The Lancet, Volume 354, Number 9182
11 September 1999
By Andrew J Wakefield
Departments of Medicine and Histopathology, Royal Free and
University College Medical School, Hampstead, London NW3 2PF, UK
Sir--Hypothesis testing and presentation of the outcome--either positive or
negative--is a fundamental part of the scientific process. Accordingly we have
published studies that both do,1 and do not2 support a
role for measles virus in chronic intestinal inflammation: this is called
integrity. The latest of these studies was strongly positive,3 and
was accepted by the MRC Review in February, 1998. By contrast, Brent Taylor and
colleagues (June 12, p 2026)4 have ignored the rules. They are
inappropriately didactic in their conclusions, despite the weakness of their
method and the contradictions in their data. A case-series analysis is unlikely
to identify a relation between exposure and disease, in which the onset is
insidious and in which, very often, there is diagnostic delay.
Taylor et al tested the hypothesis that there should be no temporal clustering
of first parenteral concerns with measles, mumps, and rubella (MMR) vaccination.
They identified a statistically significant excess risk by 6 months after MMR,
which they dismiss, post hoc, as indicating parental recall bias. Had this been
the case it should have been seen in both of their vaccine groups--those
receiving MMR and those receiving any measles-containing vaccine. The excess
risk was seen only in the MMR group; this is a fundamental flaw.
Temporal trends for autism in the USA (California*) and the UK
In 1998 the expected numbers of newly diagnosed autistic children in California
should have been 105-263 cases, according to DSM-IV; the actual figure was 1685
new cases. The temporal trend in north-west London is almost identical, although
the rise is delayed by about 10 years. The two countries use the same diagnostic
criteria. The sequential trends are consistent with the timing of introduction
of MMR to both regions.
*Data from Department of Developmental Services, Sacramento, 1987-98 (www.dds.ca.gov).
However, it pales into insignificance compared with their failure to declare the
fact of an MMR catch-up campaign that was initiated in 1988 with the
introduction of this vaccine. This campaign was targeted at children, whatever
their age, who presumably had not received either monovalent mumps or rubella
vaccine whatever their exposure status. As such it was a novel and, in terms of
safety, untested policy. On the basis of Taylor and colleagues' inclusion
criteria, and taking account of the catch-up campaign, then those first birth
cohorts who actually received MMR (circa 1986) were precisely those in whom a
doubling of the numbers of cases of autism were seen. Thereafter these numbers
continue to increase strikingly. Omission of this essential fact--the catch-up
campaign--requires explanation lest it be misconstrued.
Can the dramatic increase in autism be ascribed to change in diagnostic
practice? Data from the recent California report from the Office of
Developmental Services belie this contention. The figure juxtaposes the data
from California with those from north-west London. Identical temporal trends are
shown, with the rise in autism from a steady baseline value, coinciding with the
introduction of MMR vaccine as the single strategy in both countries that use
the same diagnostic criteria for autism.
These data expose the danger of not only setting out to prove, rather than to
test, hypotheses but also presenting the data whether they are supportive or
not. The full story has yet to unfold. In a timely BMJ newspeice,5
Begg who is described as a leading virologist, calls for MMR research to be
terminated on the basis of Taylor and co-workers' report and a non-peer-reviewed
so-called analysis in Current Problems of Pharmacovigilance. Clearly
there are some things that may end-up being terminated as a consequence of these
events: research into the possible link between MMR, autism, and bowel disease
is not one of them.
Andrew J Wakefield
Departments of Medicine and Histopathology, Royal Free and University College
Medical School, Hampstead, London NW3 2PF, UK
1 Lewin J, Dhillon AP, Sim R, Mazure G, Pounder RE, Wakefield AJ. Persistent
measles virus infection of the intestine: confirmation by immunogold electron
microscopy. Gut 1995; 36: 564-69. [PubMed]
2 Chadwick N, Bruce IJ, Schepelman S, Pounder RE, Wakefield AJ. Measles virus
RNA is not detected in inflammatory bowel disease using hybrid capture and
reverse transcription followed by polymerase chain reaction. J Med
Virol 1998; 70: 305-11. [PubMed]
3 Montgomery SM, Morris DL, Pounder RE, et al. Paramyxovirus infections in
childhood and subsequent inflammatory bowel disease. Gastroenterology 1999; 116: 796-803. [PubMed]
4 Taylor B, Miller E, Farringdon CP, et al. MMR vaccine and autism: no
epidemiological evidence for a causal association. Lancet 1999; 353: 2026-29. [Text]
5 Bower H. New research demolishes link between MMR vaccine and autism. BMJ
1999; 318: 1643.
