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Biomedical subjects

M A Carskadon

Publications and source records attributed to M A Carskadon.

At least 19 recordsLinked to original sources

Multiple sleep latency tests during the constant routine.

The "post-lunch dip" is a common behavioral phenomenon, though perhaps a misnomer. Biphasic models of the human sleep tendency rhythm suggest an alternative explanation for the afternoon decline in alertness. Sleep tendency was measured with the Multiple Sleep Latency Test (MSLT) at 2-hour intervals in 16 volunteers from three age groups (ages 10-12, ages 16-17, ages 62-74 years) during a constant routine in which small meals were given each hour. Baseline scores showed no significant Time of Day effect, although a trend for an afternoon dip was present in the eldest group. During the constant routine, a significant Time of Day effect was found for the two older groups and not for the prepubertal group. The results indicate a midday increase in sleep tendency that is unrelated to food intake but that may be related to developmental or maturational processes.

Adolescent

Studies in the genetics of obstructive sleep apnea. Familial aggregation of symptoms associated with sleep-related breathing disturbances.

Previous studies of single families have suggested that familial factors may be important in the pathogenesis of obstructive sleep apnea. In this report, the role of inheritance in obstructive sleep apnea was assessed by quantitating the degree of familial clustering of symptoms associated with sleep-related breathing disorders. In total, 272 subjects from 29 families identified through an index case with obstructive sleep apnea and 21 control families with no relative known to have sleep apnea were studied with questionnaires that ascertained health status and symptoms. The unadjusted odds ratios of habitual or disruptive snoring, breathing pauses, and excessive day-time sleepiness in subjects with a single relative with the same symptom were 1.40 to 1.53 (p less than 0.05). Odds ratios increased progressively for subjects with increasing numbers of symptomatic relatives). Adjustment for body mass index, age, and gender modestly reduced these odds ratios to 1.33 to 1.42. These data suggest a significant familial aggregation of symptoms associated with sleep-disordered breathing that appears independent of familial similarities in weight.

Adult

Sleep-disordered breathing in patients with Duchenne muscular dystrophy using negative pressure ventilators.

We studied the occurrence of nocturnal disordered breathing events and O2 desaturations in 12 patients with late-stage Duchenne muscular dystrophy (DMD) using negative pressure ventilators. We also assessed the effects of O2 supplementation and nasal continuous positive airway pressure (CPAP) on disordered breathing events in selected patients and examined sleep quality in a small subgroup. Average age was 23 + 2 years and FVC was 293 + 33 ml. Eleven of the 12 patients had more than five disordered breathing events per hour during nocturnal monitoring, and the lowest O2 saturation was < 85 percent in nine patients. Nasal O2 (2 L/min) during negative pressure ventilation in four patients did not alter the frequency of disordered breathing events, prolonged the mean and maximum durations of events, and failed to eliminate severe O2 desaturations in two patients. Nasal CPAP was used in two patients during negative pressure ventilation and completely eliminated disordered breathing events in both. Overnight polysomnography during negative pressure ventilation in three patients demonstrated frequent awakenings that fell in frequency following elective tracheostomy in two patients and use of nasal CPAP in one. We conclude that negative pressure ventilation in patients with late-stage DMD is associated with frequent disordered breathing events and severe O2 desaturations in many patients. Concomitant use of O2 supplementation may prolong the events, but a switch to positive pressure ventilation or addition of nasal CPAP is effective therapy.

Adolescent

Interactions of sleep and clonidine on daytime prolactin secretion in humans.

