The following article is really a collection of notes, re-written in a
kind of summary format so that I can get a sense of the major changes occurring
in the field of dream science related to the dreaming brain. I have decided to
put these out on Electric Dreams as I get so many questions about the brain in
sleep and this is, after all, the 50th anniversary of the discovery of REM. As
the year goes on, I will organize these notes a little more coherently. If you
have forgotten your sleep stages science and what happens, or are not familiar
with this information, there are two appendices with summaries and detailed
summaries. I haven't gone deeply into the neurochemistry of REM in the brain
stem in this article and am focusing more on the general shifts in
neuromodulation. However, many new changes in the neuro-circuitry of REM have
occurred in the last few years and if you have in mind the older models given by
Hobson, note that these are basically intact, but highly modified and expanded.
In general, this is a summary of the two articles that came out in the 2000
Behavioral and Brain Sciences journal #23. Dreaming and the Brain: Towards a
Cognitive Neuroscience of Conscious States. One article by Allan Hobson, the
other by Mark Solms. The drafts for these articles are available online.
Does and understanding of the mechanisms of the brain really make any
difference to a dreamworker? After all, what difference does it make to me if
the dream comes from the amygdala or a pre-frontal lobe? Probably none. But I
would like to make the case, [without developing it very far in this article]
that dreams are events made up of multiple forces. Understanding where these
forces come from and where we can go with them has always been part of the
In this article, I will look at a model in dream brain research called A.I.M.
and interweave this model with radically new discoveries from brain imagining
and brain lesion studies. The two major points I would like readers to get are:
1. The contributions of the higher and lower brain in dreaming.
2. There is more to the dreaming brain than just activation of areas, there is
also information gating and neurmodulatory control.
*** Three major areas that change in the dreaming brain ***
The human brain (and mammal brain) can be seen as changing in three general
ways as we move from wake to sleep to dream.
First, the general (A)ctivation of brain is at its highest during waking and
lowest during non-dream sleep. In dream sleep, the brain is almost as active as
when awake, but not quite the same way, with a shift from brain centers
associated with linear thinking and calculating to areas that are connected with
feeling and imagining.
Second, the gates for sensing the outer world (5 senses) and the gates that
allow messages for the body to move (motor movements) from the brain to the body
are the most open during wake and the most closed during dream sleep. In fact,
during normal dream sleep, the only easily observable movement are (R)rapid (E)ye
(M)ovements (REM) that can be seen behind a dreamer's closed eyelids. Almost all
other messages from the brain to the body to move are stopped before they leave
the brain, which of course protects us from moving around too much during dream
sleep. In (N)on-dream sleep (NREM), we adopt sleep-postures, we can make slight
shifts in our body position, and our ability to block out unnecessary noise and
disturbances is less than when we are in dream-sleep. But since our brain is
less activated in NREM sleep than REM dreaming sleep, the noises and lights
don't disturb and wake us very easily. (note this difference again, in REM dream
sleep we are less aware of the outside due to the input/output gates being shut
down, but in deep sleep we are not aware due to our brain being less activated.)
Finally, the third change, the neuro-chemistry of the brain at the level of our
nervous system changes from wake to sleep to dream-sleep. These neurochemical
states involve the way the brain communicates with itself and our nervous
system. Since they modulate various brain behaviors, they are often discussed as
neuromodulators. As mentioned, these impact the overall way the brain functions,
but the mind in sleep as well, just as when we take various medicines or drugs
that may alter our consciousness.
*** Picking a model for viewing the dreaming brain ***
The modern science of REM based dreaming is just about fifty years old, and
is already quite complex and full of controversy. After all, dream science
includes the study of consciousness and unconsciousness, brain and body, sleep
and wake, fantasy and reality. To grasp this complexity, scientists propose
models that generalize how dreaming works. These models are then tested and
revised as new data and research emerges. In this report on the dreaming brain,
we will be looking at the Activation/Synthesis model developed by the Hobson
group and how it has been revised in early 21st Century to include new brain
studies and research made possible by brain imaging techniques, new brain
function studies and new brain chemistry. The Activation/Synthesis model looks
at how the lower, subcortical brain activates the higher cortical brain in REM
sleep which allow the cortical brain to synthesize dreams.
I will also be toning down the causal and isomorphic parts of the
Activation/Synthesis hypothesis which have caused so much controversy and are as
yet highly speculative. That is, I will not be emphasizing the several
hypothesis that try to such things as flying in dreams being the result of
intense bursts of brainstem neurons, or paralyzed feet in the dream being the
direct result of de-activated cortical areas. Other research, such as how
aphasia or damage to higher visual centers that ruins a person's ability to
recognize faces, will be included. Also, I will be emphasizing the Synthesis
over the Activation part of the theory. Finally, I will not be giving the psi
dream factor the credit it is due for the sake of brevity. Dream psi research
explores alternative ways to the 5 senses that we may be in contact with others
and the outer world. When I say the brain is cut-off from the outer world, I
mean that we are cut off from our five senses.
