Physiology of sleep Flashcards
Atigraphy
-used to quantify circadian sleep-wake patterns and detect movement disorders during sleep; uses a motion sensor
Polysomnography
- includes EEG, EMG and EOG. ECG and other monitoring
- helps diagnosis and monitoring of sleep apnoea, narcolepsy, restless legs and REM behavioural disorder
Sleep latency
-time from ‘lights out’ to sleep
REM latency
- Time from sleep onset to first REM episode
- normally 90 mins in adults
Non-REM latency
-Time from sleep onset to first Non-REM episode
Sleep efficiency
(Total sleep time/total time in bed) x100
Multiple sleep latency test
-used to assess daytime somnolence and daytime REM onset in narcolepsy
Average length of sleep
7.5 hrs a night
sleep is made up of non-rapid eye movement and rapid eye movement phases
NREM sleep
- 75% of adult sleep
- decreased muscle tone, respiration, temp and HR
- has 4 stages
- increased parasympathetic activity, abolition of tendon reflexes, upward ocular deviation with no or few movements
- reduced recall of dreams if woken
Dreams
- dreaming occurs in all stages of sleep but the content varies
- in NREM sleep the dreams are ‘thought-like’ as thought the person is solving a problem
- in REM sleep the dreams may be illegocial and bizarre
Stage 1 NREM sleep
- 5% sleep
- drowsy period
- when woken from this stage one denies being asleep
- shows low voltage theta activity, sharp V waves
Stage 2 NREM sleep
- 45% sleep
- shows the development of sleep spindles and K complexes
Stage 3 of NREM sleep
- 12 % sleep
- <50% delta waves
Stage 4 NREM sleep
- 13% sleep
- shows >50% delta waves
- physiological functions are at the lowest
REM sleep
- 25% sleep
- darting eye movements are noted despite other muscles being paralysed
- REM sleep is characterised by high level of brain activity and physiological activity similar to wakefulness
- EEG shows low voltage, mixed frequency activity similar to an awake state. Sawtooth waves also seen
- in a typical night, we cycle through 5 cycles of NREM/REM
- REM increases in length throughout the night
- increased sympathetic activitiy, increased blood flow to genitals, increased protein synthesis, maximal loss of muscle tone with occasional myotonic jerks
- vivid recall of dream if awaken
REM sleep behavioural disorder
-muscle paralysis does not occur resulting in violent movements coinciding with brain activity
Sleep spindles
- waves with upper alpha or lower beta frequency
- seen in many stages but mainly stage 2
- duration <1 second
- symmetric and obvious in the parasagittal regions
K complexes
- large amplitude delta frequency waves, sometimes with a sharp apex
- occur throughout the brain but more prominent in the bifrontal regions
- mediated by thalamocortical circuitry
- occur when patient is partially aroused from sleep
- semiarousal follows brief noises
- runs of generalised rhythmic theta waves sometimes follow K-complexes- an arousal burst
V-waves
- v-waves are sharp waves that occur during sleep
- they are largest and most evident at the vertex bilaterally and are usually symmetrical
- multiple V waves tend to occur especially during stage 2 sleep
- occur after sleep disturbances
Suprachiasmatic nucleus
- master clock of the brain
- located in the anterior hypothalamus
- orchestrates circadian rhythms and uses signals from the retina
- in the absence of solar guidance, the 24 hour sleep-wake cycle will gradually increase to 26 hours- free-running
- pineal melatonin can also reset the SCN and promotes sleep in jet lag
Ventrolateral preoptic nucleus
- VLPO
- sleep switch nucleus
- has projections to the ascending arousal system
- VLPO induces sleep by switching off the arousal system
- people with damage to the VLPO have chronic insomnia
Waking up
- Monoaminergic system switches off the VLPO to wake people up
- negative feedback from the monoaminergic system
- arousal is then stablised by orexin (hypocretin) neurons in the hypothalamus
- orexin neurons reinforce arousal system
- patients with narcolepsy have fewer orexin neurons, leading to somnolence during the day
Acetylcholine
-cell bodies in the midbrain-pons nuclei
-activation brings on REM sleep
REM on neurons
Noradrenaline
- cell bodies in the locus coeruleus
- REM off neurons
- activation reduces REM sleep
Dopamine
- cell bodies in PAG
- D2 possibly enhances REM sleep
Serotonin
- cell bodies in raphe nuclei
- 5HT2 stimulation possibly maintains arousal
Histamine
- cell bodies in the tubermammillary nucleus
- H1 stimulation possible maintains arousal
alcohol
- increases slow wave sleep but in chronic use, loss of slow wave sleeo
- reduce initial REM but increase second half REM
alcohol withdrawal
- loss of slow wave sleep
- increased REM
- increase REM rebound
Anxiety disorders
- increased stage 1 sleep (light sleep)
- reduced REM, normal REM latency
- reduced slow wave sleep
Benzos
- decrease sleep latency
- increase sleep time
- reduce stage 1 sleep
- increase stage 2 sleep
- reduce REM and slow wave sleep
- REM rebound on cessation
- prevent transition from lighter stage 2 sleep into deep, restorative (stage 3 and 4) sleep
Cannabis
- increase slow wave sleep
- suppress REM
Carbamazepine
- increases slow wave sleep
- suppresses REM and increases REM latency
Dementia
- increased sleep latency and fragmentation
- reduced sleep time
Depression
- loss of slow wave sleep
- increased REM-leading to early wakening
- reduced REM latency
Lithium
- suppresses REM and increases REM latency
- increases slow wave sleep
Opiates
- decrease slow wave sleep and REM
- withdrawal REM bound
Schizophrenia
- inconsistent reduction in REM latency and slow wave sleep
- antipsychotics have variable effects
SSRIs
- alerting due to 5HT2 stimulation
- may reduce REM latency
- variable effects of REM suppression
Stimulants
- reduced sleep time by decreasing both REM sleep and slow wave sleep
- REM rebound on cessation (except modafinil)
Tricyclics
- REM suppression (especially clomipramine)
- increased slow wave sleep and stage 1 sleep
Z-hypnotics
- less effect on sleep architecture
- zopiclone may increase slow wave sleep
