Effects On Electroencephalographic Research Articles

EEG coherence and power spectra during REM sleep related to melatonin intake in mild-to-moderate Alzheimer’s disease: a pilot study

Introduction: It has been reported that melatonin diminishes rapid eye movement (REM) sleep latency in patients with Alzheimer’s disease (AD). Pharmacological studies suggest that melatonin promotes prompt sleep installation through interaction with GABA receptors, and that it is associated with acute suppression of neural electrical activity. Nevertheless, melatonin’s effects on electroencephalographic (EEG) activity related to REM sleep onset in AD patients have not been analyzed. Thus, in this pilot study we analyzed the effects of melatonin on EEG activity during the first episode of REM sleep in eight patients treated with 5-mg of fast-release melatonin. Methods: During a single-blind, placebo-controlled study, polysomnographic recordings were obtained from frontal, central, temporal, and occipital scalp derivations. REM sleep latency, as well as the relative power (RP) and EEG coherences of six EEG bands, were compared between the placebo and melatonin conditions. Results: Results showed that melatonin intake in AD patients decreased REM sleep onset, and that this was associated with lower RP and coherence of the β and γ EEG bands. Discussion: The possibility that the inhibitory GABAergic pathways related to REM sleep generation are well-preserved in mild-to-moderate AD is discussed. We conclude that the short REM sleep onset related to melatonin intake in AD patients is associated with a significant decrease in both RP and EEG coherence, mainly in the fast frequencies.

Neural measures of subsequent memory reflect endogenous variability in cognitive function.

Human cognition exhibits a striking degree of variability: Sometimes we rapidly forge new associations whereas at other times new information simply does not stick. Correlations between neural activity during encoding and subsequent retrieval performance have implicated such "subsequent memory effects" (SMEs) as important for understanding the neural basis of memory formation. Uncontrolled variability in external factors that also predict memory performance, however, confounds the interpretation of these effects. By controlling for a comprehensive set of external variables, we investigated the extent to which neural correlates of successful memory encoding reflect variability in endogenous brain states. We show that external variables that reliably predict memory performance have relatively small effects on electroencephalographic (EEG) correlates of successful memory encoding. Instead, the brain activity that is diagnostic of successful encoding primarily reflects fluctuations in endogenous neural activity. These findings link neural activity during learning to endogenous states that drive variability in human cognition. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Post-task Effects on EEG Brain Activity Differ for Various Differential Learning and Contextual Interference Protocols.

A large body of research has shown superior learning rates in variable practice compared to repetitive practice. More specifically, this has been demonstrated in the contextual interference (CI) and in the differential learning (DL) approach that are both representatives of variable practice. Behavioral studies have indicate different learning processes in CI and DL. Aim of the present study was to examine immediate post-task effects on electroencephalographic (EEG) brain activation patterns after CI and DL protocols that reveal underlying neural processes at the early stage of motor consolidation. Additionally, we tested two DL protocols (gradual DL, chaotic DL) to examine the effect of different degrees of stochastic fluctuations within the DL approach with a low degree of fluctuations in gradual DL and a high degree of fluctuations in chaotic DL. Twenty-two subjects performed badminton serves according to three variable practice protocols (CI, gradual DL, chaotic DL), and a repetitive learning protocol in a within-subjects design. Spontaneous EEG activity was measured before, and immediately after each 20-min practice session from 19 electrodes. Results showed distinguishable neural processes after CI, DL, and repetitive learning. Increases in EEG theta and alpha power were obtained in somatosensory regions (electrodes P3, P7, Pz, P4, P8) in both DL conditions compared to CI, and repetitive learning. Increases in theta and alpha activity in motor areas (electrodes C3, Cz, C4) were found after chaotic DL compared to gradual DL, and CI. Anterior areas (electrodes F3, F7, Fz, F4, F8) showed increased activity in the beta and gamma bands after CI. Alpha activity was increased in occipital areas (electrodes O1, O2) after repetitive learning. Post-task EEG brain activation patterns suggest that DL stimulates the somatosensory and motor system, and engages more regions of the cortex than repetitive learning due to a tighter stimulation of the motor and somatosensory system during DL practice. CI seems to activate specifically executively controlled processing in anterior brain areas. We discuss the obtained patterns of post-training EEG traces as evidence for different underlying neural processes in CI, DL, and repetitive learning at the early stage of motor learning.

Anticonvulsant effect of cannabidiol in the pentylenetetrazole model: Pharmacological mechanisms, electroencephalographic profile, and brain cytokine levels

Cannabidiol (CBD), the main nonpsychotomimetic compound from Cannabis sativa, inhibits experimental seizures in animal models and alleviates certain types of intractable epilepsies in patients. Its pharmacological profile, however, is still uncertain. Here we tested the hypothesis that CBD anticonvulsant mechanisms are prevented by cannabinoid (CB1 and CB2) and vanilloid (TRPV1) receptor blockers. We also investigated its effects on electroencephalographic (EEG) activity and hippocampal cytokines in the pentylenetetrazole (PTZ) model. Pretreatment with CBD (60mg/kg) attenuated seizures induced by intraperitoneal, subcutaneous, and intravenous PTZ administration in mice. The effects were reversed by CB1, CB2, and TRPV1 selective antagonists (AM251, AM630, and SB366791, respectively). Additionally, CBD delayed seizure sensitization resulting from repeated PTZ administration (kindling). This cannabinoid also prevented PTZ-induced EEG activity and interleukin-6 increase in prefrontal cortex. In conclusion, the robust anticonvulsant effects of CBD may result from multiple pharmacological mechanisms, including facilitation of endocannabinoid signaling and TRPV1 mechanisms. These findings advance our understanding on CBD inhibition of seizures, EEG activity, and cytokine actions, with potential implications for the development of new treatments for certain epileptic syndromes.

