Obsessive–Compulsive Behaviour: A Disorder of Decision-Making

2005 ◽  
Vol 39 (9) ◽  
pp. 757-763 ◽  
Author(s):  
Perminder S. Sachdev ◽  
Gin S. Malhi

Objective: Compulsive individuals are habitually indecisive, and indecision reaches its pathological apex in obsessive–compulsive disorder (OCD). With the increasing interest in the neurobiology of decision-making, it may be useful to conceptualize OCD as a disorder of decision-making. Method: A selective review of the neurobiological studies of the decision-making process was performed, and the convergence with the understanding of the neurobiology of OCD examined. Results: The dorsolateral, orbitofrontal and anterior cingulate cortices are engaged in multiregion neural subsystems that interact with each other to retain information online, manipulate options, make choices and maintain goals. These interact with the limbic regions, especially the amygdala, in relation to history of reward and emotional valence relating to a choice, and the basal ganglia for behavioural execution. Abnormalities in these regions also characterize OCD and related disorders, therefore leading to problems in making some decisions that are affect-laden by nature or association. Conclusion: Conceptualizing OCD as a disorder of decision-making leads to new approaches for its investigation, and novel strategies for both physical and behavioural– cognitive treatments.

2017 ◽  
Vol 47 (7) ◽  
pp. 1246-1258 ◽  
Author(s):  
T. U. Hauser ◽  
R. Iannaccone ◽  
R. J. Dolan ◽  
J. Ball ◽  
J. Hättenschwiler ◽  
...  

BackgroundObsessive–compulsive disorder (OCD) has been linked to functional abnormalities in fronto-striatal networks as well as impairments in decision making and learning. Little is known about the neurocognitive mechanisms causing these decision-making and learning deficits in OCD, and how they relate to dysfunction in fronto-striatal networks.MethodWe investigated neural mechanisms of decision making in OCD patients, including early and late onset of disorder, in terms of reward prediction errors (RPEs) using functional magnetic resonance imaging. RPEs index a mismatch between expected and received outcomes, encoded by the dopaminergic system, and are known to drive learning and decision making in humans and animals. We used reinforcement learning models and RPE signals to infer the learning mechanisms and to compare behavioural parameters and neural RPE responses of the OCD patients with those of healthy matched controls.ResultsPatients with OCD showed significantly increased RPE responses in the anterior cingulate cortex (ACC) and the putamen compared with controls. OCD patients also had a significantly lower perseveration parameter than controls.ConclusionsEnhanced RPE signals in the ACC and putamen extend previous findings of fronto-striatal deficits in OCD. These abnormally strong RPEs suggest a hyper-responsive learning network in patients with OCD, which might explain their indecisiveness and intolerance of uncertainty.


2016 ◽  
Vol 96 ◽  
pp. 1-4 ◽  
Author(s):  
Gerald Nestadt ◽  
Vidyulata Kamath ◽  
Brion S. Maher ◽  
Janice Krasnow ◽  
Paul Nestadt ◽  
...  

1998 ◽  
Vol 173 (S35) ◽  
pp. 26-37 ◽  
Author(s):  
S. Saxena ◽  
A. L. Brody ◽  
J. M. Schwartz ◽  
L. R. Baxter

Background Neuroimaging studies provide strong evidence that the pathophysiology of obsessive-compulsive disorder (OCD) involves abnormal functioning along specific frontal-subcortical brain circuits.Method A literature search was carried out for all brain imaging studies of patients with OCD. We also reviewed the basic science literature on the functional neuroanatomy of cortico-basal ganglia circuits, and integrated this information with neuroimaging data in OCD to formulate a theoretical model of brain mediation of OCD symptoms and response to treatment.Results At least a subgroup of patients with OCD may have abnormal basal ganglia development. Functional neuroimaging studies indicate that OCD symptoms are associated with increased activity in orbitofrontal cortex, caudate nucleus, thalamus and anterior cingulate gyrus.Conclusions OCD symptoms are mediated by hyperactivity in orbitofrontal-subcortical circuits, perhaps due to an imbalance of tone between direct and indirect striatopallidal pathways. We present a model which describes how frontal-subcortical brain circuitry may mediate OCD symptomatology, and suggest a hypothesis for how successful treatments may ameliorate symptoms, via their effects on circuit activity.


2008 ◽  
Vol 20 (4) ◽  
pp. 1251-1283 ◽  
Author(s):  
Tiago V. Maia ◽  
Rebecca E. Cooney ◽  
Bradley S. Peterson

AbstractFunctional imaging studies have reported with remarkable consistency hyperactivity in the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and caudate nucleus of patients with obsessive–compulsive disorder (OCD). These findings have often been interpreted as evidence that abnormalities in cortico–basal ganglia–thalamo–cortical loops involving the OFC and ACC are causally related to OCD. This interpretation remains controversial, however, because such hyperactivity may represent either a cause or a consequence of the symptoms. This article analyzes the evidence for a causal role of these loops in producing OCD in children and adults. The article first reviews the strong evidence for anatomical abnormalities in these loops in patients with OCD. These findings are not sufficient to establish causality, however, because anatomical alterations may themselves be a consequence rather than a cause of the symptoms. The article then reviews three lines of evidence that, despite their own limitations, permit stronger causal inferences: the development of OCD following brain injury, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection, and neurosurgical lesions that attenuate OCD. Converging evidence from these various lines of research supports a causal role for the cortico–basal ganglia–thalamo–cortical loops that involve the OFC and ACC in the pathogenesis of OCD in children and adults.


