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Biomedical subjects

B Saletu

Publications and source records attributed to B Saletu.

At least 109 records · Page 6Linked to original sources
PubMed1993

Clinical-pharmacological study with the two isomers (d-, l-) of fenfluramine and its comparison with chlorpromazine and d-amphetamine: psychometric and psychophysiological evaluation.

In a double-blind, placebo-controlled, crossover study, the single oral dose effects of 15, 30 mg d- and 30 mg l-fenfluramine (FEN) on psychometric and psychophysiological variables were investigated and compared with those of 50 mg chlorpromazine (CPZ) and 20 mg d-amphetamine (AMPH). Eighteen healthy young volunteers randomly (latin square) received at weekly intervals the 6 different treatments. Noopsychic, thymopsychic, psychophysiological and flexibility evaluations were carried out at 0, 2, 4, 6 and 8 h after drug administration. Either dose of d- or l-FEN induced only minimal noopsychic and thymopsychic changes. In contrast, 50 mg CPZ produced highly significant deterioration in attention, concentration, reaction time, psychomotor activity and complex reaction, as well as subjective deactivation, while 20 mg d-AMPH produced subjective activation. Critical flicker frequency was only decreased by 50 mg CPZ and increased by 20 mg d-AMPH. In regard to pupillary measurements, 15, 30 mg d-, 30 mg l-FEN and 20 mg d-AMPH produced opposite changes (widening of pupillary diameter) to those observed after 50 mg CPZ (narrowing of pupil size). Flexibility remained unchanged after FEN treatments, while it consistently decreased after both 50 mg CPZ and 20 mg d-AMPH. Time- and dose/treatment efficacy relations based on discriminant analysis (centroids) of changes in all variables showed 50 mg CPZ as the most psychoactive drug inducing significant changes from the 2nd until the 8th h, followed by 20 mg d-AMPH inducing significant changes from the 4th until the 8th h, but with opposite signs, while FEN treatments exerted only slight effects between the 2nd to 8th h postdrug.

Adult↗
PubMed1993

[Sleep disorders in neurology: hyposomnia].

Sleep disturbances are an important health problem; about 20-33% of the population suffer from hyposomnias (lack of sleep). Hyposomnias often accompany neurological disorders (head traumas, chronic cephalea, pain, cerebrovascular and neuromuscular disorders, M. Parkinson, and dementia). Slow wave sleep decreases, arousals increase, and sleep is fragmented; these types of hyposomnias are treated by treatment of the basic neurological disease. Some sleep disturbances (e.g. sleep apneas) are a risk factor for cerebrovascular disorders.

Brain↗
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↗
PubMed1992

Therapeutic efficacy of pyritinol in patients with senile dementia of the Alzheimer type (SDAT) and multi-infarct dementia (MID).

This trial was performed to investigate the efficacy of pyritinol in the treatment of senile dementia. Initially, a total of 183 inpatients were screened for eligibility. Of 164 patients who met the inclusion criteria, 156 completed the trial. Allocation of the patients to the Senile Dementia of the Alzheimer Type group or the Multi-Infarct Dementia group was based on the Hachinski Ischemic Score, computed tomography scans and electroencephalographic (EEG) findings. In a 12-week double-blind treatment phase either 200 mg pyritinol dihydrochloride-monohydrate or placebo was given 3 times daily. Confirmatory statistics included item 2 of the Clinical Global Impression, the total score of the Short Cognitive Performance Test (Syndrom Kurz Test) and the factor 'cognitive disturbances' of the Sandoz Clinical Assessment Geriatric scale. In addition, data on tolerance, of EEG brain mapping and of a responder analysis were evaluated based on descriptive statistics. The therapeutic efficacy of pyritinol was clearly demonstrated by confirmatory analysis as the drug was statistically significantly superior to placebo in all 3 target variables. The clinical relevance of the outcome was underlined by the analysis of the descriptive variables and by the convergence found at the different observation levels. The EEG mapping demonstrated significant differences between placebo and pyritinol, with the latter decreasing slow and increasing fast alpha and beta activity, which reflects improvement of vigilance. Based on the results of this trial, it can be accepted that the therapeutic effect of pyritinol is superior to placebo in patients with mild to moderate dementia of both degenerative and vascular etiology.

Aged↗
PubMed1992

Pupillometry in clinical psychophysiological diagnostics: methodology and proposals for application in psychiatry.

The change in pupillary reactions may be considered as an important parameter of the autonomic nervous system. By means of pupillometry, it became possible to measure both objectively and economically these reactions. The method of microprocessor-assisted "static" and light evoked "dynamic" pupillometry is demonstrated. A high reliability for the static variable of pupillometry was also evaluated. Variables measured during "static and dynamic" pupillometry were factor-analyzed. Four factors (static, dynamic, stimulus specific and restitution dependent) were obtained regardless of whether investigations were carried out in normals or in psychiatric patients. Examples of utilization of pupillometry in psychopharmacology and mental disorders are also described in this essay.

