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In this study, we compared the effect of group and cognitive behavioral treatment (CBT) in clinically referred patients with chronic insomnia. The participants were 32 individually treated primary insomniacs and 74 individuals with either primary or secondary insomnia treated in a group (5-7 patients per group). The primary outcome measures were subjective sleep, quality of life (QOL), and psychological well-being. CBT produced significant changes in sleep onset latency, total sleep time, sleep efficiency, and wake after sleep onset. For total sleep time and sleep efficiency, the improvements were maintained at follow-up as well. In the questionnaires, significant improvements from treatment were seen for the Sickness Impact Profile, Sleep Evaluation Form, and Dysfunctional Beliefs and Attitudes About Sleep. All these improvements remained significant at follow-up. We conclude that CBT for insomnia is effective for both individual and group treatment. Improvements were seen in subjective sleep parameters, QOL, attitudes about sleep, and sleep evaluation in general, both posttreatment and at follow-up.

In the last years, actigraphy has been used more often for clinical research and research evaluation of sleep disorders. Compared to polysomnography, actigraphy is cheap and less time-consuming. Actigraphy provides more objective information about sleep than sleep logs. Although the algorithms to score sleep and wake based on motions measured by actigraphy are still being improved, we believe that the role of actigraphy in the clinical evaluation of sleep in insomnia is limited. Instead of using actigraphy to distinguish a wakeful state from sleep in insomnia, we might better use the activity plots which the actigraph provides to get more insight into the physiological hyperarousal or restfulness of insomnia patients.

There is growing public concern about the use of gamma-hydroxybutyrate (GHB) as a party drug. This justified concern about misuse, however, should not lead to prohibition of the drug as it is efficacious in narcolepsy.

Poor sleep is a common complaint, accounting for 4-5% of all general practitioner consultations. Disorders of initiating sleep are overrated by patients compared with disorders of maintaining sleep, despite the greater effect of the latter on daytime performance. There is frequently a discrepancy between subjective observations and objective measurements of sleep. General practitioners should pay attention to sleep disorders lasting more than three weeks and should bear in mind that poor sleep is a symptom, the underlying cause of which needs to be determined. Good coordination of endogenous biorhythms and external life and working circumstances can positively influence sleeping patterns. Sleep onset latency determines the amount of deep sleep and, thus, the duration and stability of core sleep. General practitioners usually prescribe a single type of benzodiazepine drug with a half-life of 5-10 h for sleep disorders. Such drugs cause the patient to fall asleep quickly, to have a considerable period of uninterrupted sleep with little waking and to wake in the morning with a subjective feeling of having slept well. A number of less desirable changes can occur, however, that may produce, for example, anxiety dreams, increased snoring and sleep apnoea periods at night, and weakness of muscles during the day. The third generation of hypnotic agents produce less undesirable changes than the second generation. Zolpidem (an imidazoypridine), one such agent, seems to provide an effective treatment for insomnia without inducing undesirable side-effects.

In order to test the assumption that the sleep stability increases as the number of shifts and awakenings decreases, all-night sleep recordings (registered at home) were reanalyzed. The registrations belong to 10 young good sleepers, 10 adult good sleepers, 10 insomnia patients without treatment, 10 treated with a benzodiazepine and 10 treated with a nonbenzodiazepine hypnotic, 10 patients with proven narcolepsy, and 10 with obstructive sleep apnea syndrome (OSAS). For each of the categories NREM-1-2, NREM 3-4, and REM sleep, indices were defined as the number of shifts and awakenings that occurred per hour. Our results show that the indices of awakenings for the good as well for the bad sleepers were similar, whereas the indices of awakenings were very group dependent. We interpreted these results as showing that awakenings are valuable indicators for studying the quality of sleep, whereas shifts are not.

