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Clinical Psychology Review 28 (2008) 1447–1471

Contents lists available at ScienceDirect

Clinical Psychology Review

Comorbidity as a predictor and moderator of treatment outcome in youth


with anxiety, affective, attention deficit/hyperactivity disorder, and
oppositional/conduct disorders
Thomas H. Ollendick a, Matthew A. Jarrett a,⁎, Amie E. Grills-Taquechel b,
Laura D. Hovey c, Jennifer C. Wolff d
a
Child Study Center, Department of Psychology, Virginia Polytechnic Institute and State University, 460 Turner Street, Suite 207, Blacksburg, VA 24060, United States
b
University of Houston, Department of Psychology, Houston, TX, United States
c
Department of Psychology, University of Toledo, Toledo, OH, United States
d
Alpert Medical School, Brown University, Providence, RI, United States

a r t i c l e i n f o a b s t r a c t

Article history: In the present review, we examine one of the critical issues that have been raised about
Received 19 August 2008 evidence-based treatments and their portability to real-world clinical settings: namely, the
Revised 9 September 2008 presence of comorbidity in the participants who have been treated in these studies and
Accepted 11 September 2008
whether the presence of comorbidity predicts or moderates treatment outcomes. In doing so,
we examine treatment outcomes for the four most commonly occurring childhood psychiatric
Keywords: disorders: Anxiety disorders, affective disorders, attention deficit/hyperactivity disorder
Child psychotherapy
(ADHD), and oppositional defiant disorder (ODD)/conduct disorder (CD). For each of these
Comorbidity
disorders, we first review briefly the prevalence of comorbidity in epidemiological and clinical
Treatment outcome
samples and then highlight the evidence-based treatments for these disorders. We next
determine the effects of comorbidity on treatment outcomes for these disorders. For the most
part, comorbidity in the treated samples is the rule, not the exception. However, the majority of
studies have not explored whether comorbidity predicts or moderates treatment outcomes. For
the not insignificant number of studies that have examined this issue, comorbidity has not been
found to affect treatment outcomes. Notable exceptions are highlighted and recommendations
for future research are presented.
© 2008 Elsevier Ltd. All rights reserved.

Contents

1. Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1448
2. Anxiety disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1449
2.1. Anxiety and its comorbidities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1449
2.2. EBTs for anxiety disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1449
2.3. Comorbidity as a predictor/moderator of anxiety treatment outcomes . . . . . . . . . . . . . . . . . . . . . . . 1449
3. Affective disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1460
3.1. Depression and its comorbidities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1460
3.2. EBTs for affective disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1461
3.3. Comorbidity as a predictor/moderator of affective disorder treatment outcomes . . . . . . . . . . . . . . . . . . 1461

⁎ Corresponding author. Tel.: +1 540 231 2024; fax: +1 540 231 8193.
E-mail address: mjarrett@vt.edu (M.A. Jarrett).

0272-7358/$ – see front matter © 2008 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cpr.2008.09.003
1448 T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471

4. Attention-deficit/hyperactivity disorder (ADHD) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1462


4.1. ADHD and its comorbidities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1462
4.2. EBTs for ADHD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1462
4.3. Comorbidity as a predictor/moderator of ADHD treatment outcome. . . . . . . . . . . . . . . . . . . . . . . . . 1462
5. ODD/CD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1463
5.1. ODD/CD and their comorbidities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1464
5.2. EBTs for ODD/CD . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1464
5.3. Comorbidity as a predictor/moderator of treatment outcomes for ODD/CD . . . . . . . . . . . . . . . . . . . . . 1464
6. Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1465
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1467

Several evidence-based treatments (EBTs) have been identified for youth (Ollendick & King, 2004; Weisz, Jensen-Doss, &
Hawley, 2005). To date, most of these treatments have been behavioral and cognitive-behavioral ones (with the exception of
interpersonal psychotherapy for the treatment of depression in adolescents). Unfortunately, we do not really know whether other
frequently practiced treatments from different theoretical orientations work (e.g., play therapy, psychodynamic psychotherapy); in
many instances, they simply have not been evaluated sufficiently. Nonetheless, the value of identifying and promulgating
treatments that have support for their use is evident. Demonstration of efficacy of treatments in well-controlled, randomized trials
may point the way to determining the effectiveness of these treatments in real-life clinical settings (Chorpita, 2003; Weisz, Jensen-
Doss, & Hawley, 2006).
One of the concerns associated with EBTs resides in differences between what have been labeled efficacy versus effectiveness
studies (Hoagwood, Hibbs, Brent, & Jensen, 1995; Ollendick, King, & Chorpita, 2006; Southam-Gerow, Chorpita, Miller, & Gleacher,
2008). Efficacy studies demonstrate that the benefits associated with a given treatment administered in a fairly standard way
(usually with a treatment manual) are due to the treatment and not chance or other factors that threaten the internal validity of the
study. These studies are usually conducted under tightly controlled experimental conditions, typically in laboratory or university
settings. Most of these studies consist of Randomized Controlled Trials (RCTs) which involve random allocation of subjects to
treatments. Appropriate concern has been raised about the portability of these “laboratory-based” treatments to the real world —
the world of clinical practice. Arguments have been mustered that the “subjects” in RCTs do not represent real-life “clients” who are
heterogeneous in presentation and frequently comorbid with other disorders, and the “experimenters” in these trials do not
represent “clinical therapists” in applied practice settings. Moreover, the settings themselves are viewed as different — ranging
from tightly controlled laboratory conditions to less controlled conditions in everyday practice settings. In this regard, Weisz,
Donenberg, Han, and Weiss (1995) have referred to practice settings as the “proving ground” of EBTs.
Clearly, a number of differences may exist between efficacy and effectiveness studies. In the present review, we examine one of
many critical issues that have been raised in these studies: namely, the presence of comorbidity in the “subjects” treated in RCTs
and whether comorbidity predicts or moderates treatment outcomes. In doing so, we examine the treatment literature for the four
most commonly occurring childhood psychiatric disorders: Anxiety disorders, affective disorders, attention deficit/hyperactivity
disorder (ADHD), and oppositional defiant disorder (ODD)/conduct disorder (CD). For each of these disorders, we first briefly
review comorbidity in these disorders in epidemiological and clinical samples and then review the psychosocial treatment
literature to determine the effects of comorbidity on treatment outcomes.
In treatment outcome research, comorbidity can best be viewed as a potential moderator variable: a variable that influences the
strength or direction of the relationship between treatment and outcome. Treatment moderators inform “for whom” or under
“what conditions” the treatments work (Kraemer, Wilson, Fairburn, & Agras, 2002). Kraemer and colleagues further specify that a
moderator of treatment must be a baseline or pre-randomization characteristic (i.e., exists prior to treatment and not a function of
treatment) that can be shown to interact with treatment condition on outcome measures. Thus, comorbidity is a “subject”
characteristic not unlike age, sex, ethnicity or severity of the disorder that exists prior to treatment and that may help inform
whether the efficacy of the treatment is qualified by comorbidity. Finally, it should be noted that moderators of treatment outcome
are not the same as “predictors” of treatment outcome. Kraemer and colleagues, along with others (see Kazdin & Weisz, 2003;
March & Curry, 1998), specify that predictors are pre-treatment variables associated with treatment outcomes regardless of
treatment assignment. That is, such variables predict response not only to the treatment of interest but also to comparison
conditions. In contrast, a moderator variable must interact with treatment assignment to specify for whom a specific treatment
works. This distinction is an important one because not all predictor variables are moderators of treatment outcome.

1. Procedure

Standard computerized databases (PsycInfo and MEDLINE) were searched. For each of the four substantive areas (anxiety,
depression, ADHD, and conduct problems), search terms included psychotherapy, counseling, treatment, clinical trial, child,
adolescent, and comorbidity. Only articles written in English and published between 1980 and 2007 were sought. This
timeframe was selected because it coincided with the advent of DSM-III and progressed through DSM-III-R and DSM-IV and
up to the present time. In addition, published qualitative reviews and meta-analyses of the youth psychotherapy literature
were accessed to find studies not located through PsycInfo and MEDLINE. Reference trails of the reviewed studies were also
pursued.
T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471 1449

Only studies that had been subjected to peer review were included so that some degree of quality control could be assured. The
selected studies had to show a level of methodological soundness as evidenced by random assignment of participants to treatment
conditions, selection of participants who met diagnostic criteria for the indicated disorders or who surpassed clinical cutoff scores
on commonly used treatment outcome measures (e.g., clinical cutoff scores on the CBCL), and indicated use of a treatment manual
or a set of procedures that were clearly described in the study. In addition, the studies had to include post-treatment assessment.
Characteristics of the various studies can be seen in Tables 1–4. Table references not cited in the manuscript are available from the
authors by request.
Although it would have been desirable to include other measures of methodological soundness such as the qualifications of the
therapists, the quality of the outcome measures themselves, and treatment adherence and competence, it was decided not to
include these measures because of the relative state of the literature for study purposes. It might also have been desirable to
provide a meta-analysis of the studies reviewed; however, as will become evident, too few studies examined predictor/moderator
analyses to do so. Instead, a qualitative review was conducted that provides an initial foray into the state of comorbidity and its
effects on EBTs in youth.

2. Anxiety disorders

Anxiety disorders are among the most common mental health problems in children and adolescents, with prevalence rates
approximating 12% in community samples and 36% in clinical samples (cf, Kessler, Berglund, Demler, Jin, & Walters, 2005). DSM-IV
specifies that all of the anxiety disorders of adulthood are recognized in childhood (i.e., generalized anxiety disorder — GAD,
specific phobia — SP, social phobia — SOC, panic disorder — PD, agoraphobia — AG, obsessive–compulsive disorder — OCD, and
post-traumatic stress disorder — PTSD), as well as one disorder which occurs prior to age 18 (separation anxiety disorder — SAD).
However, other related difficulties are often encompassed under the anxiety-related umbrella (e.g., school refusal — SR, selective
mutism), and past research based on earlier versions of the DSM included two alternative diagnoses (i.e., overanxious disorder —
OAD, avoidant disorder — AD) that have been subsumed under GAD and SOC in DSM-IV, respectively.

2.1. Anxiety and its comorbidities

High rates of comorbidity have been reported for the childhood anxiety disorders, with other anxiety diagnoses being most
common (cf Angold, Costello, & Erkanli, 1999). Studies have also revealed broad ranges of comorbidity for anxiety disorders with
depression (17–69%; cf, Seligman, Goza, & Ollendick, 2004) and externalizing disorders (8–69%, Beidel et al., 2007). Moreover, in a
meta-analytic review of community studies of childhood disorders, Angold et al. (1999) reported comorbid rates of anxiety and
ADHD, as well as anxiety and ODD/CD, to be approximately three times greater than that expected by chance, and anxiety and
depression to be approximately eight times greater than that expected by chance.

