Differential frontal–striatal and paralimbic activity during reversal learning in major depressive disorder and obsessive–compulsive disorder

Remijnse, Peter L.; Nielen, M.; Balkom, A.J.L.M. van; Hendriks, Gert-Jan; Hoogendijk, Witte J.G.; Uylings, H.B.M.; Veltman, Dick J.

doi:10.1017/s0033291708005072

Cited by 124 publications

(106 citation statements)

References 71 publications

(94 reference statements)

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“…This is well recognized for prefrontal areas by studies showing both frontal hypo-and hyperactivity in MDD (Fitzgerald et al, 2006). Ambiguous neural responding has also been found in various other structures implicated in MDD such as the cingulate cortex (Matthews et al, 2009;Mitterschiffthaler et al, 2003), insula (Elliott et al, 2002;Mayberg et al, 1999), striatum (Knutson et al, 2008;Remijnse et al, 2009), thalamus (Fu et al, 2004;Kumari et al, 2003), (para)hippocampal areas (Bremner et al, 2004;Werner et al, 2009), amygdala (Fales et al, 2008;Lee et al, 2008), and additional subcortical and cortical regions (Fitzgerald et al, 2008a). Differences in sample characteristics, medication status, and experimental paradigms may account for observed inconsistencies in the neural signature of MDD.…”

Section: Introductionmentioning

confidence: 84%

“…Studies focusing on cognitive alterations used a variety of paradigms targeting executive function (Continuous Performance Test (Holmes et al, 2005;Hugdahl et al, 2004), Tower of London (Elliott et al, 1997(Elliott et al, , 1998, gambling Steele et al, 2004) and guessing tasks (Elliott et al, 1998), Stroop task (Mitterschiffthaler et al, 2008;Wagner et al, 2006), stop signal task (Matthews et al, 2009;Remijnse et al, 2009), oddball Wang et al, 2008) and go/no go tasks (Elliott et al, 2002), verbal fluency (Audenaert et al, 2002;Okada et al, 2003), incentive delay task (Knutson et al, 2008)), learning (associative learning (Werner et al, 2009), reversal learning (Taylor Tavares et al, 2008)), and memory (retrieval (Bremner et al, 2007), n-back working memory (Fitzgerald et al, 2008b;Harvey et al, 2005;Matsuo et al, 2007)). Tasks in this domain also included emotional targets Elliott et al, 2002;Wang et al, 2008), words (Bremner et al, 2007;Mitterschiffthaler et al, 2008), motivational feedback (Elliott et al, 1998;Taylor Tavares et al, 2008), and gain/ loss (Knutson et al, 2008;Remijnse et al, 2009;Smoski et al, 2009) conditions.…”

Section: As Shown Inmentioning

confidence: 99%

“…Tasks in this domain also included emotional targets Elliott et al, 2002;Wang et al, 2008), words (Bremner et al, 2007;Mitterschiffthaler et al, 2008), motivational feedback (Elliott et al, 1998;Taylor Tavares et al, 2008), and gain/ loss (Knutson et al, 2008;Remijnse et al, 2009;Smoski et al, 2009) conditions. Brain regions with altered activity during cognitive-emotional challenge in subjects with major depressive disorder (MDD) relative to healthy subjects (from left to right in coronal slices) for (a) neocortical regions, (b) the anterior cingulate, and (c) subcortical regions (including Brodmann Areas (BA) when possible) based on Activation Likelihood Estimation (ALE) analyses.…”

Section: As Shown Inmentioning

confidence: 99%

See 2 more Smart Citations

A meta-analysis of neurofunctional imaging studies of emotion and cognition in major depression

et al. 2012

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Section: Introductionmentioning

confidence: 84%

Section: As Shown Inmentioning

confidence: 99%

Section: As Shown Inmentioning

confidence: 99%

See 1 more Smart Citation

A meta-analysis of neurofunctional imaging studies of emotion and cognition in major depression

et al. 2012

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“…In addition, a reduced FN in depressed adults is specifically related to the severity of clinically rated anhedonia (Liu et al 2014). fMRI studies of reward processing in adolescents and adults have also found that depression is associated with decreased activation following positive feedback (i.e., reward) in reward-related brain areas such as the caudate, the putamen, the ACC, and the insula (Knutson et al 2008;Kumar et al 2008;Pizzagalli et al 2009;Remijnse et al 2009;Smoski et al 2009;Gradin et al 2011;Robinson et al 2012Zhang et al 2013). Such reductions have been specifically associated with anhedonia symptoms (Gradin et al 2011;Stoy et al 2012), have been detected in individuals at risk for depression (Gotlib et al 2010;McCabe et al 2012;Olino et al 2013), and predict the development of depression in adolescents (Morgan et al 2013).…”