2017 ◽  
Vol 47 (14) ◽  
pp. 2513-2527 ◽  
Author(s):  
C. O. Carlisi ◽  
L. Norman ◽  
C. M. Murphy ◽  
A. Christakou ◽  
K. Chantiluke ◽  
...  

BackgroundAutism spectrum disorder (ASD) and obsessive-compulsive disorder (OCD) share abnormalities in hot executive functions such as reward-based decision-making, as measured in the temporal discounting task (TD). No studies, however, have directly compared these disorders to investigate common/distinct neural profiles underlying such abnormalities. We wanted to test whether reward-based decision-making is a shared transdiagnostic feature of both disorders with similar neurofunctional substrates or whether it is a shared phenotype with disorder-differential neurofunctional underpinnings.MethodsAge and IQ-matched boys with ASD (N = 20), with OCD (N = 20) and 20 healthy controls, performed an individually-adjusted functional magnetic resonance imaging (fMRI) TD task. Brain activation and performance were compared between groups.ResultsBoys with ASD showed greater choice-impulsivity than OCD and control boys. Whole-brain between-group comparison revealed shared reductions in ASD and OCD relative to control boys for delayed-immediate choices in right ventromedial/lateral orbitofrontal cortex extending into medial/inferior prefrontal cortex, and in cerebellum, posterior cingulate and precuneus. For immediate-delayed choices, patients relative to controls showed reduced activation in anterior cingulate/ventromedial prefrontal cortex reaching into left caudate, which, at a trend level, was more decreased in ASD than OCD patients, and in bilateral temporal and inferior parietal regions.ConclusionsThis first fMRI comparison between youth with ASD and with OCD, using a reward-based decision-making task, shows predominantly shared neurofunctional abnormalities during TD in key ventromedial, orbital- and inferior fronto-striatal, temporo-parietal and cerebellar regions of temporal foresight and reward processing, suggesting trans-diagnostic neurofunctional deficits.


2018 ◽  
Vol 51 ◽  
pp. 1-8 ◽  
Author(s):  
William I.A. Haynes ◽  
Anne-Hélène Clair ◽  
Sara Fernandez-Vidal ◽  
Bahar Gholipour ◽  
Margot Morgiève ◽  
...  

AbstractBackground:Current neurocognitive models suppose dysfunctions of associative and limbic cortico-basal ganglia circuits to be at the core of obsessive-compulsive disorder (OCD). As little is known about the state of underlying anatomical connections, we investigated whether these connections were reduced and/or not properly organised in OCD patients compared to control.Methods:Diffusion magnetic resonance images were obtained in 37 OCD patients with predominant checking symptoms and 37 matched healthy controls. We developed indices to characterise the quantity (spatial extent and density) and the organisation (topography and segregation) of 24 anatomical connections between associative and limbic cortical (anterior cingulate, dorsolateral prefrontal, orbitofrontal cortices and the frontal pole), and subcortical (caudate nucleus, putamen and thalamus) areas in each hemisphere.Results:Associative and limbic cortico-basal-ganglia connections were reduced in OCD patients compared to controls: 19/24 connections had a reduced subcortical spatial extent, 9/24 had a reduced density. Moreover, while the general topography was conserved, the different cortical projection fields in the striatum and thalamus were hyper-segregated in OCD patients compared to controls.Conclusion:These quantitative and qualitative differences of anatomical connections go beyond the current model of a reduced cortical control of automatic behaviour stored in the basal ganglia. The hyper-segregation in OCD could also impair the integration of cortical information in the thalamus and striatum and distort the subsequent behavioural selection process. This provides new working hypotheses for functional and behavioural studies on OCD.


2015 ◽  
Vol 69 ◽  
pp. 166-173 ◽  
Author(s):  
Helen Pushkarskaya ◽  
David Tolin ◽  
Lital Ruderman ◽  
Ariel Kirshenbaum ◽  
J. MacLaren Kelly ◽  
...  

2009 ◽  
Vol 195 (5) ◽  
pp. 393-402 ◽  
Author(s):  
Joaquim Radua ◽  
David Mataix-Cols

BackgroundSpecific cortico-striato-thalamic circuits are hypothesised to mediate the symptoms of obsessive–compulsive disorder (OCD), but structural neuroimaging studies have been inconsistent.AimsTo conduct a meta-analysis of published and unpublished voxel-based morphometry studies in OCD.MethodTwelve data-sets comprising 401 people with OCD and 376 healthy controls met inclusion criteria. A new improved voxel-based meta-analytic method, signed differential mapping (SDM), was developed to examine regions of increased and decreased grey matter volume in the OCD group v. control group.ResultsNo between-group differences were found in global grey matter volumes. People with OCD had increased regional grey matter volumes in bilateral lenticular nuclei, extending to the caudate nuclei, as well as decreased volumes in bilateral dorsal medial frontal/anterior cingulate gyri. A descriptive analysis of quartiles, a sensitivity analysis as well as analyses of subgroups further confirmed these findings. Meta-regression analyses showed that studies that included individuals with more severe OCD were significantly more likely to report increased grey matter volumes in the basal ganglia. No effect of current antidepressant treatment was observed.ConclusionsThe results support a dorsal prefrontal–striatal model of the disorder and raise the question of whether functional alterations in other brain regions commonly associated with OCD, such as the orbitofrontal cortex, may reflect secondary compensatory strategies. Whether the reported differences between participants with OCD and controls precede the onset of the symptoms and whether they are specific to OCD remains to be established.


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