STAGES OF WAKEFULLNESS / SLEEP Flashcards
Electro-Encephalogram (EEG)
used to characterize brain activity during different states of wakefulness/sleep
- Gross average of the electrical potentials of the neurons in a general area of the brain (mostly Neocortex)
- Electrodes attached to scalp record Frequency & Voltage
- Simultaneous changes in potential
- Neural de-synchrony
- Neural synchrony
Simultaneous changes in potential (negative graphed above zero axis, positive below) summate such that…
- Neural de-synchrony => High Frequency
- Neural synchrony => Low Frequency,
Neural de-synchrony
High Frequency (w/variable Voltage) waves = Multiple sources of stimulation: “many pebbles”
Neural synchrony
Low Frequency, High Voltage waves = Coherent source of stimulation: “one big rock”
Awake, active
=> Beta Activity = 18-24 Hz, Very high frequency - very desynchronized
Awake, relaxed
=> Alpha Activity = 8-12 Hz, Like above, but somewhat lower frequency, somewhat desynchronized
Sleep 1
=> Theta Activity = 4-7 Hz, Lower freq, still quite irregular, significantly more synchronized
Sleep 2
=> Mostly Theta Activity, but with many interspersed Spindles and K Complexes
Sleep 3
=> Delta Activity = < 4 Hz observed in less than 50% of this stage, Very low freq, higher voltage, very synchronized
Sleep 4
=> Delta Activity, in more than 50% of this stage, hardest to wake Stages 3 and 4 = Slow Wave Sleep (SWS)
- Heart rate and breathing rate also decrease, and brain is less responsive to external stimuli
REM (Rapid Eye Movement) or “Paradoxical Sleep”
because of contradictory set of conditions that occur:
- EEG is desynchronized, High freq (like Sleep 1 or even Awake), Low voltage (only Sleep 1 is lower): “Imaginary pebbles?!”
- Heart rate, breathing rate, blood pressure more variable than in other sleep stages
- Eyes move, genitalia active, but postural muscles paralyzed, loss of muscle tonus thru most of body (=Atonia),
- External stimuli detected, will awaken if meaningful (e.g. name) but otherwise may not, incorporate into dreams instead
- Highly correlated (tho not 100%) with dreaming – i.e. with “story” dreams
- Some dream imagery in other stages: e.g. Night Terrors (scream awake, but w/out narrative nightmare) occur during Stage 4
Sleep Cycle
= 90 Minutes from Stage 1 to REM: Stage 1, 2, 3, 4, 3, 2, REM, 2, 3, 4, 3, 2, REM, 2, 3, 2, REM, 2, REM . . .
- Stage 4 becomes increasingly shorter as night goes on, drops out altogether after 2-3 cycles, then Stage 3 drops out
- REM becomes increasingly longer as night goes on
Sleep deprivation=
=> Lethargy, poor conc, irritability; Inc temp, metabolism & appetite; Decreased resistance to infection
- When allowed sleep, don’t sleep overall much longer, but longer in Stage 4 and especially REM (REM Rebound)
REM deprivation:
Wake subject when EEG = REM (or when atonia makes cat fall off platform into water)
- System attempts to enter REM more & more frequently; When allowed to REM, shows Rebound effect
- If continuously deprived =>Irritable, poor concentration, anxious => Psychosis, hallucination, death
Functions of Sleep & Dreaming
- ?! Controversial
- Sleep is restorative. But not clear why some species (e.g. prey) can sleep so much less than others (e.g. predators)
- Dreaming warms sleeping brain; Some evidence it helps consolidate memory; May help resolve psychol conflict
Neural control of sleep…
- PreOptic Area of Basal Forebrain Area
- Locus Coeruleus (=“Dark Blue Place”) in Pon
- PGO Wave
- Raphe Nuclei
- PreOptic Area of Basal Forebrain Area
which also assesses & regulates body temp, is critical in initiating sleep
-i.e. VLPA (Ventro-Lateral Preoptic Area) releases GABA, inhibiting all Brainstem and Forebrain arousal systems
- Locus Coeruleu
(=“Dark Blue Place”) in Pons is one target of this inhibition
- Its release of NE decreases radically during sleep, virtually none during REM
- Insufficient output for normal role in forming memories => perhaps why we so easily forget dreams?
PGO Waves
Sequence of activation in Pons => (Lateral) Geniculate => Occipital Cortex - initiates REM
- Excitatory ACh arouses (desynchronizes) visual (& other sensory/motor) pathways
- Also includes activation of Cranial Nerves from Tegmentum for Rapid Eye Movement
- Also sends descending signal => Medulla => Inhibit Motor Neurons in spine = Atonia (muscle paralysis)
- Prevents dreamer from acting out dreams - If malfunctioning, may result in Sleepwalking
Excitatory ACh arouses
(desynchronizes) visual (& other sensory/motor) pathways
- ACh builds up just before REM, holds steady during, then drops off radically as REM ends
- Also includes activation of Cranial Nerves
- Also sends descending signal => Medulla => Inhibit Motor Neurons in spine = Atonia (muscle paralysis)
- NOTE: Higher sensory areas of cortex all active during REM
but NOT
primary NOT projection areas (V1, A1, S1 etc) since no external input being received
and NOT Prefrontal Cortex (perhaps why dreams do not follow the “rules” of normal existence?)
activation of Cranial Nerves
from Tegmentum for Rapid Eye Movement
descending signal =>
=> Medulla => Inhibit Motor Neurons in spine = Atonia (muscle paralysis)
- Prevents dreamer from acting out dreams - If malfunctioning, may result in Sleepwalking
Raphe Nuclei
(medial Pons - Damage = no sleep)
Decreasing Serotonin (5HT) output > sleepiness, irritability if not sleep
- 5HT very low during sleep, none during REM, then Raphe produces sudden, strong burst of 5HT, shuts REM off
- 5HT gradually falls, shifting system back into Slow Wave sleep. When 5HT flat, PGO again initiated by Pons via ACh
