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Computer-based Multitaper Spectrogram Program for Electroencephalographic Data

Current web resources provide limited, user friendly tools to compute spectrograms for visualizing and quantifying electroencephalographic (EEG) data. ...

University of Tennessee

Oak Ridge National Laboratory

This systematic review with meta-analysis and trial sequential analysis of randomized clinical trials aimed to clarify the efficacy of sleep and circadian interventions on preventing postoperative delirium. The search and screening identified 13 trials with great heterogeneity in interventions, surgery types as well as methods for evaluating delirium, sleep and circadian rhythms. Meta-analyses revealed that sleep and circadian interventions were associated with decreased incidences of postoperative delirium (pooled relative risk (RR) = 0.48, 95% confidence interval (CI) = 0.29 to 0.78) compared with control. The pooled incidences of delirium for patients receiving interventions and no intervention (control) were 8.6% and 20.7% respectively. Results of the trial sequential analysis supported the interpretation that sleep and circadian interventions significantly diminished delirium compared to control. Subgroup analysis found that interventions that showed positive efficacy on sleep and circadian outcomes (p < 0.001), but not those without improvements (p = 0.114) or without assessments (p = 0.858), were associated with decreased risk of delirium. Dexmedetomidine sedation (p < 0.001) and timed bright light exposure (p = 0.006) appeared to reduce postoperative delirium. In summary, currently only limited evidence suggests strategies targeted at sleep and circadian health as a useful way to prevent postoperative delirium.

Promoting sleep and circadian health may prevent postoperative delirium: A systematic review and meta-analysis of randomized clinical trials.

This study tested the hypothesis that Regulators of G protein Signaling (RGS) proteins contribute to the regulation of wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep, and to sleep disruption caused by volatile anesthetics.

RGS Proteins and Gαi2 Modulate Sleep, Wakefulness, and Disruption of Sleep/ Wake States after Isoflurane and Sevoflurane Anesthesia.

Buprenorphine is an opiate used for pain management and to treat opiate addiction. The cytokine leptin can modulate nociception, but the extent to which buprenorphine-induced antinociception varies as a function of leptin signaling has not been characterized. Four congenic mouse lines with phenotypes that include differences in body weight and leptin status were used to test the hypothesis that the antinociceptive effects of buprenorphine vary as function of sex and leptin signaling. Each mouse line was comprised of males (n=12) and females (n=12) for a total of 96 animals. Groups included C57BL/6J (B6) mice (wild type), B6 mice with diet-induced obesity (DIO), obese B6.Cg-Lep/J (ob/ob) mice lacking leptin, and obese B6.BKS(D)-Lepr/J (db/db) mice with dysfunctional leptin receptors. The dependent measure was tail flick latency (TFL) in seconds for mouse-initiated tail removal from a warm water bath. Independent variables were intraperitoneal administration of saline (control) or buprenorphine (0.3mg/kg). Within every mouse line, buprenorphine significantly increased TFL relative to saline. Compared to the other mouse lines, db/db mice with dysfunctional leptin receptors had a significantly longer TFL after saline and after buprenorphine. TFL did not vary significantly by body weight or sex. The results provide novel support for the interpretation that acute thermal nociception is associated with altered leptin signaling.

Leptin status alters buprenorphine-induced antinociception in obese mice with dysfunctional leptin receptors.

Opiate-induced respiratory depression is sexually dimorphic and associated with increased risk among the obese. The mechanisms underlying these associations are unknown. The present study evaluated the two-tailed hypothesis that sex, leptin status, and obesity modulate buprenorphine-induced changes in breathing.

Buprenorphine Depresses Respiratory Variability in Obese Mice with Altered Leptin Signaling.

Anesthetic mechanisms that eliminate consciousness and perception of pain are products of the nervous system. Chemical approaches to the study of anesthetic mechanisms have the potential to serve as an ideal interface between basic and clinical neuroscience. There are disproportionately more basic neurochemical studies than clinical studies of anesthetic mechanisms. Even within neuroscience, the study of anesthetic mechanisms is sparse. The Society for Neuroscience hosts one of the world's largest and most vibrant scientific meetings, yet the content themes of that meeting do not include anesthesia. One goal of this chapter is to facilitate neurochemical studies of anesthetic mechanisms by outlining user-friendly descriptions of existing and emerging techniques. The introduction provides a context for chapter goals. The second portion of this chapter focuses on microdialysis methods that enable the humane acquisition of neurochemical samples from intact, behaving animals during anesthetic induction, maintenance, and emergence. No single neurotransmitter and no single brain region regulate the physiological and behavioral traits characteristic of any anesthetic state. This limitation is being addressed via application of new instrumentation and techniques in analytic chemistry. The final third of this chapter highlights selected omics approaches that are now being applied to the neurochemical study of anesthetic mechanisms. We hope that this brief chapter can stimulate basic and clinical metabolomic approaches aiming to elucidate the mechanisms of anesthetic action.

Neurochemistry of Anesthetic States.

By identifying endogenous molecules in brain extracellular fluid metabolomics can provide insight into the regulatory mechanisms and functions of sleep. Here we studied how the cortical metabolome changes during sleep, sleep deprivation and spontaneous wakefulness. Mice were implanted with electrodes for chronic sleep/wake recording and with microdialysis probes targeting prefrontal and primary motor cortex. Metabolites were measured using ultra performance liquid chromatography-high resolution mass spectrometry. Sleep/wake changes in metabolites were evaluated using partial least squares discriminant analysis, linear mixed effects model analysis of variance, and machine-learning algorithms. More than 30 known metabolites were reliably detected in most samples. When used by a logistic regression classifier, the profile of these metabolites across sleep, spontaneous wake, and enforced wake was sufficient to assign mice to their correct experimental group (pair-wise) in 80-100% of cases. Eleven of these metabolites showed significantly higher levels in awake than in sleeping mice. Some changes extend previous findings (glutamate, homovanillic acid, lactate, pyruvate, tryptophan, uridine), while others are novel (D-gluconate, N-acetyl-beta-alanine, N-acetylglutamine, orotate, succinate/methylmalonate). The upregulation of the de novo pyrimidine pathway, gluconate shunt and aerobic glycolysis may reflect a wake-dependent need to promote the synthesis of many essential components, from nucleic acids to synaptic membranes.

Metabolomic analysis of mouse prefrontal cortex reveals upregulated analytes during wakefulness compared to sleep.

This study tested the hypothesis that sleep fragmentation (SF) delays wound healing in obese B6.BKS(D)-Leprdb/J (db/db) mice with impaired leptin signaling and type 2 diabetes compared with wild-type C57BL/6J (B6) mice.

Ralph Lydic

Department of Psychology,
Department of Anesthesiology

University of Tennessee

Computer-based Multitaper Spectrogram Program for Electroencephalographic Data

Ralph Lydic

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Psychology,Department of Anesthesiology

University of Tennessee

Computer-based Multitaper Spectrogram Program for Electroencephalographic Data

Department of Psychology,
Department of Anesthesiology