申論題

     erer is in his or her late 50s, ordinarily lasts about a year, and always ends in death, as the name indicates. To make matters worse, so little about how it works is known to researchers after years of study. So far researchers have only figured out that in a patient with FFI, 12 proteins called prions attack the sufferer’s thalamus, a structure deep in the brain, and 13 a damaged thalamus interferes with sleep. But they don’t know why this happens, or how to stop it, or ease its 14 symptoms. Before FFI was investigated, most researchers didn’t even know the thalamus had anything to do with sleep. FFI is 15 rare, known in only 40 families worldwide. But in one respect, it’s a lot like the less serious kinds of insomnia 16 millions of people today: It’s pretty much a mystery

    If we don’t know why we can’t sleep, it’s 17 because we don’t really know why we need to sleep in the first place. We know we miss it if we don’t have it. And we know that no matter how much we try to resist, sleep conquers us in the end. We have known for 50 years that we divide our slumber between periods of deep-wave sleep and what is called rapid eye movement (REM), when the brain is as active as when we are awake, but our voluntary muscles are 18 . Furthermore, we know all mammals and birds sleep. Fish, reptiles and insects all experience some kind of repose too.

      Yet all this 19 comes at a price. An animal must lie still for a great stretch of time, during which it is easy prey for predators. So what possibly is the payback for such risk? As the renowned sleep researcher Allan Rechtschaffen once said, “If sleep doesn’t serve an absolutely vital function, it is the greatest mistake evolution ever made.” Not surprisingly, the 20 theory of sleep is that the brain demands it.