Module 5 - Disorders of Sleep/Wake Cycles Flashcards

1
Q

What is the modern definition of insomnia?

A

A perceived difficulty with sleep initiation, maintenance, consolidation, duration, or quality despite adequate opportunity, causing daytime impairment at least 3x/week for at least 3 months (ISCD-3).

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2
Q

How does the modern definition of insomnia differ from the literal Latin meaning?

A

The Latin root means ‘complete absence of sleep’ but insomnia today refers to reduced sleep due to inability to obtain desired sleep.

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3
Q

What circadian disorders can mimic insomnia?

A

Delayed sleep phase syndrome (trouble falling asleep) and advanced sleep phase syndrome (early morning waking).

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4
Q

How can sleep-disordered breathing be mistaken for insomnia?

A

Frequent arousals due to apnoea may be interpreted as insomnia despite the person being asleep.

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5
Q

What is the estimated worldwide prevalence of transient insomnia?

A

30–35%, with a median duration of 3 years and 56–74% having persistent symptoms after 1 year.

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6
Q

What are the three stages of insomnia and their contributing factors?

A

Predisposing (e.g., family history), precipitating (e.g., stress), and perpetuating (e.g., staying in bed longer, worry).

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7
Q

How does thought and emotional response influence insomnia?

A

Hyperarousal, worry, and emotional overreaction can maintain insomnia even if sleep is occurring.

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8
Q

What is the difference between fatigue and sleepiness?

A

Fatigue is exhaustion without sleep drive; sleepiness involves a strong tendency to fall asleep.

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9
Q

What are the PSG findings often associated with insomnia?

A

Longer sleep onset latency (SOL), reduced total sleep time (TST), increased awakenings, and reduced sleep efficiency.

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10
Q

How does insomnia relate to depression?

A

Insomnia can precede, predict, or contribute to depression. Treating insomnia improves depression outcomes.

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11
Q

What did the HUNT study find about insomnia and depression risk?

A

Untreated insomnia predicted depression with an OR of 6.1; depression predicted later insomnia with an OR of 5.

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12
Q

How is insomnia linked to anxiety?

A

Insomnia is common with anxiety, which is associated with nonrestorative sleep and increased nocturnal arousal.

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13
Q

What hormonal markers are elevated in insomnia?

A

Cortisol and ACTH are elevated, suggesting heightened physiological arousal.

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14
Q

What behavioural strategies help manage insomnia?

A

Same wake time, light exposure, wind-down routines, avoiding stimulating activities and substances before bed.

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15
Q

How do caffeine, alcohol, and food influence sleep?

A

Caffeine delays sleep; alcohol disrupts second-half sleep; large or protein-heavy meals can impair sleep.

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16
Q

What is stimulus control therapy (QHR)?

A

If not asleep in 15 mins, get out of bed. Return only when drowsy. Avoid stimulation while out of bed.

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17
Q

What is paradoxical intention therapy?

A

Trying to stay awake rather than fall asleep, reducing performance anxiety about sleep.

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18
Q

What is bed restriction therapy and how is sleep efficiency calculated?

A

Limit time in bed to match sleep time (minimum 5 hrs). Sleep efficiency = time asleep / time in bed * 100.

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19
Q

What is sleep misperception?

A

Underestimation of total sleep time; difficulty distinguishing light sleep from wakefulness.

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20
Q

What are key diagnostic criteria for insomnia (DSM-5 and ICSD-3)?

A

Difficulty initiating/maintaining sleep or early waking, 3x/week for ≥3 months, with daytime impact and adequate opportunity.

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21
Q

What are common subjective features of insomnia?

A

A persistent difficulty in falling asleep, staying asleep, early waking, or nonrestorative sleep despite adequate opportunity, often lasting ≥30 minutes.

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22
Q

What are typical PSG findings in insomnia?

A

Longer sleep onset latency, reduced total sleep time, more awakenings, reduced sleep efficiency, increased stage 1 sleep.

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23
Q

How does insomnia affect subjective vs. objective performance?

A

Objectively may perform similarly, but subjectively feel worse; more mental effort required.

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24
Q

What did Altena et al. (2008) find in elderly insomniacs?

A

They performed better on simple reaction time but worse on vigilance; cognitive behavioural therapy (CBT) reversed these effects.

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25
Q

What is the relationship between fatigue and sleepiness?

A

Fatigue is exhaustion without sleep drive; sleepiness is a drive to sleep. Sleepy insomniacs should be evaluated for OSA, depression, or circadian disorders.

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26
Q

What EEG changes occur during sleep in insomniacs?

A

Hyperactive amygdala firing during sleep; less frontal cortex activation in SWS; emotional responses may be exaggerated.

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27
Q

How was insomnia historically viewed in relation to depression?

A

Previously seen as just a symptom; now known to be a predictive and treatable factor for depression onset and recurrence.

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28
Q

What did the HUNT study show about insomnia and depression?

A

Untreated insomnia increased risk of future depression (OR 6.1); prior depression increased risk of future insomnia (OR 5).

