I. Oswald

Physiological and psychological differences between good and poor sleepers.

Eighteen poor sleepers and 18 good sleepers of mean age 52 yr, selected on the basis of their stated opinions about their sleep, were studied as pairs matched for sex, age, height and weight, on five consecutive nights and two consecutive days. Using EEG measures, the poor sleepers woke more often in the early hours of sleep and achieved half an hour less sleep. They had higher body temperatures by day and night and were more anxious. They tended to have higher urinary cortisol and adrenaline excretion. The groups did not differ in reaction time nor in excretion of urinary 3-methylhistidine. The poor sleepers over-estimated their sleep latency and both groups under-estimated their total sleep, the poor sleepers being significantly more inaccurate. It is concluded that those who complain of poor sleep have also metabolic differences from good sleepers.

Heroin and human sleep

Abstract It has been suggested that drugs of addiction, e.g. barbiturates, cause suppression of REM sleep followed by immediate withdrawal rebound. In rats it has been demonstrated that morphine will suppress REM sleep and, in a pilot study of withdrawal in humans, there was a delayed REM sleep rebound. 1.A: Four normal male volunteers had a subcutaneous injection of 7.5 mg heroin on 3 successive nights. During this period the percentage of REM sleep was decreased with respect to baseline values for these subjects and showed a trend back to control values over the 3 nights. On withdrawal there was a moderate but immediate percentage of REM sleep increase which, over the first 3 h of sleep, was significant. 2.B: Two of the subjects from A received a further 7 injections of 7.5 mg heroin some 2 months after the previous ones. Again the proportion of REM sleep was reduced in both subjects and there was the trend back to baseline values over the 7 nights. One subjects had increased REM sleep immediately on withdrawal. Evidence of withdrawal was apparent for some 2 months after stopping heroin. Other evidence of withdrawal was seen in the decreased delay to the first REM period ( 35 min). The other subject showed little evidence of withdrawal effects in sleep though there was a short delay to the first REM period on nights 4 and 11 of withdrawal. His proportion of REM sleep was never significantly above baseline values, indicating that there can be considerable individual differences in the effects of withdrawal of heroin. In both experiments it was noted that, far from giving an undisturbed sleep, heroin administration resulted in an increased frequency of shifts to stage 1 sleep (drowsiness) or wakefulness and an increased delay to the onset of the first stage 2 of the night.

Further studies of scratching during sleep.

Fifteen patients with a variety of itching skin diseases (atopic eczema, dermatitis herpetiformis, lichen planus, urticaria and psoriasis) have been studied in the sleep laboratory. Recordings were made of all‐night electroencephalogram, electro‐oculogram, submental electromyogram, and muscle potentials from both forearms.

Effects of repeated ritanserin on middle-aged poor sleepers

Nine subjects who believed themselves to be poor sleepers, of mean age 58 years, took a placebo for 7 days, then ritanserin 5 mg for 20 days, followed by 3 days on placebo. Sleep was recorded electrophysiologically on 2 nights during baseline, 2 early drug nights, 2 late drug nights and the 2nd and 3rd withdrawal nights. Ratings of sleep quality were collected each morning. Ritanserin, a 5HT2 antagonist, caused a persistent doubling of the amount of EEG show wave sleep, without altering the total duration of sleep. Ritanserin decreased the frequencies of awakening and after about a week it appeared to improve the subjective quality of sleep. Sleep was then impaired during withdrawal, as indicated by decreased duration and poorer subjective quality, being worst on the 3rd withdrawal night.

