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SLEE5101 > Module 2 - Normal Sleep > Flashcards

Module 2 - Normal Sleep Flashcards

1
Q

What is normal sleep?

A

Changes across the lifespan in terms of duration and pattern, Also changes cross-culturally.

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2
Q

Describe biphasic sleep

A

Before the industrial revolution (18-19C), we slept in two segments.

The first sleep was 2 hours after dusk.
We then woke for 1-2 hours. It was active.
Then slept until daylight.

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3
Q

Why did biphasic sleep stop?

A

The invention of light promoted socialisation in the evening outside and artificial light made bedtime later. The IR also made people more time conscious and efficinet.

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4
Q

What is the evidence to suggest that we don’t sleep less now than before?

A

Study from 1960-2013 found no differences.

Several countries increased and some decreased. But, Italy and Netherlands did have short sleeps.

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5
Q

What is Process S?

A

Sleep drive or sleep debt or homeostatic drive. The more time we spend awake the more we need recovery sleep, and the more SWS we have once asleep.

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6
Q

What is Process C?

A

Circadian rhythm that drives and entrains sleep.

Peaks mid-morning and late afternoon to maintain alertness despite Process S drive to sleep being high.

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7
Q

How does adenosine drive sleep onset?

A

Awake cells use ATP for energy which produces adenosine as waste. This adenosine builds up with more time awake (Process S), so at sleep onset we have a large drive to sleep and more SWS.

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8
Q

Where is the master mammalian clock?

A

Nucleus of the hypothalamus, the suprachiasmatic nucleus

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9
Q

What percentage of sleep is in N1?

A

3-5%

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10
Q

How long do we spend in N1 sleep each time we pass through it?

A

1-7 minutes

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11
Q

What does it mean if someone had more N1 sleep than expected?

A

Their sleep is highly fragmented as N1 is associated with arousals.

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12
Q

What percentage of sleep is in N2?

A

45-55%

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13
Q

How long do we spend in N2 sleep each time we pass through it?

A

10-25 minutes

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14
Q

What does the EEG look like for Stage N1?

A

Slow EEG mixed voltage

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15
Q

What does the EEG look like for Stage N2?

A

Spindles & K-Complexes

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16
Q

What percentage of sleep is in N3?

A

15-25%

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17
Q

How long is the first N3 sleep cycle?

A

20-40 minutes

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18
Q

What does the EEG look like for Stage N3?

A

> 20% has delta waves (>75mV amplitude) with a 0.5-4Hz frequency

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19
Q

What percentage of sleep is in REM?

A

20-25%

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20
Q

How long is the first REM cycle?

A

1-5 minutes

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21
Q

What is the arousal threshold in REM?

A

Variable

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22
Q

Describe tonic REM sleep

A

EEG Desychronisation (lower amplitude). Atonia, absent thermoregulation and pupils constrict.

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23
Q

Describe phasic REM sleep

A

PGO waves in bursts with eye movements. Irregular respiration and heart rate, and REMs.

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24
Q

What is the average sleep cycle length?

A

90-110 minutes

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25
Q

What is the first sleep cycle length?

A

70-100 minutes

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26
Q

What is the second and subsequent sleep cycle length?

A

90-120 minutes

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27
Q

How many arousals are expected per hour at 30 years old?

A

15-20 arousals

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28
Q

Describe the main sleep changes in the elderly

A

Total sleep decreases
Sleep latency decreases after 75 years (more in women)
WASO maintains from 35 years (but more in women increased)
REM latency slightly reduces
SWS reduces significantly (mainly in men)

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29
Q

What features of sleep do not change with age?

A

N1, N2 and sleep efficiency

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30
Q

What features of sleep change from adolescence to adulthood?

A

Rem sleep decreases
Sleep latency decreases
SWS decreases (especially large delta waves from childhood)
WASO decreases

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31
Q

How are arousals expected to change with age? (5, 20, 30 and 50 years old)~

A

Around 5 years: <10/hour
Around 20 years: 10-15/hour
Around 30 years: 15-20/hour
Around 50 years: ~25/hour

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32
Q

How does the AHI change with age?

