1. Study suggests insomnia linked to alcohol-use among adolescents

    November 21, 2017 by Ashley

    From the Rutgers University press release:

    Insomnia is linked to frequency of alcohol use among early adolescents, according to new Rutgers University-Camden research.

    “Parents, educators, and therapists should consider insomnia to be a risk marker for alcohol use, and alcohol use a risk marker for insomnia, among early adolescents,” writes Rutgers-Camden researcher Naomi Marmorstein in the study, published recently in the journal Addictive Behaviors.

    Marmorstein, a professor of psychology at Rutgers-Camden, examined the associations between alcohol use and four sleep-related issues: initial insomnia; daytime sleepiness; sleep irregularity, defined as the difference in weekday and weekend bedtimes; and disturbed sleep, characterized as nightmares, snoring, sleepwalking, wetting the bed, and talking in sleep.

    When sleep problems were found to be associated with frequency of alcohol use, she examined whether symptoms of mental health problems or levels of parental monitoring accounted for these associations.

    The research focused on seventh- and eighth-grade students participating in the Camden Youth Development Study, an initiative funded by the National Institute on Drug Abuse at the National Institutes of Health. The study examines the development of mental health problems and resilience among at-risk youth.

    Youth completed questionnaires in the classroom that asked how long it took for them to fall asleep, what times they usually went to bed on a weekday and on the weekend or vacation night, how often they experienced sleep disturbances, and whether they ever fell asleep in class or had trouble staying awake after school. They were also asked the frequency of any alcohol use in the previous four months.

    In addition, students answered questions which were used to assess depressive symptoms, as well as evidence of conduct disorder symptoms.

    Teachers also completed questionnaires, which were analyzed to determine the presence of attention-deficit hyperactivity disorder symptoms.

    Overall, there were associations between alcohol and both insomnia and daytime sleepiness. Importantly, Marmorstein determined that symptoms of mental health problems and parental monitoring did not account for the link between insomnia and alcohol use.

    “These findings indicate that insomnia may be a unique risk marker for alcohol use among young adolescents,” she says.

    The Rutgers-Camden researcher notes that the findings are consistent with associations found between insomnia and alcohol among older adolescents and adults.


  2. Study identifies group of brain cells responsible for keeping us awake

    November 19, 2017 by Ashley

    From the Emory Health Sciences press release:

    Scientists have identified an additional group of cells in the brain responsible for keeping us awake: the supramammillary nucleus, part of the caudal hypothalamus.

    Neurologists had suspected that a component of the “ascending arousal system” could be found in this part of the brain for more than 100 years, but the precise location had been a mystery. In mice, activating this region using targeted chemical genetic techniques resulted in prolonged wakefulness during the animals’ normal sleep periods.

    The results are scheduled for publication in Nature Communications.

    In humans, this region could be a target for bringing some brain injury patients out of a comatose state via electrical stimulation, says lead author Nigel Pedersen, MD, assistant professor of neurology at Emory University School of Medicine and an epilepsy specialist at Emory Brain Health Center.

    The supramammillary nucleus was known for its connections to the hippocampus, important for memory formation, and parts of the frontal cortex involved in focused attention, Pedersen says.

    “Given these connections, this region may be important for the voluntary maintenance of wake and attention, but more work is needed to study this,” he says.

    Pedersen conducted the research with Clifford Saper, MD, PhD, and Patrick Fuller, PhD, at Harvard Medical School and Beth Israel Deaconess Medical Center. Pedersen is continuing work at Emory on the importance of the supramammillary nucleus in memory and learning, and studying its connections to the hippocampus in relation to epilepsy control.

    For decades, neurologists had known that damage to the hypothalamus — including that seen in the mysterious post-World War I epidemic encephalitis lethargica — resulted in marked sleepiness. Now that the location and identity of the wake-promoting neurons are precisely defined, the supramammillary region joins other parts of the brain known as being involved in keeping people awake, such as the nearby lateral hypothalamus, the upper brain stem and basal forebrain.

    In the current paper, Pedersen and his colleagues used genetic engineering techniques to selectively activate particular groups of cells in the brain. They did so with a combination of a designer drug (clozapine-N-oxide) and receptors engineered to be triggered only by that drug. They injected viral vectors carrying an activation switch into the hypothalami of mice, and then gave the mice clozapine-N-oxide.

    Investigators mapped precisely where their injections went and which ones promoted wakefulness; only those involving the supramammillary nucleus did. So what does having this part of the brain stimulated “feel like” for the mice?

