Topographic brain mapping of EEG in neuropsychopharmacology--Part II. Clinical applications (pharmaco EEG imaging)

Multi-lead analysis of drug-induced changes in human brain function as monitored by the scalp-recorded electroencephalogram (EEG) and subsequent imaging of topographic pharmaco-EEG maps has become possible and practical with the advent of modern mini- and micro-computers. The present paper gives a survey about topographic analyses of pharmaco-EEG data obtained in systematic double-blind, placebo-controlled studies in normal healthy volunteers involving representative drugs of 5 different psychopharmacological classes, such as neuroleptics (chlorprothixene), antidepressants (imipramine), tranquilizers (diazepam), psychostimulants (caffeine), and antihypoxidotics/nootropics (pyritinol). The determination of cerebral bioavailability utilizing time- and dose-efficacy relations, as well as the evaluation of bioequipotency of different formulations of compounds is shown. Topographic pharmaco-EEG seems not only to confirm our previous knowledge that quantitative analysis of the human EEG in combination with certain statistical procedures ("quantitative pharmaco-EEG") is a valuable method to determine if, how, when and at which dosage a drug will be centrally effective, but also to have the potential to show effects of psychotropic drugs on the target organ--the human brain--which could not be previously picked up by single lead recordings. Topographic pharmaco-EEG imaging can be viewed as an enlargement of our armamentarium to better understand the mode of action of psychotropic drugs in human neuropsychopharmacology, as well as to monitor and (eventually) predict therapeutic efficacy in patients.     

咪达唑仑对人定量药物脑电图δ频段功率百分比的影响

目的观察咪达唑仑对人定量药物脑电图(QPEEG)δ频段功率百分比的影响。方法青年志愿者20人,每组10人,均为男性,分别静脉注射咪达唑仑0.05 mg.kg-1(Ⅰ组)、0.1 mg.kg-1(Ⅱ组),观察比较2组给药前后QPEEG的δ频段功率百分比。结果注射咪达唑仑后,Ⅱ组各导联QPEEGδ频段功率百分比均增加(P<0.01),5 min左右达高峰,约10 min恢复。Ⅰ组各导联QPEEGδ频段功率百分比有增加趋势,但与给药前比较差异无统计学意义(P>0.05)。结论咪达唑仑可剂量依赖性地增加人QPEEGδ频段功率百分比,提示QPEEGδ频段功率百分比可能成为监测咪达唑仑麻醉深度的指标。     

Classification and bioavailability studies with WE 941 by quantitative pharmaco-EEG and clinical analyses

Psychoactivity, pharmacodynamic properties and drug tolerance of 2-bromo-4-(2-chlorophenyl)-9-methyl-6H-thieno[3,2-f]1,2-(4-triazolo)[4,3-a][1,4]diazepine (WE 941), a new triazolodiazepine, were studied in 10 normal subjects utilizing quantitative pharmaco-EEG and clinical evaluation methods. In the double-blind, placebo-controlled trial, the subjects received randomized at weekly intervals oral single doses of 0.1 mg, 0.3 mg and 0.5 mg WE 941, placebo, and 30 mg flurazepam as reference substance. Measurements were obtained before and at the 2nd, 4th, 6th h post drug. EEG power spectral density analysis demonstrated no changes after placebo, while WE 941 and flurazepam induced statistically significant alterations characterized by an increase in beta-activity, a decrease in alpha-activity and increase in average frequency ("anxiolytic pharmaco-EEG profile"). In addition, 0.3 mg and 0.5 mg WE 941 and 30 mg flurazepam produced a significant augmentation of delta-activity indicating hypnotic qualities. Considering spontaneous and placebo-induced alterations, evaluation of the time- and dose-effect relationship indicated that all active substances exerted a tranquilizing effect throughout 8 h, while the hypnotic properties of 0.1 mg WE 941 were minimal (up to the 4th h), those of 0.3 mg WE 941 were moderate (up to 6 h) and those of 0.5 mg WE 941 were marked (up to 8 h). The dosage equipotent to 30 mg flurazepam is 0.3 mg WE 941. Heart rate and blood pressure exhibited no relevant changes, while side effects including fatigue, drowsiness and dizziness were mostly observed after the highest dosage of WE 941.     

