Alice in Wonderland Syndrome (AiWS), also known as Todd's syndrome or dysmetropsia, is a disorienting neuropsychological condition that affects perception. People may experience distortions in visual perception such as micropsia (objects appearing small), macropsia (objects appearing large), pelopsia (objects appearing to be closer than they are), or teleopsia (objects appearing to be further away than they are). Size distortion may occur in other sensory modalities as well.
AiWS is often associated with migraines, brain tumors, and psychoactive drug use. It can also be the initial symptom of the Epstein–Barr Virus.
AiWS can be caused by abnormal amounts of electrical activity resulting
in abnormal blood flow in the parts of the brain that process visual
perception and texture.
Anecdotal reports suggest that the symptoms are common in childhood, with many people growing out of it in their teen years. It appears that AiWS is also a common experience at sleep onset and has been known to commonly arise due to a lack of sleep.
Signs and symptoms
AiWS is often associated with migraines. AiWS affects the sense of vision, sensation, touch, and hearing, as well as one's own body image. Nausea, dizziness, and agitation are also commonly associated symptoms with Alice in Wonderland Syndrome.
Individuals with AiWS can experience hallucinations or illusions
of expansion, reduction or distortion of their own body image, such as microsomatognosia (feeling that their own body or body parts are shrinking), or macrosomatognosia (feeling that their body or body parts are growing taller or larger). These changes in perception are collectively known as metamorphosias, or Lilliputian hallucinations.
People with certain neurological diseases have experienced similar visual hallucinations. These hallucinations are called "Lilliputian", which means that objects appear either smaller or larger than reality.
Patients may experience either micropsia or macropsia. Micropsia
is an abnormal visual condition, usually occurring in the context of visual hallucination, in which the affected person sees objects as being smaller than they are in reality. Macropsia is a condition where the individual sees everything larger than it actually is.
One 17-year-old male described his odd symptoms by the following:
"Quite suddenly objects appear small and distant or large and close. I
feel as [if] I am getting shorter and smaller 'shrinking' and also the
size of persons are not longer than my index finger (a lilliputian
proportion). Sometimes I see the blind in the window or the television
getting up and down, or my leg or arm is swinging. I may hear the voices
of people quite loud and close or faint and far. Occasionally, I
experience attacks of migrainous headache associated with eye redness,
flashes of lights and a feeling of giddiness. I am always conscious to
the intangible changes in myself and my environment".
Although a person's eyes are normal, they will often 'see'
objects as the incorrect size, shape or perspective angle. Therefore,
people, cars, buildings, houses, animals, trees, environments, etc.,
look smaller or larger than they should be. Further, depth perception
can be altered whereby perceived distances are incorrect. For example, a
corridor may appear to be very long, or the ground may appear too
close.
Zoopsias is an additional hallucination that is sometimes
associated with Alice in Wonderland Syndrome. Zoopsias involves
hallucinations of either swarms of small animals (e.g. ants and mice
etc.), or isolated groups of larger animals (e.g. dogs and elephants
etc.). This experience of zoopsias is shared in a variety of conditions, such as delirium tremens.
The person affected by Alice in Wonderland syndrome may also lose a sense of time, a problem similar to the lack of spatial perspective. Time seems to pass very slowly, akin to an LSD
experience. The lack of time and space perspective also leads to a
distorted sense of velocity. For example, one could be inching along
ever so slowly in reality, yet it would seem as if one were sprinting
uncontrollably along a moving walkway, leading to severe, overwhelming
disorientation.
Sufferers of Alice in Wonderland Syndrome can often experience
paranoia as a result of disturbances in sound perception. This can
include amplification of soft sounds or misinterpretation of common
sounds.
In addition, some people may, in conjunction with a high fever,
experience more intense and overt hallucinations, seeing things that are
not there and misinterpreting events and situations.
Less frequent symptoms sometimes described in Alice in Wonderland
Syndrome patients include loss of limb control and dis-coordination,
memory loss, lingering touch and sound sensations, and emotional
instability.
It has been noted that patients are often reluctant to describe
their symptoms due to fear of being labeled with a psychiatric disorder.
It is usually easy to rule out psychosis as those with Alice in
Wonderland Syndrome are typically aware that their hallucinations and
distorted perceptions are not 'real', and they have not lost touch with
reality.
Furthermore, younger patients who frequently experience Alice in
Wonderland syndrome may struggle to describe their unusual symptoms, and
thus, it is recommended to encourage children to draw their visual
illusions during episodes.
It appears that the symptoms of AiWS do not change in severity over the
course of the syndrome, and though the symptoms may acutely impact the
patient's life, Alice in Wonderland syndrome typically resolves itself
within weeks or months.
Furthermore, AiWS symptoms occur transiently during the day for short
periods of time, with most patients describing their symptoms as lasting
anywhere between 10 seconds to 10 minutes. This, combined with the
typically short duration of the syndrome, suggests that Alice in
Wonderland Syndrome typically causes a relatively short-term disruption
of normal functioning. However, symptoms can be debilitating when
experienced, and the individual should exercise caution, for example
when driving, as the symptoms can appear rapidly. Symptom severity
influences whether or not the individual will be able to hold a job
during these periods of misperception.
Genetic and environmental influences
While
there currently is no identified genetic locus/loci associated with
Alice in Wonderland Syndrome, observations suggest that a genetic
component does exist. AiWS does appear to be passed on from parent to
child, with one case study showcasing a grandmother, mother, son, and
daughter all with Alice in Wonderland Syndrome. In addition, there is an
established hereditary trait of migraines. Examples of environmental
influences on the incidence of AiWS include the use of the drug
topiramate and potentially the dietary intake of tyramine. Further
research is required to establish the genetic and environmental
influences on Alice in Wonderland Syndrome.
Alice in Wonderland
Alice in Wonderland Syndrome was named after Lewis Carroll's famous 19th-century novel Alice's Adventures in Wonderland. In the story, Alice, the title character, experiences numerous situations similar to those of micropsia and macropsia.
