Increased EEG Power Research Articles

Changes in EEG Activity during Exercise

Few studies have systematically examined changes in brain electrical activity during an acute bout of exercise. Those that have studied changes during exercise have often found an increase in power in the alpha and beta frequency. PURPOSE: To investigate whether the increases in brain activity occur because of an increase in exercise intensity or an accumulation due to the duration of the exercise. METHODS: 30 males (Age = 22.5 ± 3.5 years; Height = 181.1 ± 7.2 cm; Weight = 83.7 ± 17.8 kg) participated in the study. Participants cycled on a recumbent cycle ergometer for 5, 5 min stages for a total of 25 min. The first stage was 50 W; the next 4 stages were randomly assigned at 50W, 100W, 150W or 200W. Brain activity was recorded via EEG (24 lead, PS YLAB EEG System, Contact Precision Instruments, Cambridge, MA) pre-exercise, at the end of each stage of exercise, immediate post exercise (IPE), and 10 min post-exercise. EEG signals were visually inspected for artifact and underwent a Fast Fourier Transform to determine power at the alpha 1 (8.00–10.49 Hz), alpha 2 (10.50–12.99), beta 1 (13.00–17.99 Hz), and beta 2 (18.00–30.00) frequency bands. RESULTS: ANOVA analyses revealed a significant effect for intensity (p <.001) for all EEG frequencies, alpha 1, alpha 2, beta 1 and beta 2. Compared to baseline levels, EEG power for the frequencies increased as exercise intensity increased and returned back to near baseline levels at 10-min post exercise. When running analyses based on the different stages, regardless of intensity, an effect for stage (p <.001) was also seen when compared to baseline levels with increased EEG power during the exercise session. CONCLUSIONS: It appears that the increase in alpha and beta power during exercise may be due to both an accumulation of duration as well as intensity. Future studies should continue to examine the influence of intensity and duration on changes in brain activity. These changes may be important in explaining perceptual, affective and cognitive responses to exercise.

Distinct Cognitive Neurophysiologic Profiles for Lamotrigine and Topiramate

To contrast the effects of lamotrigine (LTG) and topiramate (TPM) on cognitive task-related and resting-state EEG and evoked potential (EP) measures. We used a double-blind, randomized, crossover design. Healthy adults (N = 29) had two 8-week periods of dose escalation, 4 weeks of drug maintenance (300 mg daily), and 4 weeks of washout. EEG was recorded during working memory (WM) tasks and resting conditions at baseline, at the end of each maintenance phase, and after final washout. RESULTS. LTG did not affect overt performance on the tasks, although it reduced EEG power in both resting and WM task conditions, most prominently in the 6- to 12-Hz frequency range, and attenuated P300 evoked-potential amplitude equally in both WM task loads. TPM slowed responses and increased errors. It also increased EEG power below 6 Hz in all conditions, and reduced the amplitude of a slow wave observed in a difficult version of the WM task. The drugs produced both task-independent and task-related alterations in neurophysiologic measures. The EEG and EP changes produced by TPM are consistent with an impairment of WM, as evidenced by overt performance deficits on the behavioral tasks. By contrast, the reduction in synchronous cortical activity produced by LTG was not accompanied by cognitive impairment. It is unknown whether such effects would also be observed at lower doses, such as those that often are used in monotherapy for newly diagnosed patients.

Short-Wavelength Sensitivity for the Direct Effects of Light on Alertness, Vigilance, and the Waking Electroencephalogram in Humans

To assess the wavelength-dependent sensitivity of the acute effects of ocular light exposure on alertness, performance, waking electroencephalogram (EEG), and cortisol. A between-subjects design was employed to compare the effects of exposure to 460-nm or 555-nm light for 6.5 hours during the biological night. Intensive Physiological Monitoring Unit, Brigham and Women's Hospital, Boston, MA. Sixteen healthy adults (8 women; mean age +/- SD = 23.3 +/- 2.4 years). Subjects were exposed to equal photon densities (2.8 x 10(13) photons x cm(-2) x s(-1)) of either 460-nm (n = 8) or 555-nm (n = 8) monochromatic light for 6.5 hours, 15 minutes after mydriasis. Subjects underwent continuous EEG/electrooculogram recordings and completed a performance battery every 30 to 60 minutes. As compared with those exposed to 555-nm light, subjects exposed to 460-nm light had significantly lower subjective sleepiness ratings, decreased auditory reaction time, fewer attentional failures, decreased EEG power density in the delta-theta range (0.5-5.5 Hz), and increased EEG power density in the high-alpha range (9.5-10.5 Hz). Light had no direct effect on cortisol. Short-wavelength sensitivity to the acute alerting effects of light indicates that the visual photopic system is not the primary photoreceptor system mediating these responses to light. The frequency-specific changes in the waking EEG indicate that short-wavelength light is a powerful agent that immediately attenuates the negative effects of both homeostatic sleep pressure and the circadian drive for sleep on alertness, performance, and the ability to sustain attention.