The suppressive roles of adrenergic stimulation and rapid eye movement (REM) sleep on human prolactin (PRL) secretion are controversial. We examined the effects of sleep, clonidine (an alpha 2-adrenergic agonist), and their interaction on PRL secretion. Two groups of normal men (nine each) were studied in two morning sessions. Each group received either placebo or clonidine in both sessions. Subjects remained awake in the first session and in the next session they were asked to sleep for 3 h after the test dose was given. Blood samples were drawn at 30-min intervals and polysomnographic recordings were obtained at each session. PRL concentrations remained at baseline and no clonidine effect was detected while awake. PRL concentrations increased in placebo and clonidine groups during sleep. Despite significant suppression of REM sleep in the clonidine group, no differences were detected between the placebo and clonidine groups in peak PRL or mean PRL concentrations during the study. Also, no significant difference was detected in comparing PRL responses during non-REM sleep in both groups. The results suggest that alpha 2-adrenergic stimulation does not have a significant role in modulating human PRL secretion during sleep.

Adolescent

Sleepwalking precipitated by treatment of sleep apnea with nasal CPAP.

A 33-year-old man with a long history of snoring, observed apneic episodes, and excessive daytime sleepiness, underwent all-night polysomnography, which demonstrated severe obstructive sleep apnea. During the nasal CPAP trial, two episodes of sleepwalking were observed during a period of delta sleep rebound.

Adult

Sleep, clonidine, and their interactive effect on growth hormone secretion in normal men.

Central alpha 2-adrenergic function is often inferred from the growth hormone (GH) response to clonidine, despite the drug's known hypnotic effect and the accepted cholinergic mechanism for sleep-related GH secretion. We examined the effect of daytime sleep on GH secretion in normal men taking placebo or clonidine orally, using a two-group blind design (placebo, clonidine; n = 9 each). Each subject participated in two morning sessions monitored by polysomnography: wake (sleep actively prevented) and sleep (subjects asked to sleep for 3 hr after receiving placebo or clonidine). Blood samples were drawn at times -15 min, 0, and every 30 min for 3 hr after the test dose was given. The total sleep time was similar for both groups. The placebo/wake group had lower GH responses than the other three groups. None of the GH responses in the clonidine/sleep group were significantly different from those in the placebo/sleep group; and the peak GH micrograms/L, mean +/- SD) was 16.9 +/- 10.9 vs. 14.6 +/- 10.5, respectively. We conclude that the GH response to clonidine may not be indicative of alpha 2-adrenergic function if sleep is permitted during the test.

Administration, Oral

Patterns of sleep and sleepiness in adolescents.

Most studies of adolescent sleep habits show a pattern of decreasing total sleep time, a tendency to delay the timing of sleep, and an increased level of daytime sleepiness. Laboratory tests have shown that adolescents do not have a decreased need for sleep but probably need more sleep than prepubertally. A number of factors affect the development of adolescent sleep patterns. Puberty itself imposes a burden of increased daytime sleepiness with no change in nocturnal sleep. Parental involvement in setting bedtimes wanes, though they become increasingly involved in waking teenagers in the mornings. Curfews and school schedules also affect adolescent sleep patterns, seen most commonly as imposing earlier rise times as the school day begins earlier during the adolescent years. Part-time employment has a significant impact on the sleep patterns of teenagers: those who work more than 20 h each week sleep less, go to bed later, are more sleepy, and drink more caffeine and alcohol. Development of circadian rhythms may also play a role in the phase delay teenagers commonly experience. The primary conclusion is that many adolescents do not get enough sleep. The consequences of the chronic pattern of insufficient sleep are daytime sleepiness, vulnerability to catastrophic accidents, mood and behavior problems, increased vulnerability to drugs and alcohol, and development of major disorders of the sleep/wake cycle. Educational programs hold the promise of improving teenagers' sleep patterns through informing youngsters, parents, and pediatricians about proper sleep hygiene and the risks of poor sleep habits.

Adolescent

Sleepiness and nap sleep following a morning dose of clonidine.