The thorough descriptions of metamorphosis clearly described in the
novel were the first of their kind to depict the bodily distortions
associated with the condition. Speculation has arisen that Carroll may
have written the story using his own direct experience with episodes of
micropsia resulting from the numerous migraines he was known to suffer
from. It has also been suggested that Carroll may have suffered from temporal lobe epilepsy.
Gulliver's Travels
Alice in Wonderland Syndrome's symptom of micropsia has also been related to Jonathan Swift's novel Gulliver's Travels.
It has been referred to as "Lilliput sight" and "Lilliputian
hallucination", a term coined by British physician Raoul Leroy in 1909, based on the small people that inhabited the island of Lilliput in the novel.
Etiology
Complete
and partial forms of the Alice in Wonderland syndrome exist in a range
of disorders, including epilepsy, intoxicants, infectious states,
fevers, and brain lesions. Furthermore, the syndrome is commonly associated with migraines, as well as the use of psychoactive drugs. It can also be the initial symptom of the Epstein–Barr virus (see mononucleosis), and a relationship between the syndrome and mononucleosis has been suggested.
Epstein-Barr Virus appears to be the most common cause in children,
while for adults it is more commonly associated with migraines.
Cerebral hypotheses
AiWS
can be caused by abnormal amounts of electrical activity causing
abnormal blood flow in the parts of the brain that process visual
perception and texture. Nuclear medical techniques using technetium,
performed on patients during episodes of Alice in Wonderland syndrome,
have demonstrated that AiWS is associated with reduced cerebral
perfusion in various cortical regions (frontal, parietal, temporal and
occipital), both in combination and in isolation. It has been
hypothesized that any condition resulting in a decrease in perfusion of
the visual pathways or visual control centers of the brain may be responsible for the syndrome. For example, one study used single photon emission computed tomography to demonstrate reduced cerebral perfusion in the temporal lobe in patients with AiWS. Other theories exist that suggest the syndrome is a result of unspecific cortical dysfunction (e.g. from encephalitis, epilepsy, decreased cerebral perfusion), or reduced blood flow to other areas of the brain.
Other theories suggest that disordered body image perceptions stem from
within the parietal lobe. This has been demonstrated by the production
of disturbances of body image through electrical stimulation of the posterior parietal cortex.
Other researchers suggest that metamorphopsias may be a result of
reduced perfusion of the non-dominant posterior parietal lobe during
migraine episodes.
Throughout all the neuroimaging studies, several cortical regions (including the temporoparietal junction
within the parietal lobe, and the visual pathway, specifically the
occipital lobe) are associated with the development of Alice in
Wonderland syndrome symptoms.
Migraines
The
role of migraines in Alice in Wonderland syndrome is still not
understood, but both vascular and electrical theories have been
suggested. For example, visual distortions may be a result of transient,
localized ischaemia
(an inadequate blood supply to an organ or part of the body) in areas
of the visual pathway during migraine attacks. In addition, a spreading
wave of depolarization of cells (particularly glial cells) in the cerebral cortex during migraine attacks can eventually activate the trigeminal nerve's
regulation of the vascular system. The intense cranial pain during
migraines is due to the connection of the trigeminal nerve with the thalamus
and thalamic projections onto the sensory cortex. Alice in Wonderland
syndrome symptoms can precede, accompany, or replace the typical
migraine symptoms.
Diagnosis
Alice
in Wonderland syndrome is a disturbance of perception rather than a
specific physiological change to the body's systems. The diagnosis can
be presumed when other causes have been ruled out and if the patient
presents symptoms along with migraines and complains of onset during the
day (although it can also occur at night). As there are no established
diagnostic criteria for Alice in Wonderland syndrome, there is likely to
be a large degree of variability in the diagnostic process and thus it
is likely to be poorly diagnosed.
Prognosis
Whatever
the cause, the bodily related distortions can recur several times a day
and may take some time to abate. Understandably, the person can become
alarmed, frightened, and panic-stricken throughout the course of the
hallucinations—maybe even hurt themselves or others around them. The
symptoms of the syndrome themselves are not harmful and are likely to
disappear with time. The outcome is typically not harmful, especially in
children, and most patients outgrow these episodes. The long-term
prognosis typically depends on the root cause of the syndrome, and it is
the underlying condition which must be evaluated and treated. Often,
the difficulty lies within the patient's reluctance to describe their
symptoms out of fear of being labeled with a psychiatric disorder.
Treatment
At
present, Alice in Wonderland syndrome has no standardized treatment
plan. Often, treatment methods revolve around migraine prophylaxis, as
well as the promotion of a low tyramine diet. Drugs that may be used to prevent migraines include: anticonvulsants, antidepressants, calcium channel blockers, and beta blockers. Other treatments that have been explored include repetitive transcranial magnetic stimulation (rTMS). Further research is required to establish an effective treatment regime.
Epidemiology
The
lack of established diagnostic criteria or large-scale epidemiological
studies on Alice in Wonderland syndrome means that the exact prevalence
of the syndrome is currently unknown. One study on 3,224 adolescents in
Japan demonstrated the occurrence of macropsia and micropsia to be 6.5%
in boys and 7.3% in girls, suggesting that the symptoms of AiWS may not
be so rare.
It appears that the male/female ratio is dependent on the age
range being observed. Studies showed that younger males (age range of 5
to 14 years) were 2.69 times more likely to experience AiWS than girls
of the same age, while there were no significant differences between
students of 13 to 15 years of age. Conversely, female students (16- to
18-year-olds) showed a significantly greater prevalence.
The average age of the start of Alice in Wonderland syndrome is
six but it is very normal for some to experience the syndrome from
childhood to their late 20's. It is also thought that this syndrome is hereditary because many parents who have AiWS report their children having it as well.
History
The
syndrome is sometimes called Todd's syndrome, in reference to an
influential description of the condition in 1955 by Dr. John Todd
(1914-1987), a British Consultant Psychiatrist at High Royds Hospital at Menston in West Yorkshire.
