[Evening television and sleep. Polysomnographic, psychometric and psychopharmacologic studies in sleep disordered patients (II)].
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Anti-Anxiety Agents↗
Biomedical subjects
P Anderer
Publications and source records attributed to P Anderer.
[Nightly television and sleep. Polysomnographic, psychometric and psychopharmacologic studies of patients with sleep disorders].
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Adolescent↗
Topographic brain mapping of EEG after acute application of ergotalkaloids in the elderly.
In a double-blind, placebo-controlled, crossover study the encephalotropic and nootropic effects of single doses of two ergotalkaloids (30 and 60 mg nicergoline and 5 mg co-dergocrine mesylate (CDM)) were investigated in 12 elderly subjects (mean age 67 years), utilizing topographic brain mapping of the EEG. Evaluation of EEG, memory, pulse and blood pressure were carried out at 0, 2, 4, 6 and 8 h. Topographic brain maps demonstrated an augmentation of total power, an acceleration of the centroid of the total activity, a decrease of delta/theta and an increase of beta activity (mostly in the alpha-adjacent frequency bands), as well as an acceleration of the centroid of the delta/theta and a slowing of the beta centroid. These changes are indicative of improvement in vigilance of elderly subjects after ergotalkaloids, which was also reflected in the significant improvement of memory after nicergoline. Topographically, the main effect was found over the frontal, central and temporal regions. Timewise, the pharmacodynamic peak fell into the 4th h, although with 60 mg significant encephalotropic effects could be observed in the 2nd and in the 6th h. The drugs were well tolerated.
Clinical Trial↗
Amantadine infusions in mild dementia: acute double-blind placebo-controlled EEG mapping and psychometric studies.
In a double-blind, placebo-controlled study, the acute central effects of amantadine infusions (200 mg for 1 h) were studied in 20 mildly demented patients (DSM-III-R) utilizing EEG mapping as well as psychometry and psychophysiology at the hours 0, 2, 4, 6 and 8. Multivariate analysis of the EEG demonstrated a significant CNS effect of 200 mg amantadine as compared with placebo mostly at the 4th and 6th hour. These effects were primarily over temporo-occipital, fronto-temporal and temporal regions. Univariate analysis showed a decrease of total power and of absolute power in all frequency bands. Furthermore, an increase of relative delta and beta activities, a decrease of theta and alpha activities, as well as an acceleration of the respective centroids of the alpha, beta and total activity were observed. The delta/theta centroid showed initially a slight increase and thereafter a clear decrease. The changes were similar to those seen after psychostimulants. Multivariate analysis of noopsychic variables showed an improvement in the 6th hour after amantadine and no changes after placebo, but inter-drug differences did not reach significance. Univariate analyses revealed differential results which included improvement in digit span and deterioration in the speed related test such as DSST and reaction time. In thymopsychic variables, de-activation was observed after amantadine as compared with placebo in the 2nd to the 6th hour with a maximum in the 4th hour. As patients felt themselves slightly over-activated before treatment, de-activation may be regarded as improvement of vigilance in the narrow sense of the word. There were no psychophysiological changes.
Clinical Trial↗
Effect-kinetics on brain protection of two codergocrine-mesylate preparations (Aramexe retard and Hydergine) by EEG mapping and psychometry under hypoxia.
In a double-blind, placebo-controlled study the effect-kinetics on brain protection of a new retard formulation of codergocrine-mesylate (CDM) (Aramexe retard, 5 mg) were investigated and compared with a standard CDM drug (5 mg Hydergine) utilizing blood gas analysis, EEG mapping and psychometry. A transient, reversible hypoxic hypoxidosis (i.e. impairment of cerebral metabolism due to hypoxia) was experimentally induced by a fixed gas combination of 9.8% oxygen (O(2)) and 90.2% nitrogen (N(2)) (found at an altitude of 6000 m), which was inhaled for 23 min under normobaric conditions by 18 healthy volunteers. After an adaptation session they received randomized 5 mg Aramexe retard, 5 mg Hydergine and placebo. Evaluation of blood gases, EEG mapping and psychometry was carried out at 0,2, 4,6, and 8 h after oral drug administration - each time under normoxic and hypoxic conditions. Blood gas analysis demonstrated a drop in SaO(2) from 99% under normoxia to 70% under hypoxia, in Po(2) from 100 to 33 mmHg, and in Pco(2) from 36 to 31 mmHg, while pH increased from 7.43 to 7.48. Base excess and standard bicarbonate remained stable. Under hypoxia EEG mapping exhibited an increase in delta/theta, a decrease of alpha and increase of beta activity, as well as a slowing of the centroid of the total power spectrum, which reflects deterioration of vigilance. Both CDM preparations significantly attenuated this vigilance decrement, with 5 mg Hydergine showing its encephalotropic peak effect in the second hour, 5 mg Aramexe retard in the sixth and eighth hours. At the behavioral level, hypoxic hypoxidosis induced a deterioration of the noo- and thymopsyche (by 53% under placebo), which was significantly mitigated by both 5 mg Aramexe retard (19%) and Hydergine (32%).
