Posts tagged depression

ScienceDaily (July 3, 2012) — When a person injures their knee, it becomes inflamed. When a person has a cold, their throat becomes inflamed. This type of inflammation is the body’s natural and protective response to injury.

Interestingly, there is growing evidence that a similar process happens when a person experiences psychological trauma. Unfortunately, this type of inflammation can be destructive.

Previous studies have linked depression and inflammation, particularly in individuals who have experienced early childhood adversity, but overall, findings have been inconsistent. Researchers Gregory Miller and Steve Cole designed a longitudinal study in an effort to resolve these discrepancies, and their findings are now published in a study in Biological Psychiatry.

They recruited a large group of female adolescents who were healthy, but at high risk for experiencing depression. The volunteers were then followed for 2 ½ years, undergoing interviews and giving blood samples to measure their levels of C-reactive protein and interleukin-6, two types of inflammatory markers. Their exposure to childhood adversity was also assessed.

The researchers found that when individuals who suffered from early childhood adversity became depressed, their depression was accompanied by an inflammatory response. In addition, among subjects with previous adversity, high levels of interleukin-6 forecasted risk of depression six months later. In subjects without childhood adversity, there was no such coupling of depression and inflammation.

Dr. Miller commented on their findings: “What’s important about this study is that it identifies a group of people who are prone to have depression and inflammation at the same time. That group of people experienced major stress in childhood, often related to poverty, having a parent with a severe illness, or lasting separation from family. As a result, these individuals may experience depressions that are especially difficult to treat.”

Another important aspect to their findings is that the inflammatory response among the high-adversity individuals was still detectable six months later, even if their depression had abated, meaning that the inflammation is chronic rather than acute. “Because chronic inflammation is involved in other health problems, like diabetes and heart disease, it also means they have greater-than-average risk for these problems. They, along with their doctors, should keep an eye out for those problems,” added Dr. Miller.

"This study provides important additional support for the notion that inflammation is an important and often under-appreciated factor that compromises resilience after major life stresses. It provides evidence that these inflammatory states persist for long periods of time and have important functional correlates," said Dr. John Krystal, Editor of Biological Psychiatry.

Further research is necessary, to extend the findings beyond female adolescents and particularly in individuals with more severe, long-term depression.. However, findings such as these may eventually help doctors and clinicians better manage depression and medical illness for particularly vulnerable patients.

Source: medicalxpress.com

June 28, 2012

In a process akin to belling an infinitesimal cat, scientists have managed to tag a protein that regulates the neurotransmitter serotonin with tiny fluorescent beads, allowing them to track the movements of single molecules for the first time.

This is a microphotograph of neurons with their serotonin transporter protein labeled with red quantum dots. Credit: Jerry Chang, Vanderbilt University

The capability, which took nearly a decade to achieve, makes it possible to study the dynamics of serotonin regulation at a new level of detail, which is important because of the key role that serotonin plays in the regulation of mood, appetite and sleep.

The achievement was reported by an interdisciplinary team of Vanderbilt scientists in the June 27 issue of the Journal of Neuroscience.

The regulatory protein that the scientists successfully tagged is known as the serotonin transporter. This is a protein that extends through the membrane that forms the nerve’s outer surface and acts like a nano-sized vacuum cleaner that sucks serotonin molecules into the cell body and away from serotonin target receptors on other cells. In this fashion it helps regulate the concentration of serotonin in the area around the cell. Serotonin transporters are an important research subject because they are the target for the most common drugs used to treat depression, including Prozac, Paxil and Lexapro.

"If you are interested in mental health, then serotonin transporters are an ideal subject," said Sandra Rosenthal, the Jack and Pamela Egan Chair of Chemistry, who directed the study with Randy Blakely, the Allan D. Bass Professor of Pharmacology and Psychiatry.

Problems with serotonin transporter regulation have also been implicated in autism. Two years ago, Blakely and geneticist James Sutcliffe, associate professor of molecular physiology and biophysics, reported the discovery of multiple changes in the serotonin transporter protein that cause the transporter to become “overactive” in subjects with autism. Recently, Blakely and Assistant Professor of Psychiatry Jeremy Veenstra-VanderWeele reported that mice expressing one of these high-functioning transporters exhibit multiple behavioral changes that resemble changes seen in kids with autism.

