Basic Science And Sleep Knowledge Flashcards

1
Q

What are the 3 distinct states of the sleep system?

A

Wakefulness, NREM, REM

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2
Q

Ascending arousal systems in the brain stem and posterior hypothalamus, what are they?

A
pedunculopontine (PPT)
laterodorsal tegmental (LDT)
locus coeruleus (LC)
tuberomammillary nucleus (TMN)
substantia nigra (SN)
ventral tegmental (VTA)
basal forebrain (BF)
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3
Q

Wakefulness

A

excitatory neurons relay sensory input to the thalamus, hypothalamus, and basal forebrain and activate cortex to increase wakefulness; suppressed during sleep.

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4
Q

What are the Neurotransmitters and neuropeptides that modulate and influence wakefulness promotion?

A
Acetylcholine
Histamine
Dopamine
Serotonin 
Norepinephrine
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5
Q

Acetylcholine, what stages is it present?

A

increased in wakefulness and REM sleep

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6
Q

Histamine,
what stage in the sleep system is it present?
Where in the brain is it released?
What is it’s main action?

A

Released from tuberomammillary nucleus (posterior hypothalamus) (TMN)

increased in wakefulness and very low in REM

histamine appears to be the major arousal-promoting neurotransmitter at wake onset

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7
Q

Dopamine
Where in the brain is it released?
What stages in the sleep system is it increased?
What is it’s main actions?

A

ventral tegmental area, substantia nigra, posterior hypothalamus, and brain stem

increased in wakefulness and very low in REM

more likely to promote wakefulness under conditions of motivation or physical activity

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8
Q

Serotonin
What part of the brain is it released from?
What stages in the sleep system is it present?

A

median and dorsal raphe

increased in wakefulness and very low in REM

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9
Q

Norepinephrine (NE)
Where in the brain is it released?
What stages in the sleep system is it present?
What is it primary actions?

A

locus coeruleus (midbrain)
increased in wakefulness and very low in REM
increased cortical activation, particularly under conditions of stress and in the presence of novel stimuli

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10
Q

what is hypocretin (also called orexin)?
A deficiency of Orexin is associated with what condition?
What functions is orexin linked to?

A

Neurons in the lateral or posterior hypothalamus that produce hypocretin (also called orexin) are also active during the wake state
Orexin is a peptide that projects to cortex and subcortical arousal systems to promote awake state.
Plays important role in stabilizing wakefulness and sleep
Neuropeptide that regulates arousal, wakefulness and appetite
deficiency of hypocretin/orexin primary etiology of EDS and cataplexy in narcolepsy.
Hypocretin/orexin function linked to control of feeding behaviors, locomotion, autonomic functions.

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11
Q

What is the ventrolateral preoptic area (VLPO)?

A

major sleep-promoting area located in anterior hypothalamus
controls REM and NREM sleep
During sleep (especially SWS) – VLPO neurons active, high firing rates.
VLPO is active during sleep, releases inhibitory neurotransmitters (GABA, galanin), which inhibit neurons of ascending arousal system that are involved in wakefulness and arousal.
VLPO activated by adenosine and prostaglandin D2 (somnogens).
VLPO inhibited during awake state by NE and ACH.

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12
Q

VLPO neurons send projections to where?

A
wake-promoting regions:
tuberomammillary nucleus (TMN)
locus ceruleus (LC)
LDT and PPT 
these inhibitory neurons are believed to induce sleep by coordinating the inhibition of all the wake-promoting cholinergic and aminergic regions.
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13
Q

Most VLPO neurons release what neurotransitters?

A

inhibitory neurotransmitter g-aminobutyric acid (GABA) at their sites of projection
some utilize the inhibitory neurotransmitter galanin.

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14
Q

What controls REM sleep?

A

The control of REM sleep involves the interaction of brain stem cholinergic and aminergic neurons in a complex feedback loop

neurons releasing acetylcholine (LDT/PPT region) are disinhibited by the suppression of aminergic neurons (e.g., NE, histamine) during REM.

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15
Q

REM-associated muscle atonia is linked to?

