number of children who tried each of these foods and thenumber who responded adversely are shown. No child triedevery food. Some parents did not introduce foods that weredisliked, whereas others refused to introduce additive-contain-ing foods that they felt would cause a problem.

parental control, or anomalous family situa-tions. Forty three children were already receiv-ing some dietary restriction when first referredto the study.

ResultsSeventy eight children completed the few fooddiet. The parents of 59 of these children (76%)felt there had been a worthwhile improvementin behaviour, two children (3%) became worse,and 17 (22%) did not respond. The 59 childrenwhose behaviour had improved (fig 1) enteredthe second phase of the trial, the open sequen-tial reintroduction of foods to establish targetfoods for the double blind phase. For three(5%) of the 59 children it was not possible toprovoke a relapse with any food and theyremained well. For the parents of nine (15%)children the demands of the diet proved impos-sible to meet and they abandoned it. The foodsimplicated in the deterioration of behaviourare therefore described for the remaining 47children (referred to hereafter as responders).A large number of foods were implicated

during the reintroduction phase and table 1shows the number of children reactingadversely to the most common provokingfoods. All the relapses to food includedworsening ofbehaviour except for four relapsescaused by cows' milk and two by cheese, whichgave rise to physical symptoms only. Thesebehavioural problems were sometimes accom-panied by the reappearance of the physicalsymptoms which were reported to haveimproved on the few food diet.

It is difficult to obtain a complete picture ofintolerance to specific food additives as theyoften occur in mixtures in manufactured foods.Just four children were found to react only tofoods containing additives. When food colourswere suspected, we asked parents to give theirchildren colour capsules. Sixteen agreed to dothis; three children were not affected, two hadbehavioural and physical symptoms, eight hadbehavioural problems only, and three hadphysical symptoms only. Of 19 who tried coladrink, 16 reported problems.

Failed to complete double blindw--

Completed double blind[K1

Figure 1 Allocation of children to the trials. Values in boxes are numbers of children.

DOUBLE BLIND PHASEEleven of the 47 responders reacted adverselyto foods which could not be given in the

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a) 20 Active

-=- Placebo

loe) 5

Iol01 2 3 4 5 6 7Day of trial

Figure 2 Daily Conners' scale scores (parents'hyperactivity ratings). The mean scores, on thehyperactivity factor of the Conners' behaviour rating scale,are separately shown for the placebo period and the periodduring which a potentially active food was given.

double blind phase. Usually this was becausethe amount (for example of wheat) thatinduced symptoms was too great to disguise, or

because no suitable placebo and excipientcould be identified (for example, for cola). Theparents of a further 10 children refusedbecause of particular family circumstances atthat time and three children had entered thestudy too late to reach this stage.Twenty three children were accepted into

the double blind phase of the trial. On the firstday of each phase the families were asked toguess whether they had been given the provo-cation or placebo food. The appearance andtaste did not make the foods obvious; 50% ofthe guesses were correct and 50% were wrong.Four of the children who met the criteria for

entering the double blind phase did not com-

plete it satisfactorily (two were withdrawn bytheir families and two broke their diet).Nineteen children therefore formed the groupwhose course in the crossover trial will now bedescribed.The global rating made by parents favoured

the placebo period in 14 children. The activeperiod was favoured in three children and no

preference was expressed in two others; thesefive children were combined as treatmentfailures. There were fewer such failures thanpredicted by chance (Fisher's exact test prob-ability 0.03).

Figure 2 shows the course over a week forthe group mean on the short form of the

Conners' scale in the active and placebophases. The differences at the end of eachphase were greatest for the items 'restless','disturbs others', 'cries often', and 'temperoutbursts', suggesting a possibly greater effecton irritability than on attention deficit.

Table 2 shows behavioural ratings and testscores. Each of the outcome measures was

tested for order, treatment, and interactioneffects as described earlier. No effect of order,

Table 2 Test measures during blind trial

Difference (SE)Mean (SD) Mean (SD) Mean (SD) betweenpretrial active placebo active -placebo

Test* result result result result

CPRS scoreObservationPALT errorsMFF errorsMFF time (sec)

8-1 (7-7)0-60 (0 3)15-2 (14)1-3 (0 7)

12-3 (11-5)

13-9 (91)0-80 (0 4)14-9 (14)1-6 (0-7)9 0 (9-5)

8-8 (7 4)0 57 (0-4)14-6 (13)1-4 (0-8)

11 9 (12-3)

5-2 (2 5)0-23 (0-1)0-31 (1-5)0-21 (0-1)2-9 (1-0)

Observations were made by the psychologist testing the children.CPRS=Conners' parent rating scale; PALT=paired associate learning test; MFF=matchingfamiliar figures test.

or interaction between order and treatmentwas fourd.

