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发表于 2008-11-10 13:38
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During rapid-eye-movement sleep, when we dream, the brain is thought to be processing stored memory. The memory of a newborn infant is dominated by its fetal experience, and the infant is likely to dream about its life in the womb. Research with lucid (or conscious) dreaming has shown that dream images are supported by the corresponding body actions, using those muscles which remain active during rapid-eye-movement sleep. We suggest that sudden infant death syndrome or cot death may be a result of an infant dreaming about its life (or memory) as a fetus. In the course of that dream, since a fetus does not breathe (in the usual sense) the infant may cease to breathe and may die. This simple hypothesis is consistent with all of the known facts about sudden infant death syndrome (pathological and epidemiological), such as the age at death curve (the observed exponential decay and possibly the peak at 2–3 months), the higher risk with the prone sleeping position (but not excluding the supine position), and the observed climatic variation (seasonal and regional) in the incidence of sudden infant death syndrome. Many of these well-established facts have no other known explanation and other theories can generally only account for a few of the known facts about sudden infant death syndrome. Our hypothesis is also supported by recent findings that, as a group, sudden infant death syndrome infants have a higher proportion of rapid-eye-movement sleep, and also that they have an average higher heart rate (corresponding to possible fetal dreams) but only during rapid-eye-movement sleep. The infant dreaming hypothesis also offers an explanation of why all of the chemoreflexes, and other protective mechanisms, that would normally awake the infant, may fail simultaneously. On the basis of our theory, we make suggestions as to how the infant dreaming hypothesis can be tested further and how the risk of sudden infant death syndrome may be reduced.
只看了一下上面的摘要,没看全文。觉得是作者经验推导+主观臆断,实验设计不严谨。
1、睡眠的两种不同时相,是根据脑电图波形来区分的。一是脑电波呈现同步化慢波的时相,常称为慢波睡眠(slow wave sleep,SWW);另一种是脑电波呈现去同步化的时相,称为异相睡眠(paradoxical sleep,PS)或快波睡眠、快速眼球运动睡眠。
人睡眠一开始首先进入慢波睡眠,慢波睡眠持续约80~120分钟左右后,转入异相睡眠;异相睡眠持续约20~30分钟左右后,又转入慢波睡眠;以后又转入异相睡眠。整个睡眠期间,这种反复转化约4~5次,越接近睡眠后期,异相睡眠持续时间逐步延长。在异相睡眠期间,如将其唤醒,被试者往往会报告他正在做梦,“做梦”被认为是异相睡眠的特征之一。 既然是特征之一,也就是说还有其他的重要特征:呼吸加快、血压升高、心率加快、四肢肌肉抽动,男性生殖器官充血等,其实每一种功能的改变都可以成为新生儿猝死的原因,并且有客观指标可以证明,为什么文章作者Christos先生,非把梦境,这个说不清道不明的指标拎出来呢? 不过,脑的高级功能,思维、感觉、意识、记忆之类的确实是既吸引人又让人无从下手研究。
2、梦境虽说一般出现在快速眼球运动睡眠,但是,慢波睡眠期也有做梦。 早些年,这方面的研究比较多。简单搜索一下,某研究:在191例被试者异相睡眠期间唤醒后,报告正在做梦的有152例,占80%左右;在160例被试者慢波睡眠期间唤醒后,报告正在做梦的只有11例,占7%左右。 所以,Christos好像只选取了他所需要的结果,反正不是科学态度就是了。
3、还有一点比较搞笑。俺严重怀疑作者最基本的生理常识都不懂。 呼吸是个极其复杂的过程,多因素参与:基本呼吸节律产生于延髓,延髓是自主呼吸的最基本中枢,脑桥是呼吸调整中枢。 呼吸的外周调控更是复杂:化学感受性反射、机械感受性反射和防御性反射。其中仅化学性反射,又分为,氢离子浓度、PCO2、H2CO3、HCO3、PO2…… 嘿嘿,我一下子也说不清。 只认为做梦便可引发呼吸停止,也太太太简单了。
4、文章发表在MED HYPOTHESES,影响因子0.92。 在医学和生物学领域,我认为影响因子小于6的文章都不值得细读,Hypotheses,很多时候让人误入歧途。 推荐小榔头妹妹可以找PQDD和你研究方向类似的硕士博士论文来看,或者追踪一下你专业领域的牛人发表的大综述。应该会有事半功倍的效果的,也会给自己一个相对高的起点。 还有,这篇文章是95年的,有点儿老。 我自己看的文献,基本上05年以后的我才会细看。
呵呵,很不容易在燕谈看到跟我专业相关的讨论,正巧我以前对睡眠、记忆等感兴趣。有点儿掉书袋之嫌 |
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