    “It’s hard to say, but they display a normal repertoire of behavior,” Pedersen says. “They’re not as wound up, and they don’t show stereotyped repetitive behaviors, as they would with stimulants. The main difference between these and normal mice is that there is no ‘quiet’ wakefulness or napping during the normally sleep-enriched daytime period.”

    Inhibiting the same area of the brain with similar techniques increased the amount of time mice slept, especially non-REM (rapid eye movement) sleep, although sleep was not instant upon drug administration, as has been shown for other parts of the arousal system, Pedersen says.

    “The effects of inhibition of the supramammillary region is to increase sleep, but not dramatically,” he says. “Disruption of other components of the arousal system typically has relatively mild effects. This may amount to some redundancy in the arousal network, but may also relate to the way in which different components of the arousal system have a role in particular types or components of wakefulness. We are actively exploring this idea.”

    Genetic manipulations also allowed the scientists to determine that the brain chemical glutamate was critical for wake signals. When the gene for a glutamate transporter VGLUT2 was snipped out of the supramammillary nucleus, artificial stimulation had no effect on wake and sleep.

    The presence of the enzyme nitric oxide synthase was used to identify an especially potent wake-promoting group of neurons, but their functions still depend on glutamate release. The role of the gaseous neurotransmitter nitric oxide in this brain network is not yet known, Pedersen adds.


  3. Study suggests sleep apnea may increase risk of developing Alzheimer’s disease

    by Ashley

    From the American Thoracic Society press release:

    Obstructive sleep apnea (OSA) may put elderly people at greater risk of developing Alzheimer’s disease (AD), according to new research published online in the American Thoracic Society’s American Journal of Respiratory and Critical Care Medicine.

    In “Obstructive Sleep Apnea Severity Affects Amyloid Burden in Cognitively Normal Elderly: A Longitudinal Study,” researchers report that biomarkers for amyloid beta (Aß), the plaque-building peptides associated with Alzheimer’s disease, increase over time in elderly adults with OSA in proportion to OSA severity. Thus, individuals with more apneas per hour had greater accumulation of brain amyloid over time.

    According to the authors, AD is a neurodegenerative disorder that afflicts approximately five million older Americans. OSA is even more common, afflicting from 30 to 80 percent of the elderly, depending on how OSA is defined.

    “Several studies have suggested that sleep disturbances might contribute to amyloid deposits and accelerate cognitive decline in those at risk for AD,” said Ricardo S. Osorio, MD, senior study author and assistant professor of psychiatry at New York University School of Medicine.

    “However, so far it has been challenging to verify causality for these associations because OSA and AD share risk factors and commonly coexist.”

    He added that the purpose of this study was to investigate the associations between OSA severity and changes in AD biomarkers longitudinally, specifically whether amyloid deposits increase over time in healthy elderly participants with OSA.

    The study included 208 participants, age 55 to 90, with normal cognition as measured by standardized tests and clinical evaluations. None of the participants was referred by a sleep center, used continuous positive airway pressure (CPAP) to treat sleep apnea, was depressed, or had a medical condition that might affect their brain function. The researchers performed lumbar punctures (LPs) to obtain participants’ cerebrospinal fluid (CSF) soluble Aß levels, and then used positron emission tomography, or PET, to measure Aß deposits directly in the brain in a subset of participants.

    The study found that more than half the participants had OSA, including 36.5 percent with mild OSA and 16.8 percent with moderate to severe OSA. From the total study sample, 104 participated in a two-year longitudinal study that found a correlation between OSA severity and a decrease in CSF Aß42 levels over time. The authors said this finding is compatible with an increase in amyloid deposits in the brain; the finding was confirmed in the subset of participants who underwent amyloid PET, which showed an increase in amyloid burden in those with OSA.

    Surprisingly, the study did not find that OSA severity predicted cognitive deterioration in these healthy elderly adults. Andrew Varga, MD, PhD, study coauthor and a physician specializing in sleep medicine and neurology at the Icahn School of Medicine at Mount Sinai in New York, said this finding suggests that these changes were occurring in the preclinical stages of AD.

    “The relationship between amyloid burden and cognition is probably nonlinear and dependent on additional factors,” he added. This study finding may also be attributable to the study’s relatively short duration, highly educated participants and use of tests that fail to discern changes in cognitive abilities that are subtle or sleep-dependent, the authors wrote.