The brain’s other key neurotransmitters have their own transporter proteins, so scientists can use the capability to track the motion of individual transporter molecules to determine how they are regulated as well.

Attempts to understand how these transporters work have been limited by the difficulty of studying their dynamic behavior. “In the past, we have been limited to snapshots that show the location of transporter molecules at a specific time,” said chemistry graduate student Jerry Chang, who developed the tagging technique. “Now we can follow their motion on the surface of cells in real time and see how their movements relate to serotonin uptake activity.”

The fluorescent tags that the researchers used are nanoscale beads called quantum dots made from a mixture of cadmium and selenium. These beads are only slightly bigger than the proteins they are tagging: You would have to string 10,000 together to span the width of a human hair.

Quantum dots emit colored light when illuminated and have the useful property that small changes in their size cause them to glow in different colors. Team member Ian D. Tomlinson, assistant research professor of chemistry, developed a special molecular string that attaches to the quantum dot at one end and, on the other end, attaches to a drug derivative that binds exclusively with the serotonin transporter. When a mixture that contains these quantum dots is incubated with cultured nerve cells, the drug attaches to the transporter. As the protein moves around, it drags the quantum dot behind it like a child holding a balloon on a string. When the area is illuminated, the quantum dots show up in a microscope as colored points of light.

"Until now, neurobiologists have had to rely on extremely low resolution approaches where it takes the signals coming from thousands to millions of molecules to be detected," said Blakely, "We really had no idea exactly what we were going to see."

Putting their new procedure to use, the researchers looked at extensions of the nerve cell that are involved in secreting serotonin on the presumption that transporters would be localized there as well. From previous research, the investigators suspected that the transporters would be concentrated in cholesterol-rich parts of these extensions, termed rafts, although the level of resolution with standard approaches was inadequate to provide any clues as to what they were doing there.

The quantum dot studies demonstrated that there were two distinct populations of transporters in these areas: Those that can travel freely around the membrane and those that act as if they are unable to move. They found that the immobile transporters were located in the rafts. When they stimulated the cell to increase transporter activity, they were surprised at what happened. “We found that the transporters in the rafts began to move much faster whereas the motion of the other population didn’t change at all,” Rosenthal reported. Since the mobilized transporters do not leave the rafts, they appear to whizz around inside a confined compartment, as if released from chains that normally keep them subdued. These observations suggest it is likely that the two populations are controlled by different regulatory pathways.

"Now that we can watch transporter regulation actually happening, we should be able to figure out the identity of the anchoring proteins and the signals these proteins respond to that permit transporters to switch back and forth between low and high activity levels," said Blakely.

"Currently, antidepressant drugs must fully shut down the brain’s serotonin transporters to achieve a clinical benefit," the pharmacologist said. Such a manipulation can produce a number of unpleasant side-effects, such as nausea, weight gain, sexual problems, fatigue and drowsiness.

"By understanding the basic mechanisms that naturally turn serotonin transporter activity up and down, maybe we can develop medications that produce milder side-effects and have even greater efficacy," he said. "Our sights are also focused on transferring what we have learned with normal serotonin transporters to an understanding of the hyperactive transporters we have found in kids with autism.”

Provided by Vanderbilt University

Source: medicalxpress.com

June 27, 2012 by Bob Yirka

(Medical Xpress) — Research teams from the US and Korea have together been studying depression and other mood disorders and have found that chronic stress can block a gene whose job it is to maintain healthy neuron connections in the brain, which in turn can lead to mental ailments. In lab experiments they have found that rats show lowered levels of neuritin gene activity when driven to depression, and that rats with depression tended to do better when given treatment that boosted neuritin activity, suggesting that another means of treating people with mood disorders might be on the horizon. The team has published a paper describing their experiments and results in the Proceedings of the National Academy of Sciences.

Prior research has shown that people who suffer from chronic depression tend to lose plasticity, or the ability to organize new information in their brains, specifically in the hippocampus, leading to a degree of atrophy, a condition that makes it difficult for such people to recover from their disorder even when given drugs to help treat the symptoms. Until now however, most drugs that are used to treat mood disorders work by blocking the re-absorption of the brain chemical serotonin. In this new research, the team looked at the role of neuritin gene activity instead.

