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Biomedical subjects

P Anderer

Publications and source records attributed to P Anderer.

At least 73 records · Page 4Linked to original sources
PubMed1994

Clinical, EEG mapping and psychometric studies in negative schizophrenia: comparative trials with amisulpride and fluphenazine.

Based on recent quantitative EEG findings of increased slow activity in negative schizophrenia indicating organicity, it was hypothesized that neuroleptics decreasing delta/theta activity should be beneficial for schizophrenics with predominantly negative symptoms. Thus, a double-blind, clinical, psychometric and neurophysiological study was carried out in 40 hospitalized patients with unproductive schizophrenia (mean age: 31 years; ICD diagnoses: 295.0, 295.1 and 295.6) who were treated randomly either with the benzamide amisulpride (AMI; n = 19) or low doses of fluphenazine (FLU; n = 21). In the first 2 weeks the daily doses were 50 mg AMI or 2 mg FLU, respectively, from the third week on up to the sixth week 100 mg AMI and 4 mg FLU. Clinical evaluations, psychometry and EEG mapping were performed on day 1 (hours 0 and 4--acute effect), on day 14 (hour 0--subacute effect) and on day 42 (hours 0 and 4--chronic and superimposed effects). Three AMI patients discontinued therapy prematurely because of productive symptoms (days 14, 28 and 35), while in the FLU group 2 patients dropped out due to depressive symptoms (days 21, 28), 1 due to productive symptoms (day 35), 1 due to ineffectiveness (day 28), and 1 because of an akinetic crisis (day 6). Statistical evaluation demonstrated a significant improvement in the AMDP apathy and Andreasen SANS score in both groups with the patients remaining severely ill as rated by the CGI. FLU-treated patients needed significantly more anticholinergic medication than the AMI-treated group. Psychometric evaluation showed in regard to the noopsyche significant improvement after subacute, chronic and superimposed AMI, while FLU-treated patients showed significant improvement only after subacute treatment. AMI was significantly superior to FLU at the hours 0 and 4 of day 42. The thymopsyche improved after subacute, chronic and superimposed administration of both compounds with a significant superiority of AMI on days 14 and 42 (4 h postdrug). EEG mapping showed a decrease of delta/theta and increase of beta activity as well as an acceleration of the centroid after acute and superimposed AMI on day 42 as compared with baseline; FLU patients exhibited a decrease of delta/theta activity and an acceleration of the total centroid too, while alpha activity was augmented and beta activity tended to be reduced. Our study demonstrated that, in addition to the new benzamide AMI, FLU in low doses may also be regarded as a neuroleptic with activating properties and may be utilized in the treatment of schizophrenics with predominantly negative symptoms.

Adult↗
PubMed1994

Automatic sleep-spindle detection procedure: aspects of reliability and validity.

The paper describes a reliable and valid method for the automatic detection of sleep spindles in whole night polygraphy. The recording of a multi-channel EEG during sleep polysomnography was performed in 10 healthy volunteers aged 20-35 years. This objective method should improve the time-consuming and subjective visual evaluation by increasing the accuracy and allowing the calculation of quantitative variables (i.e., frequency and amplitude), thereby facilitating scientific work with quantitative data. An important part of the method is the treatment of artifacts (i.e., muscle and spindle-like alpha activity). Compared to hardware solutions, our software method has the advantage of higher flexibility in regard to artifact identification and usual spindle definitions.

Adult↗
PubMed1993

Topographic mapping of EEG during sleep.

Topographic aspects of all night sleep EEG were investigated in 10 healthy volunteers (age 20-35 years). EEG brain maps showed an increase of delta power from stage 1 to 4, a decrease of alpha power most pronounced parieto-occipitally and a slowing of the dominant alpha frequency. Differences of EEG power in different sleep stages (as compared to wakefulness) are displayed topographically. Analysis of the course of stage 2 showed an increase of delta power and a decrease of theta power in the first sections of the night, and an increase of beta power later in the night.

Adult↗
PubMed1993

Acute effects of the novel antidepressant venlafaxine on cognitive event-related potentials (P300), eye blink rate and mood in young healthy subjects.