Todd discovered that several of his patients experienced severe
headaches causing them to see and perceive objects as greatly out of
proportion. They have altered sense of time and touch, as well as distorted perceptions
of their own body. Although having migraine headaches, none of these
patients had brain tumors, damaged eyesight, or mental illness that
could have caused similar symptoms. They were also all able to think
lucidly and could distinguish hallucinations from reality, however,
their perceptions were skewed.
Since Lewis Carroll had been a well-known migraine sufferer with
similar symptoms, Todd speculated that Carroll had used his own migraine
experiences as a source of inspiration for his famous 1865 novel Alice’s Adventures in Wonderland. Carroll's diary reveals that in 1856 he consulted William Bowman, an eminent ophthalmologist, about the visual manifestations of the migraines he regularly experienced. Since Carroll had these migraine symptoms for years before writing Alice’s Adventures, it seemed reasonable that Carroll had used his experiences as inspiration.
Artist's depiction of the separation stage of an out-of-body experience, which often precedes free movement
An out-of-body experience (OBE or sometimes OOBE)
is an experience in which a person seems to perceive the world from a
location outside their physical body. An OBE is a form of autoscopy (literally "seeing self"), although the term autoscopy more commonly refers to the pathological condition of seeing a second self, or doppelgänger.
Those experiencing OBEs sometimes report (among other types of immediate and spontaneous experience) a preceding and initiating lucid-dream
state. In many cases, people who claim to have had an OBE report being
on the verge of sleep, or being already asleep shortly before the
experience. A large percentage of these cases refer to situations where
the sleep was not particularly deep (due to illness, noises in other
rooms, emotional stress, exhaustion from overworking, frequent
re-awakening, etc.). In most of these cases subjects perceive themselves
as being awake; about half of them note a feeling of sleep paralysis.
Near-death experiences
Another form of spontaneous OBE is the near-death experience (NDE).
Some subjects report having had an OBE at times of severe physical
trauma such as near-drownings or major surgery. Near-death experiences
may include subjective impressions of being outside the physical body,
sometimes visions of deceased relatives and religious figures, and
transcendence of ego and spatiotemporal boundaries.
Typically the experience includes such factors as: a sense of being
dead; a feeling of peace and painlessness; hearing of various
non-physical sounds, an out-of-body experience; a tunnel experience (the
sense of moving up or through a narrow passageway); encountering
"beings of light" and a God-like figure or similar entities; being given
a "life review", and a reluctance to return to life.
Resulting from extreme physical effort
Along
the same lines as an NDE, extreme physical effort during activities
such as high-altitude climbing and marathon running can induce OBEs. A
sense of bilocation may be experienced, with both ground and air-based perspectives being experienced simultaneously.
Falling
asleep physically without losing awareness. The "Mind Awake, Body
Asleep" state is widely suggested as a cause of OBEs, voluntary and
otherwise. Thomas Edison
used this state to tackle problems while working on his inventions. He
would rest a silver dollar on his head while sitting with a metal bucket
in a chair. As he drifted off, the coin would noisily fall into the
bucket, restoring some of his alertness. OBE pioneer Sylvan Muldoon more simply used a forearm held perpendicular in bed as the falling object. Salvador Dalí was said to use a similar "paranoiac-critical"
method to gain odd visions which inspired his paintings. Deliberately
teetering between awake and asleep states is known to cause spontaneous
trance episodes at the onset of sleep which are ultimately helpful when
attempting to induce an OBE.
By moving deeper and deeper into relaxation, one eventually encounters a
"slipping" feeling if the mind is still alert. This slipping is
reported to feel like leaving the physical body. Some consider
progressive relaxation a passive form of sensory deprivation;
Deep trance, meditation and visualization.
The types of visualizations vary; some common analogies include
climbing a rope to "pull out" of one's body, floating out of one's body,
getting shot out of a cannon, and other similar approaches. This
technique is considered hard to use for people who cannot properly
relax. One example of such a technique is the popular Golden Dawn "Body of Light" Technique.
Mechanical induction
Brainwave synchronization via audio/visual stimulation. Binaural beats can be used to induce specific brainwave frequencies,
notably those predominant in various mind awake/body asleep states.
Binaural induction of a "body asleep" 4 Hertz brainwave frequency was
observed as effective by the Monroe Institute,
and some authors consider binaural beats to be significantly supportive
of OBE initiation when used in conjunction with other techniques. Simultaneous introduction of "mind awake" beta frequencies (detectable
in the brains of normal, relaxed awakened individuals) was also observed
as constructive. Another popular technology uses sinusoidal wave pulses
to achieve similar results, and the drumming accompanying Native
American religious ceremonies is also believed to have heightened
receptivity to "other worlds" through brainwave entrainment mechanisms;
Magnetic stimulation of the brain, as with the God helmet developed by Michael Persinger;
Sensory deprivation. This approach aims to induce intense disorientation by removal of space and time references. Flotation tanks or pink noise played through headphones are often employed for this purpose;
Sensory overload, the opposite of sensory deprivation. The subject can for instance be rocked for a long time in a specially designed cradle, or submitted to light forms of torture,
to cause the brain to shut itself off from all sensory input. Both
conditions tend to cause confusion and this disorientation often permits
the subject to experience vivid, ethereal out-of-body experiences;
Strong g-forces that causes blood to drain from parts of the brain, as experienced for example in high-performance aircraft or high-G training for pilots and astronauts;
An apparatus that uses a head-mounted display and a touch that confuses the sense of proprioception (and which can also create the sensation of additional limbs).
Charles Richet (1887) held that OBEs are created by the subject's memory and imagination processes and are no different from dreams. James H. Hyslop (1912) wrote that OBEs occur when the activity of the subconscious mind dramatizes certain images to give the impression the subject is in a different physical location.
Eugéne Osty (1930) considered OBEs to be nothing more than the product of imagination. Other early researchers (such as Schmeing, 1938) supported psychophysiological theories. G. N. M. Tyrrell interpreted OBEs as hallucinatory constructs relating to subconscious levels of personality.
