All cases and lectures of course 3: sleep & sleep disorders
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Course
Sleep & sleep disorders (PSY3349)
Institution
Maastricht University (UM)
I followed this course for my minor in psychology. This is a course that belongs to the AMIP programme and elective courses of psychology. I got an 8 for my exam based on my notes. Good luck!
1. What is a normal sleep cycle?
Sleep Architecture sleep cycle → repeats itself during sleep.
Non-REM sleep stage 1 (N1) → when you fall asleep, lightest sleep, theta-waves
and brain activity. Slow eye movement → eyes rolling back. Easy to be awakened.
Non-REM sleep stage 2 (N2) → muscles become more relaxed, light sleep but you
have delta-brain activity, sleep spindles (short bursts of activity), K-complexes (sharp
spikes in the EEG). Memory consolidation takes place in this stage.
Non-REM sleep stage 3 (N3)→ slow-wave sleep (SWS), low frequency, deepest
sleep stage, delta-brain activity, sleep-walking can happen during this stage. This is
the most restful sleep. It is strongly related to process S (sleep drive). The amount of
slow-wave activity in the brain is used as an index of the strength of process S.
REM-sleep (Rapid Eye Movements)→ still a lot of oxygen consumption → the brain
is very active (can even be more active than during waking), muscle tensions, vivid
dreaming, muscle atonia. Your eyes move rapidly during this stage of sleep. Activity
as high as someone being awake. Strongly associated with process C and
predominates the second half of the night (when the core body temperature is near
its lowest point).
- PGO waves & oscillatory activity in the theta band range.
Actively awake = bèta activity
Getting drowsy → alpha activity → alpha waves disappear when you enter nREM
sleep stage 1.
Sleep paralysis → disturbance between REM-sleep and waking. Having dreams
while being awake and conscious.
Time until first REM episode occurs about 70 minutes. Duration of subsequent
cycles is roughly 90 minutes.
Sleep is regulated. Some physiological mechanism monitors the amount of sleep that
an organism needs it keeps track of the sleep debt we incur during hours of
wakefulness.
- The amount of slow-wave sleep that a person obtains during a daytime nap is
deducted from the amount of slow-wave sleep he or she obtains the next
night,
- An organism deprived of slow-wave sleep or REM sleep will make up at least
part of the missed sleep when permitted to do so.
One possible explanation is that the body produces a sleep-promoting substance
(adenosine) that accumulates during wakefulness and is destroyed during sleep.
The longer someone is awake, the longer he or she has to sleep to deactivate this
substance. This substance would be produced within the brain and act there.
Adenosine is a nucleoside neuromodulator which might play a primary role in the
control of sleep. Astrocytes maintain a small stock of nutrients in the form of
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,glycogen, an insoluble carbohydrate that is also stocked but the liver and muscles.
In times of increased brain activity this glycogen is converted into fuel for neurons;
thus, prolonged wakefulness causes a decrease in the level of glycogen in the
brain. A fall in the level of glycogen causes an increase in the level of extracellular
adenosine, which has an inhibitory effect on neural activity. This accumulation of
adenosine serves as a sleep-promoting substance. During slow-wave sleep,
neurons in the brain rest, and the astrocytes renew their stock of glycogen.
During prolonged wakefulness even more adenosine accumulates, which inhibits
neural activity and produces the cognitive and emotional effects that are seen during
sleep deprivation.
Adenosine is released by astrocytes when neurons are metabolically active, and the
accumulation of adenosine produces drowsiness and sleep.
Circuits of neurons that secrete at least five neurotransmitters play a role in some
aspect of an animal’s level of alertness and wakefulness arousal.
- Acetylcholine (ACh) one of the most important neurotransmitters involved in
arousal. High during wake and low during sleep.
o Acts in cortex and hippocampus;
- Norepinephrine (NE) released by Locus Coeruleus (LC) throughout the
neocortex, hippocampus, thalamus, cerebellar cortex, pons, and medulla.
Close to behavioural arousal.
o High firing of NE during wakefulness;
o Low firing during slow-wave sleep (almost 0 during REM sleep);
- Serotonin (5-HT) in raphe nuclei. Stimulation of the raphe nuclei causes
locomotion and cortical arousal (preventing synthesis of 5-HT reduces
cortical arousal).
o Activated during waking and declines during slow-wave sleep.
- Histamine in tuberomammillary nucleus (TMN) of hypothalamus. It
increases cortical activation (it provokes wakefulness).
o Can cause drowsiness.
- Orexin (or hypocretin) it plays a role in the control of eating and
metabolism, physiological and behavioural effects of drugs. It has an
excitatory effect on all regions involved in arousal and wakefulness.
o Lateral hypothalamus.
Homeostatic control of sleep:
If we go without sleep for a long time, we will eventually become sleepy, and once we
sleep, we will be likely to sleep longer than usual and make up at least some of our
sleep debt.
- The primary homeostatic factor that controls sleep is the presence or absence
of adenosine.