Venlafaxine is a novel non-tricyclic antidepressant, which preclinically has demonstrated serotonin, norepinephrine, and dopamine reuptake inhibiting effects. In this study acute effects of single oral doses of placebo, 12.5 mg, 25 mg, and 50 mg venlafaxine on event-related potentials (ERPs), eye blink rate and mood were studied in 16 healthy subjects. ERPs were investigated in an auditory odd-ball paradigm before as well as 3 h after each drug intake. In addition to 17 EEG leads, vertical and horizontal EOGs were recorded. After EOG minimization and visual artefact rejection the peak latencies of the spatial average were determined by an automatic procedure. The applied methods of data acquisition, artefact processing, objective component determination and statistical analysis were successful in describing acute effects of venlafaxine on ERPs in normals. N1 and P2 latencies were not affected. An increase in P2 amplitude in the relevant central and frontal regions was seen, reflecting some effect on automatic information processing. Stimulus evaluation time was not affected, as P300 latency remained unchanged. P300 amplitude was not affected at the relevant central and parietal region. Blink rate was not changed. By means of the adjective checklist a dose-dependent decrease of "extroversion" and "high spirits" and an increase of "introversion" was observed. Our findings suggest that venlafaxine affects human information processing less than would be expected from the more centrally inhibiting classical antidepressants.

Adult↗
PubMed1993

Treatment of the alcoholic organic brain syndrome: double-blind, placebo-controlled clinical, psychometric and electroencephalographic mapping studies with modafinil.

In a double-blind study 40 abstinent hospitalized male patients with an alcoholic organic brain syndrome (OBS; ICD 9: 291.2) were treated for 6 weeks with either placebo or 200 mg modafinil b.i.d. Modafinil (CRL 40476) is a vigilance-promoting, putative central alpha 1-adrenergic agonist with a pharmacological profile quite different from that of amphetamine. Clinical investigations demonstrated that the spontaneous remission of the alcoholic OBS was augmented and accelerated by modafinil, which was found significant as compared with placebo by confirmatory statistics in the target variable, the Clinical Global Impression scale. The drug was well tolerated. Psychometric tests revealed significant improvement of the noopsyche after modafinil as compared with placebo, while the thymopsyche and psychophysiological measurements were not affected. Electroencephalographic mapping showed significant differences between the central effects of modafinil and placebo indicating an improvement of vigilance under modafinil. Typical vigilance-promoting properties were seen after acute drug administration, were less evident before the morning dose after chronic treatment but re-occurred after super-imposed daily drug administration. Thus, our clinical, psychometric and neurophysiological investigations in alcoholic OBS patients demonstrated a therapeutic effect of modafinil in the early phase of abstinence.

Adult↗
PubMed1993

Restriction to a limited set of EEG-target variables may lead to misinterpretation of pharmaco-EEG results.

The number and types of target variables quantified from the spectrally analyzed EEG used in topographic pharmaco-EEG studies are still being discussed. Drug-induced changes of target variables obtained in the alpha frequency band--four absolute and four relative powers as well as three frequency measures--were utilized to assess the effects of xantinolnicotinate in demented patients using a parallel group design and the effects of buspirone in a double-blind, placebo-controlled crossover design. We conclude that for the proper evaluation of the different drug effects on the alpha activity, all these target variables should be considered. Descriptive p values of multiple comparisons within the framework of descriptive data analyses are important tools in interpreting drug effects.

Adolescent↗
PubMed1993

Clinical-pharmacological study with the two isomers (d-, l-) of fenfluramine and its comparison with chlorpromazine and d-amphetamine: blood levels, EEG mapping and safety evaluation.