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29
Q

How does anxiety contribute to insomnia?

A

Leads to nonrestorative sleep, increased nocturnal arousal, and sleep anxiety. Most frequently associated mental disorder.

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30
Q

What are PSG changes seen in anxious insomniacs?

A

Increased stage 2 sleep, increased awakenings, reduced TST and sleep efficiency, minor REM reduction.

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31
Q

What hormonal and neuroimaging findings support hyperarousal in insomnia?

A

Elevated cortisol and ACTH; functional imaging shows persistent alertness suggesting incomplete flip-flop switch deactivation.

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32
Q

What cognitive factors maintain chronic insomnia?

A

Worry about sleep, hypervigilance, distorted sleep perception, and unhelpful beliefs about sleep needs or consequences.

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33
Q

How does CBT for insomnia address behaviour and cognition?

A

Targets unhelpful behaviours first, then thinking patterns, then mood; behaviour improves quickly, cognition catches up over time.

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34
Q

What are examples of unhelpful pre-bed behaviours?

A

Exercise, stimulating conversations, screen use, caffeine, nicotine, alcohol, large or protein-rich meals before bed.

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35
Q

How does caffeine affect sleep?

A

Delays sleep onset and disrupts sleep quality; takes up to 8 hours to be cleared from the body.

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36
Q

What are the effects of alcohol on sleep?

A

Helps with sleep onset initially, but disrupts second half of sleep with more REM and lighter sleep; also dehydrating.

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37
Q

How can food before bed impact sleep?

A

Large meals cause discomfort and circadian disruption; proteins increase alertness. A small snack is best if hungry before bed.

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38
Q

What is the “stages of change” model in insomnia treatment?

A

Recognises readiness for change varies; interventions should be matched to current stage (e.g., precontemplation, contemplation, action).

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39
Q

What is actigraphy and how is it used in insomnia assessment?

A

Actigraphy involves using wrist-worn accelerometers to estimate sleep-wake patterns. It is especially useful in populations who can’t complete sleep diaries or self-report, like children or cognitively impaired individuals.

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40
Q

How does actigraphy compare with PSG in assessing insomnia?

A

Actigraphy is less accurate in detecting sleep stages but provides reliable long-term behavioral data. It doesn’t assess sleep architecture.

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41
Q

What are limitations of actigraphy?

A

Different scoring algorithms across devices, lower accuracy with more nighttime wakefulness, and inability to assess sleep architecture.

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42
Q

How are consumer sleep devices used in insomnia?

A

They track sleep via wearables (e.g., Fitbit, Oura) or nonwearables (e.g., Beddit), offering convenience but limited clinical accuracy.

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43
Q

What are the limitations of consumer sleep trackers in clinical use?

A

Poor validation, small studies, and limited reliability. They may provoke anxiety and are not a substitute for PSG or FDA-approved actigraphy.

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44
Q

How does clinical setting impact insomnia assessment?

A

Primary care may focus on quick diagnosis and medication, while sleep clinics offer comprehensive evaluation with possible PSG.

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45
Q

What is the value of interdisciplinary insomnia care?

A

Combines physical and psychological expertise — physicians assess medical contributors, while psychologists explore cognitive-behavioural factors.

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46
Q

How can bed partner input aid in insomnia assessment?

A

They can report on symptom frequency, severity, and screen for SRBD, PLMD, or parasomnias.

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47
Q

Which populations are at greater risk for insomnia?

A

Women (especially pregnant), older adults, people with lower income, those unemployed or with disability, and certain ethnic groups.

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48
Q

What are objective short sleep duration phenotypes in insomnia?

A

Patients with objectively short sleep (via PSG/actigraphy) may have greater physiological arousal, comorbidities, and worse prognosis.

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49
Q

How might wearable EEGs support future insomnia research?

A

They allow multi-night home monitoring, aiding phenotype identification and personalised treatment planning.

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50
Q

What are examples of insomnia phenotypes from data-driven clustering?

A

High subjective wakefulness, mild insomnia, insomnia-related distress, highly distressed, reward-sensitive, and high/low reactivity groups.

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51
Q

What is the prevalence of chronic insomnia in Australia?

A

12.2% (DSM-5) and 14.8% (ICSD-3), with only 7.5% formally diagnosed — highlighting underdiagnosis.

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52
Q

Which factors are linked to insomnia prevalence in Australia?

A

Higher in rural areas, English-speaking households, lower income, those with disability, and unemployed individuals.

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53
Q

How often do Australians seek help for insomnia?

A

Only 30% discussed sleep with a provider in the past year; even among those with chronic insomnia, under 50% sought help.

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54
Q

What treatments are underutilised for insomnia in Australia?

A

Only 8.7% use CBTi regularly. Medications used more often but still low (e.g., 12.3% use prescribed meds ≥3 nights/week).

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55
Q

What does ‘circadian’ mean?

A

Processes with an approximately 24-hour period.

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56
Q

What is the intrinsic human circadian period (tau)?

A

About 24.2 hours.

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57
Q

What structure serves as the master circadian pacemaker?