Allostatic control of sleep:
This refers to reactions to stressful events in the environment it is important to stay
awake under certain conditions (e.g., dangerous situation). This overrides
homeostatic control.
- Mediated by hormonal and neuronal responses to stressful situations and by
neuropeptides that are involved in hunger and thirst.
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,Circadian factors (or time of day factors):
These are factors that tend to restrict our period of sleep to a particular portion of the
day / night cycle.
The preoptic area region of the anterior hypothalamus. Patients who display
insomnia have damage in this region. The preoptic area is most involved in control of
sleep. It contains neurons whose axons form inhibitory synaptic connections with the
brain’s arousal neurons. When preoptic neurons (sleep neurons) become active, they
suppress the activity of our arousal neurons, and we fall asleep.
- The majority of preoptic neurons are located in the ventrolateral preoptic area
(vlPOA). Damage to these neurons causes suppressed sleep.
Source: Carlson (chapter 9).
Sleep homeostasis is a basic principle of sleep regulation. A sleep deficit elicits a
compensatory increase in the intensity and duration of sleep, while excessive sleep
reduces sleep propensity. Slow waves in the electroencephalogram (EEG), a
correlate of , serve as an indicator of sleep homeostasis in non-REM sleep, also
referred to as slow-wave sleep.
The homeostatic mechanism regulates sleep intensity (slow-wave activity).
The circadian clock regulates timing of sleep (duration).
Source: Tobler & Achermann.
Percentage of the different stages of sleep:
NREM sleep stage 1: 5%
NREM sleep stage 2: 50%
NREM sleep stage 3+4: 15-20%
REM sleep stage: 20-25%
Measurements:
Polysomnography → measures electrical brain activity and muscle tone.
PSG is the golden standard of objective sleep measurement. This can inform
about aspects of sleep quality: minutes to fall asleep, number of awakenings,
duration of each awakening, total sleep time and sleep efficiency. The most
common clinical use of PSG is for the diagnosis of sleep-related breathing
disorders.
Actigraph → measures movement (of the wrist) during the day. It measures
when you are awake or asleep, how long you slept, how many times you wake
up. Gives a more general idea of sleep pattern it provides information on
day-to-day variability in sleep (not feasible with PSG). It is cost effective (low
costs).
Sleep diary provide daily sleep data;
Sleep questionnaires retrospectively assess sleep behaviours and
symptom severity.
Multiple Sleep Latency Test MSLT)→ measurement of physiological
sleepiness. It measures sleepiness as defined by the propensity to fall asleep.
The MSLT score is the average number of minutes to fall asleep (How easy it
is for someone to fall asleep). It’s a full day test, consists of 5 scheduled
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, measurements → measure quality and duration of sleep. And they look at how
fast a person falls asleep.
Maintenance of Wakefulness Test (MWT) → measures a persons’ ability to
maintain wakefulness under conditions that are conductive to sleep (dark,
quiet and boring). Do the same as MSLT → but do not ask person to fall
asleep → they instruct people to stay awake. The MWT score is the average
time to fall asleep across the nap opportunities.
2. What determines the quality of sleep?
Evidence suggests that genetic factors affect the typical duration of a person’s slow-
wave sleep. One genetic factor is the variability in the gene that is involved in the
breakdown of adenosine.
G/A allele breaks down adenosine more slowly causes prolonged slow-
wave sleep (as compared to G/G allele).
Slow-wave activity increases as a function of the duration of prior wakefulness.
- The longer you are awake the higher level of EEG slow-waves is measured
higher sleep intensity.
3. How is age involved in the sleep cycle?
Normative aging is associated with a reduced ability to initiate and maintain sleep.
Both the macro-level structure of sleep (such as sleep duration and sleep stages),
and the micro-level architecture of sleep (including the quantity and quality of sleep
oscillations), change as we progress into our older age.
Macro-changes in sleep architecture when people age 50+
1. Advanced sleep timing (earlier bedtimes and rise times);
2. Longer sleep-onset latency (longer time taken to fall asleep);
3. Shorter overall sleep duration;
4. Increased sleep fragmentation (less consolidated sleep with more
awakenings, arousals, or transitions to lighter sleep stages);
5. More fragile sleep (higher likelihood of being woken by external sensory
stimuli);
6. Reduced amount of deeper nREM sleep known as slow-wave sleep (SWS);
7. Increased time spent in lighter nREM stages 1 and 2;
8. Shorter and fewer nREM-REM sleep cycles;
9. Increased time spent awake throughout the night.
Age-related reductions in REM sleep are more subtle as compared to (more drastic)
changes in nREM sleep. Often REM sleep impairments only emerge as adults
progress into their 80s and beyond.
The frequency of daytime naps also increases later in life.
- 10% of adult ages 55-64 years;
- 25% of adult ages 75-84 years.
One factor that appears to determine whether older adults are prone to daytime
napping and excessive daytime sleepiness is the presence of comorbid conditions
(such as chronic pain, depression, sleep disorders, and frequent night time urination
breaks).
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