Bed-wetting and the stages of sleep
Problem: To state the obvious, bed-wetting is no fun. When parents handle it poorly, and if it’s frequent and lasts beyond age 5 or so, the condition can have a devastating effect on a child’s sense of self, social relationships, and strivings for independence. Treatment is slow and frequently unsuccessful. On the upside, eventually the problem often cures itself: Only 10 percent of 7-year-old children wet the bed, and as every additional year passes, another 15 percent of the remaining sufferers stop.
Theories: A genetic component has long been suspected because there is a high likelihood that one or both parents of a bed-wetting child have a similar history. Emotional stress may also play a role. But the best-accepted theory has been that the central problem is a developmental disorder of sleep. Superdeep sleep seems a likely culprit because parents almost always say that it is virtually impossible to rouse a child who has wet the bed. In addition, parents who have outfitted their children with bed-wetting-treatment alarms (which ring as soon as they detect drops of moisture) often report that the child sleeps blissfully while the alarm wakes everyone else in the house (though, I should add, these alarms are the single most effective treatment).
New study: Recent research now casts doubt on the superdeep-sleep theory. The researchers studied 35 children between ages 6 and 14 who wet the bed almost every night, comparing them with 21 children who stayed dry. The research involved the use of the new tools in the study of sleep, including brainwave measurements, bladder measurements, and detection of bed-wetting without disturbing the child under study.
Findings: Contrary to expectations, children with severe bed-wetting problems spent more of their night hours in light sleep and fewer of them in the deep stages of sleep than children who do not have this problem. Instead, the children who habitually wet the bed all had significantly smaller bladder capacity than the children with whom they were compared. When nerve endings in their bladder walls detected a sense of fullness, a signal stimulated the bladder wall to contract and at the same time sent an activation signal to the brain, decreasing the depth of sleep. Yet the children couldn’t make the final step and wake completely. The researchers speculate that perhaps this is a side effect of the bladder’s long-term overstimulation of the brain’s arousal center.
Implications: If that speculation is correct, perhaps we should move away from bed-wetting treatments that aim to wake the child—clearly a difficult task if the overloaded brain is blocking the final transition to wakefulness. An alternative might be treatments that minimize the signals sent from the bladder to the brain, so as to allow the bladder wall to tolerate a little more filling and to decrease the frequency of signals sent to the brain’s centers that control arousal. Bladder capacity increases as children age (by about an ounce with every year of age) and, gradually, in response to stretching, but increased capacity alone doesn’t reliably end bed-wetting.
SIDS and infection
Problem: Sudden infant death syndrome is one of the most terrifying possibilities new parents face. Despite a great deal of research, we still have no clear idea of the mechanism (or mechanisms) for the sudden death of a baby. Nonetheless, epidemiological research points to certain practices to avoid. For example, it is clear that an infant put to sleep on his back, without any props or supports, is much safer than a baby who is allowed to sleep face down. It is also clear that putting a sheepskin in the baby’s crib or allowing a sleeping baby’s face to be covered increases the risk of SIDS, as does exposure to tobacco smoke. (The use of pacifiers, on the other hand, reduces the risk.)
Question: What other risk factors are there? In England and Wales, all SIDS cases are deeply and intensively studied, and a recent report based on this research suggests that an undetected bacterial infection might sometimes play a role.
New study: The researchers examined the autopsy records of about 550 infants who died suddenly, of unexplained causes, in a recent 10-year period. The cases were divided into three piles. One group contained the babies whose death could be explained, after autopsy, as a result of a noninfectious cause. For instance, these infants may have died as a result of a congenital heart defect or the result of a physical injury. Another group consisted of infants whose death was demonstrably due to a bacterial infection—perhaps pneumonia or meningitis or a blood infection, not detected before death but showing up at autopsy. Finally, for the third and largest cohort of infants, no physical findings could clearly establish a cause of death.
Findings: The autopsy protocol included the isolation of any bacteria found in all the babies’ blood, spinal fluid, or tissues. The study looked at the differences between bacteria from infants who died of physical causes (with little reason to think that the baby also had an infection) and bacteria obtained from babies with known infections. Then the researchers compared these patterns with the bacteria from infants whose cause of death was unknown. The results were striking. On average, the kind of bacteria found in infants with an unknown cause of death were much like those from children who died of bacterial infections (and the bacteria found in both of these groups were similar, and often the kinds of germs known to cause deadly infections). On the other hand, the unknown-cause bacterial cultures did not resemble those of the children whose death was caused by injury or congenital heart disease.
Implications: Needless to say, the studies don’t prove that infection caused the unexplained deaths. But the suggestive associations point to a new line of research. If unrecognized bacterial infections turn out to play a greater role in SIDS than previously thought, we might gain new ways to identify infants at risk and, perhaps, even to prevent this dreaded occurrence.
The best emergency contraception
Issue: When proper contraception isn’t available or for whatever reason isn’t used, there’s another alternative: emergency contraception. It isn’t intended to be a replacement for the real thing (for one thing, it’s not quite as effective), but for many women it’s a far better choice than nothing at all. An estimated 50 million pregnancies worldwide are terminated every year, a solution statistically safer than pregnancy, in terms of mortality rates, but less safe and more costly (in many ways) than preventing pregnancy in the first place.
Question: What is emergency contraception? What are the choices? Which method is best? How effective is it, and how safe? An extensive review of the literature, pulling together the results of 81 studies that included almost 46,000 women, compared most of the available regimens.
Methods: Emergency contraception usually involves the administration of one or two doses of a medication sometime in the three days following unprotected sex. (Calling it the “morning after pill” gives the wrong idea of the potential time frame.) The first available method was the Yuzpe regimen, introduced in the 1970s: two doses of a hormone combination similar to that contained in some birth control pills. It’s not available in American drugstores, but some doctors keep an office supply and give the pills to patients as needed. Plan B, which is available in the United States, uses levonorgestrel, a hormone similar to one produced by the body during pregnancy. And then there’s mifepristone (RU-486 or Mifeprex), a medication that blocks the activity of an important hormone needed to sustain pregnancy. Though this drug is licensed in the United States for medical abortions, it isn’t licensed for emergency contraception (a before- and after-pregnancy distinction). In addition to these medications are a few other measures that are rarely used, such as a copper IUD called ParaGuard, which can be inserted in the five days following sex and offers effective emergency contraception (as well as ongoing birth control, if it’s left in place).
Findings: The review clearly showed that the most effective medical option for emergency conception is mifepristone, which has a failure rate between 0.5 percent and 1 percent. Mifepristone also had the lowest incidence of side effects (some nausea and vomiting and sometimes a slight delay in the resumption of menses). The hormonal methods (Yuzpe and Plan B) carried an increased risk of nausea and vomiting and sometimes caused headaches. Yuzpe and Plan B were half as effective as mifepristone. The ParaGuard was also effective, with a failure of roughly 0.1 percent, though a smaller number of women were tested with this method. Also, IUD insertion requires special skills and is much more expensive. For all the methods, no serious side effects were reported among the 46,000 women in the study. A total of eight healthy babies were born after the emergency contraception failed.
Conclusion: The superior safety and efficacy of mifepristone means that the FDA, which regulates the drug, is denying women in the United States the best method of emergency contraception. My speculation, of course, is that the decision not to extend the drug’s license for this use was made more on political (and perhaps religious) grounds than on the basis of good science or good medicine. What’s to be done? As usual, beats me, but I wish a different decision had been made.