The electroencephalographic substratum of the awakening

The aim of the present study was to characterize the regional electroencephalographic substratum of the awakening process by means of a Hz-by-Hz EEG spectral power analysis. For this purpose, we recorded a group of 25 female subjects who slept for at least two consecutive nights in the laboratory. The postsleep waking EEG was compared to the one recorded during the presleep wakefulness from four midline derivations (Fz–A1, Cz–A1, Pz–A1, Oz–A1). Results indicated that the first 10 min after awakening are characterized by an increase of EEG power in the low-frequency range (1–9 Hz) compared to the corresponding presleep waking period, and by a significant decrease of EEG power in the beta range (18–24 Hz). As regards topographic differences, the increase of EEG power upon awakening in the delta–theta range showed a parieto-occipital prevalence. Moreover, the occipital derivation showed a larger decrease of power in the beta range as compared to the other derivations. In conclusion, the EEG substratum of the sleep offset period is characterized by a pattern of increased EEG power in the delta–theta and low-alpha bands, and of decreased power in the beta range. This pattern could be considered as the spectral EEG signature of the sleep inertia phenomenon. The state of postsleep EEG hypoarousal does not subside in the first 10-min period after awakening considered in the present analysis. Finally, according to our results, the more posterior scalp locations show stronger EEG signs of sleep inertia, and could be the last ones to properly wake up.

Increased EEG power and slowed dominant frequency in patients with neurogenic pain

To study the mechanisms of chronic neurogenic pain, we compared the power spectra of the resting EEG of patients (n = 15, 38-75 years, median 64 years, 6 women) and healthy controls (n = 15, 41-71 years, median 60 years, 8 women). On an average, the patient group exhibited higher spectral power over the frequency range of 2-25 Hz, and the dominant peak was shifted towards lower frequencies. Maximal differences appeared in the 7-9 Hz band in all electrodes. Frontal electrodes contributed most to this difference in the 13-15 Hz band. Bicoherence analysis suggests an enhanced coupling between theta (4-9 Hz) and beta (12-25 Hz) frequencies in patients. The subgroup of six patients free from centrally acting medication showed higher spectral power in the 2-18 Hz frequency range. On an individual basis, the combination of peak height and peak frequency discriminated between patient and control groups: discriminant analysis classified 87% of all subjects correctly. After a therapeutic lesion in the thalamus (central lateral thalamotomy, CLT) we carried out follow-up for a subgroup of seven patients. Median pain relief was 70 and 95% after 3 and 12 months, respectively. The average EEG power of all seven patients gradually decreased in the theta band and approached normal values only after 12 months. The excess theta EEG power in patients and its decrease after thalamic surgery suggests that both EEG and neurogenic pain are determined by tightly coupled thalamocortical loops. The small therapeutic CLT lesion is thought to initiate a progressive normalization in the affected thalamocortical system, which is reflected in both decrease of EEG power and pain relief.

Role of astrocytes and gap junctions in seizure-induced pial arteriolar dilations in rats

