Poster No:
660
Submission Type:
Abstract Submission
Authors:
Teresa Sousa1,2,3, Ana Araújo1,2,4,5,3, Catarina Duarte1,2, Ana Telma Pereira4,1, António Macedo5,4,1, Miguel Castelo-Branco1,2,6
Institutions:
1Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra, Coimbra, Portugal, 2Institute for Nuclear Sciences Applied to Health (ICNAS), University of Coimbra, Coimbra, Portugal, 3Shared co-first authorship, ., 4Institute of Psychological Medicine, Faculty of Medicine, University of Coimbra, Coimbra, Portugal, 5Department of Psychiatry, Coimbra Hospital and University Centre, Coimbra, Portugal, 6Faculty of Medicine, University of Coimbra, Coimbra, Portugal
First Author:
Teresa Sousa
Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra|Institute for Nuclear Sciences Applied to Health (ICNAS), University of Coimbra|Shared co-first authorship
Coimbra, Portugal|Coimbra, Portugal|.
Co-Author(s):
Ana Araújo
Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra|Institute for Nuclear Sciences Applied to Health (ICNAS), University of Coimbra|Institute of Psychological Medicine, Faculty of Medicine, University of Coimbra|Department of Psychiatry, Coimbra Hospital and University Centre|Shared co-first authorship
Coimbra, Portugal|Coimbra, Portugal|Coimbra, Portugal|Coimbra, Portugal|.
Catarina Duarte
Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra|Institute for Nuclear Sciences Applied to Health (ICNAS), University of Coimbra
Coimbra, Portugal|Coimbra, Portugal
Ana Telma Pereira
Institute of Psychological Medicine, Faculty of Medicine, University of Coimbra|Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra
Coimbra, Portugal|Coimbra, Portugal
António Macedo
Department of Psychiatry, Coimbra Hospital and University Centre|Institute of Psychological Medicine, Faculty of Medicine, University of Coimbra|Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra
Coimbra, Portugal|Coimbra, Portugal|Coimbra, Portugal
Miguel Castelo-Branco
Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra|Institute for Nuclear Sciences Applied to Health (ICNAS), University of Coimbra|Faculty of Medicine, University of Coimbra
Coimbra, Portugal|Coimbra, Portugal|Coimbra, Portugal
Introduction:
Obsessive-compulsive disorder (OCD) is a common and potentially debilitating condition that affects approximately one person out of 40 at some point during their lifetime. It causes significant distress and can also lead to substantial disability by disrupting various aspects of daily life, including occupation and social activities [1]. Recent computational models [2,3] have suggested that individuals with OCD implicitly reinforce maladaptive behaviors. These models propose an explanation for the repetitive cycle of obsessions and compulsions, which are core features of OCD symptoms, within a framework of reinforcement learning. However, they have yet to be tested at the neuronal level. The aim of this study was to examine brain connectivity related to inhibitory learning using an actor-critic architecture. We hypothesized that patients with OCD would exhibit altered connectivity between the critic, the reward system, and the associated regulating networks.
Methods:
Functional magnetic resonance imaging (fMRI) data were collected from 40 adult males, consisting of 19 OCD patients and 21 age-matched healthy subjects, during a Stop-Signal Task (SST). The analysis followed the actor-critic model [4], wherein the dopaminergic midbrain regions-the ventral tegmental area (VTA) and the substantia nigra (SN)-were considered as the critics, while the dorsal striatum served as the actor [5]. Functional connectivity was evaluated within the actor-critic network nodes using ROI-to-ROI correlation analysis. Additionally, seed-to-voxel correlation analysis was conducted to assess connectivity between each of these regions and all other brain regions. These connectivity analyses were performed in two ways: first, comparing the patient and control group, and second, dividing the patients into two subgroups based on their stop-signal reaction time (SSRT). The division was made into groups with SSRTs either lower or higher than the average, indicating different levels of inhibitory control.
Results:
We did not find any functional connectivity differences between individuals with OCD and control subjects concerning the actor-critic regions. However, our seed-to-voxel analysis revealed reduced connectivity between the critic and several regions associated with error monitoring and cognitive control in OCD. Specifically, the VTA showed decreased connectivity with the angular gyrus/supramarginal gyrus and the superior frontal gyrus/frontal pole, while the SN exhibited decreased connectivity with the central opercular cortex/insular cortex and the anterior and posterior cingulate gyrus. When considering the actor regions (putamen or caudate) as seed regions, we did not observe any functional connectivity differences between individuals with OCD and healthy subjects. Notably, such decrease in functional connectivity between SN/VTA and error monitoring and cognitive control regions was particularly evident when comparing individuals with OCD and controls possessing high inhibitory control. When comparing patients and controls with low inhibitory control, we only found decreased connectivity between the SN and the occipital pole.
Conclusions:
These findings suggest that comparing patients and controls with similar behavioral strategies (such as high inhibitory control) better emphasizes the distinct neural dynamics of OCD patients during inhibitory control. Furthermore, the decreased functional connectivity patterns identified in OCD may contribute to explaining the hyperactivity of error monitoring and reward regions in this clinical group [6]. The poor integration of both systems, mediated by network nodes acting as critics, might lead to an overload when each system operates independently. This insight could be valuable in understanding the etiological processes contributing to OCD, as it indicates potential alterations in the dynamics of the neural circuitry associated with reinforcement learning.
Disorders of the Nervous System:
Psychiatric (eg. Depression, Anxiety, Schizophrenia) 1
Higher Cognitive Functions:
Executive Function, Cognitive Control and Decision Making 2
Keywords:
Obessive Compulsive Disorder
Other - inhibition; cognitive control; error processing; learning; functional connectivity; fMRI
1|2Indicates the priority used for review
Provide references using author date format
1. Robbins et al., 2019. Obsessive-Compulsive Disorder: Puzzles and Prospects. Neuron 102 (1): 27–47.
2. Sakai et al., 2022, Memory trace imbalance in reinforcement and punishment systems can reinforce implicit choices leading to obsessive-compulsive behavior. Cell Reports 40, 111275.
3. Zhongqiang et al., 2023 Impairment of arbitration between model-based and model-free reinforcement learning in obsessive–compulsive disorder. Front. Psychiatry 14:1162800.
4. Barto, A. G., 1995. Adaptive critics and the basal ganglia. In J. C. Houk, J. L. Davis, & D. G. Beiser (Eds.), Models of information processing in the basal ganglia (pp. 215–232). The MIT Press.
5. Lindsey, J.W., & Litwin-Kumar, A., 2022. Action-modulated midbrain dopamine activity arises from distributed control policies. ArXiv, abs/2207.00636.
6. Hampshire et al., 2020. Inhibition-Related Cortical Hypoconnectivity as a Candidate Vulnerability Marker for Obsessive-Compulsive Disorder, Biological Psychiatry: Cognitive Neuroscience and Neuroimaging 5 (2): 222-230.