Effects of loprazolam and of triazolam on sleep and overnight urinary cortisol

Nine poor sleepers of mean age 61 years were studied while they took loprazolam 0.5 mg, loprazolam 1 mg and triazolam 0.5 mg for 3-week periods. Loprazolam 1 mg and triazolam 0.5 mg increased sleep duration, but there was some tolerance to both, particularly triazolam, by the 3rd week. Withdrawal of either drug led to sleep significantly shorter than baseline. This rebound effect was significant greater after withdrawing triazolam. After withdrawing loprazolam 1 mg, the rebound was maximal on the 3rd night and after withdrawing triazolam it was maximal and severe on the 1st night. In the third week of use neither drug was associated with late-night wakefulness. Total overnight urinary cortisol was lower during drug intake and there were significant withdrawal rebounds to above baseline levels, immediately so after triazolam.

Debrisoquine, guanethidine, propranolol and human sleep

Debrisoquine in dosage of 20–60 mg continued for up to 10 days caused suppression of human paradoxical sleep and withdrawal rebound, and also increased intra-sleep restlessness. An overdose of debrisoquine 200 mg caused suppression of paradoxical sleep and a rebound of over 2 weeks duration.Guanethidine 20–40 mg for 21 days did not affect paradoxical sleep but increased intra-sleep restlessness and reduced stages 3 + 4 sleep.Propranolol 120 mg had no discernable effect on sleep and did not prevent actions of dexamphetamine sulphate 10 mg nor of imipramine 75 mg. The findings relate to theories of cerebral noradrenaline in the control of sleep mechanisms.

Two Anti-anxiety Drugs: A Psychoneuroendocrine Study

Eight males were studied during 27 weeks, including two periods of five weeks during which they received clinical doses of sodium amylobarbitone and benzoctamine. Substitution of placebo for either drug caused raised anxiety and impairment of mental concentration. The drugs reduced restlessness during sleep and reduced paradoxical sleep. By the fifth week of sodium amylobarbitone, although sleep was still less restless in the early night it was more restless than normal in the late night. Blood samples were taken half-hourly during sleep by indwelling venous catheter. Plasma growth hormone concentration was little affected during drug administration but rose temporarily after withdrawal. There was a reduction of plasma corticosteroid concentration during sleep throughout administration of the drugs and a rebound above normal during the first withdrawal week.

Viloxazine, sleep, and subjective feelings.

The sleep of eight volunteers (mean age 55) was recorded electrophysiologically while viloxazine 200mg was taken daily for 3 weeks, preceded and followed by a week of matching blanks. The volunteers also made ratings of their feelings on visual analogue scales. Another 15 volunteers (mean age 34) took viloxazine 300 mg daily for 3 weeks, preceded and followed by 3 weeks of matching blanks, and they also made daily ratings of feelings.The drug diminished sleep duration and caused more frequent and longer transitions into wakefulness and drowsiness. Slow-wave sleep decreased and stage 2 increased. REM sleep was markedly reduced, especially initially, and there was a withdrawal rebound. Viloxazine impaired subjective concentration, mood, and quality of sleep. Three volunteers, however, had striking mood elevation. The drug caused a small loss of weight, which correlated with gastrointestinal symptoms. Three older subjects experienced withdrawal vomiting and prostration. Viloxazine shares properties with imipramine and with amphetamines.

Interference with human memory by an antibiotic

Thirty-two volunteers learned a sentence after awakening from early in the first REM period of sleep and recalled it after awakening from the third REM period, under experimental conditions that controlled for state dependency. The tetracycline antibiotic doxycycline (200 mg), taken at bedtime, impaired recall possibly through a putative inhibitory action on brain protein synthesis.

Effects of loprazolam and of triazolam on psychological functions

Twelve poor sleepers of mean age 52 years performed 2 h of laboratory tests three times on 1 day during each week of nightly intake of loprazolam 0.5 mg, loprazolam 1 mg, triazolam 0.5 mg, or continued placebos. Only in the mornings did loprazolam 1 mg cause impairment in manual dexterity and card-sorting, and triazolam 0.5 mg in manual dexterity. Using difference from baseline, withdrawal of either drug after 3 weeks was associated with poorer subjective quality of sleep than following continuing placebos. The rate of spontaneous complaints (including accidents) associated with the drugs was as informative as formal testing.