Cerebral arterioles and astrocytes are physically and physiologically linked to one another. Indeed, astrocyte-related factors appear to make a significant contribution to the local regulation of CBF. For example, in recent studies we reported that topical application of L-alpha-aminoadipic acid (L-AAA), an astroglial toxin which selectively damaged the glia limitans (without affecting vascular smooth muscle, endothelium, or neurons), was associated with a reduced pial arteriolar reactivity to selected vasodilating stimuli (e.g., hypercapnia and ADP; but not acetylcholine or NO). In the present study, we examined whether the pial arteriolar dilation accompanying seizure (topical bicuculline [BC]) was influenced by L-AAA-induced glial injury. In addition, we tested whether gap junctions influence the vascular response. These experiments employed topical applications of the gap junction inhibitory peptide, gap 27. To ensure that changes in the vasodilatory magnitude were not related to reduced brain activity, the local EEG activity (total EEG power) was monitored. We used anesthetized rats, with closed cranial windows inserted 24 h prior to study. L-AAA (or aCSF, 300 ul each) was introduced into the periarachnoid space immediately after window placement. BC (100 uM) was suffused over 15 min and pial arteriolar diameters measured every minute. Arteriolar responses in L-AAA- and aCSF-treated rats were compared. To assess gap junction contributions, the rats were exposed to two BC exposures (separated by 2 h). Gap 27 was topically applied for 1 h prior to the 2nd evaluation. In controls, the gap 27 was omitted. No differences in the magnitude of the EEG power increase were observed when comparing L-AAA or gap 27-treated rats to their controls. The arteriolar responses are summarized in the figure 1. The 20-25% increase in diameter that is normally seen during seizure was completely lost in L-AAA-treated rats. Topical blockade of gap junctions was associated with a 50% reduction in pial arteriolar dilation. These results indicate that astrocytes, and, to a lesser extent, gap junctions, contribute greatly to the cerebrovasodilation accompanying seizure.

Theta activity in the waking EEG is a marker of sleep propensity in the rat

In humans, EEG power in the theta frequency band (5–8 Hz) during quiet waking increases during sleep deprivation (SD), and predicts the subsequent homeostatic increase of sleep slow-wave activity (SWA; EEG power between 0.5 and 4.0 Hz). These findings indicate that theta power in waking is an EEG variable, which reflects the rise in sleep propensity. In rodents, a number of short sleep attempts, as well as SWA in the waking EEG increase in the course of SD, but neither variable predicts the subsequent homeostatic increase of EEG SWA during recovery sleep. To investigate whether there is an EEG marker for sleep propensity also in rodents, the EEG of the rat was recorded during 6 h SD in the first half of the light period (SDL, n = 7). During SDL, power of the waking EEG showed an increase in the delta (1.5–4 Hz) and low theta (5–6.5 Hz) band. Based on the neck muscle EMG, wakefulness was subdivided into active (high EMG activity) and quiet (low EMG activity) waking. During quiet waking, the theta peak occurred at 5.5 Hz, the frequency at which the increase of EEG power during SD was most pronounced. This increase was due to higher amplitude of theta waves, while wave incidence (frequency) was unchanged. Correlation analysis showed that the rise in EEG power in the 5–7 Hz band during SD predicted the subsequent enhancement of SWA in non-rapid eye movement sleep. The analysis of data of a further batch of rats which were sleep deprived for 6 h after dark onset (SDD, n = 7) revealed a significant increase in theta-wave amplitude during the SD and a tendency for a similar, positive correlation between the increase of theta power (5–7 Hz) and subsequent SWA. The results indicate that in rats, as in humans, a specific waking EEG frequency, i.e., theta power in quiet waking is a marker of sleep propensity.

Age-dependent changes in electroencephalographic responses to alcohol consumption in subjects with aldehyde dehydrogenase-2 genetic variations.

We have recently reported that alcohol consumption resulted in a significant increase in alpha power of the EEGs in aldehyde dehydrogenase-2 (ALDH2)-normal (NN) subjects but not in ALDH2-deficient heterozygote (ND) subjects. The purpose of the present study was to investigate interactive effects of individual factors such as age and ALDH2 genotype on alcohol-induced EEG changes. We examined EEG power spectral changes induced by 0.4 ml/kg of alcohol ingestion in 53 NN and 21 ND subjects of two different age groups: younger and older groups. Blood ethanol and acetaldehyde levels were also determined in 17 NN and 13 ND subjects in separate studies. Alcohol consumption markedly increased EEG power in the NN subjects of the older group, especially in theta and slow alpha power, whereas only slight increases were noted in fast alpha and beta power in the NN subjects of the younger group. However, no such differences between the two age groups were observed in the ND subjects. It should be noted that there were no differences in blood ethanol and acetaldehyde level at 30 min after alcohol ingestion between the different age groups in both genotypes. However, there was a significant increase in frequency of alcohol intake in the older group of both genotype groups. The multiple regression analysis indicated that both alcohol use habits and genotype, as well as aging, significantly modulated EEG changes after alcohol ingestion. The results suggest that both ALDH2 genotype and age as well as alcohol use habits modify alcohol sensitivity in the central nervous system, resulting in greater increases in EEG energy in response to alcohol intake in the older group of the NN subjects.

