Posts tagged insomnia
Articles and news from the latest research reports.
Researchers Identify Brain Differences Linked to Insomnia
Johns Hopkins researchers report that people with chronic insomnia show more plasticity and activity than good sleepers in the part of the brain that controls movement.
"Insomnia is not a nighttime disorder," says study leader Rachel E. Salas, M.D., an assistant professor of neurology at the Johns Hopkins University School of Medicine. "It’s a 24-hour brain condition, like a light switch that is always on. Our research adds information about differences in the brain associated with it."
Salas and her team, reporting in the March issue of the journal Sleep, found that the motor cortex in those with chronic insomnia was more adaptable to change - more plastic - than in a group of good sleepers. They also found more “excitability” among neurons in the same region of the brain among those with chronic insomnia, adding evidence to the notion that insomniacs are in a constant state of heightened information processing that may interfere with sleep.
Researchers say they hope their study opens the door to better diagnosis and treatment of the most common and often intractable sleep disorder that affects an estimated 15 percent of the United States population.
To conduct the study, Salas and her colleagues from the Department of Psychiatry and Behavioral Sciences and the Department of Physical Medicine and Rehabilitation used transcranial magnetic stimulation (TMS), which painlessly and noninvasively delivers electromagnetic currents to precise locations in the brain and can temporarily and safely disrupt the function of the targeted area. TMS is approved by the U.S. Food and Drug Administration to treat some patients with depression by stimulating nerve cells in the region of the brain involved in mood control.
The study included 28 adult participants - 18 who suffered from insomnia for a year or more and 10 considered good sleepers with no reports of trouble sleeping. Each participant was outfitted with electrodes on their dominant thumb as well as an accelerometer to measure the speed and direction of the thumb.
The researchers then gave each subject 65 electrical pulses using TMS, stimulating areas of the motor cortex and watching for involuntary thumb movements linked to the stimulation. Subsequently, the researchers trained each participant for 30 minutes, teaching them to move their thumb in the opposite direction of the original involuntary movement. They then introduced the electrical pulses once again.
The idea was to measure the extent to which participants’ brains could learn to move their thumbs involuntarily in the newly trained direction. The more the thumb was able to move in the new direction, the more likely their motor cortexes could be identified as more plastic.
Because lack of sleep at night has been linked to decreased memory and concentration during the day, Salas and her colleagues suspected that the brains of good sleepers could be more easily retrained. The results, however, were the opposite. The researchers found much more plasticity in the brains of those with chronic insomnia.
Salas says the origins of increased plasticity in insomniacs are unclear, and it is not known whether the increase is the cause of insomnia. It is also unknown whether this increased plasticity is beneficial, the source of the problem or part of a compensatory mechanism to address the consequences of sleep deprivation associated with chronic insomnia. Patients with chronic phantom pain after limb amputation and with dystonia, a neurological movement disorder in which sustained muscle contractions cause twisting and repetitive movements, also have increased brain plasticity in the motor cortex, but to detrimental effect.
Salas says it is possible that the dysregulation of arousal described in chronic insomnia - increased metabolism, increased cortisol levels, constant worrying - might be linked to increased plasticity in some way. Diagnosing insomnia is solely based on what the patient reports to the provider; there is no objective test. Neither is there a single treatment that works for all people with insomnia. Treatment can be a hit or miss in many patients, Salas says.
She says this study shows that TMS may be able to play a role in diagnosing insomnia, and more importantly, she says, potentially prove to be a treatment for insomnia, perhaps through reducing excitability.
(Source: hopkinsmedicine.org)
Tired all the time: Could undiagnosed sleep problems be making MS patients’ fatigue worse?
People with multiple sclerosis (MS) might assume that the fatigue they often feel just comes with the territory of their chronic neurological condition.
But a new University of Michigan study suggests that a large proportion of MS patients may have an undiagnosed sleep disorder that is also known to cause fatigue. And that disorder – obstructive sleep apnea – is a treatable condition.
In the latest issue of the Journal of Clinical Sleep Medicine, researchers from the U-M Health System’s Sleep Disorders Center report the results of a study involving 195 patients of the U-M Multiple Sclerosis Center.
In all, 56 percent of the MS patients were found to be at increased risk for obstructive sleep apnea, based on a method of screening for the condition known as the STOP-Bang questionnaire. But most had never received a formal diagnosis of sleep apnea, and less than half of those who had been told they had sleep apnea were using the standard treatment for it.
