THE

COGNITIVE
NEUROSCIENCE
OF
DREAMING

NEURONAL SYSTEMS, CONSCIOUSNESS AND LEARNING

Based on J.Allan Hobson and Edward F.Pace-Schott, Nature Review
Summarized by Manvi Jain
Questions driving Sleep-based Research

What are dreams?

 Dreams

• Dreams seem to help us process emotions by encoding

and constructing memories of them 11
• Our dream stories essentially try to strip the emotion
out of a certain experience by creating a memory of it.
This way, the emotion itself is no longer active.
• This mechanism is important because when we don’t
process our emotions, especially negative ones, this
increases personal worry and anxiety.
 Dreams

• “Dreams help regulate traffic on that

fragile bridge which connects our
experiences with our emotions and
memories”
• Freud’s theory centered around the notion
of repressed longing - the idea that
dreaming allows us to sort through
unresolved, repressed wishes
 Old schools of dreams
• Freud: daytime experience-triggers emergence of
related memories- determine dream content 10,64
• Subjects assessed their dream reports- paying
attention to identifiable memory sources. The
results revealed-dream content does not
represent episodic memories (available when
awake)
• Instead, discrete fragments of narrative memory
are assembled to create the plot discontinuities
and incongruities of dream content
• This information is ‘pseudo-sensory’, there’s
no external source of it…
 Questions driving Sleep-based Research

What triggers this information into the

brain, or is it out of blue?
Levels of Organizations of Sleep

Figure 1 Depth recordings

from single neuron in the
pontine brainstem of cat
shows that there’s no
absolute external sensory
stimulation during REM.
 Levels of Organizations of Sleep

• Ponto-geniculo-occipital (PGO) waves convey

pseudo-sensory information from the REM-activated
subcortex to the neocortex during dreaming 2
• During NREM, information is conveyed from the
hippocampus to the neocortex-memories; absence
of episodic memory reflects
• Inaccessibility of hippocampally stored information
to the dreaming brain 10
Questions driving Sleep-based Research

Origin of this pseudo-sensory

information for dreaming?
 Origin of this pseudo-sensory information?
• During REM, outflow of info from
hippocampus to neocortex is blocked,
• Wake-like flow of information from
neocortex to hippocampus might be
possible, enhanced by Acetylcholine
• Figure 1 shows elevated levels of Ach
during REM
• Semantic memory stored in
neocortex provides the basic info for
dreaming that helps us recognize
even in a dream that a red, edible, Figure 2 Elevated levels of acetylcholine suppresses
spherical object is an apple 64 the flow of information from the hippocampus to the
cortex both in waking and in REM
 Questions driving Sleep-based Research

How would REM sleep explain neural

basis of ‘conscious experiences’ in the
form of Dreams?
 REM and dreaming
• This explain why we are conscious
during REM sleep, even being cut off
from external perceptions:
1. Cognition-associated gamma
frequency (30–80 Hz) oscillations,
38,41

2. Loss of their synchrony between

frontal and posterior cortices 42
• In dreams, we experience fully formed
imagery while believing ourselves to
be awake This nature of REM is
hallucinatory… 60
Figure 3 Levels of Organizations of Sleep
 Hallucinatory REM
• As the brain goes, so goes the
mind.
• Mental activity of 16 normal young
subjects was studied-The five states
of Sleep were analyzed for level of
consciousness
• Reports of hallucinatory activity
increased from waking to sleep
onset and NREM to REM sleep
• Whereas reports of directed thinking
decreased rapidly. 60
Figure 4 CONSCIOUSNESS during REM- Waking suppresses hallucinosis
in favour of thought, REM releases hallucinosis at the expense of
thought.
 Consciousness and Sleep
• Greater SWA in frontal/Conscious than
in parietal and occipital/Unconscious
regions 70 during the first NREM
episode 31,32
• Frontal areas lag behind more posterior
ones in reactivation after awakening 35
• Indicating frontal areas might be the
first to fall asleep, most dependent on
sleep homeostatic processes, and last
one to wake up Figure 5 Slow-wave activity in ADHD & normal brain.
SWA-A spectral analytic measure of total power in slow-
• frontal region is most affected by sleep oscillation and delta frequencies of EEG (0.5–4.5 Hz) in
NREM sleep, which is thought to be sensitive to degree of
inertia and working memory. pre-sleep homeostatic sleep pressure.
 Dreaming as normal delirium
• Brain-based aspects of dream
consciousness:
• lack of self-reflective awareness,
inability to control dream action
voluntarily, and impoverishment of
analytical thought.
• These cognitive deficits diagnosed
dreaming as a ‘normal delirium’, sharing
with the clinical syndrome
(schizophrenia) all of its defining Figure 6 REM dreaming constitutes a normal physiological state
features: of the brain that shares its physiological substrate and
psychological experience with such psycho-pathological
• visual hallucinosis, disorientation, conditions in which limbic hyperactivation is combined with
memory loss and confabulation. 80,90 frontal hypoactivation (see REFS 80,90)
Questions driving Sleep-based Research

If so, what is the ‘Real’ dream

mechanism?
 Models of dreaming
The activation–synthesis model 2
• Ascending cholinergic activation of ‘Off-
line, aminergically demodulated’ brain
during REM sleep
• Provides best physical substrate for
distinctive features of dreaming
• Such as loss of self-reflective
awareness, bizarreness, and memory
loss.
• So, synthesis of dream proceeds without Figure 7 Brainstem activation of cerebral
access to episodic memory cortex during REM (initial concept)
Figure 8
 Models of dreaming
The three-dimensional AIM
(activation, input source, modulation) state-space model
• Normal transitions from wake to (NREM) and to REM sleep.
• REM- in which activation (A) is high, input (I) is entirely internal, and the
forebrain is cholinergically activated and aminergically demodulated (M)
• Figure 4 shows physiological signs and phenomenological activities occurring
during dreaming.

