Week 6-Sleep Flashcards

1
Q

What are 3 Psychophysiological measures for sleep stages

A

-Looks at how we sleep and how our muscles respond

  1. Electroencephalogram (EEG): electrodes attached to the scalp record electrical activity of the brain
  2. Electromyogram (EMG): electrodes attached to the chin monitor muscle (muscle twitching/mouth opening) activity whilst sleeping
  3. Electro-oculogram (EOG): monitors eye movements (Important for REM stage as rapid fast eye movements)
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2
Q

What brain activity occurs during Stage 1 of Sleep? (alpha wake stage)

A

-Slower waves than that of alert wakefulness but still low-voltage (amplitude) and high-frequency (alpha: 8-12 Hz)

-As we progress from Stage 1 sleep through Stages 2, 3 and 4, there is a gradual increase in voltage (amplitude) and decrease in frequency

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3
Q

What are EEG recordings characterised by?

A

Frequency (number of waves per second) and amplitude (size of a wave e.g., much bigger in stage 3)

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4
Q

What brain activity occurs during Stage 2 of Sleep?

A

-Increase in theta wave activity (4-7 Hz) and the body goes into a stage of deep relaxation (heart rate slows down and blood pressure decreases)

-Theta waves are interrupted by brief bursts of activities known as sleep spindles (high-frequency)

-Spindles are 1-2 second bursts of 12-14 Hz waves (high frequency bursts)

-A K-complex can also be observed - a very high amplitude pattern of brain (large negative wave and single positive wave which goes downwards)

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5
Q

What brain activity occurs during Stage 3 of Sleep?

A

Deep sleep or slow-wave sleep is defined by the occasional presence of delta waves - largest and slowest waves (1-2 Hz)

-Large and slow delta waves in EEG phase

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6
Q

What brain activity occurs during Stage 4 of Sleep?

A

Predominance of delta waves - we stay in stage 4 for a time before retreating back through sleep stages to stage 1

Stage 3 and 4 together are referred to as slow-wave sleep (SWS)

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7
Q

How does Stage 1 differ after a full cycle of sleep?

A

-After stage 4, we return to stage 1 but sleep activity is NOT the same

Initial Stage 1: First period of stage 1, not marked by major EMG or EOG activity changes (no muscle twitches, atonia or eye movements seen)

Emergent Stage 1: Subsequent stage 1 periods, marked by loss of muscle tone and characterised by rapid eye movements (REMs)

-All other stages of sleep are known as non-REM (NREM) sleep

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8
Q

What is brain activity like in the 90 minute sleep cycle?

A

Awake and Alert: Beta brain waves (has received a lot of attention lately in terms of drugs, pharmacological treatments for anxiety etc.,)

Awake but Drowsy: Alpha brain waves

50-70 minutes:
Stage 1 NREM Sleep: Mixture of alpha and theta brain waves

Stage 2 NREM Sleep: Sleep spindles, K complexes, theta brain waves, and beginning of delta waves

Stage 3 NREM Sleep: Mixture of thelta and delta brain waves

Stage 4 NREM Sleep: Delta brain waves

5-15 minutes:
REM Sleep: Fast, active brain waves accompanied by rapid eye movements (REMs)

-Never completing a full cycle=poor quality sleep

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9
Q

What do we observe in REM sleep in terms of brain activity and dreaming?

A

-During REM sleep we observe high brain activity and lack of muscle tone

-REM sleep is thought to be the physiological correlate of dreaming as 80% of dream recalls happen during awakenings from the REM sleep - while only 7% arise from NREM (not full narratives but isolated experiences e.g., “I was falling”)

-Along the night, the proportion of REM increases and NREM decreases. REM periods increase in length and frequency towards the morning (as cycle repeats)

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10
Q

How was the 2 key brain areas in the hypothalamus involved in sleep regulation discovered?

A

-The 2 key brain areas involved in sleep regulation was discovered during World War 1 by Constantin von Economo - a Viennese neurologist

-He examined victims of a serious viral infection - encephalitis lethargica - which led to the deaths of about 1.5 million people in a 1915-1926 epidemic

-The majority of patients slept for more than 20 hours per day (lethargy), arising only to eat and drink. Their cognitive function was intact and could communicate, but they would soon return to sleep

-A minority of patients had difficulty sleeping

-The neurologist wanted to look at the difference between those who slept for 20 hours and those who struggled to sleep to determine the region responsible for sleeping too much and for being awake

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11
Q

What 2 key brain areas in the hypothalamus were found to be involved in sleep regulation?

