Neural Origin of Spontaneous Hemodynamic Fluctuations in Rats under Burst-Suppression Anesthesia Condition

Liu, Xiao; Zhu, Xiao Hong; Zhang, Yi; Chen, Wei

doi:10.1093/cercor/bhq105

Cited by 158 publications

(220 citation statements)

References 51 publications

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“…With regard to intergroup comparison, control animals were imaged once based on the assumption that consistent results will be obtained by repeated imaging, because the reliability of rsFC measurement over time has been widely confirmed with test-retest designs. Further, the reliability of rsFC in anesthetized animals is confirmed by Liu and colleagues 31 who reported a strong neurovascular coupling in isoflurane-anesthetized rats, suggesting rsFC measured by fMRI in isoflurane anesthetized rats was of neural origin. Isoflurane is a vasodilator that may change the baseline blood flow level in the brain; however, rsfMRI measurement is not sensitive to baseline blood flow level, because it assesses the temporal coherence of spontaneous fluctuations of the fMRI signal, rather than its absolute amplitude.…”

Section: Discussionmentioning

confidence: 67%

Multi-Modal Approach for Investigating Brain and Behavior Changes in an Animal Model of Traumatic Brain Injury

Heffernan

Huang

Sicard

et al. 2013

Journal of Neurotrauma

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Use of novel approaches in imaging modalities is needed for enhancing diagnostic and therapeutic outcomes of persons with a traumatic brain injury (TBI). This study explored the feasibility of using functional magnetic resonance imaging (fMRI) in conjunction with behavioral measures to target dynamic changes in specific neural circuitries in an animal model of TBI. Wistar rats were randomly assigned to one of two groups (traumatic brain injury/sham operation). TBI rats were subjected to the closed head injury (CHI) model. Any observable motor deficits and cognitive deficits associated with the injury were measured using beam walk and Morris water maze tests, respectively. fMRI was performed to assess the underlying post-traumatic cerebral anatomy and function in acute (24 hours after the injury) and chronic (7 and 21 days after the injury) phases. Beam walk test results detected no significant differences in motor deficits between groups. The Morris water maze test indicated that cognitive deficits persisted for the first week after injury and, to a large extent, resolved thereafter. Resting state functional connectivity (rsFC) analysis detected initially diminished connectivity between cortical areas involved in cognition for the TBI group; however, the connectivity patterns normalized at 1 week and remained so at the 3 weeks post-injury time point. Taken together, we have demonstrated an objective in vivo marker for mapping functional brain changes correlated with injury-associated cognitive behavior deficits and offer an animal model for testing potential therapeutic interventions options.

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Section: Discussionmentioning

confidence: 67%

Multi-Modal Approach for Investigating Brain and Behavior Changes in an Animal Model of Traumatic Brain Injury

Heffernan

Huang

Sicard

et al. 2013

Journal of Neurotrauma

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“…15 Several animal studies have combined EEG with functional neuroimaging techniques [such as blood-oxygen-level-dependent functional magnetic resonance imaging (MRI), (BOLD fMRI)] to investigate cerebral hemodynamics and neurovascular coupling during BS induced via anesthesia. [20][21] In 2014, Sutin et al 22 used a simultaneous near-infrared spectroscopy (NIRS) and EEG methodology to investigate the hemodynamic responses associated with isoflurane-induced BS in the rat. Such multimodality imaging approaches have the potential to elucidate the fundamental physiological, neurovascular and neuroenergetic characteristics of the BS and discontinuous EEG state, but can also allow the spatial characteristics of these states to be investigated.…”

