Original Research
Attention-Deficit Hyperactivity Disorder With and Without Obsessive–Compulsive Behaviours: Clinical Characteristics, Cognitive Assessment, and Risk Factors Paul Daniel Arnold, MD, FRCPC1, Abel Ickowicz, MD, FRCPC2, Shirley Chen, MD, MPH3, Russell Schachar, MD, FRCPC4 Objectives: To determine the prevalence of obsessive–compulsive behaviours (OCB) in a clinical sample of children with attention-deficit hyperactivity disorder (ADHD) and to compare ADHD children (with and without OCB) with respect to clinical and cognitive characteristics and risk factors. Method: We compared ADHD children (n = 134) with and without OCB, and we compared all ADHD children with a group of normal control subjects (n = 26) on various clinical, cognitive, and inhibitory control measures; neurobiological and psychosocial risk factors; and family histories of psychiatric illness. Results: Clinically significant OCB was identified in 11.2% (15/134) of children with ADHD. Comorbid OCB was associated with significantly increased perfectionism, improved teacher ratings of inattention, and a decreased likelihood of having a first-degree relative with ADHD. Comorbid ADHD and OCB may also be associated with increased oppositional behaviour at home and better inhibitory control, though these differences were not statistically significant. Conclusions: Comorbid OCB is common in clinically referred children with ADHD and is associated with increased impairment relative to ADHD alone. Further, children with ADHD and OCB may develop symptoms as the result of different genetic and environmental risk factors, compared with children with ADHD only. (Can J Psychiatry 2005;50:59–66) Information on funding and support and author affiliations appears at the end of the article.
Clinical Implications · Clinicians should conduct comprehensive clinical assessments to cover potential comorbid conditions, because a significant proportion of the children they assess will have obsessive–compulsive behaviours (OCB). · According to parents, children with comorbid attention-deficit hyperactivity disorder (ADHD) and OCB are more impaired and may be more oppositional in the home setting. · The etiologic determinants for ADHD symptoms appear to differ among children with ADHD, compared with children with comorbid ADHD and OCB. This may have implications for research into identification and treatment of both ADHD and obsessive–compulsive disorder.
Limitations · The relatively smalil size of our comorbid ADHD and OCB group limited the statistical power of our analyses. · Our results derived from a sample of children in a tertiary care clinic and may not generalize to community-based or primary care settings. · We did not have detailed information regarding the specific nature and severity of the obsessive–compulsive symptoms in our OCB group. · Family history findings are based on screening questions for presence of illness in first-degree relatives rather than direct psychiatric assessments of family members.
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The Canadian Journal of Psychiatry—Original Research
Key Words: obsessive–compulsive behaviour, attentiondeficit hyperactivity disorder, inhibitory control, risk factors, family history
psychosocial adversity have been associated with ADHD in various studies (27–30), with less evidence that these factors contribute to the development of OCD.
ttention-deficit hyperactivity disorder (ADHD) is a common disorder with an estimated prevalence of 3% to 5% of school-aged children (1). Obsessive–compulsive disorder (OCD) is also common in childhood, with an estimated risk before age 18 years of 2% to 3% (2). Studies of children with OCD report variable rates of ADHD, ranging between 9% and 33% (3–7). However, reports of children with ADHD are largely silent on the prevalence of OCD in this population (8,9).
Despite the important clinical and research implications posed by cooccurrence of the 2 disorders, only one published study has compared ADHD children with comorbid ADHD and OCD children. Geller and others reported that individuals with ADHD and OCD are similar in clinical characteristics to children with ADHD alone, though the children with OCD were more impaired overall (31). To our knowledge, no studies have directly compared these 2 groups with respect to cognitive characteristics, measures of executive functioning, or risk factors.