Donovan Rawcliffe (1959) connected the OBE experience with psychosis and hysteria. Other researchers have discussed the phenomena of the OBE in terms of a distortion of the body image (Horowitz, 1970) and depersonalization (Whitlock, 1978).[49][50] The psychologists Nandor Fodor (1959) and Jan Ehrenwald (1974) proposed that an OBE is a defense mechanism designed to deal with the threat of death.
According to (Irin and Watt, 2007) Jan Ehrenwald had described the
out-of-body experience (OBE) "as an imaginal confirmation of the
question for immortality, a delusory attempt to assure ourselves that we
possess a soul that exists independently of the physical body. The psychologists Donald Hebb (1960) and Cyril Burt (1968) wrote on the psychological interpretation of the OBE involving body image and visual imagery. Graham Reed (1974) suggested that the OBE is a stress reaction to a painful situation, such as the loss of love. John Palmer (1978) wrote that the OBE is a response to a body image change causing a threat to personal identity.
Carl Sagan
(1977) and Barbara Honegger (1983) wrote that the OBE experience may be
based on a rebirth fantasy or reliving of the birth process based on
reports of tunnel-like passageways and a cord-like connection by some OBErs which they compared to an umbilical cord. Susan Blackmore
(1978) came to the conclusion that the OBE is a hallucinatory fantasy
as it has the characteristics of imaginary perceptions, perceptual
distortions and fantasy-like perceptions of the self (such as having no
body). Ronald Siegel (1980) also wrote that OBEs are hallucinatory fantasies.
Harvey Irwin (1985) presented a theory of the OBE involving attentional cognitive processes and somatic sensory activity. His theory involved a cognitive personality construct known as psychological absorption and gave instances of the classification of an OBE as examples of autoscopy, depersonalization and mental dissociation. The psychophysiologist Stephen Laberge (1985) has written that the explanation for OBEs can be found in lucid dreaming. David Hufford (1989) linked the OBE experience with a phenomenon he described as a nightmare waking experience, a type of sleep paralysis. Other scientists have also linked OBEs to cases of hypnagogia and sleep paralysis (cataplexy).
In case studies fantasy proneness has been shown to be higher among OBErs than those who have not had an OBE. The data has shown a link between the OBE experience in some cases to fantasy prone personality (FPP).
In a case study involving 167 participants the findings revealed that
those who claimed to have experienced the OBE were "more fantasy prone,
higher in their belief in the paranormal and displayed greater
somatoform dissociation." Research from studies has also suggested that OBEs are related to cognitive-perceptual schizotypy.
Terence Hines
(2003) has written that spontaneous out-of-body experiences can be
generated by artificial stimulation of the brain and this strongly
suggests that the OBE experience is caused from "temporary, minor brain
malfunctions, not by the person's spirit (or whatever) actually leaving
the body." In a study review of neurological and neurocognitive data (Bünning and Blanke, 2005) wrote that OBEs are due to "functional disintegration of lower-level multisensory processing and abnormal higher-level self-processing at the temporoparietal junction." Some scientists suspect that OBEs are the result of a mismatch between visual and tactile signals.
Richard Wiseman
(2011) has noted that OBE research has focused on finding a
psychological explanation and "out-of-body experiences are not
paranormal and do not provide evidence for the soul. Instead, they
reveal something far more remarkable about the everyday workings of your
brain and body."
A study conducted by Jason Braithwaite and colleagues (2011) linked the
OBE to "neural instabilities in the brain's temporal lobes and to
errors in the body's sense of itself". Braithwaite et al.
(2013) reported that the "current and dominant view is that the OBE
occurs due to a temporary disruption in multi-sensory integration
processes."
Paranormal
Writers within the fields of parapsychology and occultism have written that OBEs are not psychological and that a soul, spirit or subtle body
can detach itself out of the body and visit distant locations.
Out-of-the-body experiences were known during the Victorian period in spiritualist literature as "travelling clairvoyance". The psychical researcher Frederic Myers referred to the OBE as a "psychical excursion". An early study which described alleged cases of OBEs was the two volume Phantasms of the Living, published in 1886 by the psychical researchers Edmund Gurney, Myers and Frank Podmore.
The book was largely criticized by the scientific community as the
anecdotal reports lacked evidential substantiation in nearly every case.
A 19th-century illustration of Robert Blair's poem The Grave, depicting the soul leaving the body
The TheosophistArthur Powell (1927) was an early author to advocate the subtle body theory of OBEs. Sylvan Muldoon (1936) embraced the concept of an etheric body to explain the OBE experience. The psychical researcher Ernesto Bozzano (1938) had also supported a similar view describing the phenomena of the OBE experience in terms of bilocation in which an "etheric body" can release itself from the physical body in rare circumstances. The subtle body theory was also supported by occult writers such as Ralph Shirley (1938), Benjamin Walker (1977) and Douglas Baker (1979). James Baker (1954) wrote that a mental body enters an "intercosmic region" during the OBE. Marilynn Hughes
states that the experiences are the projection of the spiritual body
from the physical for the purpose of the soul's purification. Robert Crookall in many publications supported the subtle body theory of OBEs.
The paranormal interpretation of OBEs has not been supported by all researchers within the study of parapsychology. Gardner Murphy
(1961) wrote that OBEs are "not very far from the known terrain of
general psychology, which we are beginning to understand more and more
without recourse to the paranormal".
In the 1970s, Karlis Osis
conducted many OBE experiments with the psychic Alex Tanous. For a
series of these experiments he was asked whilst in an OBE state to try
to identify coloured targets that were placed in remote locations. Osis
reported that in 197 trials there were 114 hits. However, the controls
to the experiments have been criticized and according to Susan Blackmore,
the final result was not particularly significant as 108 hits would be
expected by chance. Blackmore noted that the results provide "no
evidence for accurate perception in the OBE".
In April 1977, a patient from Harborview Medical Center
known as Maria claimed to have experienced an out-of-body experience.
During her OBE she claimed to have floated outside her body and outside
of the hospital. Maria would later tell her social worker Kimberly Clark
that during the OBE she had observed a tennis shoe
on the third floor window ledge to the north side of the building.
Clark would go to the north wing of the building and by looking out of
the window could see a tennis shoe on one of the ledges. Clark published
the account in 1985. The story has since been used in many paranormal
books as evidence a spirit can leave the body.
