Cited by 847Obsessive-Compulsive Spectrum DisordersAnxiety, Depression, Psychometrics, Treatment, Cognitive ProcessesNeural and Behavioral Psychology Studies

Obsessive-compulsive disorder: beyond segregated cortico-striatal pathways

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Milad, Mohammed R., Rauch, Scott L.·2012·Trends in Cognitive Sciences

Abstract

Obsessive-compulsive disorder (OCD) affects approximately 2-3% of the population and is characterized by recurrent intrusive thoughts (obsessions) and repetitive behaviors or mental acts (compulsions), typically performed in response to obsessions or related anxiety. In the past few decades, the prevailing models of OCD pathophysiology have focused on cortico-striatal circuitry. More recent neuroimaging evidence, however, points to critical involvement of the lateral and medial orbitofrontal cortices, the dorsal anterior cingulate cortex and amygdalo-cortical circuitry, in addition to cortico-striatal circuitry, in the pathophysiology of the disorder. In this review, we elaborate proposed features of OCD pathophysiology beyond the classic parallel cortico-striatal pathways and argue that this evidence suggests that fear extinction, in addition to behavioral inhibition, is impaired in OCD.

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Crossref · 10.1016/j.tics.2011.11.003

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  • Neurobiological theories implicate cortico-striato-thalamo-cortical (CSTC) circuits in the etiology of OCD.

    “These range from neurobiological theories implicating cortico‐striato‐thalamo‐cortical circuits in the etiology of the disorder (Chamberlain et al., 2005; Graybiel & Rauch, 2000; Milad & Rauch, 2012; see also, van den Heuvel et al., 2016);”

    From Obsessive-compulsive disorder: Etiology, neuropathology, and cognitive dysfunction (2023) · cites this paper as Milad & Rauch, 2012

  • Research has implicated parallel CSTC circuits in the pathophysiology of OCD, and these circuits are responsible for reward- and motivational-related processes, executive function, motor and response inhibition, and habit-based behavior.

    “Research has implicated parallel CSTC circuits in the pathophysiology of OCD (Chamberlain et al., 2005; Graybiel & Rauch, 2000; Milad & Rauch, 2012; see also, van den Heuvel et al., 2016), that is, responsible for reward‐ and motivational‐related processes, executive function, motor and response inhibition, and habit‐based behavior (Fineberg et al., 2018).”

    From Obsessive-compulsive disorder: Etiology, neuropathology, and cognitive dysfunction (2023) · cites this paper as Milad & Rauch, 2012

  • Such models have been revised over the years and now adopt a more dynamic view of CSTC circuits, for example, as functionally interacting rather than being fully segregated.

    “such models have been revised over the years and now adopt a more dynamic view of CSTC circuits, for example, as functionally interacting rather than being fully segregated”

    From Obsessive-compulsive disorder: Etiology, neuropathology, and cognitive dysfunction (2023) · cites this paper as Milad & Rauch, 2012

  • These models are now more elaborate, for example, consider specific functions of OFC subareas (lateral versus medial) in relation to affective-, reward- and fear-based computation.

    “these models are now more elaborate, for example, consider specific functions of OFC subareas (lateral versus medial) in relation to affective‐, reward‐ and fear‐based computation”

    From Obsessive-compulsive disorder: Etiology, neuropathology, and cognitive dysfunction (2023) · cites this paper as Milad & Rauch, 2012

  • Neurobiological models emphasise abnormal communication between the orbitofrontal cortex, anterior cingulate cortex, dorsolateral prefrontal cortex, basal ganglia, and thalamus in OCD.

    “Neurobiological models emphasise abnormal communication between the orbitofrontal cortex, anterior cingulate cortex, dorsolateral prefrontal cortex, basal ganglia, and thalamus, regions involved in action selection, error detection, threat evaluation, cognitive control, and habit formation [11,12,13].”

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Research works printed but not linked: 1

  1. [67]Shin LM Liberzon I The Neurocircuitry of Fear, Stress, and Anxiety Disorders Neuropsychopharmacology 2009 PMC3055419 19625997

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Authors
Milad, M. R., & Rauch, S. L.
Affiliations
Harvard University (US)
Corresponding author
Milad, Mohammed R.
Venue
Trends in Cognitive Sciences
Publisher
Elsevier BV
Published
2012-01
Volume
16
Issue
1
Pages
43-51
ISSN
1364-6613 (ISSN-L)
OpenAlex
W2159370497
Cited by
847
References
101
Citations by year
2026: 62 · 2025: 57 · 2024: 57 · 2023: 49 · 2022: 61 · 2021: 83 · 2020: 67 · 2019: 70 · 2018: 63 · 2017: 61 · 2016: 59 · 2015: 73 · 2014: 39 · 2013: 33 · 2012: 12
FWCI
4.11
Type
journal article
Language
en
Open access
Locations
  • Trends in Cognitive Sciences (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (5r01mh081975-05)
  • National Institute of Mental Health (R01-MH081975)
Topics
  • Social Sciences › Psychology › Clinical Psychology › Obsessive-Compulsive Spectrum Disorders
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
Keywords
obsessive-compulsive disorder, OCD pathophysiology, corticostriatal circuits, orbitofrontal cortex, dorsal anterior cingulate cortex, amygdala, fear extinction, behavioral inhibition, obsession, compulsive behavior
MeSH terms
Amygdala, Anxiety Disorders, Cerebral Cortex, Compulsive Behavior, Corpus Striatum, Humans, Obsessive-Compulsive Disorder, Neuroimaging

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