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Journal of Autism and Developmental Disorders, Vol. 35, No. 2, April 2005 ( 2005)
DOI: 10.1007/s10803-004-1993-7Asperger Syndrome: Familial and Pre- and Perinatal FactorsChristopher Gillberg,1,2,3 and Mats Cederlund1Objective: Study familial and pre- and perinatal factors in Asperger Syndrome (AS). Methods:
One hundred boys with AS had their records reviewed. Pathogenetic subgroups were
dened according to presence of medical syndromes/chromosomal abnormalities, indices of
familiality, and pre- and perinatal risk factors predisposing to brain damage. Results: No
major index of pathogenetic factors was found in 13%, a syndrome/chromosomal abnormality
in 8%, pre- or perinatal risk 13%, combined pre- or perinatal risk and family history in 11%,
and family history only in 55% Comment: About 50% of all boys with AS have a paternal
family history of autism spectrum disorder. Pre- and perinatal risks appear to be important in
about 25% of cases.KEY WORDS: Asperger Syndrome; familial; prenatal; perinatal.INTRODUCTIONHans Asperger believed autistic psychopathy
to be caused by genetic factors or brain damage
(Asperger, 1944). His disorder, now referred to as
Asperger Syndrome (AS) (Gillberg & Gillberg 1989;
Wing, 1981) is conceptualised as an autism spectrum
disorder believed to be closely genetically and clinically linked to ICD-10 childhood autism/DSM-IV
autistic disorder (APA, 1994; WHO, 1992). However,
the empirical data on the etiology and pathogenesis
of AS is scant, and much of current clinical consensus
derives from inferences drawn from the study of
autistic disorder. The few studies that have been
published (e.g., Ghaziuddin, Shakal, & Tsai, 1995;
Gillberg, 1989; Rickarby, Carruthers, & Mitchell,
1991) have been on samples of no more than one
or two dozen individuals. However, recently, a
genome-wide-scan for susceptibility genetic loci was
performed by a Finnish group, nding at least two
loci (on chromosomes 1 and 3) that have previously
been identied as susceptibility loci for autistic
disorder (Ylisaukko-oja et al., 2004).To our knowledge, no detailed study of 100 cases
or more of carefully clinically diagnosed cases of AS
has been published before. This new study examines
in detail the family, and pre- and perinatal background of 100 children with AS followed into late
adolescence and early adult life. Summary data from
the same set of individuals have been reported
previously (Cederlund & Gillberg, 2004), but the
present report takes the ndings one step further in