In an ongoing series of blogs designed to slice through the credulous nonsense of new age mythology and antiquated religious concepts, I present here some of the surprisingly large number of papers dealing with what neuroscience has to say about so-called “out-of-body experience” (OBE). Along with heautoscopy (the hallucination of seeing one’s own body at a distance, which can occur with schizophrenia) and the strong feeling of a presence, OBEs comprise what is known as autoscopia.
I first started this series with a look at duality and why it is utter nonsense. Commenter leo1500 didn’t like my use of Phineas Gage as an example of brain damage refuting mind-brain dualism. Too bad. Phineas Gage is representative of thousands of people with frontal lobe damage induced permanent (it’s not as if temporary helps the dualist maintain the delusion…) personality change that have been studied.
Nor is this the only type of brain damage example I could have used. Hippocampal damage can permanently end a person’s ability to form new memories. Brain damage can also cause prosopagnosia, the inability to recognize faces. Such people do not have any vision problems at all – they are as able to navigate in a complex environment as anyone. How does dualism explain these observations? In short, it doesn’t. But the computational theory of mind does -the circutry involved in processing new memories and facial information is disrupted.
In the second set of blogs I tackled contra-causal free will and why it is pure illusion. The experimental study of volition has produced some truly surprising results. I just want to add one more tidbit before moving on, and that is I most certainly hope that contra-causal free will is an illusion.
Think about it – our ability to get along with others in society is dependent on our ability to read the intentions of others. If we truly had contra-causal free will, our actions would be random and unpredictable. Imagine even driving to work in the morning unable to predict what the others around you are going to do. It would be utter chaos, far worse than it already is!
Dualists like out-of-body experiences because they superficially support their view. But I’ve got a question for dualists: if the brain is just a transceiver for sensory information, how does a disembodied mind see without eyes? Fortunately, we have a very good idea how autoscopia really happens. As one journal article stated,
Although OBEs are superficially consistent with universal dualistic and supernatural intuitions about the nature of the soul and its relation to the body, recent research increasingly offers plausible alternative naturalistic explanations of the relevant phenomenology.
Electrostimulation of the vestibular motor cortex produces experiences identical to OBEs. Yet the subject’s consciousness hasn’t gone anywhere, since they are fully conscious on the operating table. Dualists completely ignore this evidence.
Direct stimulation of the brain is not the only source of autoscopy. OBEs often happen during a state of sleep known as sleep paralysis (SP). We all go through it on our way to REM sleep, and if one tries to move during SP he/she will find that they are unable to do so. We usually don’t notice because motion is the last thing we want when we are trying to get a good night’s rest.
When we envision ourselves in the world, we typically have a third-person view of ourselves, not a first-person view. This is critical to understanding autoscopia. The difference between our imagination and what we might perceive as our mind leaving our bodies is very similar to what happens in our illusion of volition. Brain regions producing our feeling of intent in imagining ourselves are missing with autoscopic experiences. It is this information which tells us that we are simply imagining ourselves from a third-person perspective that is missing that produces the free-floating illusion.
And this is what truly bothers me about people who believe (and here I use the word in the pejoritive) in things like OBEs: they accept people’s self-reported free-floating sensations at face value without any skepticism whatsoever. It’s credulous thinking at its worst when critical thinking is required, and it simply begs the question.
In a manner similar to the field of evo/devo, where mutated regulatory genes tell us far more about the gene than does the unmutated version, brain damage tells us a great deal about how individual regions of the brain function. While I find that brain injury is a tragedy for those who suffer them and to their families and friends, sufferers are of immense scientific value in understanding the mind. Autoscopic phenomena (of which OBEs are amongst), under-studied to be sure, are no exception.Autoscopy is a disruption of the sense of self via brain damage which can result in a variety of problems in the sense of embodiment and body ownership. There are several autoscopic phenomena that are currently recognized: autoscopic hallucination (damage to the occipito-parietal cortex), heautoscopy (damage to the left emporoparietal junction), out-of-body experience (damage to the right temporoparietal junction) and feeling-of-a-presence (damage to parieto-occipital cortex). But not all causes of autoscopy are due to traumatic brain injury, as they can result from diseases affecting the central nervous system (e.g., meningitis or encephatlitis).
