Behavior Genetics, Vol. 32, No.

6, November 2002 (© 2002)

A Pilot Twin Study of Psychological Measures of Attention

Deficit Hyperactivity Disorder

Jane Holmes,1 Tracey Hever,2 Lisa Hewitt,2 Claire Ball,1 Eric Taylor,3 Katia Rubia,3
and Anita Thapar1,4

Received 26 Mar. 2001–21 June 2002

There has been much interest in the genetics of attention deficit hyperactivity disorder and mol-
ecular genetic studies are now underway. The success of genetic studies will depend on how well
the phenotype is defined. Twin studies using parent and teacher rated questionnaires or inter-
views all appear to yield highly heritable measures. Nevertheless, there is evidence to suggest
that parent measures are subject to rater bias. Consequently there has been much interest in ob-
taining more objective measures of related traits such as attention span and impulsiveness using,
computerised neuropsychological tasks. However there have been few twin studies examining
the genetic contribution to these neuropsychological measures. The present study aims to inves-
tigate whether performance on the Matching Familiar Figures Test (MFFT) and Continuous Per-
formance Task (CPT) is genetically influenced in childhood. 20 monozygotic (MZ) and 20 dizy-
gotic (DZ) twin pairs were randomly selected from the Greater Manchester Twin Register.
Preliminary data suggest that MZ twins perform more similarly than DZ twins on the MFFT, but
not the CPT. Future work needs to examine whether other neuropsychological measures com-
monly used in research on ADHD are genetically influenced using larger twin samples.

KEY WORDS: Attention-deficit hyperactivity disorder; twin study; matching familiar figures test; con-
tinuous performance task; sustained attention; impulsiveness.

