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Health Psych - Kin 2G03 > Sleep > Flashcards

Sleep Flashcards

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1
Q

sleep pressure (sleep debt)

A

the cumulative loss of sleep and the consequent pressure for sleep that results in an inadequate amount of physiologically normal sleep
- happens bc sleep-wake behaviour is under homeostatic control

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2
Q

how does sleep pressure change over 48 hours?

A
  • over the time that we spend sleeping, our sleep pressure decreases
  • once we wake, our sleep pressure begins to build again, causing us to feel sleepy until we go to sleep again
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3
Q

what happens to sleep pressure when you skip a night of sleep?

A

the pressure to sleep continues to build until you finally sleep

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4
Q

what happens to sleep pressure if you take a nap during the day?

A

some sleep pressure would be releived and the pressure would build again after that
- depends on length of nap

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5
Q

describe 3 examples of how sleep pressure can interfere with human performance

A
  • driving sleepy (>16h w/o sleep) = driving legally intoxicated
  • impairs motor control, reaction time, our ability to assess situations
    ex. truck drives, airline pilots, medical professionals (shift work)
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6
Q

how much sleep is recommended for:
children (6-13)?
teens (14-17)?
adults (18-64)?

A

children: 10-11
teens: 8.5-9.5
adults: 7-9

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7
Q

how to calculate sleep deficit (deprivation)

A

= amount of sleep we need - amount of sleep we get

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8
Q

limitations of calculating sleep deficit with equation provided in class

A
  • it doesn’t take into account the way we sleep (ie. sleep quality, or time spent in bed but not asleep)
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9
Q

sleep latency

A

the time between when we go to be and when we actually fall asleep

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10
Q

mid-sleep disturbances

A

the time when we wake up mid-sleep for awhile before falling back asleep

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11
Q

how do sleep latency and mid sleep disturbances interfere with sleep quality?

A

it affects our sleep efficiency
sleep efficiency = sleep time/time in bed which will be less than 100% if we have large latencies/disturbances in our sleep

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12
Q

sleep fragmentation

A

having multiple mid-sleep disturbances over the course of a night

ex. having sleep apnea, you stop breathing while you sleep so your body wakes you up multiple times a night to get breathing again resulting in multiple sleep disturbances
- individuals often feel sleepy throughout the day

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13
Q

sleep efficiency

A

= sleep time/time in bed

- we want to have as close to 100% as possible

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14
Q

how does sleep pressure differ for an individual who is rested vs drowsy?

A
  • pressure to sleep will be less for someone who is rested than for someone who is drowsy
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15
Q

describe the details of the study that demonstrated the correlation b/w poor sleep quality and academic performance

A

assessed the sleep quality of 400 university students and related it to their academic performance

  • found that those with low sleep quality did much poorer academically than those with high sleep quality in all of their courses
  • shows that sleeping helps us perform better academically
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16
Q

what factors should we account for when calculating the costs associated with sleep deprivation?

A
  • lost productivity and human error due to decreased attentiveness, focus and memory
  • heath care costs associated with physical and mental health disorders
  • chronic sleep disturbances increase mortality and morbidity and can lead to premature death
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17
Q

what physiological changes occur from sleep to wake?

A

during sleep:

  • body temp regulated about 1 degree lower
  • muscle tone similar to wakefulness
  • respiratory rate decreases, becomes more regular
  • HR and BP decrease
  • brain activity changes
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18
Q

what is an excitatory postsynaptic potential?

A
  • the input into a postsynaptic cell that will cause an AP (cell output)
  • they add up to produce a threshold depolarization
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19
Q

steps for depolarization

A
  1. AP reaches axon terminal of presynaptic cell, depolarizes the membrane
  2. voltage gated Ca2+ channels open and Ca2+ flows in
  3. synaptic vesicles releases neurotransmitter into synaptic cleft
  4. NT binds to receptors on target cell, usually causing +ve ions to flow in and depolarize the next cell and cause an AP
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20
Q

EEG

what does EEG measure?

A

EEG = electroencephalogram

- measures brain activity (specifically EPSPs)

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21
Q

which 2 things are necessary for EEG to record brain activity?

A

optimal conditions:

  1. synchronous activation of populations of neurons
  2. neurons must be aligned to create a dipole that can be measured by electrode on scalp (parallel to one another, perpendicular to surface) to help create summation
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22
Q

EOG

what does it measure?

A

electro oculogram

- measures electrical activity around the eyes

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23
Q

EMG

what does it measure?

A

electro magnograph

- measures electrical activity in our muscles while seated, at rest

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24
Q

what does frequency measure?

A

the rate of cycling of EEG waves

- measured in Hz (cycles per second)

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25
Q

what are the different EEG frequency bands?