A

inhibition or loss of excitation of motor neurons in the brain stem and spinal cord via the medulla

pathways originate in the LDT and PPT

involve neurotransmitters acetylcholine, glutamate, glycine

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16
Q
sleep effects of drugs, overview
Benzos?
antihistamines?
TCA's and SSRI's
Psychostimulants
A

sleep-promoting benzos enhance GABA signaling

antihistamines block histamine receptors

TCA’s and SSRI’s act as REM suppressants enhancement of aminergic signals
inhibition of REM-promoting neurons.

Psychostimulants promote wakefulness by increasing dopamine and NE signals

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17
Q
Suprachiasmatic Nucleus (SCN),
what is this?
A

Located in anterior hypothalamus, behind eyes
Major circadian pacemaker in mammals, “master clock”
Controls rhythms of CBT, sleep/wake propensity
Controls secretion of melatonin, cortisol
SCN function helps maintain alertness, alerting signal during the day, reduced signal at night
Zeitgebers entrain SCN to physical environment

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18
Q
Human Alertness
What is the circadian dip and when does it occur?
What is. The second wind phenomenon?
When is the peak of alertness
When is the lowest levels of alertness?
A

Midday decrease in alertness 2-4pm, circadian dip
Alertness peaks in early evening hours
“Second wind” right before circadian signal drops off for sleep
lowest levels of alertness occurs 4-6am

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19
Q

What are Zeitgebers?

A

Time givers (German)
External stimuli, environmental cue
Entrain the SCN to the physical environment, light-dark cycle
circadian rhythms are actually longer than 24 hrs, intrinsic clock is “entrained” by Zeitgebers
Most potent is sunlight
Other: exercise, food, social activities
In the absence of zeitgebers, circadian rhythms are desynchronized or “uncoupled” from one another “free-running”)
Other types: feeding, social, exercise, cognitive activities (work)

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20
Q

Circadian rhythm in humans?

A

Period of the rhythm is called tau
Mean value of the rhythm in humans=24.2 hrs
To maintain synchrony with light/dark cycle, external stimuli induce slight daily advance to counteract intrinsic phase delay
Zeitgebers (esp.sunlight) entrain the clock

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21
Q

What are markers of Circadian Phase?

A
CBT min (core body temp, minimum)
DLMO (Dim light melatonin onset)
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22
Q

CBT min, when does it occur?

A

2-3 hrs before spontaneous awakening from unconstrained nocturnal sleep
(4-5 am in most individuals)
Reduction in CBT during sleep period corresponds to elevation in plasma melatonin

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23
Q

DLMO, when does it occur?

How is it measured

A

DLMO occurs ~2 hrs before habitual sleep onset
Determined by interval measurement of salivary or plasma melatonin performed in dim light (5 lux) in the evening
Light inhibits melatonin secretion

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24
Q

How to estimate CBT min?

A

Can be estimated as DLMO + 7 hrs

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25
Q

Phase Shifting by Light

A

Light exposure before the CBTmin causes phase delay.
Light exposure after the CBTmin causes a phase advance
Normal light exposure during early am induces daily phase advance in circadian rhythms to compensate for intrinsic tendency to phase delay due to tau longer then 24 hrs.

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26
Q

Common light exposures

A
bright blue midday sky >100,000 lux
Sunrise or sunset ~10,000 lux
commercial light boxes up to 10,000 lux
normal room light ~200 lux
moonlight 0.1 lux
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27
Q

What are intrinsically photosensitive retinal ganglion cells (IPRGCs) ?

A

circadian photoreceptors
entry point for light/dark information into the circadian system
IPRGCs send excitatory input to SCN via retiino-hypothalamic tract (RHT)

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28
Q

What is the retinal hypothalamic tract?

A

monosynaptic pathway from eye to SCN

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29
Q

What is an epoch

A

An epoch is how sleep is staged on PSG

Sleep is staged in 30 second epochs

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30
Q

How is stage REM detected?

A

EOG (eye movement) and Chin EMG are used to detect Stage R

REMs are noted
Decreased muscle tone
Decrease in chin EMG amplitude during stage R

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31
Q

What are the stages of sleep?

A
Wake, Stage W
Stage N1 (light)
Stage N2 (spindle, K complex)
Stage N3 (SWS, Delta)
Stage R (REM)
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32
Q

What happens without sleep?

