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Biomedical subjects

P Anderer

Publications and source records attributed to P Anderer.

At least 19 recordsLinked to original sources
PubMed1998

Differential effects of normal aging on sources of standard N1, target N1 and target P300 auditory event-related brain potentials revealed by low resolution electromagnetic tomography (LORETA).

The P300 event-related potential (ERP) is considered to be closely related to cognitive processes. In normal aging, P300 scalp latencies increase, parietal P300 scalp amplitudes decrease and the scalp potential field shifts to a relatively more frontal distribution. Based on ERPs recorded in 172 normal healthy subjects aged between 20 and 88 years in an auditory oddball paradigm, the effects of age on the electrical activity in the brain corresponding to N1 and P300 components were estimated by means of low resolution electromagnetic tomography (LORETA). This distributed approach directly computes a unique 3-dimensional electrical source distribution by assuming that neighbouring neurons are simultaneously and synchronously active. N1 LORETA generators, located predominantly in both auditory cortices and also symmetrically in prefrontal areas, increased with advancing age for standards but remained stable for targets. P300 LORETA generators, located symmetrically in the prefrontal cortex, in the parieto-occipital junction and in the inferior parietal cortex (supramarginal gyrus) and medially in the superior parietal cortex, were differentially affected by age. While age did not affect parieto-occipital sources, superior parietal and right prefrontal sources decreased pronouncedly. Thus, in normal aging, P300 current density decreased in regions were a fronto-parietal network for sustained attention was localized.

Adult↗
PubMed1998

Electrical sources of P300 event-related brain potentials revealed by low resolution electromagnetic tomography. 1. Effects of normal aging.

The P300 event-related potential (ERP) is considered to be closely related to cognitive processes. Previous reports regarding major generators contributing to the scalp-recorded P300 suggested widely distributed multiple sources. Based on ERPs recorded in 172 normal healthy subjects aged between 20 and 88 years in an auditory oddball paradigm, electrical activity in the brain corresponding to N1 and P300 components was localized by means of low resolution electromagnetic tomography (LORETA). The N1 LORETA generators, located in both auditory cortices, did not change over age. On the other hand, the P300 LORETA generators, located predominantly in the frontal neocortex and less pronounced in the posterior parietal cortex, decreased over age both in frontal and parietal source strength.

Adult↗
PubMed1998

Electrical sources of P300 event-related brain potentials revealed by low resolution electromagnetic tomography. 2. Effects of nootropic therapy in age-associated memory impairment.

In a double-blind, placebo-controlled study the effects of Actovegin on frontal and parietal electrical P300 sources revealed by low resolution electromagnetic tomography (LORETA) were studied in age-associated memory impairment (AAMI) patients. Actovegin is a protein-free metabolically active hemoderivative improving oxygen and glucose utilization. Each patient had, in randomized order, a treatment of 2 weeks with 250 ml 20% Actovegin and 250 ml placebo daily. Auditory ERPs were recorded before and 5 h after drug administration on day 1 (acute effect) and on day 15 (subacute and superimposed effect). Compared to age- and sex-matched normal controls, AAMI patients showed a trend towards P300 latency prolongation and a significantly reduced P300 global field power (GFP). Maximal LORETA source strength did not differ from controls. After Actovegin parietal P300 scalp amplitudes increased, while frontal and temporal amplitudes decreased as compared to placebo. This increase in hilliness, measured by the GFP, was significant. Moreover, the parietal P300 source strength increased after acute, subacute and superimposed infusion of Actovegin as compared to placebo. This may reflect improved availability of cognitive processing resources in the parietal cortex, an area that on the one hand plays an important role in fundamental aspects of attention and on the other hand has been found to be functionally impaired in dementia.

Aged↗
PubMed1997

Sleep quality during alcohol withdrawal with bright light therapy.