*** REM Sleep Summary ***
If you are not familiar with REM and Sleep Stages, see that section below. As
a quick reminder, sleep stages range from light to deep sleep. As we go to
sleep, we slowly sink down into deeper stages of sleep (meaning here that the
brain less activated), then periodically come up via REM (Rapid Eye Movement)
dream sleep (brain more activated but cut off from outer world), then descend
again. Over the course of a usual eight hour night, we will rise into REM dream
sleep about 6 times, each period averaging 20 minutes of REM dream sleep, though
more accurately we have longer REM periods towards the end of the night,
sometimes lasting over an hour. Dreaming can occur in both REM and NREM(Non-REM
sleep, stages I-IV) though traditionally we talk about REM dreaming as being
longer, more vivid, and more story-like, while NREM dreams are traditionally
described as being more thought-like and shorter. There is constant controversy
over just how much difference there really is between REM and NREM dreams.
Reports vary from 5% to 30% of the NREM dreams being indistinguishable from REM
dreams. This issue will become important again as we look at the work Mark Solms
and his view that REM is only one of the keys to turning on dreams. For now, I
will refer to REM dreaming as a state separate from dreaming in general.
*** The Activation/Synthesis Hypothesis ***
The Activation/Synthesis Hypothesis is a fairly easy way to understand the
dynamics of the dreaming brain, though it misses the richness and depth of the
dream experience itself. Hobson's group proposed that during REM sleep the lower
brain provides enough (A)ctivation for the upper brain to (S)ynthesize
information into a dream. Further, there are 3 independent ways the brain
changes that contribute to its unique states of waking, sleeping and dreaming.
They are (A)ctivation of the brain sites, (I)nformation or input/output gating
and (M)odulation of neurotransmitter systems.
A.I.M. Model of 3 Areas of change in sleep and dreams
[chart only works in Courier New or even spaced fonts]
------------ (A)ctivation ------ (I)nput -------- (M)odulating
Level Output Neurochemicals
Waking ------- High Open Aminergic
Sleep ------- Low dampened Aminergic-Cholinergic
REM ---------- High Closed Choinergic
*** Activation in the Upper Brain vs Lower Brain ***
We aren't conscious in sleep when our brain is not activated. Researchers
used to believe that when we weren't getting enough sensory stimulation in
waking life we would fall asleep. But then the reticular activating system (RAS)
was found and we now know that brain is kept awake not by direct input from
sensory pathways, but by tonic (longer lasting activation modulated by
neurochemicals) activity in pathways from the reticular formation. This means
that sleep comes from the reduction in activity from the reticular formation and
wakefulness by the return of activity in the reticular formation. This system
seems to be regulated by an internal clock in the hypothalamus.
Humans and other mammals are tied to the outer daily or circadian clock, the sun
and to this internal circadian clock located in the hypothalamus. The
suprachiasmatic nucleus of the anterior hypothalamus is the best candidate as
any damage to this area change the sleep cycle dramatically and repair causes
the return of normal cycles. This circadian pacemaker is also sensitive to
light-dark cycles of the day but can be set or re-set to different rhythms with
some discomfort, as those who get the night-shift or experience jet-lag know.
Changes to the reticular activating system that runs up though our brainstem
causes changes in activation of higher brain functions. Damage or dampening of
activation to a variety of particular brain areas will cause dampening of
In addition to the hypothalamus and the activation levels of the reticular
system, another regular system engages during sleep, the REM-NREM cycle. Sleep
is not single process, but rather has these two distinct phases that alternate
cyclically in a very organized way through the night.
The lower brain & forebrain seems to play a critical role in the activation of
REM-NREM cycle, while the forebrain and higher brain centers play a role in the
formation of dreaming. REM sleep is generated by a region in the brainstem,
called the pons, and adjacent portions of the midbrain. More will be said of
The early presentations of the Activation/Synthesis hypothesis ran into great
resistance as the Hobson group focused mostly on the Activation side of the
equation. That is, they focused on the lower brain stem mechanisms that were
involved in the REM state. This seemed a reasonable approach. Since the
activation of the upper brain by the lower brain stem seemed to happen after
cyclical phases of random nerve firings (PGO waves in cat studies), the theory
was often characterized as dreams being the results of a sleepy (upper) brain
doing its best it could to handle random signals from the lower brain. Allan
Hobson admits that the many years of focus on the Activation side of the
research led to, what he feels, this misperception of the Activation/Synthesis
hypothesis. Now, new brain research on the involvement of upper brain structures
in dreaming have helped to fill in the Synthesis side of the equation and allow
for theories that emphasize the upper brain as more autonomous in synthesizing
its own information in dream formation.
*** A.I.M. Activation, Information input/output and Modulation of
With the general two-part notion of lower brain activation and upper brain
synthesis in dream creation, we can now look at the three major areas that
change between waking, sleeping and REM dreaming through Hobson's A.I.M. model.
This model tracks three general areas of brain, its 'A'ctivation levels, the 'I'nformation
input/ouput gates and the neurochemical 'M'odulations that change over these
states of waking, sleeping and REM dreaming.