hyperplasia, non-specific colitis, and pervasive developmental disorder in
A J Wakefield, S H Murch, A Anthony, J Linnell, D M Casson,
M Malik, M Berelowitz, A P Dhillon, M A Thomson, P Harvey, A Valentine, S E
Davies, J A Walker-Smith
Inflammatory Bowel Disease Study Group, University Departments of
Medicine and Histopathology (A J Wakefield FRCS, A Anthony MB, J Linnell
PhD, A P Dhillon MRCPath, S E Davies MRCPath) and the University Departments
of Paediatric Gastroenterology (S H Murch MB, D M Casson MRCP, M Malik MRCP,
M A Thomson FRCP, J A Walker-Smith FRCP,), Child and Adolescent Psychiatry (M
Berelowitz FRCPsych), Neurology (P Harvey FRCP), and Radiology (A
Valentine FRCR), Royal Free Hospital and School of Medicine, London NW3 2QG,
Correspondence to: Dr A J Wakefield
Patients and methods
Background We investigated a consecutive series of children with chronic
enterocolitis and regressive developmental disorder.
Methods 12 children (mean age 6 years [range 3-10], 11 boys) were
referred to a paediatric gastroenterology unit with a history of normal
development followed by loss of acquired skills, including language, together
with diarrhoea and abdominal pain. Children underwent gastroenterological,
neurological, and developmental assessment and review of developmental records.
Ileocolonoscopy and biopsy sampling, magnetic-resonance imaging (MRI),
electroencephalography (EEG), and lumbar puncture were done under sedation.
Barium follow-through radiography was done where possible. Biochemical,
haematological, and immunological profiles were examined.
Findings Onset of behavioural symptoms was associated, by the parents,
with measles, mumps, and rubella vaccination in eight of the 12 children, with
measles infection in one child, and otitis media in another. All 12 children had
intestinal abnormalities, ranging from lymphoid nodular hyperplasia to aphthoid
ulceration. Histology showed patchy chronic inflammation in the colon in 11
children and reactive ileal lymphoid hyperplasia in seven, but no granulomas.
Behavioural disorders included autism (nine), disintegrative psychosis (one),
and possible postviral or vaccinal encephalitis (two). There were no focal
neurological abnormalities and MRI and EEG tests were normal. Abnormal
laboratory results were significantly raised urinary methylmalonic acid compared
with age-matched controls (p=0·003), low haemoglobin in four children, and a
low serum IgA in four children.
Interpretation We identified associated gastrointestinal disease and
developmental regression in a group of previously normal children, which was
generally associated in time with possible environmental triggers.
Lancet 1998; 351: 637-41
We saw several children who, after a period of apparent normality, lost
acquired skills, including communication. They all had gastrointestinal
symptoms, including abdominal pain, diarrhoea, and bloating and, in some cases,
food intolerance. We describe the clinical findings, and gastrointestinal
features of these children.
Patients and methods
12 children, consecutively referred to the department of paediatric
gastroenterology with a history of a pervasive developmental disorder with loss
of acquired skills and intestinal symptoms (diarrhoea, abdominal pain, bloating
and food intolerance), were investigated. All children were admitted to the ward
for 1 week, accompanied by their parents.
We took histories, including details of immunisations and exposure to
infectious diseases, and assessed the children. In 11 cases the history was
obtained by the senior clinician (JW-S). Neurological and psychiatric
assessments were done by consultant staff (PH, MB) with HMS-4 criteria.1
Developmental histories included a review of prospective developmental records
from parents, health visitors, and general practitioners. Four children did not
undergo psychiatric assessment in hospital; all had been assessed professionally
elsewhere, so these assessments were used as the basis for their behavioural
After bowel preparation, ileocolonoscopy was performed by SHM or MAT under
sedation with midazolam and pethidine. Paired frozen and formalin-fixed mucosal
biopsy samples were taken from the terminal ileum; ascending, transverse,
descending, and sigmoid colons, and from the rectum. The procedure was recorded
by video or still images, and were compared with images of the previous seven
consecutive paediatric colonoscopies (four normal colonoscopies and three on
children with ulcerative colitis), in which the physician reported normal
appearances in the terminal ileum. Barium follow-through radiography was
possible in some cases.
