Assessing Working Memory via N-Back Task in Euthymic Bipolar I Disorder Patients: A Review of Functional Magnetic Resonance Imaging Studies

Cremaschi, Laura; Penzo, Beatrice; Palazzo, Carlotta; Dobrea, Cristina; Cristoffanini, M.; Dell’Osso, Bernardo; Altamura, Alfredo Carlo

doi:10.1159/000352011

Cited by 42 publications

(40 citation statements)

References 103 publications

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“…Consistent with the literature (Cremaschi et al, 2013, McKenna et al, 2013, Thompson et al, 2007, Torres, Boudreau, 2007), we found that euthymic bipolar subjects performed worse on working memory tasks. Additionally, both working memory and processing speed domain scores were significantly associated with corpus callosum white matter integrity (FA values) in the entire sample (the correlation was driven mostly by the bipolar subjects).…”

Section: Discussionsupporting

confidence: 92%

Connectome signatures of neurocognitive abnormalities in euthymic bipolar I disorder

Ajilore

Vizueta

Walshaw

et al. 2015

Journal of Psychiatric Research

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Objectives Connectomics have allowed researchers to study integrative patterns of neural connectivity in humans. Yet, it is unclear how connectomics may elucidate structure-function relationships in bipolar I disorder (BPI). Expanding on our previous structural connectome study, here we used an overlapping sample with additional psychometric and fMRI data to relate structural connectome properties to both fMRI signals and cognitive performance. Methods 42 subjects completed a neuropsychological (NP) battery covering domains of processing speed, verbal memory, working memory, and cognitive flexibility. 32 subjects also had fMRI data performing a Go/NoGo task. Results Bipolar participants had lower NP performance across all domains, but only working memory reached statistical significance. In BPI participants, processing speed was significantly associated with both white matter integrity (WMI) in the corpus callosum and interhemispheric network integration. Mediation models further revealed that the relationship between interhemispheric integration and processing speed was mediated by WMI, and processing speed mediated the relationship between WMI and working memory. Bipolar subjects had significantly decreased BA47 activation during NoGo vs. Go. Significant predictors of BA47 fMRI activations during the Go/NoGo task were its nodal path length (left hemisphere) and its nodal clustering coefficient (right hemisphere). Conclusions This study suggests that structural connectome changes underlie abnormalities in fMRI activation and cognitive performance in euthymic BPI subjects. Results support that BA47 structural connectome changes may be a trait marker for BPI. Future studies are needed to determine if these “connectome signatures” may also confer a biological risk and/or serve as predictors of relapse.

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Section: Discussionsupporting

confidence: 92%

Connectome signatures of neurocognitive abnormalities in euthymic bipolar I disorder

Ajilore

Vizueta

Walshaw

et al. 2015

Journal of Psychiatric Research

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“…Neurobiological differences in brain activation during working memory tasks in bipolar I disorder may be trait characteristics and are thus present outside of depressive episodes. A recent review (Cremaschi et al 2013) of n-back fMRI studies of medicated euthymic subjects diagnosed with bipolar I disorder revealed altered activation and connectivity within the ventrolateral circuit and parieto-temporal circuit dysfunction rather than dorsolateral. Although we did not include euthymic subjects with bipolar II disorder in this study, it may be that bipolar II disorder is associated more with ventrolateral circuit rather than dorsolateral circuit dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…Though there are two primary subtypes of bipolar disorder, investigations of the neuropathology of working memory impairments have focused on bipolar I disorder. For example, a recent meta-analysis (Cremaschi et al 2013) of functional magnetic resonance (fMRI) studies assessing working memory in euthymic bipolar I patients points to abnormal activation patterns in the dorsolateral pre-frontal cortex (DLPFC), ventrolateral prefrontal cortex, other prefrontal regions, as well as the parietal and temporal cortices.…”

Section: Introductionmentioning

confidence: 99%

Prefrontal hypoactivation during working memory in bipolar II depression

Brooks¹,

Vizueta²,

Penfold³

et al. 2015

Psychol. Med.