A

The suprachiasmatic nucleus (SCN) in the anterior hypothalamus.

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58
Q

What is the role of the SCN in alertness?

A

Produces an alerting signal during the day and reduces it at night to promote sleep.

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59
Q

What are zeitgebers and what is the most potent one?

A

Zeitgebers are external time cues that entrain the circadian rhythm; light is the most potent.

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60
Q

What photoreceptors communicate light to the SCN?

A

Melanopsin-containing retinal ganglion cells via the retinohypothalamic tract.

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61
Q

What is the primary neurotransmitter in the RHT?

A

Glutamate.

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62
Q

What other neurotransmitter is co-released in the RHT?

A

Pituitary adenyl cyclase-activating peptide (PACAP).

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63
Q

What thalamic structure relays non-light zeitgebers to the SCN?

A

The intergeniculate leaflet (IGL).

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64
Q

When is melatonin secreted?

A

During the dark cycle, beginning 2–3 hours before habitual bedtime.

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65
Q

What inhibits melatonin secretion?

A

Light exposure, via SCN inhibition of PVH neurons.

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66
Q

What neurotransmitter stimulates the pineal gland to secrete melatonin?

A

Norepinephrine, acting via beta-1 receptors.

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67
Q

What enzyme catalyzes the rate-limiting step in melatonin synthesis?

A

Arylalkylamine N-acetyltransferase (AA-NAT).

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68
Q

What is the half-life of melatonin?

A

About 30–45 minutes.

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69
Q

What effect does melatonin binding MT1 receptors have?

A

Decreases the SCN alerting signal (hypnotic effect).

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70
Q

What effect does melatonin binding MT2 receptors have?

A

Shifts the circadian phase.

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71
Q

What is the dim light melatonin onset (DLMO)?

A

The time melatonin surpasses a threshold (~3 pg/mL saliva), about 2–3 hours before habitual bedtime.

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72
Q

What are the two main processes in the two-process model of sleep?

A

Homeostatic sleep drive (Process S) and circadian alerting signal (Process C).

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73
Q

What is CBTmin and when does it occur?

A

Minimum core body temperature, ~2 hours before spontaneous wake time.

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74
Q

What is the relationship between DLMO and CBTmin?

A

CBTmin occurs ~7 hours after DLMO.

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75
Q

When does light exposure cause a phase advance?

A

When given after CBTmin.

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76
Q

When does light exposure cause a phase delay?

A

When given before CBTmin.

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77
Q

What type of light has the greatest effect on circadian phase?

A

Short wavelength (blue light, ~460 nm).

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78
Q

How much light is required for circadian phase shifting?

A

Depends on prior exposure, timing, and intensity — natural outdoor light is most effective.

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79
Q

What is a phase response curve (PRC)?

A

A graph that describes the direction and magnitude of circadian phase shifts in response to stimuli (e.g., light, melatonin) depending on timing.

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80
Q

What does light do when administered before CBTmin?

A

It causes a phase delay.

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81
Q

What does light do when administered after CBTmin?

A

It causes a phase advance.

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82
Q

What is the PRC for melatonin?

A

Melatonin causes phase advances when taken in the afternoon/early evening and delays when taken in the morning.

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83
Q

How is melatonin used in circadian rhythm disorders?

A

It can be used as a chronobiotic to shift the timing of the circadian rhythm or as a hypnotic to aid sleep onset.

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84
Q

What dose of melatonin is typically used for phase shifting?

A

Low doses (e.g., 0.3–1 mg), taken 5–6 hours before habitual bedtime.

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85
Q

What dose of melatonin is typically used for sleep initiation?

A

Higher doses (e.g., 2–5 mg), taken closer to bedtime.

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86
Q

How should melatonin be timed in DSWPD?

A

2–3 hours before habitual bedtime to advance sleep onset.

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87
Q

Which gene mutations are associated with familial advanced sleep phase disorder (FASPD)?

A

PER2 and CSNK1D mutations.

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88
Q

Which gene mutation is associated with familial delayed sleep phase disorder (DSPD)?

A

CRY1 mutation.

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89
Q

What are the diagnostic criteria for DSWPD?

A

Significant delay in sleep onset and wake time relative to desired times, with preserved sleep duration and quality.

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90
Q

How is DSWPD managed?

A

Chronotherapy (gradually delaying sleep), light therapy in the morning, melatonin in the evening, consistent scheduling.

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91
Q

What is non-24-hour sleep-wake rhythm disorder (N24)?

A

A circadian disorder where the sleep-wake cycle is longer than 24 hours, often seen in totally blind individuals.

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92
Q

How is N24 treated?

A

Melatonin or tasimelteon (a melatonin receptor agonist), timed light exposure in sighted individuals.

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93
Q

What is irregular sleep-wake rhythm disorder (ISWRD)?

A

Characterised by fragmented sleep across 24 hours with no consistent sleep or wake pattern.

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94
Q

What causes ISWRD?

A

Common in neurodegenerative disease, brain injury, or lack of social/environmental time cues.

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95
Q

What are treatment strategies for ISWRD?

