Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,991 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Showing posts with label sleep protocol?. Show all posts
Showing posts with label sleep protocol?. Show all posts
Will this inform your competent? doctor and change your sleep protocol? Oh, I bet you have NO SLEEP PROTOCOLS, DO YOU? So, incompetence reigns in your hospital?
Summary: Blood sugar patterns and dietary choices play a
significant role in how well adults sleep. Individuals with diabetes
were more likely to experience sleep disorders, poor sleep quality, and
irregular sleep duration, with people who have prediabetes showing
similar but milder trends. The study also found that strict diabetes
control and intense dietary restriction were associated with more sleep
difficulties.
Low-protein, high-fat eating patterns were consistently linked to
poor sleep, while low-carb, high-fat diets were tied to reduced short
sleep, regardless of blood-sugar status. The findings highlight the need
to integrate dietary strategies with sleep-health recommendations.
Key Facts
Diabetes & Sleep: People with diabetes showed higher rates of sleep problems and abnormal sleep duration compared to those without diabetes.
Diet-Sleep Link: Low-protein, high-fat diets were most consistently associated with poor sleep quality across groups.
Blood Sugar Influence: Both glucose patterns and dietary choices shaped sleep outcomes, suggesting an overlooked pathway for improving rest.
Source: George Mason University
The
average adult should get a minimum of seven hours of sleep daily,
according to Centers for Disease Control and
Prevention recommendations.
An estimated 50 to 70
million Americans are diagnosed with a sleep disorder (ex., sleep apnea,
insomnia) that prevents optimal sleep outcomes, and what we eat may
play a role.
A study by
registered dietitian and clinical nutrition researcher Raedeh
Basiri showed that blood sugar levels—whether in individuals with or
without diabetes—are linked to sleep quality.
The research found that blood glucose patterns, diabetes management,
and the types of foods people eat all were associated with how well they
sleep:
Individuals with diabetes
were more likely to have trouble sleeping, be diagnosed with sleep
disorders, and have abnormal sleep duration compared
to individuals without diabetes. Those with prediabetes showed similar
patterns, but not as strongly.
Strict dietary management and
diabetes control were associated with more sleep difficulties,
suggesting that blood-sugar status and the types of foods you eat may
play important roles in how well you sleep
Low-protein diets,
especially when combined with high-fat intake, were most consistently
linked to poor sleep across the board. On the other hand, low-carb,
high-fat diets were associated with a lower likelihood of short sleep
duration in both people with diabetes and those with normal blood sugar.
Basiri’s
research highlights the importance of considering both dietary patterns
and blood sugar status when developing strategies to improve sleep.
Key Questions Answered:
Q: How does blood sugar affect sleep quality according to the study?
A:
Fluctuations in blood glucose were strongly linked to sleep problems,
with individuals experiencing disrupted glucose patterns reporting more
sleep disturbances and irregular sleep duration. This pattern was
especially pronounced in individuals with diabetes.
Q: Which dietary patterns were most associated with poor sleep?
A:
Low-protein, high-fat diets were consistently tied to poorer sleep
outcomes across participants, regardless of diabetes status. These
patterns were linked to reduced sleep quality and more sleep complaints.
Q: Can certain diets support better sleep even in people with blood-sugar issues?
A:
Yes. Low-carb, high-fat diets were associated with a lower likelihood
of short sleepduration in both individuals with diabetes and those with
normal glucose levels. This suggests that macronutrient balance may help
support healthier sleep.
Editorial Notes:
This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.
About this diet and sleep research news
Author: Mary Cunningham Source: George Mason University Contact: Mary Cunningham – George Mason University Image: The image is credited to Neuroscience News
By Michael Merschel, American Heart Association News
(Sycomore/iStock via Getty Images)
There's no question about whether sleep is important for heart and brain health. Study after study has shown that it is.
Questions about the importance of how
you sleep – on your back, on your side, on your stomach – haven't been
asked nearly as often. But experts say sleep position can indeed matter,
at least in some situations.
In general, sleep position is a
matter of personal preference, said Dr. Rachel Salas, a sleep
neurologist at the Johns Hopkins Center for Sleep and Wellness in
Baltimore.
Initially, she said, it's like Goldilocks: People gravitate toward whatever feels just right. But that can evolve over time.
Your
bedroom, your mattress, where your windows are and who you sleep with
can all affect your choices, said Dr. Susan Redline, the Peter C.
Farrell Professor of Sleep Medicine at Brigham and Women's Hospital in
Boston. So can injuries or chronic pain, said Redline, who also is a
professor of epidemiology at the Harvard T.H. Chan School of Public
Health.
But while you can make a conscious choice about which
position you start out in each night, Salas said, "not a lot" of
research has been done on the effects of that choice.
Researchers
have looked at sleep position in people with heart failure, a condition
where the heart does not pump effectively. People with heart failure
often experience shortness of breath that worsens when they sleep on
their left side, Salas said, leading many to prefer their right. But she
said sleeping on the left side might be better for people with
gastroesophageal reflux disease, or GERD, the symptoms of which can
sometimes be confused with heart issues. Sleeping on the left side also
is known to help blood flow in pregnant women.
Some research has
looked into how sleep position might affect how the brain removes waste.
"But I don't think there's anything ready for prime time,"(Really?)said Dr.