In lab experiments they first caused rats to become depressed by exposing them to a constantly stressful environment, e.g. putting them alone in a sterile environment, limiting food and alternating their night/day cycle. After about three weeks the rats became lethargic and unresponsive to normal stimuli. Once that was done, they tested them for the degree of neuritin gene activity, and found that such levels had dropped in all of them. They then treated some of the rates with standard mood stabilizers which helped reduced symptoms as it has in previous research. But then, they treated some of the other rats by infecting them with a virus that causes an increase in neuritin gene activity and found doing so helped the rats just as much as standard therapies and also served to protect their brains from atrophy.

In another experiment the team forced lowered neuritin gene activity in a group of rats but didn’t subject them to stress and found the rats became just as depressed as had those in the first experiment.

The team notes that while their results look very promising on paper, assuming the same results would occur with people is premature as there are differences in biology. Their results do however support the notion that stress itself contributes to mood disorders, which is information people can use to help them live more mentally healthy lives right now.

More information: Neuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress, PNAS, Published online before print June 25, 2012, doi: 10.1073/pnas.1201191109

Source: medicalxpress.com

ScienceDaily (June 25, 2012) — Women with moderate to severe depression had substantial improvement in their symptoms of depression after they received treatment for their vitamin D deficiency, a new study finds.

The case report series was presented June 23 at The Endocrine Society’s 94th Annual Meeting in Houston.

Because the women did not change their antidepressant medications or other environmental factors that relate to depression, the authors concluded that correction of the patients’ underlying shortage of vitamin D might be responsible for the beneficial effect on depression.

"Vitamin D may have an as-yet-unproven effect on mood, and its deficiency may exacerbate depression," said Sonal Pathak, MD, an endocrinologist at Bayhealth Medical Center in Dover, Del. "If this association is confirmed, it may improve how we treat depression."

Pathak presented the research findings in three women, who ranged in age from 42 to 66. All had previously diagnosed major depressive disorder, also called clinical depression, and were receiving antidepressant therapy. The patients also were being treated for either Type 2 diabetes or an underactive thyroid (hypothyroidism).

Because the women had risk factors for vitamin D deficiency, such as low vitamin D intake and poor sun exposure, they each underwent a 25-hydroxyvitamin D blood test. For all three women, the test found low levels of vitamin D, ranging from 8.9 to 14.5 nanograms per milliliter (ng/mL), Pathak reported. Levels below 21 ng/mL are considered vitamin D deficiency, and normal vitamin D levels are above 30 ng/mL, according to The Endocrine Society.

Over eight to 12 weeks, oral vitamin D replacement therapy restored the women’s vitamin D status to normal. Their levels after treatment ranged from 32 to 38 ng/mL according to the study abstract.

After treatment, all three women reported significant improvement in their depression, as found using the Beck Depression Inventory. This 21-item questionnaire scores the severity of sadness and other symptoms of depression. A score of 0 to 9 indicates minimal depression; 10 to 18, mild depression; 19 to 29, moderate depression; and 30 to 63, severe depression.

One woman’s depression score improved from 32 before vitamin D therapy to 12, a change from severe to mild depression. Another woman’s score fell from 26 to 8, indicating she now had minimal symptoms of depression. The third patient’s score of 21 improved after vitamin D treatment to 16, also in the mild range.

Other studies have suggested that vitamin D has an effect on mood and depression, but there is a need for large, good-quality, randomized controlled clinical trials to prove whether there is a real causal relationship, Dr Pathak said.

"Screening at-risk depressed patients for vitamin D deficiency and treating it appropriately may be an easy and cost-effective adjunct to mainstream therapies for depression," she said.

Source: Science Daily

ScienceDaily (June 22, 2012) — Scientists have discovered that plant compounds from a South African flower may in time be used to treat diseases originating in the brain — including depression. At the University of Copenhagen, a number of these substances have now been tested in a laboratory model of the blood-brain barrier.

Crinum from South Africa. (Credit: Gary I. Stafford)

Scientists at the University of Copenhagen have previously documented that substances from the South African plant species Crinum and Cyrtanthus — akin to snowdrops and daffodils — have an effect on the mechanisms in the brain that are involved in depression. This research has now yielded further results, since a team based at the Faculty of Health and Medical Sciences has recently shown how several South African daffodils contain plant compounds whose characteristics enable them to negotiate the defensive blood-brain barrier that is a key challenge in all new drug development.

