Melanie Ritter, Christine Lykke Thoustrup, Nicole Nadine Lønfeldt, Sofie Heidenheim Christensen, Valdemar Uhre, Linea Pretzmann, Anna-Rosa Cecilie Mora-Jensen, Nicoline Løcke Jepsen Korsbjerg, Kerstin Jessica Plessen, Jens Richard Møllegaard Jepsen, Signe Vangkilde, Camilla Funch Uhre, Anne Katrine Pagsberg, Robert James Blair
These findings indicate that psychotherapeutic interventions may be associated with modest and selective changes in neurocognitive performance in pediatric OCD on a group level. However, the selective effects, together with the lack of differential treatment effects and the absence of association with symptom alleviation, raise questions about the clinical relevance of these changes and whether performance-based neurocognitive differences represent clinically meaningful mechanisms underlying pediatric OCD symptoms or their alleviation with treatment.
BACKGROUND: Atypical neurocognitive functioning is consistently reported in adults with obsessive-compulsive disorder (OCD), while studies in childhood/early-onset OCD show smaller and more selective effects. Neurobiological models of OCD implicate aberrant activation within cortico-striato-thalamo-cortical (CSTC) circuits, while related executive function (EF) alterations have been proposed as potential mechanisms underlying OCD symptomatology. However, neurocognitive correlates of treatment response in pediatric OCD have not been examined across different psychotherapeutic interventions in a randomized design.
METHODS: 130 children with OCD (aged 8-17 years) were randomized 1:1 to 14 sessions of family-based psychotherapy with either cognitive-behavioral therapy (CBT) or psychoeducation and relaxation training (PRT) and assessed with a comprehensive neurocognitive test battery before randomization (baseline) and at end-of-treatment (week 16). Of those, 90 children with relevant neurocognitive data were included in the present study. An age- and sex-matched control group of 87 children with no psychiatric diagnoses were assessed at the same time points.
RESULTS: Children with OCD showed moderate improvement after treatment, relative to controls, on one pre-selected outcome (decision-making; generalized eta squared (ges) = .020) and small improvement on one exploratory outcome (processing speed; ges =.010). However, there was no differential effect of treatment type (CBT versus PRT) and no association between neurocognitive change and OCD symptom alleviation. Symptom alleviation was neither predicted nor moderated by baseline neurocognitive performance.
CONCLUSION: These findings indicate that psychotherapeutic interventions may be associated with modest and selective changes in neurocognitive performance in pediatric OCD on a group level. However, the selective effects, together with the lack of differential treatment effects and the absence of association with symptom alleviation, raise questions about the clinical relevance of these changes and whether performance-based neurocognitive differences represent clinically meaningful mechanisms underlying pediatric OCD symptoms or their alleviation with treatment.