Week 5: Physiology, Psychology and Pathology of Sleep Flashcards
1
Q
What characterizes sleep?
A
- a state of altered consciousness
- increased threshold of sensory perception → still capable of perceiving distal stimuli
- active brain patterns → all brainwave types present but different in amplitude and frequency
2
Q
What characterizes sleep in terms of its function?
A
- evolutionary (millions of years)
- essential for:
- restoration of immune system
- restoration of skeletal system
- restoration of nervous system
- restoration of muscular system
- maintenance of mood
- maintenance of cognitive function
3
Q
What is an important mechanism of sleep?
A
- thalamic-mediated synchronization mechanisms
- give rise to large-scale integration of information across cortical circuits
4
Q
What is the sleep state?
A
- a function of neural integration
- seemingly specula role played by thalamic gap
5
Q
How do different parts of the brain interact?
A
there is a competing balance between front and back of the brain to initiate nREM and REM sleep, respectively
6
Q
What are the different sleep stages and how can you recognize them?
A
- awake: alpha waves
- REM: theta waves and sawtooth waves
- non REM 1: Theta waves
- Non REM 2: Spindles and K-complex
- Non REM 3 and 4: Delta Waves
7
Q
What is the Circadium Rhythm?
A
- almost all species exhibit 24-hour changes in behavior and physiology including sleep-wake patterns
- the 24-hour cycle is not just a response to physical environment but arises from internal timekeeping system → “biological clock”
8
Q
What characterizes the Circadian Rhythm (CR)?
A
- self- sustained: continues without external time-giving cues
- entrained: synchronized by external time-giving cues
9
Q
How is the CR coordinated?
A
by suprachiasmatic nuclei
→ their importance for sleep-wake patterns are demonstrated by lesion studies
10
Q
How does light exposure affect the CR?
A
- melanopsin-containing retinal ganglion cells are primary circadian photoreceptors
- they project to SCN via direct and indirect pathway
- SCN signals to pineal gland to inhibit melatonin production
- absence of light exposure:
- inhibition is removed → pineal gland releases melatonin
- melatonin feeds back to SCN
- SCN permits sleep drive
11
Q
What is a circadian rhythm sleep disorder?
A
= a chronic recurring pattern of sleep and wake disturbances du to:
- a dysfunction of internal circadian clock systemor
- a misalignment between timing of internal circadian rhythm and externally impose sleep-wake cycles
12
Q
What is Delayed Sleep Phase Disorder?
A
= the consistent delay of the major sleep episode
13
Q
What are different Circadian Rhythm Sleep Disorders?
A
- Delayed Sleep Phase Disorder
- Advanced Sleep Phase Disorder
- Non 24-hour Sleep Wake Disorder
- irregular Sleep-Wake Rhythm Disorder
- Shift-Work Disorder
- Jet Lag (chronic)
14
Q
What is Non 24-hour Sleep Wake Disorder?
A
sleep-wake patterns that are not entrained to 24 hours and cycle over time
15
Q
What is Insomnia according to the ICD-11?
A
- difficukty in falling and/ or remaining asleep
- subjectively causes difficulties with daytime functioning or well-being
- experience sleep problems at least 3x/week for at least 3 months
- problems arise even if circumstances/ opportunities for sleep are ideal
16
Q
What are different types of Insomnia?
A
insomnia as a primary vs second condition
17
Q
When do we talk about Insomnia as a secondary condition?
A
when insomnia is in the presence of other major diagnoses
18
Q
when do we talk about “Insomnia Disorder”?
A
- also “primary Insomnia”
- exclusionary diagnosis of poor sleep → ruling out psychiatric, medial, substance and other sleep-related pathology
19
Q
How is the Interplay between Insomnia and other disorders?
A
high comorbidities with other mental disorders
20
Q
What different types of symptoms of Insomnia do we distinguish?
A
- nighttime symptoms
- cognitive impairments
21
Q
What are nighttime symptoms?
A
- difficulty initiating sleep
- frequent awakenings
- early morning awakening
- reduced sleep efficiency
22
Q
How can Insomnia affect cognitive performance?
A
- memory deficits
- impaired executive function
- attention deficits
- emotional dysregulation
23
Q
How does stress have an impact on sleep?
A
- dynamic and complex relationship between sleep and stress
- exposure to stress and to insomnia causes changes in regulation of stress and sleep
- conditions of initial insomnia and perpetuation may differ
24
Q
What is restless REM sleep and what are its consequences?
A
- sound REM sleep is the only state during which the brain has a “time-out” of noradrenaline → the locus coeruleus is silenced
- restless REM sleep indicates insufficient silencing of locus coeruleus→ lack of noradrenaline free REM sleep period→ disrupts synaptic plasticity
25
What is hyperarousal?