Also under sedation, cerebral magnetic-resonance imaging (MRI),
electroencephalography (EEG) including visual, brain stem auditory, and sensory
evoked potentials (where compliance made these possible), and lumbar puncture
Thyroid function, serum long-chain fatty acids, and cerebrospinal-fluid lactate
were measured to exclude known causes of childhood neurodegenerative disease.
Urinary methylmalonic acid was measured in random urine samples from eight of
the 12 children and 14 age-matched and sex-matched normal controls, by a
modification of a technique described previously.2 Chromatograms were
scanned digitally on computer, to analyse the methylmalonic-acid zones from
cases and controls. Urinary methylmalonic-acid concentrations in patients and
controls were compared by a two-sample t test. Urinary creatinine was
estimated by routine spectrophotometric assay.
Children were screened for antiendomyseal antibodies and boys were screened
for fragile-X if this had not been done before. Stool samples were cultured for Campylobacter
spp, Salmonella spp, and Shigella spp and assessed by
microscopy for ova and parasites. Sera were screened for antibodies to Yersinia
Formalin-fixed biopsy samples of ileum and colon were assessed and reported
by a pathologist (SED). Five ileocolonic biopsy series from age-matched and
site-matched controls whose reports showed histologically normal mucosa were
obtained for comparison. All tissues were assessed by three other clinical and
experimental pathologists (APD, AA, AJW).
Ethical approval and consent
Investigations were approved by the Ethical Practices Committee of the Royal
Free Hospital NHS Trust, and parents gave informed consent.
Clinical details of the children are shown in tables 1 and 2. None had
neurological abnormalities on clinical examination; MRI scans, EEGs, and
cerebrospinal-fluid profiles were normal; and fragile X was negative.
Prospective developmental records showed satisfactory achievement of early
milestones in all children. The only girl (child number eight) was noted to be a
slow developer compared with her older sister. She was subsequently found to
have coarctation of the aorta. After surgical repair of the aorta at the age of
14 months, she progressed rapidly, and learnt to talk. Speech was lost later.
Child four was kept under review for the first year of life because of wide
bridging of the nose. He was discharged from follow-up as developmentally normal
at age 1 year.
Table 1: Clinical details and laboratory, endoscopic, and histological
All children were antiendomyseal-antibody negative and common enteric
pathogens were not identified by culture, microscopy, or serology. Urinary
methylmalonic-acid excretion was significantly raised in all eight children who
were tested, compared with age-matched controls (p=0·003; figure 1). Abnormal
laboratory tests are shown in table 1.
Figure 1: Urinary methylmalonic-acid excretion in patients and controls
p=Significance of mean excretion in patients compared with controls.
The caecum was seen in all cases, and the ileum in all but two cases.
Endoscopic findings are shown in table 1. Macroscopic colonic appearances were
reported as normal in four children. The remaining eight had colonic and rectal
mucosal abnormalities including granularity, loss of vascular pattern, patchy
erythema, lymphoid nodular hyperplasia, and in two cases, aphthoid ulceration.
Four cases showed the "red halo" sign around swollen caecal lymphoid
follicles, an early endoscopic feature of Crohn's disease.3 The most
striking and consistent feature was lymphoid nodular hyperplasia of the terminal
ileum which was seen in nine children (figure 2), and identified by barium
follow-through in one other child in whom the ileum was not reached at endoscopy.
The normal endoscopic appearance of the terminal ileum (figure 2) was seen in
the seven children whose images were available for comparison.
Figure 2: Endoscopic view of terminal ilium in child three and in a child
with endoscopically and histologically normal ileum and colon
Greatly enlarged lymphoid nodule in right-hand field of view. A and B=child
three; C=normal ileum. Remainder of mucosal surface of` terminal ileum is a
carpet of enlarged lymphoid nodules.Histological findings
Histological findings are summarised in table 1.
Terminal ileum A reactive lymphoid follicular hyperplasia was present
in the ileal biopsies of seven children. In each case, more than three expanded
and confluent lymphoid follicles with reactive germinal centres were identified
within the tissue section (figure 3). There was no neutrophil infiltrate and
granulomas were not present.