We treated 24 patients with narcolepsy for 4 weeks with gammahydroxybutyrate (GHB), 60 mg/kg/night, in a randomized double-blind placebo-controlled cross-over trial. Both clinical and polysomnographic criteria were used to assess the results. Compared to placebo, GHB reduced the daily number of hypnagogic hallucinations (from 0.87 to 0.28; p = 0.008), daytime sleep attacks (from 2.27 to 1.40; p = 0.001) and the severity of subjective daytime sleepiness (from 1.57 to 1.24 on a 0-4 scale; p = 0.028). The number of daily cataplexy attacks was reduced from 1.26 at baseline to 0.56 after 4 weeks of GHB intake. This reduction, however, was not statistically significantly different from the difference between baseline and placebo. GHB stabilized nocturnal rapid eye movement (REM) sleep, i.e. it reduced the percentage of wakefulness during REM sleep (p = 0.007) and the number of awakenings out of REM sleep (p = 0.016), and tended to increase slow wave sleep (p = 0.053). Adverse events were few and mild. We conclude that GHB is an effective and well-tolerated treatment for narcolepsy.

We prospectively studied the reliability and accuracy of the electroencephalogram as a predictor of the risk of recurrence within 2 years in 157 patients with untreated idiopathic first seizures. In all patients, a standard electroencephalogram and, if necessary, an electroencephalogram after partial sleep deprivation were obtained. All electroencephalograms were scored by one observer according to a fixed protocol. The finding of epileptic discharges was associated with a risk of recurrence of 83% (95% confidence interval, 69% to 97%) vs 41% (95% confidence interval, 29% to 53%) in patients with nonepileptic abnormalities and 12% (95% confidence interval, 3% to 21%) in patients in whom both electroencephalograms were normal. The sensitivity proved to be 48%. Interobserver agreement among four neurologists, who independently read 50 electroencephalograms, was found to be moderate. Predictive value for each observer, however, was good. We conclude that electroencephalogram findings may play a role in the decision to initiate or delay treatment after an idiopathic first seizure.

Eighteen non-pregnant woman complaining about insomnia were polysomnographically investigated for 3 nights with weekly intervals. They received placebo, 2 mg flunitrazepam or 10 mg zolpidem according to a cross-over double blind design. The patients were selected by general practitioners on the basis of subjective complaints. Zolpidem is a recently introduced short-acting imidazopyridine hypnotic, binding to a subunit of the benzodiazepine 1 receptor. Flunitrazepam is a well-known hypnotic, binding to both the benzodiazepine 1 and 2 receptor subtypes. Objective recording did not substantiate the subjective complaint of insomnia. Sleep patterns during placebo differed only little from that expected from age matched healthy persons. Both flunitrazepam and zolpidem significantly shortened sleep onset (5 min of continuous sleep beginning with NREM 1 sleep). The sleep composition following flunitrazepam was characterized by an increase in NREM 2, a prolongation of the time of REM sleep, a reduction of REM sleep and an increase in NREM 3-4 sleep during the first 2 h of sleep. The sleep composition following zolpidem resembled more than seen in persons without sleep complaints. However, as compared to placebo, there was a decrease of the time spent awake during sleep and an increase in NREM 3-4 during the first 2 of sleep.

A vigilance state is characterized by a particular activity state of the motorIautonomic and psychiclcognitive functional systems. S-W screening is possible through poly graphic monitoring of physiological variables and signals. Quantification of these signals introduces a set of parameters allowing the characterisation of the sleep (dys)function. There is no consensus regarding the choice or definition of these parameters. A particular cluster is presented and their informative value with respect to clinical practice and research is discussed.

In the present study children suffering from primary generalized absence epilepsy were asked to estimate time under EEG monitoring. They were asked to press a button when they thought that a fixed period of time had elapsed. Only the first response after the passage of the interval was reinforced. The dependent variable was the duration of the interval between the start of the trial and the first response, the post-reinforcement time. This parameter was used as an index for the accuracy of time estimation. The performance of the subjects in trials with and without spike wave discharges was compared. Short spike wave discharges (less than 3 s) prolonged the duration of the post-reinforcement pause while longer ones reduced its duration. The prolongation was longer than could be anticipated from the duration of the spike wave discharge. It was also found that the time between the end of an EEG paroxysm and the first response was significantly shorter in trials with long spike wave discharges than in trials with short spike wave discharges. There were no differences between subjects with and without spike wave discharges. It was concluded that this type of time estimation task is sensitive in detecting cognitive disturbances induced by both short and long spike wave discharges. Moreover, it seems that after long spike wave discharges patients behave differently and are perhaps more severely disturbed.(ABSTRACT TRUNCATED AT 250 WORDS)

