Ch 19: Sleep-Wake Disorders

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182 Terms

1
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What is the major consequence of acute or chronic sleep reduction?

excessive sleepiness, which can impact social/work functioning and increase accident/injury risk

2
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What causes sleep restriction?

shift work, sleep disorders, medications, alcohol/substance use, and medical or psychiatric disorders

3
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Define sleep deprivation.

Discrepancy between hours of sleep obtained and required for optimal functioning, accompanied by impaired functioning.

4
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Why is comprehensive sleep evaluation important in mental health disorders?

Chronic sleep deprivation can mimic psychiatric symptoms, leading to misdiagnosis or inappropriate medication changes.

5
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Give an example of sleep loss mimicking psychiatric symptoms.

A patient with psychosis may have increased hallucinations from poor sleep, but the cause could be unstable housing rather than medication need.

6
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List short-term consequences of sleep disruption

Increased stress responsivity, somatic pain, reduced quality of life, emotional distress, mood disorders, cognitive/memory/performance deficits.

7
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List long-term consequences of sleep disruption in healthy individuals.

Cardiovascular disease, weight-related issues, metabolic syndrome, type 2 diabetes, colorectal cancer, increased all-cause mortality.

8
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How does sleep deprivation affect children and adolescents differently?

Children: behavioral problems, impaired cognition.
Adolescents: emotional/social issues, poor school performance, risk-taking behaviors.

9
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How does sleep loss contribute to diabetes and obesity?

alters glucose metabolism, decreases energy expenditure, increases appetite via leptin and ghrelin dysregulation.

10
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How is sleep deprivation comparable to alcohol intoxication?

17–19+ hours awake produces psychomotor deficits equal to BACs of 0.05%–0.1%.

11
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What is microsleep?

Brief episodes (1–10 sec) of sleep during wakefulness, causing reduced performance and increased error risk.

12
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why is consistency in sleep timing important?

regular bedtime/wake-up schedules support health; irregular sleep timing is linked to negative metabolic changes

13
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What are metabolic consequences of irregular sleep patterns?

Lower HDL cholesterol, higher waist circumference, increased BP, higher total triglycerides, and fasting glucose.

14
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How is “too much sleep” defined in adults?

sleeping more than 9 hours per night

15
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How is childhood obesity linked to excessive sleep?

long sleep duration may impair metabolism and increase obesity risk

16
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How does sleeping ≥10 hours affect adult health?

Increases risk for metabolic syndrome (abdominal fat, hypertension, low HDL, high glucose, high triglycerides).

17
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What non-metabolic issues are linked to excessive sleep?

depression, headaches, and increased mortality from medical conditions

18
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What conditions can cause excessive sleep?

sleep apnea, restless leg syndrome, bruxism, pain, narcolepsy, hypersomnolence

19
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How is sleep defined behaviorally?

Low or absent motor activity, reduced response to environmental stimuli, and closed eyes.

20
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How is sleep measured neurophysiologically?

with an EEG, which identifies brain wave patterns, eye movements, and muscle tone

21
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What are the two main physiological states of sleep?

Non–rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep.

22
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what percentage of total sleep time in Stage 1 (N1) and what are its features?

2–5% of total sleep time; brief transition from wakefulness to sleep, reduced body temp, muscle relaxation, slow rolling eye movements, easily aroused.

23
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What is sleep latency?

The time it takes to fall asleep.

24
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What percentage of total sleep time is Stage 2 (N2) and what are its features?

45–55%; HR and RR decline, harder to arouse than in Stage 1.

25
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What percentage of total sleep time is Stage 3 (N3) and what are its features?

13–23%; slow wave/delta sleep, reduced HR, RR, BP, low responsiveness, restorative sleep with reduced sympathetic activity.

26
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What percentage of total sleep is NREM sleep overall?

75–80%.

27
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What percentage of total sleep is REM sleep and what are its characteristics?

20–25%; muscle atonia, bursts of REM, myoclonic twitches, dreaming, autonomic variability.

28
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Why is muscle atonia in REM sleep important?

It prevents the physical acting out of dreams and nightmares.

29
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How does NREM and REM alternate during the night?

Four to six cycles of NREM and REM occur over 90–120-minute intervals.

30
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When does the shortest REM period occur, and how long does it last?

60–90 minutes after sleep onset; lasts a few minutes.

31
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What is sleep architecture?

The structural organization of NREM and REM sleep, often shown on a hypnogram.

32
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What is sleep fragmentation?

Disruption of sleep stages with excessive stage 1 sleep, multiple arousals, and frequent stage shifts.

33
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What psychiatric changes are linked to altered sleep cycles in depression?

Reduced latency to REM sleep and decreased percentage of slow wave sleep.

34
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What is unusual about sleep onset in narcolepsy?

Patients often enter sleep directly into REM rather than NREM.

35
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How do benzodiazepines and antidepressants affect sleep stages?

Benzodiazepines suppress slow wave sleep; serotonergic antidepressants suppress REM sleep.

