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Statistical analysis was conducted s.d.s.d.¼ 6.6) and the community diagnoses and 26 without a PDD
usingStatistical analysis was conducted control6.6) and the community control diagnosis.diagnoses and 26 without a PDD
using the Statistical Package for the group (mean score 2.9, s.d.group (mean diagnosis. These correlations were
¼ 258.72,258.72,(2,346) PP 55 0.001). How-
Socialthe Statistical Package for the Social score 2.9, s.d.¼ 4.0); one-way4.0); one- modest, which is un-These correlations
0.001). How- ever, it should be noted that
(2,346)
Sciences (SPSS version 11 for way ANOVA (ANOVA (FF were modest, which is un- surprising in
Levene’s testever, it should be noted that
Windows).Sciences (SPSS version 11 for view of the fact that the itemssurprising in
Levene’s test showed that the assumption
Windows). Test–retest reliability of the view of the fact that the items that make
of equality ofshowed that the assumption
SCDC wasTest–retest reliability of the up the SCDC were not derivedthat make
of equality of variances had been violated
SCDC was assessed using intraclass Discriminant validity was had thenbeen assessed up the SCDC were not derived from the
for this analysisvariances
correlation coeffi-assessed using byDiscriminant ADI–Rand are designed to measurefrom
violated for this validityanalysiswas then statistic
(Levene assessed
intraclass correlation coeffi- cients (ICCs). by determining the power the ADI–R and are designedtomeasure
19.6,(Levene statistic 19.6,ofPPthe 55SCDC
0.001). to
One-way ICCs were used,cients (ICCs). dis-determining the power of T2 thewas
SCDC to autistic traits rather than for diagnostic
Tamhane’s0.001). Tamhane’s
One-way ICCs were used, to allow for dis- tinguish participants pur-autistic traits rather than for
therefore used forT2 was with thereforeautistic-
used
inter-individual variability.to allow for spectrumtinguish participants with diagnostic pur- poses. Correlation with the
for p ost hocpos t hoc compari-compari-
inter-individual variability. Internal autistic-spectrum disorder from social interactionposes. Correlation with
sons between groups, as this testnon-
is
consistency was evaluated byInternal autistic participants,disorder from non- the social interaction sub-scale was 0.41
speciallysons between groups, as this test
consistency was evaluated by calculating autistic participants, using ROC analysis. (sub-scale was 0.41 (PP 550.001),
is specially designed for situations in
Cronbach’scalculating Cronbach’s aa This analysis was doneusing correlation0.001), correlation with the
which populationdesigned forROC analysis.
situations in
coefficient. Con-coefficient. Con- current This analysis was variances
done in two parts. First, language/communication sub-scalewith
which population differ, and is DIS CUS S IONDIS CUS
validity
R E SULTwasSR assessed
E SULT S using one- we found thatinvalidit
the SCDCin two differ, parts. and
First,is the language/communication sub-scale
Discriminant
conservative rela-variances S ION Population
waycurrent
He r i t a b ilivalidity
t y s t uwasd assessed using we found thatinthe SCDC was 0.30 (was 0.30 scre (PP 55 0.001) and
conservative
yDiscriminant rela- tion showed
to type 1 error. enin gPopulation
one-way analysis of variance (ANOVA),
yHe r i t a b ili t y s t u impressive
Thistionyto type
validit accuracy in discriminat-
1 error. This p ost hocpost
correlation
for a utistic tr ait sf scre
with0.001) and correlation with
with clinicalanalysis of variance (ANOVA), showed impressive accuracy enin
the g
repetitive and stereotyped
Earlier
d analyses of these data showed no
y clinical h oc analysisanalysis showed in that or a u t is t ic t r a it s
with group as the factor. discriminat- ing children with an autistic- ‘Is autism onerepetitive
behaviourthe end of the normal
and stereotyped
sig-Earlier analyses of these data showed significant differences in SCDCshowed that
Tamhane’s T2 (Tam-group as the factor. spectruming children with an autistic- spectrum‘Is
behaviour autism one
sub-scale wasend0.21of(sub-scale
the normal
no sig- nificant difference in the size of significant differences in SCDC scores exist
Tamhane’s T2 (Tam- hane, 1979) was spectrum disorder from (clinical plus non- spectrum
was 0.21 (PP of behaviour,
55 0.01). The or iscorrela-0.01).