2.2. EBTs for anxiety disorders

Numerous RCTs for major anxiety disorders (GAD, SAD, SOC) using behavioral and cognitive-behavioral therapy (CBT) have
been published with significant improvements noted at post-treatment (e.g., Kendall, 1994; Kendall et al., 1997) and 1-, 3-, and
7 year follow-ups (Kendall, 1994; Kendall et al., 1997; Kendall, Safford, Flannery-Schroeder, & Webb, 2004; Kendall & Southam-
Gerow, 1996). Moreover, group CBT and CBT with parent/family involvement have also been found to be effective in treating
anxious children (see Table 1). Moreover, all of the RCTs for the anxiety disorders meeting our inclusion criteria used some variant
of CBT (e.g., individual/group, child/family). Overall, significant reductions in symptoms or diagnoses have been observed in about
60% of youth, compared with about 10% for those in waitlist or comparison groups. Importantly, although many of the above
studies excluded participants with OCD and PTSD, RCTs with these disorders reveal similar findings. For example, improvement/
remission rates of 39–88% and 60–92%, compared with 0–4% and 20–42% for waitlist comparison groups, have been reported for
CBT approaches with OCD and PTSD, respectively (Barrett, Healy-Farrell, & March, 2004; King et al., 2000; POTS Team, 2004; Smith
et al., 2007).

2.3. Comorbidity as a predictor/moderator of anxiety treatment outcomes

In all, 43 RCTs for anxiety-related disorders were identified (see Table 1, 8 follow-up studies are also presented in Table 1). For
the studies that reported sample comorbidity (37), co-occurring internalizing disorders were evident in all but two instances,
whereas this was often not true for externalizing disorders (particularly ODD/CD). In addition, many studies excluded individuals
with psychotic disorders, intellectual deficits, or pervasive developmental disorders — disorders for which these treatments were
not designed. However, only 14 of the 43 RCTs specifically examined the predictive or moderating influence of comorbidity on
treatment outcomes, and two other studies (Manassis et al., 2002; Silverman et al., 1999b) noted the influence of comorbidity in
the discussion of findings but did not clearly specify how the effects of comorbidity were examined.
Kendall (1994) andKendall et al. (1997) have explored the impact of comorbidity in five studies combining participants from
their two major RCTs and new participants not previously included in either study. No significant predictive effects were found for:
1) youth with other comorbid anxiety disorders versus non-anxiety disorders (including mood disorders and externalizing
disorders) on post-treatment measures of anxiety symptoms or distress (Kendall et al., 1997); 2) the number of pre-treatment
1450
Table 1
Anxiety disorders

Authors year N age Primary diag How sample Comorbidity type in Comorbidity exclusion Treatment conditions Results of comorbidity analysis
defined sample
1 Kendall (1994) 47 oad, sad, ad Structured interview spp, dep, adhd, odd, Psychotic sxs, primary spp dis, cbt-i, wl n/a
9–13 cd iq b 80
2 Barrett, Dadds, and 79 sad, oad, soc Structured interview spp, dep, odd Intellectual disability cbt-i, cbt-i + fam, wl n/a
Rapee (1996) 7–14
3 Kendall and 36 oad, sad, ad Structured interview, f-up of #1 above Psychotic sxs, primary spp dis f-up study (cbt) n/a
Southam-Gerow (1996) 11–18 self-reports
4 Dadds, Spence, Holland, 181 gad, sad, soc, spp, Structured interview gad, sad, spp, soc, dbd, ext dis cbt-i + fam, n/a
Barrett, and Laurens (1997) 7–14 other ext monitoring
5 Kendall et al. (1997) 94 oad, sad, ad Structured interview spp, adhd, odd, Psychotic sxs, primary spp dis cbt-i, wl Yes, pred: no differences for
9–13 mdd, cd comor anx v. non-anx dis.

T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471


6 Kendall and 190 oad, sad, ad Structured interview spp, dep, adhd, odd, Psychotic sxs, primary spp dis f-up study (cbt) Yes, pred: no differences for completers
Sugarman (1997) 8–14 cd v. terminators (anx, ext, or # diag).
7 Barrett (1998) 60 sad, oad, soc Structured interview other anx, dep Intellectual disability cbt-g, cbt-g + fam, wl n/a
7–14
8 Cobham, Dadds, and 67 sad, oad, gad, spp, Structured interview spp, soc, sad, gad, ag Non-anx comor, intellectual cbt-i, cbt-i + fam n/a
Spence (1998) 7–14 soc, ag impairment
9 de Haan, Hoogduin, Buitelaar, 22 ocd Structured interview sad, edn, tic org, psychosis, ts, aut, mr, clomipramine v. bt n/a
and Keijsers (1998) 8–18 primary mdd
10 King et al. (1998) 34 sr + anx, dep, or Structured interview odd, sad, oad, spp Antisocial characteristics, cbt-i, wl n/a
5–15 adj intellectual disability, psychotic
sxs
11 Last, Hansen, and 56 sr + spp, soc, sad, Structured interview other anx, odd, tric mdd-current cbt-i, ac n/a
Franco (1998) 6–17 ad, oad, pd
12 Muris, Merckelbach, Holdrinet, 26 spp Structured interview None Comorbid psychopathology or emdr-g, in-vivo n/a
and Sijsenaar (1998) 8–17 intellectual disabilities exposure-g,
computerized
exposure
13 Mendlowitz et al. (1999) 62 any anx Structured interview Not reported Psychotic dis cbt-g, cbt-fam, cbt-g + n/a
7–12 fam, wl
14 Silverman et al. (1999a) 81 spp, soc, ag Structured interview spp, sad, oad, adhd, pdd, psychotic sxs Exposure, csct, es n/a
6–16 other
15 Silverman et al. (1999b) 56 gad, soc, oad Structured interview Not reported pdd, psychotic sxs cbt-g, wl Yes, pred: no pred effect for comor
6–16 status on severity or child/parent outcome.
16 Beidel et al. (2000) 67 soc Structured interview other anx, adjd, sm, Unspecified cbt, non-specific tx Yes, pred: no differences for comor (yes v. no).
8–12 adhd
17 Berman et al. (2000) 106 spp, oad, soc, gad, Structured interview anx, anx/ext, ext, pdd, psychotic sxs f-up study (cbt) Yes, pred: no differences for # diag or comor;
6–17 ag anx/dep, anx/dep/ comor dep (worse outcomes).
ext, ext/dep
18 Flannery-Schroeder 37 gad, sad, soc Structured interview spp, adhd, dys, odd, Psychotic sxs, primary spp diag cbt-i, cbt-g, wl n/a
and Kendall (2000) 8–14 mdd
19 Hayward, Varady, Albano, 35 soc Structured interview past mdd mdd, current/past pd, ag, su, cbt-g v. no tx n/a
Thienemann, Henderson, and 13–17 psychosis, current psychotropic
Schatzberg (2000) meds
20 King et al. (2000) 36 ptsd or ptsd sxs Structured interview dys, odd, sad, gad, Intellectual disability, psychosis cbt-i, cbt-fam, wl n/a
5–17 cd, mdd, adhd, spp
21 Spence, Donovan, and 50 soc Structured interview sad, odd, spp, dys, ld, comor other clinically severe cbt-i, cbt-i + fam, wl n/a
Brechman-Toussaint (2000) 7–14 gad, adhd diag
22 Barrett et al. (2001) 52 sad, oad, soc Structured interview spp, dep, odd Intellectual impairment, severe f-up study (cbt) Yes, pred: no differences for no comor
13–21 physical impairment, current v. comor primary v. comor other.
meds/pt
23 Kendall et al. (2001) 173 gad, soc, sad Structured interview gad, sad, soc, spp, Psychotic sxs cbt-i, wl Yes, mod: anx v. anx/anx v. anx/ext comor
8–13 ocd, pd, dep, adhd, groups compared-only difference: those with
odd, cd post-tx comor worse tx outcomes.
24 Muris, Mayer, Bartelds, Tierney, 36 gad, sad, soc, ocd Structured interview other anx, adhd Unspecified cbt-g, cbt-i n/a
and Bogie (2001) 8–13
25 Ost et al. (2001) 60 spp Structured interview spp, mdd, soc, sad, Primary dep, su, dev dis, cbt-i, cbt-i + fam, wl Yes, pred: no effect for pre-tx comor on
7–17 gad, enu psychotic sxs outcome; comor improved post-tx.
26 Shortt et al. (2001) 71 sad, soc, gad Structured interview spp, gad, sad, soc, Intellectual impairment, severe cbt-g, wl Yes, mod: no main/mod effect of comor on
6–10 dys, mdd physical impairment, current outcome; greater post-tx comor in wl v. tx groups.
meds/pt
27 Southam-Gerow et al. (2001) 135/107 sad, gad, soc, ad Structured interview spp, gad, soc, dys Psychotic sxs f-up study (cbt) Yes, pred: good v. poor tx response examined
sad, ocd, adhd, odd, with # comor dis: unrelated to or pred of tx
enu, mdd, cd response.

T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471


28 Ginsburg and Drake (2002) 9 anx except ptsd/ Structured interview soc, spp, gad, ag, Psychiatric condition contra- cbt, ac n/a
14–17 ocd mdd indicating study tx
29 Heyne et al. (2002) 61 sr + adja, anxn, pd, Structured interview anx, dep, odd cd, mr, severe disturbance cbt-i, parent + teacher n/a
7–14 adjm, ag, sad, needing immediate attention training, combined
odd, gad, spp,
ocd, soc
30 Manassis et al. (2002) 78 gad, sad, spp, soc, Structured interview sad, gad, soc, spp, Psychotic dis, iq b 80, learning cbt-i, cbt-g No, but no difference for high v. low
8–12 pd ocd, adhd, dep, odd difficulties hyperactivity on tx outcome.
31 Muris, Meesters, and van 30 sad, gad, soc Structured interview other anx Not reported cbt-g v. psych placebo n/a
Melick (2002) 9–12 v. wl
32 Nauta, Scholing, Emmelkamp, 79 sad, soc, gad, pd Structured interview adhd, dys, dep, odd, Other primary diag, iq b 80 cbt-i, cbt-i + fam, wl n/a
and Minderaa (2003) 7–18 anx
33 Rapee (2003) 165 sad, gad, soc, spp, Structured interview anx, dep, other Unspecified cbt-g + fam Yes, mod: compared no comor v. anx comor v.
7–16 ocd, pd (mostly ext) non-anx comor grps; comor grps = fewer
therapy sessions and increased cbcl-ext from
post-tx to f-up.
34 Barrett et al. (2004) 77 ocd only Structured interview Not reported Primary mdd, other anx, ext dis, cbt-i + fam, cbt-g + No, but reduction in percentage with comor diag
7–17 ts, autism spectrum, sz, organic \ fam, wl at post-tx for both ind/grp tx grps v. wl.
mental dis, mr, iq outside
normal range
35 Gallagher, Rabian, and 23 soc Structured interview sad, spp, gad, ptsd, adhd, odd, cd, bpd, pdd, mr cbt-g, wl n/a
McCloskey (2004) 8–11 dys, sm, st, enu
36 Kendall et al. (2004) 86 oad, sad, ad Structured interview Not reported Psychotic sxs, primary spp dis f-up study (cbt) Yes, pred: # of pre-tx dis did not
15–22 pred presence of anx dis at f-up.
37 Manassis et al. (2004) 43 any anx dis Structured interview Not reported Psychosis, iq b 80 f-up study (cbt) Yes, pred: no differences for 1
pre-tx anx dis v. 2 + anx dis.
38 POTS Team (2004) 112 ocd Structured interview anx/dep, tic adhd/ mdd, bpd, primary ts, pdd, cbt, sertraline, cbt + n/a
7–17 odd/cd, psychosis sertraline, pill placebo
39 Asbahr et al. (2005) 40 ocd Structured/clinical dep, mania, ptsd, Primary mdd or adhd, bpd, pdd, cbt-g v. sertraline n/a
9–17 interview sad, spp, pd, odd, tic, ptsd, blpd, neur, aut, psychosis,
enu, adhd, an, bn org, previous or current ocd tx
40 Baer and Garland (2005) 12 soc Structured interview gad, ag, pd, ptsd, su, psychosis, organic mental cbt-g, wl n/a
13–18 spp, adhd, asp dis, current mdd
41 Masia-Warner et al. (2005) 35 soc Structured interview gad, dys, ag, edn su, cd, odd, mdd, as primary cbt-g (social skills), wl No, but comor dis significantly
13–17 diag; psychotic sxs reduced in tx v. wl grp.
42 Rapee, Abbott, and 267 gad, soc, sad, spp, Structured interview anx, ext, dep Unspecified cbt-g, bbliotx, wl n/a
Lyneham (2006) 6–12 ocd, pd

