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Biomedical subjects

F Zorick

Publications and source records attributed to F Zorick.

At least 37 records · Page 2Linked to original sources
PubMed1988

Narcolepsy in a pediatric population.

Narcolepsy, a sleep-wake disorder of unknown cause, has been reported as occurring in the pediatric population, but only two reports of cases in the literature have included polysomnographic data on children with narcolepsy. We compared the clinical and polysomnographic data on a series of eight patients 15 years of age or younger and an adult comparison group with narcolepsy. All patients presented with excessive daytime sleepiness, and no significant difference was found between groups for the incidence of cataplexy, hypnagogic hallucinations, and sleep paralysis. On polysomnographic evaluation the pediatric group had increased total sleep time, percent-stage 3/4 sleep, percent rapid eye movement sleep, and decreased stage 1 sleep, which all are expected age-related differences. The pediatric group also showed a greater degree of daytime sleepiness and an increased frequency of sleep-onset rapid eye movement periods. While pediatric patients with narcolepsy resemble adults in their mode of presentation and the incidence of accessory symptoms, the increase in severity of sleepiness highlights the importance of diagnosing narcolepsy in children as early as possible so that treatment can be initiated.

Adult↗
PubMed1988

Reversal by caffeine of triazolam-induced impairment of waking function.

Twelve, healthy normal men aged 21-25 years received each of four treatments (triazolam placebo plus caffeine placebo, triazolam 0.50 mg plus caffeine placebo, triazolam 0.50 mg plus caffeine 4 mg/kg, triazolam 0.50 mg plus caffeine 8 mg/kg), double blind, in a Latin-Square design. Triazolam or placebo was administered at 0830 and caffeine or placebo at 1000 and 1245. On two memory tasks, administered at 1015 with an immediate recall and a delayed recall at 1230 following a 90 min nap (1030-1200), both immediate and delayed recall was impaired by triazolam. Neither caffeine dose reversed the impairments. Sleep latency and sleep efficiency were improved by triazolam and not reversed by caffeine. On a performance battery presented at 1300 most measures of performance were impaired by triazolam; in general the caffeine dose of 4 mg/kg partially reversed the effect while the dose of 8 mg/kg completely restored performance.

Adult↗
PubMed1988

Daytime alertness in patients with chronic insomnia compared with asymptomatic control subjects.

Despite the subjective reports of patients with difficulty initiating and maintaining sleep (DIMS) that they are impaired during the day, consistent differences in daytime functions have not been found between normal sleepers and patients with insomnia. The present study compares polysomnography and Multiple Sleep Latency Test (MSLT) data from 70 clinic patients seeking evaluation for chronic insomnia with data from a group of 45 asymptomatic sleepers. The DIMS group was found to sleep significantly less than the control group; yet they were also significantly more alert than the control group the following day, as measured by MSLT. Within the insomnia diagnostic subgroups, a correlation of -0.67 (p less than 0.05) was found between nocturnal total sleep time and mean MSLT. The results are interpreted as supporting the existence of a tendency towards physiological hyperarousal in patients with chronic insomnia. This tendency may be exacerbated by other factors (e.g., personality disorder, periodic leg movements) also associated with insomnia.

Adult↗
PubMed1988

The effects of acute sleep restriction and extension on sleep efficiency.

This study employed a repeated measures design to assess the relationship between sleep efficiency and time-in-bed (TIB). Fourteen subjects underwent three TIB conditions: (5 hour, 8 hour, and 11 hour), which were presented in a Latin Square design. Subjects slept a total of six nights (two nights per condition) while being monitored by a wrist actigraph to determine sleep time. Sleep efficiencies (sleep time/TIB) were analyzed with a two-way repeated-measures ANOVA. The main effect of night was not significant. The main effect of TIB and the interaction of nights and TIB were significant. In the 11-hour condition, sleep efficiency fell from night one to night two, and on night two both the 5-hour and the 11-hour conditions were significantly different from the 8-hour condition. Analysis of total sleep time (TST) yielded the same results with the addition of a significant night-to-night difference in the 5-hour condition. It was concluded that sleep efficiency systematically changes with an extension or restriction of TIB from 8 hour.

