Few documented cases of Riley-Day syndrome fulfilling current diagnostic criteria have been recognized in non-Jews. In our case the diagnosis was established in a Norwegian child despite the absence of Jewish origin. It represents a report of this syndrome with bilateral pathological changes in the hypothalamus in addition to extensive abnormal findings in the spinal cord and the autonomic ganglia. These findings may have significance with regard to the pathogenesis of the disease.

In this placebo-controlled study, multiple doses of secretin did not produce any symptomatic improvement.

Dramatic effects on autistic behaviour after repeated injections of the gastrointestinal hormone secretin have been referred in a number of case reports. In the absence of curative and effective treatments for this disabling condition, this information has created new hope among parents. Although controlled studies on the effect of mainly one single dose have not documented any effect, many children still continue to receive secretin. Six children enrolled in a double‐blind, placebo‐controlled crossover study in which each child was its own control. Human synthetic secretin, mean dose 3.4 clinical units, and placebo were administered intravenously in randomized order every 4th wk, on three occasions each. The measurement instruments were the visual analogue scale (VAS) and the aberrant behaviour checklist (ABC). Statistically significant differences were found for placebo in 3 out of 6 children and for secretin in one child, using parental ratings only (VAS scores). Differences were small and lacked clinical significance, which was in accordance with the overall impression of the parents and teachers and visual inspection of graphs. Conclusion: In this placebo‐controlled study, multiple doses of secretin did not produce any symptomatic improvement.

Amniocentesis and culturing of amniotic fluid cells were performed in the sixteenth week of two subsequent pregnancies in a woman who had previously given birth to two children with metachromatic leucodystrophy. On both occasions, amniotic fluid cells deficient in arylsulphatase A were found and the diagnosis was confirmed in the aborted fetuses.

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