Pharmaco-EEG study on vincamine and on teproside in patients with chronic cerebrovascular disease

Pharmaco-EEG is a technique used in diagnostic and in neuropharmacological research. Correlations between the ageing brain and EEG spectral analysis have been discovered (1-5). Typical EEG findings of multi-infarct dementia, senile dementia and chronic cerebrovascular disease have been reported by several authors. Using this methodology, it is possible to know if a drug crosses the blood brain barrier, the period of drug action and the drug-induced enhancement or inhibition of cerebral bioelectrical activity. It is also possible to ascertain the pharmacological class of a drug through a comparison between it and another that is well known. The authors have studied the pharmaco-EEG effects of teproside and vincamine in two groups of subjects affected by chronic cerebrovascular disease. The first group (8 patients, mean age 58.3 years) were treated with vincamine 15 mg i.v. EEG spectral analysis was performed using a Hewlett-Packard 5423 A analyser with centro-occipital derivations. EEG registrations were executed by using an epoch of 5 min at times- 15, 0, +15, +45, +60, and +120 min with drug administration at zero time. In a chronic study, after a three day wash-out period, teproside 240 mg/os/day was administered to the first group, while vincamine 60 mg/os/day and 120 mg/os/day was administered to the second group. Subjects were studied with EEG spectral analysis by using the same methodology at baseline and after 10 and 20 days of treatment. The two drugs induced an enhancement of cerebral bioelectrical activity by an improvement of alpha waves mean relative power, by a shifting toward rapid rhythms of dominant frequency and by a decrease of delta and theta waves mean relative power. With the dosages used teproside appeared to be more active than vincamine.     

Pharmaco-EEG test dose response predicts cholinesterase inhibitor treatment outcome in Alzheimer's disease

Previous investigations have indicated that a single dose pharmaco-EEG may predict the outcome of 4-7 weeks of tetrahydroaminoacridine (THA) treatment in dementia of the Alzheimer type (DAT). This open trial study further examined the relationship of quantitative EEG in relation to treatment response by assessing 24 probable DAT patients at baseline, 2 h after their first oral dose (30 mg), and after 12 weeks of THA treatment. Compared to EEG norms, patients, in general, evidenced EEG slowing, as shown by excessive slow (theta) and diminished fast (alpha and beta) wave power as well as reduced mean frequencies which were present prior to treatment as well as at the end of treatment. The EEG of patients exhibiting stable or improved scores on the Mini-Mental State examination (MMSE) at 12 weeks showed a significantly faster baseline mean alpha frequency as well as a significant reduction in relative theta power following the single THA test dose compared to deteriorated patients. A discriminant analysis using test dose response EEG variables correctly classified 75-79% of these two patient groups, suggesting that this procedure may be a useful approach for optimizing patient selection for antidementia treatments.     

Central effects and effective dose determination of suriclone (double-blind,controlled, phase I safety and quantitative pharmaco-EEG study)

Suriclone, a nonbenzodiazepine drug, shown to be anxiolytic in animal pharmacology, was investigated within a single dose tolerance and efficacy study using quantitative pharmaco-EEG. The investigation showed that suriclone is tolerable in single oral doses of up to 0.8 mg, the highest dose given in healthy volunteers. The minimum effective dose producing statistically significant CNS action was 0.3 mg. Suriclone produced significant dose- and time-related CNS effects. The onset of these effects was later than that of diazepam and its duration of action was longer. Suriclone was classified by the HZI computer EEG drug data base as anxiolytic at high doses. Among a variety of anxiolytics, the CNS effect of suriclone was most similar to that of diazepam. The optimal anxiolytic effective single dose of suriclone was predicted to be 0.6 mg.     