Section: Monetary Rewardsmentioning

confidence: 99%

Mechanisms Underlying Motivational Deficits in Psychopathology: Similarities and Differences in Depression and Schizophrenia

Deanna¹,

Pagliaccio²,

Luking³

2015

Current Topics in Behavioral Neurosciences

188

151

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Motivational and hedonic impairments are core aspects of a variety of types of psychopathology. These impairments cut across diagnostic categories and may be critical to understanding major aspects of the functional impairments accompanying psychopathology. Given the centrality of motivational and hedonic systems to psychopathology, the Research Domain Criteria (RDoC) initiative includes a "positive valence" systems domain that outlines a number of constructs that may be key to understanding the nature and mechanisms of motivational and hedonic impairments in psychopathology. These component constructs include initial responsiveness to reward, reward anticipation or expectancy, incentive or reinforcement learning, effort valuation, and action selection. Here, we review behavioral and neuroimaging studies providing evidence for impairments in these constructs in individuals with psychosis versus in individuals with depressive pathology. There are important differences in the nature of reward-related and hedonic deficits associated with psychosis versus depression that have major implications for our understanding of etiology and treatment development. In particular, the literature strongly suggests the presence of impairments in in-the-moment hedonics or "liking" in individuals with depressive pathology, particularly among those who experience anhedonia. Such deficits may propagate forward and contribute to impairments in other constructs that are dependent on hedonic responses, such as anticipation, learning, effort, and action selection. Such hedonic impairments could reflect alterations in dopamine and/or opioid signaling in the striatum related to depression or specifically to anhedonia in depressed populations. In contrast, the literature points to relatively intact in-the-moment hedonic processing in psychosis, but provides much evidence for impairments in other components involved in translating reward to action selection. Particularly, individuals with schizophrenia exhibit altered reward prediction and associated striatal and prefrontal activation, impaired reward learning, and impaired reward-modulated action selection.

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“…Remijnse et al [76] analysed 20 unmedicated OCDfree patients with major depressive disorder (MDD), 20 unmedicated MDD-free patients with OCD, and 27 healthy controls. Patients underwent a self-paced reversal learning task according to an event-related design during fMRI.…”

Section: Dysfunctions Of the Orbitofrontal Cortexmentioning

confidence: 99%

Functional Neuroimaging in Obsessive-Compulsive Disorder

Casale

Kotzalidis²,

Rapinesi³

et al. 2011

Neuropsychobiology

181

111

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Background and Aim: Obsessive-compulsive disorder (OCD) is a severe, highly prevalent and chronically disabling psychiatric disorder that usually emerges during childhood or adolescence. This paper aims to review the literature on functional neuroimaging in OCD, analysing the reported dysfunctional connectivity in the corticostriatothalamocortical circuitry. Method: This study included papers published in peer-reviewed journals dealing with functional imaging in OCD. Results: Striatal dysfunction, mainly of the caudate nucleus, leads to inefficient thalamic gating, resulting in hyperactivity within the orbitofrontal cortex (intrusive thoughts) and the anterior cingulate cortex (non-specific anxiety). Compulsions consist of ritualistic behaviours performed to recruit the inefficient striatum and neutralise unwanted thoughts and anxiety. Functional neuroimaging findings are discussed against the background of specific cognitive impairments, mainly regarding visuospatial processing, executive functioning and motor speed. Cognitive deficits are partial and specific, matching imaging data. Conclusions: Several studies have targeted brain regions hypothesised to be involved in the pathogenesis of OCD, showing the existence of dysfunctional connectivity in the corticostriatothalamocortical circuitry. Improvements in spatial resolution of neuroimaging techniques may contribute to a better understanding of the neurocircuitry of OCD and other anxiety disorders.

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Differential frontal–striatal and paralimbic activity during reversal learning in major depressive disorder and obsessive–compulsive disorder

Cited by 124 publications

References 71 publications

A meta-analysis of neurofunctional imaging studies of emotion and cognition in major depression

A meta-analysis of neurofunctional imaging studies of emotion and cognition in major depression

Mechanisms Underlying Motivational Deficits in Psychopathology: Similarities and Differences in Depression and Schizophrenia

Functional Neuroimaging in Obsessive-Compulsive Disorder

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