The authors also found that patients who were more fatigued were more likely to also be at elevated risk for sleep apnea – even after taking into account other factors that might have contributed to feelings of fatigue, such as age, gender, body mass index (BMI), sleep duration, depression, and other nighttime symptoms.
The research is based on patients’ answers from a sleep questionnaire designed by the authors, and four validated instruments designed to assess daytime sleepiness, fatigue severity, insomnia severity and obstructive sleep apnea risk. Medical records also were accessed with patients’ permission, to examine clinical characteristics that may predict fatigue or obstructive sleep apnea risk.
“We were particularly surprised by the difference between the proportion of patients who carried an established diagnosis of obstructive sleep apnea – 21 percent — and the proportion at risk for obstructive sleep apnea based on their STOP-Bang scores, which was 56 percent,” says the study’s lead author, Tiffany Braley, M.D., M.S. “These findings suggest that OSA may be a highly prevalent and yet under-recognized contributor to fatigue in persons with MS.”
Braley, an assistant professor of Neurology and multiple sclerosis specialist at the U-M Medical School, conducted the study in collaboration with professors Ronald Chervin, M.D., M.S., and Benjamin Segal, M.D. Chervin is the Director of U-M Sleep Disorders Center, and Segal directs the U-M MS Center.
Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system that causes inflammation and damage of the brain and spinal cord. In addition to neurological disability, MS patients suffer from a number of chronic symptoms, the most common of which is fatigue. Fatigue is also one of the most disabling symptoms experienced by MS patients.
Braley cautions that the design of this new study does not allow for demonstration of cause and effect – that is, the researchers can’t prove based on survey results that the patients felt more fatigued because they had a high score on a sleep apnea risk survey. But, she says, “the findings should prompt doctors who treat MS patients to consider sleep apnea as a possible contributor to their patients’ fatigue, and recommend appropriate testing and treatment.”
The standard treatment for obstructive sleep apnea, called continuous positive airway pressure, or CPAP, involves a machine and mask device that applies a stream of air to the upper airway to keep it open during sleep.
The patients in the study had an average age of 47 and had lived with MS for an average of 10 years. Two-thirds were female, consistent with the prevalence of MS in the U.S., and two-thirds were taking a medication to treat their MS. Three-quarters had the relapsing-remitting form of the disease.
Shorter Sleep Duration and Poorer Sleep Quality Linked to Alzheimer’s Disease Biomarker
Poor sleep quality may impact Alzheimer’s disease onset and progression. This is according to a new study led by researchers at the Johns Hopkins Bloomberg School of Public Health who examined the association between sleep variables and a biomarker for Alzheimer’s disease in older adults. The researchers found that reports of shorter sleep duration and poorer sleep quality were associated with a greater β-Amyloid burden, a hallmark of the disease. The results are featured online in the October issue of JAMA Neurology.
“Our study found that among older adults, reports of shorter sleep duration and poorer sleep quality were associated with higher levels of β-Amyloid measured by PET scans of the brain,” said Adam Spira, PhD, lead author of the study and an assistant professor with the Bloomberg School’s Department of Mental Health. “These results could have significant public health implications as Alzheimer’s disease is the most common cause of dementia, and approximately half of older adults have insomnia symptoms.”
Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. According to the National Institutes of Health, as many as 5.1 million Americans may have the disease, with first symptoms appearing after age 60. Previous studies have linked disturbed sleep to cognitive impairment in older people.
In a cross-sectional study of adults from the neuro-imagining sub-study of the Baltimore Longitudinal Study of Aging with an average age of 76, the researchers examined the association between self-reported sleep variables and β-Amyloid deposition. Study participants reported sleep that ranged from more than seven hours to no more than five hours. β-Amyloid deposition was measured by the Pittsburgh compound B tracer and PET (positron emission tomography) scans of the brain. Reports of shorter sleep duration and lower sleep quality were both associated with greater Αβ buildup.
“These findings are important in part because sleep disturbances can be treated in older people. To the degree that poor sleep promotes the development of Alzheimer’s disease, treatments for poor sleep or efforts to maintain healthy sleep patterns may help prevent or slow the progression of Alzheimer disease,” said Spira. He added that the findings cannot demonstrate a causal link between poor sleep and Alzheimer’s disease, and that longitudinal studies with objective sleep measures are needed to further examine whether poor sleep contributes to or accelerates Alzheimer’s disease.
(Source: jhsph.edu)
Brain imaging study reveals the wandering mind behind insomnia
Study is the first to find functional MRI differences in working memory in people with primary insomnia
A new brain imaging study may help explain why people with insomnia often complain that they struggle to concentrate during the day even when objective evidence of a cognitive problem is lacking.
