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what is sleep
state of unconsciousness from which an individual can be aroused by normal stimuli, light, touch, sound etc
cyclical
what is coma
state of unconsciousness from which and individual cannot be aroused and does not respond to stimuli
what does circadian rhythm control
melatonin release by pineal gland
why does darkness allow sleep
inhibitor neurones in suprachiasmatic nuclei (SCN) are stimulated by light and inhibit pineal gland from releasing melatonin
darkness removes inhibition
stimulation of pineal gland
more melatonin
sleepiness
what causes narcolepsy
loss of orexin (hypocretin) neurones
-transitions from being awake directly into REM sleep
EEG waves - alpha waves
RELAXED AWAKE state
- high frequency medium amplitude
EEG waves - beta waves
ALERT AWAKE
- very high frequency low amplitude
EEG waves - theta waves
EARLY SLEEP
- low frequency varied amplitude
EEG waves - delta waves
DEEP SLEEP
- very low frequency high amplitude
N1
stage 1 NREM sleep
slow wave non-REM S-sleep
- absent/slow eye movements
- low muscle tone
-low voltage
HIGH AMPLITUDE LOW FREQUENCY THETA WAVES
N2
no eye movements
very low tone
frequency slows
EEG shows sleep spindles - clusters of rhythmic waves and K complexes
N3
deep sleep
slow wave sleep
no eye movement
low tone
- HIGH AMPLITUDE SLOW DELTA WAVES - interspersed with short episodes of faster waves
sleep cycle state R
delta waves ONLY
rapid eye movement
very low tone
low voltage, mixed frequency
when does sleep walking/talking occur
stages 3 and 4 deep sleep
when do dreams occur
REM
types of waves seen in REM
LOW AMPLITUDE HIGH FREQUENCY - similar to awake state
how does the sleep cycle go through the stages
1, 2, 3, 4 and cycle back through 4, 3, 2 then REM
when does deep sleep occur
first few hours of sleep
- most restful
what is deep sleep associated with
decreased vascular tone and therefore lower BP, respiratory and basal metabolic rates
what part of the brain is active during deep sleep
hippocampus - hence creating of new memories of dreams
how long is each sleep cycle
90 mins
what happens to eye muscles during REM
bursts of rapid activity
why do we not "act out" dreams during REM
there is profound inhibition of skeletal muscles due to inhibitory projections from pons to spinal cord (descending)
REM promoting pathways inhibit motor neurones which is why no movement during sleep
what is REM dependent on
cholinergic pathways within reticular formation and projections to thalamus, hypothalamus adn cortex
what increases REM time
anti-cholinesterases drugs
what does REM waves mimic
beta waves associated with alert awake state
W state
wakefulness
EEG - alpha rhythm first then low voltage
EOC - variable eye movements - both rapid and slow
EMG - normal or high muscle tone
significance of amplitude and frequency of EEG waves
Useful for diagnosis of epilepsy and altered states of consciousness, measures brain electrical activity
polysomnography
sleep study measures:
Brain activity – EEG electroencephalogram
Eye movement – EOC electro-oculogram
Muscle tone – EMG electromyogram
typical pattern of a night’s sleep in an adult
On falling asleep – transition is from wakefulness → non-REM sleep
Non-REM sleep alternates with REM sleep
Sleep cycles take about 90 min
With each cycle the NREM becomes lighter and REM periods become longer
Vivid dreams during REM sleep
People usually wake up spontaneously from an episode of REM sleep
with age there is less…
REM sleep
glymphatic hypothesis
NREM sleep allows clearance of metabolites from the brain, remodelling of synapses, preserve energy
homeostatic sleep drive
substance (somnogen) accumulates during wakefulness, induces sleep, is degraded during sleep, best known candidate is adenosine
circadian regulation
24-biological clock, endogenous cycles of physiology and behaviour with a period of 24 hours
Circadian system requires light
Circadian rhythms regulate the timing of the function, not the function itself
where do EEG rhythms in non-REM sleep result from?
cortico-cortical and thalamo-cortical oscillations
When awake cells active – inhibit asleep cells
Asleep cells activate – inhibit awake cells
symptoms of narcolepsy
Chronic disease
Daytime sleepiness
Cataplexy (loss of muscle control - not always)
sleep stages in narcolepsy
Non-REM sleep fragmentation
Reduced wakefulness
Sleep-onset REM
Transitions from being awake directly into REM sleep
obstructive sleep apnoea
Pharyngeal collapse during sleep, leads to oxygen desaturation, hypercapnia and sleep fragmentation
symptoms of obstructive sleep apnoea
Snoring
Witness apnoeas
Waking up with choking sensation
Excessive daytime sleepiness
consequences of obstructive sleep apnoea
Cardiovascular
Metabolic
Neurocognitive
diagnosis of obstructive sleep apnoea is done by?
polysomnography
-SOA more common than narcolepsy
what is circadian rhythm
endogenous cycles of physiology and behaviour with a period of about 24 hours
role of suprachiasmatic nucleus in circadian rhythmicity
Circadian rhythms regulated by the suprachiasmatic nucleus
The removal of SCN abolishes circadian rhythms, transplanted SCN restores rhythms, SCN cells maintain rhythm in vitro
circadian rhythms are the…
results of feedback loops in clock genes and SCN output coordinates local clocks
what type of disorder is chronic insomnia disorder
insomnia disorder
what type of disorder is obstructive sleep apnoea and obesity hypoventilation syndrome
sleep related breathing disorders
what type of disorder is narcolepsy
central disorders of hypersomnolence
what type of disorder is jet lag and shift work disorder?
circadian rhythm sleep-wake disorders
what type of disorder is sleepwalking, sleep terrors, recurrent isolated sleep paralysis, exploding head syndrome
parasomnias
what type of disorder is restless leg syndrome, sleep-related bruxism
sleep related movement disorders