Adult↗
PubMed1988

Increased daytime sleepiness enhances ethanol's sedative effects.

Thirty healthy men, 21 to 35 years old, received either 8.7, 13.0 or 17.4 mmol/kg (0.4, 0.6, or 0.8 g/kg) ethanol after 8 hours time in bed (TIB), one night of 5 hours TIB, and four nights of 5 hours TIB. Ethanol, administered as 80-proof vodka mixed 1:4 with tonic water, was consumed over 30 minutes (0900 to 0930 hours). Sleep latency was measured at 1000, 1200, 1400, and 1600 hours using standard sleep laboratory methodology. Breath ethanol concentration (BEC) was determined prior to each latency test. Mean latency to sleep on the four tests decreased from day 1 (8 hours TIB) to day 5 (fourth day of 5 hours TIB). On day 1 mean latency after 8.7 mmol/kg differed from that after 17.4 mmol/kg, with the 13.0 mmol/kg latency intermediate between the other two. On day 2 and day 5 during sleep restriction these dose differences were diminished. Latency on day 5 after 8.7 mmol/kg was similar to that of 13.0 mmol/kg on day 2, which was similar to that of 17.4 mmol/kg on day 1. The BEC did not change from day 1 to day 5 and significant dose differences between each dose remained consistent from day to day. These data show that increased basal levels of sleepiness enhance ethanol's sedative effects for even moderate ethanol doses.

Adult↗
PubMed1988

Daytime sleepiness in young adults.

The daytime sleepiness of a large sample (n = 129) of healthy, young (age 18-29) adults with no sleep-wake complaints was measured and compared with that of a sample (n = 47) of older (age 30-80) healthy, normal sleeping, subjects. Each spent 8 h in the laboratory on 1 night and received the Multiple Sleep Latency Test (MSLT) the following day. Sleep latency was measured at 1000, 1200, 1400, and 1600 h. Mean sleep latency ranged from 2 to 20 min within each group, but the shape of the distribution of latency between groups was different. The mean latency of young subjects (particularly college students) was shorter than that of the older subjects, with the differences occurring between the sleepiest 80% of each distribution. Among the college students, those with higher nocturnal sleep efficiencies (the previous night) were sleepier the following day than those with lower sleep efficiencies. The relation between nocturnal sleep efficiency and daytime sleepiness suggests that the increased sleepiness of average young adults is due to mild sleep restriction.

Adult↗
PubMed1987

Sedative effects of antihistamines.

The central effects of a newly developed, long-acting H1 antihistamine, loratadine (10 and 40 mg), were compared with those of a standard H1 antihistamine, diphenhydramine (50 mg three times a day) with measures of performance and daytime sleepiness (multiple sleep latency test). Sixteen healthy adults (six women and 10 men), 19 to 35 years of age, received each of the drugs and placebo for 2 days, separated by 5 days at home. Each day, the drug or placebo was administered at 8 A.M. and 12 and 4 P.M. Diphenhydramine was administered in three equal doses (50 mg), and loratadine was administered in a single dose followed by two placebo doses. Mean latency to sleep on tests done at 9 and 11 A.M. and 1, 3, and 5 P.M. was reduced significantly with diphenhydramine compared to placebo, whereas neither loratadine dose reduced sleep latency. Performance measured at 9:30 P.M. and 1:30 P.M. with a battery of tests, including reaction time, vigilance, digit symbol substitution, and symbol copying tasks demonstrated a significant reduction in symbols copied and digits substituted after diphenhydramine compared to both loratadine doses. These results demonstrate that loratadine (10 and 40 mg doses) did not have clinically significant central nervous system activity, whereas diphenhydramine increases sleepiness and disrupts performance efficiency.

Adult↗
PubMed1987

Experimental sleep fragmentation in normal subjects.