REF.129 © 1996 Appleton & Lange (activation,input source,modulation) (Present concept)

Figure 9
BRAIN ACTIVATION MODEL OF DREAMING
• Forebrain processes in normal dreaming — an integration of
neuro-physiological, neuropsychological and neuroimaging
data depicted in Figure 9.
• Regions- 1 and 2 ascending arousal systems;
• 3, subcortical and cortical limbic and paralimbic structures;
• 4, dorsolateral prefrontal executive association cortex;
• 5, motor initiation and control centres;

• REF.129 © 1996 Appleton & Lange.

BRAIN ACTIVATION MODEL OF DREAMING
• 6, thalamocortical relay centres and thalamic subcortical
circuitry;
• 7, primary motor cortex; 8, primary sensory cortex;
• 9, inferior parietal lobe; 10, primary visual cortex;
• 11, visual association cortex; 12, cerebellum.
• BA, Brodmann area; LGN, lateral geniculate nucleus; PGO,
ponto-geniculo-occipital; RAS, reticular activating system.
 Activated areas and their roles
Regions- 1 and 2 ascending arousal systems
1: Pontine and midbrain RAS and nuclei
• Ascending arousal of multiple forebrain structures
• Dream: consciousness, eye-movement and motor-
pattern information via PGO system
Region 2: Diencephalic structures (hypothalamus, basal
forebrain)
• Autonomic and instinctual function, cortical arousal
• Dream: consciousness, instinctual element
• Activation of forebrain in REM occurs through
ascending arousal systems in the brainstem reticular
activating system 4,14,15 and basal forebrain 69; activation
is aminergically deficient and cholinergically driven 1,3.
Region 3: Anterior limbic structures
(amygdala, anterior cingulate, parahippocampal cortex,
hippocampus, medial frontal areas)
• Emotional labelling of stimuli, goal directed behaviour,
movement
• Dream: emotionality, affective salience, movement
• limbic and paralimbic areas and subcortex activation underlie
dream emotionality highly social nature of dreaming 70–72.
• Amygdala- mediates anxiety a prevalent dream emotion 3,73–76,
• anterior cingulate- emotion-related cognition such as conflict
monitoring, premotor functions 77.
• medial orbitofrontal and insular cortices 46,53- lesions can cause
dream-like confabulatory syndromes 67
• hippocampus with amygdala mediate storage of emotional
memories in waking 81; reactivation of these areas could allow
readout of emotionally salient memory fragments in REM
sleep.
 Region 4: Dorsolateral prefrontal cortex
• Executive functions, logic, planning
• Dream: loss of volition, logic, orientation, working memory
• Deactivation of executive areas in the dorsolateral prefrontal
cortex during NREM sleep 45–48,
• followed by their failure to reactivate during REM 46,47,52,
• might underlie executive deficiencies of dream mentation,
including disorientation, illogic, etc.
Region 5: Basal ganglia
• Initiation of motor actions
• Dream: initiation of fictive movement
• Basal ganglia are connected with REM-regulatory areas in the
mesopontine tegmentum 83,where they are coextensive with
gait circuitry 84
• cerebellar vermis, which is involved in motor control and is
increasingly implicated in emotion, cognition and
psychopathology 85, is also activated during REM 46
Region 6: Thalamic nuclei (e.g. LGN)
• Relay of sensory and pseudo-sensory information to
cortex
• Dream: transmits PGO information to cortex
• Occupy key sites in sensory-relay circuits, transmit
endogenous stimuli for sensory phenomena of
dreaming
• Ponto-geniculo-occipital (PGO) waves convey pseudo-
sensory information from the REM-activated subcortex
to the neocortex during dreaming
Region 7, 8, 10: Primary motor (7) and sensory (8,10)
cortices
• Generation of sensory percepts and motor commands
• Dream: sensorimotor hallucinosis
Region 9: Inferior parietal cortex (BA 40)
• Spatial integration of processed heteromodal input
• Dream: spatial organization
• Generates percept for fictive dream space necessary for
organized dreaming hallucinatory experience 67.
 Region 11: Visual association cortex
• Higher-order integration of visual percepts and images
• Dream: visual hallucinosis
• Areas of medial occipital and temporal cortices that mediate
higher visual processing generate visual imagery of dreams
47,67.

• As in waking, specific areas of visual association cortex

process specific visual features in dreaming.

• Region 12: Cerebellum

• Fine tuning of movement • Dream: fictive movement
 SUMMARY
• Neurobiological activation-synthesis hypothesis: dreams are electrical
brain impulses that pull random thoughts and imagery from our memories.
• Ascending arousal systems activate forebrain regions involved in dream
construction-is different from waking arousal processes.
• REM dreaming activates medial cortical circuits linking posterior
association and paralimbic areas. Thus, dreaming is so emotionally salient
and social 47
• Dreaming often involves a suite of emotional (limbic subcortex), motoric
(striatum) and instinctual (diencephalon) elements due to Subcortical
circuits- limbic structures, striatum, diencephalon and brainstem
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 Acknowledgment
Completion of this project has only been possible because of the
contributions of:
Dr C.M. Markan, Dept. of Physics and Computer Science, Dayalbagh
Educational Institute, Agra;
Dr. Naredla Apurva Ratan Murty, Dept. of Brain and Cognitive Science,
MIT, Boston;
Dr Arun Pratap Sikarwar, Dept. of Zoology, Dayalbagh Educational
Institute, Agra
And effortless editing of Mr. Shishank Jain, Student, CS