Devin L. Brown, a professor of neurology at the University of Michigan
Medical School in Ann Arbor.
One of the best-understood
connections between sleep position and heart and brain health involves
sleep apnea, where breathing stops and restarts during slumber, Redline
said. "Most people with sleep apnea have much, much worse sleep apnea
when they sleep on their back versus on their sides."
Sleep apnea
affects cardiovascular health in several ways, she said. As the body
works harder to pull in air, it triggers a stress response. Apnea can
also raise carbon dioxide levels in the blood and interfere with deep
sleep. Obstructive sleep apnea, a type that stems from anatomical
issues, has been associated with irregular heartbeats, high blood
pressure and other problems.
It also is a risk factor for stroke, said Brown, who, along with Redline, helped write a 2024 American Heart Association scientific statement on the role optimal sleep may have on brain health.
A 2011 clinical trial
published in the journal Sleep Medicine, co-written by Brown, found
avoiding the supine (face-up) position modestly reduced the severity of
apnea in people who'd had a stroke. "We don't know, however, if
treatment to avoid supine positioning, or any other treatment for sleep
apnea, helps reduce the risk of stroke," she said.
According to a 2021 AHA scientific statement
that both Redline and Brown contributed to, sleep apnea affects
approximately 34% of middle-aged men and 17% of middle-aged women, and
many cases are undiagnosed.
"There are people who have what we
call positional obstructive sleep apnea, meaning that they only have
apnea in a certain position," Salas said. Most of the time that's when
they are back-sleepers.
To combat that problem, Salas and Redline
noted the availability of a range of products, from electronic devices
that wake people when they roll onto their backs to shirts with pockets
in the back for a tennis ball, which can encourage sleepers to shift
into another position if they roll over.
"I think the bottom line
for most people is if they have sleep apnea, sleeping on your side, in
most cases, may be very helpful," Redline said. And if you don't have
sleep apnea or snore, sleeping in a position you feel most comfortable
in and where you wake least frequently "is probably the simplest
common-sense advice."
She emphasized the importance of sleep.
Most adults should average seven to nine hours of sleep each night,
according to the AHA.
"We know now that sleep really touches
every body system, including the heart and the brain, and it does so
through influencing the health of our blood vessels, the health of our
immune system," and much more, Redline said.
Salas said people "should definitely be aware of and reflect on what position they're sleeping in."
People
get into habits and can be reluctant to experiment with position in
pursuit of better sleep, but Salas encourages them to do so. A change as
simple as replacing a decades-old pillow or putting a rolled towel
between their knees to help with back pain, can make a difference, she
said.
If you can't find a comfortable position, don't ignore
that, Salas said. If a patient tells her they can't breathe when they
sleep flat, or they have to sleep in a recliner, it's a sign that "there
definitely could be something more serious going on."
If you
feel like you're getting enough sleep at night but still fall asleep
during meetings or movies, talk to a health care professional, Salas
suggested.
No matter the position, sleep needs to be a priority,
she said, and "only you can make sleep a priority. Nobody else can do
that for you."
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Heart Association News covers heart disease, stroke and related health
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From Age 56 to 62 my sleep was incredibly bad. So with my lost 5 cognitive years from my stroke I should be cognitively age 75, but I'm definitely not anywhere near that old.
Having two to three poor sleep characteristics was linked to a 2-year increase in brain age.
Poor sleep quality and insomnia symptoms were associated with accelerated brain aging.
Poor
sleep patterns in early midlife appeared to be associated with advanced
brain age in late midlife, suggesting the importance of early sleep
interventions to preserve brain health, according to study results.
“Sleep problems
have been linked in previous research to poor thinking and memory
skills later in life, putting people at higher risk for dementia,” Clémence Cavaillès, PhD, MS,
postdoctoral researcher in epidemiology in the department of psychiatry
and behavioral sciences at the University of California, San Francisco,
said in a related American Academy of Neurology press release.
Data were derived from Cavaillès C, et al. Neurology. 2024;doi:10.1212/WNL.0000000000209988.
Previous studies have typically focused on older adults, although Alzheimer pathology begins in the brain several decades before symptoms occur, the researchers wrote in the study published in Neurology, the medical journal of the AAN.
This
inspired Cavaillès and colleagues to investigate how poor sleep
characteristics and changes in early midlife affected brain health in
late midlife.
The prospective cohort study involved 589
participants (mean age, 40.4 ± 3.4 years; 53% women; 39% Black)
recruited from the Coronary Artery Risk Development in Young Adults
study who had baseline sleep data and MRI scans. Participants completed
questionnaires that researchers used to assess sleep duration, sleep
quality and whether patients had difficulty initiating and maintaining
sleep, early morning awakening and daytime sleepiness.
The
researchers divided the participants into groups based on number of poor
sleep characteristics (0-1, 2-3 or 3+) and used brain MRIs participants
underwent 15 years later to determine brain age through a machine
learning approach based on age-related atrophy.
The researchers
found that 70% of participants reported having one poor sleep
characteristic, 22% reported two to three and 8% reported more than
three.
After mean follow-up of 15 ± 0.5 years, the participants’
mean brain age was 54.3 ±7.4 years and mean chronological age was 55.3 ±
3.5 years.
