Assessment & Research

Behavioral comparisons in autistic individuals from multiplex and singleton families.

Cuccaro et al. (2003) · Journal of autism and developmental disorders 2003
★ The Verdict

Family history of autism does not change how a child scores on the ADI-R.

✓ Read this if BCBAs writing initial treatment plans for new autism referrals.
✗ Skip if Clinicians who already rely only on direct assessment data.

01Research in Context

01

What this study did

The team looked at the kids with autism. Half came from families with only one autistic child. Half had brothers or sisters with autism too.

Every child took the ADI-R, a long parent interview about autism traits. The researchers asked: do kids from 'multiplex' families score higher or lower?

02

What they found

Scores were almost identical. Language delay, repetitive actions, social interest — no meaningful gaps showed up.

Having more autism in the family tree did not shape how severe the child’s own symptoms looked.

03

How this fits with other research

Buhrow et al. (2003) also compared two groups — babies and teens with profound ID — and found different color likes but the same face preference. Both papers say: group labels alone don’t predict behavior; you still have to test the individual.

Hsieh et al. (2014) showed that in adults with ID, the reason for self-injury shifts as cognitive level drops. That study reminds us to assess function even when diagnosis looks the same. L et al. echo the warning: family type is not a shortcut for symptom picture.

Perez et al. (2015) tracked pleasure and later self-injury in adults with ID. They proved that today’s subtle signs forecast tomorrow’s big problems. L et al. add a parallel lesson: today’s family history does not forecast today’s symptom profile.

04

Why it matters

Do not assume the only child with autism needs less support than the one with autistic siblings. Run your standard ADOS, VB-MAPP, or FA regardless of family makeup. Let assessment data, not pedigree charts, guide hours and goals.

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Erase any mental note about ‘multiplex versus singleton’ and give the full ADI-R to every new client.

02At a glance

Intervention
not applicable
Design
other
Sample size
157
Population
autism spectrum disorder
Finding
null

03Original abstract

Autistic disorder (AD) is a complex neurodevelopmental disorder. The role of genetics in AD etiology is well established, and it is postulated that anywhere from 2 to 10 genes could be involved. As part of a larger study to identify these genetic effects we have ascertained a series of AD families: Sporadic (SP, 1 known AD case per family and no known history of AD) and multiplex (MP, > or = 2 cases per family). The underlying etiology of both family types is unknown. It is possible that MP families may constitute a unique subset of families in which the disease phenotype is more likely due to genetic factors. Clinical differences between the two family types could represent underlying genetic heterogeneity. We examined ADI-R data for 69 probands from MP families and 88 from SP families in order to compare and contrast the clinical phenotypes for each group as a function of verbal versus nonverbal status. Multivariate analysis controlling for covariates of age at examination, gender, and race (MANCOVA) revealed no differences between either the verbal or nonverbal MP and SP groups for the three ADI-R area scores: social interaction, communication, and restricted/repetitive interests or behaviors. These data failed to find clinical heterogeneity between MP and SP family types. This supports previous work that indicated that autism features are not useful as tools to index genetic heterogeneity. Thus, although there may be different underlying etiologic mechanisms in the SP and MP probands, there are no distinct behavioral patterns associated with probands from MP families versus SP families. These results suggests the possibility that common etiologic mechanisms, either genetic and/or environmental, could underlie all of AD.

Journal of autism and developmental disorders, 2003 · doi:10.1023/a:1022286622534