Discrimination of mode of action of anxiolytics using an integrated computer data bank and Dynamic Brain Mapping (CNS effects of diazepam and lorazepam)

In a double-blind, placebo-controlled, crossover study, the CNS effects of intravenously administered diazepam and lorazepam were investigated in anxious subjects through the quantitative pharmaco-EEG (QPEEG) method. For up to 4 1/2 hours following administration the effects of each substance on brain function were measured using computer analyzed EEG recordings (CEEG) and a new technique called Dynamic Brain Mapping. The following observations were made: 1. Both active drugs produce statistically significant CNS effects as measured by CEEG changes. These changes were observed earlier with diazepam than with lorazepam. 2. Although both compounds are classified as anxiolytic by the routine computer EEG data base, the detailed brain mapping technology indicated that the CNS effects of diazepam and lorazepam were quantitatively and qualitatively different. 3. Clinical CNS side-effects (sedation) were seen more frequently with lorazepam than with diazepam. This was consistent with the EEG slowing producing properties of lorazepam. The EEG fast activity which is characteristic for all anxiolytics was established more with diazepam than lorazepam.     

Quantitative EEG methods and measures in human psychopharmacological research

The quantitative analysis of electroencephalographic (EEG) signals is an established methodology for objectively describing the central impact of drugs administered to human subjects. This paper outlays the essential objectives and findings of this electrophysiologic measurement model of drug action and addresses the subject, recording, analytical and statistical standards which are required to ensure valid pharmaco-EEG profiling. Copyright 2000 John Wiley & Sons, Ltd.     

Topographic pharmaco-EEG mapping of increasing doses of buspirone and its comparison with diazepam

It has been argued that representative drugs of the main psychopharmacological classes induce similar pharmaco-EEG changes within groups but different changes between groups. The aim of this double-blind, cross-over, placebocontrolled study was to evaluate the effects of single oral doses of buspirone (BUS) 5, 15 and 30 mg in 15 healthy young subjects of both sexes on topographic maps of quantiative pharmaco-EEG, using diazepam (DZP) 10 mg as reference compound. Sixteen lead recordings of three-minute vigilance-controlled EEG (V-EEG) and four-minute resting EEG (R-EEG) were assessed at 0, 1, 2, 4, 6 and 8 hours after drug intake. EOG activity (vertical and horizontal) was also recorded in order to minimize ocular artifacts before applying an automatic artifact rejection method. MANOVA/Hotelling T² maps (multivariate analysis) showed a highly significant differentiation of DZP from placebo from the 1 st until the 8th hour all over the brain. After BUS a clear dose-response was observed with effects being greater and longer lasting with increasing doses, the highest showing a peak effect in the 2nd hour which lasted until the 4th hour, mostly in central regions. Maps of drug-induced pharmaco-EEG changes as compared to placebo-induced alterations (univariate analysis) demonstrated typical ‘anxiolytic pharmaco-EEG patterns’ after DZP, characterized by a decrease of total power, attenuation of alpha activity and augmentation of beta activity, as well as by an increase of the centroid and centroid deviation of the total activity. Furthermore, a decrease of the centroid of the combined delta-theta activity and an increase of the centroid of alpha activity was seen. In contrast, BUS produced an increase of theta activity with an acceleration of the centroid of the combined delta-theta activity, no modification of alpha activity but a slowing down of its centroid and a tendency to reduce beta activity. The centroid of the total activity was also decreased. Although both compounds have proven their ability to reduce anxiety in patients, their different neurophysiological profiles suggest different neurobiological mechanisms of action after acute administration.     

A pharmaco-EEG study on antipsychotic drugs in healthy volunteers

RATIONALE: Both psychotropic drugs and mental disorders have typical signatures in quantitative electroencephalography (EEG). Previous studies found that some psychotropic drugs had EEG effects opposite to the EEG effects of the mental disorders treated with these drugs (key-lock principle). OBJECTIVES: We performed a placebo-controlled pharmaco-EEG study on two conventional antipsychotics (chlorpromazine and haloperidol) and four atypical antipsychotics (olanzapine, perospirone, quetiapine, and risperidone) in healthy volunteers. We investigated differences between conventional and atypical drug effects and whether the drug effects were compatible with the key-lock principle. METHODS: Fourteen subjects underwent seven EEG recording sessions, one for each drug (dosage equivalent of 1 mg haloperidol). In a time-domain analysis, we quantified the EEG by identifying clusters of transiently stable EEG topographies (microstates). Frequency-domain analysis used absolute power across electrodes and the location of the center of gravity (centroid) of the spatial distribution of power in different frequency bands. RESULTS: Perospirone increased duration of a microstate class typically shortened in schizophrenics. Haloperidol increased mean microstate duration of all classes, increased alpha 1 and beta 1 power, and tended to shift the beta 1 centroid posterior. Quetiapine decreased alpha 1 power and shifted the centroid anterior in both alpha bands. Olanzapine shifted the centroid anterior in alpha 2 and beta 1. CONCLUSIONS: The increased microstate duration under perospirone and haloperidol was opposite to effects previously reported in schizophrenic patients, suggesting a key-lock mechanism. The opposite centroid changes induced by olanzapine and quetiapine compared to haloperidol might characterize the difference between conventional and atypical antipsychotics.     