In a double-blind, placebo-controlled, crossover study, the blood levels and pharmacodynamic properties of single oral doses of 15 and 30 mg d-fenfluramine (d-FEN) and 30 mg l-fenfluramine (l-FEN) were investigated as compared with 50 mg chlorpromazine (CPZ) and 20 mg d-amphetamine (AMPH) utilizing pharmaco-electroencephalogram (EEG) mapping as well as prolactin and safety assessments. Eighteen healthy young volunteers randomly (Latin square) received at weekly intervals the different treatments. Blood sampling to determine AMPH, FEN and its main metabolite norFEN, as well as plasma prolactic levels, EEG recordings and evaluation of hemodynamics and spontaneous side effects were carried out at 0, 2, 4, 6 and 8 h after drug administration. Before and 24 h after drug intake morning subjective sleep quality was also assessed. Blood level investigations after d-FEN demonstrated dose-dependent blood concentrations peaking after 2-4 h and slowly declining thereafter. NorFEN, the main metabolite, exhibited a steady increase in plasma concentrations up to the 8th h. After l-FEN a similar time course was obtained but the concentrations of the parent compound were higher and those of the metabolite lower in comparison with the d-isomer, suggesting stereoselective kinetics. d-FEN induced significant and dose-dependent pharmaco-EEG changes characterized by a decrease in total power and combined delta/theta activity and by an increase in beta activity and an acceleration of the centroid of the total activity with no changes in alpha power, which were quite different from those of the reference drugs. l-FEN produced only minimal changes (of the same type as d-FEN). 50 mg CPZ and 20 mg d-AMPH produced significant changes as compared to placebo but with quite opposite patterns, the former exhibiting the typical sedative-neuroleptic profile and the latter that typical of psychostimulants. Dose/treatment- and time-efficacy calculations based on all variables showed in the V-EEG that only 30 mg d-FEN and 50 mg CPZ were different from placebo (with peak effects in the 8th and 4th h, respectively), while in the resting condition (R-EEG) all drugs/dosages but 30 mg l-FEN differed from placebo (with the peak effect occurring in the 4th-6th h after d-FEN and l-FEN, in the 2nd h after CPZ and in the 4th-6th h after AMPH). Plasma prolactin levels were only modified by CPZ (maximal increase in the 2nd h).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

[Clinical and EEG/ERP brain mapping studies with vigabatrin in therapy refractory epileptic patients].

In a single blind study the antiepileptic effects and safety of vigabatrin--a new anticonvulsant drug selectively inhibiting GABA-transaminase--was investigated in therapy resistant epilepsy, along with its central effects objectivated by mapping of EEG and event-related potentials (ERP). In addition to their current antiepileptic therapy, 10 patients with complex partial seizures (CP) (4 male, 6 female), aged between 22 and 57 years received placebo for 1 month, subsequently 2 g vigabatrin for 2 months and thereafter a titrated optimal dosage vigabatrin for another 2 months. Clinical investigations were carried out at the afore-mentioned periods, neurophysiological ones pre and post 2 months vigabatrin. After 2 months vigabatrin, 5 out of 10 patients had a 50% or greater decrease in CP frequency, after another 2 months 7 out of 10. The median number of CP per months decreased from 5.5 to 3.75 (p < 0.05) to 2.0 (p < 0.01), respectively. No clinically relevant side effects and laboratory changes were noted. EEG mapping showed decreased fast alpha and slow beta power and increased delta-theta frequency variability, reflecting most likely a decreased CP disposition. ERP mapping showed slightly increased N1 and P2 as well as reduced P300 amplitudes. Unchanged P300 latency indicated no delayed stimulus evaluation time after vigabatrin therapy.

Adult↗
PubMed1992

EEG mapping and psychopharmacological studies with denbufylline in SDAT and MID.

Computed tomography (CT), electroencephalograms (EEG), clinical and psychometric data were obtained in 96 mildly to moderately demented patients (72 women, 24 men), aged 61-96 years (mean 82), diagnosed according to DSM-III criteria. Patients were off drugs for at least 2 weeks and subdiagnosed according to the modified Marshall-Hachinski ischemic score and CT in 45 senile dementia of the Alzheimer type (SDAT) and 51 multiinfarct dementia (MID) patients. Evaluations were carried out before and 12 weeks after treatment with either 100 mg denbufylline BID or placebo and included EEG mapping, the Sandoz Clinical Assessment Geriatric (SCAG) score/factors, the Clinical Global Impression (CGI), the Digit Symbol Substitution Test (DSST), the Trail-Making Test (TMT) and the Digit Span Test (DS). Descriptive data analysis including confirmatory statements found delta/theta activity enhanced, alpha and beta activity reduced, total power augmented, and the centroid slowed down over various brain regions in patients as compared with controls. The two subtypes of dementia could be differentiated in some conventional EEG variables but mostly by means of power asymmetry indices. Denbufylline induced a statistically significant and clinically relevant improvement in both SDAT and MID patients, whereas after placebo this was not the case in CGI, the TMT, and the DS, with interdrug differences being significant in all primary target variables such as the CGI, MMS, SCAG, and DSST. Thus, both the degenerative and vascular type of dementia exhibited a therapeutic benefit that could be objectified at the neurophysiological level by EEG mapping in an improvement of vigilance.

Aged↗
PubMed1992

Dose-response studies with co-dergocrine mesylate under hypoxia utilizing EEG mapping and psychometry.