A

Can’t maintain pathways in brain that let you learn and create new memories
Everyone needs sleep, but its biological purpose remains a mystery
Quality sleep is as essential to survival as food and water

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33
Q

What is melatonin?

A

Hormone that helps regulate sleep timing, “dark hormone”; need to start falling asleep
Produced in pineal gland
Inactive during the day and switches on around 9pm
Melatonin itself doesn’t make you fall asleep; it just tells your body that it’s time to fall asleep.
Lowers alertness and decreases CBT
Works in tandem with circadian clock, let’s you know when you should rest and when you should be awake.

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34
Q

What is the impact of light exposure on melatonin?

A

Too much light exposure at night; delays release of melatonin

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35
Q

How would you use melatonin for trouble falling asleep?

A

Take melatonin 5mg 60 min. Before bedtime for trouble falling asleep.
Take before usual bedtime and same time every day

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36
Q

What is an ultradian cycle

A

Sleep cycle of typically 90-100 min. In adults
Typically NREM sleep followed by period of REM sleep
Usually 3-5 NREM/REM cycles occur per night, each lasting 90-100 min.

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37
Q

What is sleep latency and what is normal in an adult

A

SL is time to fall asleep after lights out
SL should be less than 30 min, typically about 15 min.
SL increases with age slightly
Patients with sleep onsent insomnia have SL >30 min.

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38
Q

What is a hypnogram?

A

Plot of sleep stage vs time of night

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39
Q

What is WASO?

A

Wake after sleep onset

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40
Q

What is the typical sleep pattern for 20 year old?

A
Stage N1: 5%
Stage N2: 45%
Stage N3: 20%
Stage R: 25%
Arousal index (#/hr): 5-10
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41
Q

What is typical sleep pattern for 60 year old?

A
Stage N1: 15%
Stage N2: 55%
stage N3: 10%
Stage R: 20%
Arousal Index (#/hr): 15-20
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42
Q

How does sleep change as we age?

A

TST and SE decrease with age, esp after age 50
Amount of wake increases with age (WASO)
SL increases with age

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43
Q

When does napping stop for children?

A

Napping in children uncommon after age 7

Daily napping uncommon after age 5

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44
Q

What is the normal ultradian cycle in children?

A

In children, sleep cycle duration is 45-60 min.

Greater number of NREM/REM cycles per night compared to adults

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45
Q

How do infants enter sleep?

A

In infants, entry via REM sleep (active sleep) is common

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46
Q

How do adults enter into sleep?

A

Adults enter into sleep from wakefulness via NREM (usually stage N1)

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47
Q

What is the purpose of REM sleep?

A

REM sleep provides brain form of overnight therapy
Helps process difficult emotional experiences
Heightened levels of anxiety during the day can disturb sleep

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48
Q

What is the impact of anxiety on sleep?

A

Heightened levels of anxiety during the day can disturb sleep.
Anxiety prevents falling/staying asleep
Activates sympathetic nervous system, “fight or flight”
“ A ruffled mind makes a restless pillow”, C. Bronte

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49
Q

What is the typical sleep duration in adults?

A

Most of us get 7-8 hrs sleep

1/3 of population gets 6 hrs or less

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50
Q

Nocturia and sleep

A

Nocturia disrupting sleep increases with age
Increases after age 50
Impacts equally men and women

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51
Q

Impact of leg cramps on sleep?

A

Nocturnal leg cramps impact sleep
Increases after age 50
Impacts up to 5-10% of population

52
Q

What is the impact of aging on sleep?

A

Insomnia increases with age
But getting older doesn’t necessarily mean sleeping poorly
There are accumulated health risks

53
Q

What are some concerns with using meds to control insomnia?

A

Using medication to control insomnia symptoms provides some relief.
But sleep you get on meds is more sedation than sleep

54
Q

What percent of US population has Chronic insomnia disorder?

A

5% or 12 million people

55
Q

What is the “forbidden zone” or “second wind” ?

A

Relative surge of circadian based alertness to offset the buildup of sleep drive
Time zone before bedtime when it’s almost impossible to fall asleep

56
Q

What is the circadian wake drive?

