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Biomedical subjects

A Besset

Publications and source records attributed to A Besset.

16 recordsLinked to original sources

Sleep deprivation in narcoleptic subjects: effect on sleep stages and EEG power density.

Sleep of 8 narcoleptic and 8 control subjects was recorded under baseline (i.e., prior wakefulness 16 h) and after 24 h without sleep. During both baseline and recovery total sleep time and stage 2 non-REM sleep were significantly decreased in narcoleptic subjects. Slow wave activity (i.e., EEG power density in the range of 0.75-4.5 Hz) decayed exponentially during baseline and after sleep deprivation in both narcoleptic and control subjects. During both baseline and recovery EEG power density in delta and sigma frequencies in non-REM sleep was enhanced in narcoleptic subjects relative to controls. In REM sleep differences in the same direction were present in delta and beta frequencies. After sleep deprivation EEG power density in non-REM sleep was elevated in delta and some higher frequencies in both patients and controls, but the response to sleep deprivation was stronger in narcoleptic subjects. These data show that in narcoleptic subjects regulatory processes underlying non-REM sleep homeostasis are operative and indicate that the response to sleep deprivation is stronger than in control subjects.

Adolescent

Effects of zopiclone on subjective evaluation of sleep and daytime alertness and on psychomotor and physical performance tests in athletes.

1. In a double-blind cross-over study 8 athletes received during 2 sessions of 2 nights zopiclone (7.5 mg) or placebo. 2. Residual effects on subsequent daytime functions were evaluated both subjectively by visual analogue scales as well as objectively by a test battery measuring psychomotor and physical skills. 3. Zopiclone had some favourable effects on self-estimated sleep quality and daytime sleepiness. 4. Psychomotor and physical performance tests did not show any significant difference between zopiclone and placebo. 5. We conclude that zopiclone has useful hypnotic activity without significant adverse effects on athletic performance.

Adult

Sleep in human narcolepsy revisited with special reference to prior wakefulness duration.

Sleep of 11 narcoleptic subjects was recorded on baseline and after 16 and 24 hours of prior wakefulness (16 and 24 hours sleep deprivation). Eleven sex- and age-matched control subjects were recorded for comparisons. All recordings in narcoleptic subjects were characterized by frequent sleep onset rapid eye movement (REM) episodes, increased amounts of wake time after sleep onset and low sleep efficiencies. Mean total sleep time (TST) was significantly decreased in narcoleptic subjects after sleep deprivation (SD). Recovery sleep after 24 hours SD showed reduced nonREM (NREM) sleep stage 2 percentage, whereas percentages of stage 4 and slow-wave sleep (SWS = stages 3 + 4) were significantly increased. The values of REM sleep percentage of TST were remarkably constant throughout and did not differ significantly as a function of experimental conditions, indicating a normal REM sleep pressure in narcolepsy. Sleep stage analysis per sleep cycles revealed significant differences between the two groups. Percentages of stage 4 and SWS were increased during the first cycle of recovery sleep in narcoleptic subjects. Stage 2 was decreased during the third cycle, and SWS decreased rapidly from cycle 1 to cycle 2 and slightly increased thereafter. These results indicate that sleep need is increased in narcolepsy, whereas its decrease over the first NREM-REM cycle is accelerated. We hypothesize that this could reflect an alteration of the homeostatic process of sleep regulation in narcolepsy.

Adolescent

Sleep organization and epilepsy.

Sleep is known to facilitate epileptic manifestations but can also protect the sleeper against the recurrence of seizures. This has been demonstrated in studies on sleep deprivation, and is particularly evident in alcoholic epilepsy and matutinal myoclonus epilepsy. Sleep organization in the epileptic patient is permanently altered by frequent awakenings and stage shifts. Nocturnal grand mal and repetitive partial seizures worsen the sleep disorder by reducing total sleep time and decreasing REM percentage by half. The cumulative effect of these sleep disorders may act on day-time vigilance in epileptics, and may even exert an influence on the recurrence of seizures.

Adult

[Hypnotics].

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Barbiturates

[Nycterohemeral variations of growth hormone and prolactin in 6 Parkinson's sufferers treated with bromocriptine (author's transl)].

Secretions of GH and of PRL studied over a period of 24 hours in 6 untreated Parkinson's patients showed slight changes. The normal secretion of PRL in the female shows no nocturnal increase in the male. The secretion of GH linked to sleep is identified in the male and not in the female. These variations related to sex are interpreted as an increase in those normally found in the adult and facilitated by age. Bromocriptine given continuously at a dose of 10 to 20 mg/day for periods of 20 days to 6 months, results in suppression or a marked decrease in the 24-hour secretion of PRL. It has virtually no effect upon the secretion of GH. These results show that the dopaminergic regulation of PRL is preserved in Parkinson's disease.

Aged

[Effect of piribedil on nocturnal sleep (author's transl)].

Piribedil, a dopamine agonist, was administered to 5 normal male subjects for two weeks. During the first two nights there was a reduction of about 17 p. 100 in paradoxical sleep (PS) and an increase of about 13 p. 100 in slow sleep II. There was a 15 p. 100 increase in PS during the third night. This increase is maintained for 8 nights in 3 subjects and 13 nights in 2 subjects. Other sleep parameters were not altered. Piribedil appears to give the impression of satisfactory sleep by reducing the subjective period before falling asleep. Piribedil also diminishes the remembrance of dreams.