INTRODUCTION ceptor DRD4 7 repeat allele with ADHD that have been
shown in a recent meta-analysis (Faraone et al., 2001).
Attention deficit hyperactivity disorder (ADHD) is a
However findings for other candidate genes have so far
common psychiatric disorder of childhood that is char-
not been consistent (Collier et al., 2000).
acterized by problems of inattention, impulsivity, and
The definition of the phenotype is critical for the
hyperactivity (Taylor, 1994). In recent years there has
success of molecular genetic studies (Leal, 2001). In
been increased interest in the genetic basis of ADHD.
psychiatry and psychology, phenotypes are defined on
Family, twin, and adoption studies have provided con-
the basis of reported behavioral symptoms rather than
sistent evidence that hyperactivity and inattention are
on objective measures. Twin studies of ADHD, for ex-
influenced by genetic factors (Thapar et al., 1999).
ample, have focused on parent and teacher reports of
Molecular genetic studies are underway with replicated
children’s ADHD symptoms. Although there has been
findings of association and linkage of the dopamine re-
consistent evidence that measures of ADHD symptoms
are greatly influenced by genetic factors (Goodman and
1
Child and Adolescent Psychiatry Section, Department of Psycho- Stevenson, 1989; Edelbrock et al., 1995; Thapar et al.,
logical Medicine, University of Wales College of Medicine, Cardiff,
U.K. 1995; Gjone et al., 1996; Eaves et al., 1997; Levy et al.,
2
Department of Child and Adolescent Psychiatry, University of Man- 1997; Sherman et al., 1997; Neuman et al., 1999;
chester, Manchester, U.K. Hudziak et al., 2000; Thapar et al., 2000), extremely
3
Institute of Psychiatry, King’s College, London, U.K.
4
To whom correspondence should be addressed. Fax: 029-20747839. low or even negative DZ twin correlations for mater-
e-mail: Thapar@cardiff.ac.uk nally rated ADHD symptom scores have been observed
389
0001-8244/02/1100-0389/0 © 2002 Plenum Publishing Corporation
390
in some of these studies (Goodman and Stevenson,
1989; Thapar et al., 1995; Eaves et al., 1997). The
evidence suggests that this is likely to be explained by
maternal rater bias (Simonoff et al., 1998) whereby
mothers tend to contrast twins.
Given this difficulty in defining the phenotype,
there is considerable appeal in examining the value of
more objective measures of behavior and associated
neuropsychological deficits for genetic studies of
ADHD. A number of neuropsychological tasks have
been devised to assess attention span, impulsiveness,
and response inhibition (Barkley, 1998). Although tasks
such as the Continuous Performance Task (CPT) and
Matching Familiar Figures Test (MFFT) do not provide
measures that can be equated with clinical disorder,
they can be a useful adjunct to clinical assessment tools
and may be regarded as more objective. If such mea-
sures are found to be heritable as well as related to a
particular disorder, they may be helpful in defining phe-
notypes for molecular genetic studies of psychiatric dis-
order. However, little is known on whether neuropsy-
chological measures are genetically influenced.
In an adoption study of ADHD (Alberts-Corush
et al., 1986), the biological parents of children with
hyperactivity showed greater attentional difficulties
than adoptive parents and control parents, but there
was no evidence of greater impulsivity. To our knowl-
edge, there have been only two twin studies of chil-
dren using objective measures of attention (Goodman
and Stevenson, 1989; Kuntsi and Stevenson, 2001). In
the first study, using a population-based sample of
13-year-old twins, two indices of attentiveness (“free-
dom from distractibility” and “E” scan attentiveness)
were found to be moderately influenced by genetic fac-
tors (32% to 42%). In a more recent study (Kuntsi and
Stevenson, 2001), bivariate twin analysis showed no
evidence of a common genetic influence on reported
hyperactivity symptoms and neuropsychological task
measures of delay aversion and working memory but
a significant common genetic contribution to hyper-
activity and variability of reaction times on the Stop
task was detected.
It is clearly essential to first demonstrate that
neuropsychological task derived measures of attention,
hyperactivity and impulsiveness are influenced by ge-
netic factors before including them as phenotypes in
molecular genetic studies. In this paper, we present
the preliminary results of a pilot study in which we
sought to examine whether measures of attention,
using the CPT and impulsiveness, using the MFFT
appear to be influenced by genetic factors.
Holmes et al.
METHODS
Sample
The sample consisted of 20 MZ and 20 DZ male
twin pairs that were randomly selected (using SPSS for
Windows random sampling technique) from the popu-
lation-based Greater Manchester Twin Register (for de-
tails, see Thapar et al., 2000). The twin register con-
tains 2846 school aged twin pairs born between 1980
and 1991 identified from the Community Child Health
Databases for 9 health districts in Greater Manchester
and Lancashire, UK. The figures for ethnicity and so-
cial class for the register (Thapar et al., 2000) are in
keeping with those expected for a population from
Greater Manchester and Lancashire, UK (Public Health
Common Data Set, 1993). The selected sample was
aged between 8 and 12 years (mean ⫽ 10.48; SD ⫽
1.27) and included males of European ethnic origin
only. The mean age (and standard deviation) for MZ
twins and DZ twins at the time of assessment was 10.8
(1.18) and 10.19 (1.32) years, respectively.
Testing
Continuous Performance Task (CPT)
The CPT was originally designed to detect and
study brain damage in children and adults (Rosvold
et al., 1956) but was refined to measure sustained at-
tention. The CPT has frequently been used in the as-
sessment of attention deficits and has been demon-
strated to be of particular use in distinguishing children
who display behaviors described as inattentive, dis-
tractible, fidgety, restless, and impulsive from controls
(Cantwell, 1972). The present study used a comput-
erised version of the CPT identical pairs (CPT-IP) from
the Maudsley Attention and Response Suppression task
battery (MARS) (Rubia et al., 2001). This version is a
DOS-based program that sequentially displays 192
playing cards that differ in terms of number (1–9) and
suit (club or diamond). The participant is requested to
press the spacebar on the computer keyboard when a
playing card is immediately followed by another card
that is identical in both number and suit. This CPT-IP
contains 24 matches. The duration for each stimulus is
1 sec, the duration between each stimulus is 1.5 sec and
the duration for completing the task is fixed at 8 min.
The scores derived from the CPT are the number of
successful matches, the number of false alarms (the
number of responses following incorrect stimuli) and
mean response time. The number of correct matches is
considered to be a measure of sustained attention,
Twin Study of ADHD Measures 391

