We compared neurocognitive functioning in children and adolescents with moderate to severe OCD and non-psychiatric controls aged 8–17 years on neurocognitive measures assessing cognitive flexibility, planning and decision-making, WM, fluency, and processing speed. Analyses revealed that the patients with OCD showed markedly reduced neurocognitive performance relative to non-psychiatric controls, even after controlling for IQ as a potential covariate. These group differences were particularly driven by group performances on the AST, TMT, CGT, and WMI.

The extent to which children and adolescents with OCD show reduced neurocognitive performance relative to non-psychiatric controls has been debated with one meta-analysis reporting no significant group differences [12] while a recent review argued that they could be seen for visual WM, planning, decision-making under uncertainty and abnormal action monitoring [13]. Much of the older evidence was hampered by relatively small sample sizes. However, this has been less of a concern in recent work [11, 18,19,20] which, like the current study, has found evidence of group differences in neurocognitive performance.

Several important points are worth noting regarding the current results. First, the main effect of group, even for the MANCOVA including IQ and age as covariates, was highly significant. This indicates that children and adolescents with OCD do struggle with neurocognitive difficulties. Second, while groups differed in IQ—and IQ is a major determinant of neurocognitive performance (e.g., [42]), as was also seen in our data—the group difference in neurocognitive performance remained stable even after the influence of this variable was covaried out. Third, some have suggested that reduced processing speed underlies the neurocognitive underperformance seen in adults with OCD [42–44]. However, exploratory analyses with the current data indicated that the group differences in performance existed over and above group differences in processing speed. Fourth, despite the marked group differences in neurocognitive performance, our MANCOVA in the patients examining task performance and OCD symptom severity, as indexed by the CY-BOCS, revealed no significant association. In short, and consistent with previous work with adults and children/adolescents with OCD [6, 11, 45, 46], the neurocognitive difficulties indexed in the current study were not major contributors to patient symptom severity. Fifth, patients with OCD showed group differences with the non-psychiatric control participants whether these the patients presented with comorbidities or not while patients with versus without comorbidities did not differ in neurocognitive performance. These results are consistent with prior work in children/adolescents [11, 45, 46] and adults with OCD [6] and suggest that the neurocognitive difficulties identified cannot be attributed to comorbid conditions. Sixth, the neurocognitive difficulties shown by the children and adolescents with OCD were potentially particularly marked for decision-making and WM.

Difficulties in decision-making in the participants with OCD could be seen on the CGT. In line with this finding, recent studies have reported that children/adolescents with OCD, relative to comparison participants, were slower to learn response–outcome relationships and worse at adapting response strategy when previously rewarded actions were devalued compared to non-psychiatric control children [47, 48] and show poorer decision-making ability [49, 50]. The Wechsler WMI revealed group differences while the SWM index did not. Reduced working verbal and visual memory has been relatively consistently seen in adults with OCD [5] and also reported in child/adolescent samples (for a review, see [13]). Recently, reduced verbal WM was reported in one larger N study [11], whereas spatial WM was not in another [19].

Our study has several strengths: (i) the N was relatively large, (ii) the patients were not receiving pharmacological interventions or psychotherapy for OCD (nor had for the last 6 months) thereby avoiding potential confounding treatment effects [22, 23]; and (iii) the patient sample included a broad range of comorbidities (i.e., it was representative of real-world clinical populations). Moreover, and importantly, we could show groups of patients with and without comorbidities differed in neurocognitive performance relative to typically developing children/adolescents but did not differ from each other; i.e., the neurocognitive performance difficulties seen in the patients cannot be attributed to pathology associated with the comorbidities.

Our study also has several limitations. First, since the data presented here are cross-sectional, we were unable to evaluate if the observed neurocognitive underperformance is moderated by e.g., illness duration, earlier pharmacological or therapeutic intervention, or age of onset. Second, we cannot ensure that the patients were naïve to pharmacological and/or psychotherapeutic interventions for OCD as we did not assess if patients received antidepressants or antipsychotics before 6 months prior to testing. Third, we included patients with a variety of comorbidities that are known to be associated with neurocognitive underperformance. As such, it could be argued that some of our findings might relate to pathology associated with these comorbidities. Importantly, though, follow-up MANOVAs indicated that the results were not likely to be attributed to these comorbidities. Fourth, the groups differed in IQ, which is in itself a determinant of neurocognitive performance [42]. However, controlling for intelligence in secondary analyses led to results that largely mirrored those of our main analysis.

The results have clinical implications. While the atypical neurocognitive functioning observed in patients was not associated with patient symptom severity, it was highly significant and as such likely conferring some detrimental impact on patients’ lives. Moreover, this atypical neurocognitive functioning may interfere with particularly psychosocial interventions. Knowing that forms of neurocognitive dysfunction which are seen in adult patients, are already present in childhood OCD, stresses the need for studying their developmental trajectory in patients with OCD.

In conclusion, the current study indicates that many pediatric patients with OCD show a degree of atypical neurocognitive function even if the forms of atypical functioning identified here, and in previous work, do not appear to be associated with the specific symptoms associated with OCD. As such, a more precise neurocognitive model of OCD is clearly required such that it can be tested in the future with specifically designed target tests. Moreover, it will be important to determine the extent to which the neurocognitive difficulties observed here are ameliorated by treatment for OCD or, indeed, moderate treatment efficacy.