Generally speaking, when we go to sleep the brain becomes deactivated,
desensitized to outer sounds and sensations and switches over from an aminergic
neurochemical system that keeps us alert and focused on the outer world to a
cholinergic system that allows for relaxation. We are sleeping. Then something
strange occurs, the aminergic system stops almost completely and the cholinergic
system becomes hyperactive.
(To see the brain parts impacted by sleep and dreams, see):
During this time, many parts of the brain become active, the body becomes
rigid, and we begin to dream (or more accurately, dreamers that are awakened
from this state are more likely to report dreams and longer, richer dreams, than
most other dream states.) It is as though the brain were like a computer that
has been taken offline but kept running. While dreaming, it is functioning much
in the same way as waking, but the inputs and outputs and connections to normal
feedback from the environment are missing or dampened.
Activation includes the electrical output of the brain's surface as measured
by EEG Electroencephalograms and micro-flows of blood into active areas of the
brain as measured by imaging machines such as PET and MRI. This allows us to
determine what areas of the brain are in operation and active. Unfortunately,
EEGs only show general surface areas and only a handful of brain imaging studies
have been done on dream sleep, and all of these (as of 2003) within REM. (As
mentioned above, dreaming can occur outside of REM sleep and we are waiting for
brain imaging studies with NREM focus as well as in dreaming, lucid dream
See "Sleep Stages: A More Detailed Summary" in the appendix for descriptions
of EEG in sleep and dreams and details on what brain parts are active.
In general, when awake, our brain shows low-voltage(how high) fast pattern,
which print out like the line of an eyebrow. During REM, the brain will show
waves similar to waking; low-voltage, fast pattern. Specific brain areas that
have been shown to be active from brain imaging studies are discussed below in
the Specific Forebrain Structures Activated in Dreaming, however a general
description might be as follows: The main areas activated in the upper brain
during dreaming are 1. the hunting, seeking, desiring system, the 2. heteromodal
3-D imaging system and the 3. higher visual cortex. There is some evidence that
these areas are activated without the regular arousal of REM, but it is clear
that these areas are always activated by the lower brain in REM. Thus we might
say that that REM is the main key to the driving our dream car, though there are
other ways to start the car.
(I) Information input/output
Sensory input and motor output are dampened during REM, open or high I/O
during waking and slightly dampened during NREM sleep. This means signals from
the brain to the body are pretty much cut off and we are paralyzed during REM
(some theorize so that we don't act out our dreams) with some exceptions, such
as eye movement, flow of blood to the genital regions increases, and a few other
"I" is measured by EMG postural muscle tone (how relaxed our body is) and EOG,
Sensory isolation during REM comes from the inhibition of the Ia afferent
terminals (endings of the sensory nerves that form synapse with neurons in the
brain itself). The source seems to be in the brain stem, the pontomedullary
reticular formation that hyperpolarizes the motoneurons (makes them less
responsive to commands from the brain to act, ie, motor commands). Loss of
muscle control is from tonic postsynaptic inhibition of spinal anterior horn
cells by the pontomedullary reticular formation.
In general, most of the outgoing motor messages from the brain are cut off to
the body at the medulla and incoming sensory data from the five senses are
inhibited. This is not a black and white situation. Alan Worsely, for example,
reports that during the first lucid dream signaling experiments, he was able to
vibrate his hands from dream lucid dream sleep. This indicates that the outgoing
motor-muscle messages are dampened rather than being fully shut off.
Of course, the eyes move rapidly during REM dreaming and many structures and
neural routes have been suggested between the lower brain and eye movement.
In REM Behavior Disorder (RBD) people act out there dreams. This is not
sleepwalking, which occurs in NREM. "The inhibition of movement or motor output,
which normally quells the movement commands of dreams, is only quantitatively
greater than the excitation of neurons that is the embodiment of these commands.
If either inhibition declines or excitation increases, or both, movement will
result." (p96 Dreaming Brain, Hobson)
In other words, when there is an imbalance in the brain stem (due to
neurological problems or perhaps in lucid dreaming to active pre-frontal lobe
commands) one can break the REM-barrier! Hobson reports in the Dream Drugstore
(2001) one patients flailing arms, hitting his bed partner, only to wake up and
recall having to turn the wheel on his car to avoid a cliff. Another patient
dreams of swimming and crawls right off the bed.
The suspected cause is an imbalance in dopamine, a neurotransmitter involved in
one brain system with the condition of parkinsonism, and in another part of the
brain with the activation of the hunting, seeking, desiring system. (Solms 2000)
Hobson reports that sometimes the prolonged use of anti-depressants corresponds
to the RBD condition.
As mentioned above, sleepwalking occurs in NREM, as well as sleep-talking and
tooth-grinding. People awakened from these activities don't recall dreaming.
They are automatic behaviors coming from the lower brain areas called motor
pattern generators. Hobson says its fine to wake these people up without
psychological damage, if you can. They are usually in stage IV deep sleep and
very difficult to arouse.