"We found that insomnia subjects did not properly turn on brain regions critical to a working memory task and did not turn off ‘mind-wandering’ brain regions irrelevant to the task," said lead author Sean P.A. Drummond, PhD, associate professor in the department of psychiatry at the University of California, San Diego, and the VA San Diego Healthcare System, and Secretary/Treasurer of the Sleep Research Society. "Based on these results, it is not surprising that someone with insomnia would feel like they are working harder to do the same job as a healthy sleeper."
The research team led by Drummond and co-principal investigator Matthew Walker, PhD, studied 25 people with primary insomnia and 25 good sleepers. Participants had an average age of 32 years. The study subjects underwent a functional magnetic resonance imaging scan while performing a working memory task.
Results published in the September issue of the journal Sleep show that participants with insomnia did not differ from good sleepers in objective cognitive performance on the working memory task. However, the MRI scans revealed that people with insomnia could not modulate activity in brain regions typically used to perform the task.
As the task got harder, good sleepers used more resources within the working memory network of the brain, especially the dorsolateral prefrontal cortex. Insomnia subjects, however, were unable to recruit more resources in these brain regions. Furthermore, as the task got harder, participants with insomnia did not dial down the “default mode” regions of the brain that are normally only active when our minds are wandering.
"The data help us understand that people with insomnia not only have trouble sleeping at night, but their brains are not functioning as efficiently during the day," said Drummond. "Some aspects of insomnia are as much of a daytime problem as a nighttime problem. These daytime problems are associated with organic, measurable abnormalities of brain activity, giving us a biological marker for treatment success."
According to the authors, the study is the largest to examine cerebral activation with functional MRI during cognitive performance in people with primary insomnia, relative to well-matched good sleepers. It also is the first to characterize functional MRI differences in working memory in people with primary insomnia.
The American Academy of Sleep Medicine reports that about 10 to 15 percent of adults have an insomnia disorder with distress or daytime impairment. Most often insomnia is a comorbid disorder occurring with another problem such as depression or chronic pain, or caused by a medication or substance. Fewer people suffering from insomnia are considered to have primary insomnia, which is defined as a difficulty falling asleep or maintaining sleep in the absence of a coexisting condition.
(Source: eurekalert.org)
Insomnia may cause dysfunction in emotional brain circuitry
A new study provides neurobiological evidence for dysfunction in the neural circuitry underlying emotion regulation in people with insomnia, which may have implications for the risk relationship between insomnia and depression.
“Insomnia has been consistently identified as a risk factor for depression,” said lead author Peter Franzen, PhD, an assistant professor of psychiatry at the University of Pittsburgh School of Medicine. “Alterations in the brain circuitry underlying emotion regulation may be involved in the pathway for depression, and these results suggest a mechanistic role for sleep disturbance in the development of psychiatric disorders.”
The study involved 14 individuals with chronic primary insomnia without other primary psychiatric disorders, as well as 30 good sleepers who served as a control group. Participants underwent an fMRI scan during an emotion regulation task in which they were shown negative or neutral pictures. They were asked to passively view the images or to decrease their emotional responses using cognitive reappraisal, a voluntary emotion regulation strategy in which you interpret the meaning depicted in the picture in order to feel less negative.
Results show that in the primary insomnia group, amygdala activity was significantly higher during reappraisal than during passive viewing. Located in the temporal lobe of the brain, the amygdala plays an important role in emotional processing and regulation.
In analysis between groups, amygdala activity during reappraisal trials was significantly greater in the primary insomnia group compared with good sleepers. The two groups did not significantly differ when passively viewing negative pictures.
“Previous studies have demonstrated that successful emotion regulation using reappraisal decreases amygdala response in healthy individuals, yet we were surprised that activity was even higher during reappraisal of, versus passive viewing of, pictures with negative emotional content in this sample of individuals with primary insomnia,” said Franzen.
The research abstract was published recently in an online supplement of the journal SLEEP, and Franzen will present the findings Wednesday, June 5, in Baltimore, Md., at SLEEP 2013, the 27th annual meeting of the Associated Professional Sleep Societies LLC.
The American Academy of Sleep Medicine reports that about 10 to 15 percent of adults have an insomnia disorder with distress or daytime impairment. According to the National Institute of Mental Health, 6.7 percent of the U.S. adult population suffers from major depressive disorder. Both insomnia and depression are more common in women than in men.
