Persistent default‐mode network connectivity during light sedation

Greicius, Michael D.; Kiviniemi, Vesa; Tervonen, Osmo; Vainionpää, Vilho; Alahuhta, Seppo; Reiss, Allan L.; Menon, Vinod

doi:10.1002/hbm.20537

Cited by 500 publications

(420 citation statements)

References 36 publications

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“…The CO 2 -induced reduction in sensorimotor connectivity is also in good agreement with a previous report by Biswal et al (1997). In our study, we have taken special precaution to minimize the influence of basal vascular state on BOLD signals, which were not accounted for in previous studies comparing fcMRI data across physiologic states (Biswal et al, 1997;Deshpande et al, 2010;Greicius et al, 2008;Horovitz et al, 2009). We have used visual-evoked fMRI signal as a reference with the assumption that the alterations in fMRI signal is solely due to a change in vascular state (Jones et al, 2005;Zappe et al, 2008a).…”

Section: Discussionsupporting

confidence: 89%

The Influence of Carbon Dioxide on Brain Activity and Metabolism in Conscious Humans

Xu¹,

Uh²,

Brier³

et al. 2010

J Cereb Blood Flow Metab

275

289

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A better understanding of carbon dioxide (CO 2 ) effect on brain activity may have a profound impact on clinical studies using CO 2 manipulation to assess cerebrovascular reserve and on the use of hypercapnia as a means to calibrate functional magnetic resonance imaging (fMRI) signal. This study investigates how an increase in blood CO 2 , via inhalation of 5% CO 2 , may alter brain activity in humans. Dynamic measurement of brain metabolism revealed that mild hypercapnia resulted in a suppression of cerebral metabolic rate of oxygen (CMRO 2 ) by 13.4% ± 2.3% (N = 14) and, furthermore, the CMRO 2 change was proportional to the subject's end-tidal CO 2 (Et-CO 2 ) change. When using functional connectivity MRI (fcMRI) to assess the changes in resting-state neural activity, it was found that hypercapnia resulted in a reduction in all fcMRI indices assessed including cluster volume, cross-correlation coefficient, and amplitude of the fcMRI signal in the default-mode network (DMN). The extent of the reduction was more pronounced than similar indices obtained in visualevoked fMRI, suggesting a selective suppression effect on resting-state neural activity. Scalp electroencephalogram (EEG) studies comparing hypercapnia with normocapnia conditions showed a relative increase in low frequency power in the EEG spectra, suggesting that the brain is entering a low arousal state on CO 2 inhalation.

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Section: Discussionsupporting

confidence: 89%

The Influence of Carbon Dioxide on Brain Activity and Metabolism in Conscious Humans

Xu¹,

Uh²,

Brier³

et al. 2010

J Cereb Blood Flow Metab

275

289

View full text Add to dashboard Cite

show abstract

“…This decrease of connectivity was correlated to the level of consciousness, mostly affecting the precuneus, a brain area considered to be a critical hub within this network with a massive degree of interconnectivity [34]. Similar decreases in DMN connectivity were observed in healthy controls during deep sleep [35], sedation, and general anesthesia (Fig. 2) [27].…”

Section: Disorders Of Consciousness and Neural Correlates Of Awarenesssupporting

confidence: 52%

Functional neuroanatomy of disorders of consciousness

Perri

Stender

Laureys

et al. 2014

Epilepsy & Behavior

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This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. Our understanding of the mechanisms of loss and recovery of consciousness, following severe brain injury or during anesthesia, is changing rapidly. Recent neuroimaging studies have shown that patients with chronic disorders of consciousness and subjects undergoing general anesthesia present a complex dysfunctionality in the architecture of brain connectivity. At present, the global hallmark of impaired consciousness appears to be a multifaceted dysfunctional connectivity pattern with both within-network loss of connectivity in a widespread frontoparietal network and between-network hyperconnectivity involving other regions such as the insula and ventral tegmental area. Despite ongoing efforts, the mechanisms underlying the emergence of consciousness after severe brain injury are not thoroughly understood. Important questions remain unanswered: What triggers the connectivity impairment leading to disorders of consciousness? Why do some patients recover from coma, while others with apparently similar brain injuries do not? Understanding these mechanisms could lead to a better comprehension of brain function and, hopefully, lead to new therapeutic strategies in this challenging patient population.This article is part of a Special Issue entitled Epilepsy and Consciousness.

