Lecture 7: Sleep and nightmares Flashcards

1
Q

How can sleep be defined?

A

Sleep is a reversible behavioural state of perceptual disengagement from and unresponsiveness to the environment. Strange behaviours like sleepwalking, sleep talking and teeth grinding can occur.

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2
Q

How can different types of sleep be distinguished?

A

Between REM which is desynchronized, atonic muscles and dreaming, rapid bursts of eye movement and NREM which has consistent EEG activity (sleep spindles, K-complexes and high-voltage slow waves), low muscle tonus and minimal psychological activity.

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3
Q

What are the NREM stages?

A

1, 2, 3, 4 which are the same in the depth of sleep and the lowest arousal threshold in stage 1 and highest in stage 4

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4
Q

What is the difference between tonic vs phasic activity in REM?

A

Can be distinguished by the occurrence of rapid eye movements, muscle twitches and cardiorespiratory differences. Tonic activity has no rapid eye movements, muscle atonia and steady brain activity while phasic activity has intermittent bursts of activity, rapid eye movements, muscle twitches, and more variable physiological responses.

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5
Q

How is muscle atonia achieved?

A

Through inhibition of spinal motor neurons by brainstem mechanisms

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6
Q

How can sleep onset be defined by 3 different ways of measuring?

A

EMG: shows a gradual decline of muscle tonus as sleep approaches but not discrete and difficult to distinguish between pre-sleep
EOG: slow and asynchronous eye movements, which disappear after a few minutes. The onset of these coincide with perceived sleep onset
EEG: can move from clear alpha activity to a low-voltage mixed-frequency pattern. Specific EEG patterns like K complex or sleep spindles are needed for sleep onset. Sleep onset is more gradual so a single variable cannot mark this change

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7
Q

What are the behavioural correlates of the wake-to-sleep transition?

A

Simple behavioural task: when asked to do a simple task, the behaviour continues after the onset of slow eye movements and stops when EEG has a waking pattern
Visual response: bright light in front of eyes and in stage 1 or 2 of sleep reflect that they did not see the light-> perceptual disengagement
Auditory response: reaction times longer to tones while onset of stage 1 sleep and absent from change in EEG to sleep
Olfactory response: pleasant stimuli and unpleasant stimuli responses were maintained in stage 1 sleep. Peppermint was not recalled in stages 2 and 4, and pyridine never smelled in stage 4 but sometimes in stage 2
Response to meaningful stimuli: arousability shows differential responses to auditory stimuli, different responses to meaningful stimuli using K-complexes or arousal.
Hypnic Myoclonia: general or specific muscle contraction linked to vivid visual imagery, can occur with stress and irregular sleep

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8
Q

What has research found about the response to meaningful stimuli?

A
  • lower arousal threshold needed for own name compared to another’s name
  • likelihood of an appropriate response during sleep improved when nonmeaningful stimulus was made meaningful by linking absence to response to punishment
  • regional brain activation occurs in response to stimuli and that different brain regions (temporal gyrus and OFC) were activated in response to meaningful stimuli
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9
Q

Why do hypnic myoclonias occur?

A

Can happen with dissociation of REM sleep components as the imagery components of REM can occur without the motor inhibitory component, which results in movements in response to the image

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10
Q

What is the usual transition into sleep?

A

For adults through NEM, while for infants is the REM portal

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11
Q

How does memory change near sleep onset?

A

The transition from wake to sleep produces a memory impairment. Word pairs were presented to volunteers at a 30 seconds or 10 mins after the onset of sleep and were asked to recall words, performance for 30 sec group was similar to before sleep onset-> STM and LTM stores were accessible but for 10 min group only LTM was inaccessible. Two interpretations: sleep inactivates transfer of storage from short to long-term memory or that encoding does not have enough strength to allow for recall. Sleep important for consolidation of perceptual and motor learning

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12
Q

Pattern of sleep in a healthy young adult

A

Enters sleep through NREM sleep, REM sleep occurs around 80 mins or longer after, then NREM and REM which alternate through the night with a 90 minute cycle. REM sleep episodes become longer through the night, with stage 3 and 4 taking less time in the second cycle and can disappear in later stages.

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13
Q

What occurs in the first sleep cycle?