Quantitative EEG abnormalities in recently abstinent methamphetamine dependent individuals.

Methamphetamine exposure is associated with long-lasting reductions in markers for dopaminergic neurons in preclinical models and probably in humans. Quantitative electroencephalography (EEG) has been used to characterize abnormalities in brain function in a number of disorders, including cocaine dependence, but this technique has not been used to characterize abnormalities associated with methamphetamine dependence. The sample included 11 methamphetamine dependent subjects and 11 non-drug using volunteers. Methamphetamine dependent subjects were hospitalized for 4 days to document abstinence; non-drug using volunteers were studied as outpatients. EEGs were recorded in the eyes-closed resting state, and absolute EEG power in each frequency band (0.5-4, 4-8, 8-12, and 12-20 Hz) was quantitated using a fast Fourier transform. EEG power was log-transformed prior to analysis. Conventional, EEG tracings were interpreted by a qualified electroencephalographer who was blinded to the subjects' identity. Methamphetamine dependent volunteers with 4 days of abstinence had increased EEG power in the delta and theta bands. Power in the alpha and beta bands did not differ between the groups. Within the methamphetamine dependent group, a majority of the conventional EEGs were abnormal (64%), compared to 18% in the non-methamphetamine using group. Recently abstinent methamphetamine dependent subjects demonstrate QEEG abnormalities that are consistent with a generalized encephalopathy. Encephalopathic changes in brain electrical activity, as found here in methamphetamine dependence, are frequently associated with a range of cognitive and psychiatric abnormalities, suggesting further avenues of investigation.

Reflection of the intelligence structure in the spatiotemporal features of baseline EEG

The EEG correlates of the verbal, numerical, and figural IQ components according to the power and coherence characteristics of the baseline EEG in six frequency bands were studied taking into account personality traits of subjects (extroversion, neuroticism, psychoticism, and anxiety). Analysis of variance and correlation showed that a decreased power of the low-frequency θ1, 2and α1 rhythms and increased EEG power in the β2 band with the right-hemispheric dominance were characteristic of persons with higher intelligence. These EEG characteristics were associated with increased interhemispheric interaction according to the coherence indices and increased coherence within the right hemisphere. Each of the intelligence components (verbal, numerical, and figural) was characterized by a specific baseline frequency–spatial EEG pattern distinguished by specific interactions, predominantly, between the frontal and caudal cortical regions in the θ and/or β2 frequency bands.

Sleep states and sleep electroencephalographic spectral power in mice lacking the β 3 subunit of the GABA A receptor

Mice lacking the GABA A receptor β 3 subunit exhibit a profound disruption in thalamic circuitry. We have studied sleep in these mice under baseline conditions and following treatment with the benzodiazepine midazolam. Under baseline conditions, NREM sleep time did not differ between β 3 subunit knockout mice and wild type mice, while REM sleep time was significantly lower in knockout mice than in wild type mice during the light portion of a 24-h light–dark cycle. In constant dark conditions, circadian rhythmicity remained intact in mutant mice for a period of at least 9 days. EEG delta power (1–4 Hz) was significantly greater in the knockout than in wild type mice during NREM sleep but not during other states. A transient increase in EEG power in the 12–16 Hz range that occurred in wild type mice just prior to the transition from NREM to REM sleep was present but significantly blunted in the knockout. Midazolam decreased NREM delta power and REM time in wild type mice. The former but not the latter response to midazolam was intact in the knockout. These results further support a role for GABAergic transmission in regulating REM sleep and EEG spectral phenomena associated with NREM sleep.