This is the strength of chemical systems modulating the brain. For Hobson,
this is measured in the ratio of cholinergic to aminergic neruomodulator
release. In the Reciprocal Interaction Model of REM, these two systems switch in
waking and dreaming, with aminergic systems dominant in waking and the
cholinergic system dominant in dreaming. In NREM, all three tend to be
More accurately, in waking, the aminergic system is at its height of
influence and inhibits the cholinergic system. As we go to sleep, the aminergic
inhibition loosens it control slowly and the cholinergic system slowly gains in
strength. In REM the aminergic inhibition is shut off and the cholinergic system
is at its peak of influence.
Other researchers, like Mark Solms, feel that neuromodulation of dopamine to
be more important to upper brain structures involved in dreaming (the synthesis
part of the model), while cholinergic systems have more to do with only one of
many activation systems.
Very little research with humans have been done in this area, but Hobson
feels quite confident that this physiology that is common to all other mammals
will be also be at work in humans.
*** Specific Forebrain Structures Activated in Dreaming ***
To summarize before looking into the specific brain areas involved in
dreaming, the dreaming brain appears to have its own (M) neuromodulatory system
that involves [at the level of the brainstem/Pons] a shutting down of the
aminergic system and activation of the cholinergic system. The thalamus (basal
forebrain) and amygdala are cholinergically modulated. The cortex is
aminergically demodulated, especially in terms of dampening recent memory and
Activated Upper Brain Areas in Dreaming
The dreaming brain shows (A)ctivation of many areas as in waking, with the
major exceptions of the prefrontal cortex (linear thinking, calculating) and the
primary (V1 and some of V2) visual centers, though higher visual centers are
activated. This makes sense as V1 is where information from an eye would first
go if one were awake. At the level of the brainstem, the pontine tegmentum is
active, involving reticular information (general arousal) the PGO system (may
initiate REM) and activation of cholinergic centers (sleep and dream
neuromodulators). There is particularly high activation of the amygdala and
paralimbic cortex (Emotion and Recent Memory). The parietal operculum (visual-spacial
imagery) is activated.
(I)nput-output gating is in effect in the dreaming brain. At the level of the
lower brain stem motor output is blocked, leaving the body paralyzed. Sensory
input is blocked, making the outer world unavailable through the five senses.
Hobson theorizes from cat studies and newer evidence that the PGO system is
turned-on, producing input of fictive visual and motor data from the geniculate
bodies to the occipital cortex. That is, as the parts of the brain that deal
with motor movements and sense data are turned on, we begin to be able to dream
about movement and sensorial scenes.
Upper Brain Activation and Synthesis
This may be a good place to give a summary of the areas in the dreaming brain
that Mark Solms research has revealed. Solms feels that the upper brain can
synthesize dreams without the help of the lower brain stem REM system.
The paradigmatic assumption that REM sleep is the physiological equivalent of
dreaming is in need of fundamental revision. A mounting body of evidence
suggests that dreaming and REM sleep are dissociable states, and that dreaming
is controlled by forebrain mechanisms.
Solms combined recent neuropsychological, radiological and pharmacological
findings with his own brain damaged patients and other extensive neurological
research in the past to suggest that the cholinergic brainstem mechanisms which
Hobson's group shows control the REM state can only create dreams with the help
of a second, probably dopaminergic, forebrain mechanism that activates a series
of higher brain systems. Hence, Solms proposes a Dream-on instead of the Hobson
group's REM-on theory of dreaming. In the Dream-on theory, dreaming can be
initiated by many influences outside of REM activation.
In Solms theory, dreaming begins in the higher brain when a particular area
of the forebrain is activated, the mediobasal frontal cortex. Here the hunting,
seeking, desiring, wanting system is deeply networked with the limbic system
(emotions, sensory info) and mesocortical dopamine systems. There are deep
connections of dopanminergic cells from this ventral tegmental area to the
hypothalamus, the septal area, the cingulated gyrus and the frontal cortex, and
amygdala. In other words, this frontal cortex area of motivation connects with
many other parts of the higher brain, the sensory brain and the emotional brain.
When activated in sleep (by REM, drugs, seizures and perhaps other systems)
the extensive connections begin a sequence of activation that includes the (I)
input/output gating of the motor cortices (M) a dopamine modulation of brain in
general and (A) and activation of the emotional systems, the limbic system
(sensory, emotions), the PTO junction or inferior parietal cortex (heteromodal
imagination and 3-D space), and the medial-occipital temporal cortex (higher
Interestingly, the higher visual centers can be destroyed and we can still
dream, through with noticeable differences (such as missing faces in aphasia).
But other areas seem essential to dreaming. Lesions in the PTO junction where we
create or have heteromodal, 3-D space sense is essential to dreaming and no
dreams are reported from patients with lesions in this area, even after many
years follow up. Also, extreme damage to the above mentioned ventral mesial
quadrant of the frontal lobes removes any dreaming (or reports of dreaming) from
the patients. Solms theorizes that just like the patients of old who have had
leucotomies (lobotomy of this area), they just can't reach the arousal level
needed for dreaming. Patients can still perform acts in waking with lesions in
this area, but only upon request, as they lose all initiative to act on their
own volition. I asked Solms if this couldn't just be lack of motivation to
remember, and he didn't feel it was a memory issue as all the memory systems are
intact and the patient's memories function perfectly well in other situation.