A
The paucity of information may be due to the exclusion of children with OCD from large studies of children with ADHD (10), the belief that these 2 disorders have incompatible phenomenological features (11), or the assumption that cases of combined ADHD and OCD result from ADHD symptoms that are secondary to OCD (for example, inattention secondary to intrusive obsessive thoughts). However, these assumptions have received scant empirical investigation. From a clinical perspective, it is important to know the prevalence and clinical features of comorbid ADHD and obsessive– compulsive behaviours (OCB), because the comorbid group may have increased morbidity and pose unique treatment challenges to clinicians. For example, stimulants effectively treat ADHD, but they are ineffective in treating OCD and may exacerbate obsessions or compulsions in some cases (12,13). Serotonin reuptake inhibitors effectively treat OCD but are ineffective for ADHD and may worsen ADHD symptoms by causing behavioural activation in some children (14,15). These 2 common childhood disorders share certain general pathophysiological and etiologic features. Abnormal activation of cortico-striatal–thalamic circuits (CSTCs) has been demonstrated for both disorders in neuroimaging studies, though the specific brain regions activated differ between ADHD and OCD (16,17). Problems with executive functioning, likely resulting from underlying CSTC dysfunction, have also been demonstrated for both children and adults with ADHD (18) and for adults with OCD (19). In the case of children with OCD, there have been comparatively few neuropsychological studies (19), though a recent study failed to demonstrate impairment on measures of executive functioning (20). Genetic risk factors likely play a major role in the etiology of both ADHD and OCD, according to evidence from family (21–23) and twin (24–26) studies. There is little evidence that ADHD and OCD cooccur in families. One exception to this is individuals with tic disorders, among whom increased rates of both OCD and ADHD are found in first-degree relatives (23). Neurobiological risk factors (especially perinatal factors) and 60
Therefore, the first objective of this study was to determine the prevalence of OCB in a clinic-referred sample of children with ADHD. The second objective was to compare ADHD children (with and without OCB) to each other and to normal control subjects with respect to behavioural characteristics, intellectual and academic functioning, executive function, neurobiological and psychosocial risk factors, and family history.
Methods Subjects The clinical sample consisted of children with ADHD drawn from 269 consecutive referrals to an outpatient clinic for assessment of learning or behavioural disorders at a tertiary care pediatric hospital serving a large metropolitan area. We recruited normal control subjects (n = 26) by posting advertisements in the hospital. Parents of all subjects gave written consent for their children to participate in the study, and all subjects gave verbal assent. An independent institutional research ethics board approved the study. The sample was predominantly white and broadly representative of the community from which it was drawn. Diagnostic Assessment We assessed all participants, both clinic-referred cases and control subjects, using the same procedure. Parents and children attended a full-day diagnostic assessment consisting of two, 3-hour evaluation sessions with a 1-hour lunch break. We based clinical diagnoses on DSM-IV criteria, as informed by semistructured interviews conducted with the children’s parents (Parent Interview for Child Symptoms [PICS], 32) and their classroom teacher (Teacher Telephone Interview-IV [TTI-IV], 33). The PICS covers the child’s development and current behaviour, including the DSM-IV diagnostic criteria for externalizing and internalizing disorders of childhood. The TTI-IV focuses on 3 diagnostic areas in detail (ADHD, oppositional defiant disorder [ODD], and conduct disorder [CD]) and only screens for internalizing disorders. Both W Can J Psychiatry, Vol 50, No 1, January 2005
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parent and teacher interviews were administered by trained masters or doctoral mental health professionals; the PICS was administered on the day of assessment, whereas the TTI-IV was arranged at a time convenient to the teacher but within 2 weeks of the clinic visit. Parent and teacher versions of the Conners’ Rating Scale-Revised (34,35) were administered prior to the assessment to provide information on home and school functioning. We established the diagnosis of ADHD according to DSM-IV criteria. According to the PICS semistructured interview, individuals diagnosed with ADHD were deemed to have significant OCB only if they met the following requirements: presence of either obsessions or compulsions and presence of symptoms associated with either marked distress or significant functional impairment. Because of a lack of information regarding the specific OCB, we conservatively classified these children as having OCB rather than full-blown OCD. Further, all diagnoses required consensus