1451
(continued on next page)
1452
Table 1 (continued)

Authors year N age Primary diag How sample Comorbidity type in Comorbidity exclusion Treatment conditions Results of comorbidity analysis
defined sample
43 Spence, Holmes, March, and 72 gad, sad, soc, spp Structured interview other anx, odd, Intellectual or dev. dis, cbt-g, cbt-g + internet, n/a
Lipp (2006) 7–14 adhd, dys currently in pt or on meds wl
44 Wood, Piacentini, Southam- 40 sad, gad, soc Structured interview adhd, dys, mdd, sm, Unstable/started/changed cbt-f v. cbt-i n/a
Gerow, Chu, and Sigman 6–13 ocd, spp, sad, gad, psychiatric meds, current child
(2006) soc or fam pt or psychosis

T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471


45 Lyneham and Rapee (2006) 100 gad, sad, soc, ocd, Structured interview other anx, dep, ptsd, Unstable/changed psychiatric bblio w/varying n/a
6–12 spp, pd odd, enu, st, adhd, meds contact v. wl
asp, ts
46 Chalfant, Rapee, and Carroll 47 aut/asp + pd, sad, Structured interview other anx, adhd odd, cd, intellectual delay, cbt-g/fam v. wl Yes, mod: # of anx dx sig reduced
(2007) 8–13 gad, spp, soc, physical disability, currently on for cbt group only
anti-anxiety or depressant
meds, marital breakdown
47 Masia-Warner, Fisher, Shrout, 36 soc Structured interview gad, ocd, sad, mdd, su, cd, primary diag other than cbt-g (social skills), ac n/a
Rathor, and Klein (2007) 14–16 dys, adjd, edn, adhd, soc, psychotic sxs
anxn
48 Smith et al. (2007) 24 ptsd Structured interview Not reported Learning difficulty cbt-i, wl Yes, pred: response during sx
8–18 monitoring phase less likely to have
comor dis at initial evaluation.
49 Storch et al. (2007) 40 ocd Clinical/structured gad, tics, mdd, adhd, Psychosis, pdd, bpd, primary cbt-fam (intensive v. n/a
7–17 interview odd, soc, asp, pd, diag other than ocd, caregiver weekly)
tric, ag, diagnosis of mr, psychosis or
similar
50 Levy, Hunt, and Heriot (2007) 69 sad, gad, soc, spp, Structured interview All comorbid with Currently in tx for anx/ext, pdd, Anxiety tx v. anxiety + n/a
8–14 pd AND agg agg; other anx, aut aggression
adhd, odd, cd, ld
51 March et al. (2007) 112 Ocd Structured interview f-u study of ADHD f-u study cbt, sertraline, cbt + Yes, mod: presence of comorbid
7–17 MTA trial sertraline, pill placebo tic dis. sig. mod, worsened outcome for
sertraline than cbt condition

Note: ac = attention control, ad = avoidant disorder, adhd = attention deficit/hyperactivity disorder, adja = adjustment with anxiety, adjd = adjustment with depression, adjm = adjustment disorder mixed with conduct, ag =
agoraphobia, agg = aggression, an= anorexia nervosa, anx = anxiety, anxn = anxiety disorder not otherwise specified, asp = Asperger's disorder, aut = autism, bblio = bibliotherapy, blpd = borderline personality disorder, bn =
bulimia nervosa, bpd = bipolar disorder, bt = behavior therapy, cbcl = child behavior checklist, cbt-i = cognitive-behavioral therapy in individual format, cbt-f = cognitive-behavioral therapy in family format, cbt-g = cognitive-
behavioral therapy in group format, cd = conduct disorder, comor = comorbid/comorbidity, cpd = compulsive personality disorder, csct = cognitive self-control therapy, dbd = disruptive behavior disorder, dep = depressive
disorder, dev = developmental, diag = diagnosis, dis = disorder, ds = delusional system, dys = dysthymia, ed = eating disorder, edn = eating disorder not otherwise specified, enu = enuresis, erp = exposure with response
prevention, es = education support, ext = externalizing, fam = family, f-up = follow-up, gad = generalized anxiety disorder, grp(s) = group(s), ind = individual, iq = intelligence quotient, mdd = major depressive disorder, mod =
moderator, mr = mental retardation, n = sample size, n/a = not applicable, neur = neurologic condition, oad = overanxious disorder, ocd = obsessive–compulsive disorder, odd = oppositional defiant disorder, org = organic
mental disorder, pd = panic disorder, pdd = pervasive developmental disorder, pred = predictor, psych = psychological, pt = psychotherapy, ptsd = post-traumatic stress disorder, sad = separation anxiety disorder, scpd =
schizotypal personality disorder, sm = selective mutism, soc = social phobia, spp = specific phobia, sr = school refusal, st = sleep terror, su = substance use/abuse/dependence, sxs = symptoms, sz = schizophrenia, td = thought
disorder, tic = tic disorder, tric = trichotillimania, ts = Tourette's syndrome, tx = treatment, v. = versus, wl = waitlist.
Table 2
Affective disorders

Authors year N age Primary diag How sample Comorbidity type Comorbidity exclusion Treatment conditions Results of comorbidity analyses
defined in sample
1 Butler, Miezitis, 56 Depression Teacher referral, Not reported None reported Role play, cognitive n/a
Friedman, and Cole (1980) 5th and 6th symptoms self-reports restructuring, attention placebo,
grade no treatment
2 Reynolds and Coats (1986) 30 Depression Self-reports, Not reported None reported cbt, relaxation training, wl n/a
Mean = 15.7 symptoms clinician rating
3 Stark, Reynolds, and Kaslow 29 Depression Self-report Not reported None reported Self-control therapy (cbt), n/a
(1987) 9–12 symptoms behavioral problem solving, wl
4 Kahn, Kehle, Jenson, and Clark 68 Depression Self-reports, Not reported None reported cbt, relaxation training, self- n/a
(1990) 10–14 symptoms clinician rating modeling, wl
5 Lewinsohn et al. (1990) 59 mdd, minor Structured See Clarke et al. bpd with mania or cbt-i, cbt + parent, wl Yes, pred: better outcome pred by greater #

T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471


14–18 dep, or interview (1999) hypomania, pd, gad, cd, of past diag; higher state anx associated with
intermittent su, mdd — psychotic, less likelihood of recovery (see also Clarke
dep dis organic brain syndrome, et al., 1999).
mr, history of sz
6 Liddle and Spence (1990) 31 Depression Self-report and Not reported None reported Social competence training (cbt), n/a
7–11 symptoms clinician rating attention placebo, no
treatment
7 Fine, Forth, Gilbert, and Haley 66 mdd or Structured Not reported Neurological damage, Social skills, tsg n/a
(1991) 13–17 dysthymia interview and borderline intelligence
clinical diagnosis
8 Reed (1994) 18 mdd or Method for Not reported None reported Structured learning therapy n/a
14–19 dysthymia diagnosis not (cbt), placebo control
reported, self-
report
9 Vostanis, Feehan, Grattan, 57 mdd, dys, or Structured anx, odd/cd ld cbt, nfi Yes, pred: self-reported anx pred psychiatric
and Bickerton (1996) 8–17 minor dep interview dis at 2 years. comor at end of tx pred dep at
2 year f-up.
10 Wood, Harrington, and Moore 53 mdd or minor Structured oad, cd Psychosis, autism, ld Brief cbt, relaxation training n/a
(1996) 9–17 dep interview and
rating scale
11 Brent et al. (1997) 107 mdd Structured dd, anx, dbd Psychosis, bpd I or II, ocd, cbt, sbft, nst Yes, mod: anx predicted non-recovery at post;
13–18 interview and eating dis, su within past greater differences between cbt and nst when
rating scale 6 months anx present. cbt N sbft and nst in absence of
maternal dep but not if maternal dep present.
12 Weisz, Thurber, Sweeney, Proffitt, 48 Depression Self-report and Not reported None reported pascet (cbt), no treatment n/a
and LeGagnoux (1997) Mean = 9.6 symptoms clinician rating
13 Clarke et al. (1999) 123 mdd or dys Structured dd, lifetime: anx, Current mania/ cbt, cbt + parent, wl Yes, mod: lifetime comor related to higher dep
14–18 interview dbd, su hypomania, pd, gad, cd, scores at intake and greater changes in dep
su, organic brain post-tx. comor did not interact with tx
syndrome, mr, sz condition to predict change in dep sxs or
recovery at post-tx.
14 Mufson et al. (1999) 48 mdd Clinical interview dd, anx Psychosis, bpd, cd, su, ipt, clinical monitoring n/a
12–18 and rating scale eating dis, ocd
15 Rosselló and Bernal (1999) 71 mdd or dys Structured dd Psychotic sxs, bpd, su, cd, cbt, ipt, wl n/a
13–17 interview organic brain syndrome,
hyperaggression

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Table 2 (continued)

T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471


Authors year N age Primary diag How sample Comorbidity type Comorbidity exclusion Treatment conditions Results of comorbidity analyses
defined in sample
16 Asarnow, Scott, and Mintz (2002) 23 Depressive Self-report Not reported None reported Stress-busters (cbt + family n/a
4th–6th symptoms education), wl
grade
17 Clarke et al. (2002) 88 mdd or dys and Structured Unspecified Unspecified tau, tau + cbt n/a
13–18 parent dep interview
18 Mufson et al. (2004) 63 mdd, dys, adjd, Structured/ dd, anx, odd, su, su, psychosis, sz, mr ipt, tau Yes, mod: comor group had higher dep at
12–18 or dep dis nos clinical interview adhd intake but not lower global functioning. ipt
and rating scales better for those with comor anx but not
different from tau for noncomor group.
19 Rohde, Clarke, Mace, Jorgensen, 93 mdd and cd Structured dd, adhd, su, anx Psychotic sxs cbt, life skills/tutor n/a
and Seeley (2004) 13–17 interview
20 The TADS Team (2004) 439 mdd Structured dd, anx, dbd, bpd, severe cd, pdd, cbt, flx, cbt + flx, placebo Yes, mod: comor anx dis and # comor diag
12–17 interview and adhd, ocd/tic, su thought dis pred worse outcome as did number of comor
rating scale diagnoses. No mod effect.

