60 Sleep Flashcards

(78 cards)

1
Q

Which brain waves are the fastest? Slowest?

A

Fastest: Gamma (>30Hz), Slowest: delta (<4Hz)

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2
Q

What is the order of brain frequencies from fastest to slowest?

A

Gamma (30Hz) > Beta > Alpha > Theta > Delta (4Hz)

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3
Q

Which brain waves predominate during wake? Sleep? Deep sleep?

A

Wake: alpha/beta (14-30Hz) Sleep: theta (4-7Hz) Deep sleep: Delta (<4Hz)

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4
Q

What do EEG recordings represent?

A

continuum of frequencies

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5
Q

What are the 3 primary brain states?

A

Wake, Non-REM sleep, REM sleep

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6
Q

Which brain waves predominate during wake? Non-REM sleep? REM sleep?

A

Wake: alpha/beta (14-30Hz) Non-REM Sleep: theta/delta (<7Hz), REM sleep: alpha/theta: (13-4Hz)

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7
Q

What 3 characteristics are typical of Wake in terms of brainwaves, eyes, and muscle tone?

A

Brainwaves: ALPHA (8-13Hz) Eyes: RAPID EYE. Muscle tone: NORMAL

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8
Q

During wake, where are ALPHA frequencies best seen and how are they attenuated?

A

occpital regions; alpha waves attenuate with eye opening

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9
Q

What are the sleep stages? (4)

A

Non-REM: N1 (light sleep/transition) N2 (filler sleep), N3 (deep sleep, slow-wave, delta sleep) and REM

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10
Q

What characterizes the Non-REM N1 stage? (4)

A

1) alpha waves (8-13Hz) are replaced with theta waves (4-7Hz), 2) slow eye movements, 3) muscle relaxation, 4) central apneas (neural transitions of wake-sleep)

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11
Q

What is the hypnic jerk?

A

sensation of falling/flash of light - whole body jerk that is normal at the sleep/wake transition stage

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12
Q

What characterizes the Non-REM N2 stage? (3)

A

1) Theta activity that progressively slows 2) sleep spindles (13-14Hz), 3) K complex (large amp/biphasic evoked response)

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13
Q

What characterizes the Non-REM N3 stage? (2)

A

1) delta waves (<4Hz), with 20% being slow wave activity (0.5-2Hz with 75uV amplitude), 2) highest arousal threshold (hardest to wake up from)

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14
Q

What is slow wave sleep parasomnia?

A

sleep disorders; involves abnormal and unnatural movements, behaviors, emotions, perceptions, and dreams that occur while falling asleep, sleeping, between sleep stages, or during arousal from sleep.

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15
Q

What key components characterizes the REM stage? (6)

A

1) reticular activation - desynchronization, 2) stage-1 like EEG (theta range) with saw-tooth waves and phasic/tonic components 3) rapid eye movements, 4) muscle atonia (paralysis) and twitches, 5) cognitive activity, 6) PGO (pontine-geniculate-occpital) spikes

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16
Q

What are the phasic/tonic components that are characteristic of the REM stage?

A

PHASIC REM: phasic eye movements and muscle twitches + saw-tooth theta waves. High SYMPATHETHIC state. TONIC REM: no eye or motor movements, no alpha or theta. High PARASYMPATHETHIC state

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17
Q

During REM sleep, where is most of the brain activity localized to?

A

in occipital lobe (VISUAL cortex) not in our olfactory cortex - reason why our dreams are visual and not olfactory

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18
Q

What is muscle atonia and when is this most prominent?

A

muscle atonia occurs during REM sleep - important so that we don’t act out our dreams during sleep. If this doesn’t get turned on, the body will act out whatever is in the cortex (normally associated with older age and neurodegenerative disorders)

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19
Q

Sleep enters through this phase:

A

N1

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20
Q

What is the ultradian rhythm?

A

Non-REM and REM sleep cycle with approximately 90 min period

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21
Q

What stage predominates in the first 1/3 of the night? Last 1/3 of the night?

A

First 1/3: N3. Last 1/3: REM

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22
Q

Which stage of sleep do most sleep medications act on?