Overall, results of multivariable linear regression
analyses showed that having more than one poor sleep characteristic was
associated with older brain age, including by 1.61 years for two to
three characteristics (B = 1.61, 95% CI, 0.28-2.93); and 2.6 years for
three or more characteristics (B = 2.64, 95% CI, 0.59-4.69) compared
with participants with one or fewer poor sleep characteristics.
Further,
the researchers found that when examining individual sleep
characteristics, older brain age could be linked to bad sleep quality (B
= 1.84; 95% CI, 0.26-3.43), difficulty initiating sleep (B = 2.38; 95%
CI, 0.75-4.02), difficulty maintaining sleep (B = 1.14; 95% CI,
0.03-2.25) and early morning awakening (B = 2.45; 95% CI, 0.99-3.9).
These
findings were supported by a subsample of 566 participants with
repeated sleep data 5 years after baseline. Specifically, researchers
found increased brain age was linked to persistent bad sleep quality
(2.8 years), difficulty initiating sleep (3.8 years), difficulty
maintaining sleep (1.8 years), early morning awakening (3.8 years) and
daytime sleepiness (2.4 years).
The researchers noted several
limitations to this study, including the potential for misclassification
bias due to using self-reported sleep measures and limited
generalizability of the findings due to the selectivity of the study
sample.
“Our finding suggests that poor sleep in early midlife may
have effects on brain health already by midlife,” Cavaillès and
colleagues wrote.“Moreover, advanced brain aging has been associated with worse cognitive functions and AD-related atrophy patterns.”
The findings suggest that poor sleep could be targeted by early interventions, according to the researchers.
“Future
research should focus on finding new ways to improve sleep quality and
investigating the long-term impact of sleep on brain health in younger
people,” study author Kristine Yaffe, MD, professor of
psychiatry, neurology and epidemiology and director of Center for
Population Brain Health at the University of California, San Francisco,
said in the release.
Well you already lost 5 cognitive years from your stroke and your competent? doctor has NOTHING that will recover that, so ask your doctor for an EXACT SLEEP PROTOCOL so you don't lose even more cognitive ability.
Poor
sleep – which includes having difficulty falling or staying asleep – may
age the brain by nearly three years, scientists have said.
Scans of nearly 600 middle-aged people showed sleeping badly was associated with poorer brain health years later.
This was despite adjusting for factors such as age, sex, high blood pressure and diabetes, the scientists said.
Kristine
Yaffe, of the University of California San Francisco and a member of
the American Academy of Neurology, said: “Our findings highlight the
importance of addressing sleep problems earlier in life to preserve
brain health, including maintaining a consistent sleep schedule,
exercising, avoiding caffeine and alcohol before going to bed and using
relaxation techniques.
“Future
research should focus on finding new ways to improve sleep quality and
investigating the long-term impact of sleep on brain health in younger
people.”
For
the study, published in the journal Neurology – the medical journal of
the American Academy of Neurology, people with an average age of 40 at
the start of the study filled in sleep questionnaires at the beginning
and then again five years later.
The
questions focused on six main sleep characteristics: short sleep, bad
sleep quality, difficulty falling asleep, difficulty staying asleep,
waking up early, and daytime sleepiness.
Those
in the low group had no more than one poor sleep characteristic while
people in the middle group had two to three, and those in the high group
had more than three, the researchers said.
People taking part also had brain scans 15 years after the study began to see how much their brain structures had changed.
Results
showed people in the middle group had an average brain age that was 1.6
years older than those in the low group, while those in the high group
had an average brain age 2.6 years older.
Dr
Clemence Cavailles, of the University of California San Francisco,
said: “Sleep problems have been linked in previous research to poor
thinking and memory skills later in life, putting people at higher risk
for dementia.
“Our
study which used brain scans to determine participants’ brain age,
suggests that poor sleep is linked to nearly three years of additional
brain aging as early as middle age.”
Sleep comprises one third of our adult life. It is essential for
normal functioning; without it, we experience memory lapses, have
difficulty with concentration, experience mood alterations, become more
prone to accidents, perform poorly at work, experience breaches in
interpersonal relationships and develop more medical and psychiatric problems.
Animals deprived of sleep will experience metabolic abnormalities and
eventually die. Despite all of this information, however, we do not
fully understand the whys of sleep.
Scientists have yet to determine how physical and psychological
restorative processes are coordinated during sleep and why such a
behaviorally disconnected state is necessary to accomplish these tasks.
The clearance of beta-amyloid, a neurotoxic waste product that
accumulates in the brain during wakefulness, is enhanced during sleep.
This and similar information suggests that the restorative function of
sleep is a result of its importance in maintaining metabolic homeostasis
through the removal of toxins that accumulate during wakefulness.
From a behavioral standpoint, sleep is characterized by diminished
responsiveness to, and perceptual disengagement from, the environment.
In these ways, it is similar to coma, with the exception that it is
readily reversible. However, from a neurophysiologic standpoint, it
bears no resemblance to comatose state at all. During sleep, the brain
is highly active and undergoes characteristic changes that translate
into parallel changes, not just in the central nervous system (CNS), but
throughout the body. The apparent quiescence of the sleeper is a
product of active processes that diminish responsiveness to
environmental stimuli. Sleep seems to be an important aspect of the 4
Rs: rest, restore, rejuvenate and repair.