Note: adhd = attention deficit/hyperactivity disorder, adjd = adjustment with depression, anx = anxiety, bpd = bipolar disorder, cbt = cognitive-behavioral therapy, cbt-i = cognitive-behavioral therapy in individual format, cd =
conduct disorder, comor = comorbid/comorbidity, dbd = disruptive behavior disorder, dd = double-depression, dep = depressive disorder, diag = diagnosis, dis = disorder, dys = dysthymia, flx = fluoxetine, f-up = follow-up, gad =
generalized anxiety disorder, ipt = interpersonal therapy, ipt-a = interpersonal therapy for adolescents, ld = learning disorder, mdd = major depressive disorder, mod = moderator, mr = mental retardation, n = sample size, n/a = not
applicable, nfi = non-focused control intervention, nos = not otherwise specified, nst = nondirective supportive treatment, oad = overanxious disorder, ocd = obsessive–compulsive disorder, odd = oppositional defiant disorder, pd =
panic disorder, pdd = pervasive developmental disorder, pred = predictor, sbft = systemic behavior family therapy, su = substance use/abuse/dependence, sxs = symptoms, sz = schizophrenia, tau = treatment as usual, tic = tic disorder,
tx = treatment, wl = waitlist.
Table 3
ADHD

Authors year N age Primary diag How sample defined Comorbidity type in Comorbidity exclusion Treatment conditions Results of comorbidity analyses
sample
1 Horn et al. (1987) 24 add + h Behavior checklists comor sx ratings Intellectual deficits or pt, cbsct, combined Yes, pred: pre-tx conduct
7–11 psychosis in child or problems did not pred tx outcome
parent (data collapsed across conditions).
2 Pisterman et al. (1989) 46 add + h Structured interview, comor sx ratings iq b 80 pt (immediate v. delayed; wl) n/a
3–6 behavior checklists,
behavior assessment
3 Horn, Ialongo, Greenberg, 42 adhd Clinical interview, comor sx ratings; Intellectual deficits or pt, cbsct, combined, control No, but: sample grouped based on
Packard, and Smith- 7–11 behavior checklists most aggressive psychosis in child or ext behavior change;
Winberry (1990) parent group (3 groups) ) × responder (yes
or no) interaction —

T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471


combined best for responders.
4 Horn et al. (1991); 96 adhd Clinical interview, cd, odd anx, dep, intellectual med placebo, med low dose, n/a
Ialongo et al. (1993) 7–11 behavior checklists deficits, psychosis med high dose, med placebo +
pt/cbsct, med low dose + pt/
cbsct, med high dose + pt/cbsct
5 Barkley et al. (1992) 61 adhd Clinical interview, odd and cd sxs Psychosis, iq b 80 bm, psct, ft Yes, pred: odd sxs did not pred
12–18 behavior checklists mother or child-reported
outcomes (data collapsed across
conditions).
6 Anastopoulos, Shelton, 34 adhd Clinical interview, odd, oad, enu low iq, pdd, psychosis pt, wl n/a
DuPaul, and Guevremont 6–10 behavior checklists
(1993)
7 Pelham and Hoza (1996) 258 adhd Structured interview odd and cd sxs None stp Yes, pred: aggression pred better
5–12 or same response to tx.
8 Frankel et al. (1997) 47 adhd Structured interview odd Developmental pt + sst, wl Yes, pred: presence of odd did not
6–12 disorder, psychosis affect response to tx.
9 Klein and Abikoff (1997) 86 adhd Clinical interview, comor sx ratings; few Neurological dis, bt, med, combined n/a
6–12 behavior checklists sxs psychosis, iq b 85, cd
10 Pfiffner and McBurnett 27 adhd Semi-structured odd, cd, sad, oad, dys None sst-pg, sst, wl n/a
(1997) 8–10 interview, behavior
checklists
11 Kolko et al. (1999) 16 adhd + odd or Structured interview odd, cd, anx, dep, ied, None med, bm, med + bm Yes, mod: no difference between
7–13 cd dad med and bm for odd v. cd. odd
showed greater decline in
behavior problems in the bm
condition than cd. med + bm
associated with greater mood
improvement in cd than odd.
12 MTA Cooperative 579 adhd-c Structured interview anx, cd, odd, dep, tic, Conditions requiring txs bm, med, bm + med, cc Yes, mod: odd/cd did not mod tx
Group (1999a,b) 7–9 mania, other not used in study outcome. enhanced response to
bm (i.e., parent-reported adhd and
internalizing sxs) for children with
comor anx.
13 Pelham et al. (2000) 117 adhd-c Structured interview odd, cd Conditions requiring txs stp, stp + med Yes, pred and mod: presence of
7–9 not used in study odd/cd predicted increased
whining/complaining. overall,
limited evidence for pred or mod

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T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471
Table 3 (continued)

Authors year N age Primary diag How sample defined Comorbidity type in Comorbidity exclusion Treatment conditions Results of comorbidity analyses
sample
14 Barkley, Edwards, Laneri, 97 adhd and odd/ Structured interview, odd/cd Language delay, psct, bm + psct n/a
Fletcher, and Metevia (2001) 12–18 cd behavior checklists epilepsy, autism,
psychosis
15 Jensen et al. (2001); MTA 579 adhd-c Structured interview adhd, adhd + anx, Conditions requiring bm, med, bm + med, cc Yes, mod: adhd + anx responded
Study 7–9 adhd + odd/cd, adhd treatments not used in equally to med and bm. adhd or
+ odd/cd + anx study adhd + odd/cd responded best to
med (with or without bm). adhd
+ odd/cd + anx responded best to
combined.
16 Sonuga-Barke, Daley, 78 adhd Structured interview Conduct sxs reported ld, unrelated mental pt, pcs, wl n/a
Thompson, Laver-Bradbury, 3 health condition
and Weeks (2001)
17 Bor, Sanders, and Markie- 87 adhd Clinical interview, Not reported Developmental ebfi, sbfi, wl n/a
Dadds (2002) 3 behavior checklists disorder, intellectual
deficits
18 Antshel and Remer (2003) 120 adhd-i, adhd-c Structured interview, odd, anx, tic None sst, control Yes, pred: odd symptoms
8–12 behavior checklists predicted poorer treatment
outcome
19 Owens et al. (2003); MTA 579 adhd-c Structured interview anx, cd, odd, dep, tic, Conditions requiring txs bm, med, bm + med, cc Yes, mod: comor anx and
Study 7–9 mania, other not used in study oppositionality/aggression did not
pred or mod tx outcome.
20 Abikoff et al. (2004) 103 adhd Structured interview, odd, anx, dep Neurological dis, med, med + mpt, med + ac n/a
7–9 behavior checklists psychosis, tic/ts, ld, cd
21 Sonuga-Barke, Thompson, 89 adhd Structured, interview, Not reported None pt, wl n/a
Daley, and Laver-Bradbury 3 behavior checklists
(2004)
22 Ercan, Varan, and 81 adhd-c + odd, Structured interview, odd, cd Comor disorders other pt, med + pt n/a
Deniz (2005) 7–13 adhd-c + cd behavior checklists than odd and cd
23 Evans, Langberg, Raggi, Allen, 27 adhd-c, adhd-i Structured interview, Not reported Bipolar, psychosis chp, control n/a
and Buvinger (2005) 11–14 behavior checklists
24 Owens et al. (2005) 42 adhd Behavior checklists odd, cd iq b 70 yess, wl n/a
25 DuPaul et al. (2006) 167 167 mean = 8 Structured interview, odd, cd None iai, gai n/a
behavior checklists
26 Evans, Serpell, Schultz, and 79 adhd Structured interview, Not specifically Psychosis, pdd chp-c, control n/a
Pastor (2007) 10–14 behavior checklist reported, majority
comorbid
27 Jensen et al. (2007) ; MTA 485 adhd-c Structured interview Not reported Conditions requiring txs bm, med, bm + med, cc Yes, mod: baseline comor (odd/cd
Study 10–13 not used in study without anx, anx without odd/cd,
odd/cd and anx, no odd/cd or anx)
pred poorer tx response. no mod
effect.
28 Jitendra et al. (2007) 167 adhd Structured interview, odd, cd None idia, tdai n/a
mean = 8 behavior checklists
29 Pfiffner et al. (2007) 69 adhd-i Structured interview odd, cd, dep, anx, elim Language delay, Clasp, control n/a

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7–11 neurological illness,
psychosis, pdd
30 van der Hoofdakker et al. 94 adhd Structured interview odd, cd, anx, dep, tic, Conditions requiring txs pt, cc n/a
(2007) 4–12 not used in study
31 van der Ord, Prins, 50 adhd Structured interview odd/cd None bm, bm + med n/a
Oosterlaan, and Emmelkamp 8–12
(2007)

Note: ac = attention control, add + h = attention deficit disorder plus hyperactivity, adhd = attention deficit/hyperactivity disorder, adhd-c = attention deficit/hyperactivity disorder, combined type, adhd-i = attention deficit/
hyperactivity disorder, inattentive type, anx = anxiety, bm = behavior management, bt = behavior therapy, cbsct = cognitive-behavioral self-control therapy, cc = community control, cd = conduct disorder, clasp = child life and
attention skills program, chp = challenging horizons program, chp-c = challenging horizons program, consultation model, comor = comorbid/comorbidity, dad = developmental articulation disorder, dep = depressive disorder,
diag = diagnosis, dis = disorder, dys = dysthymia, ebfi = enhanced behavioral family intervention, elim = elimination disorder, enu = enuresis, ext = externalizing, ft = family therapy, gai = generic academic intervention, gpt =
group parent training, iai = individualized academic intervention, idai = intensive data-based academic intervention, tdai = traditional data-based academic intervention, ied = intermittent explosive disorder, iq = intelligence
quotient, ld = learning disorder, med = medication, mod = moderator, mr = mental retardation, mpt = multimodal psychosocial treatment, n = sample size, n/a = not applicable, oad = overanxious disorder, odd = oppositional
defiant disorder, pcs = parent counseling and support, pdd = pervasive developmental disorder, pred = predictor, psct = problem solving and communication training, psteg = parent skills training and education group, pt =
parent training, sbfi = standard behavioral family intervention, ssg = social skills group, sst = social skills training, sst-pg = social skills training with parent-mediated generalization, stp = summer treatment program, sxs =
symptoms, tic = tic disorder, ts = Tourette's syndrome, tx = treatment, wl = waitlist, yess = youth experiencing success in school.

