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Biomedical subjects

F Zorick

Publications and source records attributed to F Zorick.

At least 19 recordsLinked to original sources

Neuropsychological function in obstructive sleep apnea syndrome (OSAS) compared to chronic obstructive pulmonary disease (COPD).

Forty-nine men, 25 with obstructive sleep apnea syndrome (OSAS) and 24 with chronic obstructive pulmonary disease (COPD), were evaluated with a standard 8-hour nocturnal polysomnogram, multiple sleep latency test the following day and a neuropsychological test battery. The OSAS patients had more respiratory disturbances per hour of sleep, more stage 1 sleep and greater daytime sleepiness than COPD patients. The OSAS patients were as impaired as the COPD patients in neuropsychological test functioning, with the pattern of impairment nonspecific as to hypoxemic-sensitive versus sleepiness-sensitive tasks, with two exceptions. The OSAS patients performed more poorly on a test requiring sustained attention and considered sensitive to sleepiness, whereas the COPD patients performed more poorly on a test requiring motor skills and sensitive to hypoxemia. These deficits in psychomotor and attention appear to be specifically related to patients group (OSAS vs. COPD), but the other deficits found in complex reasoning and memory are nonspecific.

Attention

Sleep disorders in patients on continuous ambulatory peritoneal dialysis.

Sleep complaints, habits, and medical history were surveyed in 81 patients chronically receiving continuous ambulatory peritoneal dialysis. Seventy-three percent of the sample reported insomnia, and 52% reported unintentional napping during the day. Behavioral factors (such as caffeine or alcohol use) or the severity of concurrent medical disease did not account for the sleep problems. Eighteen of these patients subsequently underwent polysomnography and objective measurement of daytime sleepiness. Clinically significant sleep apnea syndrome was present in 11. The presence of sleep apnea was associated with increased levels of psychological distress and daytime sleepiness. Periodic leg movements during sleep were also frequently observed but had minimal effect on sleep quality. Implications of these findings for clinical practice are discussed.

Adult

Sedative, memory, and performance effects of hypnotics.

The sedative, amnestic, and performance disruptive effects of benzodiazepine (Bz) receptor selective and non-selective hypnotics were studied in 23 healthy, normal subjects, aged 26.8 +/- 1.0 years. Triazolam (0.25 and 0.50 mg), zolpidem (10 and 20 mg) and placebo were administered, double-blind, at bedtime in a repeated measures design. During an awakening 90 min later (at approximate peak concentration of each drug) a 30-min performance battery which included memory, vigilance, and psychomotor tasks was completed. Each drug and dose impaired memory (both immediate and delayed), vigilance, and psychomotor performance relative to placebo. Among active drugs impairment was greatest with zolpidem 20 mg, next triazolam 0.50 mg, then zolpidem 10 mg, and finally triazolam 0.25 mg. Next morning delayed recall was also impaired by all drugs and doses (i.e. anterograde amnesia). The amnestic and performance-disruptive effects paralleled the relative hypnotic effects of the drugs and doses. No receptor selectivity in these pharmacodynamic effects was observed.

Adult

Sleepiness and ethanol effects on simulated driving.

Twelve healthy young men were assessed in each of four experimental conditions presented in a Latin Square design: 8-hr time in bed (TIB) and placebo, 4-hr TIB and placebo, 8-hr TIB and ethanol, and 4-hr TIB and ethanol. After consuming ethanol (0.6 g/kg) or placebo (0900-0930 hr) with 20% supplements at 1030 and 1100 hr, subjects were tested for sleepiness (Multiple Sleep Latency Test at 1000, 1200, 1400, and 1600 hr) and divided attention (1030 hr) performance on day 1, and for simulated driving and divided attention (1000-1200 and 1400-1600 hr) performance on day 2. In the morning testing, with breath ethanol concentrations (BECs) averaging 0.049%, sleepiness was increased, divided attention reaction times increased (on both days), and simulated driving performance was disturbed in the ethanol and 4-hr TIB relative to placebo. Similarly in the afternoon, with BECs averaging 0.013%, the ethanol and 4-hr TIB condition increased sleepiness and disrupted divided attention and simulated driving performance. The results show that sleepiness and low-dose ethanol combine to impair simulated automobile driving, an impairment that extends beyond the point at which BEC reaches zero. They provide a possible explanation for the incidence of alcohol-related automobile accidents at low BECs.

Adult

Rebound insomnia and hypnotic self administration.

Twenty-one (three groups of seven), men and women, 25-50 years of age were studied to determine whether or not rebound insomnia would increase the likelihood of self administering a benzodiazepine (triazolam 0.25 mg) hypnotic. The groups compared were patients with insomnia and disturbed sleep, insomnia and normal sleep, and healthy normals. Rebound insomnia, by both subjective and polysomnographic assessment, was induced. The experience of rebound insomnia did not increase the likelihood of self administering a benzodiazepine hypnotic in any of the groups. There were clear group differences in pill self administration with normals rarely and insomnia patients frequently, but not differentially (placebo versus active drug) self administering pills.