At the same time, there is a perceptual disengagement from the
environment. However, this disengagement is not complete when important
environmental sensory information is monitored, again emphasizing the
active nature of the brain during sleep. An example is the mother who
responds to the infant’s whimper yet sleeps through other loud noises of
lesser significance.
Decades of sleep research have confirmed Aserinsky and Kleitman’s
original discovery of rapid eye movement (REM) sleep in 1953 and have
conclusively demonstrated that sleep is comprised of two fundamentally
distinct states, REM and non-REM (NREM) sleep, which repeat in cyclical
(ultradian) fashion throughout the night, forming a pattern widely known
as sleep architecture (Figure 2-1).
Proper characterization of sleep stages necessitates the simultaneous
monitoring of the numerous physiologic parameters, a process known as
polysomnography. Minimally required are the electroencephalogram (EEG),
electro-oculogram (EOG) and electromyogram (EMG) of skeletal muscle,
usually the submentalis.
The Rechtschaffen and Kales (R & K) sleep scoring manual was
published in 1968, 15 years after REM sleep was discovered. For several
decades, the manual has provided the methodology for human sleep
research, dictating the scoring of sleep stages. Advances in the field
have warranted a re-appraisal of these evaluation systems for sleep. In
2007, the American Academy of Sleep Medicine (AASM)
standards manual provided revised criteria for scoring sleep stages,
including standardizing epoch length, redefining sleep terminology and
criteria, and simplifying certain scoring rules. Table 2-1 shows a comparison of the R&K and AASM sleep stage scoring systems.
In the American Academy of Sleep Medicine (AASM) Visual Scoring system,
sleep is classified into four stages: stages N1-N3 (NREM), and stage R
(REM). Patterns for each of these parameters during the sleep of a young
adult are depicted in Figures 2-2 through 2-4.
In addition to sleep scoring, the AASM criteria also include scoring of
arousals, respiratory events, sleep-related movement disorders and
cardiac abnormalities.
The relative distribution of sleep stages changes with age (Figure 2-5).
N3 sleep is maximal in children and diminishes markedly with age,
especially during adolescence. Seniors may have little or no N3 sleep.
The loss of N3 sleep with age may be a consequence of the diminution in
cortical synaptic activity. In contrast, N1 sleep increases with age.
With aging, there is a general tendency toward sleep fragmentation,
characterized by an increase in the frequency of awakenings and brief
arousals. Older adults with specific EEG sleep characteristics (sleep
latency >30 minutes, sleep efficiency <80%, REM sleep percentage
in the lowest or highest 15% of the total sample distribution) have an
excess risk of dying beyond that associated with age, gender, or medical
burden.
Cognitive mental processes seem to be at a low level during N1 sleep
since sleepers who are awakened from it usually report experiencing
thought fragments or vague images. Most individuals awakened from delta
(N3) sleep report no mental activity at all. In contrast, most sleepers
report dreams when awakened from REM sleep.
Sleep needs are quite variable from individual to individual.
Although the average nightly sleep duration is approximately 8 hours,
children obtain about 10 hours, and the elderly <7 hours. Sleep
lengths vary even within similar age groups, with some individuals
reportedly requiring as little as 3 hours of nightly sleep. The most
prudent answer to the question of “How much sleep do I need?” is that
amount of sleep that results in optimal daytime alertness, no need to
“catch up” on sleep on non-work days, and no tendency to fall asleep
unintentionally during the course of normal daytime hours. Achieving
sleep needs should lead to a sense of mental efficiency and well-being.
Enlarge Figure 2-1: Sleep Architecture of a Normal Adult. The horizontal axis portrays hours of sleep. Source: Kryger MH, et al, eds. Principles and Practice of Sleep Medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2022.
Enlarge Figure 2-2: Polysomnography of
Wake to Sleep Transition. Notes: The most marked change is visible on
the two electroencephalographic (EEG) channels (C3/A2 and O2/A1), where a
clear pattern of rhythmic α activity (8 cps) changes to a relatively
low-voltage, mixed-frequency pattern at about the middle of the figure.
The level of electromyographic (EMG) activity does not change markedly.
Slow eye movements (right outer canthus [ROC]/left outer canthus [LOC])
are present throughout this episode, preceding the EEG change by at
least 20 seconds. In general, the change in EEG patterns to stage N1 as
illustrated here is accepted as the onset of sleep. Source: Kryger MH,
et al, eds. Principles and Practice of Sleep Medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2022.
Enlarge Figure 2-3: FIGURE 2.3 —
Polysomnography of Non-REM Sleep. Notes: The four electroencephalogram
tracings depicted here are from a 19-year-old female volunteer. Each
tracing was recorded from a referential lead (C3/A2) on a Grass
Instruments (West Warwick, RI) Model 7D polygraph with a paper speed of
10 mm/sec, time constant of 0.3 sec, and 12-amplitude high-frequency
setting of 30 Hz. On the second tracing, the arrow indicates a K-complex
and the underlining shows two sleep spindles. Stages 1 and 2 correspond
to stages N1 and N2 in the current AASM scoring system, while stages 3
and 4 correspond to stage N3. Source: Kryger MH, et al, eds. Principles and Practice of Sleep Medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2022.
