Spontaneous Brain Electrical Activity Research Articles

Accelerated Aging Characterizes the Early Stage of Alzheimer's Disease.

For Alzheimer’s disease (AD), aging is the main risk factor, but whether cognitive impairments due to aging resemble early AD deficits is not yet defined. When working with mouse models of AD, the situation is just as complicated, because only a few studies track the progression of the disease at different ages, and most ignore how the aging process affects control mice. In this work, we addressed this problem by comparing the aging process of PS2APP (AD) and wild-type (WT) mice at the level of spontaneous brain electrical activity under anesthesia. Using local field potential recordings, obtained with a linear probe that traverses the posterior parietal cortex and the entire hippocampus, we analyzed how multiple electrical parameters are modified by aging in AD and WT mice. With this approach, we highlighted AD specific features that appear in young AD mice prior to plaque deposition or that are delayed at 12 and 16 months of age. Furthermore, we identified aging characteristics present in WT mice but also occurring prematurely in young AD mice. In short, we found that reduction in the relative power of slow oscillations (SO) and Low/High power imbalance are linked to an AD phenotype at its onset. The loss of SO connectivity and cortico-hippocampal coupling between SO and higher frequencies as well as the increase in UP-state and burst durations are found in young AD and old WT mice. We show evidence that the aging process is accelerated by the mutant PS2 itself and discuss such changes in relation to amyloidosis and gliosis.

Modulation of Task-Related and Resting-State Oscillatory Responses in Primary Progressive Aphasia

Event Abstract Back to Event Modulation of Task-Related and Resting-State Oscillatory Responses in Primary Progressive Aphasia Aneta Kielar1*, Regina Jokel2 and Jed A. Meltzer2 1 University of Arizona, Speech, Language and Hearing Sciences, United States 2 Baycrest Hospital, Rotman Research Institute, Canada Introduction: Patients with PPA respond to linguistic stimuli differently than healthy controls, reflecting degeneration of language networks and engagement of compensatory mechanisms1,2,3,4,5. Although the location of neurodegeneration is thus far the best predictor of individual variation in linguistic performance across patients, alterations in network function beyond the regions of major atrophy may provide valuable information on how the brain copes with ongoing neurodegeneration. Aims: We used magnetoencephalography (MEG) to evaluate patterns of oscillatory responses during sentence comprehension and spontaneous brain electrical activity related to impairment and preservation of linguistic function in PPA. We asked whether impaired language processing in PPA is associated with altered patterns of induced and spontaneous oscillatory responses, and whether spared language functions can be associated with recruitment of preserved brain regions in the left and right hemispheres. Methods Participants: MEG data were acquired from 13 patients with PPA (Age: M = 69.62 years, SE = 2.08; Education = M = 14 years, SE = .85; 7 females) and 15 age-matched healthy controls (Age: M = 69 years, SE = 1.77; Education: M = 17 years, SE = .69, 4 females). Materials and Procedure: Participants performed a visual sentence comprehension task while their neural responses were examined using (MEG). The sentences included semantic anomalies (e.g., She went to the bakery for the loaf of books*/bread) and syntactically anomalous words (She going*/went to the bakery for the loaf of books) that evoked distinct electrophysiological responses. Results: Patients with PPA showed altered patterns of induced oscillations, characterized by delayed latencies and attenuated amplitude (Figure 1 A and B). In the left parietal region, PPA patients exhibited reversed sensitivity to semantic anomalies, with greater event-related desynchronization for control words instead (Figure 1 D). The recruitment of right hemisphere temporo-parietal areas (also found in controls) was correlated with preserved semantic processing abilities (Figure 1 E). In addition, delayed peak latencies of oscillatory responses to language stimuli were associated with lower accuracy for detecting semantic anomalies, suggesting that language deficits observed in PPA may be linked to delayed or slowed information processing. Patients with PPA exhibited altered spontaneous electrical activity, with a general shift to slower oscillations and decreased power at higher frequencies. These resting-state oscillatory abnormalities were correlated with slowed neural responses to language stimuli (Figure 1G), suggesting that degenerative pathology is linked with slower brain dynamics in both task-related and spontaneous activity. Discussion and Conclusions: The present results indicate that neuropathological changes in the brains of PPA patients result in slowed information processing, which, in turn, is linked with progressive cognitive decline. Preserved semantic processing is supported by the functionality of preserved right hemisphere regions. In contrast, syntactic processing seems to be more sensitive to the degeneration in left hemisphere language regions. The combination of spontaneous and language related oscillatory responses can reveal the extent of the neural tissue that is not directly atrophied, but is functionally compromised. Abnormalities in both resting-state and task-evoked oscillations can serve as sensitive indicators of neuronal damage associated with neurodegenerative conditions such as PPA. Figure 1 Acknowledgements This work was supported by a Basic Science Grant from the Ontario Brain Institute Ontario Neurodegenerative Disease Research Initiative (ONDRI) to JAM and RJ, an Alzheimer’s Association New Investigator Research Grant to JAM, and a postdoctoral research award from the Ontario Research Coalition to AK. We thank the participating volunteers and their families.