    The high prevalence of OSA the study found in these cognitively normal elderly participants and the link between OSA and amyloid burden in these very early stages of AD pathology, the researchers believe, suggest the CPAP, dental appliances, positional therapy and other treatments for sleep apnea could delay cognitive impairment and dementia in many older adults.

    “Results from this study, and the growing literature suggesting that OSA, cognitive decline and AD are related, may mean that age tips the known consequences of OSA from sleepiness, cardiovascular, and metabolic dysfunction to brain impairment,” Dr. Osorio said. “If this is the case, then the potential benefit of developing better screening tools to diagnose OSA in the elderly who are often asymptomatic is enormous.”


  4. ‘Morning larks’ have weaker sleep spindles during night than ‘night owls’

    November 12, 2017 by Ashley

    From the University of Helsinki press release:

    A new study from the University of Helsinki, Finland, shows that individual circadian preference is associated with brain activity patterns during the night.

    Sleep spindles are bursts of oscillatory brain activity visible on an EEG that occur mainly during stage 2 sleep. Sleep spindles are linked for example to sleep maintenance and strengthening of the memory traces during sleep.

    The study explored the association between individual circadian preference and sleep spindle activity among 170 17-year-old participants, who underwent a sleep EEG monitoring at their home environment.

    “We observed a significantly weaker spindle activity among the morning preference group compared to other groups. The spindle activity also decreased more towards the morning hours, explains the principal investigator,” Professor Anu-Katriina Pesonen. “This might be a potential facilitator underlying earlier circadian rhythm.”

    The study published in Scientific Reports shows for the first time a link between circadian preference and sleep maintaining sleep microstructures, indicated by sleep spindle activity.


  5. How memories ripple through the brain

    November 11, 2017 by Ashley

    From the NIH/National Institute of Neurological Disorders and Stroke press release:

    Using an innovative “NeuroGrid” technology, scientists showed that sleep boosts communication between two brain regions whose connection is critical for the formation of memories. The work, published in Science, was partially funded by the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a project of the National Institutes of Health devoted to accelerating the development of new approaches to probing the workings of the brain.

    “Using new technologies advanced by the BRAIN Initiative, these researchers made a fundamental discovery about how the brain creates and stores new memories,” said Nick Langhals, Ph.D., program director at NIH’s National Institute of Neurological Disorders and Stroke.

    A brain structure called the hippocampus is widely thought to turn new information into permanent memories while we sleep. Previous work by the new study’s senior author, New York University professor György Buzsáki, M.D., Ph.D., revealed high-frequency bursts of neural firing called ripples in the hippocampus during sleep and suggested they play a role in memory storage. The current study confirmed the presence of ripples in the hippocampus during sleep and found them in certain parts of association neocortex, an area on the brain’s surface involved in processing complex sensory information.

    “When we first observed this, we thought it was incorrect because it had never been observed before,” said Dion Khodagholy, Ph.D., the study’s co-first author and assistant professor at Columbia University in New York.

    Using a cutting-edge NeuroGrid system they invented, along with recording electrodes placed deeper into the brain, the researchers examined activity in several parts of rats’ brains during non-rapid eye movement (NREM) sleep, the longest stage of sleep. Their NeuroGrid consists of a collection of tiny electrodes linked together like the threads of a blanket, which is then laid across an area of the brain so that each electrode can continuously monitor the activity of a different set of neurons.

    “This particular device allows us to look at multiple areas of the brain at the same time,” said Jennifer Gelinas, M.D., Ph.D., the study’s co-first author and assistant professor at Columbia University.

    The team was also surprised to find that the ripples in the association neocortex and hippocampus occurred at the same time, suggesting the two regions were communicating as the rats slept. Because the association neocortex is thought to be a storage location for memories, the researchers theorized that this neural dialogue could help the brain retain information.

    To test that idea, they examined brain activity during NREM sleep in rats trained to locate rewards in a maze and in rats that explored the maze in a random fashion. In the latter group of animals, the ripples in the hippocampus and cortex were no more synchronized before exploring the maze than afterwards. In the trained rats, the learning task increased the cross-talk between those areas, and a second training session boosted it even more, further suggesting that such communication is important for the creation and storage of memories.

    The group hopes to use the NeuroGrid in people undergoing brain surgery for other reasons to determine if the same ripples occur in the human brain. The researchers also plan to investigate if manipulating that neural firing in animals can boost or suppress memory formation in order to confirm that ripples are important for that process.

