Validity of Subtypes of ADHD
A Component of the Colorado Learning Disability Research
Center (CLDRC) funded by the National Institute of Child Health
and Human Development
Principal Investigators:
Bruce F. Pennington, Ph.D. and Erik
Willcutt, Ph.D.
This twin study extends our previous work on the genetics
and neuropsychology of ADHD (see selected annotated publications),
by testing the validity of subtypes of ADHD using converging
methods. Despite recent progress in identifying neurobiological
mechanisms in ADHD, there is considerable heterogeneity both
within and across the clinical phenotypes of ADHD defined
by the DSM-IV. This heterogeneity is evident in situational
and reporter differences, patterns of comorbidities, neuropsychological
correlates, medication response, and possibly genetic mechanisms.
Some of this heterogeneity is likely due to genuine biological
differences, whereas some of it may reflect errors in measurement.
This continuing twin study will test the validity of
- DSM-IV subtypes,
- Those defined by comorbidities,
- Those defined by situational and reporter differences,
and
- Those defined by age and gender.
Internal validity will be tested by factor analyses and by
whether subtypes are familial within twin pairs. External
validity will be tested using both behavioral and molecular
genetic methods, neuropsychological measures, and measures
of clinical correlates and functional impairments.
To accomplish these goals, we will administer a battery of
neuropsychological and psychiatric measures to the samples
of RD, ADHD, and control twin pairs (100 pairs in each group,
half MZ and half DZ) and their siblings who will also be tested
in other projects of the CLDRC.
The neuropsychological battery of our study is designed to
test further the executive deficit hypothesis of ADHD by pitting
it against a motivational deficit hypothesis. While a deficit
on measures of inhibition, such as the Stop task, is a well-replicated
correlate of ADHD, the relation between inhibitory and other
executive measures and ADHD is far from perfect. Thus, an
executive deficit may only characterize a subtype of ADHD,
or it may only be a correlate of a more fundamental deficit,
or the executive deficit may interact with a second deficit.
To test these possibilities, we have added measures to test
the motivational deficit hypothesis, in addition to continuing
to collect data on executive measures correlated with ADHD. A
particular focus of this study is the comorbidity between ADHD
and dyslexia. We are testing which genetic and cognitive risk
factors are shared and not shared by these two disorders.
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