Long-term effects of an organophosphate upon the human electroencephalogram.

The brain electrical activity of workers exposed to the organophosphate compound (OP), sarin, was compared to that of control subjects. Exposed workers had a history of one or more documented accidental exposures to toxic levels of sarin. However, no exposed subject had exposure within 1 year of his examination. The comparison included standard clinical electroencephalograms (EEGs), computer-derived EEG spectral analysis, and standard overnight sleep EEGs. It was not possible to diagnose subjects individually by expert visual inspection of their EEGs. However, statistically significant between-group differences for both the visually inspected and computer-derived data were reported by both univariate and multivariate statistical methods. Different EEG changes revealed by visual inspection and computer-derived spectral analysis appear to reflect the differing sensitivites of these two analytic techniques. Statistically significant group differences included increased beta activity, increased delta and theta slowing, decreased alpha activity, and increased amounts of rapid eye movement sleep in the exposed population. It is suggested that the above findings represent an unexpected persistence of known short-term OP actions. It is also suggested that these results, when taken along with the reported long-term behavioral effects of OP exposure, provide parallel evidence that OP exposure can produce long-term changes in brain function.     

Valproate monotherapy in juvenile myoclonic epilepsy: dose-related effects on electroencephalographic and other neurophysiologic tests

A neurophysiologic test battery (consisting of a 24-hour, seven-channel electroencephalogram [EEG], EEG spectral analysis, multiple sleep latency test, visual evoked potentials, critical flicker fusion, and visual contrast sensitivity) was administered twice to 16 patients with juvenile myoclonic epilepsy (JME) in a double-blind, randomized, crossover study comparing two daily doses of sodium valproate (VPA), 1000 mg and 2000 mg. Clinical observation time was 6 months for each dose. Mean total VPA concentration during low-dose treatment was 470.4 mmol/L and during high-dose treatment was 700.0 mmol/L. Ten patients had seizures during low-dose treatment, but only three of these showed spike-wave activity on EEGs. During high-dose treatment, nine patients had seizures; five of these had spike-wave activity. EEG power spectrum did not change between doses. The other tests also showed no change between doses. Our results suggested that EEG and our selection of other neurophysiologic tests were of limited value for monitoring seizure frequency and clinical effects of VPA.     

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.     

Pharmacodynamic modeling of thiopental anesthesia

We have pharmacodynamically modeled the relationship between the thiopental serum concentration and its effects on the electroencephalogram (EEG). Power spectral analysis was used to calculate the spectral edge, a measure of the underlying EEG frequency that characterizes the progressive slowing of the EEG induced by thiopental. Eight male volunteer subjects had venous thiopental serum concentrations measured, and 10 surgical patients had arterial serum concentrations measured. Thiopental was infused at a rate of 75 to 150 mg/min until a burst suppression EEG pattern was evident. Frequent blood samples were obtained during and after the infusion for measurement of serum thiopental concentrations, and the EEG was recorded for subsequent off-line power spectral analysis to calculate the spectral edge. With venous blood sampling, it was not possible to demonstrate significant hysteresis between the thiopental serum concentration and the spectral edge, allowing thiopental concentrations to be directly related to the spectral edge. With arterial blood sampling, significant hysteresis was present, requiring an effect compartment to relate concentration to effect. The half-time for equilibration (mean +/- SD) between concentration and response for the arterial data was 1.2 +/- 0.30 min. This value for Keo is consistent with known values for cerebral blood flow and thiopental brain: blood partition coefficient. Arterial-venous concentration differences cause the apparent lack of hysteresis with venous blood sampling. An inhibitory sigmoid Emax pharmacodynamic model optimally characterized the relationship between thiopental concentrations and the spectral edge. This model allows estimation of the thiopental serum concentration that causes one-half of the maximal EEG slowing (IC50), which is a measure of an individual's sensitivity to thiopental. Except for the hysteresis, there was no statistical difference in the parameters of the inhibitory sigmoid Emax pharmacodynamic model when venous and arterial blood samplings were compared. Arterial blood sampling offers some distinct advantages when pharmacodynamically modeling continuous, rapidly changing measures of drug effect, such as the EEG.     

