Basic Sleep Science Flashcards

1
Q

What are the 5 theories of why we sleep, according to Deepak Shrivastava?

A
  1. Memory consolidation
  2. Energy conservation
  3. Brain restoration
  4. Protective behavioral adaptation
  5. Immune function regulation
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2
Q

What is the theory of memory consolidation as a reason for sleep?

A

Information acquired during the day is stored in the short-term memory and is transferred to long-term memory during sleep.

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3
Q

What is the sleep theory of energy conservation and why has it been refuted?

A

Based on the premise that the brain needs to rest

Refuted - Studies have found that the brain does not rest during sleep, and during REM it can be as active or even more active than when awake

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4
Q

What is the sleep theory of brain restoration?

A

Plasticity of the brain is maintained because of sleep - this is the most prevalent theory today.

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5
Q

What is the sleep theory of protective behavioral adaptation and why has it been refuted?

A

Old-fashioned theory: before light bulb, we slept because it was dark - sleep protected us from what we couldn’t see in the dark (predators, etc.)

Refuted: we now know that all organisms, even plants, sleep.

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6
Q

What is the sleep theory of immune function regulation?

A

We know that stress (can be caused by sleep-deprivation, OSA, etc.) decreases efficiency of immune system

Mice - sleep deprived - lost fur, then ulcers, then died - immune cells were affected (leukocytes, etc.)

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7
Q

Why does OSA result in sleep-deprivation?

A

Because the apnea interrupts sleep so often.

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8
Q

Why does our body temperature drop at the time we should be falling asleep?

A

This is due to the increase in melatonin production.

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9
Q

What is the relationship between body temperature and sleep (2 things)?

A

Decreasing body temperature 1) helps us to fall asleep more easily and 2) increases the proportional amount of delta sleep (e.g. both of these happen when one takes a hot shower or bath right before bedtime).

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10
Q

Homeostatic drive of sleep is also known as __________.

A

Sleep load.

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11
Q

Describe the pattern of homeostatic drive/sleep load.

A

It is almost zero when we awaken (after a good night’s sleep) and grows throughout the day until it reaches very high levels (“unsustainable”) at bedtime and the need to sleep is very strong

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12
Q

What is the relationship between Circadian drive and homeostatic drive/sleep load?

A

Circadian drive 1) increases alertness so that the increasing sleep load is not overwhelming during the day - it increases in opposition to the sleep load; 2) it peaks shortly before bedtime (around 9:00) allowing the sleep load to be greatest after the Circadian drive has begun to diminish which allows us to fall asleep; 3) during sleep (night) the Circadian drive continues to diminish even though sleep load is diminishing, thereby allowing sleep to be maintained.

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13
Q

How long does it take for homeostatic drive to change?

A

Changes to homeostatic drive are immediate/day-to-day.

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14
Q

How long does it take for Circadian rhythm to change?

A

1 hour per day per time zone (i.e. 3 days to adjust to traveling from PST to EST).

Therefore, Circadian rhythm is responsible for jet lag, shift-work tiredness, etc.

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15
Q

What is the physiological reason for insomnia?

A

Insomnia is not a lack of tiredness (i.e. sleep load/homeostatic drive). With insomnia, the body is in a state of hyperarousal - unable to fall asleep given the opportunity.

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16
Q

What percentage of sleep should be REM?

A

About 20% (20-25%).

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17
Q

When are the two peaks in Circadian drive?

A

Mid-morning and late afternoon/early evening (around 5-6).

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18
Q

What are the characteristics of Stage 1 sleep?

A

It is the “state of drowsiness.” We still have some connection with/awareness of the environment.

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19
Q

What are the characteristics of Stage 2 sleep?

A

We are completely dissociated with our environment. Virtually no sensory awareness (can’t feel spouse’s hand, the sheets, etc.).

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20
Q

What are spindles and when do they occur?

A

Spindles are a hallmark of Stage 2 sleep. The nucleus of the thalamus is responsible for relaying sensory signals to the cortex. The cortex responds by sending a signal to the motor area of the brain. The thalamus holds the signals during Stage 2 sleep(no sensation or muscle response is the result). A threshold exists, and when it is reached a volley of all the signals are sent: called spindles. Rapid burst on EEG (8-13 cycles/second).