Recent research has suggested that sleep fragmentation in the absence of sleep loss is an important cause of excessive daytime sleepiness in certain clinical populations (e.g., sleep apnea syndrome or periodic leg movements). This study experimentally varied the number and rate of arousals in sleep to define more clearly the relation of sleep fragmentation and daytime sleepiness. Five male subjects participated in the study. Data from each were recorded for three consecutive nights (one baseline followed by two experimental nights) under three experimental conditions. All nocturnal polysomnograms were followed by a Multiple Sleep Latency Test (MSLT) the next day. The experimental conditions consisted of three different schedules of arousal produced by series of tones presented to subjects over headphones. The MSLT showed statistically significant changes after two nights of fragmented sleep, but the three fragmentation schedules did not differ from each other. Arousal threshold also changed significantly with sleep fragmentation from night one to night two.

Adolescent↗
PubMed1987

Fragmenting sleep diminishes its recuperative value.

The recuperative effects of naps fragmented by different rates of electroencephalographic (EEG) arousal were evaluated. Forty healthy subjects with normal hearing and daytime sleep tendency (measured by the Multiple Sleep Latency Test at 10:00 a.m., 12:00 p.m., 2:00 p.m., and 4:00 p.m.) were randomly assigned to one of five conditions. Each was deprived of sleep for one night and then at 8:30 a.m. was given 100 min of natural sleep, sleep with arousals 1/5 min, 1/3 min, 1/1 min, or no sleep. After the recovery nap at 12:00 p.m., 2:00 p.m., 4:00 p.m., and 6:00 p.m., sleep latencies were again evaluated. Mean sleep latencies increased linearly as the rate of arousal during the recuperative nap decreased. Latency in the high-arousal condition was similar to no sleep and lower than natural sleep. The sleep latency of the low-arousal condition was similar to natural sleep and higher than no sleep, whereas latency in the medium arousal condition was intermediate to and differed from both natural sleep and no sleep. Although the natural sleep provided recuperation relative to no sleep or fragmented sleep, it did not restore daytime sleepiness to the screening level.

Adult↗
PubMed1987

Ethanol and caffeine effects on daytime sleepiness/alertness.

Eighteen normal-sleeping young (mean age 25.6 years) volunteers received either ethanol (0.75 g/kg producing blood ethanol concentrations of 71.1 +/- 24.3 mg/100 ml on average) or caffeine (4.0 mg/kg dissolved in 300 ml of 97% caffeine-free instant coffee) at 0920-0950 h after spending 5, 8, or 11 h time in bed (TIB) the previous night. Latency to sleep onset was tested at 1000, 1200, 1400, and 1600 h. Mean sleep latency differed significantly between drugs on each day of testing, with subjects being sleepier after ethanol than caffeine. On day 2 the TIB manipulation produced significant differences in latency, with the 11-h condition differing from both the 8- and 5-h conditions. The significant interaction revealed that in fully rested subjects (11-h TIB), ethanol did not produce sleepiness to the degree it did after 5 or 8 h in bed. In this condition latencies were similar to those of the caffeine and 5- or 8-h TIBs.

Adult↗
PubMed1986

Sleep-wake abnormalities in narcolepsy.

To evaluate the degree to which sleep (REM vs. NREM) intrudes into wake and wake intrudes into sleep in narcolepsy, 103 patients with narcolepsy were compared to 105 patients with other diagnoses of disorders of excessive sleep (DOES). Narcoleptic patients had more frequent REM onsets on the multiple sleep latency test (MSLT) and nocturnal polysomnograms. But the MSLT latencies to REM versus NREM in narcoleptic patients did not differ. Nocturnal measures of REM pressure, percentage of REM, and REM latency excluding the REM onsets, did not differ among patient groups. With respect to the intrusion of wake into sleep, narcoleptic patients had more and longer awakenings compared with other DOES patients, but the distribution of wake into REM and NREM sleep did not differ among groups. These data suggest that narcolepsy is not exclusively a REM-related disorder, but involves an inability to sustain a specific neural state for periods comparable to those in normal subjects or other DOES patients.

Adult↗
PubMed1986

Alerting effects of naps in patients with narcolepsy.

