Out‐of‐body experience and autoscopy of neurological origin
Olaf Blanke, Théodor Landis, Laurent Spinelli, Margitta Seeck
Brain January 15, 2004 DOI: 10.1093/brain/awh040 via OpenAlex
Summary
AI-generated from the abstractOut-of-body experiences (OBE) and autoscopy (seeing one's body from outside) share common neurological mechanisms rooted in disrupted body perception. In six neurological patients, these experiences were linked to vestibular sensations (floating, flying, rotation), visual body-part illusions (shortening or moving limbs), and the sensation of seeing only part of one's body. Body position before the experience influenced both OBE and autoscopy. Brain damage or dysfunction localized to the temporo-parietal junction (TPJ) in five patients. The findings suggest OBE and autoscopy result from a failure to integrate proprioceptive, tactile, visual, and vestibular information about one's own body, combined with a vestibular dysfunction that disconnects personal space from extrapersonal space, caused by temporary TPJ dysfunction during impaired consciousness.
Study at a glance
| Characteristics | Case series Case report Peer reviewed |
|---|---|
| Sample size | 6 |
| Population | Neurological patients with out-of-body experiences or autoscopy |
| Keywords | Psychology Medicine Neuroscience |
| Citations | 746 |
| Key finding | Out-of-body experiences and autoscopy share common mechanisms involving disrupted integration of body perception and vestibular processing, linked to dysfunction in the temporo-parietal junction. |
Abstract
During an out-of-body experience (OBE), the experient seems to be awake and to see his body and the world from a location outside the physical body. A closely related experience is autoscopy (AS), which is characterized by the experience of seeing one's body in extrapersonal space. Yet, despite great public interest and many case studies, systematic neurological studies of OBE and AS are extremely rare and, to date, no testable neuroscientific theory exists. The present study describes phenomenological, neuropsychological and neuroimaging correlates of OBE and AS in six neurological patients. We provide neurological evidence that both experiences share important central mechanisms. We show that OBE and AS are frequently associated with pathological sensations of position, movement and perceived completeness of one's own body. These include vestibular sensations (such as floating, flying, elevation and rotation), visual body-part illusions (such as the illusory shortening, transformation or movement of an extremity) and the experience of seeing one's body only partially during an OBE or AS. We also find that the patient's body position prior to the experience influences OBE and AS. Finally, in five patients, brain damage or brain dysfunction is localized to the temporo-parietal junction (TPJ). These results suggest that the complex experiences of OBE and AS represent paroxysmal disorders of body perception and cognition (or body schema). The processes of body perception and cognition, and the unconscious creation of central representation(s) of one's own body based on proprioceptive, tactile, visual and vestibular information-as well as their integration with sensory information of extrapersonal space-is a prerequisite for rapid and effective action with our surroundings. Based on our findings, we speculate that ambiguous input from these different sensory systems is an important mechanism of OBE and AS, and thus the intriguing experience of seeing one's body in a position that does not coincide with its felt position. We suggest that OBE and AS are related to a failure to integrate proprioceptive, tactile and visual information with respect to one's own body (disintegration in personal space) and by a vestibular dysfunction leading to an additional disintegration between personal (vestibular) space and extrapersonal (visual) space. We argue that both disintegrations (personal; personal-extrapersonal) are necessary for the occurrence of OBE and AS, and that they are due to a paroxysmal cerebral dysfunction of the TPJ in a state of partially and briefly impaired consciousness.