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21
Q

What is a K-complex?

A

When the burst of information is relayed from the thalamus to the cortex (spindle) in Stage 2 sleep, the cortex cannot respond to it. The K-complex is an event that is captured on the EEG that signifies that some activity occurs in the cortex in response to the spindle. It is another hallmark of Stage 2 sleep.

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22
Q

What proportion of sleep is Stage 2?

A

Almost 50%.

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23
Q

What are the synonyms for Stage N3 of sleep?

A

3-4/Delta/Deep/Slow-wave/Restorative. Stage 3 & 4 were combined by the AASM a few years ago into N3.

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24
Q

What are the characteristics of Stage N3 sleep?

A

The electrical impulse oscillates at 1.5 to 2 cycles per second - very slow electrical activity. The amplitude of the activity is high (75 mV or higher, called Delta waves in this frequency).

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25
Q

What percentage of sleep is Stage 1?

A

About 5%.

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26
Q

What proportion of healthy sleep is Stage N3?

A

About 20%.

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27
Q

What is the significance of Stage N3?

A

Stage N3 is the period of sleep that is necessary for a person to feel that they are well-rested, restored, “got a good night’s sleep.” Lack of N3 means the sleep load is not very much decreased by sleep. You still feel tired in spite of many hours of sleep.

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28
Q

What is the Alpha wave?

A

It is a slow wave (8-12 cycles/sec). As soon as we close our eyes the brain activity slows from 16-32 Hz to 8-12 Hz. Awake, but eyes closed = alpha waves.

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29
Q

What is a beta wave?

A

This is the wave during wakefulness - 16-32 Hz (although it can go faster).

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30
Q

What is the electrical activity during Stage 1?

A

Mixed frequency with low amplitude. Alpha predominates with a mixture of slower or higher frequencies. The frequency depends on what is happening in the environment (remember, the brain still engages with the environment in Stage 1). [47:00]

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31
Q

What is consistent and significant about the sleep pattern of people with chronic fatigue syndrome, chronic pain syndrome, and fibromyalgia?

A

The restorative/delta sleep is infiltrated by alpha waves. On the EEG, it is so consistent and identifiable that it is called alpha-delta [47:55].

32
Q

What is the arousal threshold like in Stage N3?

A

It is very high. Example: sleeping child in back of car, cannot wake them, they are very limp, you can change their clothes, etc., and they stay asleep and no recall of what happened, how they got there.

33
Q

How does the sleep pattern differ in someone who is sleep-deprived?

A

The early stages of sleep will be N3.

34
Q

When does the first REM cycle usually occur?

A

90-100 minutes into sleep. It is very short, sometimes as short as 30 seconds.

35
Q

Why is it important the first cycle of REM be detected on the PSG?

A

Because it is necessary to measure REM latency. REM latency can be affected by certain medical conditions, foods, or pharmaceuticals.

36
Q

How frequently do REM cycles occur in normal sleep?

A

90-100 minutes apart, beginning 90-100 minutes after falling asleep.

37
Q

How do the REM cycles change throughout the night?

A

They become progressively longer, beginning as short as 30 seconds and finishing as long as 60 minutes or more.

38
Q

What is the difference in the sleep stages in the first part of the night compared to the last part of the night?

A

Proportionally more N3 and very little REM in the first half. Proportionally more REM and Stage 2 in the second half, with little if any N3 in the second half.

39
Q

What is the typical patter of sleep stages in normal, healthy sleep?

A

1, 2, N3, 2, REM, 2, N3, 2, REM, etc. 1 always occurs after an awakening and the cycle then restarts. There is no 1 without an awakening (as shown on a hypnogram).

40
Q

How does normal sleep in the elderly differ from that in young adults?

A

The elderly have more fragmented sleep. The REM cycles are variable instead of proportionally getting longer. The total REM still remains about 20-25%. The elderly also have proportionally much less N3 sleep – there is very little N3 sleep. They still have Delta waves, but they are small enough that they are not measured or scored (the amplitude is less than 75mV so they cannot be measured).