36
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What are the two processes that regulate sleep and wakefulness?

homeostatic process (sleep drive) and circadian process (wake drive)

37
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What determines the strength of the homeostatic sleep drive?

Number of hours awake; longer wakefulness → stronger sleep drive

38
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What are circadian drives and what influences them?

near-24-hour cycles promoting wakefulness, influenced by endogenous rhythms and environmental cues

39
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Name the wake-promoting neurotransmitters.

Dopamine, norepinephrine, serotonin, acetylcholine, histamine, glutamate, hypocretin/orexin.

40
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Name the sleep-promoting neurotransmitters.

adenosine, GABA, galanin

41
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How much sleep do most adults require?

7-8 hours for optimal functioning

42
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When is sleep testing typically indicated?

when a patient has sleep disturbances or excessive sleepiness that impairs social and vocational functioning

43
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What is the most common diagnostic procedure for sleep disorders?

polysomnography

44
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What does polysomnography diagnose and evaluate?

sleep-related breathing disorders and nocturnal seizure disorders

45
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How is polysomnography performed?

One or two nights in a sleep lab with electrodes and monitors on the head, chest, and legs; records brain waves, eye movement, muscle tone, heart rhythm, and breathing.

46
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What is the multiple sleep latency test (MSLT) used for?

To objectively measure daytime sleepiness in a sleep-conducive setting.

47
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When is MSLT typically performed?

The day after a polysomnography evaluation, especially if narcolepsy is suspected.

48
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What does the maintenance of wakefulness test (MWT) evaluate?

the patient’s ability to remain awake in a situation conducive to sleep

49
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For what professions is the MWT especially important?

Jobs where sleepiness poses a public safety risk, such as airline pilots.

50
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What is actigraphy?

A wristwatch-type tracker that records body movement over time to assess sleep patterns and duration.

51
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For which conditions is actigraphy most useful?

circadian rhythm disorders and insomnia

52
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How is insomnia disorder defined?

Dissatisfaction with the quantity or quality of sleep

53
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What percentage of adults may be affected by insomnia?

up to 45% of adults

54
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Which groups are more frequently affected by insomnia?

females and older adults

55
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What assessment model is recommended for understanding causes of insomnia?

Spielman’s 3P model of insomnia

56
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What are the three factors in Spielman’s 3P model?

Predisposing, precipitating, and perpetuating factors

57
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What are predisposing factors in insomnia?

Individual factors creating vulnerability, such as prior poor-quality sleep, history of depression/anxiety, hyperarousal, being a light sleeper, or a night owl

58
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What are precipitating factors in insomnia?

External events that trigger insomnia, such as personal/vocational difficulties, medical/psychiatric disorders, grief, and role changes (e.g., retirement).

59
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What are perpetuating factors in insomnia?

Behaviors or attributes that maintain insomnia, such as excessive caffeine/alcohol use, spending too much time in bed, frequent napping, and worrying about insomnia’s consequences.

60
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What is the core complaint required for a DSM-5 diagnosis of insomnia disorder?

A predominant complaint of dissatisfaction with sleep quantity or quality.

61
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What symptoms can the dissatisfaction with sleep involve (DSM-5 Insomnia Disorder Criterion A)

  • Difficulty initiating sleep (children: without caregiver intervention).

  • Difficulty maintaining sleep (frequent awakenings or trouble returning to sleep; children: without caregiver intervention).

  • Early-morning awakening with inability to return to sleep.

62
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What functional impact is required for DSM-5 insomnia disorder?

Sleep disturbance causes clinically significant distress or impairment in social, occupational, educational, academic, behavioral, or other important areas of functioning.

63
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How often must sleep difficulties occur for a DSM-5 insomnia disorder diagnosis?

At least three nights per week.

64
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How long must symptoms persist for DSM-5 insomnia disorder?

at least 3 months

65
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What condition regarding sleep opportunity is required for DSM-5 insomnia disorder?

sleep difficulty occurs despite adequate opportunity for sleep

66
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How does DSM-5 insomnia disorder rule out other primary sleep disorders?

The insomnia is not better explained by, and does not occur exclusively during, another sleep-wake disorder (e.g., narcolepsy, breathing-related sleep disorder, circadian rhythm sleep-wake disorder, parasomnia).

67
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How does DSM-5 insomnia disorder rule out substances as a cause?

The insomnia is not attributable to the physiological effects of a substance (e.g., drug of abuse, medication)

68
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How does DSM-5 insomnia disorder rule out mental or medical disorders?

coexisting mental disorders and medical conditions do not adequately explain the insomnia complaint

69
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What are the DSM-5 specifiers for insomnia disorder?

  • With nonsleep disorder mental comorbidity (including substance use disorders)

  • With other medical comorbidity

  • With other sleep disorder

70
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What are the primary non-pharmacological interventions for insomnia disorder?