In 1996, Hayden Ebbern, Sean Mulligan and Barry Beyerstein
visited the Medical Center to investigate the story. They placed a
tennis shoe on the same ledge and discovered that the shoe was visible
from within the building and could have easily been observed by a
patient lying in bed. They also discovered the shoe was easily
observable from outside the building and suggested that Maria may have
overheard a comment about it during her three days in the hospital and
incorporated it into her OBE. They concluded "Maria's story merely
reveals the naiveté and the power of wishful thinking" from OBE
researchers seeking a paranormal explanation. Clark did not publish the description of the case until seven years after it happened, casting doubt on the story. Richard Wiseman
has said that although the story is not evidence for anything
paranormal it has been "endlessly repeated by writers who either
couldn't be bothered to check the facts, or were unwilling to present
their readers with the more skeptical side of the story."
Studies of OBEs
Early collections of OBE cases had been made by Ernesto Bozzano
(Italy) and Robert Crookall (UK). Crookall approached the subject from a
spiritualistic position, and collected his cases predominantly from
spiritualist newspapers such as the Psychic News, which appears to have biased his results in various ways. For example, the majority of his subjects reported seeing a cord
connecting the physical body and its observing counterpart; whereas
Green found that less than 4% of her subjects noticed anything of this
sort, and some 80% reported feeling they were a "disembodied
consciousness", with no external body at all.
The first extensive scientific study of OBEs was made by Celia Green (1968).
She collected written, first-hand accounts from a total of 400
subjects, recruited by means of appeals in the mainstream media, and
followed up by questionnaires. Her purpose was to provide a taxonomy of the different types of OBE, viewed simply as an anomalous perceptual experience or hallucination, while leaving open the question of whether some of the cases might incorporate information derived by extrasensory perception.
In 1999, at the 1st International Forum of Consciousness Research
in Barcelona, International Academy of Consciousness
research-practitioners Wagner Alegretti and Nanci Trivellato presented
preliminary findings of an online survey on the out-of-body experience
answered by internet users interested in the subject; therefore, not a
sample representative of the general population.
1,007 (85%) of the first 1,185 respondents reported having had an
OBE. 37% claimed to have had between two and ten OBEs. 5.5% claimed
more than 100 such experiences. 45% of those who reported an OBE said
they successfully induced at least one OBE by using a specific
technique. 62% of participants claiming to have had an OBE also reported
having enjoyed nonphysical flight; 40% reported experiencing the
phenomenon of self-bilocation (i.e. seeing one's own physical body
whilst outside the body); and 38% claimed having experienced
self-permeability (passing through physical objects such as walls). The
most commonly reported sensations experienced in connection with the OBE
were falling, floating, repercussions e.g. myoclonia (the jerking of
limbs, jerking awake), sinking, torpidity (numbness), intracranial
sounds, tingling, clairvoyance, oscillation and serenity.
Another reported common sensation related to OBE was temporary or projective catalepsy,
a more common feature of sleep paralysis. The sleep paralysis and OBE
correlation was later corroborated by the Out-of-Body Experience and
Arousal study published in Neurology by Kevin Nelson and his colleagues from the University of Kentucky in 2007. The study discovered that people who have out-of-body experiences are more likely to suffer from sleep paralysis.
Also noteworthy, is the Waterloo Unusual Sleep Experiences Questionnaire
that further illustrates the correlation. William Buhlman, an author on
the subject, has conducted an informal but informative online survey.
In surveys, as many as 85% of respondents tell of hearing loud noises, known as "exploding head syndrome" (EHS), during the onset of OBEs.
Miss Z study
In 1968, Charles Tart
conducted an OBE experiment with a subject known as Miss Z for four
nights in his sleep laboratory. The subject was attached to an EEG machine
and a five-digit code was placed on a shelf above her bed. She did not
claim to see the number on the first three nights but on fourth gave the
number correctly. The psychologist James Alcock criticized the experiment for inadequate controls and questioned why the subject was not visually monitored by a video camera. Martin Gardner
has written the experiment was not evidence for an OBE and suggested
that whilst Tart was "snoring behind the window, Miss Z simply stood up
in bed, without detaching the electrodes, and peeked." Susan Blackmore
wrote "If Miss Z had tried to climb up, the brain-wave record would
have showed a pattern of interference. And that was exactly what it did
show."
Neurology and OBE-like experiences
There
are several possible physiological explanations for parts of the OBE.
OBE-like experiences have been induced by stimulation of the brain.
OBE-like experience has also been induced through stimulation of the
posterior part of the right superior temporal gyrus in a patient. Positron-emission tomography was also used in this study to identify brain regions affected by this stimulation. The term OBE-like
is used above because the experiences described in these experiments
either lacked some of the clarity or details of normal OBEs, or were
described by subjects who had never experienced an OBE before. Such
subjects were therefore not qualified to make claims about the
authenticity of the experimentally-induced OBE.
British psychologist Susan Blackmore and others suggest that an OBE begins when a person loses contact with sensory input from the body while remaining conscious.
The person retains the illusion of having a body, but that perception
is no longer derived from the senses. The perceived world may resemble
the world he or she generally inhabits while awake, but this perception
does not come from the senses either. The vivid body and world is made
by our brain's ability to create fully convincing realms, even in the
absence of sensory information. This process is witnessed by each of us
every night in our dreams, though OBEs are claimed to be far more vivid
than even a lucid dream.
Irwin pointed out that OBEs appear to occur under conditions of either very high or very low arousal. For example, Green
found that three quarters of a group of 176 subjects reporting a single
OBE were lying down at the time of the experience, and of these 12%
considered they had been asleep when it started. By contrast, a
substantial minority of her cases occurred under conditions of maximum
arousal, such as a rock-climbing fall, a traffic accident, or
childbirth. McCreery
has suggested that this paradox may be explained by reference to the
fact that sleep can supervene as a reaction to extreme stress or
hyper-arousal.