Still, I wonder how many dreams I would recall in the morning if I lacked the
motivation to do so.
Recent brain imaging supports this theory that dreaming involves very
specific brain structures. These *activated* structures include anterior and
lateral hypothalamic areas, amygdaloid complex, septal-ventral striatal areas,
as well as the infralimbic, prelimbic, orbitofrontal, anterior cingulate,
entorhinal, insular and occipitotemporal cortical areas. *Deactivated*
structures include the primary visual cortex (where waking eye information would
go, not the same as the activated higher visual centers) and dorsolateral
prefrontal cortex (the calculating part of the brain).
Hobson has accepted much of Solms research, particularly on the specific
higher brain areas that are activated during dreaming sleep. But Hobson doesn't
feel that REM activation can ever be separated from other aspects of dreaming
and is still holding out on whether or not upper brain functioning during
dreaming is modulated by dopaminergic systems. (A separate dopamine system from
the one often related to Parkinsons).
Solms feel a variety of research lines are converging on this same issue of
the dopaninergic system in the forebrain. see:
*** Summaries of specific brain areas activated and deactivated during dream
Please use figure 7 from the online Hobson article to locate the following
brain structures. This section is unlikely to make any sense without the
++++ Zones 1 & 2, figure 7. (Subcortical) Ascending arousal systems : 1. Pons
and midbrain RAS and nuclei. PGO source. Arouses and activates brain, allowing
for consciousness and eye movements. 2. Diencephalic structures (hypothalamus,
basal forebrain). Autonomic and instinctual function, consciousness modulation.
++++ Zone 6, figure 7. (Subcortical) Thalamaocortical relay centers and
thalamic subcortical circuitry. Thalamic nuclei (e.g. lateral geniculate body).
Relays sensory and pseudosensory information to cortex.
In NREM sleep, corticothalamic waves suppress perception and mentation, but this
process is reversed in REM. In REM, the thalamic nuclei activate sensorimotor
parts of the brain and fill these parts of the brain with general activation.
Hobson feels this may present basic elements of dream scenes in the form of
++++ Zone 3, figure 7.(Cortical and subcortical) Limbic and paralimbic
Anterior limbic structures (amygdala, anterior cingulate, parahippocampal
cortex, medial frontal areas). Emotional aspects of dreaming, emotional coding,
goal directed behavior, movement,. For example, the amygdala when activated is
correlated with anxiety and high emotions, and the amygdala activates the
anterior cingulate, right parietal operculum. Deactivated are the prefrontal
cortex, parietal cortex and precuneus.
the anterior cingulate if related to emotional features in waking and dreaming
in integrating emotion with fictive actions.
As mentioned before in the section on Mark Solms research, this area also
includes motivational centers without which we would not have access to the
hunting, seeking, desiring, wanting part of ourselves.
Hobson feels this points to the notion that emotions are more the shaper of
dream plots than reaction to events in dreams being the primary force driving
emotions as in waking life.
++++ Zone 5 in figure 7. (Subcortical) Basil Ganglia. Motor initiation and
control centers. Hobson feels this lower brain area is responsible for the
modulation of movement in dreams and even adds specific features as vestibular
sensations. That is, the sensation of fictive dream movement in our dreams.
++++ Zone 11 in figure 7. (Neocortical) visual association cortex. Higher
visual processing centers that contribute visual information to dreams. We can
dream even when this area is damaged, but our dreams will be impacted, as in the
loss of face recognition in aphasia when the fusiform gyrus is damaged. At the
same time, the primary visual centers (V1 and part of V2) are deactivated. This
makes sense as the eyes are closed.
++++ Zone 9 in figure 7. (Neocortical). Inferior parietal lobe. Brodmann's
Area 40. Spatial integration of heteromodal input. Solms refers to this area as
the PTO junction (Parietal-Temporal-Occipital) and has shown that it is
essential for dreaming, allowing us to imagine inner space and without it, all
dreaming ceases. Also, it coordinates heteromodal information of all types. As
Hobson writes, it "may generate the perception of a fictive dream space
necessary for the global experience of dreaming."
Of interest to left-brain/right-brain theorists, PET studies of this area during
REM show that much of the parietal lobe is deactivated, and just this right
parietal operculum activated. That is, in some studies, the right is more
important than the left in this area during dreaming.
