The fundamental neural mechanisms of electroencephalography

Schaul, Neil

doi:10.1016/s0013-4694(97)00111-9

Cited by 143 publications

(113 citation statements)

References 35 publications

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“…It is known that atropine is a competitive antagonist of acetylcholine receptors and can block and/or limit the cholinergic pathway. These experiments concluded that cortical de-afferentation was an important factor in abnormal delta-wave production, owing to WM lesions (i.e., axonal injury) and/or defects in the cholinergic pathway (Schaul, 1998). In the human brain, the projections of cholinergic pathways highly overlap with the WM fiber tracts (Selden et al, 1998), which make the cholinergic pathways similarly susceptible as the WM tracts to TBI.…”

Section: Clinicalmentioning

confidence: 99%

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

Huang

Risling

Baker

2016

Psychoneuroendocrinology

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SummaryBackground: Pervasive use of improvised explosive devices (IEDs), rocket-propelled grenades, and land mines in the recent conflicts in Iraq and Afghanistan has brought traumatic brain injury (TBI) and its impact on health outcomes into public awareness. Blast injuries have been deemed signature wounds of these wars. War-related TBI is not new, having become prevalent during WWI and remaining medically relevant in WWII and beyond. Medicine's past attempts to accurately diagnose and disentangle the pathophysiology of war-related TBI parallels current lines of inquiry and highlights limitations in methodology and attribution of symptom etiology, be it organic, psychological, or behavioral. New approaches and biomarkers are needed. Preclinical: Serological biomarkers and biomarkers of injury obtained with imaging techniques represent cornerstones in the translation between experimental data and clinical observations. Experimental models for blast related TBI and PTSD can generate critical data on injury threshold, for example for white matter injury from acceleration. Carefully verified and validated models can be evaluated with gene expression arrays and proteomics to identify new candidates for serological biomarkers. Such models can also be analyzed with diffusion MRI and microscopy in order to identify criteria for detection of diffuse white matter injuries, such as DAI (diffuse axonal injury). The experimental models can also be analyzed with focus on injury outcome in brain stem regions, such as locus coeruleus or nucleus raphe magnus that can be involved in response to anxiety changes. * Corresponding author at: UCSD Radiology Imaging Laboratory, San Diego, CA 92121, USA. Tel.: +1 858 534 1254; fax: +1 8585346046. E-mail address: mxhuang@ucsd.edu (M. Huang). Clinical: Mild (and some moderate) TBI can be difficult to diagnose because the injuries are often not detectable on conventional MRI or CT. There is accumulating evidence that injured brain tissues in TBI patients generate abnormal low-frequency magnetic activity (ALFMA, peaked at 1-4 Hz) that can be measured and localized by magnetoencephalography (MEG). MEG imaging detects TBI abnormalities at the rates of 87% for the mild TBI, group (blast-induced plus non-blast causes) and 100% for the moderate group. Among the mild TBI patients, the rates of abnormalities are 96% and 77% for the blast and non-blast TBI groups, respectively. There is emerging evidence based on fMRI and MEG studies showing hyper-activity in the amygdala and hypo-activity in prefrontal cortex in individuals with PTSD. MEG signal may serve as a sensitive imaging marker for mTBI, distinguishable from abnormalities generated in association with PTSD. More work is needed to fully describe physiological mechanisms of post-concussive symptoms.Published by Elsevier Ltd. BackgroundBlast injuries are deemed the signature wounds of the first wars (Afghanistan and Iraq) of the 21st century (Lancet, 2007;Galarneau et al., 2008). According to a recent U.S. Department Veterans Affairs (DVA) ...

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Section: Clinicalmentioning

confidence: 99%

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

Huang

Risling

Baker

2016

Psychoneuroendocrinology

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“…The IoC and the electric suppression rate (ESR) were calculated online from the EEG by the IoC-view R monitor (Revuelta et al, 2008). The ESR reflects the isoelectric EEG activity interrupted by brief periods of highamplitude EEG activity indicating a non-specific reduction in cerebral metabolic activity (Rampil, 1998) and which appears during deep anaesthesia (Schaul, 1998). An example of the data available for each pig is presented in Figure 1.…”

Section: Facilitiesmentioning

confidence: 99%

Assessment of unconsciousness in pigs during exposure to nitrogen and carbon dioxide mixtures