Clinical Trial↗
Non-invasive localization of P300 sources in normal aging and age-associated memory impairment.
Cognitive event-related potentials were recorded from 17 EEG leads in an auditory two-tone paradigm in 43 patients aged 51-79 years with the diagnosis of age-associated memory impairment (AAMI), in age-and sex-matched normal controls and in a control group 10 years older than the AAMI patients. In addition to P300 latencies, amplitudes and topographies, three-dimensional current density distribution utilizing low-resolution brain electromagnetic tomography (LORETA) was computed. P300 latency was delayed and P300 amplitude was reduced in both AAMI and older subjects. Topographically this amplitude reduction was most pronounced frontally. LORETA revealed medial (frontal and parietal) and lateral (dorso- and ventrolateral prefrontal, middle/superior temporal, posterior superior temporal/inferior parietal) sources. Significant reductions in LORETA source strength in normal aging and in AAMI were found mainly medially frontally, right dorsolaterally prefrontally and right inferiorly parietally. Since these anatomically highly interconnected brain regions in the right hemisphere are part of a network associated with sustained attention, the results speak for a decline in attentional resource capacity in AAMI patients and elderly subjects.
Aged↗
Topographic mapping of cognitive event-related potentials in a double-blind, placebo-controlled study with the hemoderivative Actovegin in age-associated memory impairment.
In a double-blind placebo-controlled study, the effects of Actovegin on cognitive event-related potentials were studied in 18 age-associated memory impairment (AAMI) patients. Actovegin is a protein-free metabolically active hemoderivative improving oxygen and glucose utilization. Each patient was treated, in randomized order, for 2 weeks with 250 ml 20% Actovegin and 250 ml placebo daily with an interval of 3 weeks in between. Psychophysiological tests were carried out by means of the Viennese Psychophysiological Test System (VPTS) before as well as 5 h after the administration of one single infusion on day 1 (acute effect), before (subacute effect) as well as after one additional superimposed infusion on day 15 (superimposed effect). There was no effect on earlier stages of information processing measured by N1 and P2 component of nontarget ERP nor on ERP latencies. However, P300 amplitude increased after acute, subacute as well as superimposed infusion of Actovegin as compared to placebo, confirming the hypothesis that nootropic drugs may influence the P300 amplitude in the sense of an improved availability of cognitive processing resources. This increase of P300 amplitude (up to 4.8 microV), seen specifically in central and parietal regions, proved to be significant in a confirmatory test.
Aged↗
EEG brain mapping and psychometry in age-associated memory impairment after acute and 2-week infusions with the hemoderivative Actovegin: double-blind, placebo-controlled trials.
In a double-blind, placebo-controlled study the encephalotropic and psychotropic effects of Actovegin--a protein-free metabolically active hemoderivative improving oxygen and glucose utilization--were investigated in age-associated memory impairment (AAMI) patients, utilizing EEG brain mapping, psychometric and psychophysiological analyses. Each patient had a treatment of 2 weeks with 250 ml 20% Actovegin and 250 ml placebo daily with an interval of 3 weeks in between (the order of drugs sequence was randomized). Pharmacodynamic evaluations were carried out 0, 2, 4, 6 and 8 h after the administration of one single infusion on day 1 (acute effect), at 0 h on day 15 (subacute effect) as well as 2, 4, 6 and 8 h after one additional superimposed infusion on day 15 (superimposed effect). EEG brain mapping demonstrated that Actovegin exerted a significant action on the human brain function as compared with placebo characterized by a decrease of delta and theta, an increase of alpha-adjacent slow beta, a decrease of fast beta, an acceleration of the centroid of the delta/theta and alpha activity, a slowing of the beta centroid and an increase of the centroid of the total activity. Topographically the encephalotropic effects were mostly pronounced in the parietal, frontocentral and temporooccipital regions. These changes are indicative of an improvement of vigilance which was proven also by psychometric investigations at the behavioral level. Actovegin improved the noopsyche mostly in regard to attention, memory and rigidity/perseveration measures. In regard to the thymopsyche an improvement was noted in mood, affectivity, well-being and sedation. Psychophysiological evaluations demonstrated an increase in CFF, skin conductance, pupillary diameter and shortening of the latency and augmentation of the amplitude of the pupillary response. Time-efficacy calculations exhibited more effect after subacute than acute administration with the pharmacodynamic maximum in the 4th h after the superimposed dose. Evaluations of pulse, blood pressure and side effects demonstrated a very good tolerability of the drug. Our present neurophysiological, psychometric and psychophysiological findings confirm earlier results obtained in elderlies with similar methodology.
Aged↗
Paclitaxel-carboplatin chemotherapy does not cause encephalopathy in patients with ovarian cancer: a prospective EEG mapping study in 28 patients.