    “Identifying the specific neural patterns that go along with memory formation provides a way to better understand memory and potentially even address disorders of memory,” said Dr. Gelinas.


  6. Study suggests removing digital devices from the bedroom can improve sleep for children, teens

    November 9, 2017 by Ashley

    From the Penn State press release:

    Removing electronic media from the bedroom and encouraging a calming bedtime routine are among recommendations Penn State researchers outline in a recent manuscript on digital media and sleep in childhood and adolescence.

    The manuscript appears in the first-ever special supplement on this topic in Pediatrics and is based on previous studies that suggest the use of digital devices before bedtime leads to insufficient sleep.

    The recommendations, for clinicians and parents, are:

      • 1. Make sleep a priority by talking with family members about the importance of sleep and healthy sleep expectations;

    2. Encourage a bedtime routine that includes calming activities and avoids electronic media use;

    3. Encourage families to remove all electronic devices from their child or teen’s bedroom, including TVs, video games, computers, tablets and cell phones;

    4. Talk with family members about the negative consequences of bright light in the evening on sleep; and

    5. If a child or adolescent is exhibiting mood or behavioral problems, consider insufficient sleep as a contributing factor.

    “Recent reviews of scientific literature reveal that the vast majority of studies find evidence for an adverse association between screen-based media consumption and sleep health, primarily delayed bedtimes and reduced total sleep duration,” said Orfeu Buxton, associate professor of biobehavioral health at Penn State and an author on the manuscript.

    The reasons behind this adverse association likely include time spent on screens replacing time spent sleeping; mental stimulation from media content; and the effects of light interrupting sleep cycles, according to the researchers.

    Buxton and other researchers are further exploring this topic. They are working to understand if media use affects the timing and duration of sleep among children and adolescents; the role of parenting and family practices; the links between screen time and sleep quality and tiredness; and the influence of light on circadian physiology and sleep health among children and adolescents.


  7. Early age of drinking leads to neurocognitive and neuropsychological damage

    November 4, 2017 by Ashley

    From the Research Society on Alcoholism press release:

    Although drinking by U.S. adolescents has decreased during the last decade, more than 20 percent of U.S. high-school students continue to drink alcohol before the age of 14 years. This can have adverse effects on their neurodevelopment. For example, youth who initiate drinking before 14 years of age are four times more likely to develop psychosocial, psychiatric, and substance-use difficulties than those who begin drinking after turning 20 years of age. Little is known about howthe age of alcohol-use onset influences brain development. This is the first study to assess the association between age of adolescent drinking onset and neurocognitive performance, taking into account pre-existing cognitive function.

    The researchers examined data from a longitudinal study on the neurocognitive effects of substance use in adolescents: 215 adolescents (127 boys, 88 girls) with minimal alcohol use experience were administered a neuropsychological test battery, which was repeated an average of 6.8 years later. Analyses examined whether earlier ages of onset for first and weekly alcohol use adversely affected neurocognition, controlling for substance-use severity, and familial and social environment factors.

    Results showed that an earlier onset of drinking increases the risk for alcohol-related neurocognitive vulnerabilities, and that the initiation of any or weekly alcohol use at younger ages is a risk factor for poorer, subsequent neuropsychological functioning. More specifically, an earlier age of onset of first drinking predicted poorer performance in the domains of psychomotor speed and visual attention, and an earlier age of onset of weekly drinking predicted poorer performances on tests of cognitive inhibition and working memory. The authors suggested that these findings have important implications for public policies related to the legal drinking age and prevention strategies and further research on these effects is warranted.


  8. Study indicates sleep deprivation leads to mental lapses

    November 3, 2017 by Ashley

    From the University of California – Los Angeles Health Sciences press release:

    Ever sleep poorly and then walk out of the house without your keys? Or space out on the highway and nearly hit a stalled car?

    A new study is the first to reveal how sleep deprivation disrupts our brain cells’ ability to communicate with each other, leading to temporary mental lapses that affect memory and visual perception.

    “We discovered that starving the body of sleep also robs neurons of the ability to function properly,” said senior author Dr. Itzhak Fried, professor of neurosurgery at the David Geffen School of Medicine at UCLA and Tel Aviv University. “This paves the way for cognitive lapses in how we perceive and react to the world around us.”

    Fried led an international team in studying 12 UCLA epileptic patients who had electrodes implanted in their brains in order to pinpoint the origin of their seizures prior to surgery. Because lack of sleep can provoke seizures, these patients stay awake all night to speed the onset of an epileptic episode and shorten their hospital stay.

