Article

Competition between functional brain networks mediates behavioral variability. Neuroimage, 39(1), 527-537

NYU Langone Medical Center, New York, New York, United States
NeuroImage (Impact Factor: 6.36). 02/2008; 39(1):527-37. DOI: 10.1016/j.neuroimage.2007.08.008
Source: PubMed

ABSTRACT

Increased intraindividual variability (IIV) is a hallmark of disorders of attention. Recent work has linked these disorders to abnormalities in a "default mode" network, comprising brain regions routinely deactivated during goal-directed cognitive tasks. Findings from a study of the neural basis of attentional lapses suggest that a competitive relationship between the "task-negative" default mode network and regions of a "task-positive" attentional network is a potential locus of dysfunction in individuals with increased IIV. Resting state studies have shown that this competitive relationship is intrinsically represented in the brain, in the form of a negative correlation or antiphase relationship between spontaneous activity occurring in the two networks. We quantified the negative correlation between these two networks in 26 subjects, during active (Eriksen flanker task) and resting state scans. We hypothesized that the strength of the negative correlation is an index of the degree of regulation of activity in the default mode and task-positive networks and would be positively related to consistent behavioral performance. We found that the strength of the correlation between the two networks varies across individuals. These individual differences appear to be behaviorally relevant, as interindividual variation in the strength of the correlation was significantly related to individual differences in response time variability: the stronger the negative correlation (i.e., the closer to 180 degrees antiphase), the less variable the behavioral performance. This relationship was moderately consistent across resting and task conditions, suggesting that the measure indexes moderately stable individual differences in the integrity of functional brain networks. We discuss the implications of these findings for our understanding of the behavioral significance of spontaneous brain activity, in both healthy and clinical populations.

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    • "The probably best known example is negative coupling between the task-positive network (TPN), which typically shows activations during tasks that require externally directed attention , and the default-mode network (DMN), which is characterized by task-related deactivations [Fox et al., 2005; Fransson, 2005; Greicius et al., 2003; Kelly et al., 2008; Uddin et al., 2009]. This negative coupling has been discussed to represent a suppression mechanism that inhibits unwanted processes or thoughts and to increase the reliability of behavioral responses [Anticevic et al., 2012; Kelly et al., 2008; Spreng et al., 2010]. Thus, PDrelated changes in networks that show negative coupling with the STN might also be relevant. "
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    ABSTRACT: A typical feature of Parkinson's disease (PD) is pathological activity in the subthalamic nucleus (STN). Here, we tested whether in patients with PD under dopaminergic treatment functional connectivity of the STN differs from healthy controls (HC) and whether some brain regions show (anti-) correlations between functional connectivity with STN and motor symptoms. We used functional magnetic resonance imaging to investigate whole-brain resting-state functional connectivity with STN in 54 patients with PD and 55 HC matched for age, gender, and within-scanner motion. Compared to HC, we found attenuated negative STN-coupling with Crus I of the right cerebellum and with right ventromedial prefrontal regions in patients with PD. Furthermore, we observed enhanced negative STN-coupling with bilateral intraparietal sulcus/superior parietal cortex, right sensorimotor, right premotor, and left visual cortex compared to HC. Finally, we found a decline in positive STN-coupling with the left insula related to severity of motor symptoms and a decline of inter-hemispheric functional connectivity between left and right STN with progression of PD-related motor symptoms. Motor symptom related uncoupling of the insula, a key region in the saliency network and for executive function, from the STN might be associated with well-known executive dysfunction in PD. Moreover, uncoupling between insula and STN might also induce an insufficient setting of thresholds for the discrimination between relevant and irrelevant salient environmental stimuli, explaining observations of disturbed response control in PD. In sum, motor symptoms in PD are associated with a reduced coupling between STN and a key region for executive function. Hum Brain Mapp, 2015. © 2015 Wiley Periodicals, Inc.
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    • "Future studies, combining brain stimulation with neuroimaging, could further explore the dynamic brain interactions between anterior and posterior brain areas involved in memory processes. Consistently with the inhibitory account, recent work suggests that memory maintenance and consolidation depends upon the dynamic interaction between large-scale networks and the effective formation of memory traces is associated with suppressing interference from competing networks565758(see also[59]for a discussion of the neural correlates involved in post-encoding processing). Since tDCS was applied before retrieval, its effects could have modulated these consolidation processes. "
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    ABSTRACT: The role of the Dorsolateral Prefrontal Cortex (DLPFC) in recognition memory has been well documented in lesion, neuroimaging and repetitive Transcranial Magnetic Stimulation (rTMS) studies. The aim of the present study was to investigate the effects of transcranial Direct Current Stimulation (tDCS) over the left and the right DLPFC during the delay interval of a non-verbal recognition memory task.
    Full-text · Article · Dec 2015 · PLoS ONE
    • "Intrinsic brain networks provide insight into brain abnormalities in chronic pain conditions (Davis and Moayedi 2013; Apkarian et al. 2011). An emerging concept is that the delicate balance of coordinated function between networks present in healthy individuals is disrupted in a wide range of neurological disorders (Zhang and Raichle 2010; Sharp et al. 2014; Kelly et al. 2008; Whitfield-Gabrieli and Ford 2012; Pievani et al. 2014). Thus, it is crucial to understand cross-network interactions as a window into mechanisms of brain dysfunction in chronic pain. "
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    ABSTRACT: Cortical functioning within the default mode network (DMN) and salience network (SN) is altered in chronic pain patients. The mechanisms underlying these alterations are unknown, but a novel unexamined source is cross-network communication. Aberrant functional connectivity (FC) between the DMN and SN, whose activity is normally anticorrelated, reflects disease severity in many brain disorders. Further, stronger FC between the posterior cingulate cortex (PCC) and anterior insula has been reported in chronic pain, pointing to abnormal DMN-SN interactions. Here, we tested the hypothesis that cross-network FC between the DMN and SN is abnormal in chronic pain, and is related to pain and associated symptoms. We used resting state fMRI to examine FC within and between the DMN and SN in 20 patients with chronic pain due to ankylosing spondylitis and 20 healthy controls. A whole-network analysis revealed that compared to healthy controls, patients exhibited less anticorrelated FC between the SN and DMN, and the degree of cross-network abnormality tracked pain and disease-related symptoms. This suggests that cross-network FC is a metric of functional brain abnormality in chronic pain. In a complementary seed-based analysis, the PCC was strongly connected with the SN and weakly connected with the DMN in chronic pain compared to healthy controls, suggesting that the PCC acts as a hub for altered network interaction. Sensorimotor cortex cross-network FC correlated with measures of physical function, suggesting that physical functioning also impacts brain network interaction in chronic pain. Our study implicates altered communication between brain networks as a key factor underlying chronic pain.
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