We have examined the effect of injection of 6-hydroxydopamine (6-OHDA) into the ventral tegmental area (VTA) on the changes in arterial blood pressure (AP) and heart rate (HR) during the transition from non-rapid eye movement (NREM) sleep to REM sleep. The 6-OHDA-treated rats showed suppression of the increase of AP and HR during REM sleep and of theta frequency in the cortical electroencephalogram (EEG) during wakefulness (W) and REM sleep. It is suggested that midbrain dopaminergic neurons are involved in the control of AP and HR during REM sleep and in the EEG theta activity.

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We examined the effects of cervical position on the Obstructive Sleep Apnea Syndrome (OSAS) through the use of a custom-designed cervical pillow which promoted neck extension. Twelve subjects with OSAS were recruited from a tertiary sleep disorder clinic population. Of the twelve subjects, three had mild cases of OSAS, four had moderate cases, and the remaining five had severe cases. The subjects used their usual pillows during two consecutive recorded baseline nights in our laboratory. The subjects then used the cervical pillow for five days at home, and returned for two consecutive recorded nights at our laboratory while using the cervical pillow. During the nights in our laboratory, the subjects completed questionnaires, were videotaped to record head and body position, and had their breathing parameters recorded during sleep. Subjects with mild OSAS cases had a non-significant improvement in the severity of their snoring and a significant improvement in their respiratory disturbance index with the cervical pillow, while subjects with moderate OSAS cases showed no improvement in these parameters. Subjects with severe OSAS cases showed slight improvement in some measures of their abnormal respiratory events during the experimental period.

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We have no information on snoring and obstructive sleep apnea (OSA) in our population, which is predominantly Chinese. Our perception is that sleep apnea syndrome is more common than the 2-4% prevalence (Young et al., 1993) often quoted, judging from the experience in our sleep disorder unit. We studied the snorers in an adult population in Singapore and then went on to see how many snorers suffer pathological apnea and sleep apnea syndrome. Room partners, 220 of them aged 30-60 years, were interviewed for their observation of snoring among each other. 106 consecutive habitual loud snorers of a similar age group in the same population were studied with polysomnography in our sleep laboratory. An apnea index greater than 5 was considered pathological. 24.09% were loud habitual snorers. 87.5% of loud habitual snorers had significant obstructive apneas on the polysomnogram and 72% of these apneics complained of excessive daytime sleepiness (EDS). Given the clinical observation that all apneics snored, by extrapolating these figures, we guess that sleep apnea syndrome affects about 15% of the population. Multiple Sleep Latency Tests validated EDS in our cases with clinical hypersomnia. Hypersomnolence was significantly related to the poor delta wave sleep. Contrary to what was believed, OSA occurred predominantly in stage 1 and 2 non-rapid eye movement (NREM) sleep rather than in REM sleep. The frequent arousals prevented sleep going beyond stage 1 and 2.

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Visually scored delta activity (stages 3 and 4, SWS) as well as computerized delta activity measures increase after total and selective sleep deprivation. It is, however, still controversial if SWS amount is only a function of prior waking duration, or if it is related to the structure of the previous sleep period (i.e., to the time spent in SWS). In order to clarify if the amount of SWS is crucial in determining SWS recovery, we selectively deprived SWS during two nights to assess the presence of a compensatory SWS rebound in the following recovery night. Ten normal males slept for 6 consecutive nights in the laboratory. After an adaptation and two baseline nights (BSL; BSL-A), selective SWS deprivation was accomplished for two consecutive nights (DEP-1; DEP-2), by means of an acoustic stimulation technique. A recovery (REC) night then followed. An almost complete selective SWS suppression during both deprivation nights was achieved. A significant increase of S4 and SWS in the REC as compared to the BSL-A paralleled a significant shortening of S3 and S4 latencies. S2 percentage significantly increased during both DEP nights with respect to the other experimental nights. There was no significant difference among nights with regard to total sleep time, percentage of REM sleep, stage 1, movement time, number of awakenings and number of movement arousals, indicating that the acoustic stimulation technique did not dramatically disrupt normal sleep continuity and architecture. These results indicate that SWS rebound after selective SWS deprivation can be ascribed to the loss of SWS accumulated during two consecutive nights, further supporting the idea that the delta sleep amount is more linked to SWS in the previous sleep periods than to the total sleep duration.

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