Tutorial 05 Flashcards

1
Q

What does the thalamic-mediated Synchronisation mechanisms do?

A

They give rise to large-scale integration of information across cortical circuits

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2
Q

Which sleep stage is the alpha waves?

A

Awake

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3
Q

Which sleep stage are theta waves?

A

REM and Non REM1

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4
Q

Which sleep stage are delta waves?

A

Non REM 3 – deep sleep

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5
Q

Which sleep stage are spindles and K-complexes?

A

Non REM 2

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6
Q

Sleep is a state of consciousness characterised by …

A

… low awareness and alertness with a higher threshold for sensory perception

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7
Q

The sleep stage is a function of …

A

… neural integration, with seemingly special role played by the gap junctions

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8
Q

What can we characterize to figure out the different Stages of sleep and how many sleep stages are there?

A

We can identify brain wave features, which characterize the 4 stages of sleep

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9
Q

Where is a competing balance in the brain to initiate nREM and REM sleep?

A

There is a competing balance between the front and back of the brain to initiate nREM and REM sleep

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10
Q

Is CR self sustained or entrained?

A

Both, CR is self-sustained; continues without external time-giving cues
CR is also entrained: synchronized by external time-giving cues

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11
Q

What is the circadian rhythm coordinated by?

A

CR is coordinated by Suprachiasmic Nuclei (SCN), lesion studies demonstrate their importance for sleep-wake patterns

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12
Q

What are the primary circadian photoreceptors? And where do they project to?

A

Melanopsin-containing retinal ganglion cells and they project to the SCN via a direct and an indirect pathway

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13
Q

Where does the suprachiasmatic nuclei signal to?

A

SCN signals to pineal gland to inhibit melatonin production

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14
Q

What happens to the pineal gland by an absence of light exposure?

A

Absent of light exposure, inhibition is removed and pineal gland releases melatonin
-> melatonin feeds back to SCN: permits sleep drive

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15
Q

Circadian rhythm sleep disorder?

A

A chronic recurring pattern of sleep and wake disturbances due to a) a dysfunction of the internal circadian clock system
B) a misalignment between timing of internal CR and externally imposed sleep wake cycles

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16
Q

Examples of circadian rhythm sleep disorders

A

Delayed sleep phase disorder
Non 24-hour sleep wake disorder
Advanced phase sleep disorder
Irregular sleep-wake rhythm disorder
Jet lag (chronic)

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17
Q

ICD-11 definition of insomnia

A

○ Disorder is characterized by difficulty in falling asleep and/or remaining asleep
○ Subjectively causes difficulties with daytime functioning or well-being
○ Experience sleep problems at least three times a week for at least three months
○ Even if circumstances/opportunities for sleep are ideal

18
Q

Insomnia Disorder (Primary Insomnia)

A

constitutes an exclusionary diagnosis of poor sleep, ruling out
psychiatric, medical, substance, and other sleep-related pathology

19
Q

Nighttime symptoms of insomnia

A

Difficulty initiating sleep, frequent awakenings, early morning awakening, reduced
sleep efficiency

20
Q

Cognitive impairments

A

Memory and Attention Deficits, Impaired Executive Function, Emotional
Dysregulation

21
Q

Sleep and stress

A

● Literature presents a dynamic and complex
relationship between stress and sleep
● Exposure to stress and even to insomnia itself causes
changes in the regulation of stress and sleep
● As a result, the conditions under which the initial
episode of insomnia develops may differ from the
conditions that perpetuate its course or give rise to
recurrent episodes

22
Q

Restless REM sleep

A

Sound REM sleep is the only state during which the brain has a “time-out” of noradrenaline (NA): the
locus coeruleus (LC) is silenced
● Restless REM sleep, however, indicates insufficient LC silencing
→ The resulting lack of a NA-free REM sleep period disrupts synaptic plasticity