Adult

Rebound insomnia in normals and patients with insomnia after abrupt and tapered discontinuation.

Rebound insomnia was studied in subjects, aged 25-50 years, with insomnia complaints and normal sleep, insomnia complaints and disturbed sleep, and normal sleep with no complaints (N = 21, n = 7 per group). Standard sleep recordings were collected on a baseline night and after abrupt discontinuation of 6 nights of 0.50 mg triazolam, tapered discontinuation (3 nights of 0.50 mg, 2 nights of 0.25 mg, and 1 night of 0.125 mg triazolam) and 6 nights of placebo. Significantly disturbed sleep on the discontinuation night compared to the baseline night was found. The relative degree of rebound insomnia was greater in the abrupt condition than in either the tapered or placebo conditions. The tapered condition reduced sleep time by half that of the abrupt condition which was twice the reduction found in the placebo condition. An overall (regardless of group or condition) difference in baseline versus discontinuation sleep was found, suggesting that pill discontinuation itself leads to sleep disturbance. Subjects did not differ in rebound insomnia as a function of pre-existing sleep disturbance.

Adult

Long-term study of the sleep of insomnia patients with sleep state misperception and other insomnia patients.

OBJECTIVE: The objectives were 1) to investigate differences among patients with subjective insomnia (sleep state misperception), patients with objective findings of insomnia, and normal volunteers and 2) to assess the consistency of the sleep findings during a 2-month period. METHOD: Twenty-one subjects were studied. Subjects with sleep state misperception (N = 7) had insomnia complaints for more than 1 year, no objective sleep disturbance, and sleep efficiency of 90% or greater (on the diagnostic screening sleep recording), while subjectively estimating that sleep time was less than 6.5 hours. Subjects with objective insomnia (N = 7) met the same subjective criteria, but objectively sleep efficiency was 85% or less. Normal subjects (N = 7) had no insomnia complaints and objective sleep efficiency of 90% or greater. All subjects were recorded on 2 consecutive nights three times with a 3-week period between each pair of nights (6 standard all-night polysomnographic sessions of 8 hours). A subjective sleep questionnaire was administered after each sleep recording night. RESULTS: Sleep stage variables (percentages) were similar between the two insomnia groups, and both were different from the normal subjects. Sleep continuity variables were disturbed in the objective insomnia group, but they were similar in the sleep state misperception and normal groups. Both insomnia groups rated their sleep as inadequate on the questionnaires and differed from the normal subjects. The distinct sleep patterns of each of the three groups did not vary over the 6 nights of assessment. CONCLUSIONS: Sleep state misperception may be a prodromic or transitional state of sleep dysfunction between normal sleep and the sleep pattern of objective insomnia.

Adult

Rebound insomnia: duration of use and individual differences.

This study assessed consistency, duration of use, and individual difference in rebound insomnia. Eleven healthy men, 20-30 years old, with normal sleep by both subjective and polysomnographic criteria, received each of four treatments in a double-blind Latin Square design (triazolam 0.50 mg for 1, 6, and 12 nights and placebo for 12 nights), followed by two placebo discontinuation nights. Triazolam increased sleep compared with placebo without differences in effects between the first and last nights of treatment. On discontinuation following active drug, sleep efficiency was reduced compared with placebo, but duration of administration did not alter the likelihood or intensity of rebound insomnia. Those subjects (5) showing poorer sleep on discontinuation from the 12-night treatment also had poorer sleep in the 1- and 6-night treatment. Subjects with rebound insomnia had poorer baseline sleep and a greater drug effect than did subjects without.

Adult

Sleep extension, enhanced alertness and the sedating effects of ethanol.

Twelve, healthy young men (mean age 25.6 years) consumed either ethanol (0.75 g/kg producing a peak breath ethanol concentration, BEC, of 0.060% on average) or placebo at 0900-0930 hr after spending 8 hr time-in-bed (TIB) the previous night and once again after 7 or 8 consecutive nights of 10 hr TIB. Latency to sleep onset (on the Multiple Sleep Latency Test, a standard measure of daytime sleepiness/alertness) was tested at 1000, 1200, 1400 and 1600 hr and divided attention performance was assessed at 1100 hr. Ethanol reduced sleep latency and divided attention performance and the sleep extension improved both sleep latency and divided attention performance. Sleep extension attenuated the sedating effects of ethanol; sleep latency after extending sleep did not differ between placebo and ethanol. While the effects of ethanol on performance still were detectable after sleep extension, the level of performance was at the 8-hr TIB placebo level. BEC peak and decline (determined before each latency test) did not change with the sleep extension. Hence, reduced BECs do not account for the reduction in the disruptive effects of ethanol with sleep extension.