A
  1. Stage 1 persists for a few minutes at the onset and can be easily discontinued, linked to a low arousal threshold. Can also be a transitional stage throughout the night
  2. Stage 2 is shown by sleep spindles or K-complexes in EEG and continues for 10-25 mins in first cycle. More intense stimulus needed for arousal (K-complex can be evoked but no awakening)
  3. As high voltage slow wave activity increases, can result in stage 3 NREM sleep. Lasts for few mins but transitional to stage 4
  4. Stage 4 involves more high-voltage slow wave activity and a larger stimulus needed for arousal
  5. REM sleep in first cycle is short-lived and has a variable arousal threshold, selective attention to internal stimuli precedes a response or included in the dream
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14
Q

How does synchronized sleep affect the sleep cycle?

A

SWS dominates the NREM part of the sleep cycle at the start of the night, as a response to the length of wakefulness before, but diminishes later in the night. REM episodes longest near the end of the night, and brief episodes of wakefulness intrude later in the night

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15
Q

What is the length of sleep?

A

Lots of variability, can be determined by genetics and staying up late can impact. Length of prior waking can affect how much one sleeps, due to circadian rhythm processes. The amount of REM sleep can increase as the sleep is extended

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16
Q

What are generalizations about sleep in the healthy young adult (this amount of detail not needed)?

A
  • Sleep is entered through NREM sleep.
  • NREM sleep and REM sleep alternate with a period near 90 minutes.
  • SWS predominates in the first third of the night and is linked to the initiation of sleep and the length of time awake
  • REM sleep predominates in the last third of the night and is linked to the circadian rhythm of body temperature.
  • Wakefulness in sleep usually accounts for less than 5% of the night.
  • Stage 1 sleep generally constitutes about 2% to 5% of sleep.
  • Stage 2 sleep generally constitutes about 45% to 55% of sleep.
  • Stage 3 sleep generally constitutes about 3% to 8% of sleep.
  • Stage 4 sleep generally constitutes about 10% to 15% of sleep.
  • NREM sleep, therefore, is usually 75% to 80% of sleep.
  • REM sleep is usually 20% to 25% of sleep, occurring in four to six discrete episodes.
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17
Q

How does age affect sleep stage distribution?

A
  • adults have longer cycles than newborns (have around 50/60 mins but up to 90 for adults)
  • not fully developed EEG patterns of NREM not present at birth like the ability to support high-voltage slow wave and NREM stages 3 and 4 become prominent
  • SWS is maximal in children but decreases with age
    -REM sleep as a proportion of total sleep is maintained throughout, with absolute amount of REM linked to intellectual functioning
  • arousals during sleep increase with age
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18
Q

How does prior sleep history impact sleep distribution?

A
  • sleep loss can result in recovery sleep which is longer and deeper with a higher arousal threshold
  • REM shows a rebound on the following nights after an episode of sleep loss
  • an irregular sleep schedule or sleep disturbances can result in a strange distribution of sleep states like premature REM like hypnagogic hallucinations, sleep paralysis etc
  • lab sleep evaluation linked to more arousals, delayed REM and disruption of normal distribution of REM sleep, skipping of REM sleep
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19
Q

How can circadian rhythms affect sleep?

A
  • REM sleep occurs with a circadian distribution which peaks in morning hours
  • if sleep onset is delayed then the REM sleep can predominate and occur at onset of sleep
  • sleeping in environments without cues show that the timing of sleep onset and length of sleep are in accordance with circadian phases
20
Q

How can temperature affect sleep?

A

REM is more sensitive to temperature-related disruption than NREM sleep. Research has shown that mammals have minimal ability to thermoregulate during REM. Temperature related responses are more likely to occur in NREM sleep than REM sleep

21
Q

How can drug ingestion affect sleep?

A
  • Benzos suppress SWS and no effect on REM
  • antidepressants suppress REM sleep and linked to greater motor activity, fluoxetine is linked to rapid eye movements-> REM has no motor inhibition and more periodic limb movements in sleep
  • withdrawal from these drugs which suppress sleep is linked to rebound of sleep
  • acute alcohol intake increases SWS and suppression of REM sleep early in the night which rebounds later in the night
  • acute effects of weed has little sleep distribution but a reduction of REM sleep but chronic THC ingestion can produce long-term suppression of SWS
22
Q

What is narcolepsy?

A
  • characterized by an abnormally short delay to REM sleep can also be NREM sleep onset
  • includes opportunities to fall asleep across a day, dissociation of components into waking state like hypnagogic hallucinations, sleep paralysis and cataplexy
23
Q

When does sleep fragmentation occur?