He proposes that OBEs under both conditions, relaxation and
hyper-arousal, represent a form of "waking dream", or the intrusion of
Stage 1 sleep processes into waking consciousness.
Olaf Blanke studies
Research
by Olaf Blanke in Switzerland found that it is possible to reliably
elicit experiences somewhat similar to the OBE by stimulating regions of
the brain called the right temporal-parietal junction (TPJ; a region
where the temporal lobe and parietal lobe
of the brain come together). Blanke and his collaborators in
Switzerland have explored the neural basis of OBEs by showing that they
are reliably associated with lesions in the right TPJ region and that they can be reliably elicited with electrical stimulation of this region in a patient with epilepsy.
These elicited experiences may include perceptions of transformations
of the patient's arms and legs (complex somatosensory responses) and
whole-body displacements (vestibular responses).
In neurologically normal subjects, Blanke and colleagues then
showed that the conscious experience of the self and body being in the
same location depends on multisensory integration in the TPJ. Using event-related potentials,
Blanke and colleagues showed the selective activation of the TPJ
330–400 ms after stimulus onset when healthy volunteers imagined
themselves in the position and visual perspective that generally are
reported by people experiencing spontaneous OBEs. Transcranial magnetic stimulation
in the same subjects impaired mental transformation of the
participant's own body. No such effects were found with stimulation of
another site or for imagined spatial transformations of external
objects, suggesting the selective implication of the TPJ in mental
imagery of one's own body.
In a follow up study, Arzy et al. showed that the location and
timing of brain activation depended on whether mental imagery is
performed with mentally embodied or disembodied self location. When
subjects performed mental imagery with an embodied location, there was
increased activation of a region called the "extrastriate body area"
(EBA), but when subjects performed mental imagery with a disembodied
location, as reported in OBEs, there was increased activation in the
region of the TPJ. This leads Arzy et al. to argue that "these data show
that distributed brain activity at the EBA and TPJ as well as their
timing are crucial for the coding of the self as embodied and as
spatially situated within the human body."
Blanke and colleagues thus propose that the right
temporal-parietal junction is important for the sense of spatial
location of the self, and that when these normal processes go awry, an
OBE arises.
In August 2007 Blanke's lab published research in Science demonstrating that conflicting visual-somatosensory input in virtual reality
could disrupt the spatial unity between the self and the body. During
multisensory conflict, participants felt as if a virtual body seen in
front of them was their own body and mislocalized themselves toward the
virtual body, to a position outside their bodily borders. This indicates
that spatial unity and bodily self-consciousness can be studied
experimentally and is based on multisensory and cognitive processing of
bodily information.
Ehrsson study
In August 2007, Henrik Ehrsson, then at the Institute of Neurology at University College of London (now at the Karolinska Institute in Sweden), published research in Science demonstrating the first experimental method that, according to the scientist's claims in the publication, induced an out-of-body experience in healthy participants. The experiment was conducted in the following way:
The study participant sits in a
chair wearing a pair of head-mounted video displays. These have two
small screens over each eye, which show a live film recorded by two
video cameras placed beside each other two metres behind the
participant's head. The image from the left video camera is presented on
the left-eye display and the image from the right camera on the
right-eye display. The participant sees these as one "stereoscopic" (3D) image, so they see their own back displayed from the perspective of someone sitting behind them.
The researcher then stands just beside the participant (in their
view) and uses two plastic rods to simultaneously touch the
participant's actual chest out-of-view and the chest of the illusory
body, moving this second rod towards where the illusory chest would be
located, just below the camera's view.
The participants confirmed that they had experienced sitting behind their physical body and looking at it from that location.
Both critics and the experimenter himself note that the study fell
short of replicating "full-blown" OBEs. As with previous experiments
which induced sensations of floating outside of the body, Ehrsson's work
does not explain how a brain malfunction might cause an OBE.
Essentially, Ehrsson created an illusion that fits a definition of an
OBE in which "a person who is awake sees his or her body from a location
outside the physical body."
Awareness during Resuscitation Study
In 2001, Sam Parnia
and colleagues investigated out of body claims by placing figures on
suspended boards facing the ceiling, not visible from the floor. Parnia
wrote "anybody who claimed to have left their body and be near the
ceiling during resuscitation attempts would be expected to identify
those targets. If, however, such perceptions are psychological, then one
would obviously not expect the targets to be identified."
The philosopher Keith Augustine, who examined Parnia's study, has
written that all target identification experiments have produced
negative results. Psychologist Chris French wrote regarding the study "unfortunately, and somewhat atypically, none of the survivors in this sample experienced an OBE."
In the autumn of 2008, 25 UK and US hospitals began participation in a study, coordinated by Sam Parnia and Southampton University known as the AWARE study (AWAreness during REsuscitation). Following on from the work of Pim van Lommel in the Netherlands, the study aims to examine near-death experiences in 1,500 cardiac arrest survivors and so determine whether people without a heartbeat or brain activity can have documentable out-of-body experiences.
As part of the study Parnia and colleagues have investigated out of
body claims by using hidden targets placed on shelves that could only be
seen from above. Parnia has written "if no one sees the pictures, it shows these experiences are illusions or false memories".
In 2014 Parnia issued a statement indicating that the first phase
of the project has been completed and the results are undergoing peer
review for publication in a medical journal. No subjects saw the images mounted out of sight according to Parnia's early report of the results of the study at an American Heart Association
meeting in November 2013. Only two out of the 152 patients reported any
visual experiences, and one of them described events that could be
verified. The two NDEs occurred in an area were "no visual targets had been placed".
On October 6, 2014, the results of the study were published in the journal Resuscitation.
Among those who reported a perception of awareness and completed
further interviews, 46 per cent experienced a broad range of mental
recollections in relation to death that were not compatible with the
commonly used term of NDEs. These included fearful and persecutory
experiences. Only 9 per cent had experiences compatible with NDEs and 2
per cent exhibited full awareness compatible with OBEs with explicit
recall of 'seeing' and 'hearing' events. One case was validated and
timed using auditory stimuli during cardiac arrest. According to Caroline Watt
"The one 'verifiable period of conscious awareness' that Parnia was
able to report did not relate to this objective test. Rather, it was a
patient giving a supposedly accurate report of events during his
resuscitation. He didn't identify the pictures, he described the
defibrillator machine noise. But that's not very impressive since many
people know what goes on in an emergency room setting from seeing
recreations on television."