Regional Differences of the Human Sleep Electroencephalogram in Response to Selective Slow-wave Sleep Deprivation

The purpose of this study was to assess the topographic changes in sleep recuperative processes in response to selective slow-wave sleep (SWS) deprivation. SWS was suppressed on two consecutive nights by means of acoustic stimulation. The electroencephalogram (EEG) power of baseline, deprivation and recovery nights was analysed in 1 Hz bins. During the SWS deprivation nights, large decreases of EEG power were found at frontopolar, central and parietal derivations encompassing the delta, theta and alpha range, while only slow delta (0.5-2 Hz) was affected at the frontal derivation. Recovery sleep was characterized by a generalized increase of power during non-REM sleep encompassing the delta, theta and alpha bands, with a clear antero-posterior gradient. The coherent behaviour of different EEG bands with traditionally different electrophysiological meanings during non-REM sleep suggests that, in light of the recent advances in sleep neurophysiology, a re-examination of the functional role of EEG rhythms during sleep is needed. The 'resistance' to selective SWS deprivation of the frontal area, together with its larger increase of EEG power during recovery, may be interpreted as a sign of a greater sleep need of the frontal cortical areas, confirming that some aspects of the regulatory processes of human sleep are local in nature and may show use-dependent characteristics.

Effects of phencyclidine (PCP) and MK 801 on the EEGq in the prefrontal cortex of conscious rats; antagonism by clozapine, and antagonists of AMPA-, alpha(1)- and 5-HT(2A)-receptors.

1. The electroencephalographic (EEG) effects of the propsychotic agent phencyclidine (PCP), were studied in conscious rats using power spectra (0 - 30 Hz), from the prefrontal cortex or sensorimotor cortex. PCP (0.1 - 3 mg kg(-1) s.c.) caused a marked dose-dependent increase in EEG power in the frontal cortex at 1 - 3 Hz with decreases in power at higher frequencies (9 - 30 Hz). At high doses (3 mg kg(-1) s.c.) the entire spectrum shifted to more positive values, indicating an increase in cortical synchronization. MK 801 (0.05 - 0.1 mg kg(-1) i.p.) caused similar effects but with lesser changes in power. 2. In contrast, the non-competitive AMPA antagonists GYKI 52466 and GYKI 53655 increased EEG power over the whole power spectrum (1 - 10 mg kg(-1) i.p.). The atypical antipsychotic clozapine (0.2 mg kg(-1) s.c.) synchronized the EEG (peak 8 Hz). The 5-HT(2A)-antagonist, M100907, specifically increased EEG power at 2 - 3 Hz at low doses (10 and 50 microg kg(-1) s.c.), whereas at higher doses (0.1 mg kg(-1) s.c.) the profile resembled that of clozapine. 3. Clozapine (0.2 mg kg(-1) s.c. ), GYKI 53655 (5 mg kg(-1) i.p.), prazosin (0.05 and 0.1 mg kg(-1) i.p.), and M100907 (0.01 and 0.05 mg kg(-1) s.c.) antagonized the decrease in power between 5 and 30 Hz caused by PCP (1 mg kg(-1) s.c.), but not the increase in power at 1 - 3 Hz in prefrontal cortex.

Interhemispheric asymmetry of human sleep EEG in response to selective slow-wave sleep deprivation.

Recent evidence suggests that the human sleep electroencephalogram (EEG) shows regional differences over both the sagittal and coronal planes. In the present study, in a group of 10 right-handers, the authors investigated the presence of hemispheric asymmetries in the homeostatic regulation of human sleep EEG power during and after selective slow-wave sleep (SWS) deprivation. The SWS deprivation was slightly more effective over the right hemisphere, but the left hemisphere showed a markedly larger increase of EEG power in the 1.00-24.75 Hz range during recovery-night non-REM sleep, and a larger increase of EEG power during both deprivation-night and recovery-night REM sleep. These results support the greater need for sleep recuperative processes of the left hemisphere, suggesting that local sleep regulation processes may also act during REM sleep.

Eptastigmine: ten years of pharmacology, toxicology, pharmacokinetic, and clinical studies.

