科研之友
微信
新浪微博
Facebook
分享链接
摘要
Electroencephalographic (EEG) delta waves during non-rapid eye movement sleep (NREMS) after sleep deprivation are enhanced. That observation eventually led to the use of EEG delta power as a parameter to model process S in the two-process model of sleep. It works remarkably well as a model parameter because it often co-varies with sleep duration and intensity. Nevertheless there is a large volume of literature indicating that EEG delta power is regulated independently of sleep duration. For example, high amplitude EEG delta waves occur in wakefulness after systemic atropine administration or after hyperventilation in children. Human neonates have periods of sleep with an almost flat EEG. Similarly, elderly people have reduced EEG delta power, yet retain substantial NREMS. Rats provided with a cafeteria diet have excess duration of NREMS but simultaneously decreased EEG delta power for days. Mice challenged with influenza virus have excessive EEG delta power and NREMS. In contrast, if mice lacking TNF receptors are infected, they still sleep more but have reduced EEG delta power. Sleep regulatory substances, e.g., IL1, TNF, and GHRH, directly injected unilaterally onto the cortex induce state-dependent ipsilateral enhancement of EEG delta power without changing duration of organism sleep. IL1 given systemically enhances duration of NREMS but reduces EEG delta power in mice. Benzodiazepines enhance NREMS but inhibit EEG delta power. If duration of NREMS is an indicator of prior sleepiness then simultaneous EEG delta power may or may not be a useful index of sleepiness. Finally, most sleep regulatory substances are cerebral vasodilators and blood flow affects EEG delta power. In conclusion, it seems unlikely that a single EEG measure will be reliable as a marker of sleepiness for all conditions.
- 出版日期2011
