Researchers may now have gained a better understanding of how the brain causes the disorienting, disruptive sensation of being outside of one’s body.
Most of the time, the mind and body operate seamlessly as a single entity. At times, however, a person may experience a disconcerting sense of “disassociation,” during which they feel as if they are somewhere outside of their body looking in.
According to Dr. Karl Deisseroth — who is a professor of bioengineering, psychiatry, and behavioral sciences at Stanford University in California — almost 3 out of 4 people who experience trauma report this phenomenon occurring either during or some time afterward.
Also, around 2–10% of the general population experience it at some point in their lives, he adds.
Recently, Dr. Deisseroth and colleagues conducted a study that allowed them to identify, for the first time, the brain mechanism that initiates disassociation.
They have now reported their findings in the journal Nature.
The feeling of disassociation begins with nerve cells in the brain’s posteromedial cortex firing synchronously at a specific rate.
Disassociation can be both troubling and disruptive, and it may become chronic. “In order to develop treatments, and to understand the biology, we needed to know more,” says Dr. Deisseroth.
Now, he adds, “This study has identified brain circuitry that plays a role in a well-defined subjective experience.”
“Beyond its potential medical implications, it gets at the question, ‘What is the self?’ That’s a big one in law and literature, and important even for our own introspections.”
The study also describes the molecular foundation underlying the mechanism that causes disassociation.
Dr. Deisseroth describes disassociation metaphorically “as the perception of being on the outside looking in at the cockpit of the plane that’s your body or mind — and what you’re seeing you just don’t consider to be yourself.”
Indeed, the study is, in part, based on observations of a person who described the experience as being “outside the pilot’s chair, looking at, but not controlling, the gauges.”
The study authors were working with this individual as part of the Stanford Comprehensive Epilepsy Program. He experienced disassociation during preseizure “auras,” which refers to the time period directly preceding seizures.
The researchers recorded electrical signals from the individual’s cerebral cortex in an attempt to identify the brain activity causing his seizures. They noticed a particular pattern of electrical activity that coincided with the aura. It was occurring in the posteromedial cortex.
The researchers observed a particular rhythm being generated by nerve signals firing synchronously. The signal pulsed at 3 Hertz (Hz), or three times per second.
They subsequently found that if they deliberately stimulated this area of the brain electrically, the individual experienced a disassociation aura but no subsequent seizure.
Previous research has suggested that mice experience disassociation as indicated by changes in their behavior.
For example, if a mouse located on an uncomfortably warm surface simply lifts its foot without licking it to soothe it — as would be expected — it is likely experiencing disassociation. Scientists can induce this state using the drug ketamine.
In the recent study, the researchers attempted to cause disassociation in mice by using light to optogenetically stimulate neurons in the rodent equivalent of the human posteromedial cortex.
When they applied stimulation at the same 3-Hz rate they saw in the human brain, they saw disassociative behavior without the presence of ketamine.
Additional research led to the discovery that a specific protein type called an ion channel is necessary for the generation of the 3-Hz pulse.
Recognizing the role of these proteins could lead to the development of new therapies that more effectively address disassociation and the conditions with which it is often associated, such as epilepsy, borderline personality disorder, and PTSD.