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Table 4
Conduct problems

T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471


Authors year N age Primary diag How sample defined Comorbidity type Comorbidity exclusion Treatment conditions Results of comorbidity analyses
in sample
1 Bernal, Klinnert, and 36 odd/cd Behavior checklists None Psychosis, history of pt, cc, wl n/a
Schultz (1980) 5–12 psychological referral
for other than social
aggression
2 Lochman, Burch, and 76 odd/cd Behavior checklists Unspecified None ac, gs, ac + gs, control n/a
Lampron (1984) 9–12
3 Kazdin, Esveldt-Dawson, 56 cd Behavior checklists add, depression, Dementia, seizure psst, rt, control n/a
French, and Unis (1987) 7–13 adjustment disorder, disorder, neurological
other impairment
4 Webster-Stratton, Kolpacoff, 114 odd Behavior checklists Unspecified Psychosis ivm, gdvm, gd, wl n/a
and Hollinsworth (1988) 3–8
5 Kazdin, Bass, and Siegel (1989) 112 odd/cd Structured interview, adhd, adjustment Dementia, seizure psst, psst-p, rt n/a
7–13 behavior checklists disorder, other disorder, neurological
impairment
6 Kazdin et al. (1992) 97 odd/cd Structured interview, adhd, adjustment Dementia, seizure psst, pt, psst + pt n/a
7–13 behavior checklists disorder, other disorder, neurological
impairment
7 Webster-Stratton (1994) 85 odd Behavior checklists Unspecified Psychosis pt, pt n/a
3–8
8 Prinz and Miller (1994) 147 odd/cd Behavior checklists Unspecified None pt, pt n/a
4–9
9 Tremblay, Pagani-Kurtz, 166 odd/cd Behavior checklists Unspecified None pt + ss, obs, control n/a
Masse, Vitaro, and Phil (1995)
10 Kazdin and Crowley (1997) 120 odd/cd Structured interview Unspecified None psst Yes, pred: comor was a sig pred such that those
7–13 with fewer sxs on cbcl responded better to tx.
11 Webster-Stratton and 97 odd/cd Structured interview adhd None pt, ct, ct + pt, wl n/a
Hammond (1997) 4–7
12 Schuhmann, Foote, Eyberg, 64 odd Structured interview adhd Severe mental pcit, wl n/a
Boggs, and Algina (1998) 3–6 impairment
13 Barkley et al. (2001) 97 adhd and Structured interview, adhd Language delay, psct, bm + psct n/a
12–18 odd/cd behavior checklists epilepsy, autism,
psychosis
14 Webster-Stratton 99 odd/cd Structured interview adhd Psychosis ct, wl Yes, pred: presence of adhd did not pred tx outcome.
et al. (2001) 4–8
15 CPPRG (2002) 891; odd/cd Behavior checklists Unspecified None Fast track Yes, pred: hyperactivity (defined by cbcl)
mean = 6 intervention, control did not alter tx outcome.
16 Lochman and Wells (2002) 245 odd/cd Behavior checklists Unspecified None cp ci, cp cpi, control n/a
5th–6th
grade
17 Hartman et al. (2003) 81 odd/cd Structured interview adhd Psychosis pt Yes, pred: presence of adhd did not pred tx outcome.
4–7
18 Nixon, Sweeney, and 54 odd Behavior checklists Unspecified None pcit, mpcit, wl n/a
Erickson (2003) 3–5
19 Lochman and Wells (2004) 245 odd/cd Behavior checklists Unspecified None cp ci, cp cpi, control n/a
5th–6th
grade
20 Webster-Stratton 159 odd Structured interview adhd Psychosis pt, ct, pt + ct, pt + tt, ct + n/a
et al. (2004) 4–8 tt, pt + ct + tt, wl
21 Greene et al. (2004) 47 odd Structured interview dep, bp, adhd, anx None cps, pt n/a
4–12

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22 Beauchaine et al. (2005) 514 odd/cd Structured interview Unspecified Psychosis pt, ct, pt + ct, pt + tt, ct + Yes, mod: comor was sig mod; pt resulted in better
3–8 tt, pt + ct + tt, wl 1-year outcomes for children scoring below median on
cbcl anx/dep; those above median on cbcl attn probls
had better long-term outcomes when tt was included.
23 Kazdin and Whitley (2006) 183 odd Structured interview Unspecified Psychosis pt, psst Yes, pred: those with greater # of comor diag showed
(Sample 1) 3–14 greater improvement.
24 Kazdin and Whitley (2006) 132 cd Structured interview Unspecified Psychosis, pdd pt, psst Yes, pred: those with greater # of comor diag showed
(Sample 2) 7–14 greater improvement.
25 Werba, Eyberg, and Boggs 99 odd Structured interview cd, adhd Severe mental pcit, wl Yes, pred: treatment was as effective for those with
(2006) 3–6 impairment comorbid cd and/or adhd
26 Bagner and Eyberg (2007) 34 odd/mr Structured interview, Unspecified pdd pcit, wl n/a
3–6 intelligence test
27 CPPRG (2007) 891; odd/cd Behavior checklists Unspecified None Fast track, control n/a
mean = 6
28 Costin and Chambers 94 odd Structured interview adhd, anx, dep, cd No pt Yes, pred: tx was as effective or more effective for those
(2007) 5–13 with comor diagnoses.

Note: ac = anger coping, adhd = attention deficit/hyperactivity disorder, agg = aggression, anx = anxiety, cbcl = child behavior checklist, cc-client centered, cd = conduct disorder, comor = comorbid/comorbidity, cp ci = coping
power child intervention, cp cpi = coping power child plus parent intervention, cpprg = conduct problems prevention research group, cps = collaborative problem solving, ct = child treatment, dd = dina dinosaur program,
dep = depressive disorder, diag = diagnosis, gct = group cognitive therapy, gpt = group parent training, gd = group discussion, gdvm = group discussion videotape modeling, gs = goal setting, ivm = individually administered
videotape modeling, mod = moderator, mr = mental retardation, n = sample size, n/a = not applicable, obs = observation, odd = oppositional defiant disorder, pdd = pervasive developmental disorder, pred = predictor, psst =
problem solving skills training, psst-p = problem solving skills training plus practice, pt = parent training, rt = relationship therapy, ss = social skills training, sxs = symptoms, tt = teacher training, tx = treatment, wl = waitlist.

1459
1460 T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471

diagnoses on the presence of post-treatment anxiety disorder (Kendall et al., 2004); 3) the number of pre-treatment diagnoses or
parent/teacher-reported internalizing and externalizing symptoms (i.e., CBCL/TRF) on treatment termination/completion status
(Kendall & Sugarman, 1997); 4) youth who had one anxiety diagnosis, two or more anxiety diagnoses, or an anxiety diagnosis and
an externalizing diagnosis on youth self-report measures of anxiety and depression, parent/teacher measures of internalizing and
externalizing problems (i.e., CBCL/TRF), or primary anxiety disorder presence at post-treatment or follow-up (Kendall, Brady, &
Verduin, 2001); and 5) the number of parent- or youth-reported comorbid diagnoses at post-treatment and 1-year follow-up for
those grouped into good and poor treatment response groups (Southam-Gerow, Kendall, & Weersing, 2001).
Others have also examined the predictive influence of comorbid diagnoses on treatment outcomes for youth with various anxiety
disorders, with similar null effects revealed for post-treatment diagnostic status (Shortt, Barrett, & Fox, 2001) and child/parent self-
report measures of internalizing and externalizing symptoms (e.g., CBCL, RCMAS; Silverman et al., 1999b). Likewise, researchers have
confirmed Kendall and colleagues' findings that the number and type of comorbid diagnoses do not significantly predict anxiety
treatment outcomes. For instance, treatment outcome differences were not differentially predicted by one versus multiple pre-
treatment anxiety diagnoses at long-term (6–7 years) follow-up (Manassis, Avery, Butalia, & Mendlowitz, 2004). Further, in their
treatment study of anxious youth, Barrett, Duffy, Dadds, and Rapee (2001) found that children with no comorbid diagnoses, other
anxiety target diagnoses only (OAD, SAD, SOC), or non-target anxiety (e.g., OCD, PTSD, SP) diagnoses did not differ on diagnostic status,
parent-report of internalizing and externalizing symptoms, or child-reported internalizing symptoms at 6-year follow-up. In another
study, Manassis et al. (2002) similarly noted no treatment outcome differences for participants grouped as high or low on hyperactivity.
Three additional studies have revealed non-significant effects for comorbidity on treatment outcomes in children with other
anxiety disorder diagnoses (SOC, SP, PTSD). Regarding SOC and SP, no significant treatment outcome differences (e.g., child/parent-
reported anxiety, behavior tests) were found for those with, compared to those without, comorbid diagnoses (Beidel, Turner, &
Morris, 2000; Ost, Svensson, Hellstrom, & Lindwall, 2001). For PTSD, the only predictive influence found was that participants who
had a comorbid diagnosis (and less overall impairment) were less likely to respond during the monitoring phase; however, this
difference was not reported at post-treatment (Smith et al., 2007).
Finally, three RCTs reported significant, albeit small, differences for participants with anxiety and comorbid diagnoses. First,
Berman, Weems, Silverman, and Kurtines (2000) created treatment success and failure groups from two previous RCTs conducted
by Silverman et al. (1999a,b). No differences were found between the success and failure groups with regard to total number of
diagnoses, presence/absence of comorbidity overall, or presence of comorbidity with externalizing disorders specifically. However,
differences were found for those who evidenced comorbidity with depression, such that those who had comorbid depression
diagnoses were significantly more likely to be in the treatment failure group. The second study (Rapee, 2003) grouped anxious
youth by comorbidity type: no comorbid diagnoses, comorbid with other anxiety diagnoses, and comorbid with non-anxiety
diagnoses. Comparisons were made for pre-treatment, post-treatment and follow-up ratings of internalizing and externalizing
symptoms by parents and child self-reported anxiety symptoms. The only significant findings were a significant group × time
interaction from post-treatment to follow-up on maternal ratings of externalizing symptoms (slight increases for those in the
comorbid groups versus continued decrease for the non-comorbid group) and those with comorbid diagnoses attended
significantly fewer therapy sessions. In the third study, March et al. (2007) investigated the impact of comorbid tic disorders on
treatment outcome from a prior study (POTS Team, 2004). Four treatment conditions were compared for the treatment of OCD:
psychiatric medication (sertraline) alone, CBT alone, a combined group, and placebo. A significant moderational effect
(treatment × tic disorder) was found, such that medication effectiveness was reduced to no longer being significantly different
from placebo for those with OCD and comorbid tic disorder in the sertraline group only. Thus, comorbidity in this case did not
impact the groups which included CBT. Notably, this is the only study that specifically tested for moderation effects.
In summary, of the 16 RCTs for anxiety disorders that addressed or noted the predictive/moderating impact of comorbidity, 13
failed to find significant differences on post-treatment outcomes, one reported a difference only for the medication group (March
et al., 2007) and the other two reported small differences (Berman et al., 2000; Rapee, 2003). These findings suggest that the
addition of comorbid disorders in the diagnostic profile does not typically have a significant influence on treatment outcomes
among youth treated for anxiety disorders. For the two CBT studies where differences were noted (Berman et al., 2000; Rapee,
2003), the majority of findings failed to support such effects.

3. Affective disorders

Affective disorders evidenced by children and adolescents include major depressive disorder (MDD) and dysthymia. Epidemiological
studies suggest the prevalence of unipolar affective disorders in youth to be between 1.5% and 8.0% (Angold et al., 1999; Costello et al.,
1996). The diagnostic criteria for MDD and dysthymia in youth are similar to those specified for adults, except that children may
experience irritability instead of depressed mood. In addition, weight and appetite disturbances may be manifested by failure to make
developmentally appropriate weight gains and dysthymia can be diagnosed in children after one year of symptoms — as opposed to the
two years required for adults (American Psychiatric Association, 2000). Overwhelmingly, research suggests that depression in youth is
characterized by significant distress and interference and, left untreated, negative long-term outcomes.