among team members. We excluded individuals with a full-scale IQ score of less than 80; history or evidence of a neurological disorder, poor physical health, or uncorrected sensory impairments; or history of a chronic tic disorder, Tourette syndrome (TS), psychotic disorder, major mood disorder, or pervasive developmental disorder. We excluded those with a chronic tic disorder or TS because we were interested in the presentation of OCB independent of tic disorders. However, we did include individuals with tics who did not meet criteria for TS or a chronic tic disorder. Measures of intelligence, academic attainment, language abilities, and self-report measures of anxiety and depression were administered to children individually by a masters- or doctoral-level psychologist. The Wechsler Intelligence Test for Children-3rd edition (WISC-3, 36) was used to measure intellectual abilities. Academic attainment was evaluated with the Wide Range Achievement Test-3rd edition (WRAT-3, 37) and the Word Attack and Word Identification subtests of the Woodcock Reading Master Tests-Revised (WRMT-R, 38). The Clinical Evaluation of Language Fundamentals-3rd edition (CELF-3, 39) was used as a measure of language abilities. The Revised Children’s Manifest Anxiety Scale (RCMAS, 40) and the Child Depression Inventory (CDI, 41) were selected as measures of anxiety and depression, respectively. A modified version of the stop signal paradigm stop task was used to measure inhibitory control (42). The stop signal paradigm requires subjects to stop their response to a simple primary task. For example, in the forced-choice reaction time task, subjects are asked to distinguish 2 letters on a computer monitor when given a signal (such as an auditory tone). This model provides a way of estimating the latency of an internally generated act of control (that is, the stop-signal reaction time [SSRT]). Can J Psychiatry, Vol 49, No 11, November 2004 W
Assessment of Impairment and Risk Factors Parents completed the Ontario Child Health Survey scales (OCHS) family and household form (43,44) prior to the clinic visit and reviewed the form at the time of assessment. The OCHS contains a rating scale that assesses social, behavioural, and academic impairment. In addition, the OCHS contains items reflecting exposure to neurobiological and psychosocial risk factors. These items, which were given equal weight, were combined into 2 multivariate risk indexes, described elsewhere (45). Examples of factors included in the risk indexes are perinatal events (neurobiological risk index) and separation from parents before age 3 years (psychosocial risk index). We obtained family history, an indicator of possible genetic risk, during the PICS interview. Through the parent interview, we obtained information on the presence or absence of a history of psychiatric, emotional, or learning problems in a participant’s first-degree relative (that is, a parent or sibling). Family history of either ADHD or OCB or tics was coded as present if these disorders were identified in a first-degree relative. Tics and OCB were examined together, based on evidence that these 2 disorders share genetic susceptibility (23). Statistical Analyses Group means and standard deviations (SDs) for each dimensional variable were determined. We analyzed dichotomous variables by cross-tabulation chi-square procedure (using Fisher’s exact test when expected cell sizes were less than 5). We first analyzed continuous variables, using analysis of variance (ANOVA), and then conducted 2 orthogonal planned comparisons: 1) ADHD and OCB compared with ADHD alone and 2) both ADHD groups together (ADHD with and without OCB), compared with normal control subjects.
Results Of the 269 children referred to the clinic, 135 were excluded because criteria for ADHD were not met or one of our exclusion criteria was present (for example, having an IQ less than 80). Thus we included 134 children with ADHD in the study; 15 subjects (11.2%) met criteria for both ADHD and OCB, and 119 (88.8%) met criteria for ADHD alone. There were 26 children in the normal control group. The mean age of participants was 8.5 years, with no significant between-group differences for age or sex distribution. The comorbid ADHD and OCB (ADHD–OCB) group had significantly more impairment on the OCHS impairment scale, compared with the ADHD group, according to parent ratings (t = – 2.55, P = 0.012) but not teacher ratings (t = – 0.89, P = 0.378). Results from the Conners’ Rating Scales (CRS) are summarized in Table 1. In all the subscales shown, ANOVA revealed significant differences between the control group, the ADHD 61
The Canadian Journal of Psychiatry—Original Research
Table 1 Mean T scores for Conners’ rating scales ADHD compared with ADHD + OCB
Mean (SD)
Healthy control subjects compared with ADHDa P values
64 (13.0)
73 (15.8)
< 0.001
0.059
74 (9.8)
70 (9.1)
< 0.001
0.144
50 (8.1)
72 (13.3)
78 (12.5)
< 0.001
0.115
48 (7.0)
52 (9.7)
63 (14.7)
0.001
0.010
Healthy control subjects n = 26
ADHD n = 119
ADHD + OCB n = 15
Mean (SD)
Mean (SD)
Oppositional
51 (8.5)
Cognitive
53 (8.4)
Hyperactivity Perfectionism
P values
1. Parents
Social
51 (9.7)