1. Alcohol withdrawal is a complex syndrome that ranges from anxiety, insomnia to delirium tremens. Common treatment is the application of sedative medication. Exposure to bright light in the daytime should advance the normal sleep/wake cycle and moreover it should improve the availability of man's adaptive behavior during alcohol withdrawal. 2. This pilot study describes bright light therapy (BL) during alcohol withdrawal in ten alcohol dependent patients (DSM-III-R: 291.80) without any sedative medication. BL (3000 Lux) was administered on day 3 of abstinence between 7.00-9.00 a.m. and 5.00-9.00 p.m. Total-sleep-polysomnography (recordings between 10.30 p.m.-6.00 a.m.) and self-rating scale were performed to compare intraindividual changes during three nights. After one adaptation night (immediately after alcohol withdrawal), one baseline night and one "BL-night" and one "post-BL night" were analysed. 3. At baseline, total sleep time and sleep efficiency were severely deteriorated, but tended to improve in the following nights after BL. Sleep onset latency showed a significant decline after BL. Stages 3 and 4 were reduced at baseline. Latencies to slow wave sleep were significantly shortened after BL. REM increased in the nights after BL. Subjective sleep quality improved after BL. Although the present results, bright light having a possible stabilizing effect on sleep maintenance and sleep architecture during acute alcohol withdrawal, the authors could only derive hypotheses for further ongoing controlled investigations using placebo light, to receive final verification.

Adult↗
PubMed1997

Topographic distribution of sleep spindles in young healthy subjects.

The application of an automatic sleep spindle detection procedure allowed the documentation of the topographic distribution of spindle characteristics, such as number, amplitude, frequency and duration, as a function of sleep depth and of recording time. Multichannel all-night EEG recordings were performed in 10 normal healthy subjects aged 20-35 years. Although the interindividual variability in the number of sleep spindles was very high (2.7 +/- 2.1 spindles per minute stage 2 sleep), all but two subjects showed maximal spindle activity in centro-parietal midline leads. Moreover, this topography was seen in all sleep stages and changed only slightly--to a more central distribution--towards the end of the night. On the other hand, slow (11.5-14 Hz) and fast (14-16 Hz) spindles showed a completely different topography, with slow spindles distributed anteriorly and fast spindles centro-parietally. The number of sleep spindles per min was significant depending on sleep stages, with the expected highest occurrence in stage 2, and on recording time, with a decrease in spindle density from the beginning towards the end of the night. However, spindle amplitude, frequency and individual duration was not influenced by sleep depth or time of the night.

Adult↗
PubMed1997

Nonorganic insomnia in generalized anxiety disorder. 1. Controlled studies on sleep, awakening and daytime vigilance utilizing polysomnography and EEG mapping.

Objective and subjective sleep and awakening quality as well as daytime vigilance of insomniac patients with generalized anxiety disorder (GAD) were investigated, as compared with normal controls. Forty-four outpatients (25 females, 19 males), aged 24-65 (mean 43) years, diagnosed with non-organic insomnia (ICD-10: F 51.0), related to mild GAD (F 41.1), with a Hamilton anxiety (HAMA) score of 22 +/- 6 and a Zung self-rating anxiety (SAS) score of 37 +/- 6 were included. After 1 adaptation night, sleep induction, maintainance and architecture were measured objectively by polysomnography, subjective sleep and awakening quality were assessed by self-rating scales and visual analog scales, objective awakening quality was measured by a psychometric test battery, and diurnal tiredness was measured by a 3-min vigilance-controlled EEG (V-EEG) and a 4-min resting EEG mapping. In polysomnography patients demonstrated-as compared with normals-significantly increased wake time during the total sleep period and more early-morning awakening, decreased total sleep and sleep efficiency. Subjective sleep quality was deteriorated as well, as were well-being, drive, mood, and wakefulness in the morning. In noopsychic performance, GAD patients did rather well in attention, concentration, attention variability, and numerical memory, while fine-motor activity and reaction time were deteriorated. In psychophysiology, critical flicker frequency was decreased in the morning, while muscle strength, blood pressure and pulse rate showed no differences. EEG mapping during the late morning hours (10.00-12.00 h) demonstrated hypervigilance in the V-EEG, while in the resting recording an increased sleep pressure was detected. The latter was correlated significantly to the SAS score, but less so to the observer-rated Hamilton anxiety score. Our findings suggest that CNS hypervigilance and hyperarousal, as actual symptoms of GAD, lead to nocturnal insomnia, which in turn may cause-as a consequence of sleep pressure not slept off-diurnal tiredness.

