Stroop performance in bipolar disorder: further evidence for abnormalities in the ventral prefrontal cortex

Kronhaus, Dina M.; Lawrence, Natalia; Williams, A. Mark; Frangou, Sophia; Brammer, Michael; Williams, Steve; Andrew, Christopher; Phillips, Mary L.

doi:10.1111/j.1399-5618.2006.00282.x

Cited by 147 publications

(135 citation statements)

References 58 publications

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“…However, our findings are consistent with previous Stroop studies that reported reduced activation to conflict trials in IFG/MFG, medial SFG/SMA, parietal cortex, and basal ganglia in euthymic BD patients (Malhi et al, 2005;Strakowski et al, 2005;Kronhaus et al, 2006;Roth et al, 2006;Pompei et al, 2011). Stroop-like conflict has rarely been studied during affective episodes, but decreased activity in the IFG, together with hypoactivation of the basal ganglia, thalamus and/or parietal areas, was reported during inhibition and emotion categorization tasks in manic and depressed patients, as well as euthymic patients Foland-Ross et al, 2012;Vizueta et al, 2012).…”

Section: Discussionsupporting

confidence: 93%

“…Most notably, when they were euthymic, the patients exhibited a selective deactivation of rostral ACC on the conflict trials. Interestingly, deactivation of ventromedial prefrontal areas and subgenual ACC has been previously reported in euthymic patients during a color-word Stroop task (Kronhaus et al, 2006). A central involvement of the rostral ACC in the pathophysiology of both unipolar and bipolar mood disorders has been documented (e.g.…”

Section: Discussionmentioning

confidence: 84%

“…In previous studies of conflict processing in bipolar disorder, euthymic patients demonstrated decreased activation in frontalparietal networks and basal ganglia structures when processing non-emotional conflict (Kronhaus et al, 2006;Pompei et al, 2011) and task-irrelevant emotional information (Malhi et al, 2005). In addition, abnormal connectivity between prefrontal and limbic/ paralimbic areas has been reported in euthymic patients during a Stroop task (Pompei et al, 2011b).…”

Section: Introductionmentioning

confidence: 90%

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Modulation of brain response to emotional conflict as a function of current mood in bipolar disorder: Preliminary findings from a follow-up state-based fMRI study

Rey¹,

Desseilles²,

Favre³

et al. 2014

Psychiatry Research: Neuroimaging

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a b s t r a c tWe used functional magnetic resonance imaging (fMRI) to examine affective control longitudinally in a group of patients with bipolar disorder (BD). Participants comprised 12 BD patients who underwent repeated fMRI scans in euthymic (n ¼ 11), depressed (n ¼9), or hypomanic (n ¼9) states, and were compared with 12 age-matched healthy controls. During fMRI, participants performed an emotional face-word interference task with either low or high attentional demands. Relative to healthy controls, patients showed decreased activation of the cognitive control network normally associated with conflict processing, more severely during hypomania than during depression, but regardless of level of task demand in both cases. During euthymia, a decreased response to conflict was observed only during the high load condition. Additionally, unlike healthy participants, patients exhibited deactivation in several key areas in response to emotion-conflict trials -including the rostral anterior cingulate cortex during euthymia, the hippocampus during depression, and the posterior cingulate cortex during hypomania. Our results indicate that the ability of BD patients to recruit control networks when processing affective conflict, and the abnormal suppression of activity in distinct components of the default mode network, may depend on their current clinical state and attentional demand.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 84%

Section: Introductionmentioning

confidence: 90%

See 1 more Smart Citation

Modulation of brain response to emotional conflict as a function of current mood in bipolar disorder: Preliminary findings from a follow-up state-based fMRI study

Rey¹,

Desseilles²,

Favre³

et al. 2014

Psychiatry Research: Neuroimaging

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show abstract

“…Although, similar to other fields, few studies have examined simultaneous changes in different cortical regions, studies of individual regions have reported disrupted activation of OFC and dlPFC (Matsuo et al, 2007). A recent study by Phillips and co-workers showed that during performance of a cognitive task, there is dissociation between activation of OFC and dlPFC in bipolar patients (Kronhaus et al, 2006). These limited studies suggest that similar to schizophrenia and addictive disorders, the pathophysiology of PFC in mood disorders may involve abnormal dynamic interactions of ventral and dorsal regions of the PFC.…”

