The Role of Stress in the Pathogenesis and Maintenance of Obsessive-Compulsive Disorder

Individuals with obsessive-compulsive disorder often identify psychosocial stress as a factor that exacerbates their symptoms, and many trace the onset of symptoms to a stressful period of life or a discrete traumatic incident. However, the pathophysiological relationship between stress and obsessiv...

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Main Authors: Thomas G. Adams, Benjamin Kelmendi, C. Alex Brake, Patricia Gruner, Christal L. Badour, Christopher Pittenger
Format: Article
Language:English
Published: SAGE Publishing 2018-02-01
Series:Chronic Stress
Online Access:https://doi.org/10.1177/2470547018758043
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author Thomas G. Adams
Benjamin Kelmendi
C. Alex Brake
Patricia Gruner
Christal L. Badour
Christopher Pittenger
author_facet Thomas G. Adams
Benjamin Kelmendi
C. Alex Brake
Patricia Gruner
Christal L. Badour
Christopher Pittenger
author_sort Thomas G. Adams
collection DOAJ
description Individuals with obsessive-compulsive disorder often identify psychosocial stress as a factor that exacerbates their symptoms, and many trace the onset of symptoms to a stressful period of life or a discrete traumatic incident. However, the pathophysiological relationship between stress and obsessive-compulsive disorder remains poorly characterized: it is unclear whether trauma or stress is an independent cause of obsessive-compulsive disorder symptoms, a triggering factor that interacts with a preexisting diathesis, or simply a nonspecific factor that can exacerbate obsessive-compulsive disorder along with other aspects of psychiatric symptomatology. Nonetheless, preclinical research has demonstrated that stress has conspicuous effects on corticostriatal and limbic circuitry. Specifically, stress can lead to neuronal atrophy in frontal cortices (particularly the medial prefrontal cortex), the dorsomedial striatum (caudate), and the hippocampus. Stress can also result in neuronal hypertrophy in the dorsolateral striatum (putamen) and amygdala. These neurobiological effects mirror reported neural abnormalities in obsessive-compulsive disorder and may contribute to an imbalance between goal-directed and habitual behavior, an imbalance that is implicated in the pathogenesis and expression of obsessive-compulsive disorder symptomatology. The modulation of corticostriatal and limbic circuits by stress and the resultant imbalance between habit and goal-directed learning and behavior offers a framework for investigating how stress may exacerbate or trigger obsessive-compulsive disorder symptomatology.
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spelling doaj.art-e8562d96fdba4eef98b60a1fef402c912022-12-21T23:58:42ZengSAGE PublishingChronic Stress2470-54702018-02-01210.1177/2470547018758043The Role of Stress in the Pathogenesis and Maintenance of Obsessive-Compulsive DisorderThomas G. Adams0Benjamin Kelmendi1C. Alex Brake2Patricia Gruner3Christal L. Badour4Christopher Pittenger5Clinical Neuroscience Division, VA National Center for PTSD, West Haven, CT, USAClinical Neuroscience Division, VA National Center for PTSD, West Haven, CT, USADepartment of Psychology, University of Kentucky, Lexington, KY, USADepartment of Psychiatry, School of Medicine, Yale University, New Haven, CT, USADepartment of Psychology, University of Kentucky, Lexington, KY, USADepartment of Psychology, Yale University, New Haven, CT, USAIndividuals with obsessive-compulsive disorder often identify psychosocial stress as a factor that exacerbates their symptoms, and many trace the onset of symptoms to a stressful period of life or a discrete traumatic incident. However, the pathophysiological relationship between stress and obsessive-compulsive disorder remains poorly characterized: it is unclear whether trauma or stress is an independent cause of obsessive-compulsive disorder symptoms, a triggering factor that interacts with a preexisting diathesis, or simply a nonspecific factor that can exacerbate obsessive-compulsive disorder along with other aspects of psychiatric symptomatology. Nonetheless, preclinical research has demonstrated that stress has conspicuous effects on corticostriatal and limbic circuitry. Specifically, stress can lead to neuronal atrophy in frontal cortices (particularly the medial prefrontal cortex), the dorsomedial striatum (caudate), and the hippocampus. Stress can also result in neuronal hypertrophy in the dorsolateral striatum (putamen) and amygdala. These neurobiological effects mirror reported neural abnormalities in obsessive-compulsive disorder and may contribute to an imbalance between goal-directed and habitual behavior, an imbalance that is implicated in the pathogenesis and expression of obsessive-compulsive disorder symptomatology. The modulation of corticostriatal and limbic circuits by stress and the resultant imbalance between habit and goal-directed learning and behavior offers a framework for investigating how stress may exacerbate or trigger obsessive-compulsive disorder symptomatology.https://doi.org/10.1177/2470547018758043
spellingShingle Thomas G. Adams
Benjamin Kelmendi
C. Alex Brake
Patricia Gruner
Christal L. Badour
Christopher Pittenger
The Role of Stress in the Pathogenesis and Maintenance of Obsessive-Compulsive Disorder
Chronic Stress
title The Role of Stress in the Pathogenesis and Maintenance of Obsessive-Compulsive Disorder
title_full The Role of Stress in the Pathogenesis and Maintenance of Obsessive-Compulsive Disorder
title_fullStr The Role of Stress in the Pathogenesis and Maintenance of Obsessive-Compulsive Disorder
title_full_unstemmed The Role of Stress in the Pathogenesis and Maintenance of Obsessive-Compulsive Disorder
title_short The Role of Stress in the Pathogenesis and Maintenance of Obsessive-Compulsive Disorder
title_sort role of stress in the pathogenesis and maintenance of obsessive compulsive disorder
url https://doi.org/10.1177/2470547018758043
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