Adult↗
PubMed1997

Nonorganic insomnia in generalized anxiety disorder. 2. Comparative studies on sleep, awakening, daytime vigilance and anxiety under lorazepam plus diphenhydramine (Somnium) versus lorazepam alone, utilizing clinical, polysomnographic and EEG mapping methods.

Previous human pharmacological and toxicological studies demonstrated advantages of the combination drug Somnium [SOM, lorazepam (LOR) 1 mg plus diphenhydramine 25 mg] over 1 mg LOR alone, as it showed synergistic effects in hypnotic properties and antagonistic effects in regard to toxicity. In the present double-blind, parallel-group study, hypnotic and anxiolytic effects of SOM were studied in 44 patients with non-organic insomnia related to mild generalized anxiety disorder (GAD), as compared with LOR alone. After a placebo run-in phase of 1 week, they received active treatment (1 tablet SOM or LOR 1 mg) for 4 weeks and thereafter placebo again for 1 week. Clinical evaluations included the physician's general assessment of efficacy, tolerance and adverse effects, the Hamilton anxiety rating scale (HAMA), the Zung self-rating anxiety scale (SAS) and depression scale, the withdrawal symptom scale (WSS), hematology and blood chemistry. Sleep laboratory evaluations included objective and subjective sleep and awakening quality, measured by polysomnography, self-rating of sleep and awakening quality (SSA) and a psychometric test battery in the morning, as well as measurement of daytime brain function, objectivated by EEG mapping. Physicians' global evaluation of insomnia demonstrated no changes in the pre-drug placebo period, moderate improvement under both drugs, with a marginal advantage of SOM over LOR in the first 2 weeks, and a return to pre-drug values in the post-drug placebo period. Anxiety improved in observer ratings (HAMA) under both drugs, in self-rating (SAS) under the combination drug only, with the scores returning to pre-drug placebo values after post-drug placebo substitution. There were no significant findings in the self-rating depression scale and the WSS, with the exception of an improvement in the WSS score 4 weeks after SOM, as compared with pre-drug placebo. There were no rebound phenomena. Both drugs were well tolerated-in regard to both adverse effects and laboratory findings. Confirmatory statistics on the polysomnographically recorded target variable latency to sleep onset stage 2 demonstrated a significant shortening of sleep latency after SOM and a significant superiority of the combination drug SOM over LOR after acute dosing, as compared with pre-drug placebo. Descriptive statistics demonstrated further a significant improvement of sleep efficiency and total sleep time after SOM and of wakefulness time and number of awakenings during the total sleep period after both drugs, but no interdrug differences. Sleep architecture remained unchanged. Subjective sleep quality improved with both drugs, morning drowsiness and the total SSA score only with SOM, while LOR was superior to SOM regarding morning somatic complaints. There were neither changes nor interdrug differences in the morning noopsyche. In psychophysiology, critical flicker frequency decreased more under SOM than LOR. After 4 weeks therapy, no significant findings in polysomnography and subjective sleep and awakening were seen, except for an increase in movement time under LOR (tolerance development). In objective awakening quality, psychometry revealed an improvement of reaction time under SOM and a decrease of attention variability and an increase in fine-motor activity under LOR, with an interdrug comparison showing a significant superiority of SOM over LOR in regard to reaction time, reaction time variability and reaction time performance. After placebo substitution, rebound phenomena were seen in polysomnography and subjective sleep and awakening in the 1st night of the SOM group only, which were gone in the 7th placebo night, however. Noopsychic performance remained improved in both groups, with a superiority of SOM to LOR in regard to reaction time and reaction time variability. (ABSTRACT TRUNCATED)

Adult↗
PubMed1996

Comparative pharmacodynamic studies with the novel serotonin uptake-enhancing tianeptine and -inhibiting fluvoxamine utilizing EEG mapping and psychometry.