whereas the number of false alarms is thought to re- vironmental influences on sustained attention and im-
flect both sustained inattention and impulse control. pulsiveness. An information sheet was also posted to the
families which provided full details of the study. Each
The Matching Familiar Figures Test (MFFT) family was then telephoned and asked whether they
would like to participate in the study. Once verbal con-
The MFFT was originally developed by Kagan
sent was gained, an appointment was scheduled to visit
(1965) for the assessment of impulse control. Hyperac-
the twins in their home. All selected families consented
tive children’s performance on this task is characterized
to participate in the pilot study (i.e., 100% response rate).
by fast, inaccurate, “impulsive” responding (Barkley,
Twins were independently assessed on a portable
1998). This computerized version of the MFFT is a
computer in a quiet room of the house. Prior to the com-
DOS-based program (version 2.0; Sonuga-Barke et al.,
mencement of each task, the researcher read standard-
1994), which consists of 20 trials and 2 practice trials.
ised instructions for the MFFT and CPT. Participants
For each trial, a picture is displayed at the top of the
also engaged in a practice trial to ensure they under-
computer screen and then six similar pictures are pre-
stood the requirements of each task.
sented directly below. The participant is required to
choose the identical matching picture from the six vari-
ants using the computer mouse. The specified duration Statistics
for each trial is 45 sec. Once the participant responds
Between-subject associations for the CPT and
the next trial is immediately presented. If the partici-
MFFT were analyzed using intraclass correlation co-
pant provides no response within this specified time,
efficients. Scores on the MFFT were normally distrib-
then the next trial will commence. Thus test adminis-
uted. The number of false alarms on the CPT was pos-
tration time will vary depending on how quickly the sub-
itively skewed and log transformed to approximate
ject responds to each trial. The scores derived from the
normality using the transformation Y ⫽ ln(1 ⫹ X ).
MFFT are the mean time taken to the initial response
Three outliers were also excluded. The number of suc-
(latency), the total number of errors (incorrectly identi-
cessful matches on the CPT was negatively skewed and
fied pictures), and the total number of correct responses.
Spearman’s correlations are presented for the number
of successful matches (seven outliers were excluded).
Portable Computer
All statistical tests were considered significant at
A UMAX multimedia portable computer (model p ⬍ .05. Two-tailed p values are presented. Statistics were
290) was used to carry out the computer tasks. Stimuli carried out using the Statistical Package for the Social
were displayed on a 10-inch computer screen in a black, Sciences version 9.0 (SPSSW; Norusis/SPSS Inc.).
white, and red format. A computer mouse was exter-
nally attached for administration of the MFFT.
RESULTS
Table I shows the mean scores and standard devi-
Questionnaires
ations for MZ and DZ twins on the MFFT and CPT.
The zygosity of twin pairs was determined on the Table II displays the intraclass correlation coeffi-
basis of parental responses on the Twin Similarity cients for scores on the MFFT and CPT. MZ correla-
Questionnaire (Cohen et al., 1975). This questionnaire tions are higher than DZ correlations for the number of
contains items that refer to the physical similarities of
twins, for example whether or not the twins share the Table I. Mean Scores (and Standard Deviations) for MZ
same hair color or eye color. This method of deter- and DZ Twins on the MFFT and CPT
mining zygosity is reported to be over 95% accurate
(Cohen et al., 1975; Thapar et al., 2000). MZ DZ

MFFT
Procedure No. of correct responses 8.95 (3.28) 8.53 (1.9)
No. of incorrect responses 10.48 (3.40) 10.58 (2.32)
The present study was commenced over a 3-month Mean reaction time (in sec) 16.07 (5.55) 18.13 (5.47)
period. Families that were selected for the pilot study CPT
No. of successful matches 21.15 (2.48) 21.58 (1.87)
were sent a standard letter inviting the twins to partici- No. of false alarms 7.85 (14.22) 7.37 (1307)
pate in a research study investigating the genetic and en-
392 Holmes et al.