41
Q

What happens to the upper airway (laryngeal) dilator muscles with normal, wakeful, unproblematic breathing?

A

The genioglossus is the major laryngeal dilator muscle.

They increase their tone coincident with inspiration, when awake or asleep. This prevents the collapse of the airway coincident with the decrease in pressure as the diaphragm contracts. The normal pressure of breathing results in -8 to -10 mmHg. In the absence of this increased tone, the airway collapses (OSA).

42
Q

What happens to the upper airway (laryngeal) dilator muscles with the onset of sleep?

What are the outcomes because of this (e.g. proportional changes of airflow)?

A

There is a reduction in the activity of these muscles – i.e. there is a reduction in tone to counter the airway collapse. In those with OSA, the reduction is much more significant than in those without. We do not at this time know why.

The airway becomes narrower and airflow is exponentially reduced (squared, because A=pi*rsquared) – so, if the airway diameter is reduced by half, resistance is quadrupled.

43
Q

What happens to pCO2 during normal, healthy sleep?

When is this significant?

A

Increases by 2-8 mm Hg. This is an insignificant rise in CO2 for a healthy adult.

COPD: can cause respiratory failure

44
Q

What happens to pO2 levels in normal sleep?

A

Decreases by 3-19 mm Hg. A healthy adult has enough reserve that this is inconsequential.

COPD or other disorders resulting in borderline oxygen levels: can cause respiratory failure.

45
Q

What happens to SpO2 levels during normal, healthy sleep?

A

It drops by <2%.

46
Q

What is nocturnal dip? When does it occur?

A

Nocturnal dip is a decrease in BP of 10%, decrease of HR.

It occurs in NREM sleep.

47
Q

What happens to BP and HR in REM sleep? Why is this significant?

A

Both are fluctuant in REM sleep. This puts the CV system at risk if one has cardiopulmonary disease or other cardiac conditions.

48
Q

What happens to cardiac output during NREM sleep and why?

A

It decreases because the BP and HR decrease.

49
Q

What happens to bloodflow to the brain during NREM sleep?

What happens to brain bloodflow during REM sleep?

A

It decreases during NREM.

Some areas of the brain are as active as during the wakeful state during REM, therefore bloodflow increases during REM in those areas.

50
Q

What is the relationship between sleep and hormone levels?

A

Hormones are affected/controlled, without exception, by sleep.

51
Q

What is the relationship between prolactin and sleep?

A

If there is no sleep, there is no prolactin secretion.

52
Q

What is the relationship between sleep and cortisol (adrenal insufficiency)?

A

Cortisol is glycogenic and renders poor glycemic control in SA patients. It is very important to overall health: CV, stress levels, etc. It takes 3 weeks of poor sleep before cortisol levels are affected.

53
Q

What is the relationship between sleep and growth hormone levels?

A

GH is directly linked to N3 sleep. It is pulsatile, but if there is no N3 there is no GH production. It is responsible for growth of tissue in children and is important in adults for repair and body functions.

54
Q

Thyroid hormone and sleep.

A

TSH is inhibited by sleep. With sleep deprivation, more TSH, thyroid is overstimulated (thyroid burns out, hypothyroidism results). In endocrine clinic, many of the hypothyroid patients have OSA. However, not many OSA patients are not hypothyroid.

55
Q

Testosterone and sleep.

A

Testosterone increases with sleep. There are many studies that correlate impotence with SA. Men blame age, etc., but SA is a major confounder. It is also important for bone density and other things.

56
Q

What happens to our swallowing frequency when sleeping?

A

Swallowing frequency decreases when sleeping.

57
Q

What are the implications of slower gastric emptying and decreased swallowing on the airway?

A

Risk of aspiration is higher because GERD introduces more liquid into the esophagus which is not being swallowed with enough frequency. This is especially problematic in asthmatics as it can inflame the airway and render the asthma uncontrolled.

58
Q

How is gastric acid secretion related to the Circadian rhythm?

A

Gastric acid secretion is much higher in the late evening.