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“…45 Contemporary networks consisted of regions identified from resting-state fMRI experimental results. 42,[46][47][48][49][50][51][52] Sizes of classic networks varied from B11% (medial limbic area) to 35% (frontal lobe) of gray-matter space, whereas sizes of contemporary networks varied substantially, for example, a frontal network Table 2). The dashed blue line represents the best-fit linear regression of all human data (i.e., CMR glc ¼ 0.003 BIS þ 0.06, R 2 ¼ 0.984), which is insignificantly different if the two vegetative state data points are removed (i.e., CMR glc ¼ 0.003 BIS þ 0.04, R 2 ¼ 0.986).…”

Section: Regional Oxidative Demand For Glutamatergic Activity In the mentioning

confidence: 99%

Glutamatergic Function in the Resting Awake Human Brain is Supported by Uniformly High Oxidative Energy

Hyder

Fulbright

Shulman

et al. 2013

J Cereb Blood Flow Metab

109

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Rodent 13 C magnetic resonance spectroscopy studies show that glutamatergic signaling requires high oxidative energy in the awake resting state and allowed calibration of functional magnetic resonance imaging (fMRI) signal in terms of energy relative to the resting energy. Here, we derived energy used for glutamatergic signaling in the awake resting human. We analyzed human data of electroencephalography (EEG), positron emission tomography (PET) maps of oxygen (CMR O2 ) and glucose (CMR glc ) utilization, and calibrated fMRI from a variety of experimental conditions. CMR glc and EEG in the visual cortex were tightly coupled over several conditions, showing that the oxidative demand for signaling was four times greater than the demand for nonsignaling events in the awake state. Variations of CMR O2 and CMR glc from gray-matter regions and networks were within ±10% of means, suggesting that most areas required similar energy for ubiquitously high resting activity. Human calibrated fMRI results suggest that changes of fMRI signal in cognitive studies contribute at most ± 10% CMR O2 changes from rest. The PET data of sleep, vegetative state, and anesthesia show metabolic reductions from rest, uniformly 420% across, indicating no region is selectively reduced when consciousness is lost. Future clinical investigations will benefit from using quantitative metabolic measures. Keywords: astrocytes; baseline; field potentials; glutamate; multiunit activity; resting state INTRODUCTIONThe human brain consumes 20% of the body's energy at rest despite being only 2% of total body mass. 1 Normally glucose oxidation is the source of energy production supporting brain function 2 in which gray-matter signaling (i.e., events associated with neuronal firing) is dominated by glutamatergic neurons. 3 Estimates of the fraction of resting brain energy devoted to signaling were originally quite low. 4 But recent experimental studies in rodents and theoretical modeling have converged on the conclusion that majority of the resting energy consumption supports glutamatergic signaling and the energy demand changes linearly with pyramidal neuron firing rates and glutamate neurotransmitter release and reuptake. [5][6][7][8][9] Therefore in rodent models it is possible, to a first order, to show that the resting energy is primarily dedicated to total glutamatergic signaling, and the changes in neuronal signaling relative to a well-defined resting activity level can be used to calibrate changes in energy consumption during functional magnetic resonance imaging (fMRI) experiments. 10,11 In the awake human brain, however, the fraction of resting energy usage devoted to glutamatergic signaling is less well understood. The magnitude of neuronal signaling in the human brain, and by inference the commensurate energy demand, underscores the functional relevance of resting activity and has profound implications for interpreting fMRI experiments in humans. [12][13][14] Given the rapidly increasing use of resting-state fMRI in mapping networks-defined as a...

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Persistent default‐mode network connectivity during light sedation

Cited by 500 publications

References 36 publications

The Influence of Carbon Dioxide on Brain Activity and Metabolism in Conscious Humans

The Influence of Carbon Dioxide on Brain Activity and Metabolism in Conscious Humans

Functional neuroanatomy of disorders of consciousness

Glutamatergic Function in the Resting Awake Human Brain is Supported by Uniformly High Oxidative Energy

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