A

24 hr pattern of alertness

57
Q

What is the circadian nadir and when does it occur?

A

Lowest period of alertness

Occurs typically at 3-5 am

58
Q

What is a chronotype?

A

Phase preference

Propensity of individual to sleep or feel most awake at particular times in 24 hr period

59
Q

What is an evening chronotype associated with?

A
Increased risky behaviors
Depression
Academic failure
Obesity
Metabolic dysfunction
60
Q

What changes happen to sleep pattern during puberty?

A

All adolescents experience normal shift in circadian rhythm with age and onset of puberty.
Eveningness chronotype
Biologically based shift (delay) of up to several hrs in natural fall asleep & morning wake times
changes in sleep drive make it easier for teens to stay up later
Hard for teens to fall asleep before 11pm

61
Q

How much sleep should Teens get?

A

Teens should ideally get ~9 hrs sleep
Insufficient sleep is very common
Teens are prone to weekend oversleep and social jet lag

62
Q

What are some important environmental factors in Teen sleep?

A

Evening light exposure causes more phase delay
Suppresses release of melatonin
Increased sensitivity to evening light at puberty onset

63
Q

What is the definition and impact of “weekend oversleep”

A

Practice of “making up” sleep
Marker of chronic insufficient sleep
Doesn’t reverse or compensate for impairments

64
Q

What is social jet lag?

A
Shift in bedtime and wake times on non-school or work days
Leads to “circadian misalignment”
Shift melatonin onset
Permanent state of jet lag
Adjustment 1 day per time zone crossed
65
Q

What is the impact of early school start time on Teens (before 8:30am)?

A

Students are required to wake for the day and function during the circadian nadir
Circadian nadir is lowest level of alertness during 24hr period
Early wake times decreases amount of REM sleep
REM sleep is critical for learning of new info and memory
Unable to meet most sleep needs (should be getting 8-10 hrs sleep)

66
Q

What is an ideal start time for School for Teens?

A

8:30am or later school start time is considered the sleep and circadian “sweet spot” for middle schoolers and High school students

67
Q

Why do we sleep?

A
Immune function
Hormone regulation
Clearing toxins from the brain
Mood regulation
Learning and memory
Maybe be critical for prevention of AD
68
Q

What is considered the optimal time to wake up?

A

End of REM cycle

69
Q

what is melanopsin?

A

a photopigment sensitive to short-wave (blue-green) light

70
Q

Night owl eveningness chronotype, what outcomes is it associated with?

A
associated with a number of adverse health, behavioral, and performance outcomes:
lower physical activity
depression
impulsivity
aggressive and antisocial behavior
Substance Use disorder
lower academic achievements
increased perceived stress level
71
Q

what is the proper dosing and timing of melatonin for Delayed Sleep phase d/o?

A

3 to 5 mg. Melatonin should be taken in the early evening, at least 1.5 hours before the desired bedtime.

72
Q

what are assessments of Circadian/biological rhythms?

A
Sleep logs
Actigraphy
Questionnaires
AM-Evening questionnaire
Munich chronotype questionnaire
Melatonin: Dim light melatonin onset (DLMO); Urinary 6-sulfatoxymelatonin (aMT6s)
Core body temperature (CBT)
PSG: not indicated
73
Q

What is the pathway of melatonin synthesis?

A
L-tryptophan
5-hydroxytryptophan
serotonin
N-acetylserotonin
melatonin

Melatonin is released by pineal gland

74
Q

What are important characteristics of sleep homeostasis, Process S

A

Regulated length and depth of sleep
During each hour you are awake, somnogens build up in the brain (adenosine)
Wake-promoting substances are used up in the brain (NE, 5-HT)
During sleep somnogens are cleared and wake promoting substances are replenished
Caffeine is receptor antagonist for adenosine, i.e. alerting

75
Q

What are characteristics of process S in infants and young children

A

Sleep pressure builds more quickly
The duration of sustained wakefulness during the day is limited
Reason for short periods of daytime sleep (naps)

76
Q

What are characteristics of Circadian rhythm (process C)

A

Process Influences internal organization of sleep and timing and duration of daily sleep-wake cycle
24 hr in the brain
Master circadian clock = SCN (in ventral hypothalamus)
Regulate timing of appetite, urine, CBT
Circadian drive is strongest at wake time and 2 hrs after wake time

77
Q

Characteristics of Process C in infants and children

A

Circadian timing system develops rapidly in 1st 6 months of life
Combined influence of neurodev. Maturation and social/environ. Cues (light-dark cycles)

78
Q

What determines level of sleepiness in a 24 hr period?