A

Structured routines, scheduled light exposure, melatonin, behavioural intervention.

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96
Q

How does N24SWRD differ between blind and sighted individuals?

A

Blind individuals typically have normal tau and fail to entrain due to lack of light; sighted individuals often have long tau and poor light entrainment.

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97
Q

What is the typical tau in sighted individuals with N24SWRD?

A

Usually 24.5 to 25.5 hours, but can be as long as 26.5 hours.

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98
Q

How does melatonin dosing affect entrainment in N24SWRD?

A

Lower doses (0.5 mg) may be more effective than high doses (e.g., 10 mg) in some patients.

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99
Q

What is tasimelteon and its role in N24SWRD?

A

A melatonin agonist (Hetlioz) approved for N24SWRD; dose: 20 mg 1 hour before bedtime. More selective for MT2 receptors.

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100
Q

What are tasimelteon side effects?

A

Headache, vivid dreams, ALT elevation, respiratory/urinary infections. Not to be taken with CYP1A2 inhibitors.

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101
Q

How is N24SWRD treated in sighted individuals?

A

Timed melatonin (0.5–4 mg) and morning light exposure. Treatment is difficult and long-term adherence is low.

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102
Q

What neural pathway transmits circadian signals from the SCN?

A

SCN → vSPZ → DMH, which regulates sleep propensity, temperature, and cortisol.

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103
Q

What is required for diagnosing N24SWRD according to ICSD-3?

A

At least 14 days of sleep logs documenting a free-running rhythm.

104
Q

What is the most reliable circadian phase marker in N24SWRD?

A

Melatonin midpoint (DLMO), due to societal influences on sleep times.

105
Q

What are key features of advanced sleep-wake phase disorder (ASWPD)?

A

Early sleep onset and awakening, more common in elderly, worsened by early morning light.

106
Q

How is ASWPD treated?

A

Evening light exposure, avoiding naps, possibly avoiding early morning walks.

107
Q

What defines irregular sleep-wake rhythm disorder (ISWRD)?

A

≥3 sleep episodes scattered across 24 hours, often with neurodegenerative disorders.

108
Q

How is ISWRD treated?

A

Daytime light, structured routines, quiet/dark nights. Melatonin in children with neuro conditions. Avoid hypnotics.

109
Q

What is shift work disorder (SWD)?

A

Daytime sleep difficulty and impaired alertness at night due to work schedule misalignment.

110
Q

How is SWD treated?

A

Pre-shift nap, light at shift start, caffeine or modafinil, dark glasses for drive home, melatonin before day sleep.

111
Q

What is jet lag and what causes it?

A

Circadian misalignment from travel across ≥2 time zones. Eastward travel requires harder phase advance; westward requires easier phase delay.

112
Q

How is jet lag managed?

A

Light avoidance at wrong times, light exposure at correct times, melatonin before desired sleep, and allowing 1 day of adaptation per time zone.

113
Q

What is lifestyle-driven hypersomnolence?

A

Hypersomnolence caused by social and lifestyle factors, not physiological issues, leading to insufficient sleep.

114
Q

What are common causes of insufficient sleep?

A

Family responsibilities, studying, socialising, media use, and overcommitting daily tasks.

115
Q

What percentage of Australians are not getting the sleep they need according to a 2019 parliamentary inquiry?

A

Four in ten Australians.

116
Q

What causes jet lag?

A

Circadian misalignment due to crossing time zones; sleep and wake cycles are out of phase with local time.

117
Q

Why is travelling west easier than travelling east?

A

Because it is easier to delay the circadian rhythm (sleep later) than to advance it (sleep earlier).

118
Q

What strategies help reduce jet lag?

A

Gradual pre-adjustment of sleep before departure, adapting to local time slowly, avoiding critical tasks soon after arrival.

119
Q

What is Shift Work Sleep Disorder (SWSD)?

A

A condition in shift workers involving difficulty adjusting to sleep-wake schedules, leading to fatigue, headaches, and cognitive issues.

120
Q

What cognitive processes are impaired by shift work?

A

Vigilance, attention, decision making, psychomotor function, and affect regulation.

121
Q

What are the two biological processes governing sleep?

A

Process S (homeostatic sleep pressure) and Process C (circadian rhythm for sleep propensity).

122
Q

Why is night shift sleep often fragmented?

A

Circadian alerting signals increase at night, making it harder to fall asleep and stay asleep during the day.

123
Q

What happens to alertness during night shifts?

A

Alertness declines as melatonin rises and the circadian alerting signal dissipates, impairing performance.

124
Q

What percentage of the U.S. workforce works shifts outside the typical day shift?

A

Between 17.7% and 25.9%.

125
Q

What are examples of shift types?

A

Early morning (4–7am), night (6pm–4am), evening (2–6pm), and rotating shifts.

126
Q

Why are permanent night shifts common in North America?

A

They provide perceived stability and are often assigned to newer employees.

127
Q

Which age group has more difficulty with shift work?

A

Older adults, due to reduced adaptability to circadian changes.

128
Q

How much less sleep do shift workers typically get?