![A Sleep Aid Without the Side Effects
Insomniacs desperate for some zzzs may one day have a safer way to get them. Scientists have developed a new sleep medication that has induced sleep in rodents and monkeys without apparently impairing cognition, a potentially dangerous side effect of common sleep aids. The discovery, which originated in work explaining narcolepsy, could lead to a new class of drugs that help people who don’t respond to other treatments.
Between 10% and 15% of Americans chronically struggle with getting to or staying asleep. Many of them turn to sleeping pills for relief, and most are prescribed drugs, such as zolpidem (Ambien) and eszopiclone (Lunesta), that slow down the brain by binding to receptors for GABA, a neurotransmitter that’s involved in mood, cognition, and muscle tone. But because the drugs target GABA indiscriminately, they can also impair cognition, causing amnesia, confusion, and other problems with learning and memory, along with a number of strange sleepwalking behaviors, including wandering, eating, and driving while asleep. This has led many researchers to seek out alternative mechanisms for inducing sleep.
Neuroscientist Jason Uslaner of Merck Research Laboratories in West Point, Pennsylvania, and colleagues decided to tap into the brain’s orexin system. Orexin (also known as hypocretin) is a protein that controls wakefulness and is missing in people with narcolepsy. Past studies successfully induced sleep by inhibiting orexin, but had not looked into its effects on cognition. The researchers developed a new orexin-inhibiting compound called DORA-22 and confirmed that it could induce sleep in rats and rhesus monkeys as effectively as the GABA-modulating drugs.
Then the researchers went about testing the drugs’ effects on the animals’ cognition. They measured the rats’ cognition and memory by assessing the rodents’ ability to recognize objects. They presented the rats with a new object—say, a cone or a sphere—that the rats then sniffed and explored. Then they took the object away for an hour. After that hour, the rats were exposed to a new object and the one they’d already gotten to know; if the rats remembered, they spent less time checking out the familiar object. With the primates, Uslaner’s team tested their ability to match colors on a touchscreen and to pay attention to and identify the origin of a flashing light. In all the cases, the researchers found the GABA-modulating sleeping pills caused both the rats and the primates to respond more slowly and less accurately. Monkeys taking the memory and attention tests, for example, were 20% less accurate on the highest dose of each of the GABA-modulating drugs. But DORA-22 had no such effect on cognition, the team reports today in Science Translational Medicine.
"We were very excited," Uslaner says. "Folks who take sleep medications need to be able to perform cognitive tasks when they awake, and this [compound] could help them do so without impairment."
Although DORA-22 has not yet been tested in humans, it holds tremendous promise for helping people suffering from sleep disorders, says Emmanuel Mignot, a sleep researcher with the Stanford University School of Medicine in Palo Alto, California. “This study is encouraging and exciting, because there’s good reason to believe it would work differently from what we’ve used in the past,” says Mignot, who helped discover the link between orexin (or its absence) and narcolepsy. “Not every drug works for everyone, so it’s really, really good news to have a potential new drug on the horizon.”](http://41.media.tumblr.com/ec7d58bff47f9cfe77e5a11284a658a0/tumblr_mks52vgAk71rog5d1o1_500.jpg)
A Sleep Aid Without the Side Effects
Insomniacs desperate for some zzzs may one day have a safer way to get them. Scientists have developed a new sleep medication that has induced sleep in rodents and monkeys without apparently impairing cognition, a potentially dangerous side effect of common sleep aids. The discovery, which originated in work explaining narcolepsy, could lead to a new class of drugs that help people who don’t respond to other treatments.
Between 10% and 15% of Americans chronically struggle with getting to or staying asleep. Many of them turn to sleeping pills for relief, and most are prescribed drugs, such as zolpidem (Ambien) and eszopiclone (Lunesta), that slow down the brain by binding to receptors for GABA, a neurotransmitter that’s involved in mood, cognition, and muscle tone. But because the drugs target GABA indiscriminately, they can also impair cognition, causing amnesia, confusion, and other problems with learning and memory, along with a number of strange sleepwalking behaviors, including wandering, eating, and driving while asleep. This has led many researchers to seek out alternative mechanisms for inducing sleep.
Neuroscientist Jason Uslaner of Merck Research Laboratories in West Point, Pennsylvania, and colleagues decided to tap into the brain’s orexin system. Orexin (also known as hypocretin) is a protein that controls wakefulness and is missing in people with narcolepsy. Past studies successfully induced sleep by inhibiting orexin, but had not looked into its effects on cognition. The researchers developed a new orexin-inhibiting compound called DORA-22 and confirmed that it could induce sleep in rats and rhesus monkeys as effectively as the GABA-modulating drugs.