Figure 3: Biopsy sample from terminal ileum (top) and from colon (bottom)
A=child three; lymphoid hyperplasia with extensive, confluent lymphoid
nodules. B=child three; dense infiltration of the lamina propria crypt
epithelium by neutrophils and mononuclear cells. Stained with haematoxylin and
Colon The lamina propria was infiltrated by mononuclear cells (mainly
lymphocytes and macrophages) in the colonic-biopsy samples. The extent ranged in
severity from scattered focal collections of cells beneath the surface
epithelium (five cases) to diffuse infiltration of the mucosa (six cases). There
was no increase in intraepithelial lymphocytes, except in one case, in which
numerous lymphocytes had infiltrated the surface epithelium in the proximal
colonic biopsies. Lymphoid follicles in the vicinity of mononuclear-cell
infiltrates showed enlarged germinal centres with reactive changes that included
an excess of tingible body macrophages.
There was no clear correlation between the endoscopic appearances and the
histological findings; chronic inflammatory changes were apparent histologically
in endoscopically normal areas of the colon. In five cases there was focal acute
inflammation with infiltration of the lamina propria by neutrophils; in three of
these, neutrophils infiltrated the caecal (figure 3) and rectal-crypt
epithelium. There were no crypt abscesses. Occasional bifid crypts were noted
but overall crypt architecture was normal. There was no goblet-cell depletion
but occasional collections of eosinophils were seen in the mucosa. There were no
granulomata. Parasites and organisms were not seen. None of the changes
described above were seen in any of the normal biopsy specimens.
We describe a pattern of colitis and ileal-lymphoid-nodular hyperplasia in
children with developmental disorders. Intestinal and behavioural pathologies
may have occurred together by chance, reflecting a selection bias in a
self-referred group; however, the uniformity of the intestinal pathological
changes and the fact that previous studies have found intestinal dysfunction in
children with autistic-spectrum disorders, suggests that the connection is real
and reflects a unique disease process.
Asperger first recorded the link between coeliac disease and behavioural
psychoses.4 Walker-Smith and colleagues5 detected low
concentrations of alpha-1 antitrypsin in children with typical autism, and
D'Eufemia and colleagues6 identified abnormal intestinal
permeability, a feature of small intestinal enteropathy, in 43% of a group of
autistic children with no gastrointestinal symptoms, but not in matched
controls. These studies, together with our own, including evidence of anaemia
and IgA deficiency in some children, would support the hypothesis that the
consequences of an inflamed or dysfunctional intestine may play a part in
behavioural changes in some children.
The "opioid excess" theory of autism, put forward first by Panksepp
and colleagues7 and later by Reichelt and colleagues8 and
Shattock and colleagues9 proposes that autistic disorders result from
the incomplete breakdown and excessive absorption of gut-derived peptides from
foods, including barley, rye, oats, and caesin from milk and dairy produce.
These peptides may exert central-opioid effects, directly or through the
formation of ligands with peptidase enzymes required for breakdown of endogenous
central-nervous-system opioids,9 leading to disruption of normal
neuroregulation and brain development by endogenous encephalins and endorphins.
One aspect of impaired intestinal function that could permit increased
permeability to exogenous peptides is deficiency of the phenyl-sulphur-transferase
systems, as described by Waring.10 The normally sulphated
glycoprotein matrix of the gut wall acts to regulate cell and molecular
trafficking.11 Disruption of this matrix and increased intestinal
permeability, both features of inflammatory bowel disease,17 may
cause both intestinal and neuropsychiatric dysfunction. Impaired enterohepatic
sulphation and consequent detoxification of compounds such as the phenolic
amines (dopamine, tyramine, and serotonin)12 may also contribute.
Both the presence of intestinal inflammation and absence of detectable
neurological abnormality in our children are consistent with an exogenous
influence upon cerebral function. Lucarelli's observation that after removal of
a provocative enteric antigen children achieved symptomatic behavioural
improvement, suggests a reversible element in this condition.13
Despite consistent gastrointestinal findings, behavioural changes in these
children were more heterogeneous. In some cases the onset and course of
behavioural regression was precipitous, with children losing all communication
skills over a few weeks to months. This regression is consistent with a
disintegrative psychosis (Heller's disease), which typically occurs when
normally developing children show striking behaviour changes and developmental
regression, commonly in association with some loss of coordination and bowel or
bladder function.14 Disintegrative psychosis is typically described
as occurring in children after at least 2-3 years of apparently normal
Disintegrative psychosis is recognised as a sequel to measles encephalitis,
although in most cases no cause is ever identified.14 Viral
encephalitis can give rise to autistic disorders, particularly when it occurs
early in life.15 Rubella virus is associated with autism and the
combined measles, mumps, and rubella vaccine (rather than monovalent measles
vaccine) has also been implicated. Fudenberg16 noted that for 15 of
20 autistic children, the first symptoms developed within a week of vaccination.