"Several of our plant compounds can probably be smuggled past the brain’s effective barrier proteins. We examined various compounds for their influence on the transporter proteins in the brain. This study was made in a genetically-modified cell model of the blood-brain barrier that contains high levels of the transporter P-glycoprotein. Our results are promising, and several of the chemical compounds studied should therefore be tested further, as candidates for long-term drug development," says Associate Professor Birger Brodin.

"The biggest challenge in medical treatment of diseases of the brain is that the drug cannot pass through the blood-brain barrier. The blood vessels of the brain are impenetrable for most compounds, one reason being the very active transporter proteins. You could say that the proteins pump the drugs out of the cells just as quickly as they are pumped in. So it is of great interest to find compounds that manage to ‘trick’ this line of defence."

The results of the study have been published in the Journal of Pharmacy and Pharmacology.

It will nonetheless be a long time before any possible new drug reaches our pharmacy shelves: “This is the first stage of a lengthy process, so it will take some time before we can determine which of the plant compounds can be used in further drug development,” says Birger Brodin.

Yet this does not curb his enthusiasm for the opportunities from the interdisciplinary cooperation with organic scientists from the Department of Drug Design and Pharmacology and the Natural History Museum of Denmark.

"In my research group, we have had a long-term focus on the body’s barrier tissue — and in recent years particularly the transport of drug compounds across the blood-brain barrier. More than 90 per cent of all potential drugs fail the test by not making it through the barrier, or being pumped out as soon as they do get in. Studies of natural therapies are a valuable source of inspiration, giving us knowledge that can also be used in other contexts," Birger Brodin emphasises.

Source: Science Daily

ScienceDaily (June 13, 2012) — Wake up, America, and lose some weight — it’s keeping you tired and prone to accidents. Three studies being presented June 13 at sleep 2012 conclude that obesity and depression are the two main culprits making us excessively sleepy while awake.

Researchers at Penn State examined a random population sample of 1,741 adults and determined that obesity and emotional stress are the main causes of the current “epidemic” of sleepiness and fatigue plaguing the country. Insufficient sleep and obstructive sleep apnea also play a role; both have been linked to high blood pressure, heart disease, stroke, depression, diabetes, obesity and accidents.

"The ‘epidemic’ of sleepiness parallels an ‘epidemic’ of obesity and psychosocial stress," said Alexandros Vgontzas, MD, the principal investigator for the three studies. "Weight loss, depression and sleep disorders should be our priorities in terms of preventing the medical complications and public safety hazards associated with this excessive sleepiness."

In the Penn State cohort study, 222 adults reporting excessive daytime sleepiness (EDS) were followed up 7½ years later. For those whose EDS persisted, weight gain was the strongest predicting factor. “In fact, our results showed that in individuals who lost weight, excessive sleepiness improved,” Vgontzas said.

Adults from that same cohort who developed EDS within the 7½-year span also were studied. The results show for the first time that depression and obesity are the strongest risk factors for new-onset excessive sleepiness. The third study, of a group of 103 research volunteers, determined once again that depression and obesity were the best predictors for EDS.

"The primary finding connecting our three studies are that depression and obesity are the main risk factors for both new-onset and persistent excessive sleepiness," Vgontzas said.

In the Penn State cohort study, the rate of new-onset excessive sleepiness was 8 percent, and the rate of persistent daytime sleepiness was 38 percent. Like insufficient sleep and obstructive sleep apnea, EDS also is associated with significant health risks and on-the-job accidents.

Source: Science Daily

June 5, 2012

Researchers studying stroke patients have found a strong association between impairments in a network of the brain involved in emotional regulation and the severity of post-stroke depression. Results of the study are published online in the journal Radiology.

"A third of patients surviving a stroke experience post-stroke depression (PSD),” said lead researcher Igor Sibon, M.D., Ph.D., professor of neurology at the University of Bordeaux in Bordeaux, France. “However, studies have failed to identify a link between lesions in the brain caused by ischemia during a stroke and subsequent depression.”

Instead of looking for dysfunction in a specific area of the brain following a stroke, Dr. Sibon’s study was designed to assess a group of brain structures organized in a functional network called the default-mode network (DMN). Modifications of connectivity in the DMN, which is associated with internally generated thought processes, has been observed in depressive patients.