A

Sleep propensity is determined by duration and quality of previous sleep
Time awake since last sleep period

79
Q

What are the 2 periods of max sleepiness (circadian troughs)

A

3-5 pm (typically 7-9 hrs after awakening)

3-5 am

80
Q

What are 2 periods of max alertness (circadian peaks)

A

Mid morning

Just prior to sleep onset (second wind, forbidden zone)

81
Q

What is sleep inertia?

A

Period of incomplete arousal characterized by confusion, disorientation, cognitive slowing and irritability occurring immediately upon waking in the am or after a nap, esp. from SWS, may further compromise alertness levels

82
Q

What is sleep architecture?

A

Structure/stages of sleep:
REM
NREM (stages 1-3)
WAke

3 distinct states each with distinct EEG, eye movements and muscle tone

83
Q

What is the ultradian rhythm?f

A

The nocturnal cycle of sleep stages

84
Q

What is the circadian rhythms?

A

24 hour rhythm of sleep/wakefulness and physical systems

85
Q

What is sleep regulation?

A

Determinants of sleepiness and alertness levels

86
Q

What determines our sleep patterns?

A
Biology
Learning
Maturation
Culture
Environment
87
Q

What are characteristics of NREM stages

A

Slow wave sleep
Low brain activity
Brain continues to be active
Body movements are preserved
Still able to process external info and assess its salience
Resp and CV parameters are regular
After 6 mos of age, NREM divides into Stages 1, 2, 3

88
Q

What are characteristics of Stage 1 sleep?

A

Theta waves
Sleep wake transition, “bridge” to deeper sleep
30 sec to 5 min.
Recall of fragmented visual imagery (hypnogogic hallucinations)
Brief involuntary muscle contractions (hypnic jerks)
Lowest arousal threshold
Easiest to awaken

89
Q

What are characteristics of stage 2 sleep?

A

Sleep spindles and K Complexes
Initiation of true sleep
Bursts of rhythmic rapid EEG activity (sleep spindles; fluctuating episodes of fast activity, occurring after 4 weeks of age)
High amplitude slow-wave spikes (K complexes, first occurring at 6 months)
Lasts 5-25 min

90
Q

What are characteristics of stage 3 (delta sleep)

A

Deepest
Slow wave sleep
Delta sleep
High voltage, low frequency activity
Respiration is slowes and most regular during SWS
Parasympathetic activity is high
Highest arousal threshold (most difficult to awaken)
Initial SWS period is about 30-45 min, followed by brief arousal (transition to wakefulness or to a lighter sleep stage

91
Q

What are characteristics of REM sleep?

A

Active or rapid eye movement
EEG pattern: sawtooth waves
Bursts of rapid eye movements
Muscle atonia
Desynchronized cortical activity: low voltage, high freq EEG
Highest brain metabolic rate
Dreaming
Absence of skeletal muscle tone (except for diaphragm, middle ear, erectile muscles)
Lack of normal thermoregulation
Episodic bursts of phasic eye movement, hallmark of REM

92
Q

What is the typical REM latency in adults?

A

1st REM period occurs ~70-100 min. After sleep onset

Lasts about 5 min.

93
Q

What are the characteristics of REM in infant sleep?

A

In infants REM equals “active sleep”
Until 3 mos of age, infants enter sleep through REM
Muscle twitches and grimaces are normal

94
Q

What are the characteristics of sleep cycle during the night?

A

Normal REM latency is 90 min.
20-25% of sleep is REM
More REM episodes as the night progresses
NREM and REM sleep alternate throught the night in cycles of ~90-110 min
Sleep cycles in infancy are 50 min and lengthen to adult level at about school age

95
Q

What is the typical pattern of arousals during sleep?

