Sleep Flashcards

1
Q

Components of sleep

A
  • Behavioural state
  • Marked by quiescence and low attention
  • Recurrent and reversible
  • Dreams and mentation
  • Amnesia
  • Expressions vary
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2
Q

Why sleep?

A
  • Brain and body restoration
  • Energy conservation
  • Memory and learning
  • Emotional regulation
  • Housekeeping/ clearance
  • Xie et al. (2013): metabolite clearance
  • Yang et al. (2014): formation of dendrite spines
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3
Q

Structure of sleep

A
  1. Awake
  2. NREM (75%)
    - Stage N1 light sleep (5%)
    - Stage N2 (50%)
    - Stage N3 deep sleep/ slow-wave sleep (20%)
  3. REM paradoxical sleep (25%)
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4
Q

Characteristics of sleep cycles

A
  • Alternate in a cyclical fashion
  • Cycles gradually get longer (~70-100min to ~90-120min)
  • Deep sleep reduces in later cycles
  • Stage 2 and REM become longer across the night
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5
Q

Physiological changes during sleep

A
  • Motor response
  • Heart rate and blood pressure
  • Blood flow to brain
  • Respiration
  • Body temperature
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6
Q

Neural basis of sleep/wake regulation

A

Superchiasmatic nucleus (SCN)

  • Hypothalamus
  • Controls circadian cycles
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7
Q

Ascending arousal system

A
  • To stay awake
  • Hypothalamus sends signals to stimulate cerebral cortex to maintain consciousness
  • With the help of orexin neurons/hypocretin
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8
Q

Ventrolateral pre optic area (VLPO)

A

Releases NTs to switch from wakefulness to NREM by inhibiting activity in arousal centers

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9
Q

Two process model

A
  • Process S: homeostatic process (tracking need for sleep by prior sleep and duration of waking)
  • Process C: circadian process (tracking environmental time: light-dark)
  • Interplay of these processes determines timing, duration and structure of sleep
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10
Q

Light in circadian rhythm

A
  • Circadian pacemaker/ zeitgeber
  • Synchronisation of retina and optic nerve
  • Might have desynchrony in people born blind, shift workers, travellers, old people
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11
Q

Behavioral changes in sleep

A
  • Reduced attention and response to visual stimuli
  • May wake up from auditory stimuli
  • May wake up from olfactory stimuli in stage 1
  • Loss of muscle tone
  • Memory impairment
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12
Q

Polysomnography (PSG)

A
  • Electroencephalography (EEG): brain neurons
  • Electroculography (EOG): voltage changes induced by eye rotation
  • Electromyography (EMG): muscle activity from chin

Pros:
• Gold standards
• Precise rich information

Cons:
• Expensive, labour-intensive, training
• Short duration, lab based
• Intrusive (could interfere with sleep- i.e. first night effect, reversed effect for insomnia)

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13
Q

Actigraphy

A

Indirect measure (estimates sleep): algorithm used affects accuracy

Pros: 
•	Affordable
•	User friendly 
•	Ecological manner 
•	Suitable for long observations 
•	Good validation with PSG for time slept but not onset 
Cons: 
•	Indirect measure 
•	Doesn’t detect moment of onset 
•	Less information than PSG 
•	Varying data depending on device, algorithm etc. (also need to use sleep diary)
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14
Q

Sleep quality questionnaire

A

Types: Pittsburgh Sleep Quality Index; Insomnia Severity Index; Jenkins Sleep Questionnaire

Pros:
• Convenient
• Cost-effective
• Benchmarked against diagnostic criteria

Cons: 
•	Subjective 
•	Retrospective 
•	Recall bias 
•	Further assessment required
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15
Q

Sleep diary

A

Sleep parameters: sleep onset latency, time in bed, wake after sleep onset

Pros: 
•	Intuitive 
•	Stable picture with 1-2 weeks of use 
•	Information can help to reconstruct sleep experience 
Cons: 
•	Burden on sleeper; missing data 
•	Training for data collection 
•	Training to interpret 
•	Subjective and retrospective; recall bias
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16
Q