61 (13.3)
69 (16.8)
< 0.001
0.085
ADHD Index
51 (9.6)
74 (8.9)
74 (7.4)
< 0.001
0.772
Oppositional
52 (9.3)
62 (20.1)
66 (25.1)
0.004
0.513
Cognitive
51 (10.8)
66 (9.3)
59 (8.0)
< 0.001
0.014
Hyperactivity
53 (7.7)
70 (12.6)
69 (12.2)
< 0.001
0.851
ADHD Index
52 (9.0)
72 (10.8)
71 (9.8)
< 0.001
0.775
2. Teachers
ADHD = attention-deficit hyperactivity disorder OCB = obsessive–compulsive behaviours a
Healthy control subjects were compared with all ADHD patients, that is, patients with ADHD or ADHD and OCB
group, and the ADHD–OCB group (P < 0.05), and the ANOVA analysis was followed up by planned comparisons. There was a trend for parents to rate children with ADHD and OCB more highly in the oppositionality domain (Scale A), compared with the ADHD group. Increased perfectionism (Scale E) differentiated the ADHD and OCB from the ADHD group, according to parents’ reports on the CRS. Teachers rated students in the ADHD group significantly higher than the ADHD–OCB group on the Cognitive Problems/Inattention subscale (Scale B) on the teacher version of the CRS. No significant differences were found between the children with ADHD and those with ADHD and OCB on measures of depression (Children’s Diagnostic Inventory [CDI]) or anxiety (RCMAS or the Anxious/Shy subscale of the CRS). The proportion of individuals in the DSM-IV diagnostic subgroups (inattentive, hyperactive-impulsive, or combined) was not statistically different between the ADHD and the ADHD–OCB groups, though there was a trend for increased prevalence of the hyperactive-impulsive subtype in the ADHD–OCB group (40% vs 19%, P = 0.09). Of the 15 children with ADHD and OCB, ODD was present in 8, and CD was present in 4. Although the rates of these 2 disorders were relatively high, compared with the ADHD group (43 of 119 children with ODD and 20 of 119 with CD), these differences were not statistically significant. There were no differences in rates of anxiety disorders between the 2 groups. All measures of intellectual, academic, and language functioning shown in Table 2 were associated with significant (P < 0.05) between-group differences, according to ANOVA. According to planned comparisons, the combined ADHD and 62
ADHD–OCB group had significantly lower scores on measures of intellectual abilities (full-scale IQ) and on the WRAT-Arithmetic but not on the WRAT-Reading, compared with the control group. However, the ADHD–OCB group was not significantly different on any of the measures, compared with the ADHD group (including the Verbal Intelligence Quotient, Performance Intelligence Quotient, and Clinical Evaluation of Language Fundamentals scores, which are not shown in Table 2). Results from the WRMT-R are also not presented; they revealed no significant between-group differences. ANOVA revealed trends for differences among the control, ADHD, and ADHD–OCB groups for the SSRT (P = 0.06) and the Go Reaction Time (Go RT, P = 0. 08) scores. Results of the planned comparisons are shown in the second part of Table 2. On the stop signal task, the combined ADHD group (with and without OCB) had significantly longer SSRT scores, compared with normal control subjects. The mean SSRT score of the ADHD–OCB group fell approximately halfway between the ADHD group and the control group, though it did not differ significantly from the ADHD group. Table 3 summarizes the results from the OCHS neurobiological and psychosocial risk indixes and the family history of ADHD and OCB or tics from the PICS interview. No significant between-group differences were found for neurobiological and psychosocial risk factors. Family history of ADHD was significantly different between groups, with 44% of parents of the ADHD group reporting ADHD in a parent or sibling, compared with 13% for the ADHD–OCB group and 11.5% for normal control subjects. A follow-up analysis W Can J Psychiatry, Vol 50, No 1, January 2005
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Table 2 Cognitive and academic measures Healthy control subjects n = 26 Mean (SD)
ADHD n = 119 Mean (SD)
ADHD + OCB n = 15 Mean (SD)
Healthy control subjects compared with ADHDa P values
ADHD compared with ADHD + OCB P values
114 (13.1)
101 (11.9)
105 (14.6)
< 0.001
0.239
Reading
104 (13.7)
96 (14.7)
102 (12.3)
0.187
0.142
Arithmetic
103 (10.5)
93 (14.6)
97 (6.7)
0.003
0.054
WISC: FSIQ WRAT
Inhibitory control SSRT (m)
263.6 (77)
340.9 (171)
304.9 (325)
0.010
0.272
Go RT (ms)
572.0 (117)
620.0 (122)
669.0 (238)
0.071
0.444
See Table 1 for abbreviations. WISC = Wechsler Intelligence Scale for Children; FSIQ = Full-scale IQ; WRAT = Wide Range Achievement Test; SSRT = Stop signal reaction time; Go RT = Go reaction time. a
Healthy control subjects were compared with all ASDHD patients, that is, patients with ADHD or ADHD and OCB
comparing the 2 clinical groups revealed that the increased rate of ADHD in families of the ADHD group, compared with the ADHD–OCB group, was also statistically significant (P = 0.026). Conversely, there were no significant between-group differences in family history of tics or OCB, and the clinical groups had nominally lower rates of OCB or tics in first-degree relatives, compared with control subjects.