Enlarge Figure 2-4: Polysomnography of
Patient in REM Sleep. Notes: On the left side is a burst of several
rapid eye movements (out-of-phase deflections in right outer canthus
[ROC]/A1 and left outer canthus [LOC]/A2). On the right side, there are
additional rapid eye movements as well as twitches on the
electromyographic (EMG) lead. The interval between eye movement bursts
and twitches illustrates tonic REM sleep. Source: Kryger MH, et al,
eds. Principles and Practice of Sleep Medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2022.
Enlarge Figure 2-5: Sleep and Age.
Notes: Age-related percentile curves for sleep macrostructure and
arousals in 100 healthy Caucasian volunteers. (A) N1%. (B) N2%. (C) N3%.
(D) REM%. Circles represent women, squares represent men; figures show
10th, 25th, 50th, 75th and 90th percentile. Key: REM, rapid eye
movement. Source: Adapted from Mitterling T, et al. Sleep. 2015;38(6):867-875.
Polysomnography
Polysomnography is typically performed in specialized facilities called sleep disorders centers and laboratories. In preparation for polysomnography,
patients are introduced to their sleeping quarters during their initial
office-based evaluation and provisions are made for special needs. On
the night of the test, they arrive at the laboratory well in advance of
the study time to acclimate to the new environment. Studies are
conducted in noise-free and private rooms and comfort is maximized by
making rooms aesthetically pleasing.
As noted earlier, characterization of sleep stages requires, at the
minimum, an EEG, EOG and EMG of the submentalis. However, a typical
clinical polysomnogram also includes monitors for airflow at the nose
and mouth, respiratory-effort strain gauges placed around the chest and
abdomen, and noninvasive oxygen-saturation monitors that function by
introducing a beam of light through the skin. Other parameters include
the electrocardiogram and EMG of the anterior tibialis muscles, which
are intended to detect periodic leg movements (PLMs). Finally, a
patient’s gross body movements are continuously monitored by audiovisual
means (Figure 2-6).
Enlarge Figure 2-6: Patient Undergoing Polysomnography. Public domain image. Source: National Heart Lung and Blood Institute (NIH).
Mechanisms Underlying Sleep and Wakefulness
Sleep and wakefulness are believed to be the net effect of the
interaction of two opposing, mutually inhibitory, interdependent
processes (Figure 2-7).
Enlarge Figure 2-7: Brain Regions
Involved in Regulation of Sleep and Wakefulness. Source: Adapted from
Atkin T, et al. Pharmacol Rev. 2018;70(2):197-245.
Arousal Neurophysiology
The wake-promoting system is consists of noradrenergic, cholinergic
(ACh), serotoninergic (5-HT), dopaminergic and histaminergic (His)
neurons, which produce cortical arousal via two pathways: a dorsal route
through the thalamus and a ventral route through the hypothalamus and
basal forebrain (Table 2-2). The
dorsal branch of ascending neurons receives input from cholinergic cell
groups in the upper pons, the pedunculopontine and laterodorsal
tegmental nuclei, which facilitate transmission of signals from the
thalamus to the cerebral cortex.
The second branch of ascending neurons receives input from the
monoaminergic neurons in the upper brainstem and caudal hypothalamus.
This pathway also receives contributions from peptidergic neurons in the
lateral hypothalamus (LH) containing orexin and from basal forebrain
neurons containing acetylcholine and γ-aminobutyric acid (GABA). All of
these ascending arousal pathways traverse the region at the
midbrain-diencephalic junction, where it was observed that lesions
caused hypersomnolence.
The neuropeptide hypocretin/orexin plays an important role as a
stabilizer and maintainer of wakefulness, minimizing unplanned
transitions to the sleep state through the reinforcement of
wake-promoting signaling in the brain (Figure 2-8).
Orexin deficiency results in narcolepsy in many species, suggesting
that this system is particularly important for maintenance of
wakefulness, although not necessarily its initiation. Orexin neurons
receive abundant input from the limbic system and activate waking active
monoaminergic and cholinergic neurons in the hypothalamus and brainstem
regions to maintain a long, consolidated waking period. These neurons
also interact with systems that regulate emotion, reward and energy
homeostasis to maintain appropriate vigilance states.
After the identification of arousal centers more than 3 decades ago,
it remained unclear how the arousal system was turned “off” so that
sleep could be initiated and maintained. It was not until the mid-1990s
that the identity of this sleep-promoting circuitry was revealed. It was
demonstrated that wake-promoting neurons are inhibited during sleep by a
system of ventrolateral preoptic nucleus (VLPO) neurons, which contain
sleep-active cells that contain the inhibitory neurotransmitters GABA
and galanin.
Primarily active during sleep, VLPO neurons project to all of the
main cellular components in the hypothalamus and brainstem that
participate in arousal. Inhibition of the arousal system by the VLPO
during sleep is critical for the maintenance and consolidation of sleep.
Work by Batini and colleagues has provided support for the concept that
an active sleep-promoting area is located near the nucleus of the
solitary tract in the medulla, but this remains largely unconfirmed.
Because the VLPO neurons do not have orexin receptors, actions of the
orexin neurons are primarily to reinforce the wake-promoting systems
rather than to directly inhibit the VLPO (Figure 2-8).