In a double-blind, placebo-controlled trial, human brain function and mental performance were studied under two different degrees of hypoxia after administration of two different doses (6 mg and 9 mg) of co-dergocrine mesylate (CDM) utilizing blood gas analysis, EEG mapping and psychometry. Hypoxic hypoxidosis (i.e. impairment of cerebral metabolism due to hypoxia) was experimentally induced by a fixed gas combination of 9.8% oxygen (O2) and 90.2% nitrogen (N2) (found in 6000 m altitude), and of 8.6% O2, 91.4% N2 (found in 7000 m altitude), which was inhaled for 23 min under normobaric conditions by 18 healthy volunteers. They received randomized after an adaptation session placebo, 6 mg and 9 mg co-dergocrine mesylate (CDM). Evaluation of blood gases, brain mapping and psychometry was carried out at 0, 2, 4, 6, 8 h after oral drug administration. Blood gas analysis demonstrated a drop in PO2 to 42 and 32 mm Hg 23 min after inhalation of the 9.8% and 8.6% gas mixture, respectively, PCO2 decreased to 32 and 31 mm Hg, pH increased to 7.46 and 7.47 and base excess increased to 0.50 and 0.90 nmol/l, respectively. EEG mapping demonstrated an increase in delta and decrease of alpha power and a slowing of the centroid over almost the whole brain. 6 mg and slightly less so 9 mg CDM attenuated this deterioration of vigilance (i.e. dynamic state of the neuronal network determining adaptive behavior). At the behavioral level, moderate hypoxia induced a deterioration of noopsychic performance, which was mitigated by 6 mg, but not by 9 mg CDM. A deepening of the hypoxia resulted in a loss of these brain protective effects of both doses. Decrement of the thymopsyche increased after both doses in the moderate hypoxic condition, while under marked hypoxia 6 mg CDM attenuated and 9 mg aggravated this deterioration. Time-wise, brain protective effects reached the level of statistical difference between the 2nd and the 6th hour. Somatic complaints like feeling dazed, giddiness and headache were mitigated dose dependently by CDM in the moderate, but not in the marked hypoxic hypoxidosis.

Adult↗
PubMed1992

Topographic mapping of long latency "cognitive" event-related potentials (P 300): a double-blind, placebo-controlled study with amantadine in mild dementia.

Amantadine is generally used in the prophylaxis of infection with influenza A, in the treatment of Parkinson's disease and in the treatment of neuroleptic side effects. In this study acute effects of amantadine infusions on event-related potentials (ERP) were studied in 20 mildly demented patients diagnosed according to DSM-III-R criteria. Each patient was treated, in randomized order, with 0.2 g amantadine-sulfate in 500 ml NaCl and 500 ml NaCl placebo, i.v. over one hour with an interval of two weeks in-between. ERPs were investigated in an auditory odd-ball paradigm before as well as 5 hours after the infusion. In addition to 17 EEG records, vertical and horizontal EOGs were recorded. After EOG-minimization and visual artifact rejection the peak latencies of the spatial average were determined by an automatic procedure. There was no effect of amantadine on ERP latencies. N1 of the non-target showed a trend towards amplitude augmentation, P2 amplitude was reduced. As compared to placebo, P300 amplitude of targets was significantly augmented by 3.1 microV (30% of pre-treatment value), confirming the hypothesis that amantadine may influence the P 300 amplitude in the sense of an improved availability of cognitive processing resources.

Aged↗
PubMed1992

Artifact processing in topographic mapping of electroencephalographic activity in neuropsychopharmacology.

Mapping of the electroencephalogram (EEG) has been found to be a valuable method in clinical neuropsychopharmacology. It is evident that careful treatment of artifacts is of utmost importance for EEG data processing, as artifacts that contaminate the EEG data can lead to spurious results. The artifact-processing method described in this article splits signal analysis into a preprocessing step, yielding individual electro-oculographic (EOG) regression factors for EOG minimization, and into a processing step, yielding target variables. The combination of avoiding, minimizing, and identifying artifacts, as well as visual checking of face validity, will help remove artifactual effects from the EEG.

Aged↗
PubMed1992

Pharmacodynamics of venlafaxine evaluated by EEG brain mapping, psychometry and psychophysiology.