Section: Mood Disordersmentioning

confidence: 99%

Divergent Plasticity of Prefrontal Cortex Networks

Moghaddam

Homayoun

2007

Neuropsychopharmacol

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The 'executive' regions of the prefrontal cortex (PFC) such as the dorsolateral PFC (dlPFC) and its rodent equivalent medial PFC (mPFC) are thought to respond in concert with the 'limbic' regions of the PFC such as the orbitofrontal (OFC) cortex to orchestrate behavior that is consistent with context and expected outcome. Both groups of regions have been implicated in behavioral abnormalities associated with addiction and psychiatric disorders, in particular, schizophrenia and mood disorders. Theories about the pathophysiology of these disorders, however, incorporate abnormalities in discrete PFC regions independently of each other or assume they are one and the same and, thus, bunch them under umbrella of 'PFC dysfunction.' Emerging data from animal studies suggest that mPFC and OFC neurons display opposing patterns of plasticity during associative learning and in response to repeated exposure to psychostimulants. These data corroborate clinical studies reporting different patterns of activation in OFC versus dlPFC in individuals with schizophrenia or addictive disorders. These suggest that concomitant but divergent engagement of discrete PFC regions is critical for learning stimulus-outcome associations, and the execution of goal-directed behavior that is based on these associations. An atypical interplay between these regions may lead to abnormally high or low salience assigned to stimuli, resulting in symptoms that are fundamental to many psychiatric and addictive disorders, including attentional deficits, improper affective response to stimuli, and inflexible or impulsive behavior.

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“…HCs were shown previously to recruit the ventrolateral prefrontal cortex (vlPFC; which includes part of the lateral orbitofrontal cortex; OFC), the dorsomedial prefrontal cortex (dmPFC) and the ventral striatum during switch trials where negative feedback precipitated behavioral reversal (Cools et al, 2002;Evers et al, 2005). Based on research showing hypofrontality in depression during tasks of cognitive control (Blumberg et al, 2003;Goethals et al, 2005;Kronhaus et al, 2006;Okada et al, 2003), we predicted reduced signal change in vlPFC and dmPFC in the unmedicated mood disorder groups during reversal switches. In addition, previous work has shown greater amygdala responses to negative words (e.g.…”

Section: Introductionmentioning

confidence: 99%

Neural basis of abnormal response to negative feedback in unmedicated mood disorders

et al. 2008

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Depressed individuals show hypersensitivity to negative feedback during cognitive testing, which can precipitate subsequent errors and thereby impair a broad range of cognitive abilities. We studied the neural mechanisms underlying this feedback hypersensitivity using functional magnetic resonance imaging (fMRI) with a reversal learning task that required subjects to ignore misleading negative feedback on some trials. Thirteen depressed subjects with major depressive disorder (MDD), 12 depressed subjects with bipolar disorder (BD) and 15 healthy controls participated. The MDD group, but not the BD group, demonstrated enhanced sensitivity to negative feedback compared to controls, as indicated by the rates of rule reversal following misleading negative feedback. In the control and BD groups, hemodynamic activity was significantly higher in the dorsomedial and ventrolateral prefrontal cortices during reversal shifting, and significantly lower in the right amygdala in response to negative feedback. The extent to which the amygdala showed less activity during negative feedback correlated inversely with the behavioral tendency to reverse after misleading feedback. This effect was not present in the MDD group, who also failed to recruit the prefrontal cortex during behavioral reversal. Hypersensitivity to negative feedback is present in unmedicated depressed patients with MDD. Disrupted top-down control by the prefrontal cortex of the amygdala may underlie this abnormal response to negative feedback in unipolar depression.

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Stroop performance in bipolar disorder: further evidence for abnormalities in the ventral prefrontal cortex

Cited by 147 publications

References 58 publications

Modulation of brain response to emotional conflict as a function of current mood in bipolar disorder: Preliminary findings from a follow-up state-based fMRI study

Modulation of brain response to emotional conflict as a function of current mood in bipolar disorder: Preliminary findings from a follow-up state-based fMRI study

Divergent Plasticity of Prefrontal Cortex Networks

Neural basis of abnormal response to negative feedback in unmedicated mood disorders

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