A

Brief arousals normally followed by rapid return to sleep often occur at the end of each sleep cycle (4-6 times per night)

96
Q

How does REM and NREM stages change through the night?

A

SWS predominates in the first 3rd of the night
REM predominates in the last 3rd
partial arousal parsomnias that occur during NREM sleep primarily occur beginning of night (sleep terrors, etc.)
REM is compromised in forced early wake times (i.e. teenagers)

97
Q

What are the factors that affect the amount and timing of SWS?

A

Prior sleep loss
Time of sleep onset
Length of prior wakefulness
SWS is “protected” by its appearance early in noctural sleep period
SWS is preserved at expense of other sleep stages when TST is restricted
Marked increase in SWS (rebound) during night of recovery sleep following restriction

98
Q

What are factors that impact REM?

A

Rebound phenomenon in recovery sleep
Increased arousals (osa, PLM) result in sleep fragmentation and reduced amounts of SWS, REM sleep
Increase in REM may lead to more vivid dreams

99
Q

What is normal sleep architecture in newborns?

A
Three sleep states:
REM-like, 50% of sleep
Quiet (non-REM like)
Indeterminate
Enter sleep through active state
100
Q

What is normal sleep architecture in infants (3-12 mos)

A

Increasing nighttime sleep compared to newborns
Amount of active/REM sleep declines
Development of 3 stages of NREM sleep at ~6 months
Sleep cycles every 50 min
Enter sleep through non-REM
Transition to 2 naps ~6 months
“Sleeping through the night” defined variably

101
Q

What is normal developmental changes in sleep architecture for toddlers (1-3y)

Toddler sleep characteristics (1-3 years)

A

Transition to 1 nap: average ~ 18 months
Advanced circadian rhythm
High prevalence (25-30%) of bedtime problems and night wakings
REM sleep amounts continue to decline

102
Q

What are Normal developmental changes in sleep architecture preschool (3-6 y)?

Preschool Sleep characteristics (3-6 years)

A
REM sleep amounts continue to decline
Sleep cycles every 90 min
High levels of SWS, peak levels
Transition to no nap: 3-5 years
Peak pediatric prevalence of OSA
Difficulties with sleep onset and night wakings continue: 15-30%
103
Q

What are Normal developmental changes in sleep architecture middle childhood (6-12 y)?

A

Latency from sleep onset to REM sleep increases

High sleep efficiency (time asleep/time in bed)

104
Q

What are normal developmental changes in sleep architecture for teens (>12 y)?

A

40% decline in SWS

REM sleep at adult levels (25-30%)

105
Q

Waht is normal sleep? (Normal, optimal, not disordered?)

A

Most people get 7-8 hrs of sleep
1/3 get 6 hrs or fewer
Insufficient sleep in areas where there are other health comorbidities
Sleep duration trends are decreasing over time, esp. since 2012

106
Q

What is the most significant modern study of sleep and age?

A

How sleep changes over the lifespan, by Ohayon and Carskadon
Published 2004
Meta-analysis of 65 studies from 1960-2003, normal patients of all ages, looked at PSG data

107
Q

What were the findings of Ohayon’s study?

A
TST, general decline
SL: no change, slight increase
SE: decline starting in middle age
Stage 1%: highly variable
Stage 2 %: slight increase over the lifespan (lighter sleep as people get older)
REM %: decline over lifespan
SWS %: decline over lifespan (young kids larger % that drop off)
WASO: increase over lifespan
108
Q

What are age-related changes we see with sleep?

A

Loss of SWS/delta sleep with aging
Teens need more sleep than adults (9-10 hrs)
Hypnogram shows more sleep consolidation in younger years
More sleep fragmentation with age
About 55% of 18 yo get 7+ hrs sleep
Long sleep more common in teens
Lowest amout of TST seen age 30-65, working age adults
Sleep apnea risks increase with age, increasing BMI
Nocturia becomes a bigger issue at age 50, men and women; related to poor sleep quality

109
Q

What medical issues impact sleep quality?

A

OSA
Nocturia
Nocturnal leg cramps

110
Q

How does nocturia impact sleep?

A

More time getting up to go to bathroom: results in poor sleep quality
Issue present in men and women
Inflection point at age 50
Present across the lifespan

111
Q

What happens with the incidence of insomnia as we age?

