Sleep Flashcards
organization of sleep
continuum - specific stages but no distinct divisions
nREM and REM sleep alternate - each cycle ~90min
4-6 cycles in sleep period
EEG
observe changes on scalp - define sleep stages
neurophysiology of specific wave forms
measures oscillations in voltage transmitted from the brain
brain rhythms
delta: 0-3.99 Hz
theta: 4-7.99 Hz
alpha: 8-13 Hz
beta: >13 Hz
states of sleep
awake: presence of alpha rhythm
nREM sleep: N1, N2, N3
REM sleep: no muscle tone and rapid eye movement
nREM sleep
N1 - alpha drop out (no alpha rhythms)
N2 - sleep spindles and K complexes - 11-16 Hz
N3 - slow wave sleep
sleep spindles
represent hypersynchronicity (risk for seizures if epileptic)
in central temporal region
increased reticular neuron activity hyperpolarizes relay neurons via GABA-B receptors (inhibitory input)
hyperpolarization activates T-type Ca2+ channels → low threshold depolarization + bursts of thalamo-cortical activation by relay neurons
- circuit is active in absence seizures = excessive synchronous activity
relay neurons
excitatory input to cortex
inside thalamus (reticular neurons are outside of thalamus)
low threshold depolarization: can depolarize from hyperpolarized state
benzodiazepines
associated with increased stage N2 sleep, increased spindle activity - possibly due to increased GABA-ergic signalling
slow waves
delta waves - implicated in learning and memory
REM sleep
rapid eye movements = dreams
lighter phase of sleep - EEG looks awake (absence of sleep waves)
progressively increases through night - about half of U5 stage
neurobiology of sleep
glutamate = excitatory → wakefulness
GABA = inhibitory → sleepiness
Wakefulness
glutamate is secreted by
1. parabrachial/precoeruleus nuclei (pons)
2. supramammillary nuclei (midbrain)
excitatory transmission from brainstem nuclei
1. causally to motor neurons in the spinal cord
2. rostrally to neurons throughout the cortex
thalamo-cortical transmission is supported via dorsal pathway using acetylcholine to maintain consciousness
acetylcholine
maintain consciousness
secreted from the basal forebrain
cholinergic neurons in pons (pedunculopontine tegmentum and laterodorsal tegmentum) project to thalamus
highly active during wakefulness
population in pons is active in REM sleep
rostral excitatory transmission
from brainstem nuclei to neurons in cortex
histamine - from tuberomammillary nucleus
dopamine - from ventral tegmental area
serotonin - from raphe (pons)
norepinephrine - from locus ceruleus (pons)
nREM sleep transmission
inhibitory synaptic transmission (GABA) from the ventrolateral preoptic nucleus (hypothalamus) to all of brainstem nuclei important in wakefulness → inhibition of normal wakefulness pathway
REM sleep transmission
REM-on neurons in the PPT and LDT (cholinergic)
1. excitatory connection to thalamus = awake-looking EEG
2. excitatory connection to glycinergic neurons in medial medulla - inhibit motor neurons in the spinal cord = muscle atonia
hypocretin (orexin)
produced by cells in hypothalamus
provide inputs to various nuclei important in sleep to support and stabilize sleep states
1. promotes wakefulness
2. stabilize wake-sleep transitions
3. maintenance of skeletal tone during wakefulness
lower levels in narcolepsy
adenosine
mediator of sleepiness after prolonged wakefulness
promotes transition to slow wave sleep by inhibiting basal forebrain neurons (= maintenance of wakefulness)
caffeine = adenosine antagonist
melatonin
release from pineal inhibited by light stimulating suprachiasmatic nucleus in hypothalamus
darkness releases the pineal from SCN inhibition = melatonin release
acts across neuronal population to suppress glutamatergic neurons → less activity
symptoms of abnormal sleep
excessive daytime sleepiness
insomnia
abnormal movements during sleep
awakenings (parasomnias)
abnormal breathing during sleep (sleep apnia)
sleep paralysis
hallucinations
insufficient sleep syndrome
most common cause of sleepiness
affects body + brain → weight gain, high blood pressure, diabetes, altered activity of hormones can lead to obesity
hippocampus, seizures, memory, mental health
Obstructive Sleep Apnea Syndrome
second most common cause of sleepiness
temporary pause in breathing while sleeping - muscle tone diminishes + airway collapses
awakened by effort of breathing against closed airway
obesity and snoring
increased risk of heart attack and stroke
treat with CPAP
narcolepsy
excessive daytime sleepiness with sleep attacks
cataplexy - sudden temporary loss of muscle tone (no loss of awareness)
sleep paralysis
hallucinations - hypnogogic: while falling asleep; hypnopompic: while waking up
low levels of hypocretin (stabilizing sleep-wake transitions) = frequent + inappropriate transitions between sleep and wakefulness
REM-on neurons turn on inappropriately = paralysis of REM sleep while awake (cataplexy)
abnormal movements during sleep
classified by timing during sleep period
- N1-N2: sleep-wake transition movements
- N2-N3: disorders of arousal
- REM: REM sleep behaviour disorder, nightmares, sleep paralysis
restless legs syndrome
when attempting to fall asleep
uncomfortable sensations in legs with urge to move them
family history
iron-deficiency anemia; pregnancy
treatable by treating symptoms - commonly iron supplementation
parasomnias
abnormal movements or behaviours intruding into sleep
nREM sleep - disorders of arousal: confusional arousals, sleep terrors, sleepwalking
REM sleep: REM sleep behaviour disorder
sleep terrors
arise out of slow wave sleep
more common in kids
associated with sleep-walking and confusional arousals
family history
REM sleep behaviour disorder
loss of REM atonia
act out dreams
more common in elderly - associated with Parkinson’s disease and dementia with Lewy bodies
degeneration of glycinergic neurons in medulla → loss of REM atonia