A
  • beta
  • alpha
  • theta
  • delta
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26
Q

beta wave frequency

A

14-30 Hz

- represent mental activity while awake

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27
Q

alpha wave frequency

A

8-13 Hz

- represent mental activity while awake resting

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28
Q

theta wave frequency

A

4-7 Hz

- represent mental activity while asleep

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29
Q

delta wave frequency

A

< 3.5 Hz

- mental activity during deep sleep

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30
Q

how do the EEG recordings differ for awake and NREM sleep?

what frequencies are most dominant?

A

wake: beta and alpha waves observed
- fast, low amplitude waves that are desynchronized

sleep: theta and delta waves
- slow, high amplitude waves that are desynchronized

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31
Q

amplitude

A

the number of cells that are synchronized

- the more synchronized cells, the higher the amplitude of the signal

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32
Q

why is the amplitude of the EEG signal larger during NREM than during wake?

A

because the waves are slower in NREM, and when the frequency of cycles decrease, the amplitude of the waves get larger representing that there are more cells that are synchronized

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33
Q

what is the ascending activating system (AAS) and what brain regions are involved?

A

signals travel through the reticular formation, medulla, pons and sends EPSPs to the thalamus which activates the cerebral cortex, waking us up
- AAS is activated by vision, sounds, touch, and movement stimuli

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34
Q

reticular formation

A

a collection of nuclei in the brain centre that is a part of the brainstem where ascending general sensory info travels through to the rest of the AAS
- activation of reticular formation is critical for switching brain waves from synchronized (sleep) to desynchronized (wake)

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35
Q

how does the sound of your alarm clock have an impact on the activity of the reticular formation and cortex?

A

it travels through the AAS, to the thalamus which relays the info to wake up the cortex

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36
Q

what would happen if the reticular formation were damaged?

A

we may become comatose - unresponsive and unconscious (not desynchronized by afferent - aka incoming - stimuli)
- also observed: slow, high amplitude EEG

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37
Q

what would happen if the reticular formation were always activated?

A

we wouldn’t be able to fall back asleep ?

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38
Q

which nuclei are involved in arousal promoting and what NT do they release?

A
  • locus coeruleus (norepinephrine)
  • raphe - dorsal and median (serotonin)
  • tuberomamillary nucleus (histamine)
39
Q

what nuclei are involved in sleep promoting and what NT do they release?

A
  • ventrolateral preoptic area - VLPO - releases GABA which causes inhibitory signal to activation promoting NT when activated
  • insomnia is caused by damage to VLPO
40
Q

how does the interaction b/w the VLPO and the AAS impact sleep/wake behaviour?

A

GABA from the VLPO inhibit activation of the activating nuclei so that cortex stays in sleep state
- we don’t need all 3 activating nuclei to wake up, just the LC is enough to function

41
Q

how does orexin impact sleep/wake behaviour?

A

orexin is released from the lateral hypothalamic area (LHA)

- it is an arousal promoting NT that reinforces arousal activating system

42
Q

how would a deficit of orexin impact sleep/wake behaviour?

A

it would cause us to fall asleep randomly (narcolepsy)

43
Q

what roles does the thalamus play in sleep/wake transition? describe burst mode and spike mode - which state is dependent upon inputs from the AAS?

A

burst mode: random bursts of AP fire in thalamus to cause synchronized activity in the cortex, observed while sleeping

spike mode: continuous APs are send from AAS to the thalamus, causing desynchronized activity in the cortex, observed when awake

44
Q

what would happen if the thalamus was stuck in spike mode?

A

we would be awake all the time, unable to sleep

45
Q

what would happen if the thalamus was stuck in burst mode?

A

?

46
Q

fatal familial insomnia

A

a genetic condition where the thalamus is damaged (degenerates) and your thalamus is stuck in spike mode, causing you to be awake all the time
- your whole life deteriorates rapidly and you die

47
Q

what brain region controls our circadian rhythm?

A

the suprachiasmatic nucleus (SCN)

48
Q

what is the PER gene? why is it not the same for everyone and hoe does this have an impact on our sleep/wake behaviour?

A

PER gene = period gene
is set to roughly 24hr period of transcription and translation and controls on and offset of certain functions
- people with faster PER gene (<24h) are early birds
- people who have slow PER gene (>24h) are night owls

49
Q

zeitgerbers

A

they are responsible for resetting circadian rhythm based on external cues
ex. melanopsin - a light sensitive pigment that detects short wavelength visible light (blue) and signals SCN to wake (regulates light dark cycle)

50
Q

light/dark cycle

A

light phase: SCN is active, alerting pulses sent to AAS, works to counteract homeostatic pressure

dark phase: SCN produced melatonin, promotes sleep

51
Q

melatonin

A

a hormone produced by the SCN during the dark phase

- induces sleepiness by suppressing alerting pulses of the AAS system, promoting sleep

52
Q

what homeostatic factor causes sleepiness and hoes does it build up? how does this relate to the pressure to sleep?

