Effects of physostigmine infusion on healthy volunteers deprived of rapid eye movement sleep.

Rapid eye movement sleep (REMS) deprivation is believed to alter the sensitivity of various neurotransmitter systems. In the present article, we studied 20 healthy volunteers divided into three groups. Group A attended the sleep laboratory for three nights: acclimatization, a baseline night, and one night of physostigmine infusion. Group B attended for eight nights; acclimatization, baseline, four nights of REMS deprivation, and two recovery nights. With the exception of the first recovery night, when group C volunteers were administered physostigmine, group C's schedule was identical to group B's. The infusions received by group A and C were composed of 1.0 mg of physostigmine, dissolved in 100 ml of saline solution. These were administered 5 min after sleep onset and thereafter every hour, except when the subjects were either awake or in REMS. All of the subjects receiving the cholinomimetic infusion were given a peripheral anticholinergic. Group A experienced a great number of awakenings with a decrease in REMS percentage. Group B recovery occurred over two nights, with an increase in the average length of REMS. Group C exhibited maximum REMS rebound on the first recovery night with an increased number of REMS episodes, as well as significant reductions in the first REMS latency. Our findings suggest that physostigmine alters REMS rebound following REMS deprivation.

Timing discontinuation of antiepileptic treatment in childhood epilepsies--the role of the sleep deprivation EEG: a preliminary study.

Sleep deprivation EEGs can help us in timing discontinuation of antiepileptic treatment of childhood epilepsy. After 3-5 seizure-free years, a negative sleep deprivation EEG (i.e., the lack of any epileptiform potentials) is a good predictor of terminal remission of the seizures after cessation of the drug. In the drug-free follow-up period (in average 2 years) only 2/40 patients relapsed, 38/40 (= 95 percent) remained free of seizures. The results and limits of the study as well as the theoretical background are discussed briefly.

[Changes in membrane proteins in the brain stem of the rat after deprivation of the paradoxical stage of sleep and prolongation of this stage during subsequent free behavior]. / Izmeneniia membrannykh belkov v stvole golovnogo mozga krys pri lishenii ikh paradoksal'noi fazy sna i prodolzhitel'nost' étoi fazy pri posleduiushchem svobodnom povedenii.

In REM-sleep-deprived rats, phenazepam (1.0 mg/kg) prevented the SH-group content increase in the brain stem membrane proteins, but induced undesirable sedative phenomena which, however, could be eliminated by simultaneous injections of sydnocarbum. The data obtained suggest that if the brain stem membrane proteins are protected against a denaturation-like alteration (characterized by the increase of SH-group content of these proteins) during REM-sleep deprivation, there is no "rebound" of this sleep phase after the end if the experiment in the condition of the unrestrained behavior of the rats.