About three years ago Eva Salem got into some trouble with a crocodile. It snapped her hand in its jaws. In a panic, she managed to knock out the crocodile and free herself. Then, she woke up.

"I imagine that's what it's like when you're on heroin. That's what my dreams were like—vivid, crazy and active," she says. Salem, a new mother, had been breast-feeding her daughter for five months before the croc-attack dream, living on four hours of sleep a night. If she did sleep a full night, her dreams boomeranged, becoming so vivid that she felt like she wasn't sleeping at all.

Dreams are amazingly persistent. Miss a few from lack of sleep and the brain keeps score, forcing payback soon after eyelids close. "Nature's soft nurse," as Shakespeare called sleep, isn't so soft after all.

"When someone is sleep deprived we see greater sleep intensity, meaning greater brain activity during sleep; dreaming is definitely increased and likely more vivid," says neurologist Mark Mahowald of the University of Minnesota and director of the Minnesota Regional Sleep Disorders Center in Minneapolis.

The phenomenon is called REM rebound. REM refers to "rapid eye movement," the darting of the eyes under closed lids. In this state we dream the most and our brain activity eerily resembles that of waking life. Yet, at the same time, our muscles go slack and we lie paralyzed—a toe might wiggle, but essentially we can't move, as if our brain is protecting our bodies from acting out the stories we dream.

Sleep is divided into REM and four stages of non-REM; each has a distinct brain wave frequency. Stage one of non-REM is the nodding off period where one is between sleeping and waking; it's sometimes punctuated with a sensation of falling into a hole. In stage two the brain slows with only a few bursts of activity. Then the brain practically shuts off in stages three and four and shifts into slow-wave sleep, where heart and breathing rates drop dramatically.

Only after 70 minutes of non-REM sleep do we experience our first period of REM, and it lasts only five minutes. A total non-REM–REM cycle is 90 minutes; this pattern repeats about five times over the course of a night. As the night progresses, however, non-REM stages shorten and the REM periods grow, giving us a 40-minute dreamscape just before waking.

The only way scientists can study REM deprivation is by torturous sleep deprivation. "We follow the [electroencephalogram] tracing and then when we see [subjects] moving into REM, we wake them up," says psychologist Tore Nielsen, director of the Dream and Nightmare Lab at the Sacré-Coeur Hospital in Montreal. "As soon as you start to rob them of REM, the pressure for them to go back into REM starts to build." Sometimes Nielsen will have to wake them 40 times in one night because they go directly into REM as soon as they are asleep.

Of course there is non-REM rebound as well, but the brain gives priority to the slow-wave sleep and then to REM, suggesting that the states are independent of each other.

In a 2005 study published in Sleep, Nielsen showed that losing 30 minutes of REM one night can lead to a 35 percent REM increase the next night—subjects jumped from 74 minutes of REM to a rebound of 100 minutes.

Nielsen also found that dream intensity increased with REM deprivation. Subjects who were only getting about 25 minutes of REM sleep rated the quality of their dreams between nine and eight on a nine-point scale (one being dull, nine being dynamite).

Of course, REM deprivation, and the subsequent rebound, is common outside the lab. Alcohol and nicotine both repress REM. And blood pressure drugs as well as antidepressants are also well known REM suppressants. (Take away the dreams and, curiously, the depression lifts.) When patients stop the meds, and the vices, they're rewarded with a scary rebound.

But the persistence of REM begs the question: Why is it so insistent? When rats are robbed of REM for four weeks they die (although the cause of death remains unknown). Amazingly, even though we spend about 27 years dreaming over the course of an average life, scientists still can't agree on why it's important.

Psychiatrist Jerry Siegel, head of the Center for Sleep Research at the University of California, Los Angeles, recently proved that REM is nonexistent in some big-brained mammals, such as dolphins and whales. "Dying from lack of REM is totally bogus," Siegel says. "It's never been shown in any species other than a rat."

Some theories suggest that REM helps regulate body temperature and neurotransmitter levels. And there is also evidence that dreaming helps us assimilate memories. Fetuses and babies spend 75 percent of their sleeping time in REM. Then again, platypuses experience more REM than any other animal and researchers wonder why, because, as Minnesota's Mahowald puts it, "Platypuses are stupid. What do they have to consolidate?"

But, given that rats run through dream mazes that precisely match their lab mazes, others feel that there must be some purpose or meaningful information in dreams.

John Antrobus, a retired professor of psychology and sleep research at the City College of New York says that dream content is tied to our anxieties. But he never found the extreme vividness in REM rebound that others assume is there, based on a higher level of brain activity which likely means more action-packed dreams.

"The brain is an interpretive organ, and when regions are less connected as they are in sleep, we get bizarre narratives," he says. "But its purpose? For that we have to ask what is the purpose of thought. We can't answer one without answering the other."