Gupta17 commented on the striking association between measles, mumps,
and rubella vaccination and the onset of behavioural symptoms in all the
children that he had investigated for regressive autism. Measles virus18,19
and measles vaccination20 have both been implicated as risk factors
for Crohn's disease and persistent measles vaccine-strain virus infection has
been found in children with autoimmune hepatitis.21
We did not prove an association between measles, mumps, and rubella vaccine
and the syndrome described. Virological studies are underway that may help to
resolve this issue.
If there is a causal link between measles, mumps, and rubella vaccine and
this syndrome, a rising incidence might be anticipated after the introduction of
this vaccine in the UK in 1988. Published evidence is inadequate to show whether
there is a change in incidence22 or a link with measles, mumps, and
rubella vaccine.23 A genetic predisposition to autistic-spectrum
disorders is suggested by over-representation in boys and a greater concordance
rate in monozygotic than in dizygotic twins.15 In the context of
susceptibility to infection, a genetic association with autism, linked to a null
allele of the complement (C) 4B gene located in the class III region of
the major-histocompatibility complex, has been recorded by Warren and
colleagues.24 C4B-gene products are crucial for the activation
of the complement pathway and protection against infection: individuals
inheriting one or two C4B null alleles may not handle certain viruses
appropriately, possibly including attenuated strains.
Urinary methylmalonic-acid concentrations were raised in most of the
children, a finding indicative of a functional vitamin B12 deficiency. Although
vitamin B12 concentrations were normal, serum B12 is not a good measure of
functional B12 status.25 Urinary methylmalonic-acid excretion is
increased in disorders such as Crohn's disease, in which cobalamin excreted in
bile is not reabsorbed. A similar problem may have occurred in the children in
our study. Vitamin B12 is essential for myelinogenesis in the developing central
nervous system, a process that is not complete until around the age of 10 years.
B12 deficiency may, therefore, be a contributory factor in the developmental
We have identified a chronic enterocolitis in children that may be related to
neuropsychiatric dysfunction. In most cases, onset of symptoms was after
measles, mumps, and rubella immunisation. Further investigations are needed to
examine this syndrome and its possible relation to this vaccine.
Up to Jan 28, a further 40 patients have been assessed; 39 with the syndrome.
A J Wakefield was the senior scientific investigator. S H Murch and M A
Thomson did the colonoscopies. A Anthony, A P Dhillon, and S E Davies carried
out the histopathology. J Linnell did the B12 studies. D M Casson and M Malik
did the clinical assessment. M Berelowitz did the psychiatric assessment. P
Harvey did the neurological assessment. A Valentine did the radiological
assessment. JW-S was the senior clinical investigator.
This study was supported by the Special Trustees of Royal Free Hampstead NHS
Trust and the Children's Medical Charity. We thank Francis Moll and the nursing
staff of Malcolm Ward for their patience and expertise; the parents for
providing the impetus for these studies; and Paula Domizo, Royal London NHS
Trust, for providing control tissue samples.
1 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). 4th edn.
Washington DC, USA: American Psychiatric Association, 1994.
2 Bhatt HR, Green A, Linnell JC. A sensitive micromethod for the routine
estimations of methylmalonic acid in body fluids and tissues using thin-layer
chromatography. Clin Chem Acta 1982; 118: 311-21. [PubMed]
3 Fujimura Y, Kamoni R, Iida M. Pathogenesis of aphthoid ulcers in Crohn's
disease: correlative findings by magnifying colonoscopy, electromicroscopy, and
immunohistochemistry. Gut 1996; 38: 724-32. [PubMed]
4 Asperger H. Die Psychopathologie des coeliakakranken kindes. Ann
Paediatr 1961; 197: 146-51. [PubMed]
5 Walker-Smith JA, Andrews J. Alpha-1 antitrypsin, autism and coeliac
disease. Lancet 1972; ii: 883-84.