Table II. MZ and DZ Intraclass the Correlation Coefficients (and 95% Confidence Intervals)
for the MFFT and CPT

MZ DZ

MFFT
No. of correct responses
No. of incorrect responses
Mean reaction time
CPT
No. of successful matches
No. of false alarms
0.79*** (0.48 to 0.92)
0.73** (0.32 to 0.89)
0.80*** (0.49 to 0.92)
⫺0.181a
⫺0.10(⫺1.33 to 0.65)
⫺0.42(⫺2.59 to 0.44)
⫺0.08(⫺1.74 to 0.57)
0.31(⫺0.75 to 0.73)
0.53*,a
0.38(⫺0.65 to 0.77)

*p ⬍ .05, two-tailed.
**p ⬍ .01, two-tailed.
***p ⬍ .001, two-tailed.
a
Spearman’s correlations were calculated as data were negatively skewed. The wide confidence
intervals (some are ⬎ 1 or ⬍ ⫺1) are attributable to the small sample size.
Note: The wide confidence levels (some are >1 or <–1) are attributable to the small sample size.

correct responses, incorrect responses and mean reac-
tion time on the MFFT.
However, for the CPT, MZ correlations are lower
than DZ correlations for the number of matches and false
alarms. There is no biologically plausible explanation for
higher correlations in the DZ twins compared to the MZ
twins on the CPT. However as displayed in Figure 1,
there was a ceiling effect for successful matches on the
CPT which suggests that this version of the CPT may not
have been age appropriate for the twins.
DISCUSSION
As mentioned earlier there is now a wealth of ev-
idence from twin studies showing that ADHD symp-
tom scores are highly heritable (Thapar et al., 1999).