Apps and wearable tech

A
  • Similar to actigraphy
  • Algorithm and validation unclear
  • Settling of sensitivity unclear
  • Interaction errors (i.e. forget to wear)
  • Interpretation hard (sleep stages not possible)
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17
Q

Sleep perception

A
  • Sometimes objective sleep for insomniacs and normal sleepers overlaps but discrepancies are due to sleep perception
  • Insomniacs have a high tendency to underestimate their actual sleep (overestimate sleep onset latency and underestimate total sleep time)
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18
Q

Hypotheses for sleep misperception

A
  1. Challenge of context
  2. Interpreting sleep as wake
  3. Worry/ selective attention
  4. Physiological arousal
  5. Transient awakenings
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19
Q

Clock monitoring (Tang et al., 2007)

A
  • Clock monitoring lead to more reports of pre-sleep worry and longer sleep onset latency
  • Found this even when they controlled by monitoring a digital display that wasn’t time
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20
Q

Driving drowsy

A
  • 20% of all traffic accidents are sleep related

* 37% reported they have fallen asleep while driving

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21
Q

Cost of bad sleep

A
  • Total: $6.6 billion (Canadian $) direct and indirect

* A&E: $31 billion: 7.2% of all accidents

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22
Q

Define epidemiology

A

Quantitative study of frequency, distribution, determinants and control of health problems and disease
• Cross sectional: snapshot
• Case-control: retrospective
• Longitudinal cohort: prospective

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23
Q

Basic concepts in epidemiology

A
  • Exposure and outcome
  • Prevalence, incidence, persistence, remission\morbidity and mortality rate
  • Risk and odds ratio
  • Cofounder and adjusted odds ratio
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24
Q

Pros and cons of epidemiology

A
  • Representative
  • Sufficient power
  • Longer time frame
  • Temporal order
  • Expensive
  • Few items for assessment
  • Harder to use objective measures
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25
Q

How well is the world sleeping?

A
  • Large percentage of people have insomnia complaints: 30-48% (Ohayon, 2005)
  • Symptoms (37%) Diagnosis (5%) (Stewart et al., 2006)
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26
Q

Sleep deprivation and rat studies

A

Use plexiglas cage with rotating platform

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27
Q

Total sleep deprivation studies

A
  • (TSD): baseline, experimental (36 hours of wakefulness), recovery
  • Lost in one night: 2 hours REM, 2 hours SWS, 4 hours N1 and N2
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28
Q

Partial sleep deprivation studies

A

Postponed bed time and forced awakening (increase SWS and reduced N 1 & 2 and REM)

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29
Q

Partial: Sleep fragmentation

A
  • Forced arousal: transient (doesn’t affect sleep duration); outright (decreases sleep duration)
  • Leads to shallower sleep
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30
Q

Measures of cognition

A
  1. Simple attention
  2. Complex attention
  3. Processing speed
  4. Memory
  5. Reasoning and crystallized attention
  6. Verbal fluency
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31
Q

Findings of meta-analysis on short term TSD on cognition

A
  • Significant negative effect in all cognitive domains (excluding speed and reasoning accuracy)
  • High effect size for simple attention and vigilance; moderate for complex attention and WM; weak to no for reasoning and crystallised intelligence
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32
Q

Monk’s conceptual model (2012)

A

Provides possible outcomes of TSD that can affect poor performance

  • Loss of motivation
  • Cognitive rigidity
  • Cognitive slowing
  • Lapses and microsleeps
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33
Q

Complex tasks less affected than simple ones

A
  1. Vigilance hypothesis
  2. Controlled attention hypothesis
  3. Compensation hypothesis
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34
Q

Junior doctors and sleep deprivation

A
  • 300% more adverse events if 5 or more extended shifts (Barger et al., 2006)
  • Increased number of errors and time to complete task if hours of sleep decreased and fatigue increased (Eastridge et al., 2003)
  • Effects of sleep deprivation are larger in non-physicians but doctors still had decreased performance (Philibert, 2005)
  • Doctors with heavy call had higher speed variability than doctors who had alcohol before driving simulation study (Arnedt et al., 2005)
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35
Q

Hill’s criteria of causal inference

A
  1. Strength
  2. Consistency
  3. Specificity
  4. Temporality
  5. Bio gradient
  6. Plausibility
  7. Coherence
  8. Experiment
  9. Analogy
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36
Q