Comparative bioavailability studies with a new mixed-micelles solution of diazepam utilizing radioreceptor assay, psychometry and EEG brain mapping

In a double-blind, placebo-controlled study the pharmacokinetic and pharmacodynamic properties of a standard solution of diazepam (DZ) (ValiumR) were compared with those of a novel diazepam mixed-micelles solution (DZ MM) (Valium MMR) both after i.v. and i.m. application utilizing radioreceptor assay, quantitative pharmaco-EEG and brain mapping techniques as well as psychometric and psychophysiological methods. The local tolerance was studied as well. The subjects received randomized and, in weekly intervals, following injections: (1) 10 mg DZ i.v. + placebo i.m.; (2) 10 mg DZ MM i.v. + placebo i.m.; (3) placebo i.v. + 10 mg DZ i.m.; (4) placebo i.v. + 10 mg DZ MM i.m.; (5) placebo i.v. + placebo i.m. Blood sampling, EEG-recordings, psychometric and psychophysiological tests as well as tolerance evaluations were carried out at 0, 1/2, 1, 2, 4, 6 and 8 h. Blood level evaluation demonstrated after i.m. application a significantly shortened tmax, a higher Cmax and generally higher plasma concentrations in the first and second hour following the mixed-micelles solution than the standard formulation, which suggests better absorption of the former than the latter in the muscle. Subsequent to i.v. administration, lower blood levels were observed between 30 min and 2 h after DZ MM than DZ. Power spectral density analysis of the EEG resulted in typical anxiolytic-sedative pharmaco-EEG profiles after all 4 active substances as compared with placebo. However, there were significant inter-drug differences as far as topographic aspects (pharmaco-EEG maps) were concerned. DZ MM i.v. induced significantly more initial but also late delta augmentation, alpha attenuation and centroid slowing than DZ i.v. which suggests more sedative effects at those times. Following i.m. application, a significantly more pronounced delta/theta attenuation, beta augmentation and centroid acceleration after DZ MM than DZ suggested more anxiolytic effects of the novel than the standard formulation. Discriminant analysis of changes in 6 thymopsychic, 12 noopsychic and 17 psychophysiological variables demonstrated the best discrimination of the 4 substances based on thymopsychic effects. Considering the latter, all 4 active compounds differed significantly from placebo, with no inter-drug differences after i.v. application but a marked superiority of the novel mixed-micelles solution over the standard solution after i.m. application. Specifically, DZ MM i.m. induced more desactivation and affect-attenuation than DZ i.m.(ABSTRACT TRUNCATED AT 400 WORDS)     

EEG and blood level of the potential antidepressant paroxetine after a single oral dose to normal volunteers

The quantitative electroencephalogram (EEG) and plasma concentration of the antidepressant paroxetine were monitored in five normal volunteers after a single oral dose of 70 mg paroxetine and placebo. Peak plasma concentration occurred 4–6 h post-dose. Placebo had little effect on the EEG but the effects of paroxetine were statistically significant at 6 h post-dose. The EEG changes after treatment consisted of a decrease in delta and theta activity (< 8 Hz) and increase in beta activity (>12 Hz). These changes were still evident 72 h after treatment. The EEG profile obtained with 70 mg paroxetine is similar to that reported for other antidepressant 5-HT uptake inhibitors, but dissimilar to the classical, sedative antidepressants.     

