Limited research has investigated the possibility of impaired social and communicative behaviors in the siblings of children with autism spectrum disorders (ASD). Studies comparing children with autism to their siblings and to typically developing children using psychometric and behavioral indices have pointed to a broad phenotype of ASD. Social and communication behaviors of phenotypically normal siblings were found to resemble the ASD children more than they did those of typically developing children. SRS scores of siblings of children with autism have been shown to be significantly increased relative to those of probands with PDD-NOS or a psychopathology unrelated to autism. These findings suggest that subsyndromal social impairment may be prevalent among children with an affected sibling.
This study compares the communication and socialization skills of children with ASD to their siblings and to those of typically developing children. The SRS and the Vineland II are being used to assess symptom expression and adaptive functioning, respectively. The results of this investigation will provide additional information regarding the broad autism phenotype in which “unaffected” siblings demonstrate greater communication and social impairments in relation to their typically developing peers.
To date, 28 children and adolescents (mean age 9.68 years, FS IQ= 92.86) were characterized with an ASD according to performance on the ADOS, ADI-R, SRS, and Vineland II, as well as by the assessment of expert clinicians. Twenty-five unaffected siblings (mean age 10.65 years, FS IQ=115.36) met stringent exclusionary criteria to rule out ASD or other neuropsychological disorders. In addition those with scores of 70 or below on the Adaptive Behavior Composite or any subdomain of the Vineland II were excluded.
Independent samples t-tests indicated that these two groups differed significantly on full scale IQ (t=4.87, p<.001) but not on age (t=1.13, p=.265). Independent samples t-tests demonstrated that probands and their siblings differed significantly on the Communication (Proband M=77.08, Sibling M= 104.61; t=7.44, p<.001) and Socialization (Proband M= 70.60, Sibling M= 100.18; t=9.45, p<.001) domains of the Vineland II. Results from a Mann-Whitney U test also demonstrated that probands and their siblings differed significantly on the SRS (M=82.50, M=43.96; z=-6.07, p<.001). As expected, siblings showed less socialization and communication impairments than did probands. SRS and Vineland II subscores for typically developing children (age and IQ matched to the siblings) are currently being collected, with the hypothesis that siblings will show more impaired scores than typically developing children.
Unaffected siblings demonstrated higher adaptive skills and lower symptom severity scores on the Vineland II and SRS rating scales, respectively, than did their ASD siblings. It is likely that the siblings of ASD children will show communication and socialization skills intermediate between the proband and typically developing individuals. The addition of a control group will allow for the potential differences between typical children and siblings of children with ASDs to be explored. In sum, these findings would support the notion of a genetic susceptibility of social deficits demonstrated in ASD.