Characteristics of narcolepsy in preteenaged children.

Narcolepsy is rarely diagnosed in preteenaged children. Its clinical and polysomnographic manifestations, some of which are unusual, are described in four children who were observed prospectively. The mean age at onset of hypersomnia was 10.2 years (range 8.4 to 11.2 years). Daytime naps among these children were lengthy, ranging from 20 to 120 minutes, and generally were considered unrefreshing. Cataplexy was present at the onset in all four children. Three of the four children were obese, with the concurrent nocturnal snoring prompting a misleading concern about obstructive sleep apnea syndrome in two children. The histocompatibility DR2 antigen was present in all four children. Significant behavioral manifestations appeared in all of them. The response to stimulant medications was, at best, modest. Narcolepsy may be difficult to diagnose in this age group. However, a careful history eliciting sleep/wake dysfunction (including cataplexy), leukocyte assays for the histocompatibility DR2 antigen, and serial polysomnographic studies may enable early recognition and treatment of this disease.

Ventral hippocampus spikes during sleep, wakefulness, and arousal in the cat.

The relationship between high amplitude (100--300- micro V) spike potentials (50--100 msec duration) in the ventral hippocampus (VH) and sleep-wakefulness stages was investigated. Forty-eight hours of continuous recordings taken from 5 chronically implanted cats were quantitatively scored for stage by digitized outputs of integrated EEG and electromyographic signals and for VH spikes by automatic devices. (1) A very strong relationship was observed between VH spike rates and EEG stage. Spikes were rare during wakefulness and paradoxical sleep (PS). They were always most frequent during nonrapid eye movement (NREM) sleep stages, progressively increasing through drowsiness, moderate amplitude slow wave activity, and high amplitude slow wave activity. (2) VH spike rates varied inversely with level of behavioral arousal within wakefulness. Rates were lowest during the presentation of novel experimental stimuli, higher during spontaneous movement, and highest during quiet wakefulness. (3) VH spikes anticipated stage changes independent of the quantified EEG. Spike rates increased from previous baseline levels in the 30 sec epoch of waking immediately preceding NREM sleep onset and in the transition period between PS and NREM sleep. They decreased significantly from previous base-line levels in the 30 sec epoch of NREM sleep preceding either waking or PS. These results show that the VH spike is a potentially useful noncortical indicator of NREM sleep. Within wakefulness and in the anticipation of stage changes it can be a more sensitive indicator of sleep processes or arousal level than the EEG.

The indications for polysomnography and related procedures.

This paper is a review of the literature on the use of polysomnography in the diagnosis of sleep disorders in the adult. It is based on a search of MEDLINE from January 1966 through April 1996. It has been reviewed and approved by the Board of Directors of the American Sleep Disorders Association and provides the background for the accompanying ASDA Standards of Practice Committee's Parameters for the Practice of Sleep Medicine in North America. The diagnostic categories reviewed are: sleep-related breathing disorders; other respiratory disorders; narcolepsy; parasomnias and sleep-related epilepsy; restless legs syndrome and periodic limb movement disorders: insomnia; and circadian rhythm sleep disorders. Where appropriate, previously published practice parameters papers are cited and discussed. The relevant published peer-reviewed literature used as the basis for critical decisions was compiled into accompanying evidence tables and is analyzed in the text. In the section on the assessment of sleep apnea syndrome, options for estimating pretest probability to select high risk patients are also reviewed. Sleep-testing procedures other than standard polysomnography are also addressed (daytime polysomnography, split-night studies, oximetry, limited full respiratory recordings, and less-than-full respiratory recording) and treatment-related follow-up studies are discussed.

The effects of flurazepam, lorazepam, and triazolam on sleep and memory.

This study evaluated the effects of flurazepam 30 mg, lorazepam 4 mg, triazolam 0.5 mg, and placebo upon sleep and memory in eleven normal male subjects continuously monitored for nighttime EEG, EOG, and EMG recording. Subjects received each drug or placebo for two consecutive nights per week for 4 weeks in a repeated measures, double-blind, Latin Square design. Three hours post-administration, subjects were awakened and presented with a series of tasks. Recall was assessed immediately following task presentation and after the final morning awakening. The results showed that every drug significantly decreased stage 1, increased stage 2, and produced no change in stage 3--4 sleep in comparison to placebo. Only lorazepam significantly decreased REM percent. Post-drug recall was significantly decreased in comparison to placebo at night and was further decreased in the morning. Morning recall was significantly poorer when the return to sleep was 2.5 min or less than when the return to sleep was greater than 5 min following the nighttime awakening in all drug conditions. These results indicate that 1. failure of memory consolidation rather than failure of retrieval is the most likely explanation for the morning memory loss and 2. hypnotic drug properties, measured by latency to fall back asleep, affect memory consolidation.

The differential effects of short- and long-acting benzodiazepines upon nocturnal sleep and daytime performance.

Hypnotic drugs are the most frequent medical intervention for providing symptomatic relief of insomnia. Both effective amelioration of the insomnia complaint and the minimization of residual effects upon daytime performance must be considered in the selection of these medications. Data are presented here which compare the effects of short- and long-acting benzodiazepines upon sleep and upon waking performance. Unlike short-acting hypnotics with half-lives of up to 10 h (lorazepam, triazolam and temazepam), long-acting hypnotics with half-lives of up to 100 h (flurazepam, ketazolam) produce suppression of both REM and Stage 3--4 sleep which persists during the drug withdrawal (recovery) period. The half-life of hypnotics is also directly related to the duration of residual effects upon daytime performance. Hypnotics with long half-lives (flurazepam) produce more prolonged performance decrements than hypnotics with short half-lives (temazepam). In insomniacs, both effects upon sleep and upon walking performance must be considered in the selection of a hypnotic.

Effects of brotizolam, flurazepam and placebo upon nocturnal auditory arousal thresholds.

Auditory awakening thresholds (AAT) and the back-to-sleep latency (BSL) after nocturnal awakenings from Stage 2 sleep were studied in normal male subjects after placebo, brotizolam (0.25, 0.375 and 0.50 mg) and flurazepam (30 mg). AAT (dB) was measured in five trials spaced across the night in a 'double awakening' procedure with the second awakening in each trial made from Stage 2 sleep. Each drug condition was associated with elevated mean AAT across the five trials in comparison with placebo. In a trial-by-trial analysis only 0.50 mg brotizolam and 30 mg flurazepam were consistently higher in the first three trials compared with placebo. All active drug conditions decreased the mean BSL across all trials in comparison with placebo, but only 30 mg flurazepam and 0.50 mg brotizolam consistently shortened BSL in the first three trials. Brotizolam (0.50 mg) and 30 mg flurazepam are similar in their effects. The subjective improvement reported in insomniac subjects following hypnotic administration may be related to elevation in arousal thresholds and a quick return to sleep after nocturnal sleep disruption.