    The team asked the patients to categorize a variety of images as fast as possible while their electrodes recorded the firing of nearly 1,500 single brain cells across the group in real time. The scientists zeroed in on the temporal lobe, which regulates visual perception and memory.

    Performing the task grew more challenging as the patients grew sleepier. As the patients slowed down, their brain cells did, too.

    “We were fascinated to observe how sleep deprivation dampened brain cell activity,” said lead author Dr. Yuval Nir of Tel-Aviv University. “Unlike the usual rapid reaction, the neurons responded slowly, fired more weakly and their transmissions dragged on longer than usual.”

    Lack of sleep interfered with the neurons’ ability to encode information and translate visual input into conscious thought.

    The same phenomenon can occur when a sleep-deprived driver notices a pedestrian stepping in front of his car.

    “The very act of seeing the pedestrian slows down in the driver’s over-tired brain,” he explained. “It takes longer for his brain to register what he’s perceiving.”

    In a second finding, the researchers discovered that slower brain waves accompanied sluggish cellular activity in the same regions of the patients’ brains.

    “Slow sleep-like waves disrupted the patients’ brain activity and performance of tasks,” said Fried. “This phenomenon suggests that select regions of the patients’ brains were dozing, causing mental lapses, while the rest of the brain was awake and running as usual,” said Fried.

    The study’s findings provoke questions for how society views sleep deprivation.

    “Inadequate sleep exerts a similar influence on our brain as drinking too much,” said Fried. “Yet no legal or medical standards exist for identifying over-tired drivers on the road the same way we target drunk drivers.”

    Fried and his colleagues plan to dive more deeply into the benefits of sleep. Future studies aim to unravel the mechanism responsible for the cellular glitches that precede mental lapses.

    Previous studies have tied sleep deprivation to a heightened risk of depression, obesity, diabetes, heart attacks and stroke, as well as medical errors.


  9. Study identifies neurons that rouse the brain to breathe

    November 1, 2017 by Ashley

    From the Beth Israel Deaconess Medical Center press release:

    A common and potentially serious sleep disorder, obstructive sleep apnea affects at least one quarter of U.S. adults and is linked to increased risk of diabetes, obesity and cardiovascular disease. In a paper published in the journal Neuron, researchers at Beth Israel Deaconess Medical Center (BIDMC) identified specific neural circuitry responsible for rousing the brain of mice in simulated apnea conditions. The findings could lead to potential new drug therapies to help patients with obstructive sleep apnea get more rest.

    Often but not always marked by loud snoring, sleep apnea occurs when a sleeping person’s airway collapses and closes off breathing. Dipping oxygen (O2) levels and rising carbon dioxide (CO2) levels in the blood alert the sleeping brain to the problem, rousing the sleeper just long enough to re-establish breathing.

    “A person with apnea wakes up and starts breathing again and this cycle can repeat hundreds of time per night, so the person never gets very deeply asleep,” said senior author Clifford B. Saper, MD, Chair of the Department of Neurology at BIDMC. “In the morning, they may not remember that they have not had a restful night’s sleep but will feel very tired.”

    Fragmented sleep can leave people with apnea with significant impairments to cognition, mood and daytime alertness; it may also increase cardiovascular risk. But what if scientists could prevent the brain from rousing itself hundreds of times per night in response to rising CO2 levels, while allowing it to reestablish regular respiration again?

    “Our goal was to identify the circuitry responsible for waking the brain up during sleep apnea, which is distinct from the part of the brain that controls breathing,” said Saper, who is also the James Jackson Putnam Professor of Neurology and Neuroscience at Harvard Medical School. “If we could keep the brain from waking up during apneas and activate only the part of the brain that opens up the airways, people with obstructive sleep apnea would still be able to get a good night’s rest.”

    Using an enclosure with adjustable atmospheric levels of O2 and CO2, Saper and colleagues mimicked the effects of OSA in mice by changing the ratio of the two gases every five minutes for 30 seconds.

    Then, Saper and colleagues focused on a subset of neurons — called PBelCGRP cells- known to show activity in response to elevated CO2 levels. The team used mice with these cells genetically-altered in such a way that researchers could activate or suppress the neurons at will using light or drugs to trigger genetic switches. Known as optogenetics and chemogenetics, these experiments demonstrated that activating these cells will wake mice up and keep them up for hours. They also showed that suppressing PBelCGRP cells’ activity would let mice sleep even as CO2 levels in the air around them rose. Taken together, these findings show that the PBelCGRP cells wake up the brain and are necessary for arousal.