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Background Patterns of abnormal neural activation have been observed during working memory tasks in bipolar I depression, yet the neural changes associated with bipolar II depression have yet to be explored. Method An n-back working memory task was administered during a 3T functional magnetic resonance imaging scan in age- and gender-matched groups of 19 unmedicated, bipolar II depressed subjects and 19 healthy comparison subjects. Whole-brain and region-of-interest analyses were performed to determine regions of differential activation across memory-load conditions (0-, 1- and 2-back). Results Accuracy for all subjects decreased with higher memory load, but there was no significant group × memory load interaction. Random-effects analyses of memory load indicated that subjects with bipolar II depression exhibited significantly less activation than healthy subjects in left hemispheric regions of the middle frontal gyrus [Brodmann area (BA) 11], superior frontal gyrus (BA 10), inferior parietal lobule (BA 40), middle temporal gyrus (BA 39) and bilateral occipital regions. There was no evidence of differential activation related to increasing memory load in the dorsolateral prefrontal or anterior cingulate cortex. Conclusions Bipolar II depression is associated with hypoactivation of the left medio-frontal and parietal cortex during working memory performance. Our findings suggest that bipolar II depression is associated with disruption of the fronto-parietal circuit that is engaged in working memory tasks, which is a finding reported across bipolar subtypes and mood states.

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“…A third theme is abnormal activity in emotion processing circuitry, including amygdala, orbitofrontal cortex and temporal cortex, during non-emotional, cognitive task performance in bipolar disorder(23,24)(Table 1;ST1). For example, studies reported abnormally elevated amygdala activity in adults with bipolar disorder across different mood states during performance of a variety of cognitive tasks(25-27), and increased amygdala activity during motor response inhibition in manic versus remitted adults with bipolar disorder(28).…”

Section: Introductionmentioning

confidence: 99%

A Critical Appraisal of Neuroimaging Studies of Bipolar Disorder: Toward a New Conceptualization of Underlying Neural Circuitry and a Road Map for Future Research

Phillips¹,

Swartz²

2014

AJP

537

415

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Objective This critical review appraises neuroimaging findings in bipolar disorder in emotion processing, emotion regulation, and reward processing neural circuitry, to synthesize current knowledge of the neural underpinnings of bipolar disorder, and provide a neuroimaging research “roadmap” for future studies. Method We examined findings from all major studies in bipolar disorder that used fMRI, volumetric analyses, diffusion imaging, and resting state techniques, to inform current conceptual models of larger-scale neural circuitry abnormalities in bipolar disorder Results Bipolar disorder can be conceptualized in neural circuitry terms as parallel dysfunction in bilateral prefrontal cortical (especially ventrolateral prefrontal cortical)-hippocampal-amygdala emotion processing and emotion regulation neural circuitries, together with an “overactive” left-sided ventral striatal-ventrolateral and orbitofrontal cortical reward processing circuitry, that result in characteristic behavioral abnormalities associated with bipolar disorder: emotional lability, emotional dysregulation and heightened reward sensitivity. A potential structural basis for these functional abnormalities are gray matter decreases in prefrontal and temporal cortices, amygdala and hippocampus, and fractional anisotropy decreases in white matter tracts connecting prefrontal and subcortical regions. Conclusion Neuroimaging studies of bipolar disorder clearly demonstrate abnormalities in neural circuitries supporting emotion processing, emotion regulation and reward processing, although there are several limitations to these studies. Future neuroimaging research in bipolar disorder should include studies adopting dimensional approaches; larger studies examining neurodevelopmental trajectories in bipolar disorder and at-risk youth; multimodal neuroimaging studies using integrated systems approaches; and studies using pattern recognition approaches to provide clinically useful, individual-level data. Such studies will help identify clinically-relevant biomarkers to guide diagnosis and treatment decision-making for individuals with bipolar disorder.

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Assessing Working Memory via N-Back Task in Euthymic Bipolar I Disorder Patients: A Review of Functional Magnetic Resonance Imaging Studies

Cited by 42 publications

References 103 publications

Connectome signatures of neurocognitive abnormalities in euthymic bipolar I disorder

Connectome signatures of neurocognitive abnormalities in euthymic bipolar I disorder

Prefrontal hypoactivation during working memory in bipolar II depression

A Critical Appraisal of Neuroimaging Studies of Bipolar Disorder: Toward a New Conceptualization of Underlying Neural Circuitry and a Road Map for Future Research

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