  大約三年前，Eva Salem開始被一條鱷魚困擾。它下頜強壯有力，一口就咬住了她的手。慌亂之中，她居然打暈了鱷魚，這才得以脫身。然后，她醒了。

     她說：“我的夢真切，瘋狂，驚心動魄。我猜吸食毒品后的幻覺大概就會是這樣。”Salem當時剛做媽媽，夢見鱷魚襲擊的時候，正是給她女兒哺乳的第五個月，當時她每晚只能睡上4個鐘頭。就算難得有個整覺可睡，又會做這些夢，夢境像是真的一樣，弄得她覺得自己像是根本不是處在睡眠中。

     令人驚訝的是，夢會一再重復出現。缺乏睡眠的人，大腦不得不持續工作，所以等人一合上眼，它就開始報復。所以，夢，莎士比亞筆下“大自然的溫情的保姆”，并不是那么的溫情。

     “當人睡眠不足，睡眠強度就會增加，也就是說睡眠期間大腦會更加活躍，所以夢就會更多，也更生動。”明尼蘇達大學神經學專家、明尼蘇達睡眠失調中心負責人Mark Mahowald解釋道。

     這種現象叫做快速眼動（REM）反彈。REM是rapid eye movement（快速眼部活動）的縮寫，指眼球在眼皮下飛快運動。在這個階段我們最容易做夢，大腦活動也和清醒時驚人的相似。然而與此同時，我們肌肉放松，全身麻痹般躺著——也許能偶爾抽動腳趾，但總的來說動彈不得，這就像是大腦為防止我們身體像夢到的一樣動作而采取的保護機制。

     睡眠過程可分為快速眼動階段和四個非快速眼動階段，每個階段的腦波頻率都不一樣。非快速眼動的第一階段是瞌睡階段，人處于半睡半醒之間，有時會伴有類似落入洞中的感覺。在第二階段，大腦遲緩下來，只有少量活動。在隨后的第三第四階段，大腦才真正休息，進入慢波睡眠，此時心跳和呼吸頻率都大大降低。

     只有經過70分鐘非快速眼動睡眠，我們才開始第一次快速眼動，這一階段只持續5分鐘。一整個非快速眼動-快速眼動周期時長90分鐘，一晚大約重復5次。然而越到后來非快速眼動過程越短，快速眼動過程越長，睡醒前最后一次快速眼動可以帶來40分鐘的夢境。

     科學家目前研究快速眼動缺乏的現象只有通過人為中斷志愿者睡眠的方法。蒙特利爾圣心醫院夢境實驗室的負責人、心理學家Tore Nielsen說：“我們追蹤腦電圖，當觀察到被試者進入快速眼動，就叫醒他們。當快速眼動被人為打斷時，被試者會強迫自己重新回到這個狀態。”有時Nielsen一晚上要叫醒他們多達40次，因為他們一入睡就直接進入快速眼動狀態。

     當然也有非快速眼動的反彈，但這只是由于大腦傾向于先進入慢波睡眠，再進入快速眼動，這表明這些過程是彼此獨立的。

     在2005年發表于《睡眠雜志》的論文中，Nielsen指出，一個晚上缺少30分鐘快速眼動，會導致次日晚快速眼動增加35%——被試者快速眼動過程由74分鐘躍增至100分鐘。

     Nielsen還發現，夢的強度隨著快速眼動的缺乏而增長。給只經歷25分鐘快速眼動的被試者做夢的質量評分，在滿分9分的評價系統，可達到8～9分，其中1分為完全不活躍，9分為非常活躍。

     在生活中，快速眼動的缺乏和隨之發生的反彈非常常見。酒精和尼古丁都會抑制快速眼動。控制血壓的藥物和抗抑郁藥物也會遏制快速眼動。當停用藥物或是戒煙戒酒時，人們就會面對可怕的反彈。

     我們研究快速眼動的反復出現，同時卻回避了一個問題：為什么它會那么頑固的存在？老鼠被剝奪快速眼動過程持續四周就會死亡（其中機理仍然未知）。盡管平均人的一生按這規律做夢的時間累計長達27年，科學家對于夢何以如此重要仍各執一詞。

     洛杉磯加州大學睡眠研究中心的主任、精神病學家Jerry Siegel最近證實，某些腦部較大的哺乳動物如海豚和鯨魚沒有快速眼動現象。“缺乏快速眼動會導致死亡的論調是站不住腳的，”Siegel說，“沒有在任何除了老鼠以外的物種身上觀察到這種現象。”

     一些理論認為，快速眼動有助于調節人體體溫和神經傳導素水平。有證據顯示做夢能幫助鞏固記憶。胎兒和嬰兒有75%的睡眠時間處于快速眼動。動物中鴨嘴獸快速眼動時間最長，對此科學家卻表示不解，因為，用明尼蘇達的Mahowald的話說，“鴨嘴獸很笨，它們有什么好鞏固的？”

     也有人考慮到老鼠睡夢質量和實驗室表現高度匹配，認為夢一定具有一定的含義，能傳達某種信息。

     紐約市大學心理與睡眠研究所的退休教授John Antrobus認為，夢的內容和我們的焦慮有關。然而，理論上大腦活動加劇，可能造成夢的內容更加豐富，但他并沒有觀察到這種有人認為在快速眼動反彈階段會出現的夢境異常生動的現象。

     他說：“大腦是一個解釋性的器官，當我們睡著，大腦各部分聯系不再那么緊密，我們就會夢見千奇百怪的故事。但要問這有什么目的性，我們就得先問問自己思想的目的是什么。回答不了這個問題，也就回答不了前一個問題。”