Transitioning Between Wakefulness and Sleep
Transitions between the discrete states of wakefulness and sleep are
rapid and complete and can be described as a “flip-flop” switch. As
signaling from one side increases, so does its inhibitory influence on
the signaling of the opposing process (Figure 2-9).
As long as signaling from one side exceeds the other, that state is
maintained. While the flip-flop switch avoids prolonged intermediate
states between sleep and wakefulness, transitions can also occur with
little warning and may have negative consequences. To minimize unplanned
transitions from wake to sleep, wake signaling consists of redundant
pathways that are stabilized via orexin neuropeptides, collectively
making wake asymmetrically favored.
Enlarge Figure 2-9: The “Flip-Flop”
Switch Model of Arousal and Sleep. The mutual inhibition between VLPO
neurons and the monoaminergic cell groups forms a flip-flop switch,
which produces sharp transitions in state but is relatively unstable.
Source: Modified from Saper CB, et al. Nature.
2005;437(7063):1257-1263.
Factors Modulating Arousal and Sleep
There are many influences that affect the activity of the wake-sleep
circuit, which can be categorized within three major factors — circadian
rhythms, homeostatic drive and allostatic signaling.
The homeostatic influence is believed to be based on the accumulation
of the drive for sleep during prolonged wakefulness and relief of this
need during sleep. The mechanism for this homeostatic regulation may be
linked to the accumulation of a sleep-promoting substance (believed to
be adenosine) that enhances the activity of sleep-promoting cells and
reduces the activity of wake-promoting neurons.
Circadian rhythms are governed mainly by the suprachiasmatic nucleus
(SCN) area in the brain, which serves as a biological clock of roughly
24 hours. Signals from various areas in the body connect to the dorsal
and ventral subparaventricular zones, as well as the dorsomedial nucleus
of the hypothalamus (DMH). Neurons in these regions relay information
necessary for organizing daily cycles of wake–sleep and rhythms of body
temperature (Table 2-3). DMH neurons drive circadian
cycles of sleep, activity, feeding and corticosteroid secretion. These
integrative connections allow circadian rhythms to mold the daily cycles
of sleep-wakefulness in accordance with internal and external cues.
Rather than maintaining a rigid sleep/wake schedule, the physiologic
systems within the body are able to fluctuate to meet demands from
external forces via allostatic signaling. Allostatic signaling adapts
sleep and wakefulness to external behavioral events, such as
environmental, sensory, cognitive and emotional inputs. These are
thought to be mediated in part by cues from visceral sensory systems and
feeding regulatory systems to the arousal systems, involving inputs to
the SCN, VLPO and orexin neurons from corticolimbic sites.
The process of sleep is important for physical and mental restoration
and normal functioning, although the mechanism by which sleep produces
these effects is a matter of ongoing research. Nevertheless, the complex
array of changes that is seen both in the brain and the peripheral
organs during sleep is proof that sleep represents an active state that
is highly regulated. The states of sleep and wakefulness are governed by
different, but interconnected neural circuits in the brain, which are
mutually interdependent and inhibitory. The transition between the
distinct sleep/wake states is fast and complete, governed by many
factors, such as circadian rhythms, homeostatic drive and allostatic
signaling.
Doghramji K, Doghramji PP. Clinical Management of Insomnia, 3rd ed. Professional Communications Inc. 2023.
Dew MA, Hoch CC, Buysse DJ, et al. Healthy older adults’ sleep predicts all-cause mortality at 4 to 19 years of follow-up. Psychosom Med. 2003;65(1):63-73.=
Improving
sleep for patients with stroke is vital due to the importance of sleep
for neuroplasticity and functional recovery. While sleep interventions
have been successful in reducing nocturnal disruptions for hospitalized
patients, few interventions have been tested for patients with stroke in
an acute rehabilitation setting. We aimed to adapt the successful
hospital protocol SIESTA (Sleep for Inpatients: Empowering Staff to Act)
to an acute stroke rehabilitation setting.
Methods
Surveys
and focus groups with nurses caring for patients with stroke on
inpatient floors at Shirley Ryan AbilityLab informed the development of
the adapted protocol, SIESTA-Rehab. The protocol included educational
video modules for nurses regarding sleep hygiene and sleep apnea
screening, sleep enhancing measures (eye masks, quiet signs), a nurse
badge card with a checklist reinforcing protocol components, and
advocacy for patient sleep at shift handoff. Two nurse champions were
recruited to monitor protocol implementation. Periodic re-education was
conducted to account for nurse turnover. Ongoing fidelity interviews
using the Consolidated Framework for Implementation Research (CFIR)
framework assessed intervention perceptions.
Results
We
initially trained 27 (93%) nurses using the training module. Fidelity
interviews of over 20 nurses in the years post-implementation
demonstrated over 57% of nurses recalled sleep masks and “cluster care”
as part of the protocol. Moreover, more than 75% of nurses considered
the protocol to be “straightforward” and “part of the workflow.” Nurses
perceived the protocol positively, noting it “could be really beneficial
for patients and their long-term health,” and have incorporated
behavioral changes into their routine since being educated on sleep
hygiene. Nurses also reported understanding the importance of sleep for
stroke patients, stating sleep “helps in their recovery and feeling well
rested for the day so that they can participate in therapy” and
understood “how [they] affect that in [their] roles” as nurses.