  • Improving sleep hygiene

  • Shutting off electronics before bed

  • Avoiding exercise and meals immediately prior to sleep

  • Practicing relaxation techniques

  • Cognitive behavioral therapy (CBT)

  • CBT-I (specialized CBT for insomnia)

71
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Why is CBT-I recommended for insomnia?

CBT-I addresses the thoughts, behaviors, and habits that contribute to insomnia, providing a long-term solution without reliance on medication.

72
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What are common pharmacological interventions for insomnia disorder?

  • Antihistamines

  • Sedative-hypnotics (short-term use)

    • Zolpidem tartrate

    • Eszopiclone

    • Zaleplon

  • Melatonin

  • Melatonin agonist (ramelteon)

73
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Why are sedative-hypnotics recommended only for short-term use in insomnia?

To avoid tolerance, dependence, and potential side effects such as daytime sedation and cognitive impairment.

74
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What is hypersomnolence disorder?

A chronic sleep disorder (≥3 months) characterized by excessive daytime sleepiness despite adequate or prolonged nighttime sleep

75
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When does hypersomnolence disorder typically begin?

Young adulthood.

76
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Key symptoms of hypersomnolence disorder?

  • Recurrent periods of sleep or unintended lapses into sleep

  • Frequent napping

  • Prolonged main sleep (>9 hours)

  • Nonrefreshing, nonrestorative sleep

  • Difficulty achieving full alertness during wake periods

77
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How does hypersomnolence disorder affect functioning?

Causes significant impairment in social/vocational functioning, reduces enjoyment of relationships, decreases workplace productivity, increases cognitive impairment, and raises risk of accidents or injury

78
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Nonpharmacological treatment for hypersomnolence disorder?

Maintain a regular sleep-wake schedule with ample sleep opportunity (some benefit from 10+ hours).

79
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Pharmacological treatment for hypersomnolence disorder?

  • Long-acting amphetamine-based stimulants (e.g., methylphenidate)

  • Nonamphetamine-based stimulants (e.g., modafinil [Provigil])

80
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What is narcolepsy?

A rare sleep disorder (<0.05% prevalence) characterized by an uncontrollable urge to sleep, typically starting before young adulthood and persisting for life.

81
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Is narcolepsy more common in men or women?

Slightly more common in men.

82
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Key symptoms of narcolepsy?

  • Disturbed nighttime sleep with multiple awakenings

  • Automatic behaviors with memory lapses

  • Feeling refreshed upon waking but sleepy again in 2–3 hours

  • Hypocretin deficiency in cerebrospinal fluid (objective marker)

83
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How does narcolepsy differ from other hypersomnia disorders?

narcolepsy patients feel rested after sleep; other hypersomnia disorders do not

84
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What is cataplexy?

Brief episodes of bilateral muscle weakness without loss of consciousness, often triggered by strong emotions (e.g., laughter, anger, fear, joy).

85
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What causes cataplexy?

Likely due to REM sleep paralysis occurring during wakefulness.

86
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Other classic symptoms of narcolepsy besides cataplexy?

  • Hypnagogic hallucinations: false sensory perceptions at sleep onset.

  • Sleep paralysis: inability to move or speak during sleep–wake transitions.

87
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Nonpharmacological treatments for narcolepsy?

scheduled naps, exercise, and a balanced diet

88
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FDA-approved stimulant medications for excessive daytime sleepiness in narcolepsy?

Modafinil, armodafinil, methylphenidate, amphetamine.

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Nonstimulant medications for narcolepsy-related daytime sleepiness?

  • Pitolisant (Wakix): histamine-3 receptor antagonist/inverse agonist; side effects—insomnia, nausea, anxiety.

  • Solriamfetol (Sunosi): dopamine & norepinephrine reuptake inhibitor; contraindicated with MAOIs; monitor BP & HR.

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FDA-approved medication for both excessive daytime sleepiness and cataplexy in patients ≥7 years old?

Sodium oxybate (Xyrem).

91
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How does sodium oxybate help in narcolepsy?

restores normal sleep architecture at night, improving daytime alertness

92
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Off-label medications for cataplexy?

certain SSRIs and TCA, which may suppress REM sleep paralysis

93
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What is the most common breathing-related sleep disorder?

Obstructive sleep apnea hypopnea syndrome.

94
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Which gender is more affected by obstructive sleep apnea hypopnea syndrome?

Men

95
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What condition is strongly associated with obstructive sleep apnea?

obesity

96
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What causes obstructive sleep apnea hypopnea syndrome?

repeated episodes of upper airway collapse and obstruction, leading to sleep fragmentation

97
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Why can’t patients with obstructive sleep apnea sleep and breathe at the same time?

airway obstruction prevents breathing during sleep, causing repeated awakenings

98
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What are the hallmark symptoms of obstructive sleep apnea?

loud disruptive snoring, witnessed apnea episodes, and excessive daytime sleepiness

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How is obstructive sleep apnea diagnosed?

clinical evaluation and polysomnography

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What is the primary treatment for obstructive sleep apnea?

Continuous positive airway pressure (CPAP) therapy.