News for the practitioner
European Journal of Pediatrics
(1992) 151: 864-865

Hyposensitisation in children
with food-induced hyperkinetic syndrome

Background. The hyperkinetic syndrome is a childhood disorder chracterized by short attention span, distractibility, impulsivity and poorly organised overactivity. Food intolerance has been reported as one of its causes and improvement has been reported to result from the avoidance of provking foods. Based on th hypothesis tat the hyperkinetic syndrome is an allergic reaction to certain foods, desensitisation was attempted in 40 hyperkinetic children.1

Subjects and methods. Diagnosis was established according to the criteria of the diagnostic and statistical manual of mental disorders of the American Psychiatric Association. The children had a more than 1-year history of hyperactive behaviour and a score of more than 15 on the short form of the Conners' scale. This scoring system consists of ten items of behaviour and assesses behaviour at home. A score of more than 14 indicates abnormal hyperkinetic behaviour.

A group of 185 patients with hyperkinetic syndrome received an oligo-antigenic diet for 4 weeks. Those patients (116) whom parents and teachers judged to have improved with a fall of the Conners' score below 15, were challenged with varying types of foods. Provoking foods were identified by their sequential reintroduction into the oligo-antigenic diet. If hyperkinetic behaviour reappeared with a certain type of food, it was subsequently avoided.

Out of this group, 40 patients with impressive change on diet entered a double-blind, placebo-controlled trial of enzyme-potentiated desensitisation. All but 4 had associated symptoms such as recurrent headaches or recurrent abdominal symptoms in addition to overactivity. Every patient received three intradermal injections of ß-glucuronidase and a mixture of specific food extracts or three injections of placebo. Three weeks after the third injection, foods shown to provoke symptoms before the trial were reintroduced and children's behaviour was again assessed. Parents were told that when food-related symptoms recurred and persisted for 24 h they should stop the food. Results were analysed for stopping the first food given in the active and placebo group. When all foods were reintroduced the parents were asked whether the treatment had been successful.

Results. Of the 20 actively treated patients, 15 were able to continue the first reintroduced food compared to 7 in the placebo-treated group. At the end of the study parents of 16 actively treated patients thought the treatment successful versus 4 in the placebo group. Both differences were statistically significant. Offending foods included chocolate, colourings, cow milk, egg, citrus, wheat, nuts, cheese, banana, tomato, apple, pears, beef, pork and beans.

Conclusion. The results support the notion that food allergy is a possible mechanism of the hyperkinetic syndrome. Enzyme-potentiated desensitisation seems to suppress adverse effects of provoking foods.

Comments. Various mechanisms have been suggested to account for hyperactive reactions to foods or food ingredients. Results of the present study suggest that allergic mechanisms may be involved. However, hyperactive behaviour with increased impulsivity and decreased attention span is by no means an aetiologically or pathogenetically defined entity but a heterogeneous symptom complex. Even if organic brain damage has been excluded and the diagnosis has been restricted to mentally normal children with 'true' (primary) hyperactivity, the therapeutic success of behaviour modification or psycho-stimulant medication in many patients points to the importance of psychogenic factors as does the apparent effect of placebo treatment in the present study.

Reference:
1. Egger J, Stolla A, McEwen LM (1992). Controlled trial of hypo-sensitisation in children with food-induced hyperkinetic syndrome. Lancet I: 1150-1153.