Section: Introductionmentioning

confidence: 99%

Hemodynamic response to burst-suppressed and discontinuous electroencephalography activity in infants with hypoxic ischemic encephalopathy

et al. 2016

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Abstract. Burst suppression (BS) is an electroencephalographic state associated with a profound inactivation of the brain. BS and pathological discontinuous electroencephalography (EEG) are often observed in term-age infants with neurological injury and can be indicative of a poor outcome and lifelong disability. Little is known about the neurophysiological mechanisms of BS or how the condition relates to the functional state of the neonatal brain. We used simultaneous EEG and diffuse optical tomography (DOT) to investigate whether bursts of EEG activity in infants with hypoxic ischemic encephalopathy are associated with an observable cerebral hemodynamic response. We were able to identify significant changes in concentration of both oxy and deoxyhemoglobin that are temporally correlated with EEG bursts and present a relatively consistent morphology across six infants. Furthermore, DOT reveals patient-specific spatial distributions of this hemodynamic response that may be indicative of a complex pattern of cortical activation underlying discontinuous EEG activity that is not readily apparent in scalp EEG.

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“…Moreover, the mechanism outlined herein is almost certainly related to secondary effects such as the aforementioned regulation of extracellular calcium. The autoregulation of physiological processes such as cerebral blood flow may also be important in burst suppression (39,43).…”

Section: Discussionmentioning

confidence: 99%

A neurophysiological–metabolic model for burst suppression

Ching

Purdon

Vijayan

et al. 2012

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

248

303

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Burst suppression is an electroencepholagram (EEG) pattern in which high-voltage activity alternates with isoelectric quiescence. It is characteristic of an inactivated brain and is commonly observed at deep levels of general anesthesia, hypothermia, and in pathological conditions such as coma and early infantile encephalopathy. We propose a unifying mechanism for burst suppression that accounts for all of these conditions. By constructing a biophysical computational model, we show how the prevailing features of burst suppression may arise through the interaction between neuronal dynamics and brain metabolism. In each condition, the model suggests that a decrease in cerebral metabolic rate, coupled with the stabilizing properties of ATP-gated potassium channels, leads to the characteristic epochs of suppression. Consequently, the model makes a number of specific predictions of experimental and clinical relevance.B urst suppression-an electroencephalogram (EEG) pattern in which high voltage activity (burst) and flatline (suppression) periods alternate systematically but quasiperiodically (almost periodic but with variations in inter-and intra-burst duration) (1)-is a state of profound brain inactivation. It is frequently observed in deep general anesthesia (2). It is also observed in a range of pathological conditions including hypothermia (3-5), hypoxic-ischemic trauma/coma (6), and the so-called Ohtahara syndrome (7,8), a type of early infantile encephalopathy. These etiologies indicate that the burst suppression pattern represents a low-order dynamic mechanism that persists in the absence of higher-level brain activity. Indeed, the fact that many different conditions produce similar brain activity suggests that there may be a common pathway to the state of brain inactivation and may indicate fundamental properties of the brain's arousal circuits (2).The basic features of the burst suppression phenomenon have been established through a variety of EEG studies that are reviewed in ref. 9. The two most notable of these features are the spatial homogeneity of bursts and the quasi-periodic nature of the suppression. Later research has been directed at describing the phenomenon in vivo and in the specific context of general anesthesia. In particular, the early work of Steriade et al. (10) helped establish the neural correlates of burst suppression, including the differential participation of cortical and subcortical cell types. More recent studies (11,12) have suggested that burst suppression is associated with enhanced excitability in cortical networks. These studies implicate extracellular calcium as a correlate for the switches between burst and suppression.Despite the findings of these studies, a unifying mechanism for burst suppression-one that explains its prevailing features and also accounts for its range of etiologies-has not been proposed. Indeed, the existing characterizations of burst suppression in pathological situations are highly limited. Computational models offer a means of synthesizing the availabl...

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Neural Origin of Spontaneous Hemodynamic Fluctuations in Rats under Burst-Suppression Anesthesia Condition

Cited by 158 publications

References 51 publications

Multi-Modal Approach for Investigating Brain and Behavior Changes in an Animal Model of Traumatic Brain Injury

Multi-Modal Approach for Investigating Brain and Behavior Changes in an Animal Model of Traumatic Brain Injury

Hemodynamic response to burst-suppressed and discontinuous electroencephalography activity in infants with hypoxic ischemic encephalopathy

A neurophysiological–metabolic model for burst suppression

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