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who will later on be diagnosed with ASD, they also include other siblings who will be
diagnosed with other disorders, or with no disorder at all (for summaries; see Rogers,
2009; Yirmiya & Ozonoff, 2007; Zwaigenbaum et al., 2009; Zwaigenbaum & Stone,
2008). Therefore, inconsistent findings emerging from these studies are most likely
due to differences in proportions of participants who will later on be assigned to the
ASD versus other diagnoses versus typically developing groups, and cannot reliably
teach us about the prodrome of autism. Even the often made assumption that these
studies inform us about the broad autism phenotype may be questionable because
significant differences between the full group of younger siblings of children with
autism and the comparison group may (or may not) be due to the siblings who will
later on be assigned to the ASD group. The point is, without follow-up information on
outcome we do not yet know if such early indicators are ‘prodromal’ signs of ASD or
not.
However, such studies do raise some intriguing scientific questions about the
developmental trajectories that might be seen in ‘high risk’ siblings, including some
preliminary evidence of disrupted neural processing of both social and non-social
stimuli that may be indicative of neural endophenotypes of ASD (Elsabbagh et al.,
2009; McCleery, Allman, Carver, & Dobkins, 2007; McCleery, Akshoomoff,
Dobkins & Carver, in press). They also highlight the intriguing possibility that some
at risk siblings might show early perturbations (perhaps contributing to the group-
level differences found compared to siblings of typically developing children) but not
go on to develop ASDs. This ‘recovery’ pattern of development might inform us
about developmental brain plasticity and developmental trajectories, and potentially
both genetic and environmental effects on these processes (Elsabbagh & Johnson,
2007; Rogers, 2009).