Ischaemic and haemorrhagic stroke. Credit: Scientific Animations CC4.0
People who have had a stroke may be more likely to sleep too much or too little compared to those without prior stroke, according to a study published in Neurology®, the medical journal of the American Academy of Neurology. The study does not prove that stroke causes abnormal sleep; it only shows an association.
“Sleeping the right amount is considered essential for ideal brain and heart health,” said study author Sara Hassani, MD, of Duke University School of Medicine in Durham, North Carolina, and member of the American Academy of Neurology. “We know that abnormally long or short sleep after stroke can affect recovery and deteriorate quality of life, so these results should prompt us to screen for these issues and look at how we can help people improve their sleep habits.”
The study involved 39 559 participants, of whom 1572 had a stroke and 37 987 without stroke history. Every two years, participants were asked how much sleep they usually get at night on weekdays or workdays. Sleep duration was divided into three categories: short, less than six hours; normal, six to eight hours; and long, eight or more hours of sleep.
Researchers looked at how often participants had normal sleep, defined as six to eight hours. Normal sleep duration was less common for people who had a stroke than for those with no prior stroke for all age groups with 32% vs 54% for people age 18-44; 47% vs 55% for people age 45-64; and 45% vs. 54% for people over age 65.
After adjusting for factors that could affect sleep such as age, weight and high blood pressure, researchers found people who had a stroke were 54% more likely to report more than eight hours of sleep per night compared to those without stroke. Those with stroke were 50% more likely to get less than six hours of sleep per night when compared to those without stroke.
“In previous research, stroke has been linked to abnormal sleep, in particular sleep apnea,” said Hassani. “Conditions like insomnia and excessive sleepiness are common in stroke patients and may occur as a direct or indirect consequence of stroke itself. Future research should explore the links between stroke and duration of sleep and determine the effect of sleep duration on outcomes after stroke.”
One limitation of the study was that hours of sleep were self-reported, so participants may not have remembered accurately how much they slept.
Snoozing, or using intermittent alarms to get in a few more minutes of sleep in the morning, may have benefits for some people, according to research published in the Journal of Sleep Research.
In a study of 1732 adults who described their waking habits, 69% of participants reported using the snooze function or setting multiple alarms at least “sometimes.” In those who snoozed, the average time spent snoozing per morning was 22 minutes, ranging from 1 to 180 minutes. Snoozers tended to be younger than non-snoozers and were more likely to be evening types. Morning drowsiness and shorter sleep were also more common in those who snoozed.
In a second study of 31 habitual snoozers, 30 minutes of snoozing improved or did not affect performance on cognitive tests directly upon rising compared with waking up abruptly. Snoozing resulted in about 6 minutes of lost sleep, but it prevented awakening from slow-wave sleep. There were no clear effects of snoozing on stress hormone levels, morning sleepiness, mood, or overnight sleep structure.
“The findings indicate that there is no reason to stop snoozing in the morning if you enjoy it, at least not for snooze times around 30 minutes. In fact, it may even help those with morning drowsiness to be slightly more awake once they get up,” said corresponding author Tina Sundelin, PhD, of Stockholm University.
People often experience headaches and body pain after a lack of sleep, but the mechanisms behind this phenomenon are unclear. A new study published in Nature Communicationsreveals that a certain endocannabinoid neurotransmitter plays a major role.
The animal-based study, led by investigators at Massachusetts General Hospital (MGH), a founding member of Mass General Brigham (MGB), found that the heightened pain sensitivity than can result from chronic sleep disruption (CSD) – or CSD-induced hyperalgaesia – involved signalling from a part of a brain known as the thalamic reticular nucleus (TRN).
Analyses of metabolites showed that the level of N-arachidonoyl dopamine (NADA), a type of neurotransmitter called an endocannabinoid, decreased in the TRN as a result of sleep deprivation.
Activity of the cannabinoid receptor 1, which is involved in controlling pain perception, also decreased in the thalamic reticular nucleus after CSD.
Administering NADA to the TRN reduced CSD-induced hyperalgaesia in mice.
This beneficial effect of administered NADA could be countered by blocking the cannabinoid receptor 1, suggesting that both the receptor and NADA play a role in pain sensitivity due to sleep deprivation.
“We provide a mechanism as to how sleep disruption leads to exaggerated pain, suggesting that harnessing the endocannabinoid system might break the vicious cycle between pain and sleep loss,” says co-senior author Shiqian Shen, MD, the clinical director of MGH’s Tele Pain Program.
