Alcohol has a dose-related effect on parasympathetic nerve activity during sleep.

BACKGROUND: The aim of this study was to identify the acute effects of ethanol on the relationship between sleep and heart rate variability (HRV) during sleep. METHODS: Ten healthy male university students were enrolled in this study. An alcoholic beverage was given to each subject at a dosage of 0 (control), 0.5 (low dose: LD), or 1.0 g (high dose: HD) of pure ethanol/kg of body weight. All experiments were performed at 3-week intervals. On the day of the experiment, a Holter electrocardiogram was attached to the subject for a 24-hour period, and the subject was instructed to drink the above-described dosage of alcoholic beverage 100 minutes before going to bed; polysomnography was then performed for 8 hours. Power spectral analysis of the HRV was performed using the maximum entropy method, and the low- (LF: 0.04 to 0.15 Hz) and high-frequency (HF: 0.15 to 0.4 Hz) components along with LF/HF ratio were calculated. RESULTS: As alcohol consumption increased, the heart rate increased and the spectral power of HRV measured at each frequency range decreased. Higher doses of ethanol also increased the LF/HF ratio compared with the measured ratio of the control group. CONCLUSIONS: 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.

Rapid increase to double breathing rate appears during REM sleep in synchrony with REM - a higher CNS control of breathing? -.

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.

Progression of P300 in a patient with bilateral hippocampal lesions.

OBJECTIVE: To evaluate the effects of hippocampal damages on P300 of event-related potentials (ERPs). METHODS: ERPs were recorded over about 8 months using the auditory oddball paradigm in a patient with bilateral hippocampal lesions confirmed on brain magnetic resonance imaging. Findings were compared with those from clinical electroencephalography (periodic lateralized epileptiform discharges (PLEDs) or bilateral independent PLEDs (BIPLEDs)). The patient displayed no marked clinical symptoms aside from mild memory impairment during this time, and was able to fully perform the oddball task. RESULTS: Clearly identifiable P300 were present in all recordings. Furthermore, increases in the number of right PLEDs were significantly correlated with increases in P300 latency. CONCLUSIONS: Two key results were apparent. First, the appearance of P300 in all ERP recordings supports the suggestion that the hippocampus is not indispensable for P300 generation. Second, the correlation between the number of PLEDs and P300 latency supports the suggestion that the hippocampus affect the components of P300 latency. SIGNIFICANCE: This case thus offers very suggestive evidence regarding the generation of P300.