Associations with sleep problems

A
  1. Poorer perception of health
  2. More days of disability and greater service utilization
  3. Concurrent medical problem risk
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37
Q

Obese more likely to:

A
  • Sleep less than 6 hours
  • Experience at least one symptom of sleep disorder
  • Think they have sleep problem
  • Experience day time sleepiness
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38
Q

Cross-sectional data

A

Exposure and outcome measured at same time

39
Q

Prospective data

A

Cohort studies; followed up over time

40
Q

Biological mechanisms of sleep and obesity

A

Increased caloric intake:

  • Increased hunger (more Ghrelin, less Leptin)
  • Increased opportunity to eat

Reduced energy expenditure:

  • Altered thermoregulation
  • Increased fatigue
41
Q

Commonly experienced sleep disorders by obese people

A
  1. Sleep disordered breathing: crowding; collapsed airway; compromised respiratory function
  2. Restless leg syndrome: hypofunction of dopamine system; diabetic neuropathy or cardiovascular pathology
42
Q

Congenital insensitivity to pain

A
  • Rare neurological disease
  • Don’t feel extreme pain
  • Frequent accidents and often die in childhood
43
Q

Chronic vs. acute pain

A

Differs in terms of:

  • Duration
  • Pathology
  • Biological value
  • Prognosis
44
Q

Impact of chronic pain

A
  • 19% prevalence
  • Smith et al. (2000): lower level of functioning and worse quality of life than those with HIV
  • Accidental overdose
45
Q

Insomnia and chronic pain

A
  • Clinical studies: sleep is shallow, fragmented and unstable; addition of sleep disturbance worsen reports of symptoms
  • Differences: increased N1, decreased SWS, shorter St2, more shift in stages, alpha intrusion in SWS, high cyclical alternative pattern, high sleep onset REM
  • Experimental studies: sleep deprivation increased pain sensitivity and report, reduced central pain inhibitor responses, dampened mood and increased inflammation
46
Q

Diffuse Noxious Inhibitory Control (DNIC)

A
  • Conditioned pain modulation
  • Tonic: cold pressor task
  • Phasic: pressure pain threshold
  • DNIC: % change in PPTh during cold pressure relative to baselines (increase indicates normal functioning)
  • Sleep fragmentation reduces DNIC
47
Q

Sleep restriction and inflammation (Haack et al., 2007)

A

Change in bodily discomfort and tiredness possibility related to IL-6 (plasma interleukin)

48
Q

Temporal links between sleep and pain (Tang et al., 2012):

A
  • Pain didn’t predict sleep quality- mood, cognitive arousal and physiological arousal did
  • Sleep quality predicted pain next day for all day
  • BUT high SQ = low pain in morning and high in the evening
49
Q

Fibromyalgia (Mørk & Nilsen, 2011)

A
  • Dose dependent association (risk increases according to frequency of sleep problems)
  • Greater risk for women > 45 who reported sleep problems often or always
50
Q

Does positive mood buffer problems sleeping? (Steptoe et al., 2008)

A
  • Those with more sleep problems tend to acknowledge positive affect less
  • Deeper sleep= eudaimonic wellbeing
  • Association between psychological stress and sleep problems mediated by positive states
51
Q

Sleep and daily mood (Totterdale et al., 1994)

A
  • Associations are stronger and more consistent from sleep to mood than the other way
  • Positive association between sleep quality and feeling cheerful, alert and involved next day
52
Q

Acute sleep deprivation and psychopathology

A
In military (Kahn-Greene et al., 2007; Killgore et al., 2008):
•	Significant effect on somantic complaints, anxiety, depression and paranoia 
•	Decrease in emotional intelligence
53
Q

Sleep deprivation and emotional reactivity

A
  • Sleep loss intensifies negative emotions and fatigue following daytime disruptive events
  • Cognitive-energy model: sleep affects level of energy to self-regulate
54
Q

Disrupted recognition of social cues/ emotions when sleep deprived (Van der Halm, 1996)

A

Sleep deprivation blunts ability to recognize emotion (particularly anger and happiness)

55
Q

Impairment in emotional memory encoding when sleep deprived (Walker, 2012)