Discussion The first major objective of this study was to determine the prevalence of significant OCB in a clinical sample of children with ADHD. The prevalence of 11.2% in this study was elevated, compared with point prevalence estimates for childhood OCD of 0.17% to 5.5% in the general population (46,47). In another study of a clinical population (48), children with ADHD (aged 9 to 13 years) had elevated scores of OCB, compared with children with tic disorders or normal control subjects. However, Peterson and others did not find an increased risk for developing full-blown OCD in a community sample of prepubertal children with ADHD, though they found an increased risk for OCD in older adolescents and adults with ADHD (47). Comorbid OCD in patients with ADHD was also associated with increased morbidity, as reflected in increased impairment scores reported by parents but not teachers. Together, the findings of high prevalence and increased morbidity in OCD underscore the clinical importance of diagnosing OCB in children with ADHD. Our second objective was to compare the ADHD and ADHD–OCB groups with respect to behavioural correlates, intellectual and academic functioning, executive function, neurobiological and psychosocial risk factors, and family history. To answer these questions, we administered various measures, including the CRS, the WISC, the WRAT, the CELF, the stop signal task, the OCHS risk indexes, and family history questions from the PICS interview. Overall, the ADHD and ADHD–OCB groups were similar with respect to most behavioural characteristics, IQ, academic functioning, Can J Psychiatry, Vol 49, No 11, November 2004 W
expressive and receptive language abilities, and neurobiological and psychosocial risk. Statistically significant differences between the ADHD and ADHD–OCB groups were found in the domains of Perfectionism, Cognition/Inattention, and family history. In addition, our results suggest other possible differences between the 2 groups in oppositional behaviour and inhibitory control, which were not statistically significant. Oppositionality was increased according to parent (but not teacher) questionnaires in the ADHD/OCB group. However, this result was not statistically significant. Conversely, teachers but not parents rated students in the noncomorbid ADHD group as significantly more impaired on the Cognitive Problems/Inattention subscale. Teachers may be more likely to note significant impairment in cognition and (or) inattention, since there may be greater cognitive demands at school than at home. On the other hand, oppositional behaviours may be displayed in the less structured home environment rather than at school. Another difference found using the CRS was high Perfectionism scores on the Conners’ Parent Rating Scale in the ADHD–OCB group, compared with the ADHD group. Inspection of the Conners’ Parent Rating Scale reveals that many of the items on the Perfectionism subscale are consistent with OCB, including the child “has rituals he/she must go through,” is “fussy about cleanliness,” “keeps checking things over and over again,” and “gets upset if someone rearranges his/her things” (34,35). Therefore, we believe the most parsimonious explanation of the elevated perfectionism scores is that this subscale measures OCB symptoms in the ADHD–OCB group, which provides converging evidence to support our diagnosis of OCB. An alternative explanation, that the subscale reflects comorbid perfectionist personality traits, could not be ruled out from our data. The group of ADHD children with and without OCB had increased SSRT scores on the stop signal paradigm, compared 63
The Canadian Journal of Psychiatry—Original Research
Table 3 Risk factors Risk factor
Healthy control subjects n = 26
ADHD n = 119
ADHD + OCB n = 15
Analysis
Mean (SD)
Mean (SD)
Mean (SD)
F
Neurobiological risk
2.04 (1.46)
2.59 (1.97)
2.33 (1.63)
0.97
Psychosocial risk
2.16 (2.27)
2.54 (2.07)
2.53 (1.92)
0.35
n (%)
n (%)
n (%)
c2
ADHD
3 (11.5%)
51 (44.0%)
2 (13.3%)
13.3***
OCD and tics
3 (11.5%)
7 (5.9%)
1 (6.7%)
.586
OCHS Risk indices
Family history
***P < 0.001 See Table 1 for abbreviations. OCHS = Ontario Child Health Survey
with the control group, which is consistent with previous findings in ADHD (49). The ADHD–OCB and ADHD groups were not statistically different from one another on any aspect of the stop signal task, though the mean SSRT score for the children with comorbid OCB fell about halfway between the ADHD group and the control group. Interestingly, this nominal difference suggests that the ADHD–OCB group had a reduced inhibitory control deficit, compared with the ADHD group, though our study did not have sufficient statistical power to provide a conclusive answer to this question. Family history of ADHD, used as a proxy for genetic risk for ADHD, was significantly elevated in the ADHD-only group, compared with both the ADHD–OCB and control groups. The proportion of ADHD–OCB probands with a family history of OCB or tics was not different from ADHD