A

30–60 minutes less per day compared to day workers.

129
Q

Which shift tends to allow longer sleep duration?

A

Evening shifts, due to alignment with circadian delay and dark hours.

130
Q

What societal and family factors reduce shift worker sleep?

A

Parental duties, daytime obligations, and need to align with social norms.

131
Q

What is the rate of clinically significant sleep disturbance in night shift workers?

A

18.5%, over twice that of day workers.

132
Q

What is the estimated annual cost of insomnia-related work issues in the U.S.?

A

$15 to $17.7 billion.

133
Q

How does shift work impact psychomotor vigilance?

A

Reduces reaction time, slows response, increases lapses — particularly at night.

134
Q

What are ‘microsleeps’ and when are they most likely?

A

Brief intrusions of sleep into wakefulness, often lasting seconds; most common during circadian troughs.

135
Q

How does shift work affect attention and decision-making?

A

Attention lapses increase; decision-making becomes slower, more error-prone, and impulsive.

136
Q

What types of memory are affected by sleep loss?

A

Working memory, short-term recall, and long-term consolidation (especially of emotional and declarative memories).

137
Q

What brain regions are most affected by sleep deprivation?

A

Prefrontal cortex (executive function), amygdala (emotional reactivity), and hippocampus (memory consolidation).

138
Q

How does sleep deprivation affect emotional processing?

A

Increases amygdala reactivity and reduces regulation by prefrontal cortex, leading to emotional lability.

139
Q

How is empathy affected by sleep loss?

A

Reduced ability to read others’ emotions, decreased emotional sensitivity and social responsiveness.

140
Q

What real-world risks are associated with shift work and sleep loss?

A

Increased rates of workplace injuries, road accidents, medical errors, and public safety incidents.

141
Q

What time of day are fatigue-related errors most likely?

A

Between 2–6am during the circadian nadir.

142
Q

What was the role of fatigue in the Exxon Valdez disaster?

A

Crew fatigue was identified as a major contributing factor to the oil spill.

143
Q

How does sleep deprivation affect safety in healthcare?

A

Increased prescribing errors, missed diagnoses, and reduced attention to patient cues.

144
Q

What is the impact of night shift on learning and performance in students?

A

Impaired concentration, slower processing, lower academic performance, and less effective memory encoding.

145
Q

How does fatigue impair complex task performance?

A

Reduces ability to multitask, maintain focus, and make accurate judgments under pressure.

146
Q

How can strategic napping help shift workers?

A

Naps reduce sleep pressure and improve alertness; a 10–30 min nap can enhance performance without grogginess.

147
Q

When is the best time to nap before a night shift?

A

1–2 hours before starting the shift to reduce sleepiness during the first half.

148
Q

What is a ‘prophylactic nap’?

A

A nap taken before anticipated sleep deprivation to build resilience against fatigue.

149
Q

How does caffeine help shift workers?

A

Improves alertness and performance, especially when used at the start of a night shift or mid-shift.

150
Q

When should caffeine use be avoided during a shift?

A

In the second half of the shift to prevent interference with post-shift sleep.

151
Q

What medications may be used to promote wakefulness in shift workers?

A

Modafinil and armodafinil (with caution); melatonin may aid daytime sleep but with modest effects.

152
Q

How can light exposure improve circadian alignment?

A

Bright light at shift start promotes alertness and phase delay; avoiding light post-shift prevents undesired circadian shifting.

153
Q

What are light hygiene strategies for shift workers?

A

Use bright light at night, wear blue-blocking glasses post-shift, keep sleep environment dark and quiet.

154
Q

What is the best shift rotation schedule?

A

Clockwise (morning → evening → night), with at least 48 hours off between transitions.

155
Q

Why is clockwise rotation preferred?

A

It aligns with the natural circadian delay tendency and is easier to adjust to.

156
Q

What workplace strategies can reduce shift work fatigue?

A

Scheduled breaks, environmental lighting, fatigue education, reducing consecutive night shifts.

157
Q

What role can employers play in managing shift work risk?

A

Implement fatigue risk management systems, offer health screening, and promote sleep-friendly culture.

158
Q

What are policy-level recommendations for safer shift work?

A

Limit night shift duration, encourage rest breaks, regulate maximum work hours, and provide sleep education.

159
Q

What is the most important consistent habit for circadian rhythm regulation?

A

Regular wake time — even on weekends, as morning light exposure anchors circadian rhythm.

160
Q

Why is a regular lights-off time less important than a regular wake time?

A

The wake time anchors the circadian rhythm more effectively via light exposure.

161
Q

How should your bedroom environment support sleep?

A

It should be cool, dark, quiet, and free of anxiety-provoking or distracting elements.

162
Q

What should your bed be used for?

A

Only for sleep and sex — no screens, no other activities.

163
Q

Why is limiting bed use to sleep helpful?

A

It reinforces the mental association between bed and sleep, improving sleep efficiency.

164
Q

What is sleep efficiency and how is it calculated?