Fig. 1. The number of successful matches for MZ and DZ twins. The highest possible score is 24.
Twin Study of ADHD Measures
Molecular genetic studies of diagnosed ADHD are cur-
rently underway and initial results are beginning to
emerge (Thapar et al., 1999). A potential source of dif-
ficulty in the field of behavioral genetics is that phe-
notypes are based on subjective reports of symptoms
or behavior. This method of phenotypic definition con-
trasts with that used for many medical disorders such
as diabetes, for which pathophysiological measures
such as blood glucose that can be objectively defined
are available. A particular concern is that many twin
studies (Goodman and Stevenson, 1989; Thapar et al.,
1995; Eaves et al., 1997) but not all (Gjone et al., 1996;
Levy et al., 1997; Hudziak et al., 2000; Thapar et al.,
2000) have shown extremely low or negative dizygotic
twin correlations for ADHD symptom scores. This ap-
pears to be accounted for by parental rating biases (Si-
monoff et al., 1998), which raises a further concern as
to how the ADHD phenotype is defined. Neuropsy-
chological tests such as the CPT and the MFFT that
provide measures of inattention and impulsiveness are
not diagnostic instruments and are not always discrim-
inative measures. Nevertheless, these instruments may
provide more objective measures and thus, if found to
be heritable as well as related to psychopathology,
might be considered as attractive intermediate pheno-
types or “endophenotypes” (Almasy and Blangero,
2001) for genetic studies of ADHD. There has been
much interest in potential intermediate phenotypes for
psychopathology, with the hope that investigation of
these phenotypes may prove a more fruitful strategy in
elucidating the genetic aetiology of disorders. So far,
there has been little to support the success of such an
approach (e.g., smooth-pursuit eye tracking and schiz-
ophrenia). However for many disorders, including
ADHD, until further research is undertaken, there is
also insufficient evidence to warrant dismissal of such
a strategy.
In this paper, we have presented preliminary data
from a pilot twin study in which we sought to examine
to what extent measures obtained from the MFFT and
CPT are influenced by genetic factors. The pattern of
MZ and DZ correlations for the number of incorrect re-
sponses (rmz ⫽ 0.73, rdz ⫽ ⫺0.08), correct responses
(0.79, rdz ⫽ ⫺0.42) and mean reaction time (rmz ⫽
0.80, rdz ⫽ 0.31) obtained from the MFFT was strik-
ingly similar to previously reported twin correlations
for maternal-rated questionnaire and interview mea-
sures of ADHD symptom scores that have varied from
0.49 to 0.92 for MZ twins and ⫺0.16 to 0.57 for DZ
twins (Thapar et al., 1999). Although the results should
be interpreted with caution given the small sample size,
393
these findings suggest that measures of impulsiveness
obtained using a computerized version of the MFFT
may be genetically influenced. It is also of interest that
the results obtained from the MFFT, particularly for
the number of incorrect and correct responses, are so
similar to twin studies of symptom scores and in par-
ticular that DZ twin correlations are very low or neg-
ative which clearly cannot be explained by rater biases.
For the CPT measures, we found the MZ were
lower than the DZ twin correlations for which there is
no plausible biological explanation. This suggests that
measures of sustained attention, derived from this ver-
sion of the CPT, unlike impulsiveness are not strongly
genetically influenced, although clearly further work is
needed given the lack of statistical power due to our
small sample size. There are arguments that it is also
premature to conclude that the CPT is a definitive as-
sessment of sustained attention. Although numerous
studies have found deficits in sustained attention using
the CPT there are some notable exceptions that have
cast doubt upon the assertion of sustained attention
deficits in ADHD (Werry et al., 1987; Schachar et al.,
1988; Swanson et al., 1990). One study suggested that
so-called distinctive characteristics of ADHD were not
found when children were compared with both normal
children and those with another psychiatric diagnosis
(Werry et al., 1987). Meanwhile, another study has
stated that alternative explanations for poorer perfor-
mance in children with ADHD have been ignored, such
as poor understanding, co-operation and co-ordination
(Schachar et al., 1988). Additionally, Schachar et al.,
found that children’s performance on the CPT deterio-
rated with increasing time and improved with the op-
portunity to prepare, regardless of their psychiatric sta-
tus. Given these uncertainties about the validity of
using the CPT as a measure of an ADHD phenotype,
our results may not be entirely unexpected. Overall
until further work is carried out, these findings suggest
