/ Psychophysiology of sleep and dreaming Flashcards
Link between REM sleep and dreaming
Discovered by Aserinsky and Kleitman (1953)
More likely to recall dreams if woken from REM than NREM, and longer REM = longer dreams (Dement & Kleitman, 1957)
Activation-synthesis hypothesis of dreaming
Hobson & McCarthy 1977
3 factors:
- Brain stem generator
- Brain stem generates REM sleep & PGO waves provoke random memories in the cortex
- Blocks body movement & external info
- We think dreams are the real world
- brain synthesises these memories together to become more sensible - carries on into wakefulness - try to make more sense of dreams when we recall them
- Physiologica-psychological reductionism
- dream content is caused by physiology
- Aminergic demodulation
- Aminergic system is less active during sleep
- results in bizarreness of dreams
Highlights importance of REM sleep and PGO waves
- Hobson 1987 showed longer dreams = more chance of bizarreness bc more chance for PGO waves to occur
Cognitive view of dreams
Antrobus
- active brain + lack of incoming info from external environment = hallucination, believe what we are seeing is real
- During sleep, this is what dreaming is
Neuroimaging view
Desseilles et al., 2011
- increased activity in frontal lobes, emotional and visual areas of the brain during REM cause dreaming
- Relatively inactive dorsolateral prefrontal cortex = delusion from lack of reflexivity - don’t think about what’s happening, don’t spot bizarreness
- Discontinuities from sudden PGO waves triggering changes (agree with Hobson)
- Intensification of emotion
- Amnesia - Hobson says bc our neurochemical state during REM is different from wakefulness, not forming meories as strongly
Auditory stimulation during REM sleep
Stuart & Conduit, 2009
- REMs suppressed by auditory stimulation - PGO activity suppressed
- EEG arousal higher with auditory stimulation
- Decreased eye movement
- Decreased reports of dreaming
- Supportive of Hobson - Antrobus would think more activity in the brain would caused more dreams but this isn’t the case here!
The reward system and dreaming
Perogamvros & Schwartz (2012)
- Mesolimbic dopaminergic responses carry on during sleep -
- Processing emotions during sleep produces dream content - dreams are emotional but aren’t random memories like Hobson suggested
- waking motivations are processed during sleep and result in dreams - dreams are meaningful!
- memories with high emotional and motivational value are privileged to be reactivated during sleep & may amplify activation of the ML-DA system and SEEKING system
Evidence for the role of reward pathways in dreaming
Perogamvros & Schwartz, 2012
- VTA activity increased during REM
- NAcc, PFC, amygdala and ACC activity increased during REM
- Activation of HC and ventral striatum reward-related neurons during SWS
- Related to Freud - wish fulfillment view
- Related to Hobson - non-functional AIM model
- Related to Threat Simulation Theory
- Related to Stickgold & Wamsley - dreaming reflects off-line memory consolidation
Dreaming as a subsystem of the default network
Domhoff, 2011
- The default network is a resting state of synchronised activity between different areas of the brain - processing info while person isn’t deliberately processing anything (found with EEG)
- dreaming is the default network running during sleep
- like daydreaming but dreams are more intense bc there is further reduced deliberate processing of the environment - lack of external stimuli = believe dreams are real
- De-emphasises REM as being the key sleep stage for dreaming
Brain injury and dreaming
Solms, 1997 & 2000
- 100 years of records of brain damage and effects on dreaming
- Damage to parieto-temporal-occipital junction leads to aphantasia (inability to engage in mental imagery)
- Damage to ventro-mesial quadrant of the frontal lobe leads to loss of dreams, preserved REM
- frontal areas are involved in motivation –> this + mental imagery = motivations become pictured in dreams
- Brain works ‘backwards’ during sleep - cognitions cause imagery rather than what we see causing cognitions (pretty psychoanalytic view)
Fisher, Wood & Balgrove, 2004
- Frontal brain injury = increased nightmare frequency
- 23% report having repetitive nightmares
- 1/3 report complete absence of dreaming
- worse post-trauma amnesia = higher chance of this
Not having dreams or not recalling them? Solm said production is inhibited, not recall
Physiological differences between subjects with high and low dream recall frequencies
Eichenlaub et al., 2013
Evoked response method:
- high (>3/week) and low (<2/week) dream recall
- randomly present P’s own first name or random names
- Evoked Response Potentials recorded
- Higher activity to novel names for high recallers
- processing more info during sleep, causing them to have/recall more dreams
Correlation method:
- High recallers have higher cerebral blood flow in temporal parietal junction (perspective taking, language, mental imagery, episodic memory retrieval) during REM, N3 & wakefulness
- and in medial prefrontal cortex (mind representations, evaluations) during REM and wakefulness
Can’t go beyond this to say whether dreams have a function - just know there’s a physiological difference between high and low recallers
Neural correlates of dreaming
Siclari et al., 2017
- repeatedly wake P’s during the night, ask if they were/weren’t dreaming/were dreaming but can’t recall content
- Parieto-occipital region - less delta waves (1-4Hz) = dreaming
- Medial and lateral fronto-parietal areas - more activity - dreaming
- 87% accuracy when predicting if P’s were dreaming or not, based on EEG data
- dream content related to activity in areas relevant in waking life
- SO - dreaming in REM and NREM when hot-spots are activated
- pure measure of consciousness - in a single sleep state consciousness is either present (dreaming) or absent (no dreaming) & neural correlates can be assessed to determine this
