Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 16634417

Entropy.

Berthold Bein
View original source ↗Export metadata ↓

Abstract

The concept of entropy, originally derived from thermodynamics, has been successfully applied to EEG analysis. Various entropy algorithms have been used in clinical studies, but until now a commercially available monitor exists only for spectral entropy. By calculating two distinct values for the EEG dominated part of the spectrum (state entropy, SE) and the total spectrum (response entropy, RE), the M-Entropy module claims to provide useful information regarding the cortical state of the patient as well as an indirect measure of adequacy of analgesia. Generally, entropy has been studied for quantification of anaesthetic drug effect for various GABA-ergic i.v. induction agents and volatile anaesthetics like propofol and sevoflurane and overall was found comparable to the current clinical gold standard bispectral index (BIS). Entropy guidance may not be used during ketamine or nitrous oxide administration, since there is no reliable correlation to the patient's state of consciousness. The usefulness of RE as a surrogate for increased EMG activity due to painful stimulation has not been proven so far.

Explore related subjects

AnalgesiaConsciousnessElectroencephalographyEntropyFourier AnalysisHumansMonitoring, IntraoperativeJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Berthold Bein. 2006. Entropy.. https://doi.org/10.1016/j.bpa.2005.07.009

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Placebo and endogenous mechanisms of analgesia.

The discovery of the endogenous systems of analgesia has produced a large amount of research aimed at investigating their biochemical and neurophysiological mechanisms and their neuroanatomical localization. Nevertheless, the neurobiological acquisitions on these mechanisms have not been paralleled by behavioural correlates in humans--in other words, by the understanding of when and how these endogenous mechanisms of analgesia are activated. Until recent times one of the most studied behavioural correlates of endogenous analgesia was stress-induced analgesia, in which the activation of endogenous opioid systems is known to be involved. By contrast, today the placebo analgesic effect represents one of the best-described situations in which this endogenous opioid network is naturally activated in humans. Therefore, not only is placebo research helpful towards improving clinical trial design and medical practice, but it also provides us with a better understanding of the endogenous mechanisms of analgesia.

Analgesia↗
PubMed2006

A force plate study of avian gait.

OBJECTIVE: To test the force plate as a gait analysis system for broilers and to determine how the ground reaction force (GRF) patterns change in these birds with growth and administration of analgesia. MATERIALS AND METHODS: Thirty-three male Ross 308 chicks were raised on either an ad libitum or restricted-feeding regime, and subsequently treated with carprofen or a placebo. Vertical, craniocaudal and mediolateral GRFs were measured as the birds walked across a standard force plate. RESULTS: The data were easy to collect, and peak vertical forces of an equivalent percentage of bodyweight as seen in human walking were identified. Mediolateral forces were 2-3 times greater than those demonstrated in other species. GRF patterns showed significant changes during growth, but analgesia did not have a significant effect on the speed of walking, or GRF patterns. CONCLUSIONS AND CLINICAL RELEVANCE: The force plate is a suitable research tool for recording GRFs from avian bipeds. The large mediolateral forces identify a particularly inefficient aspect of avian gait; however, the role of pain remains to be determined.

Analgesia↗
PubMed2006

Molecular mechanism for analgesia involving specific antagonism of alpha9alpha10 nicotinic acetylcholine receptors.

alpha9alpha10 nicotinic acetylcholine receptors (nAChRs) have been identified in a variety of tissues including lymphocytes and dorsal root ganglia; except in the case of the auditory system, the function of alpha9alpha10 nAChRs is not known. Here we show that selective block (rather than stimulation) of alpha9alpha10 nAChRs is analgesic in an animal model of nerve injury pain. In addition, blockade of this nAChR subtype reduces the number of choline acetyltransferase-positive cells, macrophages, and lymphocytes at the site of injury. Chronic neuropathic pain is estimated to affect up to 8% of the world's population; the numerous analgesic compounds currently available are largely ineffective and act through a small number of pharmacological mechanisms. Our findings not only suggest a molecular mechanism for the treatment of neuropathic pain but also demonstrate the involvement of alpha9alpha10 nAChRs in the pathophysiology of peripheral nerve injury.

Analgesia↗