++++ Zone 4 in figure 7. (Neocortical- deactivated) Dorsolateral prefrontal
cortex, or the executive association cortex. Prominent deactivation in the
frontal cortex. This is the executive or reasoning part of the brain and the
part that we use to do math, think linearly and calculate. Hobson feels this may
contribute to many of the "dream deficiencies" such as memory loss, shifts in
scenes, disorientation. It will be interesting to see if this area of the brain
is more activated in lucid dreaming or not. Having this part of the brain
offline may contribute to better facilitation of emotional and memory
*** Final Summary - How the brain works during dreaming ***
In terms of the process of dreaming at the level of the brain/body, we have
learned quite a bit since the discovery of REM 50 years ago by Aserinsky and
Kleitmann in the Chicago University sleep labs. REM or Rapid Eye Movement sleep
occurs on a regular cycle about 20 minutes every 90 minutes of sleep. (More
accurately, we have shorter REM the first part of the night, and longer REM
periods, up to two hours, towards the end of the night). People often report
dreams if awakened from REM.
Now we look at three different levels brain dreaming, the activation of various
sites in the brain, the gating or input/output during Wake/Sleep/ REM stages and
the different neurotransmitters that are impacting these stages.
In brief, when the sleeping person enters REM sleep, much of the mind that was
quiet "wakes up", the dominate neurotransmitter changes from aminergic to
cholinergic washes, and the output from the brain is cut off at the level of the
lower brain stem. That is, messages from the activated brain go out to the body
as in waking, but never make it there and so we get a kind of REM paralysis. Two
areas of the brain that don't wake up are the parts of the pre-frontal cortex
that one usually uses to calculate the lunch bill, and the primary visual
centers used during waking site. (Higher visual centers are still activated. Its
unclear still what brain parts are activated during lucid dreaming).
According to Hobson, this whole cycle is started by the changes occurring
regularly in sleep in the brain stem. Mark Solms sees this brain stem activation
as only one of the ways the brain starts its dreaming cycle. Solms focuses on
the higher brain in dreaming and sees the beginning occurring in the frontal
part of the brain that is our hunting, seeking, goal oriented center. Without
it, (in damaged brain patients) there just isn't the motivation to dream or
recall dreaming. From there, the activation crosses over to the very important
PTO junction between our Occipital, Parietal, Temporal lobes, a place that might
be described as necessary for a human to have any kind of spacio-temporal
imagination. Without it, (in damaged brain victims) there is no dreaming
reported. Finally the activation occurs in the higher visual centers. We can
dream even without activation of these visual centers, but its unclear just what
kinds of dreams one can really have. Patients with partial damage, causing for
example aphasia, can't recall faces in people in their dreams.
Spontaneous or General?
Hobson sees this whole process modulated by the lower brain stem and
cholinergic neurotransmitters. Solms sees the brain stem as peripheral to
dreaming, as epilepsy and other events in NREM or Non-REM sleep can stimulate
dreaming as well. Solms hypothesizes that the main neurotransmitter is
serotonin. Either way, it is REM sleep from brain stem which seems to operate as
a regular starting mechanism for the activation of the higher brain, though
other spontaneous dreaming may occur outside of REM.
APPENDIX 1 *** REM and
Sleep Stages ***
We live on a planet that is light half the day and dark the other half.
Creatures adapt to this two-part cycle, active and competitive in one, resting
and asleep in the other. But the night is not as inactive as one might predict
for some of its sleeping creatures. Almost all mammals experience in sleep
complex changes in brain activation levels, sensory input, motor output and
brain chemistry. In humans these changes often set the brain-body conditions in
which we experience dreams.
Beginning of Contemporary Dream Science in REM (Rapid Eye Movement Sleep)
In 1953 at the University of Chicago, Nathaniel Kleitman and his student
Eugene Aserinsky connected eye activity in sleep to dreams. (Aserinsky &
Kleitman, 1953) Dr. Kleitman had been studying sleep difficulties in infants and
wanted to explore the slow rolling eye movements that babies have at sleep
onset. He had his student Eugene Aserinsky watch these movements of sleepy
infants. What surprised Aserinsky and changed the notion of sleep forever, was
the occasional occurrence of very rapid movements of the eyes at various times
during the sleep cycle. Though the eyes remained closed, they moved just as if
the child was awake and outside playing games. Aserinsky and Kleitman then
monitored adults and found the same thing, and that these eye movements lasted
anywhere from three to fifty-five minutes (Van De Castle, 1994).
Since the movements appeared as if the sleepers were scanning a scene, they
decided to awaken them and ask what they were looking at. They were, more often
than not, dreaming. When they woke sleepers up when there was no eye movement,
they rarely reported dreams. These discoveries were reported in _Science_ on
September 4th, 1953 and again in an expanded article in 1955. It was the
beginning of what is now 40 years of contemporary dream research in the
While Aserinsky finished his medical program and left the labs, William C.
Dement (1976) filled his place and soon was able to characterize sleep in
stages. The REM state is different physiologically than waking or other kinds of
sleep. During REM sleep, there are irregular patterns in breathing, heart rate
and blood pressure. Our muscles are tense, though they can twitch and jerk. Most
of the motor commands from the brain to the muscles are cut off during REM above
Stages of Sleep
Although sleep stages are different in every individual and vary from night
to night and differ widely from childhood to late adulthood, some
generalizations have been observed.
After a few minutes of drifting we slide into deeper and deeper levels of
what is called NREM or Non-REM sleep. The brains waves get wider and slower.