In a double-blind, placebo-controlled study, the encephalotropic and psychotropic effects of tianeptine (TIA)--a new tricyclic antidepressant, enhancing serotonin reuptake--were investigated as compared with the serotonin reuptake inhibiting antidepressant, fluvoxamine (FLU), utilizing EEG mapping, psychometric and psychophysiological measures. 16 healthy volunteers (8 males, 8 females) aged 21-35 (man 27) years received randomized and at weekly intervals single oral doses of placebo, 12.5 and 25 mg TIA and 50 mg FLU. 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 hours; blood sampling, in addition, at hour 1. TIA plasma levels rose fast to peaks at 1-2 hours and declined rapidly as well, while the MC5 metabolite peaked in the 4th hour and declined more slowly. EEG mapping demonstrated that both TIA and FLU induced significant changes in brain function between the 1st and 8th hour, which, however, differed in their time course. 12.5 mg TIA exhibited, as compared with placebo, slight activating properties in the EEG (decrease of delta and theta, increase of alpha and beta, acceleration of the centroid), parallelled by thymopsychic improvement (mood elevation). 25 mg TIA showed EEG activation up to the 4th hour, later EEG sedation, accompanied by an initial thymopsychic improvement and differential changes thereafter (improved mood, decreased vigility), with the noopsyche improving at all times (attention, Pauli test). 50 mg FLU induced initially sedation and thereafter activation, accompanied by thymopsychic deterioration and subsequent improvement, the latter also being observed in the noopsyche (attention, memory). In pupillary and skin conductance measures, generally a slight activation occurred after placebo, which was attenuated by 25 mg TIA. Correlation maps between plasma levels and EEG changes demonstrated: the higher the TIA plasma levels, the more absolute and relative beta power, the less alpha power and the faster the centroid of the total power spectrum, reflecting CNS-activation. Topographically, the correlations were mostly seen over both fronto-temporal regions. In the latter, dominant frequency signalled desactivation in the right and activation in the left hemiphere after both antidepressants which, thereby induced changes in brain function opposite to those observed in depression. Both drugs were well tolerated.

Adult↗
PubMed1996

Severe hypoglycaemia unawareness is associated with an early decrease in vigilance during hypoglycaemia.

To elucidate neurophysiological characteristics in hypoglycaemia unawareness, we investigated the relationship between electroencephalography (EEG) parameters of vigilance and awareness of various symptom categories early in response to hypoglycaemia in intensively treated diabetic patients with different degrees of hypoglycaemia unawareness. Hypoglycaemia (venous plasma glucose below 2.2 mmol/1) was induced with an intravenous insulin bolus in seven patients with insulin-dependent diabetes mellitus (IDDM) with a history of hypoglycaemia unawareness and repeated severe hypoglycaemia, as well as in a group of seven IDDM patients with good awareness of hypoglycaemia. Both groups were comparable in age, treatment strategy, glycaemic control and level of late complications. Basic cognitive performance and other symptom categories were estimated serially during a period of 2 h following the insulin bolus. A vigilance-controlled EEG was recorded continuously; its automatic analysis included the evaluation of vigilance indices. In the baseline prehypoglycaemic state, hypoglycaemia unaware patients showed higher initial vigilance (p = .05) than the aware group. Unaware patients reported fewer neurogenic (p = .002, mainly cholinergic, p = .009) hypoglycaemia symptoms during hypoglycaemia, and developed an impairment in cognitive performance over time (p = .002). EEG analysis indicated a more rapid decrease in vigilance after the hypoglycaemic stimulus for unaware patients than for aware patients. The lowering of plasma glucose to 3.06-3.89 mmol/l already induced a significant increase in delta and theta, as well as a decrease in alpha relative power only in the unaware group. Differences between groups with regards to the degree of deceleration were most pronounced early, during only slight hypoglycaemia, and topographically spread over central and parietal brain regions. Further lowering of plasma glucose induced an even more pronounced, abrupt increase in slow waves in unaware patients at higher plasma glucose levels than in hypoglycaemia aware subjects (for delta waves at 2.41 +/- 0.16 vs. 1.96 +/- 0.1 mmol/l, p = .04). This preceded the worsening of cognitive performance during hypoglycaemia in unaware patients by 19 +/- 3 min. Hypoglycaemia unawareness associated with previous unconsciousness is associated with- and may be the result of-an early hypoglycaemia-induced reduction in vigilance and an early EEG deceleration, which seems to be a teleologically effective measure for delaying eventual cerebral energy failure in hypoglycaemia.