A

Under 30 years old, AHI ~3
Increases with age
>60 years old, AHI > 10

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33
Q

List some purposes of sleep (8)

A

Memory Processing
Immunity
Waste Removal
Repair
Hormone Regulation
Mental Health
Brain Energy Restoration
Driver of Development

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34
Q

Describe how memory processing is influenced by sleep

A

Memory and learning are processed during sleep
NREM: Procedural/declarative
REM: Emotional
Frontal lobe is inactive during sleep therefore we are more creative.

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35
Q

Describe how immunity is influenced by sleep

A

Circadian variation in lymphocyte counts and immune cells

Complex relationship, but short sleep is related to increased viral infections and lower vaccine efficacy

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36
Q

Describe how waste removal of the brain is influenced by sleep

A

Glymphatic clearance “pump”
Brain reduces in size and increases CSF fluid (13-24%) during sleep to clear waste like amyloid and alpha synclein to move them out. This CSF moves along arteries into the tissue through the perivascular space of astrocytes (type of glial cell) due to the activation of aquaporin receptors.

CSF collects in the veins where it drains the waste it collected.

It does occur during wakefulness but more activity during sleep.

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37
Q

Describe how cellular repair is influenced by sleep

A

Sleep promotes systemic homeostasis and allows reallocation from high-energy neuronal function to repairing daily damage.
DNA repair and cellular structures are repaired during sleep

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38
Q

Describe how hormone regulation is influenced by sleep

A

Fluctuation in hormones occurs during sleep.
There is increased growth hormone in N3 sleep and teenagers have more N3 sleep than before and it will reduce after puberty. Growth hormone is principally produced during sleep.
In men, testosterone is highest at the beginning of the night.
The hunger hormone, ghrelin is increased with less sleep.
Sleep deprivation can influence glucose levels.

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39
Q

Describe how mental health is related to sleep

A

Neural networks for sleep and mental health overlap with a bidirectional relationship.

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40
Q

What is SWS associated with in terms of sleep purposes?

A

Neuronal repair, memory processing and GH.

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41
Q

What is REM sleep associated with in terms of sleep purposes?

A

Growth of synapses, adrenergic receptor homeostasis and long-term memory.

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42
Q

Describe how the brain energy restoration is influenced by sleep

A

Adenosine builds up throughout the day with more time awake, this accumulation may promote transition to sleep as it is cleared during sleep.

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43
Q

Describe how sleep may be a driver of development

A

Brain, bone and growth development.
Newborns have 50% of sleep in REM and they sleep 18 hours/day to drive brain development, learn and adapt.

44
Q

What modules our circadian rhythm?

A

Light
Melatonin
Zitgebers
Temperature

45
Q

How does light impact the circadian rhythm?

A

Primary entrainer of the circadian rhythm

Light -> photosensitive ganglion cells -> retinohypothalamic tract -> SCN

Earlier light = phase advance
Later light = phase delay

Stronger and longer light, bigger phase changes

46
Q

What wavelength of light is the more influential to the circadian rhythm?

A

Blue spectrum (short wavelength) due to melanopsin

47
Q

What secretes melatonin and where is it in the brain??

A

The pineal gland

Cerebellum end of hypothalamus

48
Q

Describe the relationship between melatonin and light

A

Melatonin secretion is suppressed by light

49
Q

How does the concentration of melatonin change throughout the day?

A

Highest concentration overnight
Starts to increase a few hours before sleep onset (DLMO), roughly 7 hours before lowest body temperature drop

50
Q

How does light influence melatonin secretion physiologically?

A

The SCN receives input about light -> intermediolateral cell column of upper thoracic spinal cord which passes through superior cervical ganglion cells -> pineal gland

51
Q

What are some examples of photic and non-photic zeitgebers?

A

Photic: reduction of light before sleep and sleeping in the dark.

Non-photic: evening shower, brushing teeth

52
Q

How does core body temperature fluctuate throughout the day?

A

Minimum CBT occurs around 2 hours before waking
Sleep onset occurs with fall of CBT
NREM: slight reduction of CBT
Prior to waking, slight increase in CBT

53
Q

What are delta waves and what sleep stage are they associated with?