The effects of a single oral dose of clonidine on morning nap sleep and daytime sleepiness were evaluated in 18 normal young adult male volunteers aged 18-21 years. Polysomnography and subjective sleepiness (Stanford Sleepiness Scale and linear analog sleepiness rating scale) measures were obtained on 2 mornings. Half the subjects received placebo and half clonidine (0.25-0.3 mg) on both occasions. Subjects were instructed to stay awake on the first morning (wake) and to sleep on the second (sleep). Efforts were made to help subjects maintain arousal on the wake day. Results from the wake morning showed that clonidine subjects were significantly sleepier than placebo subjects as measured by introspection. In addition, clonidine subjects tended to have more polysomnographic signs of sleepiness (microsleeps) when not actively aroused. On the sleep morning, clonidine and placebo subjects slept for approximately 90% of the 3-h nap. Stage 1 and rapid-eye-movement (REM) sleep were significantly reduced and stage 2 sleep significantly increased in the clonidine group. In conclusion, a morning dose of clonidine produced profound sedation in waking subjects and marked REM suppression in sleeping subjects.

Adolescent

REM sleep episodes during the Multple Sleep Latency Test in narcoleptic patients.

Forty narcoleptic patients were given the Multiple Sleep Latency Test, consisting of 20 min opportunities to sleep offered at 10.00, 12.00, 14.00, 16.00 and 18.00 o'clock. Eleven patients had 2 episodes of REM sleep, 5 had 3, 11 had 4, and 13 had 5 before they were awakened. Fourteen control subjects given similar opportunities to sleep (reported in a companion article (Richardson et al. 1978)) had no REM sleep episodes. For the 10.00-18.00 o'clock opportunities respectively, there were 32, 29, 30, 28 and 27 REM sleep episodes. We conclude that this procedure can provide physicians with data useful in the diagnosis of narcolepsy.

Adult

Hypnotic efficacy of temazepam: a long-term sleep laboratory evaluation.

1 Temazepam was evaluated in a strictly defined insomniac patient population under sleep laboratory conditions. Two protocols were used: a short-term (26-night) and a long-term (54-night) protocol evaluated the efficacy of the drug administered at night at 15 mg (short-term study) and 30 mg (long-term study), respectively. 2 Temazepam seemed to be both safe and effective at doses of 15 and 30 mg with up to 5 weeks of ingestion. 3 Suppression of slow wave sleep was observed at the high dose, but no suppression of REM sleep, found in studies with other benzodiazepines, was noted. 4 No evidence was found for development of tolerance or rebound effects.

Adult

Effects of total sleep loss on sleep tendency.

Effects of two nights of sleep loss were assessed in six young adult (18--21 yr.) volunteers (2 women, 4 men). Performance on the Wilkinson Addition Test fell significantly below baseline values during the sleep-loss procedure and recovered after one or two full nights of sleep. Performance on a Serial Alternation Task also declined during sleep loss. Mood and sleepiness, assessed by subjective self-rating scales, showed a significantly less positive mood and a greater degree of sleepiness during sleep loss, with a recovery to baseline levels after one full night of sleep. Sleep tendency, measured at 2-hr. intervals during all waking periods, was assessed using an objective measure of latency to sleep onset, the Sleep Latency Test. The scores fell to about 1 min. at 0600 on the first night of sleep loss and remained at similarly low values throughout the sleep loss period. After one night of recovery sleep the scores remained significantly below baseline levels, which were not achieved until after the second recovery night. The multiple sleep latency test appears to be a valuable operationally defined tool for measuring daytime sleepiness.

Achievement

Sleep habits of children and the identification of pathologically sleepy children.

Sleep disorders and daytime sleepiness have been investigated only minimally in children. The sleep habits of 218 children, ages 10-13 years, were surveyed by a sleep habits questionnaire (SHQ). Our results demonstrate that total night time sleep on school nights begins to fall in early adolescence, whereas it remains relatively stable on non-school nights. Daytime sleepiness is not a common problem in this age group, in contrast to a college age population. We conclude that in adolescence chronic sleep deficits begin to occur which cumulatively affect later functioning. The potential use of the SHQ for depicting pathological sleepiness is also discussed.

Adolescent

Excessive daytime sleepiness in man: multiple sleep latency measurement in narcoleptic and control subjects.