1. In a double-blind, placebo-controlled study the effects of venlafaxine--a novel nontricyclic compound inhibiting neuronal uptake of serotonin, noradrenaline and to a lesser extent dopamine--were investigated utilizing EEG brain mapping, psychometric and psychophysiological measures. 2. Sixteen healthy volunteers (eight males, eight females) aged 21-36 years received randomized and at weekly intervals single oral doses of placebo, 12.5 mg, 25 mg and 50 mg venlafaxine. EEG recordings, psychometric and psychophysiological tests, and evaluation of pulse, blood pressure and side-effects were carried out at 0, 2, 4, 6, and 8 h. 3. EEG brain mapping demonstrated that venlafaxine exerted a significant action on human brain function as compared with placebo at all three doses, characterized mostly by attenuation of absolute power, increase of relative delta/theta and beta, and decrease of alpha power, as well as by an acceleration of the total centroid fronto-temporally and by its slowing centrally and parietally. These findings are similar to antidepressants such as imipramine. Topographically, drug-induced alterations were most pronounced over both fronto-temporal and the right temporal to temporo-occipital regions. 4. Psychometric and psychophysiological investigations demonstrated significant dose-dependent psychotropic properties of the drug. Multivariate statistics exhibited an improvement of both the noopsyche (e.g. attention, concentration, attention variability, memory, fine motor activity, reaction time performance) and thymopsyche (e.g. drive, wakefulness)) but also significant psychophysiological activation (e.g. in c.f.f., pupillary and skin conductance measures). 5. Time-efficiency calculations showed significant central effects from the 2nd hour onwards, with increasing differences between placebo and treatment up to the 8th hour. Nausea was the most frequent complaint and appeared dose dependent.

Adult↗
PubMed1991

[Relation between blood levels and average quantitative EEG and psychometrically assessed pharmacodynamic changes following zotepine].

In a double-blind, placebo-controlled study, the relationships between blood levels and pharmacodynamics of zotepine were investigated in 15 healthy subjects. They received randomized at weekly intervals single oral doses of 25, 50 and 100 mg zotepine and 50 mg clozapin as reference substance. Blood sampling for zotepine and prolactin plasma levels, quantitative EEG analyses, psychometry and tolerability measures were carried out at the hours 0, 1, 2, 4, 6 and 8. There was a dose-dependent increase in zotepine plasma levels with a tmax between 2-4 hours post-drug and cmax: 6.9, 14.8 and 19.6 ng/ml for the 3 doses, respectively and a slow decline thereafter. Prolactin levels also rose dose dependently, peaking in the 4th hour. Regression and correlation analyses demonstrated: the higher the zotepine plasma levels, the more delta/theta, the less alpha activity and the slower the centroid in the spectral analysed EEG and the more decrease in reaction time performance, numerical memory and CFF in psychometry. Neurophysiological changes started at 8 ng/ml, psychometric ones at 9 ng/ml. Our pharmacodynamic findings suggested zotepine to be a sedative broad-band neuroleptic, which was also reflected in the side effects.

Adult↗
PubMed1991

Sleep laboratory studies on the single-dose effects of serotonin reuptake inhibitors paroxetine and fluoxetine on human sleep and awakening qualities.

Paroxetine is a novel antidepressant drug with selective serotonin (5-HT) reuptake inhibitory properties. In a double-blind placebo-controlled crossover sleep laboratory study the single-dose effects on objective and subjective sleep and awakening qualities were investigated after paroxetine 20, 30 and 40 mg morning doses (PX 20, 30, 40), paroxetine 30 mg evening dose, fluoxetine 40 mg morning dose (FX 40) and placebo in 18 healthy young volunteers. The drugs were orally administered in 2-wk intervals. In addition to each drug night, the adaptation night and washout night were recorded. Polysomnographic investigations (10:30 p.m. to 6:00 a.m.) showed a delayed sleep onset only after the morning intake of paroxetine, PX 40 being statistically different from placebo. Total sleep time and sleep efficiency deteriorated under morning PX 30, PX 40 and evening PX 30 as compared to placebo. The nocturnal wake time and sleep stage 1 increased under the paroxetine. Rapid eye movement (REM) reduction (min and %) occurred dose dependently after all paroxetine doses, but the REM latency was lengthened only after the morning intake. The suppressant effect on REM sleep is characteristic for antidepressants and was still significant in the washout nights following PX 40 and evening PX 30. The only statistically relevant finding under 40 mg fluoxetine referred to the increase of REM latency in both drug and washout nights. In contrast to objective results, subjective sleep quality remained generally unchanged. Attention, concentration and reaction performance improved under paroxetine as compared to baseline. The deterioration of well-being under PX 40 might be related to the appearance of drowsiness and nausea. Blood pressure and pulse rate were unaffected.