it an
genetic influ-nificant difference in the size between all three clinical groups:scores
used as ahane, 1979) was used as a po st clinical)disorder abnormal
The correla- condi-of behaviour, or is it an
of genetic influ- ence in males and exist between allfrom three(clinical
clinicalplus non-for
groups:
hocpost h oc test totest to see which clinical) controls (AOCcontrols (AOC¼ abnormal condi- tion?’ (Medical Research
tionbetweentheSCDCtotalandthe3ditotaltio
females and no evidenceence in males each group comparison,for each group
diagnostic groups differed fromsee which 0.86,0.86, PPPP5555 0.001). Maximal0.001). Council, 2001).tion?’ (Medical Research
nbetweentheSCDCtotalandthe3ditotal
and females and no evidence of separate comparison, 0.001.0.001.
diagnostic groups differed from each Maximal discrimination between all Council,
score was2001). To date,
0.38 (score wasno0.38
whole (PP 55
non-additive genetic effects inof separate
other in terms of mean SCDC score.each pervasive devel-discrimination between population screen forTo date, no whole
0.001).0.001).
non-additive genetic effects in females
other in terms of mean SCDC score. all pervasive devel- opmental disorder population screen for autistic traits has
(Scourfieldfemales (Scourfield et alet al ,
(PDD) diagnoses andopmental disorder been published. Weautistic traits has been
1999). Here, addi-, 1999). Here, addi-
(PDD) diagnoses and non-PDD published. We simply do not know
tional analyses have further examined
diagnoses/normal comparisonsnon-PDD whether autisticsimply do not know
thetional analyses have further examined
diagnoses/normal comparisons was whether
Autism isautistic
a highlybehaviours are
heritable disorder, but
the question of gender differences and
obtained at a cut-off score of 9 pointswas continuous
ofAutism is with a highlya normalbehaviours
heritable disorder, arebut
have in-question of gender differences
obtained at a cut-off score of 9 points (a continuous
of the various screening instruments of
with a normal distribution
and have in- cluded the influence of a
score of 9 or above implied a case). Sen- severity,
availablethe as the workscreening
various ofdistribution of
scalar amplificationcluded the influence of
(a score of 9 or above implied a case). severity,
instruments as the work of
available SpikerSpiker
only the Social et
a scalar amplification or dampening of the
Sen- sitivity was 0.90 and specificity was alet al (2002) and
Responsiveness Constantino
Scale hasonly the &(2002)
Social
phenotype in either gen-or dampening of
0.69sitivity was 0.90 and specificity was and
Responsiveness Scale has been implies;
Constantino & Todd (2003) evaluated or
the phenotype in either gen- der.This
0.69 with this cut-off; the positive whether
in terms autism
of formal isTodd (2003) implies; or
heritabil-been
allows for comparison withanotherder.
predictivewith this cut-off; the positive whether
evaluated autism
in terms is distinct,
of formal either in terms
heritabil- ity
This allowsfor comparisonwith another
predictive validity was 0.75 and the He
of r i t a b
bimodality ili t y o f t h
ofdistinct,e S C D
either
by means of a twin study. Constantinoity in terms of
twin study of an autism trait measure
negative predic-validity was 0.75 and the bimodality
CHe r i t a bof
by means of
iliatquantitative
y o f tstudy.
twin heSC trait
D distribution
Constantino &
(Con-twin study of an autism trait
negative predic- tive validity was 0.86. Of or
C
Toddin qualita-quantitative
(2003) report a besttrait fittingdistribution
model&
measure (Con- stantino & Todd, 2003).
the 61 falsetive validity was 0.86. Of the or in qualita-
Todd (2003) report tive difference frommodel
a best fitting normal
These additionalstantino & Todd, 2003).
61 false positives obtained with this cut- development.tive
heritability estimate difference
of 0.48, from
with a normal
These additional analyses have shown no
off, 19positives obtained with this cut-off, development.
sampleheritability The estimate
SCDC may ofbe used
0.48, fora
with
evidence of separateanalyses have shown
19 (31%) were clinical control cases a first-stageThe
sample size of 788 SCDC twin may be The
pairs. usedbestfor a
no evidence of separate additive genetic
selected(31%) were clinical control cases first-stage
fittingsize of screen
788 twinof school-aged
pairs. The best
effects in males or femalesadditive
selected from children attending the populations
fitting modelinfor orderscreen
SCDC dataof school-aged
showed no
genetic
Int ern aleffects
a n dinemalesxt ernorafemales
l relia and no
Great Ormondfrom children attending the populations infor
signifi-model order
SCDC to data
provide an answer
showed no
evidence of scalar
bilit yIntern al and amplification
extern al orand no Great Ormond Street clinic. These were to thesecant
signifi- questions.to provide anand,
gender differences answer
using
evidence of scalar amplification or
reliabilit y of th e S CDCof
Cronbach’sCronbach’s
th e S for
aa coefficient cases of socialStreet clinic. These were to these questions.