    In the final experiment, the researchers followed the PBelCGRPneurons’ long-reaching branches (called axons) to the cells they connect with in other regions of the brain. Without disrupting the cells’ entire activity, the researchers switched off PBelCGRPneurons’ connection to a key site in the basal forebrain. That resulted in a nearly complete loss of sensitivity to CO2 arousal.

    Saper and colleagues note that rising CO2 levels may not be the only factor that repeatedly rouses people with sleep apnea throughout the night. Negative air pressure in the collapsed upper airway may also send “wake-up” messages to the brain via another neuronal circuit. Or PBelCGRP neurons may rouse a sleeping brain in response to a variety of stimuli, not just rising CO2 levels, the researchers suggest. Learning which neurons regulate arousal could allow scientists to develop drugs to treat obstructive sleep apnea and other sleep disorders.

    “The long-term goal of this research is to come up with drugs that will affect specific pathways in the brain,” Saper said. “The next step is to see if we can use drugs to prevent the wake-up response while augmenting the opening of the airway. That way, having an apnea won’t wake a person up.”


  10. Study suggests sleepwalkers may have multitasking advantage over non-sleepwalkers when awake

    October 31, 2017 by Ashley

    From the Ecole Polytechnique Fédérale de Lausanne press release:

    Try counting backwards from 200 in steps of 7 while walking en-route to your favourite café. Chances are, you will slow down or even freeze mid-stride, unless you are a sleepwalker.

    Breakthrough research using virtual reality has revealed significant differences in how the brains of sleepwalkers and non-sleepwalkers control and perceive body movement — a first in cognitive science. Sleepwalkers exhibit increased automation in their movements with respect to non-sleepwalkers. The results are published in Current Biology on October 23, 2017.

    Wearing a full-body motion capture suit in a room full of IR-tracking cameras at EPFL (Ecole polytechnique fédérale de Lausanne), sleepwalkers and non-sleepwalkers were asked to walk towards a target object, in this case a virtual cylinder. The subject was shown a life-size avatar that could truthfully replicate or deviate from the subject’s actual trajectory in real-time. Participants could therefore be tricked into walking along a modified trajectory to compensate for the avatar deviation. Their walking speed and accuracy of movement along with their movement awareness were then recorded and analysed.

    There was no difference between sleepwalkers and non-sleepwalkers while performing this first task — just as previous research would have suggested. When the researchers added a layer of complexity, however, a clear distinction emerged between the two groups.

    Subjects were asked to count backwards in steps of 7 starting from 200. Non-sleepwalkers significantly slowed down when having to count backwards while walking, yet sleepwalkers maintained a similar walking velocity in both conditions, showing a strong link between sleepwalking and automatic control of locomotion not during nocturnal episodes of sleepwalkers, but during full wakefulness. Furthermore, sleepwalkers were more accurate at detecting changes in the virtual reality feedback when faced with the mental arithmetic task.

    “We found that sleepwalkers continued to walk at the same speed, with the same precision as before and were more aware of their movements than non-sleepwalkers,” says EPFL neuroscientist Olaf Blanke. “The research is also a first in the field of action-monitoring, providing important biomarkers for sleepwalkers — while they are awake.” Sleepwalkers are known to perform complex movements such as walking in the absence of full consciousness. This ability may translate into a multi-tasking advantage for sleepwalkers while awake. Somnambulism, or sleepwalking, currently affects between 2-4% of adults and over 10% in children. The condition can cause movements ranging from small gestures, to complex actions such as walking and even behaviours like getting dressed, driving a car, or playing a musical instrument, — all while asleep.

    Sleepwalking is caused by a partial arousal from slow-wave or deep sleep, however it is not know which functional brain mechanisms are affected by this pathophysiology. The new relationship between sleepwalking and conscious movement control offers new insights into the brain mechanisms of sleepwalking and could potentially be used to aid diagnosis of sleepwalking while the subject is awake, rather than requiring an overnight stay in a sleep laboratory. “Traditionally, little has been known about daytime markers of sleepwalking, mostly because of the difficulty in investigating this condition experimentally,” explains Oliver Kannape from the University of Central Lancashire (UCLan) and lead author of the study. “Our research offers novel insight into this common sleep disorder and provides a clear scientific link between action monitoring, consciousness, and sleepwalking.”