International Meeting for Autism Research: A Genetic Epidemiological Approach to the Sensory Over-Responsivity Phenotype

A Genetic Epidemiological Approach to the Sensory Over-Responsivity Phenotype

Saturday, May 22, 2010: 9:45 AM
Grand Ballroom CD Level 5 (Philadelphia Marriott Downtown)
9:45 AM
H. H. Goldsmith , Psychology, The University of Wisconsin-Madison, Madison, WI
C. Van Hulle , The University of Wisconsin-Madison, Madison, WI
N. L. Schmidt , The University of Wisconsin-Madison, Madison, WI
Background: Strong responses to seemingly mild sensory stimulation are frequently reported as a non-diagnostic feature of the autism spectrum. A thorough understanding of this phenomenon requires investigation of sensory symptoms per se. We previously evaluated 1394 toddler-aged twin pairs using parental report of auditory and tactile over-responsivity (Goldsmith et al., 2006). We observed fairly strong genetic effects for tactile over-responsiveness (83% of MZ--genetically identical--pairs, compared with 32% of DZ pairs were concordant for tactile symptoms).

Objectives: We investigated the phenotypic and genetic distinctiveness of sensory symptoms and common features of childhood behavioral problems in middle childhood.

Methods: Twins were identified from statewide birth records, and 2095 children (all twins) were screened at age 6-7 years on the Health and Behavior Questionnaire (HBQ), a survey of DSM symptoms in the internalizing and externalizing domains and Miller’s sensory screener. Follow-up data on a subsample enriched for behavioral problems were available on 765 participants, mostly aged 7-8 yrs. Probable diagnoses were obtained using the DISC, which is a structured psychiatric interview (of parents) that yields DSM-IV diagnoses and symptom counts.

Results: Almost half (44%) of children who screened positive for SPD did not qualify for any DISC diagnoses. When we examined symptoms rather than diagnoses, we found overlap between behavior problem symptoms and sensory symptoms. This indicates that sensory issues are problematic for children with other recognized behavioral problems. We also examined mother reports of physical health for children who screened positive for SPD and qualified for a DISC diagnosis, children who only screened positive for SPD, children who only qualified for a DISC diagnosis, and non-diagnosed children. In general, children who screened positive for SPD only did not have more major health problems than other groups.

We examined the relationship between symptoms of SPD and symptoms of DISC diagnoses and explored possible genetic and environmental factors that contribute to both. We collapsed the psychiatric symptoms into two broad factors: anxiety and externalizing (impulsivity, conduct problems).  Then, we conducted quantitative genetic analyses to answer a series of questions: Are there genetic influences on sensory symptoms? Yes. Are there genetic influences on anxiety symptoms? Yes. Are there genetic influences on externalizing symptoms? Yes.  Then, we asked whether the more critical question: do the genetic influences on sensory symptoms overlap with genetic influences on anxiety and externalizing symptoms. Briefly, bivariate genetic modeling indicated that sensory symptoms were only weakly correlated with anxiety and externalizing, but the correlation that did exist could be accounted for by genetic factors.

Conclusions: Our analyses generally supported the phenotypic distinctiveness of the high standing on sensory symptoms. Given that the genetic factors for sensory symptoms and other common (anxiety, externalizing) symptoms largely did not overlap, we also have evidence for the genetic distinctiveness of sensory symptoms. We discuss various qualifications to these analyses.

We are currently expanding this line of research to examine sensory symptoms in a sample of twins, one or both of whom have an autism spectrum diagnosis. Preliminary results will be presented.

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