Behavioural ratings by parents on the finalday of each treatment period showed astatistically significant effect of the foods(p<0 05). Errors on the paired associate learn-ing test were not significantly different betweengroups, but there was a difference on thematching familiar figures test for latencyand errors (p<001). The psychologist'sbehavioural observations also showed dif-ferences for the scale of hyperactive behaviour(p<O-Ol), with the greatest difference on theitem rating fidgetiness.These results suggest that children whose

behaviour is 'diet responsive' on an open trialcan also be shown to respond by a blindobserver using standardised tests.

RESPONDERS V NON-RESPONDERSOf great value to the clinician would be infor-mation about which children are likely torespond to diet and some hints may beobtained from the open phase of the trial. The47 responders and 17 non-responders did notdiffer in terms of age or sex, socioeconomicstatus, number of physical symptoms, or thirst.There was, however, a marked differencebetween the two groups in the number ofchildren on a restricted diet before the study.The parents of 90% of the responders hadalready noticed a reaction to food, whereasonly 6% of the non-responders had done so.Cravings were reported by 85% of the parentsof responders and 30% of non-responders.Dietary management also seemed less likelyto produce a change where there were dis-cordant marital relations (present in 13% ofresponders, 53% of non-responders).

In the blind phase of the trial, children hadalready been selected as 'responders', so theprediction of response at this stage is lessfeasible. It was, however, possible to dividethe 16 children with complete rating scalesinto six with trivial or absent physical symp-toms and 10 whose physical symptoms werejudged to be significant. The differencebetween the means for active and placebo wascalculated for parental ratings, separately forthose with and without physical symptoms.Those with symptoms (mean (SD) difference5-5 (10-8)) were not significantly differentfrom those without (mean (SD) difference 4-7(9 6)).

DiscussionThis trial indicates that diet can contribute tobehaviour disorders in children and that thiseffect can be shown in a double blind, placebocontrolled trial. The effects of diet were not aslarge as in some stimulant drug trials, but mayhave been underestimated by the design asamounts of food given blind were necessarilysmall. The important conclusion is that theparents' reports of a behaviour change withdiet can, in a selected group of children, beconfirmed by double blind, placebo controlledtrial with objective tests.

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It is not possible to conclude that diet is asatisfactory treatment for all hyperactivechildren. Although efforts were made to recruitan unbiased sample in our second study, thiswas only partially successful. Our group stillincluded a high proportion of children withphysical symptoms and of parents who wereparticularly interested in following a dietaryapproach.

Diagnostic uncertainties also lead to somedoubt about the group of children to whom theresults can be generalised. We chose the DSMIII definition of attention deficit disorder withhyperactivity as a robust and widely studieddefinition. Some people, however, will applythe word 'hyperactivity' either to a wider groupof children with high scores on questionnaireratings, or to a narrower group of children withhyperkinetic disorder who are also more bio-logically impaired.22 It is not likely that theprecise psychiatric manifestation is the key toidentifying a diet sensitive group, however.Severity of hyperactivity did not predict out-come in this series. European clinicians shouldnote that the group with 'attention deficit' inthis report would often receive a clinical diag-nosis of conduct disorder.23The ways in which diet worked remain

unclear. Toxic, pharmacological, or allergicmechanisms could be involved, and thephysiological effects of different foods may

vary. It is conceivable that foods might inducechanges in brain perfusion similar to thosereported in attention deficit disorder by Lou etal.24 These results argue against the notion thatthe only mechanism involved is the 'placeboeffect' of expectation and suggestion, and test-ing this was a main purpose of the study. Theresults do not exclude the possibility of indirectmechanisms via bodily symptoms rather thaneffects on brain function. The finding of asimilar effect size in children with and withoutphysical symptoms is circumstantial evidenceagainst such an explanation, but does not ruleit out because full physical evaluation mightreveal worsening of physical illness due tofoodstuffs with behavioural changes secondaryto feeling ill and because the children hadalready been selected as responders by theopen phase of the trial.The treatment, as applied in this study, has

disadvantages. It is a difficult and exactingregimen which puts a considerable strain on thewhole family. It is not yet clear whether modi-fied diets can also be effective. In this study andour previous work,4 the same foods were foundto be most commonly implicated. It may there-fore be possible to devise a less restricted dietwith similar levels of success. It seems clear,from the small number of children reactingonly to additives at the open stage, that an addi-tive free diet by itself would be of little benefit.

There are some indications from this studythat the symptoms showing change are not theattention deficit that is considered to be thecore of hyperactivity, but rather irritability.Many parents commented after the few fooddiet phase that their children had become moremanageable and more amenable to reasoning

rather than less active or better able to concen-trate.