59
Q

How strong is the relationship between psychological disorders and sleep?

A

Almost 50% of psych disorders have a cross-relationship with sleep. Bi-directional.

60
Q

How many sleep disorders have been identified?

A

60 (over 100 if you count the subcategories).

61
Q

Wisconsin sleep study: prevalence of apnea in males and females.

A
Take home: 1 in 4
Males AHI >5: 1 in 4
Males AHI >15: 1 in 10
Females AHI >5: 1 in 10
Males AHI >15: 1 in 25
62
Q

Spain study prevalence of SA in males and females

A
Take home: 1 in 4
Male >5: 1 in 4
Male >15: 1 in 7
Female >5: 1 in 4
Female >15: 1 in 15
63
Q

How long does it take to recover sleep debt?

A

1-2 weeks to fully recover

64
Q

How much sleep do teens get on weekdays versus weekends when school is in session?

A

Weekdays: 7.8 hours
Weekends: 9.5

65
Q

How does sleep affect risk behaviors in youth?

A

CDC Youth Risk Survey
N= 12,154 students in grades 9-12 Sleep 8 hrs
• Used 1+ cigarettes daily 24% 15%
• Used alcohol in past 30 days 50% 37%
• Used marijuana in past 30 days 23% 16%
• Currently sexually active 39% 28%
• Felt sad or hopeless 31% 22%
PMID:18528314

66
Q

Has sleep deprivation been shown to be a causative factor with increased pain levels?

A

Yes.
Sleep deprivation causes:

a) Hyperalgesia
- Thermal sensitivity
- Mechanical sensitivity
b) Spontaneous pain (Haack, 2005, Smith 2007)

67
Q

What is the relationship between chronic pain and sleep loss?

A

Bi-directional

Affleck, 1996; Stone,1997

68
Q

Does poor sleep increase the odds of widespread pain?

A

Poor sleep increases odds of developing widespread pain (WP)
In general population [Gupta (2007)] —3 fold increased risk
In those with a regional pain disorder [Mikkelsson (1999)]

69
Q

Does improved sleep quality affect pain levels?

A

“Restorative sleep” linked to 3 fold remission rate from widespread pain [Davies(2008)]

70
Q

How does insomnia affect the likelihood of chronic pain after recovery from injuries?

A

Insomnia in hospital increases risk of chronic pain after burn injury [Smith, Pain (2008)

71
Q

How does poor sleep affect Diffuse Noxious Inhibitory Controls (the brain’s natural pain management system)?

A

Restricted sleep showed no effect

Sleep fragmentation impaired pain inhibitory processes

72
Q

What chronic conditions have been associated with DNIC? Remember, DNIC is impaired by fragmented sleep, but not by restricted sleep.

A
Fibromyalgia
TMD
IBS
Low back pain
Tension headache
73
Q

What are the three mechanisms by which sleep is postulated to increase hyperalgesia?

A

1) Descending opioidergic pain inhibitory pathways 2) impaired cognitive ability to reduce pain by distraction 3) Sleep restriction may heighten pain via enhancing inflammation

74
Q

Nasal obstruction is an independent risk factor for which sleep disorders?

A
Habitual snoring
Non-restorative sleep
Daytime sleepiness
OSA
CPAP non-acceptance/intolerance
Oral appliance failure
75
Q

What did Zeng find to be the only 2 predictors of OAT failure?

A

Nasal resistance and BMI only 2 predictors of treatment response
Non-responders also had significantly increased nasal resistance in supine position
(Zeng B et al. Influence of nasal resistance on oral appliance treatment outcome in obstructive sleep apnea. Sleep 2008; 31:543-7)

76
Q

When should DISE (drug-induced sleep endoscopy) be considered?

A
  1. Baseline preoperative evaluation – especially if concern for multilevel/complex pattern of obstruction
  2. Adjunct to stage I surgical therapy to better predict proper procedure selection for later stages
  3. Persistent symptoms/OSA after prior surgical therapy
  4. Persistent symptoms/OSA with oral appliance therapy
  5. Predict oral appliance therapy outcomes?