Why ruminators won't stop: The structural and resting state correlates of rumination and its relation to depression

Kühn, Simone; Vanderhasselt, Marie‐Anne; Raedt, Rudi De; Gallinat, Jürgen

doi:10.1016/j.jad.2012.03.024

Cited by 130 publications

(98 citation statements)

References 69 publications

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“…Numerous studies using event-related and resting-state fMRI designs point to alterations in ACC activity in depressed patients (26)(27)(28)(29). The first resting-state fMRI study with MDD patients revealed a hyperconnectivity between the subgenual ACC and the DMN, confirming previous PET studies, which found resting state overactivity in ACC in these patients (30).…”

Section: Discussionsupporting

confidence: 70%

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Bosch

Rihm

Scheidegger

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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In many patients with major depressive disorder, sleep deprivation, or wake therapy, induces an immediate but often transient antidepressant response. It is known from brain imaging studies that changes in anterior cingulate and dorsolateral prefrontal cortex activity correlate with a relief of depression symptoms. Recently, resting-state functional magnetic resonance imaging revealed that brain network connectivity via the dorsal nexus (DN), a cortical area in the dorsomedial prefrontal cortex, is dramatically increased in depressed patients. To investigate whether an alteration in DN connectivity could provide a biomarker of therapy response and to determine brain mechanisms of action underlying sleep deprivations antidepressant effects, we examined its influence on resting state default mode network and DN connectivity in healthy humans. Our findings show that sleep deprivation reduced functional connectivity between posterior cingulate cortex and bilateral anterior cingulate cortex (Brodmann area 32), and enhanced connectivity between DN and distinct areas in right dorsolateral prefrontal cortex (Brodmann area 10). These findings are consistent with resolution of dysfunctional brain network connectivity changes observed in depression and suggest changes in prefrontal connectivity with the DN as a brain mechanism of antidepressant therapy action.

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Section: Discussionsupporting

confidence: 70%

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Bosch

Rihm

Scheidegger

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…The fact that the involvement of dorsal areas might be a vulnerability factor is underscored by the observation that rumination is also associated with volume and resting state reductions in brain areas that have been linked to cognitive control processes such as prefrontal areas and the ACC (Kuhn, Vanderhasselt, De Raedt & Gallinat, 2012).…”

Section: A Cognitive Framework Of Depression and The Relationship Witmentioning

confidence: 99%

Neurostimulation as an intervention for treatment resistant depression: From research on mechanisms towards targeted neurocognitive strategies

Raedt

Vanderhasselt

Baeken

2015

Clinical Psychology Review

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106

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Despite the fact that several interventions for major depression have proven efficacy, a substantial number of patients are or become treatment resistant to various forms of pharmacotherapy and psychotherapy. Biological interventions that directly target brain activity such as electroconvulsive therapy are used to treat these patients, but some of these interventions are unlikely to be easily accepted because of their more invasive nature or sideeffects. The efficacy of non-invasive neurostimulation with a favorable side effect profile, such as repetitive Transcranial Magnetic Stimulation, could not be sufficiently demonstrated for treatment resistant depressed patients (TRD). We argue that research on the working mechanisms of these neurostimulation techniques is necessary to develop more efficient treatment protocols. After an overview of current neurostimulation approaches to treatment resistance and the introduction of a neurobiological and a cognitive framework of depression, we provide an integrative review of research on both the neurobiological and cognitive working mechanisms of neurostimulation in TRD, with a specific emphasis on the work of our lab. Thereafter, we describe our own studies and studies from other labs on new neurocognitive interventions. Finally we discuss how all this knowledge can be used to further develop new strategies to deal with treatment resistance, in combining neurostimulation and cognitive interventions.

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“…Another study comparing DMN and task-positive networks in MDD showed that ruminations were associated with increased DMN dominance at rest (Hamilton et al, 2011). Finally, by computing whole-brain correlation between RRS and resting state activity, Kühn, Vanderhasselt, De Raedt, and Gallinat (2012) found a negative relation with right inferior frontal gyrus, right ACC, and sgACC. They also found increased functional connectivity of the left striatum with left inferior frontal gyrus in healthy individuals experiencing more unwanted thoughts (Kühn, Vanderhasselt, De Raedt, & Gallinat, 2013).…”

Section: Introductionmentioning

confidence: 96%

Neural substrates of rumination tendency in non-depressed individuals

Piguet

Desseilles

Sterpenich

et al. 2014

Biological Psychology

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a b s t r a c tThe tendency to ruminate, experienced by both healthy individuals and depressed patients, can be quantified by the Ruminative Response Scale (RRS). We hypothesized that brain activity associated with rumination tendency might not only occur at rest but also persist to some degree during a cognitive task. We correlated RRS with whole-brain fMRI data of 20 healthy subjects during rest and during a face categorization task with different levels of cognitive demands (easy or difficult conditions). Our results reveal that the more subjects tend to ruminate, the more they activate the left entorhinal region, both at rest and during the easy task condition, under low attentional demands. Conversely, lower tendency to ruminate correlates with greater activation of visual cortex during rest and activation of insula during the easy task condition. These results indicate a particular neural marker of the tendency to ruminate, corresponding to increased spontaneous activity in memory-related areas, presumably reflecting more internally driven trains of thoughts even during a concomitant task. Conversely, people who are not prone to ruminate show more externally driven activity.

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Why ruminators won't stop: The structural and resting state correlates of rumination and its relation to depression

Cited by 130 publications

References 69 publications

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Sleep deprivation increases dorsal nexus connectivity to the dorsolateral prefrontal cortex in humans

Neurostimulation as an intervention for treatment resistant depression: From research on mechanisms towards targeted neurocognitive strategies

Neural substrates of rumination tendency in non-depressed individuals

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