Publications by authors named "Kleinlogel H"

Modern mobile phones emit electromagnetic fields (EMFs) ranging from 900 to 2000 MHz which are suggested to have an influence on well-being, attention and neurological parameters in mobile phone users. To date most studies have investigated Global System for Mobile Communications (GSM)-EMF and only very few studies were concerned with Universal Mobile Telecommunications System (UMTS)-EMF. Consequently, we tested the effects of both types of EMF, 1950 MHz UMTS (SAR 0.

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Modern mobile phones emit electromagnetic fields (EMF) ranging from 900 to 2000 MHz which are suggested to have an influence on well-being, attention and neurological parameters in mobile phone users. Until now most studies have investigated Global System for Mobile Communications (GSM)-EMF and only very few studies have focused on Universal Mobile Telecommunications System (UMTS)-EMF. Therefore, we tested the effects of both types of unilaterally presented EMF, 1950 UMTS (0.

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Patients with schizophrenia have reduced execution functions and white matter alterations indicating cerebral disconnectivity. Here we investigated the relationship between white matter integrity and event related potentials (ERP) during a continuous performance test (CPT). Anisotropy values were correlated with the brain electrical P300 microstate duration and P300 latency associated to the NoGo- and the Go-stimuli of the CPT in 11 patients with first episode schizophrenia and 11 matched healthy controls.

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Objective: NoGo-stimuli during a Continuous Performance Test (CPT) activate prefrontal brain structures such as the anterior cingulate gyrus and lead to an anteriorisation of the positive electrical field of the NoGo-P300 relative to the Go-P300, so-called NoGo-anteriorisation (NGA). NGA during CPT is regarded as a neurophysiological standard index for cognitive response control. While it is known that patients with chronic schizophrenia exhibit a significant reduction in NGA, it is unclear whether this also occurs in patients undergoing their first-episode.

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Most studies of continuous EEG data have used frequency transformation, which allows the quantification of brain states that vary over seconds. For the analysis of shorter, transient EEG events, it is possible to identify and quantify brain electric microstates as subsecond time epochs with stable field topography. These microstates may correspond to basic building blocks of human information processing.

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Rationale: Olanzapine is an atypical antipsychotic drug with a more favourable safety profile than typical antipsychotics with a hitherto unknown topographic quantitative electroencephalogram (QEEG) profile.

Objectives: We investigated electrical brain activity (QEEG and cognitive event related potentials, ERPs) in healthy subjects who received olanzapine.

Methods: Vigilance-controlled, 19-channel EEG and ERP in an auditory odd-ball paradigm were recorded before and 3 h, 6 h and 9 h after administration of either a single dose of placebo or olanzapine (2.

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Based on an integrative brain model which focuses on memory-driven and EEG state-dependent information processing for the organisation of behaviour, we used the developmental changes of the awake EEG to further investigate the hypothesis that neurodevelopmental abnormalities (deviations in organisation and reorganisation of cortico-cortical connectivity during development) are involved in the pathogenesis of schizophrenia. First-episode, neuroleptic-naive schizophrenics and their matched controls and three age groups of normal adolescents were studied (total: 70 subjects). 19-channel EEG delta-theta, alpha and beta spectral band centroid frequencies during resting (baseline) and after verbal stimuli were used as measure of the level of attained complexity and momentary excitability of the neuronal network (working memory).

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The aim of this study was to search for differences in the EEG of first-episode, drug-naive patients having a schizophrenic syndrome which presented different time courses in response to antipsychotic treatment. Thirteen patients who fulfilled DSM-IV diagnosis for schizophrenia or schizophreniform disorder participated in this study. Before beginning antipsychotic treatment, the EEG was recorded.

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Electrophysiological approaches range from global EEG studies to single unit recordings. Quantified EEG studies indicate that cognition enhancers increase the power of fast-frequency (beta) EEG activity in humans and the duration of hippocampal theta in animals. A problem here is the distinction between improved cognition and increases in general arousal, although the two might have the same end effect.

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The characteristics of the power density spectra of the frontal and occipital cortical EEG between 1 and 31 Hz as well as the total power of the neck muscle EMG during an 8-second epoch were used to differentiate 8 vigilance stages in normal rats. The following stages and the time spent within these stages during a 6-hour recording (9.00-15.

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In order to gain a better understanding of the role of the noradrenergic system in the control of the EEG sleep-waking stages, the effects of the selective alpha 1-antagonist prazosin was investigated in the rat. Oral doses of prazosin (0.1-10 mg/kg) were administered that have been shown to enter the brain.

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The effects of oral paroxetine and zimeldine on EEG sleep-waking phases in the rat were investigated over a wide dose range. To ascertain that at the doses used for the EEG studies paroxetine and zimeldine selectively affect the serotoninergic system, their effects on brain 5-hydroxytryptamine (5-HT), dopamine and noradrenaline were determined. It was found that paroxetine and zimeldine at doses of 1-18 mg/kg dose-dependently prolonged waking and shortened slow-wave sleep and paradoxical sleep.

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Approximately 20% of Charles River rats which were chronically implanted with brain electrodes for EEG recordings exhibited within half a year of the implantation spontaneous, paroxysmally occurring, steep EEG potentials of high amplitude (spikes and waves) whilst falling asleep. These EEG paroxysms were dose dependently antagonized by the 'petit mal' drugs dipropylacetate, ethosuximide and trimethadione as well as by the anticonvulsant drugs diazepam and nitrazepam. The neuroleptics chlorpromazine, haloperidol and thioridazine prolonged the EEG paroxysms.

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The sleep-waking pattern of the isolated female rat showed a clear ultra-, circa- and infradian vigilance rhythm. The ultradian period was about 4-6 h. During the day, the amount of slow wave sleep (SWS) decreased and that of paradoxical sleep (PS) increased.

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There are distinct differences, but also marked similarities between the quantitative and qualitative sleep parameters of various species of laboratory animals. The increasing use of computers and the automatic, powerful methods of EEG analysis in sleep research give rise to the belief that in the near future the sleep of the various species may be better differentiated. However, one commonly encountered problem when attempting to compare sleep patterns of different species is the use of different brain areas as recording sites.

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A cable technique is described which allows continuous, unsupervised recording of cortical EEG and neck muscle EMG in rats over long periods. In addition, brain temperature is measured with an NTC-thermistor. After suitable adaptation the signals are computed for selected 8 s epochs into Hjorth parameters by means of a Normalised-Slope-Descriptor.

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The effects of the peripheral and central alpha-adrenoceptor stimulant and antihypertensive agents clonidine and BS 100-141 (N-amidino-2[2,6-dichlorophenyl]acetamide - HCl) on EEG sleep patterns in rats and on blood pressure in pithed rats have been investigated. Whereas both compounds abolished paradoxical sleep (PS), clonidine, in contrast to BS 100-141, markedly increased the sleeping time. Both drugs caused a dose-dependent increase in the blood pressure of pithed rats.

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