Peltier, S. J. et al. Functional connectivity changes with concentration of sevoflurane anaesthesia. Neuroreport 16, 285-288

Department of Psychology, Emory University, Atlanta, Georgia, United States
Neuroreport (Impact Factor: 1.64). 03/2005; 16(3):285-8. DOI: 10.1097/00001756-200502280-00017
Source: PubMed

ABSTRACT Low-frequency oscillations (<0.08 Hz) have been detected in functional magnetic resonance imaging studies, and appear to be synchronized between functionally related areas. The effect of anesthetic agents on cortical activity is not completely characterized. This study assessed the effect of anesthesia on the temporal relations in activity in the motor cortices. Resting-state magnetic resonance data were acquired on six volunteers under different anesthetic states (using 0.0%, 2.0% and 1.0% stable end-tidal sevoflurane). Across all volunteers, the number of significant voxels (p<2.5 x 10) in the functional connectivity maps was reduced by 78% for light anesthesia and by 98% for deep anesthesia, compared with the awake state. Additionally, significant correlations in the connectivity maps were bilateral in the awake state but unilateral in the light anesthesia state.

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Available from: Stephan B Hamann, Aug 20, 2015
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    • "( " deep anesthesia, " burst suppression pattern) FC maps also showed all of the core regions of the networks and subsequently grouped data across levels. A human study reported a breakdown of interhemispheric connectivity of homologues in the DMN at a sevoflurane concentration of 1.00% [Peltier et al., 2005] that "
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    ABSTRACT: Despite their widespread use, the effect of anesthetic agents on the brain's functional architecture remains poorly understood. This is particularly true of alterations that occur beyond the point of induced unconsciousness. Here, we examined the distributed intrinsic connectivity of macaques across six isoflurane levels using resting-state functional MRI (fMRI) following the loss of consciousness. The results from multiple analysis strategies showed stable functional connectivity (FC) patterns between 1.00% and 1.50% suggesting this as a suitable range for anesthetized nonhuman primate resting-state investigations. Dose-dependent effects were evident at moderate to high dosages showing substantial alteration of the functional topology and a decrease or complete loss of interhemispheric cortical FC strength including that of contralateral homologues. The assessment of dynamic FC patterns revealed that the functional repertoire of brain states is related to anesthesia depth and most strikingly, that the number of state transitions linearly decreases with increased isoflurane dosage. Taken together, the results indicate dose-specific spatial and temporal alterations of FC that occur beyond the typically defined endpoint of consciousness. Future work will be necessary to determine how these findings generalize across anesthetic types and extend to the transition between consciousness and unconsciousness. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 07/2014; 35(12). DOI:10.1002/hbm.22583 · 6.92 Impact Factor
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    • "The early work of Kiviniemi and associates (2005) indicated that sedative levels of the intravenous anesthetic , midazolam enhanced the amplitude and synchrony of spontaneous BOLD signal fluctuations. Greicius and coworkers (2008) found a general preservation of default mode connectivity with specific focal reductions in the posterior cingulate cortex that were different from the patterns seen with the volatile anesthetic, sevoflurane (Peltier et al., 2005). During sedation with propofol, regionally diverse, dose-dependent changes in resting-state connectivity have been found (Hudetz, 2012; Liu et al., 2013d). "
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    ABSTRACT: The richness of conscious experience is thought to scale with the size of the repertoire of causal brain states, and it may be diminished in anesthesia. We estimated the state repertoire from dynamic analysis of intrinsic functional brain networks in conscious sedated and unconscious anesthetized rats. Functional resonance images were obtained from 30-min whole-brain resting-state blood oxygen dependent (BOLD) signals at propofol infusion rates of 20 and 40 mg/kg/h, iv. Dynamic brain networks were defined at the voxel level by sliding window analysis of regional homogeneity (ReHo) or coincident threshold crossings (CTC) of the BOLD signal acquired in nine sagittal slices. The state repertoire was characterized by the temporal variance of the number of voxels with significant ReHo or positive CTC. From low to high propofol dose, the temporal variances of ReHo and CTC were reduced by 78±20% and 76±20%, respectively. Both baseline and propofol-induced reduction of CTC temporal variance increased from lateral to medial position. Group analysis showed a 20% reduction in the number of unique states at the higher propofol dose. Analysis of temporal variance in twelve anatomically defined regions of interest predicted that the largest changes occurred in visual cortex, parietal cortex, and caudate-putamen. The results suggest that the repertoire of large-scale brain states derived from the spatiotemporal dynamics of intrinsic networks is substantially reduced at an anesthetic dose associated with loss of consciousness.
    04/2014; 5(1). DOI:10.1089/brain.2014.0230
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    • "The fact that our experiments were performed in anaesthetized animals raises the question as to whether the observed effects truly reflect the functional architecture of the mouse brain in conscious states. While reduced intrinsic connectivity has been reported in deeply anesthetised subjects (Boveroux et al., 2010; Deshpande et al., 2010; Peltier et al., 2005), human and animal studies have consistently demonstrated that the effect of anaesthesia on the brain's functional connectivity is strictly dose-dependent (Boveroux et al., 2010; Deshpande et al., 2010; Liu et al., 2011; Wang et al., 2011). In keeping with this, the use of light anaesthesia or sedation have been shown to exert minimal interference on the functional topology of multiple rsFC networks in the primate, human and rat brain (Greicius et al., 2008; Hutchison et al., 2011; Margulies et al., 2009; Vincent et al., 2007b). "
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    ABSTRACT: Laboratory mouse models represent a powerful tool to elucidate the biological foundations of disease, but translation to and from human studies rely upon valid cross-species measures. Resting-state functional connectivity (rsFC) represents a promising translational probe of brain function; however, no convincing demonstration of the presence of distributed, bilateral rsFC networks in the mouse brain has yet been reported. Here we used blood oxygen level dependent (BOLD) and cerebral blood volume (CBV) weighted fMRI to demonstrate the presence of robust and reproducible resting-state networks in the mouse brain. Independent-component analysis (ICA) revealed inter-hemispheric homotopic rsFC networks encompassing several established neuro-anatomical systems of the mouse brain, including limbic, motor and parietal cortex, striatum, thalamus and hippocampus. BOLD and CBV contrast produced consistent networks, with the latter exhibiting a superior anatomical preservation of brain regions close to air-tissue interfaces (e.g. ventral hippocampus). Seed-based analysis confirmed the inter-hemispheric specificity of the correlations observed with ICA and highlighted the presence of distributed anterior-posterior networks anatomically homologous to the human salience network (SN) and default-mode network (DMN). Consistent with rsFC investigations in humans, BOLD and CBV-weighted fMRI signals in the DMN-like network exhibited spontaneous anti-correlation with neighbouring fronto-parietal areas. These findings demonstrate the presence of robust distributed intrinsic functional connectivity networks in the mouse brain, and pave the way for the application of rsFC readouts in transgenic models to investigate the biological underpinnings of spontaneous BOLD fMRI fluctuations and their derangement in pathological states.
    NeuroImage 09/2013; 87. DOI:10.1016/j.neuroimage.2013.09.050 · 6.36 Impact Factor
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