Acute ethanol intake inhibits parasympathetic nerve activity and results in predominance of sympathetic nerve activity during sleep, in a dosage-dependent manner. The results of this study suggest that ethanol interferes with the restorative functions of sleep.

Bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) usually appear transiently in patients with severe disturbances of consciousness and are indicative of a poor prognosis. Recurrent BIPLEDs have not previously been reported in the literature. We report a 64-year-old patient with bilateral hippocampal lesions (cerebral infarction) who exhibited persistent periodic lateralized epileptiform discharges (PLEDs) (chronic PLEDs) associated with recurrent BIPLEDs. Electroencephalography was recorded for more than 6 months. Left hemispheric PLEDs appeared first. Next, PLEDs shifted to the right hemisphere and BIPLEDs occasionally developed. Brain magnetic resonance imaging and single-photon emission computed tomography with technetium-99-hexamethyl-propyleneamine oxime was performed before and after the appearance of BIPLEDs. The patient had no remarkable clinical symptoms aside from mild memory impairment for this period of time. This is the first case of recurrent 'benign' BIPLEDs, that is, BIPLEDs with a positive prognosis.

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Breathing rate (BR) during rapid eye movement (REM) sleep is known to fluctuate largely, while increases in BR during REM sleep reported were small. In our mice experiments, we found that mice exhibit a rapid increase in instantaneous BR (RIBR) of >2 fold during natural sleep with accompanying atonia, laying their sides down. The RIBR was further found in a sleeping mouse attached with EEG electrodes when the EEG amplitude and delta wave power were lower. Therefore, it is likely that mice show RIBRs during REM sleep. Interestingly, similar RIBRs accompanied by atonia and REM burst during REM sleep were also found in humans by standard polysomnographic studies in 11 healthy volunteers (age: 22.3 +/- 2.8) with BR measurement by nasal/oral airflow sensors and chest/abdomen belt sensors. All subjects underwent RIBR of doubled BR at least once a night. As SpO(2) before RIBRs was a level not effective to be a respiratory stimulant (96.7 +/- 1.6 %, n = 63), the RIBR seems to be controlled by higher central nervous system rather than autonomic nervous system control on response to central and peripheral chemical sensors. In fact, tachypnea with suppressed amplitude during RIBR resulted in a slight fall in SpO(2) (96.4 +/- 1.7 %, p = 0.0007). In the present study, RIBRs accompanied by atonia and REM were not necessarily consistent in change in rate and/or amplitude, therefore, these various pattern of RIBRs may be potential indices of dreams with various emotional contents. Analysis of instantaneous BR, thus, may be a helpful tool for understanding the neural control of breathing during REM sleep.