A

Slowest waves, >75mV @ 0.5-4Hz

> 20% epoch of SWS

54
Q

Where do you see delta waves the best on an EEG?

A

Frontal

55
Q

What are theta waves and what sleep stage are they associated with?

A

4-8Hz, no required amplitude

All stages of sleep but commonly N1 and N2

56
Q

What are alpha waves and what sleep stage are they associated with?

A

8-13Hz, no required amplitude

Awake increased frequency or arousal and background in REM.

57
Q

Where do you see alpha waves the best on EEG?

A

Occipital

58
Q

What are beta waves and what sleep stage are they associated with?

A

13-30Hz, no required amplitude

Low voltage waves, individual but often seen in background frequency. Most commonly in REM and awake.

59
Q

Describe sawtooth waves and what sleep stage they’re associated with

A

2-6Hz

Small duration, <5 second wave

REM sleep

60
Q

Where do you see sawtooth waves the best on EEG?

A

Central

61
Q

Describe spindles and what sleep stage they’re associated with

A

12-14Hz

Overlap with alpha waves.

<1second waveform associated with N2 sleep but can also be seen in others.

62
Q

Where do you see spindles the best on EEG?

A

Central

But, slower (12Hz) waves are often frontal and faster (14Hz) are parietal

63
Q

What are the presumed roles of spindles?

A

They are generated in the reticular nucleus of the thalamus and associated with memory consolidation. They maintain sleep as arousal is less likely during a spindle.

64
Q

Describe K-Complexes and what sleep stage they’re associated with

A

Arousal response and no scoring requirements. Often sharp increase then decrease and return to normal.

Amplitude decreases with age.

Associated with N2 sleep.

65
Q

What are the presumed roles of K-complexes?

A

Memory consolidation and sleep maintaince.

66
Q

Describe vertex sharp waves

A

Often at sleep onset. They have a “V” shape.

67
Q

Explain the Berger effect

A

Also called alpha blocking.

When eyes are open, alpha amplitude decreases. Light reduces the alpha oscillations.
But, 10% of people do not have different EEG alpha waves from eyes open and closed.

Found in 1933.

68
Q

What is the role of orexin/HCRT?

A

Wakefulness and excitatory

69
Q

What is the role of histamine?

A

Sleepiness and inhibitory

70
Q

List the sleep waveforms in order of slowest to fastest with the associated frequency range.

A

Delta: 0.5-4
Theta: 4-8
Alpha: 8-13
Beta: 13-30

Sawtooth: 2-6
Spindles: 12-14

71
Q

What parts of the brain does orexin project to?

A

From the lateral hypothalamus:
Cerebrum
Basal forebrain
TMN
Substantia nigra
PPT/LDT
Raphe
Locus coerulus

72
Q

What parts of the brain does histamine project to?

A

From the TMN (tuberomamillary nucleus):
VLPO (ventrolateral pre optic nucleus)
Substantia nigra
PPT/LDT
Raphe
Locus coerulus

73
Q

What part of the brain is important for maintaining alertness

A

Lateral hypothalamus

74
Q

Why is there confusion around how much we sleep now from 1985?

A

A study showed that sleep has decreased since 1985 but 1985 was a significantly low sleep outlier.

75
Q

What is the difference between sleep restriction and sleep deprivation?

A

Restriction is voluntary.

76
Q

When does sleep restriction become pathologic?

A

It is unclear due to problems in self-report bias, we re bad at knowing how much we sleep.

77
Q

What is the relationship between sleep and mortality and BMI in women?

A

U-shaped

Increased mortality risk with <6.5 hours (12% risk increase) and >8 hours.

78
Q

What are some possible health consequences of insufficient sleep?

A

Obesity (causal in kids, maybe and associated in adults)
Hypertension
Coronary artery calcification

But, it’s not actually clear if chronic restriction causes ill health when by choice.

79
Q

What did the CARDIA study reveal about sleep reporting bias?

A

Used actigraphy. Demonstrated that self-report is inaccurate and is correlated to SES.
Most accurate: white women
Least accurate: black men

Race, health and sex all influenced error
But, this may be beside the point as major drivers of ill health are related and there are social and cultural determinants of health.