Adult↗
PubMed1991

EEG brain mapping in diagnostic and therapeutic assessment of dementia.

EEG brain mapping has been proven to be a valuable method in diagnostic and therapeutic assessment in dementia trials, because it is a readily available, inexpensive, high time-resolution method for objective and quantitative evaluation of the neurophysiological aspects of dementias. In 111 mildly to moderately demented patients diagnosed according to DSM-III as both degenerative [senile dementia of the Alzheimer type (SDAT)] and vascular [multi-infarct dementia (MID) type], we were interested in showing not only differences between SDAT and MID patients and normal controls but also the relationship between CT scans, EEG maps, clinical ratings and psychometric tests. CT measures included 10 cerebrospinal fluid (CSF) space variables as well as 17 cortical density measures (1.7 mm3 cubes, Hounsfield units). Clinical investigations consisted of the SCAG score/factors, the digit symbol substitution test, the trailmaking test and the digit span forward test. In brain maps, SDAT patients showed slightly to moderately more slow and less alpha and beta activity as well as a slowing of the dominant frequency (DF) and the centroid (C) than did normal controls. These findings were most prominent in parietal and temporal regions. MID patients exhibited markedly augmented delta/theta and attenuated alpha and beta activity and a slowing of the DF and C. These neurophysiological findings suggest a deterioration of vigilance. Differences between SDAT and MID patients were found mostly in measures concerning differences in the maps. Brain maps of correlation coefficients between CT and EEG variables demonstrated: the greater the anterior horn distance, lateral ventricle distance, and Evan's index, as well as the less cortical density, the more delta/theta and the less alpha and beta activity in the EEG. Moreover, the higher the delta/theta, the less alpha and beta activity, the higher the SCAG scores, and the worse the psychometric performance. From the pharmacological point of view, we observed a significant improvement in vigilance after administration of several nootropic drugs both in normal and pathologically aging subjects, which was associated also with improvement of psychopathometric scores. Based on multi-variante analysis of variance (MANOVA)/Hotlelling T2 we observed a drug's effect in different brain regions of MID and SDAT patients. Thus, pharmaco-EEG mapping mediates valuable information regarding if, how, when, in which dosage, and where a nootropic drug acts on its target organ--the aging human brain.

Aged↗
PubMed1990

Brain protection of nicergoline against hypoxia: EEG brain mapping and psychometry.

In a double-blind, placebo-controlled trial human brain function and mental performance as well as the antihypoxidotic properties of nicergoline were studied utilizing blood gas analysis, EEG brain mapping and psychometry. Hypoxic hypoxidosis was experimentally induced by a fixed gas combination of 9.8% oxygen (O2) and 90.2% nitrogen (N2) equivalent to 6,000 m altitude, which was inhaled for 23 min under normobaric conditions by 16 healthy volunteers. They received randomized after an adaptation session placebo, 10 mg, 30 mg and 60 mg nicergoline (NIC). Evaluation of blood gases, brain mapping and psychometry was carried out at 0, 2, 4, 6, 8 hrs oral drug administration. Blood gas analysis demonstrated a drop in PO2 from 95 to 35 and 34 mm Hg in the 14 and 23 min of inhalation, respectively. PCO2 decreased too (38 to 34 and 34 mm Hg), while pH increased (7.39 to 7.44 and 7.44). Base excess increased (-0.6 to 0.6 and 0.4) while standard bicarbonate decreased (24.4 to 24.1 and 23.8 mmol/l). Thus, blood gases remained stable between the 14 and 23 min of hypoxia during which time the neurophysiological and behavioral evaluations were carried out. EEG brain mapping exhibited an increase in delta/theta activity mostly over the parietal, temporal and central regions (left more than right), while alpha activity decreased (mostly over the parietal, central, frontal, fronto-temporal and temporo-occipital regions). 30 and 60 mg NIC attenuated this deterioration of vigilance. At the behavioral level, hypoxic hypoxidosis induced a deterioration of the noo- and thymospsyche which was mitigated by NIC. Based on 13 psychometric variables, the hypoxia-induced performance decrement was on the overall (2nd-8th hr) 43% after placebo as compared with pretreatment normoxic values, while only 29, 24 and 31% after 10, 30 and 60 mg nicergoline, respectively. The difference between placebo and the optimal dosage of nicergoline 30 mg reached the level of statistical significance (p less than 0.01, multiple Wilcoxon).

Adult↗