The Activation Synthesis Theory of Dreaming – Hobson & McCarley (1988)
In the 1970s, J. Allan Hobson and Robert W. McCarley developed the activation synthesis theory of
dreaming. This theory states that dreams are produced by random stimuli from the pons. The forebrain,
the "thinking" part of the brain, receives these stimuli and then makes up stories to make sense of
them. These stories are what we call dreams.
According to the activation-synthesis theory, dreams are merely the brain's reaction to random
biological processes that occur during sleep.
Various parts of the brain - in particular the pons, part of the brain stem - continue to function and
produce stimuli during sleep and REM sleep in particular. The brain then takes these internal stimuli
and attempts to make some sort of sense of them. To do this it uses other random stimuli and
memories, especially those easily accessible in the short-term memory.
Random Brainwaves
For example, the randomly produced stimuli might resemble those produced when running. The
sleeper's mind could then interpret those stimuli as a dream of running. If, in addition, they had
earlier that day been startled by a cat then the brain might latch on to that memory and produce a
dream of being chased by a lion. Thus cortical attempts to explain random signals from the lower
brain produce a random dream with no deep or hidden meanings or purpose.
As the pons continues to fire random stimuli at the forebrain, the latter constantly attempts to
interpret them. This is why dreams sometimes shift so suddenly in content. The forebrain is
attempting to respond to totally new random stimuli and needs to build a completely new situational
model to incorporate them.
The activation-synthesis hypothesis has the advantage that it renders dreams meaningless and
removes any need to understand or interpret them. Some would argue that this is also its biggest
disadvantage.
We Dream Outside of REM Sleep
The activation synthesis theory is based on the idea, which has been shared by many, that dreams are
an aspect of REM sleep. Therefore, if REM sleep is caused by activity in the pons, then dreams are
caused by activity in the pons.
However, in 1962, cognitive psychologist David Foulkes performed a sleep study. In such studies,
subjects are usually woken up at different ages of sleep and asked if they have been dreaming.
However, instead of asking subjects if they had been dreaming, Foulkes asked, "What was passing
through your mind?" Half of the subjects who were awakened during NREM sleep reported complex
mental activities that could have been considered dreams.
While the average NREM dream is less vivid than the average REM dream, between 5 and 30 percent
of NREM dreams can't be distinguished from REM dreams. Considering that about three quarters of
the time we spend sleeping is spent in the NREM stages, this means that about one quarter, at least, of
vivid dreams take place during NREM sleep.
Could some of Foulkes' subjects who claimed to have been dreaming vividly in NREM sleep really been
dreaming during an earlier REM stage and been mistaken about when they dreamed? In many cases,
that would not have been possible. Foulkes found that subjects would report dreams even before they
had entered the first stage of REM sleep.
Later research has shown that if someone is awakened during the first few minutes of sleep, they will
report a dream 50 to 70 percent of the time, and the dream will be no different from an REM dream,
except for the length.
People Who Don't Have REM Sleep Still Dream/People Who Don't Dream Still Have REM Sleep
At the end of the 20th century, Solms studied records of cases in which people suffered damage to the
pons and therefore lost most or all of their ability to experience REM sleep. He found 26 such cases. He
found that only one of these people said that they had also stopped dreaming
Solms also studied records of cases in which people stopped dreaming after suffering brain damage.
There were 111 such cases. In all but one case, there was no damage at all to the pons. A completely
different part of the brain was injured.
Further studies have shown that in these cases, people still experience REM sleep, even though they
no longer dream. To ensure that they haven't simply forgotten their dreams, patients have been
awakened during REM sleep to check that they haven't been dreaming.
Where Dreams are Made
Solms then performed a study of his own neurosurgical patients in hospitals in London and
Johannesburg. For four years, he asked every patient if they had noticed any changes to their dreams
after they had suffered brain damage. For a control group, he used patients who had been referred to
him but had been found not to have any neurological damage.
Patients reported four types of major changes to their dreams:
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Some patients stopped dreaming altogether.
Some patients stopped seeing things in their dreams
Some patients started having recurring nightmares
Some patients began to confuse dreams and reality
By looking at where these patients' brains had been injured, Solms was able to find which parts of the
brain have a part in the dreaming process.
Dreams are Made in the Forebrain
Solms found that while REM sleep is produced by the pons in the brainstem, dreams are produced in
two different areas of the forebrain.
One of these areas is in a part of the frontal lobes just above the eyes. This area contains a pathway
through which a chemical called dopamine travels from the middle of the brain to the higher parts of
the brain. When someone suffers damage to the dopamine pathway, they continue to have REM sleep,
but they stop dreaming.
In the 1940s and 1950s, a study was done of over 300 people who had undergone frontal lobotomies.
It was found that these people tended to have very few or almost no dreams.
Drugs such as L-Dopa, which stimulate the dopamine pathway, cause people to have vivid dreams.
Drugs such as haloperidol, which suppress the dopamine pathway, can cause frequent, excessively vivid
dreams to stop.
The second area of the brain that is responsible for dreaming is the occipito-temporo-parietal (OTP)
junction, which is located just behind and above the ears. We use this area of the brain for the highest
levels of thinking. This includes taking concrete information and converting into abstract ideas. If
someone experiences damage to this part of the brain, they cannot dream at all.
How Dreams Protect Sleep
Solms found that the activity of the pons during REM sleep is just one of many different triggers,
including L-DOPA and some stimulant drugs, which can cause people to dream. These triggers all have
one thing in common - they create a state of arousal.
However, these triggers only cause people to dream when they activate the dopamine pathway. If this
pathway is removed, they can't dream.
The main purpose of the dopamine pathway is to make us try to achieve our goals. People who suffer
damage to this pathway not only stop dreaming, they also lose the motivation to achieve things in their
waking lives.
Solms also found that the dorsolateral frontal convexity, a part of the frontal lobes that is one of the
most active areas of the brain when we are awake, becomes completely inactive when we dream. This
area of the brain is connected to the motor system. It is the area of the brain where thoughts are
converted to action.
Brain activity during waking life is concentrated in the dorsolateral frontal cavity. However, when we
dream, it is concentrated in the OTP region, the part of the brain that houses our memory and our
perceptual systems.
This means that when we sleep, our wishes are not converted to actions. Instead, our intentions to act
are transferred away from the motor systems and toward our perceptual systems, where they are
transformed into internal images. In addition, because parts of the limbic system that allow us to reflect
on our experiences become inactive during sleep, we mistake these images for reality.
In this way, we are prevented from physically perform goal-seeking actions while we sleep. Thus, our
sleep is protected.