A

stage N2 sleep, but some will suppress REM sleep

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23
Q

How does autonomic activity change with Non-REM sleep? REM sleep?

A

Non-REM: decreased HR and BP, REM: variable sympathetic activity

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24
Q

How does respiratory activity change with Non-REM sleep? REM sleep?

A

both: decreased

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25
How does muscle tone change with Non-REM sleep? REM sleep?
Non-REM: reduced, REM: minimal
26
How does temperature change with Non-REM sleep? REM sleep?
Non-REM: intact regulation. REM: poikilothermic (considerable variation)
27
How does cerebral blood flow change with Non-REM sleep? REM sleep?
Non-REM: reduced CBF REM: increased CBF
28
How does cognititon/cortical arousal change with Non-REM sleep? REM sleep?
Non-REM: reduced REM: abundant/bizzare
29
How do genitals change with Non-REM sleep? REM sleep?
Non-REM: ?? REM: Penile erection/vaginal blood flow
30
What does ontogeny (of sleep) mean?
how sleep develops
31
In fetuses/newborns, what sleep stage predominates?
active sleep (REM). Fetuses experiences 80% of their sleep in this stage, while newborns experience 50% of their sleep in this stage
32
When is nocturnal sleep established?
3-4 months
33
When does active sleep/REM eventually level off?
at 2 years of age, where it remains fixed at 25%
34
REM remains fixed ~25% over one's lifetime, but what decreases over adult life? Increases?
Decreases: amount of slow-wave activity. Increases: stage 1 sleep (N1)
35
What is one explanation as to why the elderly suffers from a plethora of sleep problems?
elderly makes less melatonin (or their melatonin receptors may be diminishing)
36
What regulates circadian rhythms? (2)
1) internal biological factors (biological clock), 2) external cues (Zeitgebers) light vs night
37
What 3 main bodily functions have circadian rhythms?
1) hormones (higher cortisol secretion in the MA), 2) body temperature, 3) cardiovascular system, etc
38
What is entrainment? Free-running?
ENTRAINMENT: adjustment of cycles to compensate for differences between intrinsic period and environmental cycles (day/night), such that rhythms occur at correct daily phases. FREE-RUNNING: persistance of rhythms during constant conditions (ie constant light or constant dark)
39
What is photic entrainment?
light entrains the circadian rhythm within various limits and according to specific patterns
40
What happens if light is presented near the initiation of the "dark cycle" activity (ie temperature nadir)? Near the conclusion?
Near initiation: phase delay. Near conclusion: phase advance.
41
What happens if light is presented during the typical "light cycle" activity?
nothing
42
What is the primary clock mechanism in humans?
suprachiasmatic nucleus of the hypothalamus
43
What happens if you ablate the SCN? Isolate? Stimulate?
ABLATE: loss of rhythmicity (loss of body clock). ISOLATE: autorhythmicity. STIMULATE: phase shifting
44
How does light stimulate the SCN?
light goes from the retina to the SCN via the retinothalamic tract
45
What is the pathway that induces the pineal gland to secrete melatonin?
DARKNESS > retina > SCN > Hypothalamus > Pineal gland > SCN > Basal forebrain (PPT) and Dorsal raphe (serotonin)
46
What is melatonin?
"hormone of darkness". Released by the pineal gland in response to darkness, binds to receptors on the SCN to reinforce the dark signal
47
How does melatonin secretion change with age?
decreases
48
What is the purpose of giving melatonin as a therapy to those who have trouble sleeping?
melatonin will advance the sleep stage (remember it is the hormone of darkness)
49
What is delayed vs. advanced sleep phase?
delayed: where you can't sleep. Advanced: sleep earlier than desired
50
What is the etiologies of delayed sleep phase? (4)
1) alterations in the endogenous circadian system, 2) Zeitgebergers (bright light in the evening, lack of exposure to morning light), 3) behavioral preference, 4) psychopathology/depression
51
How do you treat delayed sleep phase? (3)
1) chronotherapy/time therapy (progressive 3-hour delay to correct schedule) 2) phototherapy (bright light treatment), 3) melatonin