After an hour or two the first REM period begins and lasts a few minutes. Then
we sink back into deeper and deeper sleep. This cycle occurs about every 90
minutes. Towards the end of the night or sleep period, the REM periods get
longer and we dont sink into quite as deep of sleep.
Traditionally, three kinds of measurement used to determine the stage and
level of sleep are:
1. EEG: The electroencephalogram to determine electrical activity on the
surface of the brain. Short dense fast desynchronized waves during waking and
dreaming, tall, wide synchronized waves during NREM sleep.
2. EOG: The electrooculogram. To measure eye movements which produce REM.
3. EMG: The electromyogram. To measure muscle tone.
Now other measurements include the brain chemistry, EKG or heart rate,
respiration and PHG or genital arousal. Newer recording equipment such as the
MRI, PET and other digital imaging equipment are slowly being used in dream
research. These techniques take advantage of the fact that when a particular
area of the brain is active, there are micro-fluctuations of blood flow in that
Sleep Stage Summary:
Comparing REM with waking we find many similarities. About an hour or two
into sleep, people move back up through states three, two and one, and often
enter the first REM stage of the night. REM sleep is sometimes called
"paradoxical sleep" because it has characteristics of both light and deep sleep.
The first REM period of the night usually lasts only a few minutes. Then people
sink into the deeper stages of sleep again. As the night progresses, more REM
periods occur and become longer and longer. Near the end of a sleep period, they
can last for an hour or more. The NREM or non-REM sleep times are shortened as
the night goes on.
By the end of the night, we usually have stopped having state 4 sleep. Near
the end of the night (or sleep period) we rotate between stage two at bottom and
up to REM.
It is easy to get dream reports from people awakened from REM, but people can
dream in any stage. Sawtooth waves occur in the EEG (electroencephalogram, a
surface brain activity measurement) and eyes move rapidly back and forth.
Messages from brain are cut off at the brain stem and never reach the body. The
bodys heating system is regulated more like a reptile and cannot heat or cool
itself. It assumes the temperature of the surrounding room. Part of
understanding that the REM state is different is that it is a *physiologically*
different state than waking or other kinds of sleep. During REM sleep, there are
irregular patterns in breathing, heart rate and blood pressure.
APPENDIX 2 *** Sleep Stages: A
More Detailed Summary ***
NREM Sleep Stage 1.
Wake-Sleep Transition: As we lie down and close our eyes, (if we are tired)
we begin to de-activate and move into low voltage, mixed-frequency EEG brain
People awakened from this sleep stage often report just barely being asleep, or
just about to fall asleep. Short dreams, or dreamlets may be reported. Body
jerks and wandering thoughts can occur. This sleep stage usually lasts 3- 12
EEG: tight, fast Beta waves are replaced by looser, slower Alpha waves
characteristic of a meditating mind. Soon Theta waves [4-8 Hz, (Frequency or how
fast) 50-100 ΅V (Amplitude or how tall the waves peak)] begin to appear.
Reactions to outside stimulus diminish. We stop noticing a lot of the noise
(M)odulation of neurochemical systems
The daytime aminergic system begins to wane and slowly stops inhibiting the
cholinergic system which slowly starts coming online.
NREM Sleep Stage 2.
Not to hard to wake people here, but they usually report being really
asleep. Lasts 10-20 minutes
(A) EEG: Sleep spindles appear. That is, twice as slow Theta waves.
Occasional spikes called K-complexes and the beginning of large slow delta
[4-15 Hz , 50-150 ΅V ]
(I) EMG: Muscles have tone or tension. Reactions to outside stimulus
diminish. Unlikely to notice noise and lights unless unexpectedly strong
(M) Aminergic neuromodulation system continues to loose control and
cholinergic system gains more control.
NREM Sleep Stage 3.
Lasts about 10 minutes
(A) EEG: Slow waves [ 2-4 Hz, 100-150 ΅V
] and Delta Waves. A little less than half the waves are large, slow delta
waves. Spikes and K-complexes occur, but not as much. Slow waves + spindles + K
(I) EMG: Muscles have tone. Reactions to outside stimulus unlikely unless
strong or salient (mother hearing child's call or we hear our name). Unlikely to
notice noise and lights unless unexpectedly strong
(M) Aminergic neuromodulation system continues to loose control and
cholinergic system gains more control.
NREM Sleep Stage 4
More slow-wave activity in the EEG readings and overall neuronal activity at
it lowest. Brain temperatures lowest and sympathetic outflow, heart rate and
blood pressure down. Stages 3 and 4 in humans are sometimes called slow-wave
Sleepers hard to awaken. Children my take several minutes to awaken.
Combined with stage 3, Lasts 40-90 minutes.
(A) EEG: Delta Sleep. More than half the waves are large, slow delta waves
(I) . EMG: Muscles have tone. Sleepwalking, sleeptalking, night-terrors,
bedwetting in children.
(M) Aminergic neuromodulation system continues to loose control and
cholinergic system gains more control.