Autoscopic hallucination is the experience of seeing a double of one’s elf without the experience of leaving one’s own body. OBEs are autoscopic hallucinations with the added sensation of disembodiment. Heautoscopy lies between these two. Sufferers see a double of themselves in extrapersonal space, but are unable to determine whether they are disembodied or not. Thus, we see that OBEs lie within a spectrum of what are known as autoscopic phenomena produced by (but not limited to) localized brain injury. Each of these phenomena display different patterns of associated hallucinations and deficits, but they are clearly related. The type of phenomenon displayed is strongly dependent on the strength and type of vestibular dysfunction (disruption of balance information provided by our inner ear) produced by the brain injury. Brain damage is not the only source of vestibular dysfunction, and all of us have experienced transient forms – rapid motion of the head producing vertigo is a transient form of vestibular dysfunction. I can think of a number of other causes, including transient ischemic attacks (essentially reversible strokes), migraine (which are also known to produce hallucinations involving ‘auras’) and (no surprise here) recovery from cardiac arrest.
Currently, autoscopic phenomena are being modeled as a multi-sensory disintegration in body and self processing. That is, there is a conflict between tactil (sense of touch), proprioceptive (sense of where our body is in space), kinesthetic (sense of motion) and visual information which produces errors in assessing what and where the self is. Additionally, OBEs are associated with conflicted vestibular and visual information.
I wonder if there is also an element of a disruption of being an active agent initiating thinking about the self. Whenever we think of ourselves in the environment, we typically take a third-person perspective. We know it is a third-person perspective because we have initiated imagining ourselves this way. But remove this knowledge and what you are left with is actually seeing yourself from outside your body with the rationalization that your self is in the extrapersonal space. This is similar to the need for knowledge of initiating an action to enable our sense of volition as a conscious agent. I have not seen this in the literature and it may be an interesting line of inquiry.
Thus, it is more than possible that OBEs are purely a product of the brain, just as the mind is. Anything affecting the temporoparietal junction can induce an OBE. There is in fact a portion of the population which is susceptible to changes in the metabolic rate in this region, which could indeed induce OBEs. Such people include those suffering from anxiety, depression or depersonalization and body dysmorphhic disorders. These conditions can increase the metabolism in this and other brain regions as measured by PET. Such metabolic disturbances can easily be a cause for OBEs. In addition, electrostimulation of the vestibular motor cortex produces experiences identical to OBEs. Yet the subject’s consciousness hasn’t gone anywhere, since they are fully conscious on the operating table. OBEs often happen during a state of sleep known as sleep paralysis (SP). We all go through it on our way to REM sleep, and if one tries to move during SP he/she will find that they are unable to do so. We usually don’t notice because motion is the last thing we want when we are trying to get a good night’s rest. Dualists completely ignore such evidence.
The face-value acceptance of OBEs as really being OBEs is credulous at best, particularly when good explanations for their occurance already exist and no evidence exists for OBEs actually being real. Indeed, we have model subjects for which we can study autoscopic phenomena directly. There is no need to invoke any spiritual nonsense in order to explain them. So why do people continue to buy nonsense books on OBEs and the like in the New Age section of bookstores? Because they want to believe it. I’ve got one thing to say to such people: grow up.
Blanke O and Mohr C. Out-of-body experience, heautoscopy, and autoscopic hallucination of neurological origin.
Implications for neurocognitive mechanisms of corporeal awareness and self consciousness. Brain Res Rev 50:184-99 (2005)
Cheyne JA, Girard TA. The body unbound: vestibular-motor hallucinations and out-of-body experiences. Cortex 45:201-15 (2009)
Lopez C, Halje P and Blanke O. Body ownership and embodiment: vestibular and multisensory mechanisms. Clin Neurophysiol 38:149-61 (2008)
Mohr C and Blanke O. The demystification of autoscopic phenomena: experimental propositions. Curr Psych Reports 7:189-95 (2005)
Solenski NJ. Transient ischemic attacks: Part I. Diagnosis and evaluation. Am Fam Physician 69:1665-74 (2004)
Szirmai A. Vestibular disorders in patients with migraine. Eur Arch Otorhinolaryngol 254 Suppl 1:S55-7 (1997)