Adult↗
PubMed1996

Hormonal, syndromal and EEG mapping studies in menopausal syndrome patients with and without depression as compared with controls.

UNLABELLED: The aim of the study was to investigate brain function in menopausal depression by EEG mapping, as compared with menopausal syndrome patients without depression and normal controls, and to correlate neurophysiological with clinical and hormonal findings in order to elucidate the pathogenesis of depression in the menopause. METHODS: One hundred and twenty-nine menopausal women, aged 45-60 years, with no previous hormonal replacement therapy were investigated in regard to hormones (estradiol [E2], follicle stimulating hormone [FSH]), clinical symptomatology (Kupperman Index [KI], Hamilton depression score [HAMD]) and brain function (EEG mapping). Based on KI and DSM-III-R research criteria for major depression, 3 groups were available for statistics (after removal of protocol violators): group A had a KI of <15 and no depression (n = 29); group B had a KI of > or = 15 and no depression (n = 29) and group C had a KI of > or = 15 and fulfilled the criteria for major depression (n = 60). RESULTS: EEG maps of depressed patients demonstrated less total power and absolute power in the delta, theta and beta band, more relative delta and less alpha power as well as a slower delta/theta and faster alpha and beta centroid than controls, suggesting a vigilance decrement. Group B did not differ from group A. Correlation maps showed significant relationships between estradiol levels and EEG measures (the lower the E2, the worse the vigilance) and between the EEG measures and the Hamilton depression (HAMD) score (the worse the vigilance, the higher the depression score). There were no correlations between the hormones E2 and FSH and the syndromes KI and HAMD. In the target variable, the asymmetry index, depressed patients showed less alpha power over the right than left frontal lobe, whereas normal controls exhibited the opposite. Group B did not differ from group A. The frontal asymmetry index was significantly correlated with the Hamilton depression score and suggests right frontal hyper- and left frontal hypoactivation in depression. CONCLUSIONS: Although hormonal findings are not directly linked to psychic changes, low estradiol levels do contribute to a decreased vigilance at the neurophysiological level , which is in turn correlated with higher depressive and menopausal symptomatology at the behavioural level. Depression is further correlated to a right frontal hyper- and left frontal hypoactivation.

Brain↗
PubMed1996

Multichannel auditory event-related brain potentials: effects of normal aging on the scalp distribution of N1, P2, N2 and P300 latencies and amplitudes.

Event-related potentials (ERPs) were recorded at 17 leads in an auditory oddball paradigm in 172 normal healthy subjects aged between 20 and 88 years. With advancing age, N1 latency increased parietally (0.12 ms/year), P2 latency increased frontally (0.34 ms/ year) and N2 and P300 latencies increased all over the scalp (0.37 ms/year for N2; 0.92 ms/year for P300). P300 latency/age relationship was curvilinear with accelerated latency increase in elderlies (0.35 ms/year for subjects below 60 years; versus 2.03 ms/year for subjects above 60 years). With advancing age, standard tone ERP amplitudes were enhanced frontally (0.03 microV/year for N1; 0.07 microV/year for P2), N2 amplitudes were attenuated frontally (0.11 microV/year) and P300 amplitudes were attenuated parietally (0.15 microV/year). Multichannel analysis demonstrated that ERP latencies and amplitudes depended on electrode location. Standard tone ERP latencies changed their topographic distribution with age, whereas target tone ERP latencies did not. While N1 amplitude distribution was unaffected by age, P2, N2 and P300 topography changed significantly with age: P2 topography to a more frontal distribution and increased 'global field power'; N2 topography to a more parietal distribution: P300 topography to a more frontal and more equipotential distribution Thus, specific age effects on different ERP components were confirmed.

