This is one of the first studies to explore the relationship between traumatic life events, as captured by an expanded PTSD diagnosis, and incidence of OCD in the pediatric population, using systematic data from a large pool of carefully assessed youth seen in a specialized setting. We found that, although only a small minority of OCD subjects also had PTSD (6%), rate of concurrent PTSD was still significantly greater in children with OCD than in a comparable control group. In those children with concurrent OCD and PTSD, obsessions were experienced as more intrusive and distressing, and compulsions as more distressing and difficult to suppress than the children with OCD without PTSD. Total CY-BOCS scores were significantly higher in children with concurrent illness. In practical terms, a CY-BOCS scale score of 2 means moderate interference and distress while a score of 3 is used to record severe interference and distress. A scale score of 2 denotes moderate control over rituals while a score of 3 is used to denote little control. Most salient, a total CY-BOCS scale score of 21.3 (mean score in OCD group) is in the moderate range overall while a scale score of 25.5 (mean score OCD+PTSD group) is in the severe range. In this sample of children with OCD, a PTSD diagnosis and trauma was associated with CY-BOCS scale scores that increased in severity in clinically meaningful measures.
Our finding of a significant association between OCD and PTSD in children is consistent with the literature from adult studies over more than two decades, which provides compelling evidence of such a link. The Epidemiological Catchment Area (ECA) Study (Helzer et al., 1987
) found that among Vietnam veterans with PTSD, the relative risk (RR) of having OCD was 10.1, higher than for any other comorbid diagnosis including mood disorder (dysthymia RR 7.8, bipolar disorder RR 5.7), alcoholism (RR 1.9) and drug abuse or dependence (RR 5.0). In a survey of the extant literature, rates of OCD among adults with PTSD were found to range from 5–22%, much higher than the general population lifetime prevalence of OCD of 1–2% (Huppert et al., 2005
). Furthermore, OCD is a psychiatric disorder whose phenotype is fairly consistent across the lifespan, without the ambiguity seen in some other child psychiatric disorders. Diagnostic criteria and treatment approaches are similar in children and adults and it is reasonable to pursue significant associations derived from adult OCD research in early-onset subjects. From a clinical viewpoint, increased severity of OCD and comorbid status may have treatment and outcome implications. A recent study of the impact of trauma on treatment outcome in a comparative treatment study of depressed adolescents (Lewis et al., 2010
) found that a trauma history moderated treatment outcomes.
Cognitive-behavioral theory provides an empirically based, well-established framework for understanding a possible association between trauma and OCD and our finding that children with concurrent OCD and PTSD had more severe OCD symptoms. Central to the behavioral framework is Mowrer’s (1939)
two-factor theory, which states that the acquisition of fears is based on classical conditioning and maintained by operant principles (i.e.,
negative reinforcement). In the conditioning process, a previously neutral stimulus becomes associated with a feared stimulus (e.g. a psychological trauma) and thereby produces distress. The person engages in ritualistic behavior that reduces distress and anxiety and increases the likelihood of future ritual engagement. Threat appraisals in OCD are associated with multiple cognitive errors such as an exaggerated importance attributed to thoughts or an inflated concern about the ability to control these thoughts (Barrett & Healy, 2003
; Obsession Compulsive Cognitions Working Group, 1997
). Similar threat-based attention and interpretation biases have been observed among individuals with PTSD (Kaspi, McNally, & Amir, 1995
; Vrana, Roodman, & Beckham, 1995
). Shared psychological mechanisms underlying both disorders may therefore cause degrees of intrusiveness and distress that are additive. Biological mechanisms may also be common to both disorders. Photon emission tomography (PET) has shown both PTSD and OCD patients have reductions in right caudate blood flow (Lucey et al., 1997
) and activation of the right posterior medial orbito-frontal region (Rauch, Savage, Alpert, Fischman, & Jenike, 1997
There are good reasons to explore salience of potential environmental triggers in children with OCD. Our findings documenting an association between pediatric OCD and traumatic life events are consistent with data from genetic studies suggesting that a considerable proportion of the variance in the occurrence of OCD can be explained by non-genetic environmental
factors. For example, in a meta-analysis of family studies, (Hettema, Neale, & Kendler, 2001
) found only modest estimated heritability coefficients for OCD of 30–40%. In a cross-cultural sample of 4246 twin pairs, Hudziak et al. (2004)
used structural equation modeling using an 8-item Obsessive Compulsive scale (OCS) from the CBCL as a proxy for OCD to examine the influence of both genetic (45%-58%) and unique environmental (42%-55%) factors and concluded that both were about equally important. Even lower estimates of heritability of OCD were reported by Jonnal et al. (2000)
in a population sample of 527 female twin pairs using items from the Padua Inventory. These studies support the role of environmental risk factors that could influence the expression of OCD and underscore the importance of seeking to understand such triggers.