similarcant gender differences and, using
dampening of the phenotypic trait in
CDC
the SCDC wascoefficient
eitherdampening for the SCDC
of the phenotypic was
trait in cases of social communication difficulty similar analyses, a substantially greater
0.93, showing
either gender. that the content
For both males and of the0.93,
females on referral thatcommunication difficulty heritabilityanalyses, a substantially
showing
thegender. thatForthebothcontent
malesofand thefemales on referral that had already been greater heritability of 0.76 with unique
instrument
the influence has of high internalenvironment
the shared assessed locally and werehad already environmental influ-of 0.76 with unique
consistency.instrument
wasinfluence of the shared has environment
high internal been assessed locally and were referred environmental influ- ences of 0.24. A
consistency. The ICCand
was non-significant for the
test–retest SCDC
best fitting to our national centre for a secondreferred heritability of 0.76 is closeences of 0.24. A
scores on aThe ICC forand
modelnon-significant test–retest
the best SCDC
fitting to our national centre for a second (or heritability of 0.76 is close to the
scores showed,
model on a clinical sample
for both of 188achildren
genders, even a third) opinion. Their presence is(or heritability estimates (about 0.9)to the
(Skuseclinical sample of
heritability ofshowed, for188
bothchildren
genders, a even a third) opinion. Their presence is heritability estimates (about 0.9) reported
(Skuse etetof alal , 1997) with a mean
Crit
likelye ri
toohave
n valiraised the false-positive in twin studies of clinical cases ofreported
heritability 0.74andnon-
Validit y of th e S
retest interval of, 1997) with a mean
sharedenvironmentalinfluence0.74andnon dit yCri t e to
rate;likely rio n raised the false-positive
have in twin studies of clinical cases of autism
Finally, criterion validity was assessed
CDCValidit
retest
C urr eynof
o n cinterval of th eyears
t 2.7
-sharedenvironmentalinfluence S (s.d.2.7 years
of 0.26 v a
rate;li d i t
amongy
byFinally, criterion validityfrom
comparisons the
was assessed (Baileyautism (Bailey et alet al , 1995). No
CDC
(s.d.¼
(summary
vali dit 0.5,
yCo range
ofncdata
urre1.51–5.39)
presented was0.5,
as a dataof general
by comparing popu-among
total scorescomparisons
on the SCDC from significant, 1995). No significant influence
The
range mean SCDC score
1.51–5.39) for the autistic-The the general popu- lation theon false-positive of the shared environmentinfluence of the
0.26 (summary
nt validit y score ofwas
data0.81 (95%
presented CIas0.76–
a withcomparing total scores the SCDC
mean SCDC for the autistic- rate
0.86).0.81
data (95% CI
supplement to0.76–0.86).
the online version of with was only 9%.lation
the ADI–R equivalent thealgorithm
false-positive shared environment emerged in our
spectrum group was 16.6 (s.d.spectrum rate was only 9%.equivalent
We repeated the ROC study, although the upperemerged in our
thissupplement to the online version of outputthe ADI–R algorithm
group was 16.6 (s.d.¼ 5.7), which5.7), analysisgenerated
excludingWe repeated
this paper).paper). output by the 3di, forthe theROCGreat study, although the upper 95% confidence
which was significantly higher than that analysis excluding data from
Ormondgenerated by the 3di,the for general
the limit of these estimates95% confidence
ofwas significantly higher than that of the population sample.data from (Street
the general limit of these estimates was 0.26 in
Great Ormond Street sample
clinical control group (mean score population sample. The sensitivity of the females and 0.45 in males;was 0.26 in
sample (nn¼ 230), comprising 73 chil-
11.6,the clinical control group (mean instrument (with theThe
230), comprising 73 chil-sensitivity
dren with of the females and 0.45 in males; therefore, it is
score 11.6, instrument
5705 autism, 131(with with theotheridentical
PDDdren cut-off)
with was possible that a larger sampletherefore, it
7 0 the same
autism, 131(0.9)withbutidentical
other PDD cut-off) was is possible that a larger sample size might
the same (0.9) but the specificity was have detected a more significantsize
reduced to 0.35.the specificity was might have detected a more significant
reduced to 0.35. effect.effect.
The instrument compares well with
existingThe instrument compares well
with existing autism screening tools in
S O C I A L A N D C O M M U N I C AT I O N D I S O R D E R S C H E C
terms of its psy-autism screening tools in K L I S T S O C I A L A N D C O M M U N I C AT I O N D I S
terms of its psy- chometric properties. O R D E R S C H E C K L I S T
57
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