Adult

[Secretion of gonadotropins during sleep. Changes during secondary amenorrheas].

4 females with secondary amenorrheas underwent sleep polygraphic recordings together with blood samples for measurements of LH, FSH and GH, 3 normal females served as controls. Among normal subjects LH and FSH secretion showed a pulsating pattern around the time of ovulation, appearing as secretory episodes throughout the night, without any relationship with sleep stages. In amenorrheas, 3 types of abnormalities could be identified: the first was a lack of secretory episodes of LH and FSH associated with an abnormal pattern of GH (9 subjects). The second was an hypersecretion of LH and a decrease of FSH secretion together with a normal secretion of GH in 4 subjects with a Stein-Leventhal syndrome. The last one was an hypersecretion of LH and FSH together with a normal pattern of GH in a subject with an early menopause. These results are discussed according to the present data on the part of neurotransmission in the regulation of ovulation and the 2 types of sleep. Furthermore secretory abnormalities of LH and FSH together with a disconnection between GH secretion and the stages of sleep lead to question the possibility of interrelationships in the secretory mechanisms of these different hormones.

Adolescent

[Secretions of GH, FSH and LH during sleep of the normal child and the child with retarded growth].

In normal children the major GH release begins during NREM sleep of first cycle. At puberty secretion of gonadotropins is enhanced and secretion of LH occurs with the same periodicity as the sleep cycles. Two groups of dwarfish are seen: the first lacks both GH secretion during sleep and the increase of gonadotropins at puberty. The second group exhibits GH, LH and FSH secretion patterns similar to normal children. Study of secretion patterns of GH, FSH and LH during sleep in children can document the degree of maturation of the hypothalamic pituitary hormonal system.

Adolescent

[Insomnia in bismuth encephalopathy (author's transl)].

Myoclonic encephatopathy caused by the insoluble salts of bismuth may be accompanied by a state of total insomnia. This insomnia has been confirmed by polygraphic recordings in 3 subjects. The recovery of sleep has a stereotyped course, with a step-wise reappearance over time of sucessive stages of NREM sleeps tarting with stage age I, and parallel re-establishment of REM sleep. Return to normal sleep lags behind clinical recovery. A pharmacological analysis with the phobenecid test was attempted in 2 of the 3 subjects. The results were the same in both as regards renewal of lumbar 5 HIAA, which paradoxically is not changed much; as regards the rate of lumbar HVA renewal, the results were quite different.

Adult

[Sleep organization by subjects in chronical post-traumatic inconscience (author's transl)].

Nine subjects who underwent a severe head traumatism with a brainstem dysfunction at the acute stage, were polygraphically recorded at the chronic stage under strict conditions of drug withdrawal and light-dark periods. Two groups of subjects were identified. The first one (5 subjects) showed normal NREM sleep and REM sleep morphologic patterns as well as a partly preserved architecture of sleep. The synchronisation of sleep with dark periods was lost in 4 out of 5 cases. In the second (4 subjects) NREM sleep morphologic patterns were lost and REM sleep was either uncertain or absent in 3 subjects. The synchronisation of sleep with dark periods was lost in 3 out of 4 cases. The morphologic alterations of sleep are connected with different types of encephalic lesions whereas the anomalies of the architecture of sleep and of its synchronisation with dark periods are referred to the numerous endogennous and exogenous stimuli undergone by these subjects. At the chronic stage of post-traumatic comas a 24-hour polygraphic recording supplies no definite information with regards to the prognosis.

Adult

Circadian patterns of growth hormone and cortisol secretions in narcoleptic patients.

Narcolepsy, a disorder which is clinically characterized by recurring episodes of sleep during the day, frequently associated with nocturnal disrupted sleep and polygraphically by sleep onset REM periods, has been studied in regard to the relationships between GH, cortisol secretion and sleep. Ten narcoleptics were polygraphically recorded during 24 h after one night's adaptation. Blood samples were taken every 20 min for GH and cortisol immuno-assays. Three narcoleptics were recorded twice 2 months later and 2 normal subjects served as controls. The following results were obtained: GH secretory pattern was different in narcoleptics and controls; two groups were identified: the first one showed a very low basal GH secretion with rare and small secretory peaks not clearly linked with sleep. One subject of this group recorded twice showed a similar pattern. The second group exhibited a higher basal secretion with many peaks without any well-defined relationship to sleep stages. The pattern was again consistent in two recordings of 2 subjects in this group. Furthermore GH secretion rose significantly (p less than 0.01) between 2100 and 0000 with no apparent relationship to sleep stages. The cortisol secretory pattern showed a significant rise (p less than 0.01) between 0400 and 1000 and was not different in narcoleptics and controls. In narcolepsy the monophasic sleep-wakefulness cycle is disrupted. The GH secretion pattern is modified whereas the circadian pattern of cortisol secretion is normal and independent of the sleep-wakefulness cycle of the narcoleptic patient.

Adult