Does our I-function sleepwalk?

mkhilji's picture

There are countless stories of sleepwalkers suddenly waking up and finding themselves naked in their backyards. Between 1 and 15% of the population are prone to sleepwalking, which involves people getting up and walking around while asleep and often doing bizarre things (1). Frequent sleepwalking can lead to health problems since it interrupts normal patterns of sleep. But what causes sleepwalking and are there ways to control it? How does this relate to the structural mechanisms of neurobiology that we have learned over the semester?

Sleepwalking (also know scientifically as somnambulism) is defined as a series of complex behaviors that are initiated during partial awakenings from sleep. People walk around in a state, which is of partial consciousness and often exhibiting impaired judgment. Knowledge about sleepwalking is quite limited-however various scientists have found that many diagnosed with sleepwalking experience disruption of slow-wave sleep. This is categorized as the deepest stage of sleep. With each of these disruptions there is an increasing vulnerability to sleepwalking.
The vast majority of sleepwalking cases have genetic basis. Sleep walking in children is considered a relatively common developmental phenomenon. In adulthood, in addition to genetics, various conditions can predispose someone to sleepwalking, such as hyperthyroidism, migraine headaches, head injury and encephalitis. Also it has been found that some psychiatric medications such as lithium and amitriptyline can increase sleepwalking (1).

It is probably considered more common that children sleepwalk because they have not fully developed and therefore their I-function has not necessarily fully gained control of it signal sending yet. It could also be related to other parts of the brain not being fully developed which can restrain the children necessarily from certain actions. This may have something to do with the part of the brain that has control of whether a child can control their bladder or not during the night-resulting in bed-wetting.

Neurologist Antonio Oliviero of the National Hospital for Paraplegics in Toledo, Spain, explains that sleep disorders such as sleepwalking can arise when normal physiological systems are active at inappropriate times. He further argues that there is no precise explanation as to why the brain may still issue commands to the muscles during certain phases of sleep. However it is known that usually such commands are suppressed by other neurological mechanisms-perhaps the suppression is incomplete (2).

It is quite possible that during sleepwalking the I-function is activated and not successfully blocking or controlling signals that it would usually pass on in the 'awakened' state of the body. Studies have proven that while we sleep there is in fact some brain activity. Therefore the effects of sleepwalking may arguably be a result of the control of the I-function of sending certain signals to the motor neurons.

Recently Oliviero's team has proposed a possible physiological mechanism underlying sleepwalking. During normal sleep the chemical messenger gamma-aminobutyric acid (GABA) acts as an inhibitor that stifles the activity of the brain's motor system. In children the neurons that release this neurotransmitter are still developing and have not yet fully established a network of connections to keep motor activity under control. As a result, many kids have insufficient amounts of GABA, leaving their motor neurons capable of commanding the body to move even during sleep. In some, this inhibitory system may remain underdeveloped-or be rendered less effective by environmental factors-and sleepwalking can persist into adulthood (2).

75% of sleepwalking episodes occur during non-REM sleep (3). The first episode of REM sleep occurs about 90 minutes after the beginning of the sleep episode, and then recurs about every 60 to 90 minutes thereafter, lasting a short time at each occurrence. One particularly interesting feature of REM sleep is that electroencephalography measurements (EEG) during this time are remarkably similar to when an individual is awake. EEG measurements then transition back into the "asleep" range when the individual abruptly resumes non-REM sleep.

Thus, sleepwalking has been hypothesized as originating from some sort of incomplete transfer from brain functions characteristic of "asleep" EEG frequency to those of an "awake" frequency. The brain is in limbo between the state of being "awake" or being "asleep". Brain areas have different functions based on the current state of consciousness, and different types of activity may lead to different outcomes as a result. This sparks new insights regarding the I-function and whether the I-function has the capability to determine the context in which it may be giving orders to the rest of the nervous system. There are already observations that support the idea that indeed there is brain activity, now it is whether that brain activity necessarily is the I-function, and whether whatever active part of the brain is capable of being limited or has ability to determine reality from a dream.

1), Hayley Birch, "Science of Sleepwalking", 11 May 2007.
2), Scientific America: By the Editors, "Why Do Some People Sleepwalk?", January 2008.
3) "Parsomnias: Managing bizarre sleep-related behavior disorders", Carlos H. Schenck, MD; Mark W. Mahowald, MD.Vol. 107, No. 3, March 2000, Postgraduate Medicine , 145-56.


Dr. A Page's picture

bedwetting sleepwalking

Through my years as an enuresis treatment specialist, I have found some interesting similarities to what you describe above, in patients that exhibit bed wetting problems. It was interesting reading about REM and non-REM sleep and the distinctions here.

Paul Grobstein's picture

Sleep walking and the I-function

If "75% of sleep walking episodes occur during non-REM sleep" and the EEG during REM sleep "is remarkably similar to when an individual is awake", doesn't that the EEG suggest that the I-function isn't active during many sleep walking episodes?

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