Efficacy and safety of midazolam in the treatment of night terrors in children.

Midazolam, in an oral dose of 15 mg, and placebo were administered to 15 children aged 6-15 years in treatment of night terrors. After an initial adaptation night, the patients received placebo for 2 nights, followed by 15 mg midazolam for 2 nights and placebo again on the final 2 nights. Eight-hour nocturnal polygraphic recordings were made after the administration of both placebo and midazolam. The patients were continuously monitored by means of closed circuit infra-red television. Ten of the patients manifested simple episodes while five had attacks associated with motor automatisms and EEG anomalies. The total sleep time was lengthened by midazolam in most of the children; sleep architecture was favourably modified, mainly in terms of the amount and proportion of REM sleep (accompanied by dreams) and stage 2 sleep. Night terrors were eliminated by midazolam in all except one patient. REM sleep latency also decreased as did the number of nocturnal arousals (clinical and/or EEG). In the five cases with a background of organic cerebral disorders, the EEG anomalies and these attacks were suppressed by midazolam especially during the first sleep cycles. Patients' subjective assessment of the quality of sleep was favourable. Midazolam was well tolerated with no side-effects.

Effects of arginine vasotocin on REM sleep in narcoleptics and in symptomatic hypersomniacs.

Arginine vasotocin (AVT), in doses of 1.5 microgram, administered intranasally to two narcoleptics (a male aged 42 years and a female aged 35 years), as well as to 5 symptomatic hypersomniacs (3 females and 2 males), aged 25-57 years, induced very rapidly in most instances in sleep with REM periods at onset and markedly increased in amount of REM sleep during a fixed period of 180 min of sleep recording. After AVT administration there was a significant shortening of the time of occurrence of the first REM sleep period both in narcoleptics (t test = 0.05 greater than P greater than 0.025) and in symptomatic hypersomniacs (t test = 0.02 greater than P greater than 0.01).

REM sleep dependent release of vasotocin into cerebrospinal fluid of narcoleptics.

The lumbar cerebrospinal fluid (CSF) collected from 6 narcoleptic patients (three males and three females) aged between 31 and 47 years, as well as from 2 patients having Pickwickian syndromes with hypersomnia attacks (two males), aged 43-51 years, contained relatively high amounts of arginine vasotocin (AVT) only if the CSF was removed after a REM sleep period. The release was not induced by darkness since the same release of AVT occurred when the CSF was removed after a REM sleep period during daylight hours. No detectable AVT levels have been found in the CSF samples of four narcoleptics collected after a NREM period of sleep, either during night or daylight hours. The present results suggest a possible alteration of the rhythmical release of AVT both in narcolepsy and in narcoleptic syndromes.

Pineal vasotocin: REM sleep dependent release into cerebrospinal fluid of man.

Lumbar cerebrospinal fluid (CSF) of seven healthy male volunteers contains detectable levels of arginine vasotocin (AVT) when CSF was removed after awakening from rapid eye movement (REM) sleep. No detectable levels of AVT were found in the CSF of the same subjects when CSF WAS removed after awakening from non rapid eye movement (NREM) sleep. The amount of AVT detected in CSF after REM sleep was significantly higher if the subjects experienced vivid and emotive dreams. The present results provide the first evidence for a REM sleep dependent release of AVT into CSF of man.