Conclusion
The
SIESTA protocol can be successfully adapted to an acute rehabilitation
setting for stroke patients, as evidenced by positive staff responses to
sleep-promoting interventions, ease of protocol incorporation, and high
staff compliance. Ongoing work is investigating patient perceptions and
outcomes following implementation of this sleep protocol.
Your doctor and hospital should have a
sleep protocol, otherwise they are contributing to your risk of
dementia. Nurses would pass out sleeping pills like candy at 10pm. Does
using them count as real sleep? I got woken up almost every morning by
the blood vampires coming for
either me or my roommates at 7am. Do they now know about needleless
blood draws, only out since May 2016? Needle free blood draws or microneedles? I had mild sleep apnea but can't use a CPAP, don't know if I still have it, don't have a partner to tell me about it.
Inaugural Sleep and Dementia Consortium analysis points to associations with sleep apnea
by
Judy George, Deputy Managing Editor, MedPage Today
July 19, 2023
AMSTERDAM -- Better sleep consolidation and
the absence of sleep apnea were associated with better global cognition
over 5 years, a pooled analysis of sleep studies in nearly 6,000 adults
showed.
An
apnea-hypopnea index (AHI) score of 5 or more, indicating mild to
severe obstructive sleep apnea, was associated with poorer global
cognition (pooled β -0.06, P=0.01) compared with an AHI less
than 5. Comparable results were found for moderate to severe apnea.
Sleep stage percentages were not associated with global cognition across
cohorts.
"Most of our knowledge on sleep, cognition, and dementia
relationships comes from studies using subjective sleep or analysis of
activity patterns using actigraphy," Pase said. "We used in-home,
gold-standard sleep studies to clarify the aspects of sleep that are
most strongly related to cognitive function in almost 6,000 persons."
"The significance of mild asymptomatic sleep apnea has previously
been unclear as studies tend to examine participants who have presented
with sleep complaints," Pase pointed out. "Since participants in this
community-based study did not present with any specific sleep
complaints, the association between even mild obstructive sleep apnea
and poorer cognition is an important observation."
"Approximately
half our sample had evidence of at least mild obstructive sleep apnea,"
he added. "Treatment trials are needed to determine whether sleep
treatment can mitigate cognitive decline."
The inaugural analysis included 5,946 participants with no history of
stroke or dementia who underwent overnight, home-based type II
polysomnography (PSG) and neuropsychological assessments over 5 years of
follow-up. Results were adjusted for demographic variables, time
between PSG and neuropsychological testing, BMI, antidepressant use, and
sedative use.
"The use of five pooled independent community cohorts enabled us to
draw robust conclusions, as compared to any single study alone," Pase
said.
Across cohorts, 31.5% of participants were women, and mean ages
ranged from 58 to 89 at the time of PSG. The median wake after sleep
onset time ranged from 44 to 101 minutes, and the prevalence of moderate
to severe apnea ranged from 17% to 29%.
The
percentage of people with at least mild obstructive sleep apnea ranged
from 45% to 64%, reflecting differences in age and sex of the cohorts,
Pase noted.
Pooled estimates showed short total sleep time was associated with
poorer attention and processing speed. Pooled effects did not show
overall associations between sleep and learning and memory or
visuospatial abilities.
A limitation of the study was that sleep and cognition were assessed
at one time point. Given that associations between sleep and brain
health are likely bidirectional, longer follow-ups may be needed to
unravel temporal associations between poor sleep and cognitive
impairment, Pase noted.
"Having established the Sleep and Dementia Consortium, we now have a
resource to examine other important questions, including which aspects
of sleep are most strongly related to the risk of dementia up to 20
years in the future," he said.
Judy George
covers neurology and neuroscience news for MedPage Today, writing about
brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy,
autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep,
pain, and more. Follow
Disclosures
The Sleep and Dementia Consortium is funded by a grant from the National Institute on Aging.
Pase reported no disclosures.
Co-authors
reported relationships with Biogen, Eisai, National Institutes of
Health, Jazz Pharmaceuticals, Eli Lilly, and Apnimed.
Primary Source
JAMA Network Open
Source Reference: opens in a new tab or windowPase
MP, et al "Sleep architecture, obstructive sleep apnea, and cognitive
function in adults" JAMA Netw Open 2023; DOI:
10.1001/jamanetworkopen.2023.25152.
Your doctor and hospital should have a sleep protocol, otherwise they are contributing to your risk of dementia. Nurses would pass out sleeping pills like candy at 10pm. Does using them count as real sleep? I got woken up almost every morning by the blood vampires coming for
either me or my roommates at 7am. Do they now know about needleless
blood draws, only out since May 2016? Needle free blood draws or microneedles?
Pretty bad, say Dutch researchers, but fixable with "simple changes" in nightly routines
by Nicole Lou, Contributing Writer, MedPage Today
Good sleep was hard to come by for Dutch hospital patients, but the study authors said many noises and disruptions could be reduced fairly easily.
One day across 39 Dutch hospitals, 2,005 patients said in a survey that they spent the night before in the general wards sleeping an average 83 fewer minutes than at home (P<0.001); that they had more nocturnal awakenings during sleep (3.3 vs 2.0, P<0.001); and that they woke up that morning 44 minutes earlier than usual (P<0.001), according to Prabath Nanayakkara, MD, PhD, of VU University Medical Center in Amsterdam, and colleagues found.