Eptastigmine (heptyl-physostigmine tartrate) is a carbamate derivative of physostigmine in which the carbamoylmethyl group in position 5 of the side chain has been substituted with a carbamoylheptyl group. In vitro and ex vivo results suggest that eptastigmine has a long-lasting reversible brain cholinesterase (i.e., acetylcholinesterase and butyryl-cholinesterase) inhibitory effect. When administered in vivo to rodents by various routes, eptastigmine inhibits cerebral acetylcholinesterases (AChE) and increases acetylcholine (Ach) brain levels by 2500-3000%, depending on the dose. This effect leads to an improvement in the cerebral blood flow in the ischemic brain, excitatory and inhibitory effects on the gastrointestinal tract and to a protection from acute soman and diisopropylfluorophosphate intoxication. Eptastigmine, by either acute or chronic administration, has been found to have memory enhancing effects in different species of normal, aged and lesioned animals. It also restored to normal the age-related increase of EEG power without affecting spontaneous motor activity. Clinical investigations on more than 1500 patients with Alzheimer's disease demonstrated that eptastigmine significantly improved cognitive performance (as assessed by the cognitive subscale of the Alzheimer's Disease Assessment Scale) as compared with placebo. This improvement was most evident in patients with more severe cognitive impairment at the baseline. The relationship between patient performance and average steady-state AChE inhibition was described by an inverted U-shaped dose-response curve. Pharmacokinetic studies have revealed that after oral administration eptastigmine is rapidly distributed to the tissues and readily enters the CNS, where it can be expected to inhibit AChE for a prolonged period. Eptastigmine is generally well tolerated and the majority of adverse events (cholinergic) were mild to moderate in intensity. However, the adverse hematologic (granulocytopenia) effects reported in two studies have resulted in the suspension of further clinical trials.

Seasonal affective disorder: spatial organization of EEG power and coherence in the depressive state and in light-induced and summer remission

The present study analyzed EEG power and coherence in subjects with seasonal affective disorder (SAD) during depressive episodes and during light-induced and summer remission. Baseline EEG activity was recorded during the winter period before light treatment (31 SAD patients, 30 control subjects); after 10 days of 2-h morning light treatment (10 SAD subjects); and during the summer period (14 SAD subjects, 27 control subjects). EEG power and coherence were calculated for the delta, theta-1, theta-2, alpha, beta-1 and beta-2 frequency bands. Compared with control subjects, SAD subjects had lower than normal EEG power in most frequency bands; asymmetrical distribution of delta, theta-1, theta-2 and alpha activity in parietal and temporal regions due to increased EEG power over the left electrode sites; and beta activity in the lateral frontal region due to increased beta power over the right electrode site. The foci of decreased EEG coherence were mainly in the right and left frontal and the right posterior regions. Remitted SAD subjects showed normalization of inter-hemispheric asymmetry in lateral frontal areas; increases of delta, theta-2, and alpha activity compared with control values; theta-1 activity in excess of control values; and disappearance of the foci of decreased coherence in anterior areas of the left hemisphere.

EEG mapping in seasonal affective disorder

Given that the nature of hemispheric dysfunction is different in heterogeneous disorders, in the present investigation EEG power mapping was applied to establish neurophysiological profiles that might potentially discriminate patients with seasonal affective disorder (SAD) among other affective disorders. The baseline resting EEG activity was recorded from 31 depressed SAD patients and 30 controls. Power in the delta, theta-1, theta-2, alpha, beta-1 and beta-2 frequency bands was extracted by Fourier transformation. Patients were found to have a lower delta (in central, parietal, occipital, temporal, posterior-temporal areas), theta-1 (in central and parietal), theta-2 (in anterior-frontal, parietal, occipital) and alpha activity (in anterior-frontal, midfrontal, central, parietal and occipital areas) than controls. SAD subjects showed, compared to controls, an asymmetrical distribution of delta, theta-1, theta-2 and alpha activity in parietal and temporal regions due to an increase of EEG power over the right electrode sites, and beta activity in the lateral frontal region due to an increase of beta power over the right electrode site. It is assumed that differential hemispheric contributions of EEG spectra may discriminate between the varieties of depression or different depressive states.

Electroencephalogram Spectral Characteristics After Alcohol Ingestion in Japanese Men With Aldehyde Dehydrogenase-2 Genetic Variations: Comparison With Peripheral Changes