A

Percentage of time in bed spent asleep. E.g., 6h sleep/9h in bed = 67%; 6h sleep/7h in bed = 86%.

165
Q

What should you do if you’re awake in bed for more than 15 minutes?

A

Get out of bed, do something non-stimulating, and return when sleepy.

166
Q

What does it mean to ‘respect sleep’?

A

Allocate enough time to sleep, but don’t obsess over it. Pressure can worsen insomnia.

167
Q

What are examples of effective wind-down cues?

A

Showering, brushing teeth, reading a boring book, using low light, doing low-cognitive activities.

168
Q

Why avoid stressful tasks before bed?

A

They raise cortisol, which should peak in the morning and disrupt sleep onset.

169
Q

Why should caffeine be avoided in the second half of the day?

A

It has a half-life of 5–6 hours; 150 mg at 3pm means ~75 mg still active by 9pm.

170
Q

How does alcohol affect sleep?

A

May help with falling asleep, but disrupts second half of the night and suppresses REM.

171
Q

What are practical tips when co-sleeping with a partner?

A

Agree on who handles child wakeups, discuss noise/light levels, address pets, phones, and blanket sharing.

172
Q

What should you do about clock-watching?

A

Avoid it. If you’ve set an alarm, trust it. Clock-watching increases cognitive arousal.

173
Q

Who is Randy Gardner and why is he significant in sleep research?

A

Randy Gardner stayed awake for 11 days (264 hours) in 1964 as part of a school science experiment, demonstrating the extreme cognitive and physiological effects of sleep deprivation.

174
Q

What symptoms did Randy Gardner experience during his 11-day wakefulness?

A

Mood changes, memory issues, hallucinations, cognitive lapses, and microsleeps. He showed surprisingly fast recovery after sleep.

175
Q

What did the Randy Gardner case teach us about sleep deprivation?

A

That while extreme sleep loss is survivable short-term, it causes profound cognitive and perceptual dysfunction, and recovery occurs but does not fully compensate hour-for-hour.

176
Q

What was the outcome of the 2019 Australian Parliamentary Inquiry into Sleep?

A

It formally recognised sleep as a public health priority and called for increased awareness, though many recommendations have not yet been implemented.

177
Q

What media example highlighted sleep awareness and public neglect?

A

The documentary ‘The Sleep Revolution’ emphasised society’s undervaluation of sleep despite known health risks.

178
Q

What is jetlagrooster.com and how is it used?

A

An online tool that generates personalised jet lag management plans based on flight details and destination.

179
Q

What kinds of apps or tools can help manage jet lag?

A

Apps that provide personalised light exposure and sleep timing schedules to help reduce jet lag (e.g., Timeshifter, Jet Lag Rooster).

180
Q

How long did Randy Gardner stay awake and what were the effects?

A

264 hours (11 days); experienced extreme drowsiness, irritability, reduced stress tolerance, but no psychosis. Recovery sleep occurred over several days.

181
Q

What did the Randy Gardner case demonstrate?

A

That prolonged sleep deprivation causes significant functional impairment but is not necessarily permanently damaging.

182
Q

What were the findings of Kollar et al.’s 205-hour sleep deprivation study?

A

Participants showed impaired attention, reduced concentration, cognitive slowing, and personality changes on the MMPI.

183
Q

How did Kollar et al.’s findings differ from Gardner’s?

A

Kollar’s participants were monitored in clinical settings and exhibited more profound and measurable cognitive changes.

184
Q

What did the 1896 Patrick & Gilbert study show about sleep loss?

A

90 hours of sleep deprivation led to psychomotor slowing, sluggish thinking, and increased reaction times.

185
Q

What did Legendre and Pièron observe in dogs after sleep deprivation?

A

Drowsiness, slowed responses, and physiological signs of accumulating sleep pressure.

186
Q

What was observed in Kleitman’s puppy sleep deprivation study?

A

Puppies remained awake longer with social stimulation but eventually showed signs of fatigue and sleepiness.

187
Q

What key principle was illustrated in the puppy sleep study?

A

Environmental stimulation can temporarily mask sleepiness, but homeostatic pressure builds and ultimately forces sleep.

188
Q

What are the three pillars of good health for adolescents?

A

Good sleep, regular exercise, and good nutrition.

189
Q

What is the most Googled personal health question?

A

‘Why am I always tired?’

190
Q

Why are teens particularly vulnerable to sleep deprivation?

A

Because of a combination of late body clocks, academic and social pressures, screen use, and under-recognition of sleep needs.

191
Q

What is the ‘perfect storm’ of factors that sabotage teen sleep?

A

Late body clocks, inflexible school start times, social media, part-time jobs, homework, hormones, stress, ambition, screen addiction, reduced parental control.

192
Q

What percentage of teens are chronically sleep deprived on school days?

A

70% — more than triple any other age group.

193
Q

Which countries are the most sleep-deprived according to data?

A

South Korea, the United States, and Australia (3rd worst globally).

194
Q

What societal factor is closely linked to national sleep deprivation?

A

Rate and speed of adoption of new screen technology.

195
Q

What are some physical and mental health consequences of teen sleep deprivation?