Acoustic Stimulation↗
PubMed1996

On the cerebro-protective effects of caroverine, a calcium-channel blocker and antiglutamatergic drug: double-blind, placebo-controlled, EEG mapping and psychometric studies under hypoxia.

1. In a double-blind, placebo-controlled study, the acute antihypoxidotic properties of the calcium-channel blocking and antiglutamatergic caroverine were investigated utilizing blood gas analysis, EEG mapping and psychometry under a transient, reversible, hypoxic hypoxidosis. 2. The latter was induced by a fixed gas combination of 9.8% oxygen (O2) and 90.2% nitrogen (N2) (found in 6000 m altitude), which was inhaled for 23 min under normobaric conditions by 16 healthy, young volunteers. They received randomized after an adaptation session, single oral doses of placebo, 40, 80 and 120 mg caroverine. Evaluation of blood gases, EEG mapping and psychometry were carried out 0, 2, 4, 6 and 8 h post-drug, during hypoxia. 3. Blood gas analysis demonstrated a drop in PO2 from 95 to 33 and 30 mmHg, in PCO2 from 38 to 30 and 30 mmHg in the 14th and 23rd minute of inhalation, respectively, while pH increased from 7.41 to 7.50 and 7.51. Base excess and standard bicarbonate remained stable. 4. EEG mapping under hypoxia exhibited a marked increase of delta/theta, decrease of alpha and an increase of superimposed beta activity, which reflects deterioration of vigilance. 5. Caroverine attenuated this hypoxia-induced vigilance decrement in a dose- and time-dependent manner 6-8 h after 80 mg and 2-8 h after 120 mg. 6. Hypoxic hypoxidosis induced a deterioration of memory and attention variability, which was mitigated by 80 and 120 mg caroverine. However, there was an augmentation of the hypoxia-induced decrement in psychomotor performance after 120 mg. 7. The drug was well tolerated, and there were no significant differences compared with placebo with regard to pulse and blood pressure.

Adult↗
PubMed1996

EEG topography during insulin-induced hypoglycemia in patients with insulin-dependent diabetes mellitus.

A group of young patients with insulin-dependent diabetes mellitus (n = 14; 8 men, 6 women; 33.1 +/- 8.9 years) were examined by topographic EEG mapping under normoglycemic and hypoglycemic conditions (glucose levels after intravenous insulin injection down to 32.6 +/- 7.6 mg/dl). From the clinical aspect, 7 of them had a good and 7 had a poor awareness of hypoglycemia. During hypoglycemia, a decrease in alpha activity (p < 0.05), an increase in delta (p < 0.05), and especially in theta activity (p < 0.05) were found. The most sensitive parameter was the alpha/theta ratio. In the range of slight hypoglycemia (50-60 mg/dl) the increase in delta and theta activity showed a topographic maximum in lateral frontal regions. During deep hypoglycemia there was a topographic maximum of slow frequencies in posterior parts of the brain (centrotemporal to parieto-occipital regions). The differences between the group with good and with poor awareness of hypoglycemia were most pronounced during slight hypoglycemia in C3, C4, and Pz (p < 0.05). At lower glucose levels group distinction was no longer possible. These EEG changes correspond to a temporary organic brain syndrome.

Adult↗
PubMed1996

First-night-effects on generalized anxiety disorder (GAD)-based insomnia: laboratory versus home sleep recordings.