A

Less likely to remember positive words when sleep deprived

56
Q

Possible neurological underpinnings in sleep deprivation and emotions (Yoo et al., 2007)

A

Sleep deprivation increased amygdala activation and decreased functional connectivity with medial prefrontal cortex

57
Q

Sleep and depression

A
  • Lower REM sleep latency, less SWS (particularly in first cycle), more awakenings, longer periods of awakenings
  • 63% had significant sleep disturbances (hypersomnia or insomnia)
58
Q

Sleep and bipolar

A
  • Depression phase: REM dysregulation, less SWS, hypersomnia
  • Mania/ hypomania: less need for sleep, delayed sleep onset, less REM latency, more REM intensity
  • Inter-episodes: acute sleep deprivation can trigger a switch into mania; more sleep fragmentation and greater night-to-night variability
59
Q

Sleep and anxiety

A
  • Difficulty falling and staying asleep: more sleep onset latency, more frequent or lengthier awakenings, less total sleep time, less sleep efficiency
  • Poor quality of sleep: restless and unsatisfying
60
Q

Sleep and PTSD

A
  • Hyperarousal
  • Fragmented sleep, short sleep duration, motoric reactivity, REM short and rare
  • Small-medium effect size for increased REM density, increased N1 and reduced SWS
61
Q

How does pre-sleep stress affect sleep?

A
  • Decreasing REM latency
  • Increasing REM density and duration
  • Increasing in arousal occurrence in sleep
62
Q

Sleep and suicide

A
  • Insomnia increases risk of completed suicide
  • Time of suicide peaks in the morning
  • 45.4% of participants who had committed suicide had recorded sleep disturbance
63
Q

REM and mental health

A
  • REM as abnormality marker

- Rem affects emotional memory processing

64
Q

Sleep to forget sleep to remember model (SFSR)

Walker & Van der Helm

A

Remember:
• Theta oscillations: carriers to connect brain regions
• Acetylcholine: important long term consolidation and abundant in REM

Forget:
• Reduction in affective tone associated with recall (but information contained)

65
Q

REM dreams

A
  • Cartwright et al. (1984): divorcees that were not depressed had longer dreams, dealt with wider time frame and had dreams with themes of marital status
  • Cartwright et al. (1998): significant reduction in POMS (profile of mood states) depression score overnight; especially females in non clinical sample
66
Q

Clinical insomnia

A

Sleeping problem in own right and difficulties despite adequate opportunity (not just sleepiness)

67
Q

Insomnia ICD-10

A
  • 16 sleep disorder codes
  • Organic or non-organic
  • Largely irrelevant to psychology
68
Q

Insomnia DSM-IV

A
  • 2 categories: Primary and secondary
  • Duration: 1 month
  • Severity: Significantly impaired
  • No frequency criterion
69
Q

Insomnia DSM-5

A
  • Removed secondary and primary
  • Removed ‘non-restorative’
  • Added ‘early morning awakening with inability to return to sleep’
  • Frequency 3 nights/week
  • Duration 3 months
  • Specifications: 1. With non-sleep disorder mental comorbidity 2. With other medical comorbidity 3. With other sleep disorders
70
Q

Insomnia ICSD-2

A
  • 73 diagnoses
  • Requires testing with PSG and expertise
  • 11 subtypes: i.e. paradoxical, idiopathic
71
Q

Insomnia ICSD-3

A
  • Simplified
  • Three: chronic, short term, other
  • People with and without comorbidity
72
Q

Convergence of DSM and ICSD for insomnia

A
  • Elimination of other sleep disorders
  • No primary or secondary categories
  • Frequency, duration and severity
  • Subjective complaint
  • Daytime consequences and dissatisfaction with sleep
  • ICSD allows for observers
73
Q

Hard to differentiate insomniacs on objective measures

A
  1. Appearance
  2. TSD
  3. Daytime sleepiness
  4. Daytime functioning
74
Q

Insomniacs and psychological characteristics

A
  • MMPI links: hypochondriacs, depression, hysteria, psychopathic deviation, gender rigidity, social introversion
  • Personality: neuroticism, internalisation, anxious concerns, perfectionism
75
Q

