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Flashcards in Sleep Deck (51)
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1
Q

What does sleep polysomnography measure?

A

Brain activity EEG, eye movements EOG, muscle activity EMG, and heart activity ECG

2
Q

What does EEG measure?

A

Measures the potential differences between two points on the scalp

3
Q

Wakefulness EEG

A

Low amplitude fast rhythms

A relaxed subject with eyes closed is differentiated from sleep by the presence of alpha EEG activity in 50% or more of the time.

4
Q

Stage 1 EEG

A

Similar to wakefulness, very superficial, small eye movements, slow, slightly higher amplitude EEG.

Alpha activity 50% or less of the time

5
Q

Stage 2 EEG

A

Spindles and K complexes:

Characteristics include sleep spindles and K-complexes occurring on a low-voltage, mixed-frequency background EEG and minimal (<20% of the time) slow-wave activity.

6
Q

Stage 3 EEG

A

High amplitude slow waves

Contains delta EEG activity with a 75 µV or greater amplitude enduring for 20% or more of the duration

7
Q

REM EEG

A

Similar to wakefulness EEG, sensory disconnected from environment

Saccadic eye movements occur during epochs with low-voltage, mixed-frequency EEG in association with a very low level of EMG activity.

8
Q

Proportions spent in each sleep phase?

A

REM sleep accounts for approximately 20% to 25% of total sleep time, stage N2 accounts for 50%, N3 accounts for 12.5% to 20%, and N1 accounts for the remainder.

9
Q

Sleep oscillations

A

Rhythmic and/or repetitive electrical activity generated spontaneously and in response to stimuli by neural tissue in the central nervous system

10
Q

Slow waves divided into

A

Slow oscillation (0.2-1 Hz)
Delta (1-4 Hz)
Spindle (7-15 Hz
Theta (4-10 Hz)

11
Q

Three areas controlling sleep oscillations

A

Cortex, thalamus, reticular nucleus of thalamus

12
Q

Thalamus sends what signals to RTN and cortex

A

Glutaminergic

13
Q

Cortex sends what signals to RTN and thalamus

A

Glutaminergic

14
Q

Reticular neurons sends what signals to where

A

GABAergic inhibitory output to the thalamocortical neurons

15
Q

What is a sleep spindle

A

0.5-second (or longer) burst of 12- to 14-Hz activity

16
Q

What initiates spindles

A

Thalamic reticular nucleus and regulated by thalamo-reticular and thalamo-cortical circuits.

17
Q

What disorder leads to deficits in spindle activity?

A

Schizophrenia

18
Q

What diffuse subcortical neuromodulatory systems regulate global brain states

A
Cholinergic 
Adrenergic 
Histaminergic 
Dopamine 
Serotonin 
Orexin/Hypocretin
19
Q

Where are orexin neurons

A

Lateral nucleus of the hypothalamus

20
Q

Cholinergic nuclei are located?

A

Lateral dorsal tegmentum and posterior pontine tegmentum

Basal forebrain

21
Q

Cholinergic neuron effect on arousal

A

Maintain awake state

22
Q

Monoaminergic nuclei that project to forebrain include

A

Noradrenergic locus coeruleus, histaminergic neurons in the TMN, serotoninergic neurons in the median raphe nuclei, dopaminergic neurons in the vPAG and VTA

23
Q

Monoaminergic in wakefulness

A

Fire during wakefulness

24
Q

Monoaminergic neuron in sleep and REM sleep

A

Decrease activity during non-REM sleep, and silent during REM sleep

25
Q

Noradrenergic neurons in

A

Locus coeruleus

26
Q

Histaminergic neurons in

A

TMN

27
Q

Serotoninergic neurons in

A

Median raphe nuclei

28
Q

Dopaminergic neurons in the

A

VTA and vPAG

29
Q

Phenelzine can

A

Eliminate REM sleep

30
Q

When do Orexin neurons fire

A

Fire predominantly during wakefulness, and particularly during motivated behaviours

31
Q

Orexin neurons inhibited by

A

Glucose, (activated when glucose is low)

32
Q

Orexin destruction leads to

A

Narcolepsy

33
Q

What is the sleep promoting area

A

VLPO (ventral lateral preoptic nucleus)

34
Q

What is the wake promoting area

A

TMN (histamine), LC (noradrenaline), LH (orexin), VTA (dopamine)

35
Q

How do wake promoting and sleep promoting areas communicate?

A

Inhibitory connections

36
Q

Sleep promoting neurons are

A

GABAergic neurons in preoptic hypothalamus

37
Q

Why do benzodiazepines make you sleepy?

A

Potentiate GABA (preoptic sleep promoting area)

38
Q

How is REM sleep controlled?

A

REM-on cells and REM-off cells

39
Q

What is a circadian rhythm?

A

Natural, internal process that regulates the sleep–wake cycle and repeats on each rotation of the Earth roughly every 24 hours.

Any biological process that displays an endogenous, entrainable oscillation of about 24 hours.

40
Q

Master circadian clock is?

A

SCN

41
Q

SCN input

A

Light information by a direct retinohypothalamic tract (RHT) to entrain the clock to the 24-h day.

42
Q

What is a zeitgeber?

A

Cue in the regulation of the body’s circadian rhythms.

43
Q

What regulates the timing of melatonin synthesis?

A

The SCN clock

44
Q

Where is melatonin released from?

A

Pineal

45
Q

When is melatonin secreted?

A

At night

46
Q

What does it mean to be able to synchronise and reset biological oscillations?

A

Chronobiotic effects

47
Q

Responsiveness of SCN neurons to melatonin is greatest

A

Around subjective dusk

48
Q

Role of melatonin

A

Chronobiotic, feedback to SCN clock

49
Q

Sleep after sleep deprivation is

A

Deeper, not necessarily longer

50
Q

Elderly sleep

A

Advanced sleep timing (i.e. earlier bedtimes and rise times)

Longer sleep-onset latency (i.e longer time taken to fall asleep)

Shorter overall sleep duration

Increased sleep fragmentation (i.e. less consolidated sleep with more awakenings, arousals, or transitions to lighter sleep stages)

More fragile sleep (i.e. higher likelihood of being woken by external sensory stimuli)

Reduced amount of deeper NREM sleep known as slow wave sleep (SWS), increased time spent in lighter NREM stages 1 and 2, shorter and fewer NREM-REM sleep cycles, increased time spent awake throughout the night.

51
Q

Consequences of sleep deprivation

A

Decreased alertness

Increased attentional lapses

Decreased hand-eye coordination

Decreased attention and sustained vigilance

Decreased olfactory discrimination

Impaired verbal learning, deficit in temporal memory, impairment in working memory

Reduced verbal fluency

Reduced capacity to modify behaviour rapidly and flexibly to changing demands

Reduced inhibitory control

Impaired capacity to integrate emotional cues into the decision-making process, impaired judgement.