6 D'Eufemia P, Celli M, Finocchiaro R, et al. Abnormal intestinal
permeability in children with autism. Acta Paediatrica 1996; 85: 1076-79. [PubMed]
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8 Reichelt KL, Hole K, Hamberger A, et al. Biologically active
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hyperplasia, non-specific colitis, and pervasive developmental disorder in
The Lancet, Volume 352, Number 9123,
18 July 1998
J Wakefield and co-workers1 have
identified a new relation between gastrointestinal
disease and developmental disorders in children; it
opens a new avenue for the study of the gastrointestinal
tract and other diseases that may be immunologically
mediated. Their findings of ileal-lymphoid-nodular
hyperplasia and non-specific colitis gastrointestinal
manifestations in connection with autistic-spectrum
disorders is the first description of this relation,
with strong data suggesting the anatomical and
histological alteration of the gut in such disorders.
Although these workers suggest possible mechanism(s) of
increased permeability for exogenous molecules they do
not offer any explanation for these gastrointestinal
alterations. The endoscopic and histopathological
findings of ileal-lymphoid-nodular hyperplasia and
non-specific colitis have so far escaped explanation and
have evaded pathogenetic definition.
In support of the findings of Wakefield et al are
several behavioural and clinical features known to be
related to the central nervous system (CNS), such as
migraine,2 infantile colic,3
abdominal epilepsy,4 allergic-tension-fatigue
syndrome, and attention-deficit-hyperactivity disorder,5
which have been related to food allergy, although the
precise relation is still unclear. IgE-mediated food
allergy is plainly not the only mechanism of tissue
injury, and these specific disorders could involve other
A major investigative effort of our laboratories has
been directed to the study of food allergy and the
immunological involvement of the gut as a central focus
for injury of other target organs (skin, lungs, and
gastrointestinal tract). We have noted a striking
appearance of ileal-lymphoid-nodular hyperplasia in
patients with non-IgE-mediated food allergy who present
with asthma, atopic dermatitis, and
attention-deficit-hyperactivity disorder. We have also
studied two patients with this hyperactive disorder who
were allergic to various foods, and our findings
obtained by colonoscopy of their terminal ileum, shown
in the figure, match with those reported by Wakefield
Endoscopic view of terminal ileum in child with
Greatly enlarged lymphoid nodules in both fields of
In our study, ileal-lymphoid-nodular hyperplasia is the
hallmark lesion of the gastrointestinal tract, which
allows entry of antigens across the inflamed mucosa of
the bowel as a result of the reactive inflammatory
response in the adjacent lymphoid tissue of Peyer's
patches in patients with non-IgE-mediated food allergy.
We propose that similar mechanism(s) may be involved in
the pathogenesis of the CNS dysfunction in the patients
described by Wakefield and co-workers.1
Although Wakefield's study, which suggests a
connection between the CNS and the gut in patients
previously immunised with measles, mumps, and rubella
vaccine, did not prove an association, it has stimulated
further discussion and opened unanticipated lines of
investigation concerning the role of ileal-lymphoid-nodular
hyperplasia as a predictive marker of gastrointestinal
inflammation responsible for immunologically mediated
tissue injury in other target organs sites.
*Aderbal Sabra, Joseph A Bellanti, Angel R Colón
*International Center for Interdisciplinary Studies
of Immunology, and Department of Pediatrics, Georgetown
University Medical Center, Washington, DC 20007, USA
1 Wakefield AJ, Murch SH, Anthony A, et al. Ileal-lymphoid-nodular
hyperplasia, non-specific colitis, and pervasive
developmental disorder in children. Lancet 1998; 351: 63741. [Text]
2 Egger G, Carter CM, Wilson J, Turner MW, Soothill JF.
Is migraine food allergy? Lancet 1983 ii: 86569.
3 Hewson P, Oberklaid F, Menahen S. Infant colic,
distress and crying. Clin Pediatr 1987; 26: 6976. [PubMed]
4 Senanayake N. "Eating epilepsy"--a
reappraisal. Epilepsy Res 1990; 5: 7479. [PubMed]
5 Egger G, Stolla A, McEven L. Controlled trial of
hyposensitization in children with food induced
hypercinetic syndrome. Lancet 1992; 339: 115053. [PubMed]