health

Why Do We Dream? Here’s A New Theory About Dreams

By  | 

Are we dreaming to protect the cerebral cortex? Why do we dream? Although psychologists and neurologists have debated the function of dreaming in humans for years, they still cannot give a definitive answer. Recently, two authors named David M. Eagleman and Don A. Vaugh came up with a new theory. With the article titled “Defensive Activation Theory: Dreaming as a mechanism to prevent the capture of the visual cortex”, we come up with a new theory about dreaming.

In my opinion, although this theory is a very original and innovative idea, I am not completely convinced. According to Eagleman and Vaugh, our dreams keep the visual cortex of the brain to be stimulated during sleep. The reason for this; He argues that if the visual cortex in the brain remains passive all night, this will lead to permanent dysfunction.

If there is no signal input to the visual cortex located in the occipital lobe of the brain, the brain begins to respond to non-visual signals. In people who cannot see, this situation is formed by sensitivity to touch. Inadequately used brain areas can be reused in this way. This condition is called neuroplasticity. Although neuroplasticity is generally considered a good thing, Eagleman and Vaughn point out that the sense of sight, unlike other senses, is not always active, so it can pose a threat in this situation.

When we are in a dark room or at night, we get little or no visual input. Therefore, according to this theory, our visual cortex will be vulnerable to ‘capture’ by other senses at night or in the dark. According to this theory, dreams are the defense mechanism of our brain by keeping the visual system active.

As I mentioned before, although I like the theory, it didn’t seem very convincing to me. This is because we already know that dreams are associated with the stimulation of the occipital cortex during a sleep phase called “REM sleep”. As a result, dreams indeed activate the visual system, but I am not convinced of the theory that this is the main reason.

First of all, Eagleman and Vaugh’s theory can only work if reuse in neuroplasticity occurs very quickly.


The harmful neuroplasticity must occur within a few hours for the visual cortex to need defense. According to the article, evidence that neuroplasticity can occur is discussed. However, this does not show any evidence that rapid change could be harmful.

Eagleman and Vaugh do not even portray dreams as a direct defense mechanism. Rather, it provides evidence of the relationship between REM sleep and rate of development. Primates whose babies learn to walk faster and mature sooner tend to have less REM knowledge. (Humans, known as the slowest maturing primates, have the most REM.)

The main idea here is; rapid development means slower neuroplasticity and this means less need to protect the visual cortex. The authors cite other evidence and argue that their current hypothesis can be measured directly by cortical plasticity.

This hypothesis can be easily tested. We can voluntarily recruit a group of people and give them an fMRI scan to determine the extent of their visual cortex and how visually selective they are. (Only visual input, no other senses are important for the reliability of the test.)

For 24 hours, half of the volunteers will be blindfolded to create visual deprivation, the other half will undergo a second fMRI scan with disturbed REM sleep and the data will be compared. According to the theory of Eagleman and Vaugh, it predicts that visually impaired persons will have less selective visual cortex visually and most importantly, REM impairment will increase this effect.