A

Poor academic performance, suicide risk, motor vehicle accidents, anxiety, depression, emotionality, drug use, impaired judgment, obesity, immune dysfunction.

196
Q

What is the increase in suicide risk associated with just one hour of lost sleep?

A

58% increase in teen suicide risk.

197
Q

How does sleep deprivation affect ethical decision-making in teens?

A

It impairs prefrontal cortex function, increasing emotional and risky decisions.

198
Q

What is ‘conditioned insomnia’ in teens?

A

Inability to fall asleep due to training the brain to associate bed with stimulating activities, especially screen use.

199
Q

What is the impact of screen use before bed on adolescent sleep?

A

Suppresses melatonin, increases arousal, delays sleep onset, and reduces sleep duration and quality.

200
Q

What brain region is primarily affected by late-night screen use?

A

The prefrontal cortex, which is responsible for reasoning, judgment, and self-regulation.

201
Q

What is meant by ‘cognitive shutdown’ in teens?

A

The process where the prefrontal cortex goes offline from lack of sleep, increasing emotional reactivity and impulsivity.

202
Q

How long does it take for prefrontal function to fully return after a night of poor sleep?

A

At least 2–3 nights of sufficient recovery sleep.

203
Q

Why is prefrontal cortex vulnerability a concern for teenagers?

A

It’s still developing and is especially susceptible to sleep deprivation and overstimulation.

204
Q

How do early school start times affect adolescent sleep?

A

They reduce total sleep time, misalign with teen circadian rhythms, and increase daytime sleepiness.

205
Q

What biological shift occurs in adolescence that affects sleep timing?

A

The circadian rhythm delays by about 1–2 hours, making it harder to fall asleep early.

206
Q

What time should school ideally start to align with teen circadian biology?

A

Around 9:30am or later.

207
Q

What are the benefits observed after delaying school start times?

A

Increased sleep duration, improved attendance, mood, academic performance, and reduced car accidents.

208
Q

Why have some schools resisted later start times?

A

Concerns about sports schedules, transport logistics, parent work hours, and tradition.

209
Q

What is social jetlag?

A

A misalignment between biological sleep rhythms and social obligations, especially when weekend sleep patterns differ significantly from weekdays.

210
Q

How much of a sleep phase shift on weekends is considered harmful?

A

A shift of more than 1.5–2 hours can have negative effects on alertness, mood, and metabolic function.

211
Q

Why is weekend oversleep not a good solution to weekday sleep loss?

A

It delays the circadian rhythm further, making Sunday night sleep onset harder and perpetuating the cycle.

212
Q

What is the ‘Sunday night effect’?

A

Difficulty falling asleep on Sunday nights due to weekend sleep-ins and circadian phase delay.

213
Q

How can parental behaviour impact teen sleep?

A

Setting limits on bedtimes and screens, modelling healthy routines, and enforcing consistent wake times can improve teen sleep.

214
Q

Why is parental involvement in teen sleep declining?

A

Increased adolescent independence, busy family schedules, and lack of awareness about sleep importance.

215
Q

What are common parental misconceptions about teen sleep?

A

Believing teens are lazy, underestimating sleep need, or assuming they can ‘catch up’ on weekends.

216
Q

Why should adolescent sleep be framed as a public health issue?

A

Because it affects academic performance, mental health, driving safety, and long-term health outcomes.

217
Q

What are effective strategies to improve teen sleep at a population level?

A

Later school start times, screen curfews, public education, and accessible behavioural sleep interventions.

218
Q

What role do schools and communities play in improving teen sleep?

A

They can adjust timetables, educate students and parents, support sleep-positive policies, and foster sleep-friendly environments.

219
Q

What is the two-process model of sleep regulation?

A

It includes Process S (homeostatic sleep pressure, which builds with wakefulness) and Process C (circadian rhythm, which governs optimal sleep timing).

220
Q

How does sleep pressure change during adolescence?

A

It builds more slowly, making teens less sleepy at typical bedtimes.

221
Q

What circadian changes occur in adolescence?

A

Melatonin secretion is delayed, leading to later sleep onset and preference for later bed and wake times.

222
Q

How does light exposure impact melatonin and circadian alignment?

A

Evening light delays melatonin onset; morning light advances it but is less effective when sleep-deprived.

223
Q

What are common red flags for adolescent sleep deprivation?

A

Difficulty waking for school, excessive weekend sleep-ins, frequent naps, and morning irritability.

224
Q

Why are weekend sleep-ins counterproductive?

A

They delay the circadian rhythm and make Sunday night sleep onset harder, worsening weekday fatigue.

225
Q

What does ‘cognitive shutdown’ refer to in tired teens?

A

The reduced function of the prefrontal cortex, impairing attention, memory, and decision-making.

226
Q

Why does learning suffer after sleep deprivation?

A

New information may not be encoded effectively (‘in one ear, out the other’) and memory consolidation is impaired.

227
Q

How many nights of good sleep are needed to consolidate learning?

A

At least two nights of sufficient sleep.

