Sleep Flashcards
polysomnogram
EEG- brain activity EOG- eye movement EMG- reflects muscle tone EKG- reflects cardiac impulse conduction respiratory channels
brain waves
delta 30 Hz
three primary brain states
awake- low voltage, fast EEG
sleep- NREM- high voltage, slow EEG
REM- low voltage, fast EEG
wake
alpha rhythm- best seen in occipital regions (defined as with eyes closed)
rapid eye movements
normal muscle tone
non-rem
N1- light sleep
N2
N3- deep sleep/ slow wave sleep/ delta sleep
N1
alpha drop out- theta replaces it vertex sharp waves slow eye movements muscle relaxation sleep starts- full body jerk central apneas
N2
theta movement- progressive sllowing
eye movement stops
sleep spindles- 12-14 Hz
K complex- large amplitude bi phasic evoked response
N3
> 20% slow wave activity
frequency and amplitude- .5-2 Hz slow wave activity
high amplitude
hard to wake from
no eye movements
night terrors come from N3
ok
REM
reticular activation- desynchronization stage 1 like EEG- sawtooth wavs hippocampal theta activity phasic/tonic components rapid eye movements
muscle atonia
muscle twitches
cognitive activity
which stages dominate which parts of the night
N3 dominates first 1/3
REM dominates in the last 1/3
how much time do we spend in each sleep stage
N1 5%
N2 50%
N3- 20%
REM- 25%
compare and contrast non rem and rem sleep
nonREM- decreased HR and BP, decreased drive to low O2 and increased CO2, intact thermal regulatoin, reduced muscle tone, decreased CBF, reduced cognitive function
REM- variable sympathetic activity, lowest drive to low O2 and increased CO2, no thermal regulation, minimal muscle tone, increased genital blood flow, increased CBF, abundant, bizzare cognitive function
how does sleep change w/ age
fetus- 80% active sleep (REM) newborn- 16-18 hrs. 50% is active 3-4 months- establishment of nocturnal period 1 yr- 12-13 hrs sleep, 30% REM 2 years- 10 hrs sleep, 25% REM
second decade- marked decline in slow wave activity. continues to decrease across life
REM stays constant
elderly- sleep less, nap more, lighter sleep and increased awakening
zeitgebers
external cues that regulate circadian rhythm
entrainment
describes period and phase control of an oscillator by an environmental cycle
-adjustment of internal cycle to external cycle, and synchronization of various internal clocks
free running
persistence of rhythms during constant conditions
current evidence suggests pacemaker period is 24.2 hrs
photic entrainment
light entrains the circadain rhythm
graphic description of cycles in response to light is a phase response curve
light near initiation of dark cycle produces phase delay
light near conclusion of dark activity produces phase advance
what is responsible for humans circadian rhythm
suprachiasmatic nucleus in hypothalamus
keeps cycle in isolation
some rhythms persist after SCN removal
rhythmicity evident in what cycles?
temp, hormones, CV
melatonin
released by pineal gland in response to darkness, reinforces darkness signal at SCN
linked to control of body temp
levels decline from childhood onwards
acts as a phase shifter and sleep promotor
delayed sleep phase type
delayed sleep phase,
inability to fall asleep at approriate time, but otherwise healthy sleep
commonly seen in younger individuals
causes: endogenous rhythm, exposure to light in evening, lack of exposure to morning light, depression, behavior preference
treatment- chronotherapy- three hour progressive delay phase or thirty minute progressive phase advance
process s
homeostatic drive to sleep- related to sleeping and waking
“something” is accumulating while you were awake
exponential rise during wake, declines during sleep
correlated w/ slow wave sleep
probably adenosine driven
process c
circadian rhythm- variation of sleep tendency based on temporal schedule
adenosine
inhibits basal forebrain ACh neurons
high concentrations in wake
declining concentrations in SWS
caffeine is adenosine antagonist
where is NE secreted from?
locus coeruleus
where is serotonin secreted from?
dorsal raphe
where is ACh secreted from?
PPT/LDT (brainstem) and basal forebrain
where is histamine secreted from?
hypothalamus- tuberomamillary nucleus
where is adenosine secreted from?
basal forebrain, hypothalamus
where is orexin/hypocretein secreted from?
hypothalamus
where is DA secreted from?
brainstem/ hypothalamus
RAS
project to thalamus, basal forebrain, cortex, and hypothalamus
produce desynchronization of cortical neurons- wakefulness
LDT, locus coeruleus, raphe, and tuberomamillary bodies promote wake
orexin/hypocretin
wake active- may prevent unwanted transitions to sleep
projections to cortex and ARAS
sleep active
VLPO- acts on wake promoting areas in inhibitory fasion
also inhibits orexin, switching to sleep
switch flips w/ buildup of adenosine
REM sleep generation
decreased firing in locus coeruleus, tuberomamillary bodies and raphae neurons
increased firing in LDT and PPT (ACh)- wake centers
descending motor inhibition
sleep function
restoration energy conservation memory function promotion of CNS in young maintenance of circuitry restoration of NTs