that at present, caution is warranted in using CPT-
derived measures as intermediate phenotype measures
of ADHD.
Given more recent research (Rubia et al., 2001)
showing that children with ADHD display deficits in
more challenging response inhibition tasks such as the
go-no-go task (Mesulam, 1985) and the stop task
(Logan and Cowan, 1984), it is evident that a larger
twin study of such measures including other instru-
ments such as those that tap response inhibition is
clearly needed before substantive conclusions can be
drawn. The results of a recently published paper based
on bivariate extreme analysis on a sample of 16 to
394
19 MZ twin pairs and 26 to 28 DZ twin pairs utilised
some of these measures as well as other tasks (Kuntsi
and Stevenson, 2001). No common genetic influence
on hyperactivity symptoms and delay aversion or work-
ing memory measures was found but significant shared
genetic influences on hyperactivity and variability of
speed on the stop task were shown.
Limitations
Caution is required in interpreting our data given
the small sample size. We also question the usefulness
of the CPT data given the evidence of a ceiling effect
for scores and the skewed distribution. Finally these re-
sults apply to a population-based sample of males
within a narrow age range and could differ for those
with clinical disorder. Nevertheless twin study results
suggest that for questionnaire measures of ADHD
symptom scores, the genetic aetiology for extreme
scores is similar to that for normal variation.
In conclusion, in this pilot study we found genetic
influences on MFFT-derived measures of impulsiveness
but not for CPT measures of sustained attention. Further
twin work is needed before it can be concluded which
neuropsychological tasks yield measures that may be
useful as endophenotypes in genetic studies of ADHD.
ACKNOWLEDGMENTS
J. H. was funded by Action Research and SPARKS.
The Greater Manchester Twin Register was funded by
the Medical Research Council, UK. We thank the twins
who participated in this study.
REFERENCES
Alberts-Corush, J., Firestone, P., and Goodman, J. (1986). Attention
and impulsivity characteristics of the biological and adoptive
parents of hyperactive and normal control children. Am. J. Or-
thopsychiatr. 56: 413– 423.
Almasy, L., and Blangero J. (2001). Endophenotypes as quantitative
risk factors for psychiatric disease: Rationale and study design.
Am. J. Med. Genet. (Neuropsychiatr. Genet.) 105:42–44.
Barkley, R. (1998). Attention deficit hyperactivity disorder: A hand-
book for diagnosis and treatment. London, The Guildford Press.
Collier, D., Curran, S., and Asherson, P. (2000). Mission: not im-
possible? Candidate gene studies in child psychiatric disorders.
Mol. Psychiatr. 5:457– 460.
Cohen, N. J., Dibble, E., and Grawe, J. M. (1975). Reliably separat-
ing identical from fraternal twins. Arch. Gen. Psychiatr.
32:1371–1375.
Eaves, L. J., Silberg, J. L., Meyer, J. M., Maes, H. H., Simonoff, E.,
Pickles, A., Rutter, M., Neale, M. C., Reynolds, C. A., Erick-
son, M. T., Heath, A. C., Loeber, R., Truett, K. R., and Hewitt,
J. K. (1997). Genetic and developmental psychopathology: 2.
The main effects of genes and environment on behavioral prob-
Holmes et al.
lems in the Virginia twin study of adolescent behavioral devel-
opment. J. Child Psychol. Psychiatr. 38:965–980.
Edelbrock, C. S., Rende, R., Plomin, R., and Thompson, L. (1995).
A twin study of competence and problem behavior in childhood
and early adolescence. J. Child Psychol. Psychiatr. 36:775–786.
Faraone, S. V., Biederman, J., Weiffenbach, B., Keith, T., Chu, M. P.,
Weaver, A., Spencer, T. J., Wilens, T. E., Frazier, J., Cleaves,
M., and Sakai, J. (1999). Dopamine D4 gene 7-repeat allele and
attention deficit hyperactivity disorder. Am. J. Psychiatr. 156:5.
Faraone, S. V., Doyle, A. E., Mick, E., and Biederman, J. (2001).
Meta-analysis of the association between the dopamine D4 gene
7 repeat allele and attention deficit hyperactivity disorder. Am.
J. Psychiatr. In press.
Gjone, H., Stevenson, J., and Sundet, J. M. (1996). Genetic influ-
ence on parent-reported attention-related problems in a Norwe-
gian general population twin sample. J. Am. Acad. Child Ado-
lesc. Psychiatr. 35:588–596.
Goodman, R., and Stevenson, J. (1989). A twin study of hyperactiv-
ity: II. The aetiological role of genes, family relationships, and
perinatal adversity. J. Child Psychol. Psychiatr. 30:691–709.
Holmes, J., Payton, A., Barrett, J., Hever, T., Fitzpatrick, H.,
Trumper, A., Harrington, R., McGuffin, P., Owen, M., Ollier,
W., Worthington, J., and Thapar, A. (2000). A family-based and
case control association study of the dopamine D4 receptor gene
and dopamine transporter gene in attention deficit hyperactiv-
ity disorder. Mol. Psychiatr. 5:523–530.
Hudziak, J. J., Rudiger. L. P., Neale, M. C., Heath, A. C., and Todd,