Background : Electroencephalographic (EEG) activity induced by alcohol ingestion may be influenced by individual differences in alcohol metabolism. Specifically, an absence of the low Km isozyme of aldehyde dehydrogenase (ALDH), found in many Asians, may be related to alterations of EEGs. Methods: EEG power spectral changes induced by 0.4 ml/kg of alcohol ingestion were compared in two groups of Japanese subjects: NN (ALDH2*1/1, n= 19) and ND (ALDH2*2/1, n= 12). Peripheral changes in heart rate and facial skin temperature were evaluated after the same treatment. Blood ethanol, acetaldehyde, and catecholamine levels were determined to evaluate mediation of the ethanol metabolite, acetaldehyde, and its indirect action on EEGs through the effects on peripheral systems. Results: As expected, blood acetaldehyde was about 10-fold higher in the ND subjects compared with the NN subjects during the postingestion period. Ethanol produced characteristic EEG changes during and after ingestion. The ND subjects, however, displayed brief periods of decrease in slow α immediately after alcohol ingestion and showed no long-term EEG changes. The EEG changes were parallel to peripheral changes. Conclusions: The lack of increased EEG power in the ND subjects may be partly mediated by a direct action of the high concentration of acetaldehyde in the central nervous system that penetrates from the peripheral blood. In addition to this direct action of acetaldehyde, an indirect action, such as feedback from peripheral changes, might prevent the characteristic increase in α and β power observed in the NN subjects.

Electroencephalogram Spectral Characteristics After Alcohol Ingestion in Japanese Men With Aldehyde Dehydrogenase‐2 Genetic Variations: Comparison With Peripheral Changes

Electroencephalographic (EEG) activity induced by alcohol ingestion may be influenced by individual differences in alcohol metabolism. Specifically, an absence of the low Km isozyme of aldehyde dehydrogenase (ALDH), found in many Asians, may be related to alterations of EEGs. EEG power spectral changes induced by 0.4 ml/kg of alcohol ingestion were compared in two groups of Japanese subjects: NN (ALDH2*1/1, n = 19) and ND (ALDH2*2/1, n = 12). Peripheral changes in heart rate and facial skin temperature were evaluated after the same treatment. Blood ethanol, acetaldehyde, and catecholamine levels were determined to evaluate mediation of the ethanol metabolite, acetaldehyde, and its indirect action on EEGs through the effects on peripheral systems. As expected, blood acetaldehyde was about 10-fold higher in the ND subjects compared with the NN subjects during the postingestion period. Ethanol produced characteristic EEG changes during and after ingestion. The ND subjects, however, displayed brief periods of decrease in slow alpha immediately after alcohol ingestion and showed no long-term EEG changes. The EEG changes were parallel to peripheral changes. The lack of increased EEG power in the ND subjects may be partly mediated by a direct action of the high concentration of acetaldehyde in the central nervous system that penetrates from the peripheral blood. In addition to this direct action of acetaldehyde, an indirect action, such as feedback from peripheral changes, might prevent the characteristic increase in alpha and beta power observed in the NN subjects.

Le sommeil du fibromyalgique : revue des données cliniques et polygraphiques

Fibromyalgia syndrome is a common chronic pain syndrome that is often associated with sleep disturbances characterized by subjective experience of non-restorative sleep. The complaints of sleep disturbances are correlated with polysomnographic features showing clear abnormalities in the continuity of sleep as well as in the sleep architecture. Sleep-recording abnormalities are characterized by a reduced sleep efficiency with increased number of awakenings, a reduced amount of slow wave sleep and an abnormal alpha wave intrusion in non rapid eye movement, termed alpha-delta sleep. These data were confirmed by spectral analysis of sleep showing an increased EEG power density in the higher frequency band and a reduced EEG power density in the lower frequency bands. Moreover, other microstructural aspects of sleep were modified with high frequency of arousals and alpha-K complex reported, both indicators of fragmented sleep. The fibromyalgia symptoms may relate to a non-restorative sleep disorder associated with the alpha-EEG sleep anomalies. However, alpha-EEG sleep anomaly is non-specific for fibrositis, also seen in normal controls during stage 4 sleep deprivation. Moreover, fibromyalgia patients may also experience primary sleep disorder such as sleep apnea or periodic leg movements. The etiology of this common condition is incompletely understood and the existence of a specific entity of fibromyalgia is still a matter of debate. However, several studies have found abnormal brain metabolism of substances such as serotonin implicated in sleep arousal and pain mechanisms and administration of tricyclic antidepressants and selective serotonin reuptake inhibitors may be useful in fibromyalgia. Pain, poor sleep quality and anxiety may contribute to the clinical picture. Several factors such as psychological, environmental, genetic factor, altered serotonin metabolism and altered sleep physiology are involved in the pathogenesis of fibromyalgia.