First-night effects (FNE) were comparatively investigated in patients with disorders in initiating and maintaining sleep (DIMS) associated with generalized anxiety disorder (GAD) in laboratory (n = 22) and home sleep polysomnography (n = 21). Patients had to be drug-free for at least 2 weeks prior to the first recording. Evaluation measures included 1) objective data on sleep initiation and maintenance; 2) sleep architecture based on polysomnographic recordings, analyzed visually according to the criteria of Rechtschaffen and Kales; 3) subjectively estimated sleep and awakening quality, assessed by a self-rating scale and visual analogue scales; 4) objective awakening quality as measured by a psychometric test battery; and 5) psychophysiological data, including critical flicker frequency, muscle strength, pulse, and blood pressure. Statistical analysis using multivariate analysis of variance (MANOVA) demonstrated multiple FNE in both groups regarding sleep efficiency, total sleep time, percentage of time in stage 2 sleep, percentage of time in stage 3/4 sleep, minutes of rapid eye movement (REM) sleep, and REM sleep latency. There was a group-by-night effect in the number of awakenings. There were no significant FNE regarding subjective sleep and awakening quality in either group. Differential adaptation effects were observed in attention and fine motor activity, with improvement in laboratory-recorded patients and deterioration in home-recorded patients. Differential findings also occurred in regard to evening blood pressure, with laboratory-recorded patients showing more adaptation.

Adult↗
PubMed1995

Acute effects of the anxiolytics suriclone and alprazolam on cognitive information processing utilizing topographic mapping of event-related brain potentials (P300) in healthy subjects.

In a double-blind, placebo-controlled, cross-over study, acute effects of suriclone--a cyclopyrrolone derivative--were investigated by means of topographic mapping of event-related potentials (ERPs). Fifteen normal volunteers, aged 22-35 years, received randomized, oral single doses of placebo, 0.1 mg, 0.2 mg and 0.4 mg suriclone and 1 mg alprazolam as a reference compound. ERPs were investigated in an auditory oddball paradigm before and 3 h after intake of each drug. In addition to 17 EEG leads, vertical and horizontal electro-oculograms (EOGs) were recorded. After EOG minimization and artifact identification, the peak latencies of the spatial average were determined by an automatic procedure. Compared to placebo, no significant effects of the low and middle doses of suriclone on N1 amplitude were observed; the highest dosage reduced N1 amplitude, as did 1 mg alprazolam to an even greater extent. While no consistent effects on P2 amplitude were observed after suriclone, alprazolam reduced P2 amplitude. P300 amplitude was reduced only after the highest dosage of suriclone, but much more so after alprazolam. P300 latency was not affected significantly by suriclone, but a marked prolongation of P300 latency was observed after 1 mg alprazolam. Concerning N1 and P2 effects, alprazolam, but not suriclone, may have an inhibitory influence on stimulus-induced cortical arousal. Concerning P300 effects, the used doses of suriclone were superior to 1 mg alprazolam, which seemed to have reduced cognitive information processing capacity and prolonged stimulus evaluation time. Self-rated well-being (adjective checklist) showed subtle beneficial effects after 0.1 mg and 0.2 mg, but marked sedative effects after both 0.4 mg suriclone and 1 mg alprazolam.

Adult↗
PubMed1995

Nicergoline in senile dementia of Alzheimer type and multi-infarct dementia: a double-blind, placebo-controlled, clinical and EEG/ERP mapping study.