A

-He found that deceased victims with excessive sleep symptoms had damage in the posterior hypothalamus (wakefulness is associated with PH), whilst victims with the opposite problem had damage in the anterior hypothalamus (sleep is associated with AH)

-His findings and assumptions about the hypothalamus were later confirmed by lesion and animal experimental studies (look at fMRI studies and neuroimaging for additional reading)

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12
Q

What did Bremer (1936) discover after severing the brain stems of cats in several areas?

A
  1. Cut between the inferior and superior colliculi to disconnect their forebrains from ascending sensory input to not go to the upper part of the cortex (“cerveau isole” (upward dash on e), or isolated forebrain) –> continuous SWS (slow-wave sleep)
  2. Transection (cutting through) caudal to the colliculi (“encepale isole”) (upward dash on 2nd e and i), or isolated brain) cutting most of the same sensory fibers –> normal sleep cycle)

-This suggested that the structure involved in wakefulness was located somewhere in the brainstem between these two transections

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13
Q

What are the 4 pieces of evidence that the reticular activating system is involved in sleep? (based on Bremer’s cat study)

A
  1. Cats with a midcollicular transection (i.e., a cerveau isole preparation) displayed a pattern of continous slow-wave sleep in their cortical EEGs.
  2. Lesions at the midcollicular level that damaged the core of the reticular formation, but left the sensory fibers intact, produced a corticial EEG indicative of continous slow-wave sleep.
  3. Electrical stimulation of the pontine reticular formation desynchronised the cortical EEG and awakened sleeping cats.
  4. Cats with a transection of the caudal brain stem (i.e., and encephale isole preparation) displayed a normal sleep-wake cycle of cortical EEG.

-Together, these 4 findings suggest that a wakefulness-producing area was located in the reticular formation between the cerveau isole and the encephale isole transections

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14
Q

What were 2 more findings which indicated this structure was the reticular formation?

A
  1. Partial transections at the cerveau isole level disrupted normal sleep-wake cycles of cortical EEG BUT only when they severed the reticular formation core of the brain stem.
  2. Electrical stimulation of the reticular formation of sleeping cats awakened them

-Based on these 4 findings Moruzzi and Magoun (1949) proposed that low levels of activity in the reticular formation produce sleep and that high levels produce wakefulness –> reticular formation known as the reticular activating system.

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15
Q

What do similarities between REM and wakefulness suggest + what is REM sleep controlled by?

A

-Similarities between REM and wakefulness suggest that the same brain area might be involved in controlling both.

REM sleep is controlled by nuclei in the caudal reticular formation, each controlling a different aspect of REM:
-Atonia (loss of muscle tone)
-Rapid eye movements
-Cardiorespiratory changes

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16
Q

What is the Neurochemical control of sleep?

A

-Sleep is regulated - suggesting a monitoring mechanism

-Do sleep-promoting substances or wakefulness promoting substances exist?

-Substances do not appear to circulate in the blood just produced in the brain (NMs or NTs)

-Controlled by chemicals that are produced and act within the brain

-Because REM and NREM sleep are regulated independently there might be two substances (related to 2 brain regions mentioned prior)

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17
Q

The amount and timing of sleep is regulated by what 2 major factors?

A
  1. Homeostatic drive (the body’s need for sleep)
  2. Circadian rhythm (the body’s biological clock for the sleep-wake cycle)

-The control of sleep can also be allostatic (the need to be awake) in nature; under some circumstances it is important to stay awake, as for example when reacting to stressful events in the environment (danger, lack of water) –> override homeostatic control

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18
Q

What is adenosine?

A

-It’s a substance/ NT that accumulates with waking hours and drives the pressure to sleep

-Caffeine promotes wakefulness by acting as an antagonist of adenosine (slows it down delaying pressure to sleep)

-The need for sleep, or pressure to sleep is lowest after a good night’s sleep and then starts to build up as we awaken. The need to sleep will rise until we get to sleep.

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19
Q

What is the role of adenosine in the Neurochemical control of sleep?

A

-Adenosine is a neuromodulator that has an inhibitory (i.e., decreases) effect on neural activity

-In terms of increased brain activity glycogen stored in the astrocytes is converted into glucose to fuel neurons

-When glycogen levels start to fall (energy depletion), adenosine starts to accumulate

-Caffeine blocks adenosine receptors (to remain awake longer)

-During SWS, neurons in the brain rest and the astrocytes renew their stock of glycogen (taking adenosine levels back to normal)

-If wakefulness is prolonged even more adenosine accumulates

-Since adenosine inhibits neural activity, it can produce the cognitive and emotional effects/impairments seen during sleep deprivation.