In conclusion, this confirms and extendsresults obtained in an earlier study4 that dietcan be shown to affect some children in adouble blind placebo controlled trial, but thatdietary management is difficult to carry out. Itis still not clear how generally applicable such atreatment might be within a general group ofhyperactive children. There are indications thatif parents notice some effects of diet, effortsshould be made to support their exploration ofexclusion diets. Further research could focuson the development and assessment of a modi-fied diet based on the avoidance of the mostcommonly implicated foods, on the possibilityof mediation by physical symptoms, and on anyphysical basis of the behavioural reaction inchildren showing sensitivity to specific foods.

The authors are grateful to Action Research and the TrusteeSavings Bank for financial support, to Rowntrees plc forsupplying food colours, to Lilly Industries Ltd for supplyingcapsules for food colours, and to the children and familiesinvolved in the study who coped enthusiastically with thedemands we made on them.

1 Feingold BF. Hyperkinesis and learning disabilities linkedto artificial food flavours and colors. Am J Nurs 1975; 75:797-803.

2 Taylor E. Toxins and allergens. In: Rutter M, Casaer P, eds.Biological risk factors for psychosocial disorders. New York:Academic Press, 1992: 219-32.

3 Weiss B, Williams JH, MargenS, et al. Behavioural responseto artificial food colours. Science 1980; 207: 1487-9.

4 Egger J,Carter CM, Graham PJ, Gumley D, Soothill JF.Controlled trial of oligoantigenic treatment in the hyper-kinetic syndrome. Lancet 1985; i: 540-5.

5 David TJ. Reactions to dietary tartrazine. Arch Dis Child1987; 62: 119-22.

6 Rowe KS. Synthetic food colourings and 'hyperactivity': adouble blind crossover study. Australian PaediatricJournal1988; 24: 143-7.

7 Pollock I, Warner JO. Effect of artificial food colours onchildhood behaviour. Arch Dis Child 1990; 65: 74-7.

8 Kaplan BJ, McNicol J, Conte RA, Moghadam HK. Dietaryreplacement in preschool-aged hyperactive boys. Pediatrics1989;83:7-17.

9 EggerJ, Stolla A, McEwen LM. Controlled trial of hyposen-sitisation in children with food induced hyperkineticsyndrome. Lancet 1992; 339: 1150-3.

10 American Psychiatric Association. Diagnostic and statisticalmanual of mental disorders. 3rd Ed. Washington, DC: APA,1980.

11 Conners CK. Rating scales for use in drug studies withchildren. Psychopharmacol Bull 1973; 9: 24-8.

12 Wechsler D. The Wechsler intelligence scale for children-revised. New York: Psychological Corporation, 1974.

13 Wechsler D.The Wechsler preschool and primary scak of intel-ligence. New York: Psychological Corporation, 1969.

14 Neale MD. Neale analysis of reading ability. 2nd Ed. NewYork: Macmillan, 1968.

15 Quinton D, Rutter M, Little C. Institutional rearing,parenting difficulties and marital support. Psychol Med1984; 14: 107-24.

16 Carter CM, Egger J, SoothillFJ. A dietary management ofsevere childhood migraine. Human Nutrition: AppliedNutrition1985; 39A: 294-303.

17 Taylor E. Attention deficit. In: Taylor E, ed. The overactivechild. London: MacKeith Press/Blackwell, 1986: 73-106.(Clinics in developmental medicine No 97.)

18 SwansonJ, Kinsbourne M. Stimulant related state-dependentlearning in hyperactive children. Science 1976; 192: 1354-6.

19 Cairns E, Cammock T. Development of a more reliable ver-sion of the matching familiar figures test. DevelopmentalPsychology 1978; 14: 555-60.

20 Cohen NJ, Minde K.The'hyperactive syndrome' inlknder-garten children. Comparison of children with pervasiveand situational syndromes. J Child Psychol Psychiatry1983; 24: 443-56.

21 Hills M, Armitage P. The two period cross-over clinical_trial.BrJ Clin Pharnacol1979; 8: 7-20.22 Taylor E,SandbergS, ThorleyG, Giles S. The epidemiology

ofchidhood hyperactivity. Oxford: Oxford University Press,1991. (Maudsley monographs No 33.)

23 Prendergast M, Taylor E, RapoportJL, et al. The diagnosisof childhood hyperactivity: a US-UK cross-national studyof DSM-III and ICD-9.Y Child Psychol Psychiatry 1988;29: 289-300.

24 Lou HC, HenriksenL, Bruhn P. Focal cerebral dysfunctionin developmental learningdifficulties. Lancet 1990; 335:8-11.

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