Plenary lecture by Herman van Engeland, ESCAP 2009 Budapest
ESCAP 2009 Congress in Budapest, Hungary: original abstract by professor Herman van Engeland (Netherlands) – “Autism and Schizophrenia: a Reappraisal.” Plenary Session V., 24 August 2009, 09:00, Chaired by H. Remschmidt (Germany).
In DSM II  autism was considered to be an early form of schizophrenia. In DSM III  the concept „pervasive developmental disorder” was introduced and autism was considered to be a prototype of these pervasive developmental disorders and was unambiguously demarcated from childhood schizophrenia. The diagnosis of autism excludes a diagnosis schizophrenia and longitudinal research revealed that children with autism were not at increased risk of schizophrenia later in life. This „splitting” approach which is the basis of the current DSM classification, has led to classifying diagnostic approach practice with a high degree of interrater reliability, allowing great advances in epidemiological and biological research. However, recent research findings question the [biological] validity of the categorical classification systems in Psychiatry and the rigorous demarcation between autism and schizophrenia:
1. Parents with schizophrenia have an increased risk of offspring with autism. Youngsters with early onset schizophrenia often have a prior diagnosis in the autism spectrum.
2. Children with atypical autism have a greatly increased risk of schizophrenia.
3. In some genetic syndromes, such as Klinefelters syndrome and the 22q11.2 deletion syndrome, autism and schizophrenia do co- occur in the same child.
An increased number of Minor Physical Anomalies and Copy Number Variations were found in both disorders. There is a considerable overlap in candidate genes for autism and schizophrenia. The question is raised whether psychiatric disorders can be unambiguously demarcated. Are there only smooth transitions in our biological reality „And”. What does that mean for our current classification systems? Should we dimensionalise instead of categorise „And” if we chose to dimensionalise, on what should we base our dimension? On symptoms or on endophenotypes?
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