23 Mayıs 2013 Perşembe
The Science of Insomnia - Joseph Bennigton-Castro
We've all experienced a sleepless night or two, and for some people that's actually the norm. But why do we experience insomnia at all? What is going on in our minds and bodies, to cause this awful condition? Here's what scientists know so far.
The prevalence of insomnia in adults varies widely, depending on how the condition is defined. Most broadly, someone has insomnia if he or she simply suffers from difficulty falling asleep, waking up over and over during the night, or nonrestorative sleep — and according to that definition, up to 50 percent of adults experience insomnia. But only around 20 percent of the population deals with insomnia, if we're going by the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders, where insomnia is considered a sleeping disorder (pdf) that lasts at least a month and causes daytime distress.
In any case, our understanding of insomnia is constantly evolving. For many years, insomnia was considered just a symptom of other issues, including depression, anxiety and schizophrenia. The prevailing thought was that if you treated the dominant condition, insomnia would subside as well. Insomnia is now known to be a syndrome in its own right, one that occurs alongside (is comorbid with) other disorders. So if you suffer from depression and insomnia, both issues should be treated at the same time — rather than just treating your depression alone.
To doctors, this type of insomnia, which is not caused by other medical issues or medicines, is called primary insomnia (as opposed to its sibling, secondary insomnia). They further describe the condition by how long it lasts — acute insomnia occurs for days or weeks, while chronic insomnia goes on for a month or more.
The basic models
In the past few decades, scientists have proposed a number of models to describe how chronic primary insomnia arises. One of the foundational paradigms was the "3-P model," referring to the supposed Predisposing, Precipitating and Perpetuating factors of the condition.
The model says that certain attributes, including being highly anxious or a perfectionist, may first make you more susceptible to insomnia. Then, some precipitating event, such as a death in the family or a new job, throws your sleep out of balance, causing acute insomnia. Finally, poor attitudes and perceptions perpetuate insomnia — these can include heightened uneasiness and tension regarding sleep, or poor sleep hygiene.
Over the years, other models have come along, some of which adapted concepts of the 3-P model. For example, the cognitive model, proposed a little over a decade ago, explains that insomniacs are overly worried about sleep and about what happens if they don't get enough of it. These negative thoughts trigger arousal and emotional distress, which essentially plunges people into an anxious state, causing them to actively monitor themselves and the environment for sleep-related threats (noises, body sensations and the like). Of course, this only exacerbates sleeplessness.
But insomnia (and the models to explain it) isn't limited to the psychological realm. The neurocognitive model explains that people with insomnia show more high-frequency electrical activity in the brain (EEG) when they're going to sleep compared with normal sleepers. This cortical arousal suggests that insomniacs have enhanced sensory or information processing and long-term memory formation during a time when normal sleepers do not, which could ultimately affect sleep. For example, the enhanced sensory processing may make insomniacs more sensitive to and aware of what's going on in the environment.
A common theme in these models and others is this idea of arousal. In fact, many researchers now consider insomnia to be a state of 24-hour hyperarousal, brought on by the interplay between psychological and physiological factors.
Current models suggest insomnia is caused by an interaction between behavioral and neurobiological factors. Courtesy of Elsevier.
On the psychological side of things, we have some of what we've already discussed. One useful cognitive model called the AIE (attention–intention-effort) pathway says that people with insomnia focus their attention on sleep, which leads to an active intention and effort to fall asleep.
The idea here is that normal sleep is automatic and involuntary — it's the result of a de-arousal process that allows homeostatic and circadian factors to engage sleep. But by actively trying to engage sleep themselves, insomniacs are impeding these natural processes and actually maintaining a state of arousal.
Interestingly, scientists have seen evidence of AIE even in the daytime naps of insomniacs. Numerous studies have looked at the Multiple Sleep Latency Test, which involves four or five 20-minute nap opportunities set two hours apart. If someone has gotten poor sleep because of insomnia, it stands to reason that they would be able to fall asleep quicker than someone who slept well the night before — but test after test has shown just the opposite. Some researchers are now speculating that the increased nap latency of insomniacs is due to the demands of the test, which directly asks participants to attempt to sleep at that very moment (insomniacs have basically conditioned themselves to enter a state of arousal when they make a conscious effort to sleep).
This induced arousal, at night and during naptime, has several lines of supporting physiological evidence. For example, studies have shown that insomniacs have higher whole-body metabolic rates — measured by looking at oxygen consumption at periodic intervals throughout the day — than normal sleepers.
Using PET scans, researchers have also investigated brain metabolism differences between insomniacs and normal sleepers. They saw similar results: insomnia patients had elevated global brain metabolism, both asleep and awake. Moreover, the study showed that insomniacs had smaller metabolism declines in wake-promoting regions of the brain when going from waking to non-REM sleep. In addition to this, a recent study found that insomnia patients have increased waking EEG.
Scientists have also examined the body temperatures, galvanic skin responses and heart rates of insomniac patients (all of which are physiological indicators of arousal). The results are not entirely conclusive, but suggest insomniacs have elevated electrodermal activity during the day, and may have elevated heart rates and altered heart rate variability during sleep; also, elderly insomnia patients have elevated core body temperatures at night (given the inconsistencies in the research, we can't say much else about other insomniacs).
Studies on hormone levels have also yielded interesting results, supporting the hyperarousal theory. Patients with primary insomnia apparently secrete less nighttime melatonin, which is known to regulate sleep and wake cycles. On the other hand, norepinephrine, which helps mediate wakefulness, is increased in insomnia patients, even at night. Stress hormones, including cortisol and ACTH (adrenocorticotropic hormone) may also be elevated in insomniacs when compared with controls.
Scientists' understanding of insomnia points to the condition being a state of hyperarousal, which is mediated by cognitive and physiological factors. But the exact mechanisms behind the arousal are not clear.
Some research suggests that the neurobiology of sleep-wake regulation may provide some answers. To put it simply, the tendency to sleep is regulated by a balance between sleep-promoting neurotransmitter systems and wake-promoting neurotransmitter systems. To facilitate sleep, a group of neurons in the hypothalamus called the ventrolateral preoptic nucleus (VLPO) release the inhibitory neurotransmitters galanin and GABA to shut off the arousal (wake) system. So a faulty VLPO flip-flop switch may prevent the brain from de-arousing.
At the same time, however, other evidence suggests that sleep arises from bottom-up processes. In this sense, sleep may be a local process, an intrinsic property of individual neurons or group of neurons. This concept of local sleep would suggest that hyperarousal is not something that happens globally in the brain — it may instead be a "use-dependent dysfunction" in specific neural circuits.
Future research will no doubt tease out these finer details. And other work may elucidate the role that genetics play in chronic primary insomnia. But the ultimate goal of insomnia research, of course, is to find an effective way to stop the condition in its tracks. Given that insomnia apparently costs us billions of dollars each year, curing the syndrome could have a huge positive impact in a lot of areas.
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