From single to multiple deficit models of developmental disorders

392 B.F. Pennington / Cognition 101 (2006) 385–413
3.1.4. Cognitive overlap
In the Willcutt et al. (2001) study which used a 2 £ 2 design, we found that the cognitive
phenotype in children with both RD and ADHD was essentially the sum of the
phenotype in each disorder considered separately. Once full scale IQ and subclinical
elevations of RD or ADHD were controlled statistically, we found main eVects of
ADHD on measures of inhibition (Stop Task and Continuous Performance Test)
and main eVects of RD on measures of phoneme awareness (PA) and verbal working
memory (WM), but no signiWcant interactions. The one caveat is that there was a
trend for an RD main eVect on inhibition measures, indicating that the double dissociation
between RD and ADHD was not totally clean. So the etiology of isolated
ADHD presumably led to an inhibition deWcit but did not aVect the cognitive markers
of RD: PA and verbal WM. In contrast, the etiology of isolated RD did have
some marginal eVects on inhibition, which is the cognitive marker for ADHD. This
asymmetric pattern would be consistent with the pleiotropy hypothesis. That is, the
RD risk locus on 6p aVects two largely separate cognitive processes, phonological
processing and inhibition, and individuals with this risk locus are more likely to have
deWcits on both, thus explaining the comorbidity between RD and ADHD.
However, this cognitive pleiotropy hypothesis is less parsimonious than one in
which shared etiologic risk factors lead to shared cognitive risk factors because the
cognitive pleiotropy hypothesis must explain why the shared etiological risk factor
leads to both cognitive deWcits in some individuals and not others. So perhaps by
examining other cognitive deWcits, we might Wnd more evidence for a cognitive overlap
between RD and ADHD.
In a new sample of subjects also using a 2 £ 2 design, and now including measures
of processing speed, we found more evidence for cognitive overlap between RD and
ADHD (Willcutt, Pennington, Olson, Chhabildas, & Hulslander, 2005). The RD
only, ADHD only, and RD + ADHD groups had deWcits of similar magnitude on the
processing speed factor. So a deWcit in processing speed might be a cognitive risk factor
that is shared by RD and ADHD.
The processing speed measures in this study included the Wechsler Coding and
Symbol Search subtests, and the color and word naming baseline conditions of the
Stroop. So they included both linguistic and non-linguistic measures of processing
speed. Because rapid serial naming (RSN) tasks can also be thought of as measuring
processing speed, we included them in a follow-up study (Shanahan et al., in press). A
factor analysis of various processing speed measures found two factors: a verbal factor
(on which RSN and the Stroop baseline conditions loaded) and a motor factor
(on which Wechsler Symbol Search and Coding loaded). Again using a 2 £ 2 design,
we found main eVects of both ADHD and RD status on both factors. There was also
an ADHD x RD interaction, such that the comorbid group was less impaired on
each factor than the sum of the deWcits found in each pure group. Given these results,
we reasoned that RD and ADHD were not cognitively independent in the domain of
processing speed. So in this study we did Wnd evidence for a cognitive risk factor that
is shared by RD and ADHD.
In sum, our cognitive studies of the heterotypic comorbidity between RD and
ADHD have found both cognitive deWcits speciWc to each disorder (in phonological