23
Q

Hyperarousal

A

● Hyperarousal resembles the state of acute
anxiety or other emotional distress
● Hyperarousal in insomnia involves
imbalances in neurotransmitters like
noradrenaline, GABA, and glutamate

24
Q

Manifestations of hyperarousal

A

somatic, emotional,
cognitive, cortical

25
Sleep reactivity
● Is the trait-like degree to which stress exposure disrupts sleep, resulting in difficulty falling and staying asleep → more susceptible to hyperarousal ● Sleep reactivity is a normal phenomenon
26
Neurobiological underpinnings for sleep reactivity
involve disrupted cortical networks and dysregulation in the autonomic nervous system and hypothalamic-pituitary-adrenal axis
27
Rumination
is a form of preservative cognition that focuses on negative content, and results in emotional distress
28
Hyperarousal concept
subjects who tend to focus on the insomnia and start to ruminate about their sleep complaint are prone to develop ‘learned sleep- preventing associations’ which may explain the chronicity of the disorder
29
most classical form of treatment for insomnia?
CBT-I, non-pharmacological approaches, pharmacotherapy, (multimodal approach)
30
Cognitive (Behavioral) Therapy (CBT-I)
= combination of cognitive therapy with other techniques, multi-component approach goal: change the patient's misconceptions, beliefs, and attitudes that hinder sleep short-term treatment that includes 4 to 8 sessions (25 min every 14 days) e.g. sleep diary, psychoeducation
31
Name non-pharmacological treatments of insomnia
Paradox intervention, sleep hygiene, (Physical) daytime activation, sleep restriction, Relaxation Training, stimulus control
32
Hypnotics
= heterogenous group of substances with sedative, hypnotic, anxiolytic and sleep inducing effects - different forms of application: spray, tablets, sublingual forms
33
Common side effects of hypnotics
- anterograde amnesia, working memory impairment, attention - distortion of sleep architecture (less REM, phase 3&4) - daytime somnolence and dizziness - potential for addiction (!)
34
Examples of hypnotics
Non-Benzodiazepines “Z-Drugs”, Orexin Receptor Antagonists, Benzodiazepines, Melatonin Receptor Agonists, Antidepressants, Antipsychotics, Anticonvulsants, Antihistamines
35
How do benzodiazepines work?
- positive modulation / activation GABAa-receptors - ligand-gated ion channel (GABA) - open: Influx of Cl- (cell becomes more negative) - BZD/Non-BZD bind to α-γ / α unit of GABAa- receptors and induce a change of conformation - dependent on presence of GABA - overall inhibitory effect in the nervous system - high risk for dependency in BZD, withdrawal needs to be under medical observation! → short period
36
Melatonin
hormone, produced in pineal gland under control of circadian system in hypothalamic suprachiasmatic nucleus (SCN) - key role in regulating the sleep-wake cycle - synthesis modulated by presence of light
37
Mechanism of melatonin receptor agonists
- Melatonin Receptor Agonists activate Mt1 and Mt2 receptors and simulate the presence of Melatonin - different onset possible (release)
38
Orexin (Hypocretin)
= neuropeptide (protein made from genome) in two forms - bind to receptor OX1R and OX2R and leads in cascades to opening of Ca2+-Channel (influx of Ca2+) - effects: promote wakefulness + suppress REM sleep via excitatory projections from hypothalamus (Flip-Flop) - clinical implications in Narcolepsy
39
How do Orexin Receptor Antagonists work?
Orexin Receptor Antagonists bind to OX1R and OX2R receptors and block Orexin from activating the receptors → promote sleep
40
Stimulation therapy – results
- NIBS have potential in managing insomnia symptoms - yet, “no brain-stimulation protocol exists that could claim relevant therapeutic benefits” →“understanding how the cortex contributes to sleep regulation and which patterns of cortical activity are altered in patients with insomnia will be essential when optimizing stimulation targets and protocols” - need for further research, well established protocols, sham control group, double-blinded studies (minimizing methodological limitations