A

The incidence of insomnia increases with age

112
Q

How is sleep debt defined?

A

How much sleep you feel like you need vs how much sleep you get

113
Q

What do we see with age and resilience to sleep loss?

A

2004 study showed young people dramatically underestimate how impaired they are
Older people more resilient to sleep loss
Older people overestmate how impaired they are
Younger people more likely to crash in motor vehicle stimulator after sleep restriction than older adults

114
Q

How does SDB change with age?

A
Prevalence of SDB increases with age
Plateau around age 65
Muscle fibers may be related
Sleep apnea risk factors in older adults
Increased risk of mortality <70, but not >70
115
Q

What is prevalence of sleep disorders in older adults?

A

SDB =20%
Insomnia=15%
Hypersomnia=20%

116
Q

How does sleep change in infancy/childhood?

A

Decline in avg 24hr sleep duration
Decrease in daytime napping over 1st 5 years of life
More gradual decrease in nocturnal sleep amounts into late teens
Decrease in REM %: birth =50%, early childhood into adulthood (30-35%)
40-60% decline in SWS after puberty, further decreases over the life span
High amounts of SWS in children is reason for high prevalence of partial arousal parasomnias (sleep walking and sleep terrors)
Decrease in no. Of end of cycle arousals due to lengthening of ultradian sleep cycle
Gradual shift to later bedtime and sleep onset time begins in middle childhood and accelerated in early to mid teen years
Irregularity of sleep wake patterns begins middle childhood and peaks in teen years: big differences between school night and non-school night bedtimes and wake times.
Increased weekend oversleep in teen years

117
Q

What are the impacts of sleep deprivation on the brain?

A

Neuronal functions
Neuroplasticity: ability for brain to change structure/function in response to environment
Downscaling of synapses to compensate for net increase in synapse formation and strength during wakefulness
Gene activation/expression
Neurogenesis
Brain cell protection/ repair from stress
Neurotransmitter
Melatonin production
Cellular metabolism
Increase in stress response and stress hormones

118
Q

How much do average Americans sleep?

A

Sleep has declined from avg of 9 hrs to 7 hrs
Americans sleep ~6hr 51 min during the week and 7hr 37 min weekends
80% of teens sleep less that optimal amounts (9+ hrs)

119
Q

What are the consequences of sleep deprivation?

A

Reduced productivity
Lower cognitive performance
Accidents
Teens high risk for sleep related MVA’s (55% of fall asleep MVAs)
24 hrs of sleep deprivation impairs performance as much as 0.10 blood ETOH level

120
Q

What is Maggie’s law?

A

Law in NJ, passed 1997
If you are a motorist who has been up for 24+ hours, fall asleep and kill another driver: you can be charged with vehicular homicide

121
Q

What are long term consequences of sleep deprivation?

A
Increased risk of obesity
Hypertension
Diabetes
Mortality (too little or too much=bad)
Changes in waking activity
122
Q

How is social jet lag defined?

What is its impact?

A
Weekend oversleep
Adjustment takes 1 day per time zone crossed
Effects persist up to 3 days
Associated daytime sleepiness
Poor academic performance
Depressed mood
123
Q

Development of circadian rhythms

A

Term: sleep-wake periods occur randomly
1 month: CBT has circadian rhythm
3 months: Hormones (melatonin and cortisol) begin to cycle in circadian rhythm
3-6 months: maturation of circadian system leads to sleep consolidation (sleeping through the night)

124
Q

Nap patterns in children: summary

A

Transitions:
to 2 naps: ~6 mos
to one nap: ~ 18 mos
To no nap: ~ 3-5 years

High normative variability in timing of transitions
Transitions often happen gradually rather than abruptly, and can temporarily disrupt nighttime sleep routine

125
Q

What is the impact of sleep duration on health?

A

Short sleep duration (6 hours or less per 24-hour period) is associated with adverse outcomes, including mortality

Long sleep duration (>9 to 10 hours per 24-hour period) may also be associated with adverse health outcomes

At a population level, the optimal sleep duration in adults for good health is 7 to 9 hours, although individual variability exists