Striatal circuits, habits, and implications for obsessive-compulsive disorder
Open accessAbstract
Increasing evidence implicates abnormalities in corticostriatal circuits in the pathophysiology of obsessive-compulsive disorder (OCD) and OC-spectrum disorders. Parallels between the emergence of repetitive, compulsive behaviors and the acquisition of automated behaviors suggest that the expression of compulsions could in part involve loss of control of such habitual behaviors. The view that striatal circuit dysfunction is involved in OC-spectrum disorders is strengthened by imaging and other evidence in humans, by discovery of genes related to OCD syndromes, and by functional studies in animal models of these disorders. We highlight this growing concordance of work in genetics and neurobiology suggesting that frontostriatal circuits, and their links with basal ganglia, thalamus and brainstem, are promising candidates for therapeutic intervention in OCD.
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In CSTC circuits, the putamen interacts with core regions like the CN and OFC to modulate habit formation; disruptions in CN-putamen connectivity may amplify compulsive behaviors by reinforcing rigid motor patterns, indirectly exacerbating cognitive inflexibility through impaired feedback integration in salience network dynamics.
“In CSTC circuits, the putamen interacts with core regions like the CN and OFC to modulate habit formation (170); disruptions in CN-putamen connectivity may amplify compulsive behaviors by reinforcing rigid motor patterns (183), indirectly exacerbating cognitive inflexibility through impaired feedback integration in salience network dynamics (108).”
From Neural mechanisms underlying cognitive inflexibility in obsessive-compulsive disorder: a review (2026) · cites this paper as [170]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredDysfunction in the caudate nucleus, a key component of the striatum within the dysfunctional CSTC circuit, has been associated with over-reliance on the habitual as opposed to goal-directed system in OCD.
“Dysfunction in the CN—a key component of the striatum within the dysfunctional CSTC circuit—has been associated with over-reliance on habitual (as opposed to goal-directed) system in OCD (169–171).”
From Neural mechanisms underlying cognitive inflexibility in obsessive-compulsive disorder: a review (2026) · cites this paper as [170]
The human-studies section links caudate abnormalities and striatal-circuit dysfunction to OCD. The endophenotypes section describes a habit hypothesis and reports evidence of excessive avoidance habits in OCD, but it does not specifically link caudate dysfunction to a shift from goal-directed to habitual behavior. Page numbers are unavailable in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredConverging lines of evidence have implicated these fronto-striatal circuits in the pathophysiology of OCD.
“which converging lines of evidence have implicated in the pathophysiology of OCD (Burguière et al., 2015, Jahanshahi et al., 2015, Pauls et al., 2014).”
From Inhibitory control in obsessive compulsive disorder: a systematic review and activation likelihood estimation meta-analysis of functional magnetic resonance imaging studies (2022) · cites this paper as Burguière et al., 2015
Dysfunctions of fronto-striatal neural networks are implicated in the pathophysiology of obsessive-compulsive disorder (OCD).
“Previous research showed that dysfunctions of fronto-striatal neural networks are implicated in the pathophysiology of obsessive–compulsive disorder (OCD).”
From P300 and delay-discounting in obsessive–compulsive disorder (2022) · cites this paper as [5]
OCD symptoms may be related to increased activity in the OFC, as a consequence of diminished inhibitory effects of the striatum (especially the globus pallidus internus) on the thalamus.
“It was postulated that OCD symptoms may be related to increased activity in the OFC, as a consequence of diminished inhibitory effects of the striatum (especially the globus pallidus internus) on the thalamus.”
From P300 and delay-discounting in obsessive–compulsive disorder (2022) · cites this paper as [5]
The neuroanatomical hypothesis suggests that OCD could be associated with dysfunctional cognitive and metacognitive processing.
“Furthermore, this hypothesis suggests that OCD could be associated with dysfunctional cognitive and metacognitive processing.”
From P300 and delay-discounting in obsessive–compulsive disorder (2022) · cites this paper as [5]
The OFC is suggested to be a region functionally altered in OCD.
“The OFC activity would be of special interest in OCD since it is suggested to be a region which is functionally altered in OCD, during a task that is known to elicit deviating behaviour in OCD patients compared und unaffected individuals.”
From P300 and delay-discounting in obsessive–compulsive disorder (2022) · cites this paper as [5]
OCD is caused by abnormal activity in the cortico-striato-thalamo-cortical (CSTC) circuits, including the orbitofrontal cortex (OFC), the striatum within basal ganglia and the thalamus.
“In addition, it has been suggested that OCD is caused by abnormal activity in the cortico-striato-thalamo-cortical (CSTC) circuits, including the orbitofrontal cortex (OFC), the striatum within basal ganglia and the thalamus [5, 6], which is summarised as the neuroanatomical hypothesis.”
From P300 and delay-discounting in obsessive–compulsive disorder (2022) · cites this paper as [5]
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References 73 · Cited by 286
- Authors
- Burguière, E., Monteiro, P., Mallet, L., Feng, G., & Graybiel, A. M.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- McGovern Institute for Brain Research (US)
- Corresponding author
- Graybiel, Ann M
- Venue
- Current Opinion in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2015-02
- Volume
- 30
- Pages
- 59-65
- ISSN
- 0959-4388 (ISSN-L)
- PMC
- PMC4293232
- OpenAlex
- W2077823633
- Cited by
- 286
- References
- 73
- Citations by year
- 2026: 25 · 2025: 19 · 2024: 25 · 2023: 23 · 2022: 33 · 2021: 28 · 2020: 28 · 2019: 20 · 2018: 27 · 2017: 20 · 2016: 20 · 2015: 13 · 2014: 1
- FWCI
- 2.74
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-nd)
- PMC
- Funders
- Simons Initiative on Autism and the Brain
- NIH/NICHD (R37 HD028341)
- Defense Advanced Research Projects Agency (W911NF-10-1-0059)
- EMBO Long-term Fellowship
- NIH/NIMH (R01 MH081201)
- Simons Foundation Autism Research Initiative
- Topics
- Social Sciences › Psychology › Clinical Psychology › Obsessive-Compulsive Spectrum Disorders
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- obsessive-compulsive disorder, striatal circuits, corticostriatal circuits, frontostriatal circuits, basal ganglia, compulsive behavior, habit formation, thalamus, brainstem, therapeutic target
- MeSH terms
- Corpus Striatum, Habits, Humans, Nerve Net, Neural Pathways, Obsessive-Compulsive Disorder
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