A
  • the homeostatic factor is adenosine
  • adenosine is produced by degradation of ATP during wake (active neurons, glial cells)
  • increased adenosine drives homeostatic pressure to sleep
53
Q

what homeostatic factor causes sleepiness and hoes does it build up? how does this relate to the pressure to sleep?

A
  • the homeostatic factor is adenosine
  • adenosine is produced by degradation of ATP during wake (active neurons, glial cells)
  • increased adenosine drives homeostatic pressure to sleep
54
Q

how does coffee work to keep you awake?

A

the caffeine molecule binds to adenosine receptors to block adenosine from binding
- if the adenosine can’t bind to its receptors, this limits it sending sleepy signals so we can maintain alertness

55
Q

what impact does adenosine have on the VLPO?

A

adenosine activates VLPO, reinforces sleepiness

56
Q

what impact does adenosine have on the AAS?

A

adenosine inhibits AAS, makes us sleepy

57
Q

in the transition from NREM to REM sleep, how do the EEG, EOG and EMG signals change and what impact does this have on function?

A
  • EEG: synchronized during NREM then becomes synchronized in REM
  • EOG: v. little activity in NREM then activity increases during REM
  • EMG: some muscle activity observed during NREM but complete atonia is seen in REM
58
Q

what is atonia and why is it important?

A
  • no muscle tone (complete paralyzation) during REM sleep

- important so that we don’t act out our dreams

59
Q

changes in body temp, respiration and HR from NREM to REM transition

A
  • body temp: regulated in NREM, is not regulated in REM so body temp drifts toward that of the env’t
  • respiration: decreases during NREM, increases in REM
  • HR: slows during NREM and increases and varies in REM
60
Q

what is the EEG frequency like for each of the sleep stages:

  • awake and alert
  • awake but drowsy
  • stage 1 NREM
  • stage 2 NREM
  • stage 3 NREM
  • stage 4 NREM
  • REM sleep
A
  • awake and alert: beta brain waves
  • awake but drowsy: alpha waves
  • stage 1 NREM: mix of alpha and theta waves
  • stage 2 NREM: theta brain waves and beginning of delta waves (also K complexes and sleep spindles)
  • stage 3 NREM: mixture of theta and delta
  • stage 4 NREM: delta waves
  • REM sleep: fast active brain waves and rapid eye movement
61
Q

sleep spindles and K complexes?

A
  • appear at stage 2 NREM sleep

- they are involved in changes b/w spike and burst modes in the brain

62
Q

how long is one cycle of sleep?

A

90 mins

63
Q

what is the order of sleep stages?

A 
stage 1 NREM
stage 2 NREM
stage 3 NREM
stage 4 NREM
stage 3 NREM
stage 2 NREM
stage 1 NREM
REM sleep
repeat
64
Q

how many times does sleep cycle across the night?

A

4-5 times

65
Q

how does NREM sleep change across the night?

A

amount of time spent in NREM sleep decreases throughout the night since the pressure to sleep dissociates as adenosine is turned back into ATP

66
Q

how does REM sleep change across the night?

A

we spend more and more time in REM sleep as the night goes on
- bc we don’t need to spend as much time in restorative deep sleep (NREM) after having slept for longer amounts of time

67
Q

when are you most likely to wake up during the sleep cycle?

A

right after REM

- waking up at the wrong stages can impair motor and cognitive performance

68
Q

what are the 2 main ways that brain activity can be depicted? how do they differ?

A
  1. time series - we can see cycles per second (frequency)

2. power spectrum - we see power density plot (frequency distribution)

69
Q

what is delta power? in which sleep stage is it most dominant? how does delta power change across the night?

A
  • delta power is low frequency (Hz)
  • is most dominant in stages 3 and 4 NREM sleep (SWS)
  • we see a progressive decrease in delta power across the night
70
Q

what impact does sleep deprivation have on NREM, REM and delta power?

A
  • increases time spend in stages 3 and 4 NREM so therefore increases the delta power
  • has little effect on REM
  • spike in delta power will be less and less after sleep deprivation with full recovery by the 3rd night following the sleep deprivation
71
Q

naps and sleep latency

A

naps cause greater sleep latency (from 15 mins up to an hour)
- they make it more difficult to fall asleep

72
Q

naps and NREM, REM sleep

A

napping causes us to spend less time in NREM sleep and more time in REM and cycles 1, 2, 3, NREM (as if we jumped ahead in the sleep cycle) and REM will happen more in the following sleep cycles as normal

73
Q

naps and delta power

A

total delta wave activity is still the same after napping

- delta power at night is reduced after daytime napping

74
Q

what is the relationship b/w adenosine and delta power?