"The default-mode network is activated when the brain is at rest," Dr. Sibon said. "When the brain is not actively involved in a task, this area of the brain is engaged in internal thoughts involving self-related memory retrieval and processing.”

In the study, 24 patients between the ages of 18 and 80 underwent resting-state functional magnetic resonance imaging (fMRI) 10 days after having mild to moderate ischemic stroke. An fMRI imaging study measures metabolic changes in specific areas of the brain. Although many fMRI exams are designed to measure brain changes while a patient performs a specific task, during a resting-state fMRI exam, patients lie motionless.

The patients, which included 19 men and five women, were also clinically evaluated 10 days and three months post-stroke to determine the presence and severity of depression and anxiety symptoms. At three months post-stroke, patients were evaluated for depression using the DSM-IV diagnostic classification system.

Using the DSM-IV criteria, 10 patients had minor to moderate depression, and 14 patients had no depression. Results of the fMRI exams revealed an association between modifications of connectivity in the DMN 10 days after stroke and the severity of depression three months post-stroke.

"We found a strong association between early resting-state network modifications and the risk of post-stroke mood disorders," Dr. Sibon said. "These results support the theory that functional brain impairment following a stroke may be more critical than structural lesions."

According to Dr. Sibon, the widespread chemical changes that result from a stroke may lead to the modification of connectivity in brain networks such as the DMN. He said results of his study may contribute to the clinical management of stroke patients by providing an opportunity to investigate the effects of a variety of treatments on patients whose fMRI results immediately post-stroke indicate impaired connectivity in the DMN.

Provided by Radiological Society of North America

Source: medicalxpress.com

ScienceDaily (May 30, 2012) — Bipolar disorder is a serious and debilitating condition where individuals experience severe swings in mood between mania and depression. The episodes of low or elevated mood can last days or months, and the risk of suicide is high.

Antidepressants are commonly prescribed to treat or prevent the depressive episodes, but they are not universally effective. Many patients still continue to experience periods of depression even while being treated, and many patients must try several different types of antidepressants before finding one that works for them. In addition, it may take several weeks of treatment before a patient begins to feel relief from the drug’s effects.

For these reasons, better treatments for depression are desperately needed. A new study in Biological Psychiatry this week confirms that scientists may have found one in a drug called ketamine.

A group of researchers at the National Institute of Mental Health, led by Dr. Carlos Zarate, previously found that a single dose of ketamine produced rapid antidepressant effects in depressed patients with bipolar disorder. They have now replicated that finding in an independent group of depressed patients, also with bipolar disorder. Replication is an important component of the scientific method, as it helps ensure that the initial finding wasn’t accidental and can be repeated.

In this new study, they administered a single dose of ketamine and a single dose of placebo to a group of patients on two different days, two weeks apart. The patients were then carefully monitored and repeatedly completed ratings to ‘score’ their depressive symptoms and suicidal thoughts.

When the patients received ketamine, their depression symptoms significantly improved within 40 minutes, and remained improved over 3 days. Overall, 79% of the patients improved with ketamine, but 0% reported improvement when they received placebo.

Importantly, and for the first time in a group of patients with bipolar depression, they also found that ketamine significantly reduced suicidal thoughts. These antisuicidal effects also occurred within one hour. Considering that bipolar disorder is one of the most lethal of all psychiatric disorders, these study findings could have a major impact on public health.

"Our finding that a single infusion of ketamine produces rapid antidepressant and antisuicidal effects within one hour and that is fairly sustained is truly exciting," Dr. Zarate commented. "We think that these findings are of true importance given that we only have a few treatments approved for acute bipolar depression, and none of them have this rapid onset of action; they usually take weeks or longer to have comparable antidepressant effects as ketamine does."

Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist, which means that it works by blocking the actions of NMDA. Dr. Zarate added, “Importantly, confirmation that blocking the NMDA receptor complex is involved in generating rapid antidepressant and antisuicidal effects offers an avenue for developing the next generation of treatments for depression that are radically different than existing ones.”

Source: Science Daily

ScienceDaily (May 16, 2012) — In a new study analyzing Internet usage among college students, researchers at Missouri University of Science and Technology have found that students who show signs of depression tend to use the Internet differently than those who show no symptoms of depression.