Isoflurane and sevoflurane decrease entropy indices more than halothane at equal MAC values

Recently, bispectral index (BIS) values were demonstrated to be different for various anesthetics as a result of differential effects on electroencephalographic (EEG) signals. Entropy is similar to the BIS monitor, as both process raw EEG to derive a number. We hypothesized that entropy may also be anesthetic agent-specific. Thirty adult patients undergoing spinal surgery were randomized to receive halothane, isoflurane, or sevoflurane. Entropy indices were recorded at various minimum alveolar concentration (MAC) values-0.5, 0.75, 1.0 and 1.5-both during wash-in and wash-out of the agent. Heart rate (HR), mean arterial blood pressure (MAP), response entropy (RE), and state entropy (SE) were noted. Statistical analysis was done using a one-way analysis-ofvariance test. P values less than 0.05 were considered significant. Ten patients in each group completed the study. The demographics and baseline values of HR, MAP, RE, and SE were comparable in all three groups. During the study period, for a given MAC value, both RE and SE remained low in the isoflurane and sevoflurane groups compared to the halothane group. For a given MAC, the RE and SE were comparable during wash-in and wash-out phases. Halothane produced higher entropy values as compared to isoflurane and sevoflurane at equivalent MAC levels.

Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation

Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up. Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8x or 1.2x the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED(50)) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s). Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from approximately 6 to approximately 8.5 Hz, and the SEF from approximately 25.5 to approximately 27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED(50) propofol, only the tail clamp and 1 Hz stimuli increased MEF ( approximately 8 to approximately 10-10.5 Hz). At the higher propofol infusion rate (1.2 ED(50)) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from approximately 23 to approximately 21.5 Hz). Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.

Pharmacokinetic Studies of Intramuscular Midazolam in Guinea Pigs Challenged with Soman

Studies have demonstrated that benzodiazepine compounds are effective at antagonizing seizure activity produced by the organophosphate (OP) cholinesterase inhibitor soman. In this present study we have investigated the pharmacokinetics of midazolam and its associated effects on electroencephalographic (EEG) activity following intramuscular (im) injection to soman‐exposed guinea pigs (Crl:(HA)BR). Prior to experiments, the animals were surgically implanted with EEG leads to monitor seizure activity. For the study, animals were administered the following pretreatment/OP/treatment regimen. Pyridostigmine bromide (0.026 mg/kg, im) was given 30 min prior to soman (56 µg/kg, 2 × LD50; subcutaneously, sc), followed in one minute by atropine sulfate (2 mg/kg, im) and pralidoxime chloride (25 mg/kg, im). All animals receiving this regimen developed seizure activity. Midazolam 0.8 mg/kg, im, was administered 5 min after onset of seizure activity. Based on EEG data, animals were categorized as either seizure‐terminated or seizure not‐terminated at 30 min following anticonvulsant administration. Serial blood samples were collected for the plasma midazolam analysis; the assay was accomplished with a gas chromatograph/mass spectrometer. The mean time to seizure termination was 8.8 ± 1.6 min. The mean time‐plasma concentration data were fit to standard pharmacokinetic models. The following parameter estimates were determined from the model‐fit for seizure terminated and not‐terminated animals respectively: apparent volumes of distribution (Vd) were 1.4 and 1.7 l/kg; area under the time‐concentration curves (AUC), 15,990 and 15,120 ng · min/ml; times to maximal plasma concentration (Tmax), 1.66 and 2.91 min and maximal plasma concentrations (Cmax) 535.1 and 436.6 ng/ml. These data indicate that im injection of midazolam is effective at terminating ongoing soman‐induced seizure activity. Additionally, the relatively short Tmax and latency to seizure termination demonstrate the rapidity of drug absorption and action respectively.

Sleep in the wake of complicated grief symptoms: An exploratory study

Our aim was to explore the concept that the symptoms of complicated grief may be a form of posttraumatic distress, rather than depression, and thus may have different effects on sleep. Sixty-five recently bereaved elders with varying levels of symptoms of complicated grief and depression were stratified by high versus low levels of symptoms; a two-way analysis of variance examined main effects of level of complicated grief symptoms and depressive symptoms on selected sleep measures, as well as interactions. Complicated grief symptoms were independently associated with mild subjective sleep impairment but showed no main effects on electroencephalographic (EEG) sleep measures. In a multiple regression analysis, complicated grief symptoms interacted with depressive symptoms to increase REM sleep percent. Thus, it appears that complicated grief symptoms do not entail the changes of EEG sleep physiology seen in depression, with the possible exception of an interaction with coexisting depression to enhance REM sleep percent.