3.1. Depression and its comorbidities

There is substantial comorbidity both within the affective disorders (e.g., dysthymia coexisting with a major depressive episode)
and between affective disorders and other disorders. In fact, it is somewhat rare for a child or adolescent diagnosed with an affective
T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471 1461

disorder to not carry at least one additional diagnosis. Comorbidity tends to be associated with earlier age of onset of the depressive
episode (Lewinsohn, Rohde, & Seely, 1998) and higher frequency of suicidal behavior (Rohde, Lewinsohn, & Seeley, 1991).
In a review of 21 community surveys, Angold et al. (1999) found that up to 75% of youth diagnosed with an affective disorder
were also diagnosed with an anxiety disorder. The rate of CD/ODD in depressed youth ranged from 0–79% whereas rates of
comorbidity of ADHD in depressed youth ranged from 0–57%. Summarizing across studies, affective disorders were strongly
related to anxiety disorders and CD/ODD but less strongly related to ADHD. The rate of comorbidity in treatment-seeking samples
also suggests that comorbidity is the rule rather than the exception for youth with affective disorders. For example, substantial
comorbidity was evident in the sample of youth in the Treatment of Adolescents with Depression Study (TADS), a large RCT
comparing CBT, fluoxetine (FLX), CBT + FLX, and pill placebo (TADS Team, 2005). Although certain comorbid conditions (i.e., bipolar
disorder, severe CD, pervasive developmental disorders, and thought disorder) served as exclusion criteria for the trial, almost half
of the sample (47.8%) had at least one concurrent comorbid non-mood disorder.
In general, treatment studies investigating psychosocial interventions for youth with a diagnosis of MDD or DYS have employed
samples with substantial comorbidity and these data are routinely reported. More specifically, as can be seen in Table 2, only one of
the 11 treatment studies for youth with affective disorders failed to report on comorbidity in the sample. Further, six of the 11
studies examined comorbidity as a predictor of outcome and four investigated whether comorbidity served to moderate the effects
of treatment condition on outcome.

3.2. EBTs for affective disorders

CBT, CBT with parent involvement (CBT + parent), and interpersonal therapy (IPT) have been shown to be efficacious for youth
with depression (Chorpita et al., 2002, see Table 2). In most trials, recovery rates (i.e., percent diagnosis free) for CBT treatments
range from approximately 50% to over 80%. In a trial of IPT for adolescents, for example, Mufson, Weissman, Moreau, and Garfinkel
(1999) report that 87.5% of adolescents receiving IPT were diagnosis free at post-treatment. Moreover, there is some evidence that
positive effects for both CBT and IPT may be applicable to various ethnic and racial groups (Rosselló & Bernal, 1999).

3.3. Comorbidity as a predictor/moderator of affective disorder treatment outcomes

In general, concurrent comorbidity, particularly comorbidity with anxiety disorders and multiple comorbid diagnoses, predicts
poorer acute outcomes (Brent et al., 1998; Curry et al., 2006; Young, Mufson, & Davies, 2006). There is also some evidence that
double-depression may be a negative prognostic indicator (Brent, Kolko, Birmaher, Baugher, & Bridge, 1999). However, in a CBT
benchmarking study, Weersing, Iyengar, Kolko, Birmaher, and Brent (2006) found neither the presence of double-depression nor
the number of comorbid diagnoses to predict outcome. Additionally, lifetime comorbidity may have a different effect on outcome
than concurrent comorbidity. For example, Clarke et al. (1992) and Rohde, Clarke, Lewinsohn, Seeley, and Kaufman (2001) found
lifetime comorbidity to be related to better treatment outcome. More specifically, greater number of past diagnoses was a predictor
of better outcome (Clarke et al., 1992) and, although comorbidity was related to higher self-reported depression at intake, it was
also related to greater changes in depressive symptoms — particularly for those with a history of anxiety disorders (Rohde et al.,
2001). However, it should be noted that these studies examined the effects of lifetime comorbidity in the samples treated by
Lewinsohn, Clarke, Hops, and Andrews (1990) and Clarke, Rohde, Lewinsohn, Hops, and Seeley (1999), many of whom had few
concurrent comorbid disorders upon study entry (see Table 2).
Similarly, more research is needed on the effects of comorbidity on long-term outcomes. Studies that have addressed this issue
have resulted in mixed findings. More specifically, Birmaher et al. (2000) found that comorbidity did not predict or moderate
recovery, chronicity, or recurrence at two-year follow-up in a sample of youth treated with CBT, systemic behavioral family therapy,
or nondirective supportive therapy. However, Vostanis and colleagues (1998) found that comorbidity at the end of treatment did
predict the presence of depression at two-year follow-up in a sample of children and adolescents treated with either CBT or a non-
focused supportive intervention. Notably, the latter study determined comorbidity at the end of treatment, not prior to treatment.
In terms of the more specific question of the moderating effects of comorbidity on EBTs for depression, anxiety disorders, given
their high rate of co-occurrence with depression, have received the most attention. Interestingly, despite the concern expressed by
many that EBTs do not allow for the flexibility needed to treat youth with comorbid conditions, the evidence to date supports the
use of CBT or IPT especially in these more complicated cases. For example, Brent et al. (1998) found CBT led to higher rates of
recovery than a nondirective supportive therapy in adolescents with MDD, but that this difference was even more pronounced in
youth with comorbid anxiety disorders. Similarly, Young et al. (2006) found that IPT was superior to treatment-as-usual (TAU) for
youth with a comorbid anxiety disorder1 but the two treatments resulted in similar outcomes for youth without comorbid anxiety.
More specifically, for youth with symptoms consistent with panic disorder, those who received IPT achieved better functioning and
reported fewer depressive symptoms at post-treatment than those receiving TAU; outcomes for the two treatments were not
significantly different for those youth without panic disorder symptoms however. In this study, anxiety symptoms improved along
with the depression symptoms and for some types of anxiety this effect was moderated by treatment. That is, youth with
symptoms of GAD were over four times as likely to show improvement in their anxiety symptoms if they were treated with IPT.

1
These youth were not diagnosed with an anxiety disorder through use of a diagnostic interview. Tentative diagnoses were made on the basis of a self-report
of symptoms that mapped onto DSM diagnostic categories.
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This suggests that separate treatment to address the comorbid anxiety may not be necessary and is especially encouraging given
the high rate of GAD/OAD in depressed youth.
Similar moderating effects have not been found when examining comorbidity more broadly. For example, treatment condition
and presence of lifetime comorbidity did not interact to predict recovery or changes in self-reported depression in youth treated
with CBT, CBT + parent, or assigned to a waitlist condition (Rohde et al., 2001). Similarly, in a sample of youth all diagnosed with
MDD and CD, CBT was more effective than a life skills tutoring treatment. Although the additional diagnosis of ADHD in this study
was associated with longer time to recovery, additional comorbid conditions did not interact with treatment condition to predict
time to recovery (Rohde, Seeley, Kaufman, Clarke, & Stice, 2006).
In sum, across treatments for affective disorders in youth, youth with comorbidity, particularly comorbid anxiety disorders,
achieve poorer outcomes; however, there is some evidence that these seem to be exactly the youth who benefit most from these
EBTs when compared to youth receiving other non-EBTs.

4. Attention-deficit/hyperactivity disorder (ADHD)

ADHD is also a prevalent psychological disorder in childhood with studies typically showing prevalence rates ranging from 3%–
7% (APA, 2000). In addition, the DSM-IV delineates three subtypes of the disorder based on the two symptom dimensions of
inattention and hyperactivity-impulsivity: ADHD, predominantly inattentive type (ADHD-I), ADHD, combined type (ADHD-C), and
ADHD, predominantly hyperactive/impulsive type (ADHD-H/I; APA, 2000). ADHD is often associated with significant short-term
and long-term impairment and is a risk factor for the development of additional psychological problems across the lifespan.

4.1. ADHD and its comorbidities

Studies have found that ADHD is often highly comorbid with both internalizing (13–51%) and externalizing (43–93%) disorders.
This finding suggests that “pure” ADHD, as with the other disorders examined in this review, is the exception rather than the rule
and has led some authors to advocate for distinct comorbid subtypes of ADHD (Jensen et al., 2001; Jensen, Martin, & Cantwell,
1997). Studies to date have focused primarily on the comorbidity of ADHD and externalizing disorders with fewer studies
examining comorbidity with internalizing disorders. One reason for this lag in research is that ADHD is more often comorbid with
externalizing disorders (~50% in epidemiological studies), although the comorbidity of ADHD and anxiety and depression are also
substantial with comorbidity rates averaging 25% in epidemiological studies (Angold et al., 1999; Jensen et al., 1997).

4.2. EBTs for ADHD

To date, only a handful of treatments have been found to be effective with youth who have ADHD, at least in the short-term.
These treatments include behavioral modification, central nervous system stimulants, and the combination of these treatments
(Pelham, Wheeler, & Chronis, 1998). Although these approaches have often yielded improvement in functioning, symptomatology
often still remains outside the normal range of functioning after treatment is completed. In addition, ADHD symptoms often return
to pre-treatment levels when treatment is discontinued. Among these three treatments, pharmacotherapy has been found to be
the most effective treatment for ADHD, although it should be noted that discontinuing medication often leads to a return to pre-
treatment symptom levels (Pelham et al., 1998). In addition, there is evidence that a subgroup of children (10%–20%) with ADHD
does not respond to stimulant medication (Greenhill, Halperin, & Abikoff, 1999), suggesting that alternative treatment approaches
need to be considered.
Currently, only two psychosocial treatments have been shown to be efficacious in the treatment of youth with ADHD:
behavioral parent training and behavioral interventions in the classroom. Cognitive interventions alone have not been shown to be
effective (Pelham et al., 1998). Until recently, the question of whether treatments should be administered individually or in
combination with one another remained unanswered. In the largest RCT ever conducted for the treatment of ADHD, the
Multimodal Treatment Study of Children with ADHD (MTA Study; MTA Cooperative Group, 1999a) attempted to answer this
question by comparing behavioral treatment alone, stimulant medication alone, a combined treatment, and a community control
treatment. Overall, the study found that stimulant medication alone and the combined treatment were significantly more effective
than the behavioral treatment alone and the community control. In addition, the combined treatment did not significantly differ
from the stimulant medication alone condition for core ADHD symptoms.
Since the time of this initial publication, data from two follow-up points have been published (2 years after treatment and
3 years after treatment; MTA Cooperative Group, 2004; Jensen et al., 2007). Although the groups involving MTA medication
management (i.e., medication alone and combined) continued to show advantages at the first follow-up, the effect sizes were
approximately half compared to the initial outcome studies. Interestingly, results recently published from the 3-year follow-up
found no differences between treatment conditions, although remarkable improvements were seen in all four of the groups,
suggesting that any form of treatment may result in relatively long-term treatment gains (Jensen et al., 2007).