Using actual Internet usage data collected from the university’s network, the researchers identified nine fine-grained patterns of Internet usage that may indicate depression. For example, students showing signs of depression tend to use file-sharing services more than their counterparts, and also use the Internet in a more random manner, frequently switching among several applications.

The researchers’ findings provide new insights on the association between Internet use and depression compared to existing studies, says Dr. Sriram Chellappan, an assistant professor of computer science at Missouri S&T and the lead researcher in the study.

"The study is believed to be the first that uses actual Internet data, collected unobtrusively and anonymously, to associate Internet usage with signs of depression," Chellappan says. Previous research on Internet usage has relied on surveys, which are "a far less accurate way" of assessing how people use the Internet, he says.

"This is because when students themselves reported their volume and type of Internet activity, the amount of Internet usage data is limited because people’s memories fade with time," Chellappan says. "There may be errors and social desirability bias when students report their own Internet usage." Social desirability bias refers to the tendency of survey respondents to answer questions in a manner that will be viewed favorably by others.

Chellappan and his fellow researchers collected a month’s worth of Internet data for 216 Missouri S&T undergraduate students. The data was collected anonymously and unobtrusively, and students involved in the study were assigned pseudonyms to keep their identities hidden from the researchers.

Before the researchers collected the usage data from the campus network, the students were tested to determine whether they showed signs of depression. The researchers then analyzed the usage data of the study participants. They found that students who showed signs of depression used the Internet much differently than the other study participants.

Chellappan and his colleagues found that depressed students tended to use file-sharing services, send email and chat online more than the other students. Depressed students also tended to use higher “packets per flow” applications, those high-bandwidth applications often associated with online videos and games, than their counterparts.

Students who showed signs of depression also tended to use the Internet in a more “random” manner — frequently switching among applications, perhaps from chat rooms to games to email. Chellappan thinks that randomness may indicate trouble concentrating, a characteristic associated with depression.

The randomness stood out to Chellappan after his graduate student, Raghavendra Kotikalapudi, examined the “flow duration entropy” of students’ online usage. Flow duration entropy refers to the consistency of Internet use during certain periods of time. The lower the flow duration entropy, the more consistent the Internet use.

"Students showing signs of depression had high flow duration entropy, which means that the duration of Internet flows of these students is highly inconsistent," Chellappan says.

At the beginning of the study, the 216 participating students were tested to determine whether they exhibited symptoms of depression. Based on the Center for Epidemiologic Studies-Depression (CES-D) scale, about 30 percent of the students in the study met the minimum criteria for depression. Nationally, previous studies show that between 10 percent and 40 percent of all American students suffer from depression.

To ensure that participants were not identified during the study, each participant was assigned a pseudonym. The campus information technology department then provided the on-campus Internet usage data for each participant from the month of February 2011.

The researchers’ analysis of the month’s worth of data led Chellappan and his colleagues to conclude that students who were identified as exhibiting symptoms of depression used the Internet differently than the other students in the study.

Chellappan’s research has been accepted for publication in a forthcoming issue of IEEE Technology and Society Magazine.

The chief author of the paper is Kotikalapudi, who received his master of science degree in computer science from Missouri S&T in December 2011. His co-authors are Chellappan; Dr. Frances Montgomery, Curators’ Teaching Professor of psychological science; Dr. Donald C. Wunsch, the M.K. Finley Missouri Distinguished Professor of Computer Engineering; and Karl F. Lutzen, information security officer for Missouri S&T’s IT department.

Chellappan is now interested in using these findings to develop software that could be installed on home computers to help individuals determine whether their Internet usage patterns may indicate depression. The software would unobtrusively monitor Internet usage and alert individuals if their usage patterns indicate symptoms of depression.

"The software would be a cost-effective and an in-home tool that could proactively prompt users to seek medical help if their Internet usage patterns indicate possible depression," Chellappan says. "The software could also be installed on campus networks to notify counselors of students whose Internet usage patterns are indicative of depressive behavior."

Chellappan also believes the method used to connect Internet use and depression could also help diagnose other mental disorders like anorexia, bulimia, attention deficit hyperactivity disorder or schizophrenia.