A
  • likely with many other sleep disorders
  • brief arousals likely in rhinitis, arthritis and Parkinson’s
  • ECG arousals important for the upper airway resistance syndrome as less obvious than signs of sleep apnea
  • changes in blood pressure can signify arousals
  • can be linked to subcortical events that are seen in the EEG signal
  • disorders linked to an increase in the absolute and proportional amount of stage 1 sleep
24
Q

What are sleep apnea syndromes?

A

Can be linked to suppression of SWS or REM sleep secondary to the breathing problem. Many successful treatments can produce large rebounds of SWS or REM

25
Q

Which other conditions have a short REM sleep latency?

A
  • sleep reversal or jet lag
  • withdrawal from REM suppressant drugs
  • chronic restriction or sleep disruption
  • endogenous depression
  • higher prevalence of early REM sleep onsets in adults and adolescents
26
Q

What is nightmare disorder?

A

Nightmare= extended, dysphoric dream that involves efforts to avoid threats to survival, security or physical integrity during REM sleep and involves feelings of fear
Nightmare disorder= repeated occurrence of nightmare that cause clinically significant distress in many areas of functioning not due to coexisting mental disorders or physiological effects of a substance

27
Q

What are the different types of nightmares?

A
  • posttraumatic nightmares can be direct replications of a traumatic event or has a trauma related emotion or symbolically related to the trauma-> more severe arousal, more awakenings, stronger aggression, more helplessness
  • idiopathic nightmares depict stories more imaginative and not reflective of a traumatic event
28
Q

What is the DSM criterion for nightmare disorder?

A
  • repeated occurrences of exteneded, dysphoric and well-remembered dreams
  • waking up not a neccessary criterion
  • no frequency criterion but a mild ND involves less than an episode per week on average, moderate one or more per week, severe is every night
  • acute: 1 month or less, subacute: 1 month but less than 6, chronic: 6 months or longer
29
Q

What are the consequences of nightmare disorder?

A
  • wide range of mental complaints, sleep disruptions and insomnia
  • difficulties in sleep onset and maintenance, compromised daytime functioning
  • tiredness after getting up, daytime sleepiness, lack of energy, petulance, difficulty concentrating, worrying about having enough sleep
  • increased mental distress, anxiety, depression, poor academic performance, maladaptive personality functioning
  • increase the risk of attempting and re-attempting suicide
30
Q

How can nightmares be assessed?

A
  • Nightmare frequency questionnaire,
    -NDQ shows that nightmares strongly correlated with mental health complaints like anxiety and depression
  • Distress caused by nightmares is more relevant to mental health than the nightmare frequency
31
Q

Solms’ neurocognitive theory of dream generation

A

Not generated by the brainstem that controls REM sleep but by forebrain mechanisms that are independent of the REM sleep state. His findings confirm that the mesocortical-mesolimbic dopamine system plays a causal role in the generation of dreams. Any lesions inhibit dreaming but not REM.

32
Q

What is the role of increased hyperarousal in nightmare disorder?

A

Those with PTSD and insomnia disorder more likely to experience arousals during REM sleep than good sleepers and more fragmented REM-sleep periods than good sleepers. Increased hyperarousal said to accumulate during the day and maintained at night

33
Q

What is the role of impaired fear extinction in nightmare disorder?

A

Those with ND continue to activate arousing memory fragments during sleep to reinforce fear memories. Those high in affect load (trait-like tendency to react to stressors with negative affect) and distress are prone to this. Linked to a hyperactive amygdala and compromised mPFC. Memory fragments are incompatible with negative arousal cannot be retrieved and fear-laden memory fragments cannot fully be integrated.

34
Q

What are the factors facilitating hyperarousal and impaired fear extinction?

A
  • traumatic experiences: fear extinction capacity is impaired by consequences of trauma due to induced changes in mPFC- amygdala circuits. Linked to emotion regulation disruption and fear memory development reinforced
  • trait susceptibility: higher novelty seeking and reward-related behaviours linked to more ND and worrying, more nightmares linked to increased depth of processing of semantic stimuli, more errors in response to distractors
  • maladaptive beliefs: suppressed thoughts can recur in dreams in REM sleep, avoidance linked to more recurrent nightmares
  • physiological factors: nightmares linked to sleep apnea, which occurs more often in PTSD patients. Withdrawal from REM sleep suppressing medication linked to nightmares
  • nightmare scripts: nightmares can continue as a learned behaviour linked to loops of replaying fixed expectation patterns when the original stressor has faded, can be activated in response to dream elements
35
Q

Stress acceleration hypothesis

A

Argues that memories of early events which are suppressed after the infantile amnesia period can influence dreaming and waking memory

36
Q

Which neurotransmitters play a role in nightmares?