Effects of the South American Psychoactive Beverage Ayahuasca on Regional Brain Electrical Activity in Humans: A Functional Neuroimaging Study Using Low-Resolution Electromagnetic Tomography

Ayahuasca, a South American psychotropic plant tea obtained from Banisteriopsis caapi and Psychotria viridis, combines monoamine oxidase-inhibiting β-carboline alkaloids with N,N-dimethyltryptamine (DMT), a psychedelic agent showing 5-HT_2A agonist activity. In a clinical research setting, ayahuasca has demonstrated a combined stimulatory and psychedelic effect profile, as measured by subjective effect self-assessment instruments and dose-dependent changes in spontaneous brain electrical activity, which parallel the time course of subjective effects. In the present study, the spatial distribution of ayahuasca-induced changes in brain electrical activity was investigated by means of low-resolution electromagnetic tomography (LORETA). Electroencephalography recordings were obtained from 18 volunteers after the administration of a dose of encapsulated freeze-dried ayahuasca containing 0.85 mg DMT/kg body weight and placebo. The intracerebral power density distribution was computed with LORETA from spectrally analyzed data, and subjective effects were measured by means of the Hallucinogen Rating Scale (HRS). Statistically significant differences compared to placebo were observed for LORETA power 60 and 90 min after dosing, together with increases in all six scales of the HRS. Ayahuasca decreased power density in the alpha-2, delta, theta and beta-1 frequency bands. Power decreases in the delta, alpha-2 and beta-1 bands were found predominantly over the temporo-parieto-occipital junction, whereas theta power was reduced in the temporomedial cortex and in frontomedial regions. The present results suggest the involvement of unimodal and heteromodal association cortex and limbic structures in the psychological effects elicited by ayahuasca.

The Effects of Propofol on Brain Electrical Activity, Neurologic Outcome, and Neuronal Damage Following Incomplete Ischemia in Rats

This study compares the effects of propofol and fentanyl/N2O on spontaneous brain electrical activity, neurologic outcome, and neuronal damage due to incomplete cerebral ischemia in rats. Thirty Sprague-Dawley rats were assigned to one of three groups: group 1 (n = 10) received 70% N2O in O2 plus fentanyl (bolus 10 micrograms.kg-1, infusion 25 micrograms.kg-1.h-1); group 2 (n = 10) received 70% N2 in O2 and propofol (infusion 0.8-1.2 mg.kg-1.min-1) adjusted to maintain EEG burst suppression during ischemia; group 3 (n = 10) was anesthetized with propofol and received 6 ml.kg-1 10% glucose intraperitoneally 15 min before the start of ischemia. Incomplete cerebral ischemia was produced by right common carotid artery occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Arterial blood gases, pH, and rectal temperature were kept constant in all groups. Plasma glucose was lower during ischemia in propofol-anesthetized rats compared to that in fentanyl/N2O- (P = 0.009) and glucose-loaded propofol-treated rats (P = 0.008). Neurologic outcome and brain tissue injury were significantly better in propofol-anesthetized compared to fentanyl/N2O-anesthetized rats (P less than 0.05). Elevated plasma glucose in propofol-treated rats resulted in similar neurologic outcome and histopathologic injury as seen in propofol-anesthetized rats given no glucose. Recovery of EEG theta-alpha activity after ischemia was inversely correlated to neurologic deficit (fentanyl/N2O: r = -0.71; propofol: r = -0.83; P less than 0.01). These results show that propofol improves neurologic outcome and decreases neuronal damage from incomplete cerebral ischemia when compared to fentanyl/N2O. This effect is not dependent on plasma glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Concurrent increases in brain electrical activity and intracranial blood flow velocity during low-dose ketamine anaesthesia

