Telepathy in dreamstate and OBEs

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Re: Telepathy in dreamstate

The TPJ was mentioned as the specific location of proprioception...
No, it is mentioned as the specific location where OBE's were triggered by stimulation with an electrode. Proprioception, as far as I know is generalized throughout the parietal lobes and is also processed in the cerebellum. I have never heard it attributed to one spot. Proprioception may be got to in some different way by stimulating some other spot on the parietal lobes: touch them somewhere else and the person may feel like their nose is pointed sideways, who knows?

As well, the results of further studies of TPJ disturbance could not distinguish between an arrest and extra noise in the TPJ-

'We can postulate at least two mechanisms for
the interfering effect of TMS, either of which could explain our
results. First, TMS could have added extra noise to the neural
signals that provide input to a body/non-body discrimination pro-
cess. Additional input noise would impair discrimination. Second,
TMS could have transiently arrested the test-for-fit process itself,
reducing the difference between body and non-body processing.
Our results cannot distinguish between these two mechanisms of
action'

http://www.manostsakiris.googlepages.com/TsakirisNeuropsychologia.pdf...

...Thus, I think the evidence of lack of sensation as sole cause is inconclusive or irrelevant.
(Wrote something like this yesterday, but have had computer problems.)
Whether it's one mechanism or the other with the TMS is not too important since they have merely "suggested" a test-for-fit process here, not exactly proven one. What I would like to know is whether any of the test subjects felt their hand had turned into a spoon after TMS at the TPJ. (Such things can happen: a girl I know said she felt like she had turned into a giant muffin after eating mushrooms. Carlos Castenada reports that Don Juan slowly talked him into "becoming" a crow after smoking something, as well.)

There is clearly some higher function somewhere making decisions about what to believe in the event of sensory discrepancies but the proposal of the OBE as a disturbance of the test-for-fit process is shaky when you ask where the rubber hand (or spoon) is in the wild OBE. Also, what corresponds to the tactile deception?

The OBE is a great deal more dramatic and comprehensive than adopting a rubber hand and also happens without elaborate lab illusions: it happens spontaneously to people as they are drifting off to sleep with their eyes closed. As you may know from accounts, the experience is often preceded by a loud buzzing and strong sense of the body vibrating. This is obviously some kind of neuronal hyperactivity, be it a simple partial seizure or the kind of less organized "noise" that precedes the expanding area of spreading cortical depression in migraine aura. The loss of sense of body follows this, and is obviously something akin to post-ictal Todd's Paralysis or cortical depression in the wake of a scintillating scotoma happening in brain areas responsible for proprioception. Once it is paralyzed or depressed, some other part(s) of the brain try to make sense of this come up with the interesting "solution" to the problem which is that consciousness has left the body, complete with corroborative hallucinations of autoscopy and/or of travel.

Also, Ehrsson's repeatable experiment upon healthy people, which is anecdotally more like an anecdotally reported OBE (than the partial effects of Blanke's magnetic disturbance on an epileptic patient's TPJ) and which involves virtual sensations, seems more likely to involve more sensations than less.
Blanke did not use magnetic stimulation. He was using depth implanted electrodes which can both send and receive signals. They do this to try and provoke the seizures from which the patient normally suffers in an effort to specifically locate the problem seizure focus which will be removed in surgery. For obvious reasons they want to limit what they remove as much as possible. Depth implanted electrodes are an invasive procedure and are only used on people going to have surgery anyway.
I don't see why you find the rubber hand to be more like anecdotally reported OBE's.
 

fuzzyfelt

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Re: Telepathy in dreamstate

No, it is mentioned as the specific location where OBE's were triggered by stimulation with an electrode.
OK, that is a relief! I had been confused by the words and run-ons and thought you were saying the OBE phenomenon or proprioception is specifically located at the TPJ, which seemed a big leap. Rather you only meant that electrodes in that spot caused something-‘failure’, ‘blocking’…- affecting something around the area which has something to do with proprioception. It took me a while to get that!