Electroencephalographic sleep profiles during depression. Effects of episode duration and other clinical and psychosocial factors in older adults.

Limited evidence suggests that polysomnographic alterations may be more prominent early in a depressive episode. Whether the effects of episode duration extend beyond middle age and appear in late-life depression as well has important implications for treatment decisions and for understanding depressive illness across the life span. Furthermore, the impact of episode duration on sleep has not been examined in the context of other factors related to clinical history and psychosocial status. Eighty-three persons aged 60 years or older with recurrent depression were studied: 34 had been depressed for 2 to 16 weeks and 49 for longer periods. An age- and gender-matched group of 48 persons with no history of major depression served as controls. Initial univariate analyses examined duration effects on electroencephalographic (EEG) sleep measurements. Multivariate analyses considered the combined effects of episode duration, clinical variables, and psychosocial variables on EEG sleep profile. Episode duration was strongly associated with sleep continuity, architecture, and rapid eye movement: subjects who were earlier in their depressive episodes had their sleep impaired more than those later in their episodes, who, in turn, were more impaired than controls. Moreover, clinical characteristics of subjects' depressive illness, demographic variables, and psychosocial stressors and supports had unique effects on the EEG sleep profile. Episode duration appears to be a potent factor to consider when evaluating sleep during depression. The additional contribution of clinical and psychosocial characteristics to the prediction of the EEG sleep profile demonstrates the importance of incorporating these variables into models of the psychobiologic characteristics of depression. The results are relevant to the timing and focus of therapeutic interventions.

Comparative study of the EEG profile of neuroleptics selective for D-1 or D-2 dopamine receptors in the rabbit

The neuroleptics SCH 23390 and raclopride, which interact selectively with either D-1 or D-2 dopamine receptor, were studied for their effects on electroencephalographic (EEG) activity in the rabbit. Haloperidol (0.3 and 1 mg/kg intravenously, i.v.), which was used for comparison, induced synchronization of the cortical EEG activity. Spectral EEG analysis showed increase of power in the whole frequency range (0.1–38.5 Hz) and in all frequency bands in the cortex, whereas a slight decrease of slow and fast theta activity (3.7—7.2 and 7.2–12.2 Hz) was observed in the hippocampus. Animals appeared sedated and arousal response to somatosensory stimuli was markedly inhibited. SCH 23390 (0.03 and 0.3 mg/kg i.v.) induced periods of cortical synchronization and changes of spectral power qualitatively similar to those accompanying haloperidol administration. The drug slightly reduced the duration of arousal elicited by stimuli. Raclopride (1 and 3 mg/kg i.v.) induced weak EEG changes and little effect on arousal response to stimulation. There was an increase of slow wave activity which was particularly evident in the hippocampus. The data indicate that, although to a lesser degree, the D-1 receptor antagonist SCH 23390 induced EEG effects similar to those of haloperidol, whereas blockade of D-2 receptors by raclopride resulted in different patterns of EEG activity.

Electroencephalographic Sleep in Late-Life Neuropsychiatric Disorders

Late-life depression and dementia of the Alzheimer's type both have profound, although different, effects on electroencephalographic (EEG) sleep patterns. Thus, while depression is associated with REM sleep disinhibition and extreme sleep fragmentation (e.g., sleep onset REM periods and early morning awakenings), Alzheimer's disease is associated with deficits in the production of phasic activity during sleep (e.g., rapid eye movements and K-complexes) and with increased rates of sleep-disordered breathing. These differences have been shown to be reliable in large numbers of patients during the past five years and appear to extend to differences in sleep between depressive pseudodementia and dementia with secondary depression. Preliminary data also suggest that pretreatment sleep onset REM periods may be associated with enhanced vulnerability to recurrent depression. In summary, sleep physiological measures provide useful diagnostic and prognostic indexes in late-life neuropsychiatric disorders.

EEG AMPLITUDE CHANGES DURING DIFFERENT COGNITIVE PROCESSES INVOLVING SIMILAR STIMULI AND RESPONSES

ABSTRACTIn order to investigate the effects on electroencephalographic (EEG) amplitude of cognitive processes, as distinct from direct effects of sensory stimulation and motor response, subjects were given three different tasks in which the stimuli were always similar sets of spoken numbers and the responses were always written numbers. In response to 61 regularly occurring, randomly ordered, single‐digit numbers, seven Ss wrote, on successive trials, (1) the sum of every 4 consecutive numbers, (2) every fourth number, and (3) every “7” and “9” heard. Since the physical stimuli were the same and the movements of response were similar for the three tasks, intertask pattern differences in EEG alpha and beta amplitude would presumably be due to differences in the cognitive processes required in the tasks. No differences due to cognitive factors were found. All short‐term variations in both alpha and beta appeared related to widespread effects of response and preparation for response. Preresponse effects seemed related to motor set which was distinguished from attentional factors. The results suggest the necessity for a greater emphasis on motor effects in EEG studies.