The purpose of the present study was to assess the effects of low-dose ketamine on spontaneous brain electrical activity (EEG) and intracranial blood flow velocity. Twenty healthy volunteers were divided into two groups: Group I (n = 10) received 0.25 mg.kg-1 ketamine iv; Group II (n = 10) received 0.5 mg.kg-1 ketamine iv. Mean arterial blood pressure (MAP), heart rate (HR), end-tidal PCO2 (PETCO2), and arterial oxygen saturation (SaO2) were measured. The EEG was recorded from temporo-occipital recording sites over both hemispheres. Blood flow velocity in the middle cerebral artery was measured using a transcranial Doppler ultrasound system. All variables were evaluated at baseline and for 60 min following ketamine. Administration of ketamine resulted in increases of MAP and HR in both groups to a similar degree. The PETCO2 and SaO2 did not change in either group over time. Ketamine caused a dose-dependent, transient shift in the EEG to synchronous high-voltage slow waves with an increase in total power (Group I: 301 +/- 38%; Group II: 104 +/- 28%). These changes were associated with dose-dependent increases in mean blood flow velocity (Group I: 35 +/- 7%; Group II: 68 +/- 10%). Our data suggest that increases in intracranial blood flow velocity are closely correlated to increases in neuronal activity and are not secondary to changes in systemic haemodynamic variables.

Electroencephalographic and evoked potential monitoring in the hyperbaric environment

The purpose of this study was to investigate brain bioelectrical activity during hyperbaric oxygenation by continuous and simultaneous monitoring of electroencephalographic and bimodal (auditory, somatosensory) evoked potentials. Multivariable recordings (electroencephalogram, brainstem auditory evoked potentials, early somatosensory evoked potentials, heart rate, heart rate variability, and transcutaneous partial pressure of oxygen) were measured with a new technique in 12 healthy male volunteers 26 to 52 years old (mean +/- SD, 35.9 +/- 9.5 years). Recordings were obtained while the subjects breathed (1) air at normal atmospheric pressure, (2) 100% oxygen at normal atmospheric pressure, (3) air at 2 atm (10 meters sea water [msw]), and (4) 100% oxygen at 2 atm (10 msw). Spontaneous brain electrical activity, somatosensory evoked potentials, and heart rate variability were not significantly affected during hyperbaric oxygenation, whereas the heart rate showed a significant decrease (paired t test, P less than 0.05). Alterations in brainstem auditory evoked potentials were seen under hyperbaric conditions and did not reach statistical significance (increase of the I-V interpeak latency by paired t test; P less than 0.2). All subjects showed insignificant increases in dominant alpha frequency and decreases in delta frequency under hyperbaric situations.

Electrophysiological and sleep alterations in experimental mouse rabies

Changes in the spontaneous brain electrical activity and sleep organization were investigated in 5 mice strains during the evolution of experimental fixed rabies infection. Cortical electrodes were chronically implanted for continuous EEG recording and spectral analysis until death. Three evolutionary phases were individualized. The initial phase exhibited alterations of sleep stages, REM sleep disappearance, pseudoperiodic facial myoclonus and first clinical signs. The mature phase was characterized by a generalized EEG slowing (2–4 cycles/s). The terminal phase occurring with extinction of hippocampal rhythmic slow acticity showed a flattening of cortical activity. The brain electrical activity ceased about 30 min before the cardiac arrest. Paroxysmal activities appeared during the course of the disease as burst of rhythmic slow waves, pseudoperiodic spikes or occasionally ictal epileptic discharges. Spectral analysis revealed a progressive and characteristic clustering of the EEG frequency band power values. The spread of infection in the CNS was monitored by specific immunofluorescence studies which revealed the presence of rabies virus antigen in the pons, the cerebellum, the thalamus and the cortex during the initial phase. The pyramidal field of the hippocampus was infected during the mature phase but the gyrus dentatus was never infected even at the terminal phase. These studies show that particular neuronal functions are impaired during rabies virus infection suggesting that neuronal alterations may be involved in the pathogenic mechanisms leading to lethality.

Reversible depression of spontaneous brain electrical activity induced by actinomycin D and 7-aminoactinomycin D in rats.

Various types of actinomycin (C,D,S2, I and V) and 7-amino-analogue of actinomycin D were injected into the right lateral ventricle of the brain through a chronically implanted cannula. In rats but not in mice actinomycin D, actinomycin S2 and 7-aminoactinomycin D caused depression of EEG, while cardiac and respiratory activity were maintained. This effect of the EEG was reversible and a normal EEG pattern reappeared at least 3 h after administration.