A

Norepinephrine, serotonin, dopamine linked to occurrence of nightmares. While GABA, acetylcholine, histamine less likely to induce nightmares.

37
Q

How can treatment approaches target the meaning of nightmares?

A
  • posttraumatic nightmares described as having stereotypic replicative content
  • seen as an alarm signal of disturbance of psychic equilibrium and psychodynamic treatments could try to resolve these conflicts
  • importance of processing of multiple levels like the developmental and trauma history, similarities and differences to episodic memory traces, occurrence of nightmares to therapeutic processes, life situation and interpersonal patterns
  • changes in dream content were linked to adaptation vs maladaptation after traumatic events
38
Q

How can treatment approaches target the chronic repetition of nightmares?

A
  • seen as an overlearned behaviour which needs to be unlearned, based on desensitization, exposure, imagery rehearsal and lucid dreaming
  • desensitization: muscular relaxation when imaging the nightmare, or without relaxation-> other symptoms are overridden by other adaptive processes but can cause severe distress
  • imagery rehearsal therapy: involves rescripting the story of the nightmare in wakefulness which is then rehearsed, found to be significant in reducing nightmare frequency
  • lucid dreaming: dream with awareness of orientation and ability to make decisions. Can do so by dream recall after awakening, realizing whether you are dreaming, checking whether you are dreaming. But not everyone is able to reach the lucid state
39
Q

Which aspects of IRT were found to be the most effective?

A
  • multicomponent package-> difficult to identify which specific component is effective
  • treatments include: psychoeducation, sleep diaries, relaxation exercises, imagination techniques
  • keeping of diaries is not necessary and minimal exposure not
  • just psychoeducation was also found to be effective
40
Q

What are the treatment approaches targeting maladaptive beliefs?

A

Maladaptive beliefs can be modified through behavioural experiments and cognitive re-structuring. Assigning negative beliefs to the self can worsen negative beliefs about nightmares and paradoxical intention (encouraging nightmare sufferers to have nightmares) can be used to combat negative appraisals

41
Q

What are the active treatment mechanisms of direct nightmare treatment?

A

The belief that one is in control of nightmares involves cognitive elements and emotional processing which results in memory consolidation (reorganization of fear structures in the memory network) which is found to be important for treatment and restructuring memory content to overcome hyperarousal.

42
Q

What has been found about pharmacological treatment of nightmares?

A

Use of prazosin which is a CNS receptor antagonist, but found mixed results. Is seen as an option for treatment, but not fully recommended

43
Q

How can nightmare treatment be used in different populations?

A

PTSD: IRT found to be effective, especially when combining with CBT but lots of variability in treatment protocol
Other mental disorders: IRT effective as an add on treatment for frequency and distress, can improve general treatment outcomes
Refugees: 30% suffer from PTSD, many suffering from sleep disturbances, language and cultural differences can complicate treatment
Children and adolescents: more likely to be afraid of the dark and sleeping alone, having nightmares at 8-11 was predictive of later nightmares. Treatments found to be effective and showed decreases in nightmare symptoms

44
Q

How is there lack of knowledge about nightmare suffering and treatment availability?

A

Nightmare screenings and treatments are rare even in sleep centres. Nightmares can be treated even with a single session, but many do not seek professional help due to lack of knowledge of other options

45
Q

What are the future perspectives (not too important to learn)?

A
  • research depends on subjective criteria so more valid experimental models needed and more clearly defined nightmare criteria
  • importance of psychoneuroimmunology and endocrinology
  • interplay btw sleep-disordered breathing and nightmares
  • better understanding of thought suppression
  • alternative treatments to IRT should be considered
  • little research about the content of nightmares
46
Q

Future perspectives on sub-populations (not needed to learn as not too important)

A
  • more identification of PTSD symptoms with nightmare symptoms
  • benefits of using IRT with other psychotherapies
  • relationship btw cognitions, sleep and PTSD
  • little research on the impact of nightmare treatments on other disorders
  • nightmare treatments fail to address the needs of refugees
  • no comparison across age groups for nightmare treatment
  • many go untreated due to lack of screening-> more education and more efficient screening
  • low threshold interventions should be developed
47
Q

What are the future perspectives about the integration into healthcare?

A