AWARE Study II
As
of May 2016, a posting at the UK Clinical Trials Gateway website
describes plans for AWARE II, a two-year multicenter observational study
of 900-1500 patients experiencing cardiac arrest, with subjects being
recruited as August 1, 2014 and a trial end date of May 31, 2017.
Smith & Messier
A
recent functional imaging study reported the case of a woman who could
experience out of body experience at will. She reported developing the
ability as a child and associated it with difficulties in falling sleep.
Her OBEs continued into adulthood but became less frequent. She was
able to see herself rotating in the air above her body, lying flat, and
rolling in the horizontal plane. She reported sometimes watching herself
move from above but remained aware of her unmoving "real" body. The
participant reported no particular emotions linked to the experience.
"[T]he brain functional changes associated with the reported
extra-corporeal experience (ECE) were different than those observed in
motor imagery. Activations were mainly left-sided and involved the left
supplementary motor area and supramarginal and posterior superior
temporal gyri, the last two overlapping with the temporal parietal
junction that has been associated with out-of-body experiences. The
cerebellum also showed activation that is consistent with the
participant's report of the impression of movement during the ECE. There
was also left middle and superior orbital frontal gyri activity,
regions often associated with action monitoring."
OBE training and research facilities
The Monroe Institute's
Nancy Penn Center is a facility specializing in or out-of-body
experience induction. The Center for Higher Studies of the Consciousness
in Brazil is another large OBE training facility. The International
Academy of Consciousness in southern Portugal features the Projectarium,
a spherical structure dedicated exclusively for practice and research
on out-of-body experience. Olaf Blanke's Laboratory of Cognitive Neuroscience has become a well-known laboratory for OBE research.
Astral projection
Astral projection is a paranormal
interpretation of out-of-body experiences that assumes the existence of
one or more non-physical planes of existence and an associated body
beyond the physical. Commonly such planes are called astral, etheric, or spiritual. Astral projection is often experienced as the spirit or astral body leaving the physical body to travel in the spirit world or astral plane.
The somatosensory system is a part of the sensory nervous system. The somatosensory system is a complex system of sensory neurons and pathways that responds to changes at the surface or inside the body. The axons (as afferent nerve fibers),
of sensory neurons connect with, or respond to, various receptor
cells. These sensory receptor cells are activated by different stimuli
such as heat and nociception, giving a functional name to the responding sensory neuron, such as a thermoreceptor which carries information about temperature changes. Other types include mechanoreceptors, chemoreceptors, and nociceptors and they send signals along a sensory nerve to the spinal cord where they may be processed by other sensory neurons and then relayed to the brain for further processing. Sensory receptors are found all over the body including the skin, epithelial tissues, muscles, bones and joints, internal organs, and the cardiovascular system.
Touch
is a crucial means of receiving information. This photo shows tactile
markings identifying stairs for visually impaired people.
Somatic senses are sometimes referred to as somesthetic senses, with the understanding that somesthesis includes the sense of touch, proprioception (sense of position and movement), and (depending on usage) haptic perception.
The mapping of the body surfaces in the brain is called somatotopy. In the cortex, it is also referred to as the cortical homunculus. This brain-surface ("cortical") map is not immutable, however. Dramatic shifts can occur in response to stroke or injury.
System overview
This
diagram linearly (unless otherwise mentioned) tracks the projections of
all known structures that allow for touch to their relevant endpoints
in the human brain.
Mechanical
The four mechanoreceptors in the skin each respond to different stimuli for short or long periods.
Merkel cell nerve endings are found in the basal epidermis and hair follicles; they react to low vibrations (5–15 Hz)
and deep static touch such as shapes and edges. Due to a small
receptive field (extremely detailed info) they are used in areas like
fingertips the most; they are not covered (shelled) and thus respond to
pressures over long periods.
Tactile corpuscles react to moderate vibration (10–50 Hz) and light touch. They are located in the dermal papillae; due to their reactivity they are primarily located in fingertips and lips. They respond in quick action potentials, unlike Merkel. They are responsible for the ability to read Braille and feel gentle stimuli.
Lamellar corpuscles
determine gross touch and distinguish rough and soft substances. They
react in quick action potentials, especially to vibrations around 250 Hz
(even up to centimeters away). They are the most sensitive to
vibrations, and have large receptor fields. Pacinian reacts only to
sudden stimuli so pressures like clothes that are always compressing
their shape are quickly ignored.
Bulbous corpuscles
react slowly and respond to sustained skin stretch. They are
responsible for the feeling of object slippage and play a major role in
the kinesthetic sense and control of finger position and movement. Merkel and bulbous cells - slow-response - are myelinated;
the rest - fast-response - are not. All of these receptors are
activated upon pressures that squish their shape causing an action
potential.
Neural
Gray's Anatomy,
figure 759: the sensory tract, showing the pathway (blue) up the spinal
cord, through the somatosensory thalamus, to S1 (Brodmann areas 3, 1,
and 2), S2, and BA7
Gray's Anatomy, figure 717: detail showing path adjacent to the insular cortex (marked insula in this figure), adjacent to S1, S2, and BA7
All afferent touch/vibration info ascends the spinal cord via the
posterior (dorsal) column-medial lemniscus pathway via gracilis (T7 and
below) or cuneatus (T6 and above).
Cuneatus sends signals to the cochlear nucleus indirectly via
spinal grey matter, this info is used in determining if a perceived
sound is just villi noise/irritation. All fibers cross (left becomes
right) in the medulla.
BA3 receives the densest projections from the thalamus.
BA3a is involved with the sense of relative position of neighboring
body parts and amount of effort being used during movement. BA3b is
responsible for distributing somato info, it projects texture info to
BA1 and shape + size info to BA2.