"We could also investigate associations between other Internet features like visits to social networking sites, late night Internet use and randomness in time of Internet use with depressive symptoms," he says. "Applications of this study to diagnose and treat mental disorders for other vulnerable groups like the elderly and military veterans are also significant."

Source: Science Daily

May 14, 2012

What goes bump in the night? In many U.S. households: people. That’s according to new Stanford University School of Medicine research, which found that about 3.6 percent of U.S. adults are prone to sleepwalking. The work also showed an association between nocturnal wanderings and certain psychiatric disorders, such as depression and anxiety.

The study, the researchers noted, “underscores the fact that sleepwalking is much more prevalent in adults than previously appreciated.”

Maurice Ohayon, MD, DSc, PhD, professor of psychiatry and behavioral sciences, is the lead author of the paper, which will appear in the May 15 issue of Neurology, the medical journal of the American Academy of Neurology.

Sleepwalking is a disorder “of arousal from non-REM sleep.” While wandering around at night can be harmless and is often played for laughs — anyone remember the Simpsons episode where Homer began wandering around and doing silly things in his sleep? — sleepwalking can have serious consequences. Episodes can result in injuries to the wanderer or others and lead to impaired psychosocial functioning.

It is thought that medication use and certain psychological and psychiatric conditions can trigger sleepwalking, but the exact causes are unknown. Also unclear to experts in the field is the prevalence.

"Apart from a study we did 10 years ago in the European general population, where we reported a prevalence of 2 percent of sleepwalking," the researchers wrote in their paper, "there are nearly no data regarding the prevalence of nocturnal wanderings in the adult general population. In the United States, the only prevalence rate was published 30 years ago."

For this study, the first to use a large, representative sample of the U.S. general population to demonstrate the number of sleepwalkers, the researchers also aimed to evaluate the importance of medication use and mental disorders associated with sleepwalking. Ohayon and his colleagues secured a sample of 19,136 individuals from 15 states and then used phone surveys to gather information on participants’ mental health, medical history and medication use.

Participants were asked specific questions related to sleepwalking, including frequency of episodes during sleep, duration of the sleep disorder and any inappropriate or potentially dangerous behaviors during sleep. Those who didn’t report any episodes in the last year were asked if they had sleepwalked during their childhood. Participants were also queried about whether there was a family history of sleepwalking and whether they had other parasomnia symptoms, such as sleep terrors and violent behaviors during sleep.

The researchers determined that as many as 3.6 percent of the sample reported at least one episode of sleepwalking in the previous year, with 1 percent saying they had two or more episodes in a month. Because of the number of respondents who reported having episodes during childhood or adolescence, lifetime prevalence of sleepwalking was found to be 29.2 percent.

The study also showed that people with depression were 3.5 times more likely to sleepwalk than those without, and people with alcohol abuse/dependence or obsessive-compulsive disorder were also significantly more likely to have sleepwalking episodes. In addition, individuals taking SSRI antidepressants were three times more likely to sleepwalk twice a month or more than those who didn’t.

"There is no doubt an association between nocturnal wanderings and certain conditions, but we don’t know the direction of the causality," said Ohayon. "Are the medical conditions provoking sleepwalking, or is it vice versa? Or perhaps it’s the treatment that is responsible."

Although more research is needed, the work could help raise awareness of this association among primary care physicians. “We’re not expecting them to diagnose sleepwalking, but they might detect symptoms that could be indices of sleepwalking,” said Ohayon.

Among the researchers’ other findings:

• The duration of sleepwalking was mostly chronic, with just over 80 percent of those who have sleepwalked reporting they’ve done so for more than five years.
• Sleepwalking was not associated with gender and seemed to decrease with age.
• Nearly one-third of individuals with nocturnal wandering had a family history of the disorder.
• People using over-the-counter sleeping pills had a higher likelihood of reporting sleepwalking episodes at least two times per month. (Indeed, a sleeping pill was the trigger for Homer Simpson’s middle-of-the-night shenanigans.)

D. Le’ger, MD, PhD, from the Universite Paris Descartes in France, was senior author of the study. Researchers from the University of Minnesota Medical School, the Hopital Gui-de-Chauliac in Montpellier, France, and Duke University School of Medicine were also involved.

Provided by Stanford University Medical Center

Source: medicalxpress.com