Sleep Flashcards
Awake EEG
Fast EEG (Beta, >12 Hz) Low voltage
Desynchronized activity of eyes, muscles, etc
EEG waves
Gamma = active, >30 Hz Beta = awake, >12 Hz Alpha = eyes closed, rest, 7-12 Hz Theta = sleep, 3-7 Hz Delta = deep sleep, <3 Hz
Continuum - no clear-cut divisions
Overview of sleep EEG
NREM:
- slow, synchronized EEG
- high voltage
- Stage 1 = light, alpha -> theta transition
- Stage 2 = slowing -> K complexes, spindles
- Stage 3 = deep -> >20% slow delta waves
REM - fast, desynchronized, low voltage
90 minute cycles throughout night
- begins with more Stage 3 NREM -> more REM at end
NREM EEGs
N1 - light - very small proportion
- alpha -> theta transition (slowing)
- slow eye movement, muscle relaxation
- may have starts/jerks, apneas
N2 - most sleep time
- mostly theta waves
- K complexes - large amplitude, biphasic, periodic
- sleep spindles - 13-14Hz group, spikes
N3 - deep sleep, most in beginning
- >20% slow/delta waves (high amplitude)
- highest arousal threshold
- parasomnias (walking, nonsense, terrors)
REM sleep
EEG - low voltage, fast - “sawtooth”
Phasic rapid eye movements
Muscle atonia with twitches
Pontine-geniculate-occipital spikes -> dreams
Hippocampal theta activity
REM sleep bx disorder - not paralyzed, act out dreams
REM physiology
(vs NREM) Autonomic variable (vs dec HR, BP) Very low resp drive (vs somewhat low) Very low muscle tone (vs somewhat low) No thermal regulation Inc genital blood flow -> erection Cerebral blood flow, activity increased (vs decreased)
Dev’t of sleep
Fetal - 80% “active” (REM)
-> 50% infant
-> 25% by 2 years -> constant
Consolidation by 3-4 months (SCN develops)
Decline in slow wave (N3) during second decade
Elderly - less consolidated -> napping
- disorders more prevalent? physiologic?
Circadian rhythm
Endogenous (24.2 h) + Zeitgeibers (light) -> sleep/wake, temp, hormones, etc Process S = homeostatic - exponential increase while awake - buildup of adenosine - correlated with slow wave once asleep Process C = circadian - sinusoidal, somewhat reciprocal to S - peak at 10 pm -> "second wind"
Overall dips in late afternoon, late evening
Entrainment of circadian rhythms
Zeitgeibers - SCN free-running with daily entrainment
Light - only active at transitions
- evening -> phase delay, morning -> phase advance
Melatonin - released by pineal gland, “darkness” hormone
- decline in old age
-> night advance
SCN function
Master pacemaker - autorhythmicity - ablation -> loss of circadian, stim -> phase advance Input - direct retinal - pineal (melatonin) - hypothalamus (emotional, hunger) - basal forebrain Ach, PPT Output -> hypothalamus -> multiple systems
Sleep schedule disorders
Difficult to isolate from social-environmental factors!
Tx: can only advance 30 min vs delay 3 hrs
Delayed phase - younger, social, depression
- can’t fall asleep, can’t wake up
- normal amount of sleep if ad lib schedule
- > phototherapy in am, melatonin in pm
Advanced phase - usu older
- sleepy early, wake in early morning
- > phototherapy in evening
Neurotransmitters
Sleep promoting: - GABA - adenosine - buildup side product of neural activity in basal fore - counteracted by caffeine - endorphins - inhibit sensory - CCK (from gut) Wake promoting: - Ach - brainstem (LDT, PPT), basal forebrain - NE - locus ceruleus - DA - brainstem, hypothal - Histamine - hypothal (tuberomammilary) - Serotonin (5HT) - dorsal raphe - Orexin - hypothal
Awake physiology
Orexin/hypocretin - lateral hypothalamus = master control
-> descending to activate ARAS
-> direct activation of cortex
Ascending reticular activating system (ARAS) -> broad projections
- lat dorsal tegmentum (LDT), pedunculorpontine tegmentum (PPT), basal forebrain -> Ach
- tubero-mammilary (hypothal) -> histamine
- ventral tegmental area -> DA
- raphe nucleus -> serotonin
- locus ceruleus -> NE
ARAS inhibits VLPO (ventrolateral pre-optic area) - no GABA
Sleep physiology
Ventrolateral preoptic area (VLPO) - GABA
- > inhibits ARAS (TMN, raphe, locus ceruleus, etc)
- > thalamus -> inhibits sensory, produces slow wave, spindles
- > inhibits lateral hypothal -> no orexin release
REM:
- LDT, PPT -> high Ach
-> oculomotor, lateral geniculate, cortex
(PGO aka pontine-geniculate-occipital spikes)
-> also descending motor inhibition
- even lower activity of ARAS
- still high VLPO activity
Sleep functions
NREM: - restoration (anabolic vs catabolic, rest, repair) - conserve energy - protective? - some memory "playback" REM: - consolidation of memory - development - pruning, maintenance of circuitry - rest locus ceruleus -> NE -> vigilance while awake
Sleep loss is cumulative
- slight deficit over long term is bad (dose-response)
- > speed -> accuracy -> momentary lapses
