Clinical Cognitive Neuroscience Center

Research

Obsessive-Compulsive Disorder

Obsessive-Compulsive Disorder

Key question. How does dysfunction of the cortico-striato-thalamo-cortical (CSTC) circuit give rise to obsessions and compulsions, and why do patients with the same diagnosis differ in onset, symptoms, and course?

Approach. We study a clinical cohort of patients with OCD, including medication-free patients, using structural, diffusion and functional MRI, neurocognitive tasks, and computational models of behavior. We take part in the ENIGMA-OCD working group. Our studies of treatment response in OCD are described under Neuromodulation and Neuropsychopharmacology.

Recent Findings

Pathophysiological Mechanisms

Striatal white matter connectivity and microstructure in OCD

Patients with OCD showed reduced orbitofronto-striatal and increased motor- and parietal-striatal white matter connectivity, with altered microstructure in the corresponding striatal subregions (Park, Kim et al., Mol Psychiatry, 2022).

Fronto-pallidal and intra-thalamic dysconnectivity in OCD

In OCD, fronto-pallidal dysconnectivity was related to impaired set shifting, and intra-thalamic dysconnectivity to compulsivity (Kim et al., Brain, 2022).

Neurocomputational model of compulsivity

A neurocomputational model showed that compulsivity arises from a deviation from an uncertain goal-directed system (Kim et al., Brain, 2024).

Heterogeneity

Cortical gyrification in early-onset and late-onset OCD

Early-onset OCD showed greater cortical gyrification than both healthy controls and late-onset OCD, suggesting neurodevelopmentally distinct subtypes (Park et al., Psychol Med, 2023).

Neural networks associated with obsessions and delusions

Obsessions and delusions were associated with distinct neural networks in a connectome-wide association study (Lee et al., Psychol Med, 2021).

Foundational Work

Fronto-striatal dysfunction was linked to impaired task switching in OCD (Gu et al., Brain, 2008).