80
Q

What are the 6 types of public health studies and their benefits?

A

Community or Population Based: You go to the, not chosen by disease (e.g. location or profession).

Clinic-based: known to have disorder and already interacting with health system

Cross-Sectional: phone pole poster.

RCTs

Cohort study: follow through time

Case-control: disease vs no disease.

81
Q

Why would you do a community or population-based study?

A

To determine prevalence and aetology

82
Q

Why would you do a clinic-based study?

A

For prevalence and prognosis

Don’t over interpret.

83
Q

Why would you do a Cross-sectional study?

A

For prevalence (what is the cake made up of)

84
Q

Why would you do an RCT?

A

To answer questions about a treatment.

85
Q

Why would you do a cohort study?

A

For prognosis and disease progression.

86
Q

Why would you do a case-control study?

A

Great for rare diseases, but hard to do this study well.

87
Q

What is the difference between incidence and prevalence?

A

Prevalence: percentage with disease right now.

Incidence: percentage who will develop the disease now or in determined time frame.

88
Q

What is insomnia?

A

Difficulty maintaining or initiating sleep. Inability to obtain as much sleep as wanted.

89
Q

What did the BEACH study on the prevalence of insomnia consultations at GP clinics reveal?

A

80% of sleep consults at GPs are for insomnia

0.2% in <25 year olds
2.7% >75 year olds
60:40 female:male

95% treated pharmacology which was less common between 2007-2015

90
Q

What is the most costly sleep disorder and how much is it estimated to cost?

A

Insomnia due to a reduction in enjoyment
$1.5billion/year in direct costs including QoL and presenteeism

91
Q

What are the long-term consequences of insomnia?

A

Might be mortality in men (but single cohort effects)
Wisconsin study: depression, anxiety, CSD, reduced health and sleepiness
May have prognostic value in ADHD and renal disease

92
Q

What was the old definition of insomnia?

A

Sleep state misperception

93
Q

Why is changing of insomnia definitions problematic?

A

Prevalence estimates are untrustworthy

94
Q

What are the risk factors for sleep apnea?

A

Male: 6:1
Post-menopausal women 1:1 (MF)
Age until 65-70
Obesity
Family history
Some genetic conditions like marfans, down syndrome and upper airway cancers

95
Q

What is the most common sleep apnea?

A

Mild, but different from habitual snorers

It’s not clear if mild SA does anything medically

96
Q

Does sleep apnea increase mortality?

A

No. But, moderate-severe without treatment has 4x risk of death.

But, you are more likely to die between 12-6am unlike the average ~8am.

97
Q

What is the relationship between sleep apnea and cancer?

A

SA increases cancer signal but it may not be causal (not always = to death)

98
Q

What is the relationship between sleep apnea and diabetes?

A

None, with treatment it doesn’t increase diabetes

99
Q

What is the relationship between treating OSA and CVD?

A

None, seems to have no impact, but trial ongoing.

100
Q

How severe does OSA have to be to be a disease?

A

This isn’t clear, but likely an AHI ~20

101
Q

Describe Periodic Limb Movement Disorder

A

The nighttime version of restless leg (80-90% have PLMD).

Highly stereotyped leg movements during sleep

102
Q

What is the relationship between Periodic Limb Movement Disorder and mortality?

A

Increases risk of mortality

103
Q

What are the biggest risk factors for Periodic Limb Movement Disorder?

A

AGE (biggest)
African American may be protected
~4-10% Europeans (lots of variability in studies)
Women may have 1.5-2x risk, and might be influenced by pregnancy due to lower ferritin and/or dopamine
Genetic marker increases risk by 50-80%

Generally poor evidence due to subjective measurements and poorly defined or highly selected samples

104
Q

What is Shift Work Sleep Disorder?

A

Insomnia or excess sleepiness in work hours during sleep periods.

Not well studied, but 15-25% of working age population is exposed to shift work.

105
Q

What is the Healthy Shift Work effect?

A

Adverse effects of shift work leads to people leaving the job, leaving those who work shift work long term as those who can “handle” it.

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