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20
Q

Neurochemical control of arousal: What is the arousal spectrum?

A

-Instead of only considering one being “awake” or “asleep” we should be thinking about the arousal spectrum (with varying cognitive demands on the brain)

There are 5 key neurotransmitters that can influence where someone lies on the spectrum:
-Acetylcholine (ACh)
-Norepinephrine (NE)
-Serotonin (5HT)
-Histamine (HA)
-Orexin (Hypocretin)

21
Q

What is the role of Acetylcholine in arousal?

A

-Acetylcholine is released from the cortex and hippocampus

-It is involved in desynchronised activity in the pons and the basal forebrain

-ACh antagonists decrease EEG arousal and agonists increase it

-Important for REM sleep and waking you up is also associated with visual processing in dreams (extra reading maybe) more ACh=more vivid dreams (in theory)

-The release goes down during SWS meaning its not important for that

22
Q

What is the role of Noradrenaline (aka Norepinephrine) in arousal?

A

-It is located in the locus coeruleus (LC) of the pons (deep in the brain stem area)

-LC is a small nucleus (small cluster of neurons with similar function) in the dorsal pons that is involved in directing attention

-Activation of LC neurons increases vigilance

-Noradrenaline agonists such as amphetamines produce arousal and sleeplessness

23
Q

What is the role of Serotonin (5-HT) in arousal?

A

-Serotonin is produced by raphe nuclei (located in the pontine and medullary regions of the reticular formation)

-Stimulation of the raphe nuclei causes movement and arousal

-Serotonin is involved in the activation of continuous in automatic behaviours such as pacing, chewing and grooming in cats

-When an animal engages in orienting responses the activity of serotonergic neurons decrease

(additional reading here?)

24
Q

What is the role of Histamine in arousal?

A

-Antihistamines are medicines often used to relieve allergy symptoms but have a disruptive side-effect for daily tasks making you sleepy as they block histamine signalling (can get ones which don’t pass the BBB to prevent this)

-Histaminergic neurons are located in the tuberomammillary nucleus of the hypothalamus and are involved in maintaining wakefulness

-Histaminergic neurons ‘regulate’ wakefulness by activating neurons in the cortex that drive arousal and by inhibiting neurons that promote sleep

  • Firing activity is high during waking and low during sleep

-Blocking activity of histamine neurons increases sleep

-Most structures related to sleep tend to be deep near the brain stem which neurally project to other areas of the brain e.g., back of the cortex

25
Q

What did Lin et al., 1999 find in studying narcoleptic dogs for more than 10 years?

A

-They isolated the gene that caused narcolepsy –> this gene encodes a receptor protein that binds to a neuropeptide called orexin

Narcolepsy has been associated with problems with orexin signalling:
-Degeneration of orexin neurons in humans
-Hereditary absence of orexin receptors in dogs

26
Q

What is the role of Orexin (aka hypocretin) in arousal?

A

-Orexin neurons (only 7000) are in the lateral hypothalamus and project to almost all areas of the brain

-Cortex and areas relevant to all of the previous neurotransmitters

-Orexins have a wakefulness promoting effect

-Active during wakefulness and inactive during sleep

27
Q

Neurochemical control of SW sleep: What is the preoptic area?

A

-What controls the activity of the arousal neurons? Von Economo insomnia patients?
They had damage of the anterior hypothalamus

-Nowadays this region is called PREOPTIC AREA (AH and PH still): It contains neurons whose axons form inhibitory connections with the brain’s arousal neurons

28
Q

Neurochemical control of SW sleep: What is the ventrolateral preoptic area?

A

-The majority of ‘sleep neurons’ (inhibit arousal neurons) are located in the ventrolateral preoptic area (VLPA)

-When the VLPA neurons become active they suppress the activity of the arousal neurons:
-The VLPA induces slow-wave sleep by secreting GABA to inhibit the brainstem and forebrain arousal systems
-This suppresses alertness and we fall asleep

What happens if you lesion the VLPA?
-Total insomnia in rats (can never fall asleep)
-Animals fall into a coma and die after 3 days (highlights importance)

29
Q

Neurochemical control of SW sleep: What is the flip-flop mechanism?