probands and was lower than that in the control group. While no previous study comparing ADHD and ADHD– OCB children has included such a comprehensive range of dependent measures, our results are generally consistent with other investigators’ reports. A recent study systematically compared demographic and clinical characteristics in children with ADHD and children with ADHD and OCD (31). Their findings indicated that the 2 groups were essentially identical on all clinical characteristics, with the exception of worse overall functioning in the ADHD–OCD group. More recently, the same group has reported a similar lack of differences between children with OCD alone, compared with children with OCD and ADHD (50), with the exception of increased impairment of educational functioning in children with comorbid ADHD. Similarly, our findings indicated that the ADHD–OCB group is more impaired, compared with the ADHD group, which is not surprising given the additive burden of having 2 disorders. Further, the trend toward increased oppositionality at home may contribute to the increased impairment reported by parents. The absence of elevated neurobiological and psychosocial risk factors in ADHD, 64
compared with control subjects, is consistent with previous findings reported by our group on an overlapping sample (45). Our findings support a phenocopy model in which the susceptibility genes for ADHD play a major role in the ADHD-only group, whereas in the ADHD–OCB group, different etiologic determinants produce similar symptoms. For example, one or more genes that impact inhibitory control may predispose children in the ADHD group to ADHD, which is consistent with previous work by our group, demonstrating that a family history of ADHD is much more likely in ADHD subjects with higher scores on the stop signal paradigm, compared with those with lower scores. Further, compared with the ADHD group, ADHD–OCB subjects exhibited both nominally better inhibitory control and reduced genetic risk for ADHD. Taken together, the family history and inhibitory control results suggest that susceptibility gene(s) involved in inhibitory control may strongly predispose to ADHD, while playing a much smaller role in ADHD–OCB. Our findings also suggest that ADHD–OCB may be distinct from “pure” childhood OCB, in which genetic determinants are thought to play a major role. The proportion of ADHD–OCB probands with a family history of OCB or tics was only 6.7%, which is much lower than the rate of 52% previously reported in a well-designed family study of OCD probands (23). Overall, our family history findings underscore the need to consider comorbidity in genetic studies of neuropsychiatric disorders, because the presence of comorbid conditions may reflect underlying genetic heterogeneity. This study has several limitations. First, statistical power of our analyses was limited by the small size of our comorbid ADHD and OCB group. Second, our results were derived from a sample of children in a tertiary care clinic, and the possibility of referral bias (51) means that we cannot generalize the prevalence of comorbid OCB to the general population. However, the clinic setting enabled us to conduct detailed assessments, including semistructured interviews and computerized measures of inhibitory control, that would be extremely difficult to apply in a community or primary care W Can J Psychiatry, Vol 50, No 1, January 2005
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setting. An additional modest referral bias may have occurred in recruitment of normal control subjects through hospital advertisement. It is possible that the control subjects who were not paid to participate and did so altruistically were derived from families characterized by relatively high socioeconomic status. Another limitation of this study is that, although information was available for OCB and other childhood psychiatric disorders, based on a methodologically rigorous semistructured diagnostic interview, we did not have detailed information regarding the specific nature and severity of obsessive– compulsive symptoms. This type of information would have been provided by an instrument such as the Children’s Yale-Brown Obsessive–Compulsive Scale (CYBOCS, 52). As a result, we conservatively classified children with obsessive– compulsive symptoms as having OCB, though given our requirement for distress and impairment, it is likely that many of these children would have met criteria for OCD. It is arguable that we might have missed some children with full-blown OCD, since, according to the DSM-IV, OCD can be diagnosed in the absence of distress and impairment if symptoms take up a great deal of time (for example, over 1 hour daily). Finally, family history results were based on screening questions for presence of illness in first-degree relatives, whereas systematic psychiatric assessments of family members would be needed to confirm our finding of differences in family history of ADHD between ADHD and ADHD–OCB children.