BACKGROUND: The objective of this study was to evaluate possible effects of a paclitaxel containing chemotherapy, on the central nervous system (CNS) in women with ovarian cancer. MATERIALS AND METHODS: Twenty-eight women with histologically documented epithelial ovarian carcinoma and treated with a combination chemotherapy consisting of paclitaxel and carboplatin entered the study. Patients were tested with resting EEG (R-EEG) before and after chemotherapy. RESULTS: Twenty of the 28 patients responded to the chemotherapy (71%). Eleven patients (39%) developed peripheral neurotoxicity. A decrease of beta power and an increase of delta and theta power as well as a deceleration of the total centroid frequency clearly demonstrated a reduced vigilance in patients with ovarian cancer compared to healthy controls. On the other hand, the observed increase of beta power, a decrease of delta and theta power, and an acceleration of the total centroid from pre- to post-treatment demonstrated an improvement of vigilance in patients with ovarian cancer after treatment with paclitaxel/carboplatin. CONCLUSIONS: The results of this study suggest that chemotherapy consisting of paclitaxel and carboplatin does not cause adverse effects on the central nervous system. Improved vigilance was measured in patients with ovarian cancer after chemotherapy.
Adenocarcinoma↗
Effects of the novel neuroprotective agent, riluzole, on human brain function and behavior: I. Double-blind, placebo-controlled EEG mapping and psychometric studies under normoxia.
In a double-blind, placebo-controlled, crossover study, the encephalotropic and psychotropic properties of single oral doses of the novel neuroprotective agent, riluzole, were investigated utilizing EEG mapping and psychometry. Twenty healthy young volunteers received randomly at weekly intervals, placebo, 50, 100 and 200 mg riluzole. EEG recordings and evaluation of 9 noopsychic and 5 thymopsychic variables were carried out at 0, 2, 4, 6 and 8 h after oral drug administration. EEG maps on the multivariate analysis demonstrated that all three doses induced significant changes in human brain function, as compared with placebo, between 2 and 8 h, with effect only increasing slightly with dose. EEG maps on univariate analysis demonstrated generally an increase of delta/theta, decrease of alpha and beta power, as well as a slowing of the centroid of the total power spectrum, which suggests sedative properties of the drug. Only after the two highest doses at 6 h were some different findings observed. Multivariate statistics on psychometry failed to show any significant effects on the noopsyche, while for the thymopsyche, all three doses of riluzole produced a deterioration. The latter was characterized by a decrease in drive and wakefulness as well as deterioration in well-being, mood and affectivity. Thus, under normoxia, in all three doses riluzole produced neurophysiologically a sedative effect, accompanied at the behavioral level by a deterioration in the thymopsyche, which may be expected from a drug with antiglutamatergic effects in normals.
Adult↗
Effects of the novel neuroprotective agent, riluzole, on human brain function and behavior: II. Double-blind, placebo-controlled EEG mapping and psychometric studies under hypoxia.
In a double-blind, placebo-controlled study, the antihypoxidotic properties of the novel neuroprotective agent, riluzole, were investigated utilizing blood gas analysis, EEG mapping and psychometry under a transient, reversible, hypoxic hypoxidosis. The latter was induced by a fixed gas combination of 9.8% oxygen (O2) and 90.2% nitrogen (N2) (found at 6000 m altitude), which was inhaled for 23 min under normobaric conditions by 20 healthy, young volunteers. They randomly received, after an adaptation session, single oral doses of placebo, and 50, 100 and 200 mg riluzole. Evaluation of blood gases, EEG mapping and psychometry were carried out 0, 2, 4, 6 and 8 h postdrug, each time under the 23-min hypoxia. Blood gas analysis demonstrated a drop in PO2 from 106 to 37 and 36 mmHg, in PCO2 from 35 to 31 and 31 mmHg at 14 and 23 min of inhalation, respectively, while pH increased from 7.43 to 7.48 and 7.48. Base excess and standard bicarbonate remained stable. EEG mapping exhibited under hypoxia a marked increase of delta/theta, decrease of alpha and an increase of superimposed beta activity, as well as a slowing of the centroid of the total activity, which reflects deterioration of vigilance. Riluzole in lower doses and at early hours after higher doses did not attenuate this hypoxia-induced vigilance decrement, while with higher doses (100-200 mg) in later recording periods (6-8 h) brain protection occurred. As compared with placebo, delta/theta power increased at 2-8 h after 50 mg riluzole and up to 4 h after 100 mg riluzole, while a decrease occurred at 4 and 8 h after 100 mg and at 6-8 h after 200 mg. Alpha power showed no changes after 50 mg, an increase at 2 and 8 h after 100 mg and a decrease at 4 h after 200 mg, with no changes thereafter. Beta power decreased at various times after all three doses. At the behavioral level, hypoxic hypoxidosis induced a deterioration of the noopsyche, which was not mitigated by riluzole. In regard to the thymopsyche, there was even a slight deterioration after all three doses, as compared with placebo.
Adult↗