Adult

Characteristics of individuals who do or do not seek treatment for chronic insomnia.

Survey data have shown that a minority of people who complain of insomnia receive medical treatment for this problem. Patients who seek treatment for insomnia at medical clinics and sleep disorders centers are a self-selected group who may not be representative of all individuals with insomnia. Fifty patients presenting to a sleep disorders center with an insomnia complaint were compared to 50 subjects with insomnia recruited through the newspaper for psychopharmacological studies. No differences in sleep parameters were found, but significant differences on psychometric measures and in daytime alertness were present. The implications of these differences are discussed.

Adult

Fragmented sleep, daytime somnolence and age in narcolepsy.

This study examined whether narcoleptics experience an age-related increase in nocturnal sleep disturbance and, if so, what impact that disturbance has on daytime sleepiness. To evaluate these questions, the records of 228 patients diagnosed as narcoleptic were assessed. Total sleep time (TST) and sleep efficiency (SE) significantly decreased, and wake during sleep (WDS), number of awakenings, and percentage of stage one significantly increased across the decades. This indicates an age-related elevation in sleep fragmentation. Daytime sleepiness, however, did not exhibit age effects. These data further support the theory that narcolepsy is a basic neural defect not confounded by excessive daytime sleepiness secondary to sleep fragmentation.

Adult

Predictors of objective level of daytime sleepiness in patients with sleep-related breathing disorders.

Excessive daytime sleepiness, the most prevalent symptom associated with the OSAS, is hypothesized to result from either fragmentation of sleep or hypoxemia during sleep. Measures of nocturnal sleep, respiration during sleep, and daytime sleepiness in 466 patients with apnea were collected to evaluate these two hypotheses. The various parameters were submitted to correlation and multiple regression analyses to predict daytime sleepiness as measured by the MSLT. The RAI, which measures the number of arousals from sleep associated with respiratory disturbances (best fragmentation correlation), produced a higher correlation with MSLT scores than did TMES (best hypoxemia correlation); however, the measures were highly intercorrelated, and multiple regression analyses to determine which parameters independently predicted MSLT showed the single best predictor to be the RAI. Additional independent variance in MSLT score was explained by TST and PSG1. Measures of hypoxemia provided little or no independent predictive information. These data support the hypothesis that sleep fragmentation is an important determinant of daytime sleepiness in patients with apnea.

Female

Recovery of alertness after CPAP in apnea.

Excessive daytime sleepiness is the most common symptom in OSAS. Administering CPAP improves breathing during sleep. We evaluated the time course of the recovery of alertness following CPAP therapy in OSAS patients. Thirty-nine patients with OSAS were treated with CPAP and evaluated after one, 14, or 42 nights of treatment, 13 patients being randomly assigned to each group. All received a diagnostic polysomnogram and MSLT before treatment. The three groups had similar baseline values for nocturnal respiratory disturbance, oxygenation during sleep, fragmentation of sleep, and level of EDS. CPAP treatment was associated with a significant improvement in sleep-related respiration, oxygenation, and sleep fragmentation. The EDS showed significant improvement after one night, and further significant improvement after 14 nights, but no further significant improvement after 42 nights. The differential rate of improvement in nocturnal parameters compared with that of primary complaint of EDS suggests that OSAS patients experience a chronic functional sleep loss. As with sleep deprivation, recovery of alertness in OSAS requires several nights of normal sleep.

Adult

The dose effects of zolpidem on the sleep of healthy normals.

This study determined the dose effects of zolpidem in 12 healthy males with normal sleep patterns. Subjects spent 7 weeks, 3 consecutive nights per week, in the laboratory and had a 4-night washout between treatments. The first week was a screening and adaptation week. Then subjects received zolpidem (2.5, 5.0, 7.5, 10.0, or 20.0 mg) or placebo on the first two nights for each of the next 6 consecutive weeks. Treatments were organized in a Latin square design and administered in a double-blind fashion. On the third night of each treatment, subjects always received placebo. The 5.0 mg and larger doses of zolpidem significantly decreased latency to persistent sleep and wake before sleep. Sleep maintenance measures were not affected by zolpidem. The 7.5 mg and higher doses of zolpidem significantly increased total sleep time. The only significant sleep stage effect was a decrease in percent of rapid eye movement sleep at only the 20 mg dose. No consistent discontinuation effects were found. Zolpidem was hypnotically active at doses as low as 5.0 and 7.5 mg, and sleep stage effects occurred only at the 20 mg dose, thus separating the dose range of hypnotic and sleep stage effects.

Adult

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

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