52
What is advanced sleep phase?
when you experience sleepiness earlier than desired
53
How do you treat advanced sleep phase?
phototherapy/melatonin
54
What is Process S vs Process C in terms of sleep regulation?
Process S: adenosine-driven - the longer you've been awake, the more tired you become due to adenosine accumulation Process C: circadian clock-driven - helps us to stay awake at the end of the day (purpose is to allow one to consolidate sleep and wake periods)
55
How does Process S vs Process C change during the day?
Both Process S (adenosine) and Process C (circadian) INCREASE. Process S increase (adenosine) due to continual use of ATP for energy and Process C increase to help us stay awake at the end of the day so that we can consolidate sleep at night
56
What is adenosine?
homeostatic regulator of sleep. Increases during the wake cycle. Inhibits "wake-active" ACh neurons in the basal forebrain, thus promoting sleepiness
57
What antagonizes Process S (adenosine)?
caffeineeeeeeeeeeeeee :)
58
Where is NE released?
locus ceruleus
59
Where is Serotonin (5HT) released?
dorsal raphe
60
Where is ACh released? (2)
PPT/LDT (brainstem), basal forebrain
61
Where is Histamine released?
hypothalamus (tubero-mammillary nucleus)
62
Where is Adenosine released?
basal forebrain, hypothalamus
63
Where is Orexin/hypocretin released?
hypothalamus
64
Where is Dopamine released?
brainstem/hypothalamus
65
What is the ARAS?
Ascending Reticular Activating System (ARAS) projects to thalamus, lateral hypothalamus, basal forebrain, and diffusely throughout the cerebral cortex and produces desynchronization of cortical neurons to promote WAKEFULNESS
66
What components and hormones of ARAS are active during wake?
ACH (LDT, PPT), NE (Locus ceruleus), 5HT (dorsal raphe), Histamine (Tuberomammillary nucleus) PLLDT
67
Why does anti-histamines make you tired?
because histamines, secreted from the tuberomamillary nucleus (TMN), are active during wake
68
What hormone is deficient in narcolepsy?
orexin/hypocretin
69
What are the functions of orexin/hypocretin?
promote wake-active state by sending projections to ARAS and prevent unwanted transitions to sleep
70
What area of the brain is active during Non-REM sleep generation?
Ventrolateral preoptic area (VLPO).
71
What is the function of ventrolateral preoptic area (VLPO)? (4)
promotes sleepiness/sleep ONSET in the Non-REM sleep by: 1) reducing ARAS activity, 2) block sensory input to thalamus, 3) produce spindle activity to the reticular thalamic nuclei, 4) slow wave production at the thalamus/cortex
72
What inhibits VLPO? What is the net effect of this inhibition?
activity in the arousal systems inhibit the VLPO, which relieves its suppression of arousal centers and orexin neurons
73
When does the VLPO system become active? What is the net effect of this activity?
during sleep (when the homeostatic drive for sleep accumulates and reaches a tipping point), VLPO become active and inhibits the tuberomammillary nucleus, locus cereulus, and raphe nuclei to promote sleepiness/sleep ONSET
74
During REM sleep generation, which areas of the brain increases its activity? Which areas decreases its activity?
DECREASES: Locus ceruleus (NE), TMN (histamine), raphe nucleus (5HT). INCREASES: LDT, PPT (ACh)
75
How does the activity in the LDT/PPT (in the pons) during REM sleep cause in visual dreams?
LDT/PPT connects to 1) lateral geniculate (which connects to the occpital/visual cortex), 2) oculomotor nuclei (for eye movement), 3) spinal cord (for motor inhibition, so we don't act out our dreams)
76
What are wake-active neurotransmitters and substances?
WAKE-ACTIVE: Hypocretin/orexin, histamine, ACh, NE, dopamine, serotoin. (HHANDS SLEEP-PROMOTING: GABA, adenosine, endorphins, cholecystokinin (CAGE)
77
What is the purpose of Non-REM sleep? REM sleep?
Non-REM: restoration of physiological functions and hormones, tissue repair, energy conservation. REM: learning and memory, CNS development and maintenance, restoration of NE transmitter function
78
how does sleep deprivation affect functional performance?
negatively affects functional performance (speed, accuracy) due to REM deprivation