Then the researchers went about testing the drugs’ effects on the animals’ cognition. They measured the rats’ cognition and memory by assessing the rodents’ ability to recognize objects. They presented the rats with a new object—say, a cone or a sphere—that the rats then sniffed and explored. Then they took the object away for an hour. After that hour, the rats were exposed to a new object and the one they’d already gotten to know; if the rats remembered, they spent less time checking out the familiar object. With the primates, Uslaner’s team tested their ability to match colors on a touchscreen and to pay attention to and identify the origin of a flashing light. In all the cases, the researchers found the GABA-modulating sleeping pills caused both the rats and the primates to respond more slowly and less accurately. Monkeys taking the memory and attention tests, for example, were 20% less accurate on the highest dose of each of the GABA-modulating drugs. But DORA-22 had no such effect on cognition, the team reports today in Science Translational Medicine.
"We were very excited," Uslaner says. "Folks who take sleep medications need to be able to perform cognitive tasks when they awake, and this [compound] could help them do so without impairment."
Although DORA-22 has not yet been tested in humans, it holds tremendous promise for helping people suffering from sleep disorders, says Emmanuel Mignot, a sleep researcher with the Stanford University School of Medicine in Palo Alto, California. “This study is encouraging and exciting, because there’s good reason to believe it would work differently from what we’ve used in the past,” says Mignot, who helped discover the link between orexin (or its absence) and narcolepsy. “Not every drug works for everyone, so it’s really, really good news to have a potential new drug on the horizon.”
Drug May Offer New Approach to Treating Insomnia
A new drug may bring help for people with insomnia, according to a study published in the November 28, 2012, online issue of Neurology®, the medical journal of the American Academy of Neurology.
The drug, suvorexant, blocks the chemical messengers in the brain called orexins, which regulate wakefulness. Other drugs for insomnia affect different brain receptors.
Taking the drug suvorexant increased the amount of time people spent asleep during the night, according to the study. The study involved 254 people ages 18 to 64 who were in good physical and mental health but had insomnia that was not due to another medical condition.
The participants took either the drug or a placebo for four weeks, then switched to the other treatment for another four weeks. The participants spent the night in a sleep laboratory with their sleep monitored on the first night with each treatment and then again in the fourth week of each treatment.
While taking the drug, participants’ “sleep efficiency,” which reflects the total amount of time they slept during a fixed, eight hour time in bed, improved by 5 to 13 percent compared to those taking the placebo. They also experienced 21 to 37 fewer minutes awake during the night after they had fallen asleep than those who took the placebo. “This study provides evidence that suvorexant may offer a successful alternative strategy for treating insomnia,” said study author W. Joseph Herring, MD, PhD, of North Wales, Penn., Executive Director of Clinical Research with Merck, the maker of suvorexant, and a member of the American Academy of Neurology. “Suvorexant was generally well-tolerated, and there were no serious side effects.”
Herring said larger, longer studies have recently been conducted on suvorexant, along with studies to determine whether the drug could be safe and effective for elderly people, who make up a large percentage of those suffering from insomnia.
Can’t sleep? You could have inherited the insomnia gene
21 August 2012 by Lois Rogers
Thousands of otherwise healthy people put up with a level of sleep deprivation that would drive the rest of us insane. But they are not the usual candidates for insomnia, such as shift workers or those with severe mental illness. Instead, they belong to a newly identified group of people born without the ‘comfort’ genes needed for easy sleep.
This means they are immune to the feeling of warmth and relaxation which sends an average person off to sleep within 15 minutes. Their genes are designed instead to maintain a state of mental alertness. This makes normal, prolonged sleep impossible so they sleep fitfully, in only short bursts. Even then, their lack of ‘comfort’ genes may mean they struggle to get comfortable, fussing about the bedding or finding their sleeping position.
There are other so-called insomnia genes — some cause repeated periods of wakefulness in the small hours of the night or at the slightest disturbance, or drive an affected person to leap out of bed raring to start the day at 4am, but leave them exhausted by 4pm. Until recently, insomnia was considered a purely psychological complaint triggered by stress, grief, or sleep disruption as a result of shift work or jet lag.
But doctors are now unravelling the genetic explanation of why at least one-third of us have intermittent or constant sleep problems. Even so, it’s already thought there could be six or more different types of insomnia linked to genes. This means it will be possible to develop drugs to block the effect of the chemical signals they produce.
(Source: Daily Mail)