In a double-blind placebo-controlled trial, ritanserin (a 5-HT2 receptor blocker) 5 mg/day or placebo was added to the usual medication in 28 patients with narcolepsy during 4 wk. The effect was assessed by means of polysomnography, daily and weekly subjective evaluations, and Multiple sleep latency tests (MSLT). During the night ritanserin increased the amount of nonrapid eye movement slow wave sleep and reduced wakefulness after sleep onset. It improved the feeling of being refreshed in the morning after awakening and reduced subjective daytime sleepiness. The drug did not significantly influence sleep latency in the MSLT.

A case of an 11-year-old boy with an autosomal dominant form of paroxysmal kinesigenic choreoathetosis is presented. Routine EEG, sleep EEG recording, and registration of visual evoked potentials and somatosensory evoked potentials were normal. EEG with videomonitoring and registration of event-related potentials, however, showed abnormalities, which are discussed in detail. Our data provide further arguments in support of the hypothesis that paroxysmal kinesigenic choreoathetosis is the expression of a dysbalance in the cortico-striopallidal-thalamic loop, and has an extrapyramidal genesis.

In this paper we describe one hardware and two software automated sleep spindle detection methods, used in our laboratory. With each of the three methods at least 500 polygraphic sleep recordings were analyzed and the results compared with the outcome of the visual analysis. In this way we were able to evaluate the advantages and the disadvantages of each of the three methods and also to discuss the practical application of this method for clinical and scientific purposes, as for example a better quantification of the variation in sleep spindle density under influence of the intake of benzodiazepine derivatives.

In this study effects of temazepam on the EEGs of 10 healthy volunteers were detected using a standardized EEG registration procedure applied in a controlled environment. The EEGs were recorded both before and after administration of 20 mg temazepam as well as before and after placebo. A mean power spectrum was computed for each EEG from the 'eyes closed' condition, and the Student t test was used to detect differences in the spectra of the pre- and posttreatment EEGs in both placebo and drug conditions. For all 10 subjects the drug condition was easily distinguishable from the placebo condition based on the results of the t test.

The transient visual-evoked potentials (VEP), recorded in patients suffering from generalized epilepsy, can be characterized by a duplication of the negative peak with a latency of 70-100 ms, a strong increase in amplitude of the negative peak between 80 and 130 ms and the development of a high amplitude slow negative wave following the primary complex. In this study we have investigated to which degree these changes are influenced by the intravenous administration of clonazepam and sodium valproate. Therefore, VEPs were registered in 30 patients, suffering from generalized epilepsy, just before and immediately after the intravenous injection of 0.4-0.8 mg clonazepam and further at 15, 30 and 16 min thereafter. The same procedure was applied on 10 patients treated with an intravenous injection of 400 mg sodium valproate. In both groups we found more or less a reduction in number and degree of the mentioned VEP changes. The improvement was associated with a strong decrease in amplitude of the VEP components in the group treated with clonazepam but was not seen in the sodium valproate group.

Sleep-wakefulness patterns recorded following 1 night total sleep deprivation were studied in 15 normal subjects and in 252 epileptic patients. The patients were taking various types and combinations of antiepileptic medication. Sleep deprivation caused a reduction in sleep latency and an increase in NREM stage 3 + 4 sleep. This effect persisted in patients treated with valproate sodium and/or carbamazepine. In patients treated with diphenylhydantoin light NREM 1 + 2 sleep increased. In those treated with antiepileptics + chlorazepate, both an increase in NREM 1 + 2 and NREM 3 + 4 sleep was seen. The former probably reflects a benzodiazepine effect, the latter is due to a sleep deprivation effect. In patients treated with antiepileptics + clonazepam, a benzodiazepine effect predominated.