Clinical interviews for insomnia

A
  • Obtain: sleep history, overview of problems
  • Info: nature of complaint, current sleep pattern, development course, impact of problem, treatment received
  • Diet, substance use and medication; other psychiatric, medical or sleep problems
76
Q

Narcolepsy

A
  • 0.05% prevalence
  • Excessive daytime sleepiness (sleep attacks)
  • Disrupted night time sleep
  • Could be due to a deficiency in orexin
77
Q

Restless leg or periodic limb movement disorder

A
  • 4.4% prevalence
  • Lower extremities
  • Disrupted night time sleep
78
Q

Obstructive sleep apnea

A
  • 2-4% prevalence
  • Breathing effort
  • Sleep disruption
79
Q

Fatal familial insomnia

A
  • Genetic degenerative brain disorder
  • Pathogenic mutation of prion protein gene
  • Unarousable coma and finally death (within 8-72 months after onset)
80
Q

Factors when looking for causes for insomnia

A
  1. Predisposing: genes, biology, arousability
  2. Precipitating: noise, jet lag, life stresses
  3. Perpetuating (maintaining): cognitive, emotional, behavioural
81
Q

Single factor theories for insomnia: Sleep hygiene

A
  • Notion: lifestyle factors promote or inhibit sleep

* But no differences in sleep hygiene for good and poor sleepers

82
Q

Single factor theories for insomnia: Stimulus Control Model

A
  • Notion: sleep as a habit or conditioned behaviour (bed and bedroom is paired with non-sleeping behaviour for insomniacs)
  • Good: bed > sleep > arousal reduction and sleep onset
83
Q

Multiple factors of insomnia: Morin (1993) CBT model

A
  • Dysfunctional cognitions
  • Maladaptive habits
  • Consequences
  • Arousal
84
Q

Multiple factors of insomnia: Harvey (2002) cognitive model

A
  • Beliefs and safety behaviour
  • Negative cognitive activity, arousal/distress, selective attention and monitoring, misperception of sleep/ daytime functioning
85
Q

Multiple factors of insomnia: Lundh & Broman (2000) model

A
  • Arousal: arousability, stimulus-arousal associations, CB strategies, interpersonal relations
  • Appraisal: attributions, perfectionism, beliefs
86
Q

Multiple factors of insomnia: Espie

A
  • Attentional-intention-effort pathway
  • Assumes that normal sleep is inhibited by explicit and implicit attention to sleep, intention to sleep, and direct and indirect attempts to control it
87
Q

Hyperarousal in insomnia models

A
  • This idea is embedded into many of the theories
  • Insomnia often found in those with high (inappropriate) arousability
  • Cognitive e.g. beliefs about sleep
  • Behavioral e.g. poor stimulus control
88
Q

Format of CBT for insomnia

A
  • 4-12 weekly sessions
  • Individual or group
  • Self help book; telephone
89
Q

CBT content and AASM recommendation

A
  • Sleep hygiene education: none
  • Relaxation training: high
  • Biofeedback: moderate
  • Imagery training: none
  • Paradoxical intention: moderate
  • Stimulus control therapy: high
  • Sleep restriction: moderate
  • Cognitive therapy: none
90
Q

CBT pros and cons

A
Advantages: 
•	Suitable for persistent insomnia 
•	Patient’s preference 
•	Gains maintained at follow-ups 
•	Fewer and more tolerable side effects 

Disadvantages:
• Not a panacea
• Longer treatment duration
• Limited access to treatment

91
Q

Insomnia drug classes

A
  • Barbituates
  • Benzodiazepines
  • Non-benzodiazepines
  • Antidepressants
  • Antihistamines
  • Melatonin
  • Herbal or dietary supplements
92
Q

Drugs pros and cons

A

Advantages:
• Convenient (fast acting)
• Suitable for short term insomnia

Disadvantages: 
•	Harsh side effects 
•	Residual effects 
•	Altered sleep architecture 
•	Tolerance 
•	Lethal overdose 
•	Increased mortality and incidence of cancer 
•	NICE recommends that non-medicine treatments should be considered and tried first
93
Q

Alternative treatments

A
  • Bright light therapy
  • Exogenous melatonin
  • Exercise
  • Mindfulness