A

-VLPA activity initiated by adenosine and neurons in VLPA are inhibited by histamine, noradrenaline and serotonin

-Arousal centers are active=VLPA is inhibited (Flip-Flop on)
-VLPA is active=centers are inhibited (i.e., sleeping) =arousal (Flip-Flop off)

-The Flip-Flop mechanism is only one state at a time (mutual inhibition)

30
Q

Neurochemical control of SW sleep: Where is orexin in all of this (aka the flip-flop mechanism)?

A

-Orexin stabilises and tips the system towards the waking state - it can control the flip-flop mechanism

Stabilising function:
-During waking you won’t fall asleep because orexin excites neurons of the arousal system
-Orexin holds the arousal centers in the “on” position

31
Q

Neurochemical control of SW sleep: What controls the activity of orexin neurons?

A
  1. During the day orexin neurons receive excitatory input from the biological clock that controls the circadian rhythms
  2. Also, from brain areas that monitor the animal’s nutritional state
    Hunger signals—orexigenic neurons (being starving would keep you awake)
    Satiety signals—orexigenic neurons (being full may make you sleepy)
  3. Accumulation of adenosine overcomes excitatory input from other areas and sleep happens

Conclusion: orexigenic neurons are involved in all 3 factors that control sleep and wakefulness: homeostatic, allostatic and circadian

32
Q

What is the Neurochemical control of REM sleep?

A

-Brain metabolism during REM sleep is as high as in wakefulness

-REM sleep is also controlled by a flip-flop mechanism (REM-on and off cells)

-The sleep waking flip-flop determines when we wake and we sleep

-Once we fall asleep the REM flip-flop controls the SWS(NREM)/REM cycles

-Acetylcholine neurons in the pons fire at high rate during REM (similar to wakefulness) and they are responsible for cerebral activation during wakefulness and REM sleep

33
Q

Neurochemical control of REM sleep: What’s REM flip-flop?

A

-The switch between REM and NREM sleep is mediated by mutually inhibiting REM-on and REM-off neurons in the pons

-Only one can be present at a certain time so in which state is this when awake?

-During waking the REM off receives excitatory input from Orexin, noradrenergic and serotenergic neurons tipping the switch to the off state

-When the sleep/waking flip-flop switches into the sleep phase SWS begins

-Excitatory activity to REM off decreases, this tips the switch to REM on

34
Q

What’s the circadian rhythm?

A

-Circadian is a term derived from the Latin phrase “circa diem” meaning “around a day”.

-Circadian rhythms refer to the 24 hour cycles that form part of the human body’s internal biological clock

-The most well-known circadian rhythm is the sleep-wake cycle

-Circadian rhythms are kept on schedule by temporal cues in the environment (also known as zeitgebers)

-The most important zeitgeber is the daily cycle of day and light

35
Q

How’s Time a cognitive zeitgeber?

A

-Clocks, work and travel schedules place demands on the body to remain alert for certain tasks e.g., coursework and social events

-There is a cognitive pressure to stay on schedule

36
Q

How is melatonin a hormonal zeitgeber?

A

-Melatonin is released in a daily light-sensitive cycle (when dark melatonin levels rise)

-Levels of melatonin begin climbing after dark

-Melatonin can influence our circadian rhythm (e.g., melatonin-deficient insomnia)

-Melatonin supplements may help individuals reset their circadian rhythm

37
Q

What is the suprachiasmatic nucleus (SCN)?

A

-The SCN of the hypothalamus is considered to be the circadian clock (where our internal biological clock is meant to be)

-It receives light inputs from the retina and resets the clock everyday accordingly to the day-night cycle

-Involved in melatonin synthesis

-The SCN is most active during the day and least active at night

-The VLPA is inhibited by the SCN (remember the flip-flop)

-Light-induced activation of SCN prevents the production of melatonin by pineal gland

38
Q

Zeitgebers entrain (control the timing of) circadian rhythms, but what happens to S-W cycles in an environment that is devoid of zeitgebers?

A

Circadian rhythms persist when devoid (absent) from day-light cycle (constant environments with no temporal cues)
-Rhythms=free-running rhythms
-Duration=free-running period

-Constant illumination=24.2 hours
-Constant darkness=25 hours

39
Q

What is Jet lag?

A

-Jet lag occurs when zeitgebers are accelerated (phase advances i.e., zeitgebers occur faster) during eastbound flights (e.g., going to Thailand) or decelerated (phase delays i.e., zeitgebers occur slower) during westbound flights (e.g., going to the US)

-It results in sleep disturbances, fatigue, mood changes, deficits on tests of physical and cognitive performance

-Temporary problem (5-10 days) treatable with light exposure or melatonin administration

40
Q

What is meant by shift work?

