Sleep Flashcards

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1
Q

Disorders of Sleep

A
  • Insomnia
  • Sleep Apnea
  • Narcolepsy
  • REM sleep behaviour disorder
  • Slow-wave sleep problems
  • Fatal familial insomnia
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2
Q

Characteristics of REM sleep

A
  • Electroencephalography desynchrony (rapid, irregular waves)
  • Lack of muscle tonus
  • Rapid eye movements
  • Penile erection or vaginal secretion
  • Dreams
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3
Q

Characteristics of Slow-Wave sleep

A
  • Electroencephalography synchrony (slow waves)
  • Moderate muscle tonus
  • Slow or absent eye movements
  • Lack of genital activity
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4
Q

Functions of slow-wave sleep

A
  • Slow-wave sleep deprivation affects cognitive abilities, especially sustained attention, but not physical abilities
  • Cerebral metabolic rate and blood flow falls by about 75%.
  • This coupled with people’s unresponsiveness, and confusion if awakened suggests cerebral cortex ‘shuts down’ during sleep.
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5
Q

Functions of REM sleep.

A
  • If deprived of REM sleep, you will have more REM sleep in the next sleep period (Rebound phenomenon).
  • Highest proportion of REM sleep occurs during brain development
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6
Q

Findings of studies of the effect of sleep on learning

A
  • REM sleep facilitates consolidation of nondeclarative memories
  • Slow-wave sleep facilitates consolidation of declarative memories
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7
Q

Neurotransmitters that play a role in arousal.

A
Acetylcholine
Norepinephrine
Serotonin
Histamine
Orexin
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8
Q

Describe the neural control of slow-wave sleep.

A
  • controlled by 3 factors – homeostatic, allostatic, and circadian.
  • Primary homeostatic factor – presence or absence of adenosine.
  • Allostatic control is mediated by hormonal and neural responses to stressful situations
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9
Q

So if a high level of activity in the arousal related neurons keeps us awake and a low level puts us to sleep, what controls the activity of these neurons?

A
  • Inhibition of the arousal system is necessary for sleep
  • Group of GABAnergic neurons in the ventrolateral preoptic area (vlPOA) become active and supress activity of arousal neurons.
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10
Q

What is the sleep/wake flip-flop

A
  • The flip-flop is on when the sleep-promoting neurons in the vlPOA are inhibited and the arousal neurons are active
  • The flip-flop is off when the sleep-promoting neurons in the vlPOA are activated and the arousal neurons are inhibited
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11
Q

Describe the effect of the orexinergic neurones in the sleep/wake flip-flop

A
  • Orexinergic neurons help to stabilise the sleep/waking flip/flop
  • Motivation to remain awake or events that disturb sleep activate the orexinergic neurons.
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12
Q

What factors control the activity of the orexinergic neurons?

A
  • Biological clock
  • Hunger related signals activate them
  • Satiety related signals inhibit them
  • Orexinergic neurons receiving inhibitory input from the vlPOA because of a build-up of adenosine.
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13
Q

Describe the Neural Control of REM Sleep

A
  • Acetylcholinergic neurons also fire at a high rate in REM sleep
  • There is a REM flip-flop
  • REM-ON neurons are located in the pons
    REM-OFF neurons are located in the midbrain
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14
Q

Causes of insomnia

A
  • Age - More common in older people
  • Environmental factors
    ○ Electronic devices, noise, light–detrimental
    ○ White noise or other repetitive noise - beneficial
  • Physiology
    ○ Heightened activity in the reticular activating system
  • Circadian rhythms
  • Medical conditions and medications
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15
Q

Treatment of insomnia

A
  • drugs, mindfulness and CBT.
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16
Q

What is sleep apnea

A
  • Form of insomnia – the inability to sleep and breathe at the same time
  • Build of carbon dioxide in the blood stimulates chemoreceptors
  • Disrupts sleep affecting daytime functioning
  • If caused by obstruction can be corrected surgically or relieved by pressurised air that keeps the airway open
17
Q

Narcolepsy symptoms

A
  • Sleep attack – overwhelming urge to sleep
  • Cataplexy – muscular paralysis of REM sleep while awake
    ○ Varying degrees of muscle weakness
    ○ Can become completely paralyzed while conscious
    ○ Generally occurs when the person feels strong emotions or by sudden physical effort.
  • Sleep paralysis
    ○ REM muscular paralysis just before the onset of sleep or upon waking
  • Hypnagogic hallucinations
    ○ dreaming while awake and paralysed
    ○ can very realistic and terrifying.
18
Q

Causes of Narcolepsy

A
  • Hereditary element
  • Environmental factors play a role but are unknown
  • Orexinergic neurons are attacked by the immune system, usually in adolescence
19
Q

Treatments of Narcolepsy

A
  • Sleep attacks diminished with stimulants e.g methylphenidate (Ritalin)
  • REM sleep phenomenon (cataplexy, sleep paralysis and hypagogic hallucinations) treated with antidepressant drugs
  • Most common current treatments are modafanil and/or sodium oxybate (GHB; gamma hydroxybutyric acid), both stimulant drugs
20
Q

What is REM Sleep Behaviour Disorder

A
  • Neurodegenerative disorder with a genetic component
  • Failure to exhibit paralysis during REM sleep
  • Acting out dreams
21
Q

Name some slow-wave sleep problems

A
  • Sleepwalking (Somnambulism)
  • Night terrors (pavor nocturnus)
  • Bedwetting (nocturnalenuresis)
22
Q

What is Fatal Familial Insomnia

A
  • Neurodegenerative condition
    • Prion disease - caused by build up of abnormal prion proteins which are resistant to being broken down by enzymes = accumulation = damage to brain
    • Damage to the thalamus
    • Initially presents with insomnia and very vivid dreams when the person finally manages to sleep.
    • Psychiatric complications – panic attacks, cognitive deficits, paranoia and phobias
    • As the disease progresses it affects the autonomic nervous system (e.g. elevated blood pressure) and coordination (ataxia)
    • EEG shows disturbances and reductions in sleep spindles and K complexes
    • Disappearance of slow-wave sleep and only brief periods of REM sleep
    • Ultimately inability to voluntarily move or speak (akinetic mutism), coma, and death.