Region S2 (secondary somatosensory cortex)
divides into Area S2 and parietal ventral area. Area S2 is involved
with specific touch perception and is thus integrally linked with the
amygdala and hippocampus to encode and reinforce memories.
Parietal ventral area is the somatosensory relay to the premotor cortex and somatosensory memory hub, BA5.
BA5 is the topographically organized somato memory field and association area.
BA1 processes texture info while BA2 processes size + shape info.
Area S2 processes light touch, pain, visceral sensation, and tactile attention.
S1 processes the remaining info (crude touch, pain, temperature).
BA7 integrates visual and proprioceptive info to locate objects in space.
The insular cortex
(insula) plays a role in the sense of bodily-ownership, bodily
self-awareness, and perception. Insula also plays a role in conveying
info about sensual touch, pain, temperature, itch, and local oxygen
status. Insula is a highly connected relay and thus is involved in
numerous functions.
Structure
The somatosensory system is spread through all major parts of the vertebrate body. It consists both of sensory receptors and afferent neurons in the periphery (skin, muscle and organs for example), to deeper neurons within the central nervous system.
General somatosensory pathway
A somatosensory pathway will typically have three long neurons: primary, secondary, and tertiary (or first, second, and third):
The second neuron has its cell body either in the spinal cord or in the brainstem. This neuron's ascending axons will cross (decussate) to the opposite side either in the spinal cord or in the brainstem;
In the case of touch and certain types of pain, the third neuron has its cell body in the VPN of the thalamus and ends in the postcentral gyrus of the parietal lobe.
Touch can result in many different physiological reactions. Here, a baby laughs at being tickled by an older sister.
Photoreceptors, similar to those found in the retina of the eye, detect potentially damaging ultraviolet radiation (ultraviolet A specifically), inducing increased production of melanin by melanocytes. Thus tanning potentially offers the skin rapid protection from DNA damage and sunburn caused by ultraviolet radiation (DNA damage caused by ultraviolet B).
However, whether this offers protection is debatable, because the
amount of melanin released by this process is modest in comparison to
the amounts released in response to DNA damage caused by ultraviolet B radiation.
Tactile feedback
The tactile feedback from proprioception is derived from the proprioceptors in the skin, muscles, and joints.
Balance
The receptor for the sense of balance resides in the vestibular system
in the ear (for the three-dimensional orientation of the head, and by
inference, the rest of the body). Balance is also mediated by the
kinesthetic reflex fed by proprioception (which senses the relative location of the rest of the body to the head). In addition, proprioception estimates the location of objects which are sensed by the visual system
(which provides confirmation of the place of those objects relative to
the body), as input to the mechanical reflexes of the body.
Fine touch (or discriminative touch) is a sensory modality that
allows a subject to sense and localize touch. The form of touch where
localization is not possible is known as crude touch. The posterior column–medial lemniscus pathway is the pathway responsible for the sending of fine touch information to the cerebral cortex of the brain.
Crude touch (or non-discriminative touch) is a sensory modality
that allows the subject to sense that something has touched them,
without being able to localize where they were touched (contrasting
"fine touch"). Its fibres are carried in the spinothalamic tract, unlike the fine touch, which is carried in the dorsal column.
As fine touch normally works in parallel to crude touch, a person will
be able to localize touch until fibres carrying fine touch (Posterior column–medial lemniscus pathway) have been disrupted. Then the subject will feel the touch, but be unable to identify where they were touched.
Neural processing of social touch
The
somatosensory cortex encodes incoming sensory information from
receptors all over the body. Affective touch is a type of sensory
information that elicits an emotional reaction and is usually social in
nature, such as a physical human touch. This type of information is
actually coded differently than other sensory information. Intensity of
affective touch is still encoded in the primary somatosensory cortex and
is processed in a similar way to emotions invoked by sight and sound,
as exemplified by the increase of adrenaline caused by the social touch
of a loved one, as opposed to the physical inability to touch someone
you don't love.
Meanwhile, the feeling of pleasantness associated with affective
touch activates the anterior cingulate cortex more than the primary
somatosensory cortex. Functional magnetic resonance imaging (fMRI) data
shows that increased blood oxygen level contrast (BOLD) signal in the
anterior cingulate cortex as well as the prefrontal cortex is highly
correlated with pleasantness scores of an affective touch. Inhibitory
transcranial magnetic stimulation (TMS) of the primary somatosensory
cortex inhibits the perception of affective touch intensity, but not
affective touch pleasantness. Therefore, the S1 is not directly involved
in processing socially affective touch pleasantness, but still plays a
role in discriminating touch location and intensity.
Individual variation
A
variety of studies have measured and investigated the causes for
differences between individuals in the sense of fine touch. One
well-studied area is passive tactile spatial acuity, the ability to
resolve the fine spatial details of an object pressed against the
stationary skin. A variety of methods have been used to measure passive
tactile spatial acuity, perhaps the most rigorous being the grating
orientation task. In this task subjects identify the orientation of a grooved surface presented in two different orientations, which can be applied manually or with automated equipment. Many studies have shown a decline in passive tactile spatial acuity with age;
the reasons for this decline are unknown, but may include loss of
tactile receptors during normal aging. Remarkably, index finger passive
tactile spatial acuity is better among adults with smaller index
fingertips;
this effect of finger size has been shown to underlie the better
passive tactile spatial acuity of women, on average, compared to men. The density of tactile corpuscles, a type of mechanoreceptor that detects low-frequency vibrations, is greater in smaller fingers; the same may hold for Merkel cells, which detect the static indentations important for fine spatial acuity. Among children of the same age, those with smaller fingers also tend to have better tactile acuity.
Many studies have shown that passive tactile spatial acuity is enhanced
among blind individuals compared to sighted individuals of the same
age, possibly because of cross modal plasticity
in the cerebral cortex of blind individuals. Perhaps also due to
cortical plasticity, individuals who have been blind since birth
reportedly consolidate tactile information more rapidly than sighted
people.
Clinical significance
A somatosensory deficiency may be caused by a peripheral neuropathy involving peripheral nerves of the somatosensory system. This may present as numbness or paresthesia.