= state of acute anxiety or other emotional distress
→ can manifest in somatic, emotional, cognitive, cortical ways
26
What is hyperarousal in the context of Insomnia?
imbalances in neurotransmitters like noradrenaline, GABA, glutamate
27
What is sleep reactivity?
= the trait-like degree to which stress exposure disrupts sleep, resulting in difficulty falling and staying asleep
→ its a normal phenomenon
28
What are the neurobiological underpinnings for sleep reactivity?
- disrupted cortical networks
- dysregulation in the autonomic nervous system
- dysregulation in hypothaamic-pituitary-adrenal axis
29
What is rumination?
= a form of preservative cognition that focuses on negative content → results in emotional distress
30
How does rumination affect Insomnia?
- subjects who tend to focus on Insomnia and start to ruminate about their sleep complaints are prone to develop “learned sleep-preventing associations”
- might explain chronicity of the disorder
31
What is the prevalence of Insomnia?
~10 - 30% of the population
32
How expensive is Insomnia for us?
~92.5-107.5 billion dollars annually
33
The treatment of insomnia is dependent on…
- access to healthcare
- disposability of trained clinicians and psychologists
- addiction potential
- possible medication interactions
- diagnosis and comorbidity
34
What are the most classical forms of treatment for Insomnia?
- CBT-I
- non-pharmacological approaches
- pharmacotherapy
35
What is CBT-I?
= Cognitive Behavioral Therapy for Insomnia
- non-pharmacological treatment for insomnia
- combination of CBT with other techniques
- short-term treatment with 4-8 sessions
36
What is the goal pf CBT-I?
change the patient's misconceptions, beliefs and attitudes that hinder sleep
37
What are elements of CBT-I?
- psychoeducation
- sleep diary
- sleep hygiene
- sleep control
- sleep drive
- relaxation
- thoughts
38
What are forms of non-pharmacological treatments of insomnia other than CBT-I?
- paradox intervention
- Sleep hygiene
- (physical) daytime activation
- stimulus control
- relaxation training
- sleep restriction
39
What are Hypnotics?
- a heterogenous group of substances with sedative, hypnotic, anxiolytic and sleep inducing effects
- different forms of application: spray, tablets, sublingual forms
40
What are common side effects of Hypnotics?
- Potential for addiction
- daytime somnolence and dizziness
- distortion of sleep architecture (less REM, phase 3&4)
- anterograde amnesia
- working memory impairment
- difficulty with attention
41
How do Benzodiazepines and Non-Benzodiazepines work for Insomnia?
- positive modulation / activation of GABAa-receptors → influx of Cl, cell becomes more negative
- BZS/Non-BZD bind to a-y/ a unit of GABAa-receptors and induce a change of conformation
- overall inhibitory effect in the nervous system
42
What are side effects of BZD?
- high risk for dependency
- withdrawal needs to be under medical observation
43
What is Melatonin?
- a hormone produced in pineal gland under control of circadian system in hypothalamic suprachisamatic nucleus (SCN)
- key role in regulating sleep-wake cycle
- synthesis modulated by the presence of light
44
How do Melatonin Receptor Agonists work?
- activate Mt1 and Mt2 receptors and stimulate presence of Melatonin
- different onset is possible (slow vs fast vs pulsatile release melatonin
45
What is Orexin?
- neuropeptide (protein made from genome) in two forms
- also called Hypocretin
- binds to receptor OX1R and OX2R and leads in cascades to opening Ca2+-channel → influx in Ca2+
- promotes wakefulness and suppresses REM sleep via excitatory projections from Hypothalamus (flip-flop)
- clinical implications in Narcolepsy
46
How do Orexin Receptor Antagonists work?
bind to OX1R and OX2R receptors an block Orexin from activation the receptor → promotes sleep
47
What are NIBS?
non invasive brain stimulation techniques that are being studied as treatment options for insomnia
48
What is the current state in terms of NIBS as a treatment option for insomnia?
- have potential in managing insomnia symptoms
- no brain stimulation protocol exists that could claim relevant therapeutic benefits
49
What is needed to establish NIBS for insomnia?
- understanding how the cortex contributes to sleep regulation
- understanding which patterns of cortical activity are altered in patients with insomnia
- further research
- well established portals
- sham control group
- double-blinded studies
50
What does the American academy of sleep medicine say?
- need for greater emphasis on sleep health in education, clinical practice, inpatient and long-term care, pubs health promotion, the workplace
- more sleep and circadian research is needed