R. D. (2000). A twin study of inattentive aggressive and anxious/
depressed behaviors. J. Am. Acad. Child Adolesc. Psychiatr. 37:
848–857.
Kagan, J. (1965). Reflection-impulsivity and reading ability in pri-
mary grade children. Child Dev. 36:609–628.
Kuntsi, J., and Stevenson, J. (2001) Psychological Mechanisms in
Hyperactivity: II. The role of genetic factors. J. Child Psychol.
Psychiatr, 42:211–219.
Leal, S. M. (2001). Phenotypes and genetic analysis of psychiatric and
neuropsychiatric traits. Am. J. Med. Genet. (Neuropsychiatric
Genet.) 105:4–7.
Levy, F., Hay, D., McStephen, M., Wood, C., and Waldman, I.
(1997). Attention-deficit hyperactivity disorder: A category or
a continuum? Genetic analysis of a large-scale twin study. J. Am.
Acad. Child Adolesc. Psychiatr. 36:737–744.
Logan, G. D., Cowan, D. B., and Davis, K. A. (1984). On the abil-
ity to inhibit simple and choice reaction time responses: a model
and method. J. Exp. Psych. and Hum. Percept. Perform. 10:276–
291.
Mesulam, M. (1985). Principles of behavioral neurology. Philadel-
phia, FA Davis.
Neuman, R. J., Todd, R. D., Heath, A. C., Reich, W., Hudziak, J. J.,
Bucholz, K. K., Madden, P. A. F., Begleiter, H., Porjesz, B., Ku-
perman, S., Hesselbrock, V., and Reich, T. (1999). Evaluation
of ADHD typology in three contrasting samples: A latent class
approach. J. Am. Acad. Adolesc. Psychiatr. 38:25–33.
Palmer, C. G. S., Bailey, J. N., Ramsey, C., Cantwell, D., Sinsheimer,
J. S., Del’Homme, M., McGough, J., Woodward, J. A., Asarnow,
R., Asarnow, J., Nelson, S., and Smalley, S. L. (1999). No evi-
dence of linkage or linkage disequilibrium between DAT1 and
attention deficit hyperactivity disorder in a large sample. Psy-
chiatr. Genet. 9:157–160.
Rosvold, H. E., Mirsky, A. F., Sarason, I., Bransome, E. D., and
Beck, L. H. (1956) A Continuous performance test of brain dam-
age. J. Consult. Psychol. 20:343–350.
Rubia, K., Taylor, E., Smith, A. B., Oksannen, H., Overmeyer, S.,
Bullmore, E. T., and Newman, S. (2001). Neuropsychological
analyses of impulsiveness in childhood hyperactivity. Br. J. Psy-
chiatr. In press.
Schachar, R., Logan, G., Wachsmuth, R., and Chajezyk, D. (1988).
Attaining and maintaining preparation: A comparison of atten-
Twin Study of ADHD Measures
tion in hyperactive, normal and disturbed control group. J. Ab-
norm. Child Psychol. 16:361–378.
Sherman, D. K., McGue, M. K., and Iacono, W. G. (1997). Twin con-
cordance for attention deficit hyperactivity disorder: A com-
parison of teachers’ and mothers’ reports. Am. J. Psychiatr. 154:
532–535.
Simonoff, E., Pickles, A., Hervas, A., Silberg, J. L., Rutter, M., and
Eaves, L. (1998). Genetic influences on childhood hyperactiv-
ity: contrast effects imply parental rating bias, not sibling in-
teraction. Psychol. Med. 28:825–837.
Smalley, S. L., Bailey, J. N., Palmer, C. G., Cantwell, D. P., McGough,
J. J., Del’Homme, M. A., Asarnow, J. R., Woodward J. A., Ram-
sey, C., and Nelson, S. F. (1998). Evidence that the dopamine D4
receptor is a susceptibility gene in attention deficit hyperactivity
disorder. Mol. Psychiatr. 3:427–430.
Sonuga-Barke, E. J. S., Houlberg, K., and Hall, M. (1994). When is
impulsiveness not impulsive? The case of hyperactive children’s
cognitive style. J. Child Psychol. Psychiatr. 35:1247–1253.
Swanson, J. M., Shea, C., McBurnett, K., Potkin, S. G., Fiore, C.,
and Crinella, F. (1990). Attention and hyperactivity. In: Enns,
J. T. (ed.), The development of attention and theory. New York;
North Holland, pp. 383–403.
Swanson, J. M., Sunohara, G. A., Kennedy, J. L., Regino, R.,
395
Fineberg, E., Wigal, T., Lerner, M., Williams, L., Lahoste, G. J.,
and Wigal, S. (1998). Association of the dopamine receptor D4
(DRD4) gene with a refined phenotype of attention deficit hy-
peractivity disorder (ADHD): A family-based approach. Mol.
Psychiatr., 3:38–41.
Taylor, E. (1994). Syndromes of attention deficit and overactivity.
In: Rutter M., Taylor, E., and Hersov, L. (eds.), Child and ado-
lescent psychiatr: Modern approaches. London, Blackwell Sci-
entific Publications, pp. 285–307.
Thapar, A., Hervas, A., and McGuffin, P. (1995). Childhood hyper-
activity scores are highly heritable and show sibling competi-
tion effects: Twin study evidence. Behav. Genet. 25:537–544.
Thapar, A., Holmes, J., Poulton, K., and Harrington, R. (1999). Genetic
basis of attention deficit and hyperactivity. Br. J. Psychiatr.
174:105–111.
Thapar, A., Harrington, R., Ross, K., and McGuffin, P. (2000). Does
the definition of ADHD affect heritability? J. Am. Acad. Child
Adolesc. Psychiatr. 39:1528–1536.
Werry, J. S., Elkind, G. S., and Reeves, J. C. (1987). Attention deficit,
conduct, oppositional and anxiety disorders in children, III: Lab-
oratory differences. J. Abnorm. Child Psychol. 15:409– 428.
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