A

process S - the pressure to sleep - builds up during wake and is discharged when we sleep
- ie. adenosine accumulates during our time awake and is discharged when we sleep

75
Q

what is the function of delta power?

A

the same as the function of NREM

76
Q

why does NREM always come first? what is the function of NREM?

A
  • restore glycogen stores within the brain (process S)

- increases prior wakefulness (SWS)

77
Q

sleep paralysis

A
  • when a person cannot move/speak immediately after waking
  • temporary atonia from REM has not yet shut off
  • occurs during transition from REM to wake
78
Q

sleep walking

A
  • when a person gets out of bed and engages in motor activity but is unconscious and won’t remember the activity if awoken
  • occurs in slow wave sleep (cycles 1 and 2 NREM)
  • happens bc individual is unable to maintain SWS or their SWS is fragmented
79
Q

when do we dream?

explain the function of this sleep stage

A

during REM sleep

  • memory consolidation occurs here where important synapses are strengthened and unimportant synapses are pruned away
  • all of these synapses are firing at random which gives us a weird story (dream)
80
Q

how does dreaming differ in REM and NREM? would you be more likely to remember your dreams if woken from REM or NREM sleep?

A
  • REM dreaming is crazy vivid, and dreams are more likely to happen; motor cortex is active
  • NREM dreaming is less vivid and less emotional
  • individuals are better able to recall dreams when woken from REM
81
Q

lucid dreaming

A
  • being consciously aware that you are dreaming and control your dream
  • can occur during unique stage transitioning b/w REM and wake
  • happens bc of greater right frontal cortex activation, indicative of self awareness
82
Q

memory consolidation

A
  • measured using optogenetics where we can use light to turn different neurons in the brain on and off
  • theta rhythm happens in the hippocampus during REM sleep therefore the hippocampus is thought to be related to memory consolidation
83
Q

list 3 physical and 3 mental health issues that can arise from chronic sleep impairment

A

physical:

  • obesity
  • cardiovascular disease
  • stroke

mental:

  • anxiety
  • depression
  • dementia
84
Q

list 3 consequences of acute sleep deprivation

A
  • poor judgement & lack of focus
  • lost productivity
  • greater risk for accidents
85
Q

how does age have an impact on sleep quality and quantity?

A

for both:

  • total sleep time decreases (below recommended) w age
  • sleep latency is less affected by age
  • wake after sleep onset increases w age (sleep fragmentation is the cause of this)
  • sleep efficiency really decreases w age (makes sense given the increases in sleep disturbances seen w age)
86
Q

what are common treatments for sleep impairment? are they effective?

A
  • sleeping pills: can be effective at getting you to sleep but sleep may not be restorative and can cause daytime sleepiness; dependance is also an issue
  • cognitive behavioural therapy - takes time for people to do
87
Q

which aspects of sleep are impacted by exercise?

A

both quality and quantity:

  • total sleep time
  • SWS time (restorative time)
  • sleep latency
  • mid-sleep disturbances
88
Q

how does exercise help improve sleep in young adults?

A
  • increases total sleep time and SWS time

- decreases sleep latency and mid-sleep disturbances

89
Q

what is the optimal exercise intensity for sleep benefit for young adults?

A
  • half an hour of moderate-high aerobic exercise no closer than 3h before bedtime
  • overtraining can disrupt sleep
90
Q

what is the optimal exercise intensity for sleep benefit for older adults?

A
  • moderate intensity exercise shows the best improvement in sleep quality for older adults
  • no diff seen in sleep quantity with diff. exercise intensities
91
Q

why might high intensity exercise impair sleep?

how might the LC be involved?

A

for older adults, we see increases in stress hormones ACTH and cortisol

  • we want exercise to be stimulating enough to use ATP and build sleep pressure but we don’t want to stress ourselves out too much
  • the LC secretes norepinephrine which sense EPSPs to the cortex, maybe is overstimulated by cortisol ?
92
Q

what is a systematic review?

A
  • looking at all of the research that has been done on a topic so far and summarizing
93
Q

describe Ana’s systematic review on resistance exercise and sleep.

A
  • looking at the effects of acute and chronic resistance exercise, also chronic combined aerobic/resistance
  • results: for older adults, chronic resistance exercise is beneficial for sleep quality (older adults)
  • greater intensity, greater frequency, greater benefit
  • mood improvements observed with resistance exercise (depression and anxiety)
  • limitation: acute resistance exercise and chronic combined exercise is poorly studied

Health Psych - Kin 2G03 (3 decks)

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