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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 226 (1981), S. 63-71 
    ISSN: 1432-1459
    Keywords: Sleep disorder ; EEG ; Body temperature ; Circadian rhythm
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Ein zwölf Jahre alter Junge, der seit seinem achten Monat an Enzephalopathie litt, zeigte einen verlängerten Schlaf-Wach-Zyklus mit einer Dauer von 10–15 Tagen. Seine Körpertemperatur folgte dabei einem circadianen Rhythmus, aus dem geschlossen werden kann, daß einige normale circadianen Oszillatoren intakt waren. Dieser lange Schlaf-Wach-Zyklus konnte weder durch Gaben von Methylphenydat noch durch heftiges Wecken gestört werden, woraus man schließen kann, daß der Zyklus nicht dieselben Eigenschaften besitzt wie andere Rhythmen und die 10–15-tägige Periode des Schlafens und Wachens wahrscheinlich durch Mechanismen kontrolliert werden, die sich sehr von denen unterscheiden, welche das Verhalten im Normalzustand steuern. Das Datenmaterial belegt das Vorhandensein multipler Schwingungsrhythmen beim Menschen.
    Notes: Summary A severely brain-damaged boy of 12 years had a prolonged sleep-wakefulness cycle of 10–15 days' duration. His body temperature followed a circadian rhythm, suggesting that some normal circadian oscillators were intact. The long sleep-wakefulness cycle could not be influenced by either methylphenidate administration or enforced wakefulness, which suggests that the cycle did not have the same properties as other rhythms, and the 10–15-day periods of sleep-wakefulness were probably controlled by mechanisms different from those operating in normal state. The case shows that there are multiple oscillating mechanisms in the control of different rhythms in humans.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: EEG ; ERP ; P300 ; Benzodiazepine ; Hypnotics ; Cognition ; Sleepiness
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present study was to clarify whether cognitive impairments caused by benzodiazepines (BDZs) are a consequence of their specific direct effects on cognitive function or whether they are explained as secondary effects of increased sleepiness. Ten healthy men (mean age, 33.9 years) participated in two experimental sessions in a randomized cross-over, double-blind study: in one session subjects were given a placebo and in the other they were given 0.125 mg triazolam (TRZ). Each experimental session was conducted on 1 day. After a pre-drug EEG recording and an event-related potential (ERP) recording, under an oddball paradigm, subjects took the TRZ or placebo orally at 1000 hours. Thereafter, EEG and ERP recording sessions, following the same procedure as the pre-drug sessions, were conducted at 1, 2, 4, 6 and 8 h after drug administration. The EEG and ERP recordings from Cz and Pz referred to the bilaterally linked ear electrodes were used. We found that P300 latency was significantly prolonged in TRZ condition at 2 h (Pz) and 4 h (Cz and Pz) after TRZ, and that the P300 amplitude was significantly reduced at 2 h (Cz and Pz) and 4 h (Pz) after TRZ, compared to the same times after placebo. The absolute power values for the theta (4–7 Hz), alpha 1 (8–9 Hz), and alpha 2 (10–12 Hz) bands did not differ at any measurement time between the treatments. Only the beta band (13–19 Hz) power value was significantly elevated after the TRZ administration (versus placebo). No significant sedative effects were detected in subjective measurements. These results indicate that a single oral dose of 0.125 mg TRZ caused cortical changes without distinct general sedation or subjective sleepiness.
    Type of Medium: Electronic Resource
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