An early sign of Alzheimer’s disease is sleep disturbance – many people eventually diagnosed with Alzheimer’s start experiencing difficulty falling and staying asleep years before the emergence of cognitive problems such as memory loss and confusion. In a vicious circle, Alzheimer’s disease disrupts sleep, and poor sleep accelerates harmful changes to the brain.
Now, researchers at Washington University School of Medicine in St. Louis have identified a possible way to help break that cycle. Published in Annals of Neurology, a small, two-night study has shown that people who took a sleeping pill before bed experienced a drop in the levels of key Alzheimer’s proteins – a good sign, since higher levels of such proteins tracks with worsening disease. The study, which involved a sleeping aid known as suvorexant that is already approved by the Food and Drug Administration (FDA) for insomnia, hints at the potential of sleep medications to slow or stop the progression of Alzheimer’s disease, although much more work is needed to confirm the viability of such an approach.
“This is a small, proof-of-concept study. It would be premature for people who are worried about developing Alzheimer’s to interpret it as a reason to start taking suvorexant every night,” said senior author Brendan Lucey, MD, an associate professor of neurology and director of Washington University’s Sleep Medicine Center. “We don’t yet know whether long-term use is effective in staving off cognitive decline, and if it is, at what dose and for whom. Still, these results are very encouraging. This drug is already available and proven safe, and now we have evidence that it affects the levels of proteins that are critical for driving Alzheimer’s disease.”
Suvorexant belongs to a class of insomnia medications known as dual orexin receptor antagonists. Orexin is a natural biomolecule that promotes wakefulness. When orexin is blocked, people fall asleep. Three orexin inhibitors have been approved by the FDA, and more are in the pipeline.
Alzheimer’s disease begins when plaques of the protein amyloid beta start building up in the brain. After years of amyloid accumulation, a second brain protein, tau, begins to form tangles that are toxic to neurons. People with Alzheimer’s disease start experiencing cognitive symptoms such as memory loss around the time tau tangles become detectable.
Lucey and colleagues were among the first to show in people that poor sleep is linked to higher levels of both amyloid and tau in the brain. The question remains as to whether good sleep has the opposite effect – a reduction in amyloid and tau levels, and a halt in or reversal of the progress of Alzheimer’s disease – but mouse studies with orexin inhibitors have been promising.
As a first step to assess the effect of orexin inhibitors on people, Lucey and colleagues recruited 38 participants ages 45 to 65 and with no cognitive impairments to undergo a two-night sleep study. The participants were given a lower dose (10 mg) of suvorexant (13 people), a higher dose (20 mg) of suvorexant (12 people) or a placebo (13 people) at 9 p.m. and then went to sleep in a clinical research unit at Washington University. Researchers withdrew a small amount of cerebrospinal fluid via spinal tap every two hours for 36 hours, starting one hour before the sleeping aid or placebo was administered, to measure how amyloid and tau levels changed over the next day and a half.
Amyloid levels dropped 10% to 20% in the cerebrospinal fluid of people who had received the high dose of suvorexant compared to people who had received placebo, and the levels of a key form of tau known as hyperphosphorylated tau dropped 10% to 15%, compared to people who had received placebo. Both differences are statistically significant. There was not a significant difference between the people who received a low dose of suvorexant and those who received the placebo.
By 24 hours after the first dose, hyperphosphorylated tau levels in the high-dose group had risen, while amyloid levels remained low compared to the placebo group. A second dose of suvorexant, administered on the second night, sent the levels of both proteins down again for people in the high-dose group.
“If we can lower amyloid every day, we think the accumulation of amyloid plaques in the brain will decrease over time,” Lucey said. “And hyperphosphorylated tau is very important in the development of Alzheimer’s disease, because it’s associated with forming tau tangles that kill neurons. If you can reduce tau phosphorylation, potentially there would be less tangle formation and less neuronal death.”
The study is preliminary, since it only looked at the effect of two doses of the drug in a small group of participants. Lucey has studies underway to assess the longer-term effects of orexin inhibitors in people at higher risk of dementia.
“Future studies need to have people taking these drugs for months, at least, and measuring the effect on amyloid and tau over time,” Lucey said. “We’re also going to be studying participants who are older and may still be cognitively healthy, but who already have some amyloid plaques in their brains. This study involved healthy middle-aged participants; the results may be different in an older population.
“I’m hopeful that we will eventually develop drugs that take advantage of the link between sleep and Alzheimer’s to prevent cognitive decline,” he continued. “We’re not quite there yet. At this point, the best advice I can give is to get a good night’s sleep if you can, and if you can’t, to see a sleep specialist and get your sleep problems treated.”