4.3. Comorbidity as a predictor/moderator of ADHD treatment outcome

Prior to publication of the MTA Study, few studies examined comorbidity as a predictor or moderator of psychosocial treatment
outcome. Table 3 presents 31 RCT studies examining the efficacy of behavioral parent training or behavioral interventions in the
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classroom. 22 of the 31 studies reported that children with comorbid disorders or co-occurring symptoms were included in the
sample. Early studies tended to explore comorbidity in a more dimensional manner (i.e., behavior checklists) and examined it in
relation to prediction rather than moderation. Finally, although 22 of the studies reviewed collected information on comorbidity,
only 12 of these studies used this information for examining prediction or moderation. In addition, 5 of the 12 studies were from
the MTA Study and only 6 examined moderation (5 from the MTA Study).
Six studies were identified that examined comorbidity as a predictor of treatment outcome. Horn, Ialongo, Popovich, and
Peradotto (1987) found that pre-treatment level of conduct problems did not predict treatment outcome. Subsequently, Barkley,
Guevremont, Anastopoulous, and Fletcher (1992) indicated that the number of child ODD symptoms did not predict mother or
child-reported outcomes. Pelham and Hoza (1996) reported that co-occurring aggression (initiating fights or being physically cruel
to people) predicted better or at least the same response to treatment (depending on outcome measure) in comparison to children
without co-occurring aggression. Frankel, Myatt, Cantwell, and Feinberg (1997) found that presence of ODD did not predict
response to a social skills training treatment. Using data from the MTA Study, Pelham et al. (2000) found little evidence for
prediction but did find a small effect in which the presence of ODD/CD predicted increased/whining complaining during their
Summer Treatment Program. Finally, Antshel and Remer (2003) found that ODD symptoms predicted a poorer response to social
skills training. Overall, the studies that have examined prediction have found little evidence for comorbidity to impede treatment
gains, although the study by Antshel and Remer (2003) is a notable exception.
In relation to moderation, Kolko, Bukstein, and Barron (1999) compared medication, behavior management, and medication
plus behavior management for children with ADHD + ODD and children with ADHD + CD. Children with ADHD + ODD showed a
greater decline in behavior problems in the behavior management condition than children with ADHD + CD. In the combined
condition, medication plus behavior management was associated with greater mood improvement in children with ADHD + CD
than children with ADHD + ODD. More recently, the MTA study addressed comorbidity as a moderator of treatment outcome with
the largest sample to date. These more recent analyses of the MTA data have found that comorbidity is an important factor in
interpreting the results from the study. In two subsequent papers (MTA Cooperative Group, 1999b; March et al., 2000), the
behavioral treatment alone was found to be just as effective as the medication alone condition for children with parent-rated
anxiety. In addition, the combined treatment was found to be more effective than the stimulant medication alone condition for
children with comorbid anxiety and conduct problems on some composite outcome measures (Jensen et al., 2001). These
moderational findings suggest that children with comorbid conditions may benefit from behavioral modification as either a stand
alone treatment or as an adjunctive treatment.
Additional findings from the MTA Study have shown the importance of methodological considerations when interpreting
treatment effects. Owens et al. (2003) analyzed the MTA data specifically using receiver operating characteristics to examine what
they defined as “excellent response” (i.e., a composite score indicating the average level of parent- and teacher-reported ADHD and
ODD symptoms less than or equal to “just a little”). The study also considered conjoint effects of multiple moderators rather than
examining only one moderator at a time in predicting treatment outcome (in contrast to earlier MTA reports). In contrast to
previous analyses, comorbid anxiety was not found to moderate treatment outcome using this new outcome measure. New
findings did emerge, though, as parental depression symptoms and severity of child ADHD were found to moderate rates of
“excellent” response, as the medication and combined treatments showed poorer response while the behavioral alone and
community control treatments did not show poorer response.
In addition to the short-term effects of comorbidity, the long-term effects of comorbidity on treatment outcome have recently
been addressed. Jensen et al. (2007) examined the effect of pre-treatment comorbidity on outcome 2 years post-treatment.
Comorbidity at baseline (ODD/CD without anxiety, anxiety without ODD/CD, ODD/CD and anxiety, no ODD/CD or anxiety) did not
moderate but predicted poorer treatment response. Interestingly, this finding is in contrast to the studies presented earlier in this
section that found little evidence for comorbidity to predict poorer treatment outcome.
Although the MTA Study examined comorbid conduct problems and anxiety, additional comorbidities such as the mood disorders
will need attention in future studies. Some authors have suggested that the relationship between ADHD and depression may be
epiphenomenal in that the relationship is mediated by the presence of comorbid conduct disorders (Angold et al., 1999), while other
authors have concluded that the relationship is not epiphenomenal (Blackman, Ostrander, & Herman, 2005). In relation to psychosocial
treatments, no study was found that examined the predictive or moderating effect of depression on ADHD treatment outcome.
Finally, presence of comorbid bipolar disorder will need to be considered in future studies, as meta-analyses have shown that
approximately 60% of children with bipolar disorder also meet diagnostic criteria for ADHD (Youngstrom, Youngstrom, & Starr,
2005). Although no psychosocial treatment has been designed to specifically address ADHD and bipolar disorder, it should be
noted that one treatment, Collaborative Problem Solving (Greene et al., 2004), has been expanded beyond bipolar disorder to
address other disruptive behavior problems (e.g., ADHD, ODD) and has shown some initial evidence for efficacy (Greene et al.,
2004). No analyses examining comorbidity have been reported though.

5. ODD/CD

Children with oppositional and conduct problems comprise a heterogeneous group of youth who engage in a broad array of
problem behaviors ranging from relatively minor defiance and temper tantrums to more serious violations such as physical
aggression, destructiveness, and stealing. ODD refers to a recurrent pattern of developmentally inappropriate levels of negativistic,
defiant, disobedient, and hostile behavior toward authority figures. CD consists of more severe antisocial and aggressive behavior
that involves serious violations of others' rights or deviations from age-appropriate norms. Prevalence of these disorders is
1464 T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471

estimated to be between 2% and 16%, depending on the population, ascertainment methods, and diagnostic measures used (Loeber,
Burke, Lahey, Winters, & Zera, 2000).

5.1. ODD/CD and their comorbidities

Children with conduct problems are at increased risk for manifesting a variety of other emotional and behavior disorders
including ADHD, anxiety, and depression. A meta-analysis of general population studies found that of those with ODD or CD, 3.1–
41.0% had ADHD, 2.2–45.9% had depression, and 4.8–55.3% had a comorbid anxiety disorder (Angold et al., 1999). Similarly, the
National Comorbidity Survey found that of those with lifetime ODD, 92.4% meet criteria for at least one other lifetime DSM-IV
disorder, including: mood (45.8%), anxiety (62.3%), and ADHD (35.0%; Nock, Kazdin, & Hiripi, 2007). In a clinic-referred sample,
Greene et al. (2002) reported that over 80% of those diagnosed with a conduct problem disorder also had ADHD. In addition,
approximately 50% met criteria for depression and about 40% met criteria for an anxiety disorder. Thus, ODD and CD tend to co-occur
with other childhood disorders at rates significantly greater than chance.

5.2. EBTs for ODD/CD

As summarized by Nock (2003), treatments for oppositional and conduct problems can be classified according to each
treatment's focus on parent, child, or systemic characteristics. Parent training interventions include procedures designed to improve
coercive interactions between parents and their children. Typically, these treatments include proper use of commands, contingent
reinforcement, differential attention, and time-out (e.g., McMahon & Forehand, 2003). CBT for youth with conduct problems targets
maladaptive social-cognitive processes and focuses on improving anger control, social skills, and problem solving skills (e.g., Greene
et al., 2004; Kazdin, Sigel & Bass, 1992; Webster-Stratton, Reid, & Hammond, 2001). Finally, multisystemic treatment (MST) is based
on a social-ecological model and treats youth by reaching out to multiple layers of the youth's social environment including their
family, neighborhood, peers, and school (e.g., Henggeler, Schoenwald, Borduin, Rowland, & Cunningham, 1998). Often, elements of
these various approaches are combined into multicomponent intervention programs that target both parenting skills and children's
social skills. These combined programs have produced reductions in children's conduct problems and aggressive behavior, and
increases in problem solving skills and social-cognitive skills (Conduct Problems Prevention Research Group, 2002; Webster-
Stratton & Hammond, 1997).
Brestan and Eyberg's (1998) review of 82 treatment studies for youth with conduct problems showed that two variants of
parent training were efficacious: videotape modeling parent training programs and parent training programs based on Patterson
and Guillion's (1968) manual Living With Children. In addition, MST and several CBT programs were identified as being possibly
efficacious. In a meta-analysis, Serketich and Dumas (1996) reported a mean effect size for parent training (d = 0.86) that was
notably higher than the mean effect size for CBT (d = 0.23; Bennett & Gibbons, 2000) and the mean effect size for MST (d = 0.55;
Curtis, Ronan, & Borduin, 2004). However, a more recent meta-analysis found more comparable results with an effect size of 0.47
for parent training and 0.35 for child-focused CBT (McCart, Priester, Davies, & Azen, 2006). Thus, considerable progress has been
made toward developing effective treatments for child conduct problems.

5.3. Comorbidity as a predictor/moderator of treatment outcomes for ODD/CD

Despite the substantial empirical support for treatments of ODD and CD, relatively little is known about factors related to poor
treatment response that is typically seen in about one third to one half of treated cases (Beauchaine, Webster-Stratton, & Reid,
2005). Although Brestan and Eyberg's (1998) review of treatments for conduct problems included youth with comorbid disorders,
only 32.1% of the studies included sample demographics, including information on comorbidity. Thus, little was known about
factors that may predict or moderate treatment outcome. Since that time, more attention has been paid to these factors; however,
relatively few studies have actually examined predictors of outcome for oppositional and conduct problem interventions and even
fewer have examined moderators of outcome (see Nock, 2003). In fact, of the 28 studies reviewed here, only one examined
comorbidity as a moderator of treatment outcome and eight studies looked at comorbidity as a predictor of treatment outcome. As
can be seen in Table 4, the vast majority of studies allowed for the inclusion of youth with comorbid disorders. When comorbid
exclusion criteria were specified, it was most often on the basis of psychosis and mental retardation.
Kazdin and Whitley (2006) recently explored the effect of comorbid disorders on treatment outcome for youth with ODD or CD.
The study examined outcomes for those who completed evidence-based versions of parent management training or problem
solving skills training. Differences in treatment response were assessed with respect to whether these children had no, one, or two
or more comorbid diagnoses including ADHD, depression, and anxiety. The effects of treatment were not attenuated for children
diagnosed with multiple disorders. Although differences were found between groups with different numbers of comorbid
disorders, the number of comorbid disorders did not alter treatment outcome in the expected negative direction. Indeed, the
magnitude of change from pre-treatment to post-treatment was greater among those with at least two additional disorders.
Moreover, children with and without a comorbid disorder did not differ at the end of treatment in terms of their antisocial
behavior, problem behaviors observed in the home, or parent ratings across multiple symptom domains. Results of this study
suggest that comorbidity does not predict negative treatment outcomes for oppositional and conduct problem youth.
In a similar study, Costin and Chambers (2007) examined the role of comorbid diagnoses on the effectiveness of parent training
in community settings. Study participants were divided into three groups: (1) those with ODD alone, (2) those with ODD plus
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ADHD, and (3) those with ODD, ADHD, and an emotional disorder (either anxiety or depression). Contrary to hypotheses,
comorbidity did not predict poor treatment response. All three groups showed improvements in response to parent training as
assessed at post-treatment and 5-month follow-up. In fact, similar to Kazdin and Whitley's (2006) findings, rates of improvement
were greater for those in the comorbid groups compared to those in the ODD alone group. Moreover, these results held true when a
measure of clinically significant change was applied.
Another study examined the moderating role of dimensional symptoms associated with ADHD, anxiety, and depression on
treatment outcomes for those who received various combinations of parent, child, and teacher focused interventions (Beauchaine
et al., 2005). While analyses of moderation did not show a negative effect for increased symptoms ratings, they did reveal
differential responses to treatment based on symptom presentations. Specifically, interventions including parent training were the
most effective for children who scored below the median on the CBCL Anxious/Depressed subscale, whereas all intervention
combinations were equally effective for children with elevated Anxious/Depressed scores. Results also showed that when children
scored above the sample median on CBCL Attention Problems, they achieved better long-term outcomes when teacher training
was included in their treatment. In all, while results of this study revealed that co-occurring symptoms of Anxiety/Depression and
Attention Problems moderated treatment response, they did not generally predict negative outcomes.
Because ADHD is the most frequent co-occurring disorder with conduct problems, several studies have specifically examined
treatment outcomes for youth with this comorbid presentation. Despite early speculation that children with comorbid ADHD
would require more intensive services and be less responsive to intervention efforts (i.e., Lyman 1998), studies addressing the role
of ADHD in predicting or moderating treatment outcomes have shown little or no difference for conduct problem youth. This
finding has been consistent for parent training interventions (Beauchaine et al., 2005; Hartman, Stage, & Webster-Stratton, 2003),
social skills and problem solving training for children (Webster-Stratton, Reid, & Hammond, 2001), and MST or combined
approaches such as the Families and School Together Track project (The Conduct Problems Prevention Research Group, 2002). It
should be noted, however, that the majority of these studies have relied on dimensional symptoms of inattention, impulsivity, and
hyperactivity rather than categorical diagnoses of ADHD (e.g., Beauchaine et al., 2005; Hartman et al., 2003). Moreover, only one of
these studies conducted analyses of moderation while the others considered ADHD symptoms a predictor of treatment outcome.
Taken together, these studies indicate that treatment response is similar among youth with and without comorbid ADHD.
Overall, of the eight studies that have examined comorbidity as a predictor of treatment outcome and the one study that
examined the potential moderating role of comorbidity, the vast majority suggest that it has little or no effect on the treatment of
child conduct problems. In fact, only one study suggested that those with more comorbid symptoms had poorer treatment
outcomes (Kazdin & Crowley, 1997). Thus, contrary to concerns about use of EBTs, comorbid youth sometimes responded better to
treatment than their non-comorbid peers (e.g., Costin & Chambers, 2007; Kazdin & Whitley, 2006).

