VIII-Sleep Flashcards
sleep def
behaviorally by the normal suspension of consciuosness + electrophysiologically by specific brain wave criteria
types of behavior
- wakefulness- aware of self and environment
- Non REM (stages 1-4) = uncon with cortical synchrony
- REM = uncon with active cortex, dreaming, paralysis
theories of sleep benefits
- protection by sleeping in the dark
- recuperation to restore brain and body tissue
- remembering (consolidation) to reset brain connections
- growth by pituitary gland
- waste removal of neurotoxic products by glymphatic drainage system
circadian regulation
- retinal ganglion cells carry light-dark cycle info to SCN
- light signals hypothalamus (suprachiasmatic nucleus) to stop pineal gland releasing melatonin SO when dark melatonin inc/sleepiness
SCN signaling pathway to pineal
NOT direct
1. suprachiasmatic nucleus
2. paraventricular nucleus
3. sympathetic ganglion
4. pineal gland
how brain waves are categorized
- frequency- cycles per second
- synchrony- wave amplitude
stage 1 sleep
NON REM - quiet sleep
just drifting, fantastic images or auditory hallucinations
stage 2 sleep
NON REM - quiet
more relaxed, clearly asleep
-sleep spindles (short burst of activity) occur
stage 3 sleep
NON REM- deep, slow wave sleep
transitional stage to deeper sleep
-consolidation happens
stage 4 sleep
NON REM - deep, slow wave sleep
-deepest sleep of all, hard to awaken but only occurs during first few cycles of the night
-consolidation happens, highest synchrony
REM sleep
paradoxical sleep
-low amplitude, fast, regular beta waves similar to awake-aroused state
-rapid eye movements, vivid dreams,
-brain very active but muscles are relaxed, paralyzed
-time spent in REM increases throughout the night
EEG wave patterns
- awake = high freq beta waves
- drowsy = alpha waves (relaxed wakefullness)
- stage 1 = theta waves
- stage 2 = sleep spindles + mixed waves
- slow wave = more delta waves
- REM = high frequency beta waves like alert
stage 1>4 activity slows down but gets more synchronized
when is REM least likely to occur
during the first 60 minutes of normal adult sleep
-bc go through stages 1-4 first
physiologic changes during non REM
DEC - oxygen use by brain, metabolic rate, HR, BP, RR
physiologic changes during REM
- active brain
- bursts of eye movements
- irregular HR and RR
- depressed muscle tone thru body
mediates bursts of eye movement during REM
PGO spikes (pontine-geniculate-occipital)
REM sleep atonia
suppression of activity in LMNs + neural mechanisms so that people don’t act out dreams
-if have REM behavior disorder then no atonia
mechanism of LMN inhibition in atonia
- pons excites medullary neurons to inhibit spinal motor neurons
- glycinergic neurons in medullary reticular area send fibers to reticulospinal tract to postsynaptically inhibit motor neurons (suppress extensor activity bilaterally)
muscle relaxation contrast
relaxed in both REM and non but post synaptic inhibition of alpha motor neurons is more intense during REM
-not all muscles inhibited though (respiratory and eye)
neurotransmitters during wakefullness
- acetylcholine
- norepinephrine
- serotonin
- histamine
- orexin
neurotransmitters during sleep
- acteylcholine
- norepinephrine
- serotonin
all decrease in non REM then inactivate during REM except Ach stays active for PGO
sleep patterns with age
sleep less as get older (dec REM)
-newborns get 8 hours REM
sleep deprivation signs
- diff focusing, less productive
- inc tendency to make mistakes
- irritability and fatigue
- dec immune system
- hallucinations after 72 hours
insomnia
diff initiating or maintaining sleep during normal periods
-excessive sleepiness and sleep during normal waking period
parasomnias
- bed wetting/nocturnal enuresis
- sleep walking/somnambulism
- sleep terros
- REM sleep behavior disorder
- sleep apnea (central or obstructive)
sleep cycle disorders
narcolepsy
sleep attacks, excessive sleepiness
obstructive sleep apnea
failure to breathe when asleep = chronic loud snoring
-sleep fragmentation bc waking up in the night to breathe
-treat with weight loss and CPAP
probable cause of narcolepsy
reduction/absence of hypothalamic cells that produce orexin (hypocretin) from autoimmune attack
-orexin regs arousal and wakefullness
symptoms of narcolepsy
- sleep attacks- go directly into REM
- cataplexy- attack of muscle weakness and hypotonia triggered by emo stims
- sleep paralysis
- hallucinations
- dec voluntary sleep latency
distinguish generalized and focal seizure
generalized = entire brain involved, all of the clonic/tonics
partial = only part of brain involved, either simple or complex partial
stages of tonic-clonic seizures
grand mal
- tonic - inc muscle tone
- clonic - jerky movements
- postictal - altered state of consciousness
what type of epilepsy has EEG records of 3/sec spikes and dome pattern
absence seizures
-sudden transient interruption of consciousness so vacant stare, eyes roll, lids flutter, lack of response
-disappears by adulthood
major diffs b/t simple partial and complex partial seizures
simple does not affect general consciousness so very limited symptoms
-complex does affect so confusion or disorient (temporal or frontal lobe)