Excessive daytime sleepiness is a complaint characterizing many disorders of the wakefulness--sleep cycle. This paper addresses the complaint of sleepiness objectively by an attempt to differentiate a group of control subjects from a group of patients with unambiguous narcolepsy. Fourteen control and 27 narcoleptic subjects were evaluated by one of three protocols involving nocturnal recordings, detailed interviews, and 5 or more 20-min opportunities to sleep offered at 2-h intervals beginning at 10.00 o'clock, +/- 30 min. Each 20-min opportunity to sleep was given to subjects lying in a darkened quiet room and asked to try to fall asleep. Polysomnographic variables were monitored and sleep was scored in 30-sec epochs by standard criteria. The interval from the start of each test to the first epoch of NREM (including stage 1 sleep) or REM sleep was called sleep latency. In two of the protocols, the subjects were awakened immediately after sleep onset. In the third protocol, the subjects were awakened after 10 min of sleep. Narcoleptics consistently fell asleep much more readily than did control subjects. We conclude that the Multiple Sleep latency test, in addition to providing opportunities to clinically document sleep onset REM sleep periods, can demonstrate pathological sleepiness. Based on these data, we suggest that an average sleep latency less than 5 min be set as the minimum cutoff point for pathological sleepiness.

Adult

Respiration during sleep in children.

In 22 children (11 boys and 11 girls), aged 9 to 13 years, respiration was monitored during one night of sleep. No child had a significant history of breathing problems during sleep. Sleep was recorded using standard techniques (electroencephalography, electrooculography, electromyography), and respiration was measured with nasal thermistors and abdominal or thoracic strain gauges. Respiratory pauses (five seconds or longer) were determined for all sleep stages. Respiratory rate was scored only in the first and last sleep cycles and during ten waking minutes before sleep onset. Respiratory rate was significantly affected by wakefulness or stage of sleep: highest in wakefulness and stage 1, lowest in stage 2 of the last sleep cycle. Regularity of respiratory rate showed a similar effect. Variance of respiratory rate was significantly lower in girls than boys. Respiratory pauses during sleep were seen in every child, ranging from 3 to 40 pauses per night (average, 17.2 for boys and 18.0 for girls). Significantly greater numbers of pauses per minute were seen in stage 1 and rapid eye movement (REM) sleep than in stages 2, 3 and 4. The longest respiratory pause was 25 seconds. The conclusion is made that a small number of respiratory pauses during sleep are normal in children of this age.

Adolescent

Self-reports versus sleep laboratory findings in 122 drug-free subjects with complaints of chronic insomnia.

The authors compared the sleep laboratory recordings of 122 drug-free subjects who complained of chronic insomnia with the subjects' estimates of their habitual sleep characteristics and their estimated sleep time on the morning after sleeping in the laboratory. Most subjects consistently underestimated the amount of time they slept and overestimated the amount of time it took them to get to sleep in comparison with laboratory data. All subjects consistently underestimated the number of arousals they experienced. The authors discuss the implications of these findings for the treatment and definition of insomnia and for further research.

Adolescent

Narcolepsy. Diagnosis and treatment.

Narcolepsy may affect as many as 200,000 Americans. The illness involves a neurologic defect in the regulation of sleep and wakefulness. The chief symptoms are sleepiness, inappropriate sleep episodes, and cataplexy. A characteristic history of cataplexy establishes the diagnosis. Narcoleptic patients also frequently complain of hypnagogic hallucinations, sleep paralysis, blackouts (or automatic behavior), and disturbed nocturnal sleep. Narcolepsy usually develops in adolescence and is a life-long illness. Symptoms may also appear in young children who may be misdiagnosed as hyperactive or psychotic. No completely satisfactory treatment is available at the present time. The current treatments of choice are methylphenidate (for sleepiness and sleep episodes) and imipramine (for cataplexy). Medication dosages must be adjusted for individual patients. A careful history of the illness can rule out hypothyroidism, hypoglycemia, and epilepsy. Sleep apnea is a serious complication of narcolepsy and may be life threatening.

Adolescent