Furthermore, 70.4% of study participants reported being awakened by external causes -- and that hospital staff were part of the reason in over half of these cases, they reported in JAMA Internal Medicine.
All aspects of sleep quality from the Consensus Sleep Diary and the Dutch-Flemish Patient-Reported Outcomes Measurement Information System (PROMIS) Sleep Disturbance item bank were rated worse during hospitalization than at home.
Sleep tended to be rated worse by younger patients and those admitted to a surgical unit.
The most commonly reported disturbances of sleep were noises from other patients, medical devices, pain, and going to the toilet.
"Most of the sleep-disturbing factors found in our study seem easy to address by incorporating simple changes in nightly hospital routines," Nanayakkara's group said. "A recent pilot study demonstrated an increase in total sleep time and subjective sleep quality after offering sleep hygiene education to nurses, introducing interventions to minimize light and noise disturbances, and reducing care-related disruptions and overnight fluids."
Interventions of interest, they suggested, include dimmed lights in corridors and patient rooms, silent footwear, remote alarms in staff rooms and in the pockets of the nurses, and distribution of earplugs and eye masks at admission.
"The possibility of introducing remote measurement of vital signs and nocturnal checkups via webcams should also be explored. In addition, changing the timing and minimizing nursing activities early in the morning; avoiding unnecessary standard procedures, such as routine vital signs measurements, continuous intravenous drips at night, and diuretics in the afternoon, could potentially improve sleep," the authors suggested.
"However, to our knowledge, most of these interventions have never been tested in general wards; therefore, prospective interventional studies are needed," they cautioned.
The "flash mob" nature of the study -- having all patients fill out questionnaires on Feb. 22, 2017 -- left the researchers with lots of missing data. They acknowledged that their dataset also potentially had recall bias because they relied on patients to estimate usual sleep at home.
Even with these limitations, the impetus is there for "a much-needed hospital-wide culture change to minimize sleep disruption in the hospital setting," according to Matthew Growdon, MD, MPH, and Sharon Inouye, MD, MPH, both of Harvard Medical School in Boston.
"Sleep deprivation in the hospital has been linked to important adverse outcomes, including alteration of homeostatic functions, such as glucose metabolism, cortisol regulation, and circadian rhythmicity; difficulty weaning from mechanical ventilation; defects in cellular immunity; and increased risk of long-term sleep disorders that play a role in depression, anxiety, and posttraumatic stress disorder ... When our patients relate their difficulty sleeping in the hospital, they are not reporting only a nuisance but also a direct contributor to adverse outcomes, even mortality," Growdon and Inouye wrote in an invited commentary.
To improve hospital outcomes, Inouye developed the Hospital Elder Life Program (HELP), which has a sleep protocol -- consisting of warm drinks, massage, relaxation music, unit-wide noise reduction strategies, and effective schedule adjustments -- that has been linked with decreased use of hypnotics and better quality of sleep the more these interventions were adopted, the editorialists noted.
"HELP and related programs
have shown that it is possible to be thoughtful about addressing hospital-related factors that disrupt sleep and, of importance, that these interventions improve health care outcomes and cost-effectiveness of care. With the aging of the world's population, these programs will become more essential, particularly in the prevention of delirium and adverse cognitive outcomes," according to the pair.
Nanayakkara and Growdon disclosed no relevant relationships with industry.
Inouye disclosed holding the Milton and Shirley F. Levy Family Chair at Hebrew SeniorLife and Harvard Medical School, and being a developer of HELP.
![Figure 2-2: Polysomnography of Wake to Sleep Transition. Notes: The most marked change is visible on the two electroencephalographic (EEG) channels (C3/A2 and O2/A1), where a clear pattern of rhythmic α activity (8 cps) changes to a relatively low-voltage, mixed-frequency pattern at about the middle of the figure. The level of electromyographic (EMG) activity does not change markedly. Slow eye movements (right outer canthus [ROC]/left outer canthus [LOC]) are present throughout this episode, preceding the EEG change by at least 20 seconds. In general, the change in EEG patterns to stage N1 as illustrated here is accepted as the onset of sleep. Source: Kryger MH, et al, eds. <em>Principles and Practice of Sleep Medicine. 7th ed. </em>Philadelphia, PA: Elsevier Saunders; 2022.](https://www.healio.com/~/media/clinical-guidance/insomnia/overview/ch2normalsleep/figure22.webp)
![Figure 2-4: Polysomnography of Patient in REM Sleep. Notes: On the left side is a burst of several rapid eye movements (out-of-phase deflections in right outer canthus [ROC]/A1 and left outer canthus [LOC]/A2). On the right side, there are additional rapid eye movements as well as twitches on the electromyographic (EMG) lead. The interval between eye movement bursts and twitches illustrates tonic REM sleep. Source: Kryger MH, et al, eds. <em>Principles and Practice of Sleep Medicine. 7th ed</em>. Philadelphia, PA: Elsevier Saunders; 2022.](https://www.healio.com/~/media/clinical-guidance/insomnia/overview/ch2normalsleep/figure24.webp)