REM Sleep Stage:
Just exactly what starts REM sleep is complex and partially still being
A system of neurons generating the EEG, eye movement, twitches and underlying
muscle atonia of REM sleep have been identified in the brainstem . This system
utilizes adrenergic (noradrenergic and serotonergic) REM sleep-off neurons,
GABAergic, cholinergic, glycinergic and glutamatergic REM sleep-on cells as well
as other neurons.
In REM or Rapid Eye Movement sleep, the EEG looks similar to stage 1 NREM and
waking. Because it resembles waking, REM is often called "paradoxical" sleep.
In REM there are bursts of neural activity, expecially in the Pons. These bursts
generate high-voltage spike potentials, the ponto-geniculo-occipital or PGO
spikes. The PGO spikes are named after structures in which these spikes are most
detected (the pons, lateral geniculate nucleus, and occipital cortex). PGO
spikes are one of the phasic or short-lasting events of REM sleep, including eye
movements and cardio-respiratory irregularity.
The overall activity of the brain increases, and so the brain temperature and
metabolic rate are high, equal to or greater than during the waking state.
Atonia occurs (loss of muscle tone or outgoing motor commands to muscles) though
small, phasic twitches occur and the skeletal muscles controlling the movements
of the eyes, middle ear ossicles, and diaphragm are not atonic. The pupils are
constricted (miosis), reflecting the high ratio of parasympathetic to
sympathetic output to the pupil. Genital arousal regularly occur during REM
sleep. There is a reduction in homeostatic mechanisms. Respiration is relatively
unresponsive to changes in blood CO2, and response to heat and cold are absent
or greatly reduced. Thus the body temperature drifts toward room temperature as
(A) EEG much like waking [15-50 Hz < 50 ΅V ] and stage 1
EEG gamma frequency 30-80 cycles per second "that has been touted as denoting
sufficient temporal coherence among the widespread neuronal circuits of the
context to permit the binding necessary for the unification of conscious
Pontine tegmentum: activated retircular formation, PGO system and cholinergic
Amygdala & paralimbic cortex : activation of emotional (quantity) and remote
Parietal operculum (PTO junction) : activated visuospatial imagery
Prefontal cortex deactivated: volition, insight & judgement and working memory
EKG: Irregular heatbeat compared to NREM
(I) EOG: Rapid Eye Movements back and forth rapidly. Sometimes measured by
strain gauges as well. EMG: muscles loose and relaxed. Active suppression of
senory input and motor output. That is, stimuli from the outer world is dampened
and messages from the brain to move are cut off at the brain stem. (Eyes are an
example of the few outgoing nerves not dampened, and hence REM)
Motor output blocked: real action dampened
Sensory input blocked: outer world data unavailable
PGO system turned on: fictive visual & motor data generated
Respiration is less regular than NREM
(M) Aminergic demodulation, Cholinergic control. (suppression of firing by
locus coeruleus and raphe neurons). " REM-on cells are postulated to occur via
disinhibition (resulting from the marked reduction in firing rate by aminergic
neurons at REM sleep onselt) and through excitation (resulting from mutually
excitatory cholinergic-noncholinergic cell interactions within the pontine
Aminergic demodulation (loss of waking mental tone) may be a more or less
direct cause of the difficulty in moving dreams from short to long term memory,
as the attention needed to code memory is difficult with aminergic demodulation.
Thalamus basal forebrain & amygdale cholinergically modulated.
Cortex aminergically demodulated: recent memory and orientation down.
Pons: switch from aminergic (now off) to Cholinergic neurons (now on)
Schematic summary of REM:
"EEG dysychronization results from a net tonic increase in reticular,
thalamocortical, and cortical neuronal firing rates. PGO waves are the result of
tonic disinhibition and phasic excitation of burst cells in the lateral
pontomesencephalic tementum. Rapid eye movements are the consequence of phasic
firing by reticular and vestivular cells; the latter directly excite oculomotor
neurons. Muscular atonia is the consequence of tonic postsynaptic inhibition of
spinal anterior horn cells by the pontomedullary reticular formation. " From
Hobson et al., 2000 Behavioral and Brain Sciences 23
In cat studies, oncoming REM seems to come from the lateral geniculate bodies of
the thalamus, corresponding to the depolarization of the geniculate neurons by
excitatory impulses arising in the pontine brain stem, and depolarization of
neurons of the reticular formation and the PPT pedunculopontine region. The PPT,
a cholinergically modulated area, is thought to be the origin of the process
that initiates REM in the brain stem. signals originate in the pons (P) and
radiate to the geniculate bodies (G) and the occipital cortex (O).
REM begins when PGO waves become cholenergically hyperexcitable, a condition
that is regulated by the inner circadian clock in the thalamus.
More specifically, the " of serotonergic inhibition and neuromodulation that
results from the "Don't Act Now" signals sent down into the pons from the
hypothalamic circadian clock. "
This mode of active signals without input/output gating means we have a lot
of "fictive movement" or movement hat is centrally commanded but peripherally
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BBS Special Issue: Sleep and Dreaming