A

-In shift work, zeitgebers stay the same (not different timezones) but workers are forced to adjust their natural S-W cycles to meet the demands of changing work schedules (e.g., night shift)

-It can take 1 day for the circadian rhythm to adapt to 1 hour change in light/dark cycle

-Shift work disorder is related to fatigue, poor performance and poor memory as well as a risk of other health problems e.g., cardiovascular disease, depression and diabetes

41
Q

What type of sleep disorders are there?

A

Many sleep disorders fall into one of two categories: insomnia and hypersomnia
-Insomnia includes all disorders of initiating and maintaining sleep
-Hypersomnia includes all disorders of excessive sleep or sleepiness

-Another type of sleep disorders include those related to REM-sleep dysfunction

-Parasomnias: abnormal behaviours emanating from or associated with sleep

42
Q

What type of sleep disorders can be seen in NREM and REM?

A

NREM:
-Confusional arousals
-Sleep walking
-Sleep terrors
-Sleep related eating disorder (people eat whilst asleep)

REM:
-REM sleep behaviour disorder
-Isolated sleep paralysis

43
Q

What is Insomnia?

A

-Insomnia affects 25% of the population occasionally and 9% regularly

-Insomnia can be defined in relation to a person’s particular sleep needs

-Many cases of insomnia are iatrogenic (physician-created) and caused by an increased tolerance and later withdrawal symptoms to sleeping pills (e.g., benzodiazepines)

-Other causes of insomnia can include stress, anxiety, environmental factors (e.g., noise levels, temperature extremes), pain, medication and more

44
Q

What are some conditions in Insomnia?

A

-Insomnia can also be associated with sleep apnea where the patient stops total breathing many times each night and only wakes up to breathe again and then drift back to sleep

-Periodic limb movement disorder is characterised by periodic involuntary movements of the limbs, often involving twitches of the legs during sleep, but patients are unaware (this can result in poor sleep and daytime sleepiness)

-Restless leg syndrome is characterised by a tension and discomfort in patients’ legs that prevents them from falling asleep (aware)

45
Q

NREM parasomnias: What is confusional arousals and sleep walking?

A

CA:
-Disoriented behaviour during arousal from NREM sleep just before REM sleep
-Last for seconds to minutes
-Poor recall of events the following day

SW:
-Up to 17% in children and 4% of adult population
-Combination of moving with the persistence of impaired consciousness
-Linked with anxiety, fatigue, medications and mental disorders

46
Q

REM Parasomnias: What is REM sleeping behaviour disorder?

A

-Loss of normal atonia: dream enactment behaviour

-It can often result in injuries e.g., “fighting a bear”

-More frequent in males > 50 years old

-Associated with neurodegenerative disorders (Parkinson’s, dementia)

-Some genetic component

-Treated with clonazepam, a benzodiazepine (has to be monitored with someone with you whilst asleep)

-More serious compared to NREM

47
Q

REM Parasomnias: What is Isolated sleep paralysis?

A

-Paralysis is maintained after waking from REM sleep

-It can also occur when falling asleep

-Patients are fully aware of what is happening but have an inability to move

-It can last for seconds to minutes

-It is sometimes accompanied by hallucinations

-It first appears during adolescence but most often in 20s and 30s

-Parasomnia=symptom of something else meaning it may not happen all the time

48
Q

What is 4 things Narcolepsy is characterised by?

A

It’s the most widely studied disorder of hypersomnia:
1. Sleep attacks - overwhelming urge to sleep for a few minutes (can’t control)

  1. Cataplexy - sudden paralysis during which a person remains conscious (often triggered by an emotional experience)
  2. Sleep paralysis - inability to move just as one is falling asleep or waking up
  3. Hypnagogic hallucinations - dreams that occur during periods of sleep paralysis (can be violent and scary like nightmares)
49
Q

What is Narcolepsy associated with?

A

-Narcolepsy is associated with a lack of orexins (like dog study prior)

-This may suggest that narcolepsy is an autoimmune disease and streptococcus bacteria appears to be the trigger for the autoimmune attack (means treatments are temporary)

-Occurrence of events at a vulnerable age (childhood) makes an immune attack on the orexin system more likely

-Improvements have been made for potential treatments in narcolepsy