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

Sleep laboratory investigations on hypnotic properties of melatonin.

Melatonin (MLT), a pineal hormone, has some sedative and hypnotic properties. To explore this effect further 20 young, healthy volunteers exposed to artificial insomnia participated in a double-blind, placebo controlled, parallel group design study. They slept in a sleep laboratory for several consecutive nights and were polygraphically monitored and subjected to a battery of psychometric tests and standardized self-report questionnaires each morning. One night all subjects received only placebo (21:00 hours) and on a second night half of them were subjected to placebo and half to MLT. On the later night blood MLT levels were measured. Polygraphic recordings revealed that MLT at bedtime decreased the time the subjects were awake before sleep onset (P less than 0.025), sleep latency (P less than 0.05), and the number of awakenings during the total sleep period (P less than 0.025), and increased sleep efficiency (P less than 0.05). In addition, it decreased sleep stage 1 (P less than 0.05) and increased sleep stage 2 (P less than 0.025). On the morning following the treatment most objective and subjective measures for awakening quality showed a trend towards improvement after MLT. One hour after its oral administration, serum MLT rose to a high pharmacological level (25817 pg/ml; median), but individual peak serum MLT levels varied by a factor of 300.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
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↗
PubMed1990

On the treatment of the alcoholic organic brain syndrome with an alpha-adrenergic agonist modafinil: double-blind, placebo-controlled clinical, psychometric and neurophysiological studies.

1. In a double-blind study forty abstinent hospitalized male patients with an alcoholic organic brain syndrome (OBS) were treated for 6 weeks with either 200 mg modafinil or placebo. 2. Modafinil (CRL 40476) is a putative central alpha-1 adrenergic agonist. It's pharmacological profile is quite different from that of amphetamine, which can be seen by the lack of peripheral sympathomimetic effects. The vigilance promoting effect of modafinil has been shown previously in pharmaco-EEG and psychometric studies as well as in clinical studies involving treatment of daytime sleepiness in idiopathic hypersomniacs and narcoleptics. 3. The present clinical investigations demonstrated that the spontaneous restitution of the alcoholic OBS was significantly augmented and accelerated by modafinil. 4. Psychometric tests did not show significant intergroup differences. Modafinil- and placebo-treated patients improved continously over the 6-week period. 5. Psychophysiological and autonomous nervous system parameters were affected neither by placebo nor by modafinil. 6. Neurophysiological investigations by means of quantitative pharmaco-EEG showed partly inconsistent findings. However, superimposed dosages of modafinil (on the top of 6 weeks chronic administration) induced a decrease of slow activity and an increase of alpha activity suggesting an improvement of vigilance after the daily drug intake. 7. Considering the beneficial effects of modafinil in abstinent chronic alcoholic patients, it may be said that activation and improvement of adaptive behaviour by an alpha-adrenergic agonist could be regarded as a therapeutic principle in the treatment of the OBS, eventually due to noradrenergic deficits.

Adrenergic alpha-Agonists↗
PubMed1990

EEG-brain mapping in schizophrenics with predominantly positive and negative symptoms. Comparative studies with remoxipride/haloperidol.

EEG brain maps obtained in 48 drug-free hospitalized schizophrenics diagnosed according to DSMIII demonstrated significant differences as compared with normal controls characterized by a decrease of alpha-1 activity, increase of beta activity and acceleration of the centroid. These findings suggest a state of sustained hyperarousal in schizophrenia. While the patients with negative schizophrenia showed a bi-temporal and frontal augmentation of delta/theta activity, patients with florid symptomatology exhibited just the opposite findings. Alpha-1 activity was attenuated, beta activity augmented in both groups with the findings more pronounced in the positive schizophrenia group. The increase of slow activity suggests an organic factor in the pathogenesis of the negative syndrome, which was supported by correlation maps between EEG measures and the apathy syndrome as measured by the AMDP system. Treatment of schizophrenics with predominantly positive symptoms with 2 different neuroleptics such as remoxipride and haloperidol resulted also in differential effects on brain activity: while haloperidol augmented delta/theta and alpha activity and decreased beta activity, remoxipride produced a decrease of slow and increase of beta activity as well as an acceleration of the centroid suggesting vigilance-promoting properties of the drug. These differential effects on the neurophysiological level were also reflected at the behavioural one evaluated by psychometry, while global clinical evaluation showed, as expected, similar improvement with both drugs (apart from extrapyramidal side effects being significantly more pronounced after haloperidol than remoxipride). Our findings suggest that brain electrical signal topography is a promising method in regard to a better understanding of pathogenesis and treatment in schizophrenia.

Adult↗