Autism in Thalidomide

In the late 1950s thalidomide was synthesized and independently introduced in Germany, Great Britain and Japan as a potent sedative drug with few negative side-effects. In 1961 reports came from Germany, Australia and Great Britain (Kosenow and Pfeiffer 1961, MsBride 1961, Wiedeman 1961, Lenz 1962, Smithells 1962) that children were being born with serious malformations that might be associated with the mother's intake of thalidomide during pregnancy. The drug was withdrawn from the market in late 1961, but was still prescribed in Japan until September 1962. Approximately 5000 children with thalidomide defects were observed in West Germany; Japan and Great Britain each had around 700 cases, and thalidomide embryopathy was reported from another 26 countries (Kajii 1965). In Sweden approximately 150 children were affected, but about onethird of these died from serious birth defects in early infancy (Winberg 19640, b). Approximately 100 Swedes suffering from thalidomide embryopathy are alive today. The most frequent anomalies that affected the children were upperand lower-limb defects, but other organ systems (such as the ears, heart, kidneys and genitals) were also shown to be involved. Based on studies of the exact time of ingestion of thalidomide (Lenz and Knapp 1962, Nowack 1965), the sensitive period for the teratogenicity of the drug was considered to be 20 to 36 days after conception (35 to 51 days from the first day of the last menstrual period). The effects on different organs according to exact time of ingestion of thalidomide have been analysed in some detail (Fig. 1). Anomalies of the ears and cranial nerves, and deformities of the thumbs and upper limbs, were shown to be induced in the early teratogenic period of thalidomide, while defects of the lower limbs and triphalangism of the thumbs originated later in the sensitive period.