Llonch

Rodríguez

Jospin

et al. 2013

Animal

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The aim of this study was to assess unconsciousness in pigs during and after the exposure to gas mixtures of 70% nitrogen (N2) and 30% carbon dioxide (CO2) (70N30C), 80% N2 and 20% CO2 (80N20C) and 85% N2 and 15% CO2 (85N15C) compared with 90% CO2 in air (90C) by means of the Index of Consciousness®(IoC), their behaviour and the absence of brain stem reflexes. The experiment included three trials of 24 pigs divided into four groups according to the number of treatments. Half of the group was exposed for a short time and the other half for a long time (3 and 5 min for the N2/CO2 mixtures exposure and 2 and 3 min in 90C exposure, respectively). During exposure, the IoC and the electroencephalography suppression rate (ESR) were assessed, as well as the time to onset and percentage of gasping, loss of balance, vocalizations, muscular excitation and gagging. At the end of the exposure, the corneal reflex, rhythmic breathing and sensitivity to pain were each assessed at 10 s intervals for 5 min. Brain activity decreased significantly (P < 0.05) 37.60 s after the start of the exposure to 90% CO2, which was significantly earlier than in 70N30C, 80N20C and 85N15C exposure, (45.18 s, 46.92 s and 43.27 s, respectively). Before brain activity decreased, all pigs experienced gasping and loss of balance and a 98% muscular excitation. The duration of the muscular excitation was longer in animals exposed to 70N30C, 80N20C and 85N15C than 90C (P < 0.01). After a long exposure time, all animals exposed to 90C died, whereas the 30.4% of animals exposed to N2/CO2 gas mixtures survived. Pigs exposed to 85N15C recovered corneal reflex and sensitivity to pain significantly earlier than when exposed to 90C. Exposure to 90C causes a higher aversive reaction but a quicker loss of consciousness than N2/CO2 gas mixtures. Exposure to N2/CO2 gas mixtures causes a lower percentage of deaths and an earlier recovery of the brain stem activity than 90C, whereas the time to recover the cortical activity is similar. In conclusion, the inhalation of N2/CO2 gas mixtures reduces the aversion compared with high concentrations of CO2; however, the period of exposure for inducing unconsciousness may be longer in N2/CO2 gas mixtures, and the signs of recovery appear earlier, compared to CO2.

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“…are neuronal in origin and generated by dipole layers of cortical pyramidal cells [5]. Some literature suggests that certain types of slow waves may originate in subcortical structures [6].…”

Section: Pathological Slow Wavesmentioning

confidence: 99%

EEG, the language of the brain and its neurochemical souffleuse

Wieser¹

1999

Swiss Arch Neurol Psychiatr

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SummaryWieser HG. EEG, the language of the brain and its neurochemical souffleuse. Schweiz Arch Neurol Psychiatr 1999;150:62-71.Neurochemical correlates of EEG activity are discussed concentrating on microdialysis findings and seizure prediction by calculating Lyapunov spectra and related measures of complexity in the EEG. Some other interesting findings in relation to brain stimulation by weak D. C. electromagnetic fields i. e. evocation of epileptiform activity by weak D. C. magnetic fields and in vivo polarization (D. C. electrical stimulation) of the hippocampus are reported. In addition a few new findings are presented with regard to histochemical findings of resected epileptogenic brain specimen and proton magnetic resonance spectroscopy ( 1 H-MRS).Keywords Although it is tempting to glorify these achievements, in particular at an occasion such as this 50-year jubilee, it is fair to say that the generation of EEG potentials has proved to be extremely complex and difficult to understand. The achievements of non-invasive radiological and radionuclear methods in the field of structural diagnosis on the one hand and the feeling of doing pragmatically useful work with an ill-understood method on the other hand have been depressing for many workers in the field. The history of electroencephalography, masterly compiled by Niedermeyer [4], however, tells us that such challenges can present a stimulus for the electrophysiological field, since the function-oriented aspects of the neurological sciences will always be of paramount significance. With such an attitude we chose the title of this presentation which shall concentrate on our own Zurich work. However, let us first try to answer the question "what do we know about the nature of the EEG?" What is the EEG?Electrical activity of the brain results from ionic currents generated by biochemical processes at the cellular level. The principle EEG generators of the EEG are convoluted dipole layers of pyramidal neurons in the cortical gray matter.The EEG Congress report is due to temporal and spatial summation of postsynaptic potentials (PSPs) from cortical pyramidal cells. What are epileptiform potentials, such as spike and spike-slow waves?The epileptiform spike is an excitatory event. In focal epilepsy it represents a summation of synchronous paroxysmal depolarization shifts (PDSs), in generalized epilepsies it represents summated excitatory postsynaptic potentials (EPSPs). The following slow wave is an inhibitory event related to synchronous after hyperpolarization in focal epilepsy and recurrent inhibition in generalized epilepsy. Pathological slow wavesare neuronal in origin and generated by dipole layers of cortical pyramidal cells [5]. Some literature suggests that certain types of slow waves may originate in subcortical structures [6]. For many authors such an assumption is difficult to reconcile [7]. However, there exists evidence that for certain slow rhythms the networks responsible may be located in subcortical structures such as the thalamus [8]. Advantag...

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The fundamental neural mechanisms of electroencephalography

Cited by 143 publications

References 35 publications

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

Assessment of unconsciousness in pigs during exposure to nitrogen and carbon dioxide mixtures

EEG, the language of the brain and its neurochemical souffleuse

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