Even if a small amount of variance (in the expression of OCD) is explained by psychological trauma, all gene-environment mediators are of potential importance. Genetic models may be helpful in that, for complex psychiatric disorders, research posits many common variants, each explaining but a small amount of the variance in phenotype. The cumulative effect of multiple common genetic variants, each with small effect, may lead to a critical threshold for phenotype expression. Similarly, any significant environmental associations are of interest and merit further study.
Several limitations could affect interpretation of our data. This was a secondary analysis of existing data collected for a study whose design did not, a priori, focus on the present research question. As such the design was not ideally suited to explore the relationship between OCD and trauma in children and could have lead to potential sampling bias. The overall prevalence of PTSD in our sample was quite low making comparisons more difficult. In particular, absence of PTSD in our control group is at variance with the cited pediatric literature and is possibly explained by the relatively high SES in our sample (upper middle class and predominantly Caucasian subjects) whose risk for exposure to trauma may not be representative of the greater population at large. If true, then we would expect our findings to retain their significance as all our subjects had a similar SES. Our findings of a significant difference in the sub- and total scores of the CY-BOCS, considered the most sensitive quantitative assessment scale for pediatric OCD, (Scahill et al., 1997
) is even more noteworthy in the small cohort of OCD+PTSD subjects. Another possibility is that the DSM-III-R diagnostic criteria for PTSD used to assess the control group were less sensitive (i.e.,
more restrictive) than the DSM-IV criteria used for the OCD subjects who represented a later cohort. However, the screening question/probe that we used to elicit a trauma history did not vary between the KSADS interview instruments and with some minor variation in language, also did not differ in itemized probes for PTSD criteria B, C, D or E (distress and impairment). However, the use of sequential versions of the DSM for PTSD represents a further limitation of this work.
Another concern is that diagnoses could be confounded and that the apparent higher than expected concurrence of PTSD and OCD is an artifact caused by mis-attribution of symptoms. This assumption is at odds with the extensive literature on this subject including epidemiological studies (i.e.,
non-clinically referred subjects that avoids Berkson’s bias) (Berkson, 1946
) although the extant literature may be limited by the changing nosology of the DSM and the stringency or sensitivity of evolving PTSD diagnostic criteria. It is important to note that even if a trauma acts as a trigger for obsessions, the CY-BOCS measures syndrome-specific
symptoms and severity, not PTSD symptoms. If more severe OCD symptoms in children with concurrent OCD and PTSD represented an artifact of the PTSD diagnosis (e.g.
PTSD symptoms masquerading as OCD symptoms) we would expect fears of harm and aggression characteristic of PTSD to be overrepresented in these children. This is not the case; symptoms and symptom dimensions did not differ between groups, suggesting that increased severity of OCD is a true finding. We took particular care to include only children who met syndrome criteria for diagnoses attending to potential overlap in symptoms. Indeed a large number of plausible traumatic events including physical and sexual abuse were not
included in the PTSD sample, as they did not meet diagnostic criteria, even though we used an expanded phenotype to increase our diagnostic sensitivity to such cases.
We elected to include subthreshold cases in an expanded phenotype in our analysis as detailed in Methods. Given the criteria we used for a subthreshold diagnosis that specified a patient must have had a trauma and met all criteria for two out of the other three DSM-IIIR sections, or more than half of all criteria for all three remaining sections, this operational threshold was judged reasonable to define some quantifiable measure of trauma for an exploratory analysis. Since such an experience is largely subjective, the DSM language requiring “an event involving actual or threatened death or serious injury, or a threat to the physical integrity of self or others and intense fear, helplessness, or horror” may be excessively strict for vulnerable individuals. This may be especially true for children whose perception of serious threat is developmentally sensitive.
Another potential limitation is that our findings of a link between trauma and OCD may not be specific to the modeled variable of OCD but rather a general effect on psychopathology in youth. However, we argue that specificity of the association is demonstrated in several ways. First, the association between OCD and PTSD remained significant after controlling for common comorbid disorders that might represent proxy associations. Second the temporal link between syndrome onsets is noted, and thirdly, the nature of the symptoms is often thematically linked as seen in case descriptions in .
Finally, not every child had complete data of symptom types and scalar scores so that our denominator was slightly smaller for this analysis. Despite this, our sample is the largest ever reported using systematic expert assessments applied consistently over the duration of the data collection.
Children with OCD also had PTSD and evidence of psychological trauma at rates higher than found in a comparable non-OCD cohort and those affected with concurrent disorders had more severe OCD symptoms. Although a minority of children may be included in this association, the threshold criteria for defining a meaningful trauma for children who are vulnerable remain unclear. Since genetic influences account for only some of the expression of OCD, the search for environmental mediators (epigenetic factors) of large and small effect in genetically vulnerable individuals is important. The adult literature points towards psychological trauma as a plausible factor to study in early onset cases. In this large sample of children with OCD we found a positive signal suggesting further systematic study of this association is needed.