Drug-specific EEG frequency spectra and their time courses produced in the cat by antidepressants and a benzodiazepine

The effects of the tricyclic antidepressants imipramine, desipramine and doxepin and the anti-anxiety agent diazepam were tested for their effects on the frequency distribution of spontaneous brain electrical activity (EEG) in the cat. Multivariate statistical techniques were employed to make an objective and quantitative assessment of the results of broad-band frequency analysis in terms of certain dose-related and drug-specific variables. In spite of several clinical and pharmacological differences in their properties, the antidepressants produced remarkably similar profiles of frequency change which were unrelated to those produced by diazepam.

Neonatal electroencephalographic patterns as affected by maternal drugs administered during labor and delivery.

Effects of drugs used during labor and delivery on spontaneous (resting) and evoked brain electrical activity were studied in 45 normal human newborns 48 hours after delivery. Mothers received either anesthesia (general plus local) alone (group 1), anesthesia plus meperidine (group 2), anesthesia plus meperidine and promethazine (group 3), or anesthesia plus meperidine and diazepam (group 4). Autoregressive spectral analyses and subsequent stepwise discriminant analyses showed no differences in spontaneous brain electrical activity in the infants related to the type of drugs given to the mother. However, when auditory stimuli were reduced in intensity from 80 dB to 63 dB, a significant effect was found in newborn brain electrical activity between the anesthetic-only drug pattern (group 1) and the drug patterns of anesthetics with meperidine (group 2) and anesthetics with meperidine plus diazepam (group 4). The data suggest that this effect diminishes in the presence of promethazine (group 3). Evoked responses to visual, tactile, and olfactory stimuli remained unaffected.

An application of long-term frequency analysis in measuring drug-specific alterations in the EEG of the cat

A method is described for the quantitative measurement of “drug-specific” effects on the EEG of the cat. These effects are dose-related and are independent of the normal sources of EEG variation associated with the sleep-waking cycle. Drug-induced changes are expressed as characteristic alterations in frequency spectra and the time courses of these effects are followed for 5 h following administration of the test compounds. Atropine sulfate (0.5 and 2.0 mg/kg) and physostigmine salicylate (0.05 and 0.20 mg/kg) were administered to three unanesthetized and unrestrained cats and a broad-band frequency analysis was performed on the spontaneous brain electrical activity recorded from the prepyriform cortex, ventral hippocampus, lateral geniculate nucleus and the midbrain reticular formation. The resulting data were used as input to discriminant and canonical statistical analysis programs employed to abstract “drug-specific” patterns of frequency change. It was found that both atropine and physostigmine produce alterations in EEG frequency spectra which are clearly distinct from those patterns associated with the sleep-waking cycle and thus neither compound results in what has been characterized as an “EEG-behavioral dissociation”.

Effect of elimination of visual afferentation on electrical activity of various brain structures

Changes in spontaneous brain electrical activity were studied in experiments on rabbits totally blinded by enucleation befor acquiring vision, and on rabbits with direct vision excluded. Total exclusion of vision causes a sharp decrease in amplitude of electrical potentials in the cortex and subcortex. Depression of activity is greatest in the visual cortex and adjacent regions. Deprivation of direct vision also leads to definite changes in the EEG. The most marked changes are produced by restoration of normal vision. The possible mechanisms of the manifestation of depression in the brain electrical activity of animals with blocked visual function are discussed.

The effects of mescaline, amphetamine and four-ring substituted amphetamine derivatives on spontaneous brain electrical activity in the cat

Alterations in frequency distribution of spontaneous brain electrical activity were measured following administration of mescaline, amphetamine, trimethoxy-amphetamine (TMA), methoxy-methylenedioxy-amphetamine (MMDA), methylenedioxy-amphetamine (MDA) and dimethoxy-amphetamine (DMA) to unanesthetized and unrestrained cats. Two orthogonal patterns of frequency change were found which were correlated with dosage of the test compounds. It is proposed that one of these patterns represents central alerting in the cat, while the other is a correlate of the hallucinogenic effect produced in man by some of the drugs used. An analysis of the effects produced by individual compounds for their content of each pattern revealed that only amphetamine produced significant alerting; in terms of hallucinogenic effect, activities of the drugs decreased in the order TMA > MDA > MMDA > mescaline > DMA.