228
Q

How did COVID-19 lockdowns affect teen sleep?

A

Teens slept more with flexible schedules and later wake times during remote learning.

229
Q

What schooling model preserved sleep best during the pandemic?

A

Asynchronous online learning (vs. early start synchronous classes).

230
Q

What is the SleepShack program?

A

An online CBT-based sleep intervention for teens including assessment, bedtime fading, light therapy, and behavioural strategies.

231
Q

What are the steps included in the SleepShack intervention?

A

Online assessment, daily sleep log tracking, melatonin-safe wind-down routine, bedtime fading, bright morning light exposure, clinician support if needed.

232
Q

How does SleepShack involve parents?

A

Parents receive automated alerts and can support environment management and routine enforcement.

233
Q

What behavioural principles underlie SleepShack?

A

Stimulus control, sleep restriction (via bedtime fading), and circadian alignment via light exposure.

234
Q

Why do some teens resist sleep recovery even when tired?

A

Low motivation, underestimation of fatigue impact, screen addiction, and reward system dysfunction.

235
Q

How can families help improve adolescent sleep?

A

By promoting consistent wake times, limiting evening light exposure, using calm routines, and setting digital curfews.

236
Q

What is a key communication principle when discussing sleep with teens?

A

Avoid judgment; focus on their goals (e.g., academic, sport performance) and link sleep to those outcomes.

237
Q

Why is understanding adolescent reward systems important in sleep support?

A

Teens may prioritise immediate gratification (e.g., screen time) over long-term benefits, requiring goal-based motivation strategies.

238
Q

What role do clinicians play when behavioural strategies alone aren’t enough?

A

Providing support for co-occurring anxiety, depression, or neurodevelopmental disorders interfering with sleep improvement.

239
Q

What is slow-wave activity (SWA) and its relevance to adolescent sleep?

A

SWA reflects homeostatic sleep pressure and declines exponentially overnight. It’s used to gauge sleep need and recovery.

240
Q

What is the role of the suprachiasmatic nucleus (SCN)?

A

It acts as the brain’s master clock, regulating circadian rhythms based on light input.

241
Q

How do screens influence adolescent brain chemistry?

A

Active screen use triggers dopamine, adrenaline, and cortisol release, increasing arousal and making sleep onset harder.

242
Q

What is ‘infomania’ in the context of adolescent sleep?

A

A state of constant anticipatory alertness due to notifications and messages, contributing to conditioned arousal and sleep disruption.

243
Q

How did Australian education performance rank in recent PISA data?

A

Australia ranked 39th out of 41 developed nations in performance declines, partly attributed to student sleep deprivation.

244
Q

How did late school start time reforms compare to education spending (Gonski 2.0)?

A

Delaying school start times produced better academic improvements than $28 billion in traditional education spending.

245
Q

How does sleep interact with genetic risk for depression in teens?

A

Teens with genetic vulnerability only showed depressive symptoms during life transitions (e.g. starting uni) if they were also sleep-deprived.

246
Q

What protective role does sleep play in adolescent mental health?

A

Sufficient sleep buffers teens from developing mood disorders, even if they have genetic susceptibility.

247
Q

What are recommended guidelines for morning light therapy in teens?

A

Exposure to 2,500–10,000 lux of bright light in the morning helps shift circadian rhythms earlier.

248
Q

Why combine melatonin with light therapy?

A

The combination is more effective for circadian realignment than using either intervention alone.

249
Q

How does sleep timing differ between DSWPD and behavioural insomnia in teens?

A

DSWPD involves consistent delayed sleep onset (e.g., 2–6am), even without screens. Behavioural insomnia has variable timing linked to screen use or lack of routine.

250
Q

How is sleep duration on weekends different in DSWPD vs. screen-related insomnia?

A

DSWPD teens sleep normally when allowed to follow their body clock. Behavioural insomnia teens may still have fragmented or insufficient sleep.

251
Q

What is the weekly pattern of cognitive symptoms in DSWPD vs. behavioural insomnia?

A

DSWPD causes persistent sluggishness and sleepiness all week. Behavioural insomnia shows worse performance on weekdays with improvement on weekends.

252
Q

What distinguishes sleep quality in DSWPD vs. screen-induced insomnia?

A

DSWPD teens sleep well once asleep. Behavioural insomnia often involves fragmented sleep and difficulty winding down.

253
Q

How do weekends help differentiate the two disorders?

A

DSWPD teens continue late sleep patterns. Behavioural insomnia teens often improve with more parental control or less screen time.

254
Q

What does DLMO testing reveal in DSWPD vs. behavioural insomnia?

A

DLMO is delayed in DSWPD but normal in behavioural insomnia.

255
Q

What is the treatment response difference between DSWPD and screen-induced insomnia?

A

DSWPD requires structured light and melatonin therapy. Behavioural insomnia often improves rapidly with screen limits and routine.

256
Q

How does motivation differ in DSWPD vs. behavioural insomnia?

A

DSWPD teens are often motivated but misaligned biologically. Behavioural insomnia teens may lack motivation and have low insight.