6. Discussion

Findings from our qualitative review inform us about the current state of comorbidity and its potential effects on treatment
outcomes of EBTs. First, contrary to the assertions of many (e.g., Dulcan, 2005; Westen, Novotny, & Thompson-Brenner, 2004), the
vast majority of RCTs examined in this review included participants who had comorbid disorders. Although the majority of the
studies excluded participants with psychosis, pervasive developmental disorders, and mental retardation, other more frequently
occurring disorders were present in most of the participants, and in some studies, all of the participants. Exclusion of participants
with psychosis, pervasive developmental disorder, and mental retardation was based on the fact that effective treatments for these
disorders typically require additional treatment strategies, consistent with sound clinical practice. In addition, the percentage of
participants who were comorbid with these other disorders in the RCTs was similar to rates of comorbidity found in clinically-
referred samples. As a result, it is not likely the case that the participants were less clinically severe than those seen in routine
clinical practice. Comorbidity was the rule rather than the exception.
Second, although rates of comorbidity were high in these RCTs, only a limited number of studies examined whether comorbidity was
a predictor or moderator of treatment outcome. As noted by Kraemer et al. (2002), predictors are baseline variables that show similar
relations with outcomes in both treatment and control groups. Moderators, on the other hand, are baseline variables that show
differential degrees of association with outcome across treatments. That is, moderators help us identify which treatments work best for
which subgroups. In our review, the effects of comorbidity on treatment outcome – either as a predictor or a moderator – was somewhat
variable. In the internalizing disorder area, several RCTs addressed the potential impact of comorbidity as a predictor of treatment
outcome with CBT treatment for youth with anxiety disorders. Overall, the clear majority of studies failed to find significant differences
on post-treatment outcomes, and the findings suggested that the addition of comorbid disorders in the diagnostic profile did not have a
significant influence on treatment outcomes. However, none of the studies examined comorbidity as a moderator of treatment outcome,
using the guidelines specified by Kraemer et al. (2002). In the area of youth depression, several studies also examined the potential
impact of comorbidity as a predictor of treatment outcomes of CBT and IPT. However, unlike the findings for the anxiety area, concurrent
comorbidity tended to predict poorer post-treatment outcomes. Interestingly, however, lifetime comorbidity – not examined in the
anxiety disorder area – appeared to be related to better treatment outcome (Clarke et al., 1992; Rohde et al., 2001). In terms of
moderation, comorbidity of the anxiety disorders and the mood disorders received the most attention. The evidence was unequivocal
and supported the use of CBT or IPT especially for these more complicated cases.
Turning to the externalizing disorder area, the findings are also somewhat mixed. For ADHD, the evidence suggests that the
presence of comorbidity is not generally associated with poorer outcome, although a study by Antshel and Remer (2003) found
that the presence of ODD was associated with poorer response to social skills training. More recently, the MTA study conducted
1466 T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471

moderational analyses and found that the behavioral treatment alone was just as effective as the medication alone condition for
children with parent-rated anxiety (MTA Cooperative Group, 1999b; March et al., 2000). In addition, the combined treatment was
found to be more effective than the stimulant medication alone condition for children with comorbid anxiety and conduct
problems on some composite outcome measures (Jensen et al., 2001). These findings suggest that children with comorbid
conditions may benefit from behavioral therapy as either a stand alone treatment or as an adjunctive treatment. Interestingly,
comorbid oppositional and aggressive problems did not moderate treatment outcome in the MTA study. For ODD/CD, findings
suggest that comorbidity may have little or no effect on the treatment of child oppositional and conduct problems. Specifically,
studies examining treatment outcomes for youth with comorbid ADHD have shown little or no differences in outcomes. In
addition, in some studies, comorbid youth have responded better to treatment than their non-comorbid peers (e.g., Costin &
Chambers, 2007; Kazdin & Whitley, 2006). In terms of moderation, the study by Beauchaine et al. (2005) revealed differential
responses to treatment based on symptom presentation. Specifically, interventions including parent training were most effective
for children who scored low on the anxiety and depression measures, whereas all intervention combinations were equally effective
for children who scored high on the anxiety and depression scores. Results also showed that when children scored high on
attention problems, they achieved better long-term outcomes when teacher training was included in their treatment.
Overall then, results across the domains of anxiety, depression, ADHD, and ODD/CD indicate that the effects of comorbidity on
outcomes associated with empirically supported psychosocial treatments are not as negative or problematic as suggested by some
(e.g., Dulcan, 2005, Westen et al., 2004). Of course, this conclusion must be tempered by a number of methodological and statistical
considerations. For example, the way in which comorbidity has been operationally defined in these studies varies from study to study
and has included measures obtained from parent or teacher rating scales, self-report child measures, and structured clinical diagnostic
interviews. Thus, the very way in which comorbidity has been defined in these studies might be questioned and potentially lead to
different conclusions (see Nottleman & Jensen,1995; Rutter,1994). Still, across these various sources of information, similar conclusions
are evident (see Tables 1–4). In addition, the way in which treatment outcomes have been defined in these studies has varied. Some
studies used percent of participants who were diagnosis free following treatment as their outcome index whereas others used clinician
global ratings or parent, teacher, and self-report measures. As such, some have used dichotomous indices whereas others have used
dimensional ones. Again, variability may well exist in outcomes associated with comorbidity depending upon how the outcome is
operationally defined. Statistically, too, as noted by March et al. (2000) and Owens et al. (2003), most of the studies to date have looked
at moderators one at a time and have not looked at the complex interplay of multiple potential moderators simultaneously. The
possibility exists that multiple moderators might be related to one another and that their combined effects might differ from their
individual effects. Such possibilities suggest use of more complex statistical models including those incorporating receiver operating
characteristics (ROCs). As noted by Kiernan, Kraemer, Winkleby, King, and Taylor (2001), the ROC approach is nonparametric, highly
sensitive to possible interactions, and imposes few assumptions about normality, making it more applicable for such purposes. In
addition, such an approach is often more clinically informative.
Of course, our findings related to the effects of comorbidity on treatment outcomes for these disorders do not address the
response of the comorbid disorders themselves to the treatment interventions. For the most part, the studies have been silent on
this issue. That is, does the effective treatment of an anxiety disorder result in the amelioration of comorbid conduct problems? Or,
does the treatment of ADHD result in improvements in associated affective disorders? After all, if an intervention is effective in
reducing symptoms in the primary disorder, but the child is still functionally impaired due to the comorbid condition, can we
consider the individual and her or his family successfully treated? One of the challenges that remain for comorbidity research is to
develop efficient treatment packages that address comorbidity without engaging in a series of unrelated evidence-based
treatments. Although some limited support exists to suggest that these treatments might have “reach” beyond their intended
purposes, the findings are sparse. For example, in the MTA study (MTA Cooperative Group, 1999a) it was reported that behavioral
treatment targeting characteristics of ADHD possessed ameliorative effects on anxiety as well. This is a provocative finding and
awaits both replication and extension to the other disorders and treatment modalities. More likely, creative treatment programs
that address the complexities of comorbid disorders will be needed.
Undoubtedly, a number of other considerations are also in need of systematic inquiry before a full picture of comorbidity and its
effects on treatment outcome can be realized. For example, none of the studies to date have examined the interaction of age or
cognitive development with comorbidity in predicting or moderating treatment outcomes. Nottleman and Jensen (1995) have
documented that patterns of comorbidity change with age and that the comorbid conditions themselves might be more or less
transitory depending on the age of the child. Might it be possible that age “moderates” the effects of comorbidity in these studies?
For example, the co-occurrence of ODD with MDD might be associated with differential treatment outcomes with children versus
adolescents. Further, IPT might be more effective than CBT for comorbid adolescents but the reverse might be true for children.
Similarly, co-occurrence of GAD with ADHD might signal differential treatment outcomes for children than adolescents. In this
instance, pharmacologic interventions might be superior to a psychosocial intervention for children but a combined intervention
or perhaps a psychosocial intervention alone might be more effective with adolescents. Extant studies do not, and in many studies
cannot, speak to these issues due to the restricted age of participants in the studies (e.g., MTA study included 7 to 9 year children
only) or the limited sample size. Similarly, very little is known about the role of ethnicity, culture, and gender and how they might
interact or moderate the effects of comorbidity for EBTs or their portability to real-world clinical settings.
The task before us is a formidable one. In undertaking such investigations, it is evident that the power to detect significant
differences in treatment outcomes based on interactions of comorbidity with age, ethnicity, and gender, let alone other potentially
important subject characteristics and contextual variables (e.g., socioeconomic status, parental level of education, parental
psychopathology) would require massively large numbers of participants, far surpassing the MTA, POTS, and TADS studies
T.H. Ollendick et al. / Clinical Psychology Review 28 (2008) 1447–1471 1467

reviewed in this paper. While such massive studies are probably not feasible, in the least we urge researchers to document such
important characteristics in their studies. Only with such information will we be able to address Gordon Paul's (1967) eloquent
challenge – issued now over 40 years ago – about what treatments are most effective for which individuals with what specific
problems. Although we have a long way to go, important advances in the study of comorbidity and its effects on treatment
outcome are evident and progress is being made.

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