Conclusions The high prevalence of clinically significant OCB in children with ADHD, in addition to the possible increased functional impact of having both disorders, indicates that clinicians seeing children with ADHD should conduct comprehensive clinical assessments to cover potential comorbid disorders. Few clinical differences were found between children with comorbid OCB and children with ADHD alone. An increased rate of ADHD was found in the first-degree relatives of children with ADHD, but not in the subgroup of children with ADHD–OCB, suggesting that ADHD symptoms in children with ADHD–OCB may represent a phenocopy resulting from different etiologic determinants. Further investigations to elucidate differences between these subgroups will provide insights into the pathogenesis of both ADHD and OCD that may lead to improved diagnosis and prevention of these common childhood neuropsychiatric conditions.
Funding and Support This research was supported by a grant from Canadian Institutes of Health Research (grant number MOP44070).
Acknowledgements The authors give special thanks to the children and parent participants and acknowledge the contributions of the Neuropsychiatry Team at the Hospital for Sick Children in Toronto in the conduct of this research. Can J Psychiatry, Vol 49, No 11, November 2004 W
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Presented as part of the symposium “OCD Spectrum Illnesses: What Does It Mean?” at the American Psychiatric Association Annual Meeting; 2003 May 19; San Francisco (CA). 1 Research Fellow, Neurogenetics Section and Child Psychiatry Program, Centre for Addiction and Mental Health, Toronto, Ontario; Research Fellow, Department of Psychiatry, University of Toronto, Toronto, Ontario. 2 Staff Psychiatrist, Department of Psychiatry and the Brain and Behaviour Programme at the Hospital for Sick Children, Toronto, Ontario; Assistant Professor, Department of Psychiatry, University of Toronto, Toronto, Ontario. 3 Research Associate, Psychiatry Research, Brain and Behaviour Programme, The Hospital for Sick Children, Toronto, Ontario. 4 Director of Psychiatry Research, Brain and Behaviour Programme at the Hospital for Sick Children, Toronto, Ontario; Professor of Psychiatry, Department of Psychiatry, University of Toronto, Toronto, Ontario. Address for correspondence: Dr A Ickowicz, MD, FRCPC, Department of Psychiatry, The Hospital for Sick Children, 555 University Ave, Toronto, ON M5G 1X8 e-mail:
[email protected]
Résumé : Le trouble d'hyperactivité avec déficit de l'attention, avec et sans comportements obsessionnels–compulsifs : caractéristiques cliniques, évaluation cognitive et facteurs de risque Objectifs : Déterminer la prévalence des comportements obsessionnels–compulsifs (COC) dans un échantillon clinique d'enfants souffrant du trouble d'hyperactivité avec déficit de l'attention (THADA) et comparer les enfants souffrant du THADA (avec et sans COC) en ce qui concerne les caractéristiques cliniques et cognitives, et les facteurs de risque. Méthode : Nous avons comparé les enfants souffrant du THADA (n = 134) avec et sans COC, et nous avons comparé tous les enfants souffrant du THADA avec un groupe de sujets témoins normaux (n = 26) relativement à diverses mesures de contrôle cliniques, cognitives et inhibitrices; aux facteurs de risque neurobiologique et psychosocial; et aux antécédents familiaux de maladie psychiatrique. Résultats : Des COC cliniquement significatifs ont été constatés chez 11,2 % (15/134) des enfants souffrant du THADA. Les COC comorbides étaient associés à un perfectionnisme significativement accru, à de meilleures cotes d'inattention de l'enseignant, et à une probabilité moindre d'avoir un parent du premier degré souffrant du THADA. Le THADA et les COC comorbides peuvent aussi être associés à un comportement oppositionnel accru à la maison et à un meilleur contrôle inhibiteur, bien que ces différences ne soient pas statistiquement significatives. Conclusions : Les COC comorbides sont fréquents chez les enfants souffrant du THADA adressés en clinique et sont associés à une incapacité accrue reliée au THADA seulement. En outre, les enfants souffrant du THADA et des COC peuvent développer des symptômes en présence de facteurs de risque génétiques et environnementaux, comparativement aux enfants souffrant du THADA seulement.
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