As part of their standard diagnostic evaluation, 45 patients with narcolepsy and 45 patients with other disorders of excessive sleepiness (DOES), primarily obstructive sleep apnea, each underwent one of three nap conditions that involved manipulating time in bed on the 1600 h latency test of the standard multiple sleep latency test (MSLT) and varying the time between the 1600-h latency test and a subsequent fifth latency test. Compared with the mean of tests 1-4, a 15-min nap at 1600 h (condition 1) increased latency to stage 1 sleep on a latency test 15 min later in both groups. However, the increase was greater for patients with narcolepsy than with other DOES. A 30-min nap at 1600 h (condition 2) produced increased latency 15 min later, but the increase was greater for patients with other DOES. While narcoleptic patients showed no change in latency as a function of increased nap duration, the other DOES patients had increased latencies. When tested 30 min after a 15-min nap (condition 3), narcoleptic patients had latencies that did not differ from those of tests 1-4, while the other DOES patients sustained their increased latencies.

Adult↗
PubMed1986

Hypnotic residual effects of benzodiazepines with repeated administration.

Performance measures were compared to the multiple sleep latency test (MSLT) as indices to assess tolerance to the residual effects of benzodiazepine hypnotics during repeated nightly administration. Twelve healthy, normal sleepers received flurazepam 30 mg, temazepam 30 mg, and placebo for nine nights in a repeated measures, Latin-square design with 19 nights of recovery separating the treatments. As compared to placebo, both drugs altered sleep stage parameters in the early (nights 1-2) and late (nights 8-9) phases of the study. Hypnotic effects were found for both drugs in the early phase, but diminished for both in the late phase. The subjects' performance the next day was disrupted following treatment with flurazepam, but not with temazepam, during the early phase. Mean sleep latency on the MSLT was reduced by both drugs during the early phase. During the late phase, flurazepam did not disrupt performance but still affected the MSLT. Temazepam affected neither index the next day during the late phase.

Adult↗
PubMed1986

Chronic hypnotic efficacy of estazolam.

The chronic hypnotic efficacy of estazolam 2.0 mg was studied in five female and seven male subjects. Subjects with a complaint of insomnia verified by polysomnography were included in the study. Following a screening and adaptation period, subjects spent two consecutive nights a week in the laboratory. The protocol for medication was placebo for weeks 1, 2, 9 and 10 and estazolam for weeks 3-8. Estazolam 2.0 mg significantly improved sleep onset and total sleep time for up to six weeks of nightly administration without consistent recovery effects upon discontinuation.

Adult↗
PubMed1986

Dose effects of temazepam tablets on sleep.

The dose effects of temazepam tablets (15 and 30 mg) were studied at two sleep centres in 48 volunteers who had objective polysomnographic evidence of sleep onset insomnia. Volunteers slept in the laboratory, retiring at their usual bedtime after taking placebo or temazepam 30 min earlier, and were monitored for 8 h using standard polysomnographic techniques. Acute (nights 5-7) and short term (nights 11-13) temazepam, both 15 and 30 mg, improved the sleep of these volunteers by reducing sleep latency and increasing sleep time compared to the placebo baseline (nights 2-4). Dose differences were found primarily on the measurement of sleep staging, with 30 mg having a greater or more consistent effect than 15 mg. No residual effects were observed on the basis of questionnaires and objective tests of performance and no consistent evidence of disturbed sleep after discontinuing treatment was seen.

Adult↗
PubMed1985

Efficacy of a reduced triazolam dose in elderly insomniacs.

Elderly persons with insomnia are unique because the cause of their insomnia differs from that of younger people and their metabolism of benzodiazepine hypnotics differs as well. This study used nocturnal polysomnography and daytime sleep/wake tendency measures (Multiple Sleep Latency Test, MSLT) to assess the efficacy and safety of a reduced triazolam dosage (0.125 mg) in elderly subjects with insomnia. After 2 nights and an intervening day of screening each subject received triazolam and placebo for 2 consecutive nights presented in a counter-balanced design. Compared to placebo the reduced triazolam dose induced and maintained sleep thereby increasing total sleep time. Sleep stage distribution and the frequency of apneas and periodic leg movements was not altered. The improved sleep was associated with a restoration of the normal pattern of daytime alertness. The correspondence of this clinical data to known pharmacokinetic data is discussed.

Aged↗