Analysis of sleep EEG microstructure in subchronic paroxetine treatment of healthy subjects

Paroxetine is a selective and potent serotonin reuptake inhibitor and its efficacy for the treatment of depression has been proven. Under acute and subchronical treatment regimens, disturbances of the regular sleep pattern are a reported side effect of the drug. The present study was therefore performed to investigate the impact of subchronic treatment with the selective serotonin reuptake inhibitor paroxetine on the microstructure of the sleep EEG. The study especially addressed the question of subchronic effects of paroxetine medication (30 mg/day) in eight healthy male volunteers in a double blind, placebo-controlled crossover design. Conventional sleep EEG parameters and a spectral power analysis for different sleep stages after 4 weeks of treatment were computed. Additionally, the correlation of certain EEG rhythms across the night was calculated in order to detect subtle dynamical EEG alterations, not necessarily obvious when regarding conventional EEG analysis. Although we could not detect any alterations of the spectral power values in certain frequency bands either during NREM nor during REM sleep following subchronic paroxetine medication, the dynamical EEG attributes across the night revealed a significant enhancement of the correlation between certain EEG rhythms mainly during NREM sleep. Received: 18 July 1996 /Final version: 19 February 1997     

Effects of nonsedating histamine H1-antagonists on EEG activity and behavior in the cat

The central effects of the newly-developed antihistamines (H1-receptor antagonists) loratadine, astemizole, mequitazine and terfenadine were evaluated by studying brain electrical activity (EEG), sleep-waking patterns and behavior in the cat. The different stages of the sleep-waking cycle, i.e., wakefulness (W), spindle sleep (SS), slow wave sleep (SWS) and REM sleep (REM) were evaluated. The power spectrum analysis of the EEG was obtained by a computerized technique. For comparison, the sedating agent diphenhydramine was examined. Given at 3 mg/kg orally, a dose slightly above that effective therapeutically, diphenhydramine markedly affected behavior and all sleep stages. In particular, it depressed REM and increased SS (drowsiness). The EEG showed occasional spikes typical of subconvulsive states. Loratadine did not modify either sleep patterns or behavior over the 3-30 mg/kg dose range orally, which is far above that used clinically. The EEG, evaluated either visually or by spectral power analysis, was unaffected. Astemizole at 10 and 30 mg/kg PO reduced REM, markedly altered behavior at 30 mg/kg, but did not modify EEG activity. Mequitazine, at low doses (1-10 mg/kg PO), enhanced SS and decreased SWS and REM. Like diphenhydramine, mequitazine induced EEG changes typical of subconvulsive states and affected EEG power over the frequency range of 0.1-15.0 Hz. Terfenadine did not change sleep patterns and slightly affected behavior only at the high dose of 30 mg/kg orally; EEG activity was not influenced. These data show that: a) diphenhydramine and mequitazine appear to produce CNS effects by altering basic processes within the brain; b) astemizole and terfenadine seem to cross the blood-brain barrier at high doses only; c) loratadine has the lowest liability to produce central side effects. Of the sleep features examined, REM appeared to be the most sensitive stage to blockade of central H1-receptor pathways.     

家兔常规定量脑电图的描记

目的建立清醒状态下家兔定量脑电图(BEAM)的描记方法。方法用CFM-8型21导数字化EEG机记录126只家兔左、右脑的额、颞、顶、枕各区的BEAM。结果用本方法可成功地记录清醒兔的BEAM。与正常成人EEG以α波为主、枕区能量最高不同,兔以θ频段分布最广泛,以顶区能量最高。此外,人的β频段也低于家兔。结论清醒状态下家兔BEAM稳定可靠,可作为研究药物定量脑电图的模型。     

Acute alcohol poisoning in man: An experimental electrophysiological study

Spontaneous (EEG) and visual evoked (V.E.P.) electroencephalographic activity have been longitudinally studied during acute alcohol poisoning in 8 young voluntary subjects; a comparison with i) neuropsychiatric state of the subject, ii) alcoholic haematic rate and iii) the time of reaction to different sensorial and sensitive stimulations has been made. A spectral EEG analysis has been carried out and the temporal behaviour of four main frequency bands has been studied.

1. The V.E.P. can show alterations both in the latency and amplitude of its components as well as in morphology; such effects may alter from subject to subject.
2. EEG alterations are as follows:

1. a constant slacking of alpha rhythm (about 1 c/s) occurs, which is parallel to its amount reduction.
2. a new slow activity is always verified. Band analysis shows that it can belong to every value under the alphfa frequency, namely to the 0–3.2 c/s band.

1. EEG alterations are not timely corrlated, either with neuropsychiatric changes or the alcohol hematic level.