In a double-blind, placebo-controlled study on the therapeutic efficacy and central effects of nicergoline, an ergot alkaloid with metabolic, antithrombotic and vasoactive action, 112 patients with mild to moderate dementia, diagnosed according to DSM III-R criteria (MMS 13-25), living in pensioners' homes, were included. Fifty-six were subdiagnosed as senile dementia of the Alzheimer type (SDAT), 56 as multiinfarct dementia (MID), based on computed tomography and Hachinski scores (< or = 49 SDAT, > or = 7 MID). They received, after 2 weeks' run-in period (placebo), randomized for 8 weeks either 2 x 30 mg nicergoline (NIC) or 2 x 1 placebo (PLAC) orally. The four subgroups (SDAT/NIC. SDAT/PLAC, MID/NIC, MID/PLAC; 4 x 28 patients) were comparable in regard to age and sex. Only four, four, four and two patients of the respective groups did not finish the study for minor reasons. Confirmatory statistical analysis demonstrated in the target variable-the Clinical Global Impression (CGI)-a significant superiority of Global Impression (CGI)-a significant superiority of NIC over PLAC in both the SDAT and MID groups. Global improvement (CGI item 2) was seen in both nicergoline subgroups (3 and 3), while no changes occurred under placebo (4 and 4, respectively). The responder versus non-responder ratio was in the SDAT/NIC group 16/8, versus 8/16 in the SDAT/PLAC group (chi 2 = 4.1, P = 0.04); in the MID/NIC group 17/7, versus 7/19 in the MID/PLAC group (chi 2 = 7.96, P < 0.005). Furthermore, there was a significant improvement of the Mini-Mental State and the SCAG score in both the MID and SDAT group after 8 weeks of nicergoline, which was significantly superior to the minimal improvement or no change in placebo-treated SDAT and MID patients. EEG mapping demonstrated in NIC-treated SDAT and MID patients a significant decrease in delta and theta, increase in alpha 2 and beta activity and an acceleration of the centroid of the total power spectrum as compared with pretreatment, while opposite changes occurred in PLAC-treated SDAT and MID patients. The differences between PLAC and NIC reached the level of statistical significance. Event-related potential (ERP) recordings demonstrated a significantly shortened P300 latency under NIC treatment in both SDAT and MID patients, while there was a trend towards lengthening under PLAC. Thus, nicergoline improved vigilance and information processing at the neurophysiological level, which leads at the behavioural level to clinical improvement both in degenerative and vascular dementia.

Alzheimer Disease↗
PubMed1995

Double-blind, placebo-controlled, hormonal, syndromal and EEG mapping studies with transdermal oestradiol therapy in menopausal depression.

In a double-blind, placebo-controlled study, the antidepressant and vigilance-promoting properties of transdermal oestrogen in post-menopausal depression were investigated utilizing hormonal, syndromal and EEG mapping evaluations. Sixty-nine menopausal women, aged 45-60 years without previous hormonal replacement therapy, diagnosed as major depression without psychotic or suicidal symptoms (DSM-III-R criteria), were randomly assigned to a 3-month treatment with transdermal oestradiol [Estraderm TTS (ETTS) 50 micrograms, applied twice weekly] or placebo. No other psychoactive medication was allowed. After removal of protocol violators, 32 patients were evaluable in each group, which did not differ in age, height or weight. As five patients discontinued prematurely in both groups and in one placebo patient a post-drug EEG could not be obtained, 27 patients remained in the ETTS and 26 in the placebo group for efficacy analysis. While in the placebo group, oestradiol (E2) and follicle stimulating hormone (FSH) remained unchanged, E2 increased and FSH decreased significantly in the ETTS group. Syndromal evaluation showed a significant improvement in the Kupperman Index (KI) as well as Hamilton Depression Rating Scale (HAMD) in both groups, with no inter-group difference. However, EEG mapping demonstrated significant inter-drug differences in brain function, mostly over the left temporal region. While ETTS patients showed an increase of alpha and alpha-adjacent theta activity and a decrease of beta activity, as well as an acceleration of the delta/theta centroid and a slowing of the alpha, beta and total power centroid, no changes occurred in the placebo-treated patients. These neurophysiological findings suggest improvement of vigilance by oestrogen, previously referred to as "mental tonic" effect. There were no changes, however, in the frontal alpha asymmetry index, reflecting left frontal hypo- and right frontal hyperactivation. Thus, this neurophysiological variable represents a state-independent marker for depression. The tolerability of ETTS was very good.

Administration, Cutaneous↗