And, sorry, electrodes in Blanke’s case, and magnetism used in a further study of TPJ disturbance with results that left possibilities of arrest or noise open, but is there any reason to state that lack of sensation is a sole or necessary cause?

I don't see why you find the rubber hand to be more like anecdotally reported OBE's.
And no, I didn’t think Ehrsson’s glove experiment that you linked to was more similar to anecdotally reported OBEs, and I think that answers some of your questions. Instead I meant Ehrsson’s OBE experiment that I had linked to.

To explain, I had originally linked to Ehrsson’s OBE experiment as good reason to question Blanke’s OBE experiment since it is a repeatable experiment and unlike Blanke’s, involves healthy people. Another reason was because it may not involve TPJ disturbance. Further, it also is more similar to anecdotal descriptions of OBEs than the experience in Blanke’s case. I raised it again here because it involves virtual sensations, suggesting involvement in this seemingly better OBE experiment of more, rather than less, sensation.
 
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OK, that is a relief! I had been confused by the words and run-ons and thought you were saying the OBE phenomenon or proprioception is specifically located at the TPJ, which seemed a big leap. Rather you only meant that electrodes in that spot caused something-‘failure’, ‘blocking’…- affecting something around the area which has something to do with proprioception. It took me a while to get that!
Sorry if my wording was confusing. Yes, all I meant to say was that the TPJ had been isolated as a critical spot where an OBE could be triggered. What that means is that it's neurological. The TPJ is some kind of important point of contact with the circuit, or circuits that are involved in the OBE, but "OBE activity" in these circuits may range far from that spot.

... but is there any reason to state that lack of sensation is sole cause?
The failure of one sensation, proprioception in this case, is all we need to start a multimodal hallucination in other senses. Removing one class of information, internal sense of body, is all we need to require the brain to reprocess everything else it has to work with into the new fictional picture of the body located floating in the room near the ceiling. If you don't feel located anywhere you confabulate something plausible to account for that and outright hallucinate a view of yourself lying in bed from a perspective near the ceiling.

You may wonder why I don't suppose the visual hallucination precedes the feeling of floating: Autoscopy can, and does, happen by itself with no "floating", as in the report from Ramachandran I quoted to Neodevin. The "double" seems perfectly subject to gravity. In other reports the person's visual perspective can shift from the real position to the perspective of the double and they can look at themselves from either perspective, but neither is floating. It's not a case of being out of body, but more like suddenly having two separate bodies and one consciousnes that can shift back and forth. There is no automatic tendency for autoscopic experiences to take the form of "floating", therefore there must be some specific trigger for it when they do.

If we suppose that an unexpected failure of proprioception is the primary event, then we have good reason for the hallucinations that follow which are, in effect, answers to the question "Why don't I feel like I'm in my body?"

Interferring with some integrative process (test-for-fit) by the introduction of "noise" seems very unlikely to produce the relatively coherent (however erroneous) experience of the OBE. Failures of integration, agnosias, are incoherent, chaotic experiences. Here's what facial agnosia looks like to a migraine sufferer who has episodic experiences of it:

https://www.amazon.com/gp/product/037570406X/?tag=pfamazon01-20

Sacks describes an equally horrifying, Picasso-like, experience of his leg the first time he tried to stand on it after recuperating from having torn a major muscle loose: it's position seemed to change incoherently six times a second. Ascribing the cause of the OBE to a failure of a specific integration process doesn't fit with the much more chaotic and bewildering, choppy things that actually seem to happen when integration fails. I am more likely to suppose the integration process goes really well in an OBE. The problem with it is that it's based on incomplete data: with no internal information from the body the brain decides it is located floating in the room.

Messages from proprioceptors in the body, like all other sensory information, go first to the thalamus, and they are reworked and sent to the cortex from there. The cortex feeds info back to the thalamus, and the thalamus responds. The thalamus always controls the cortex and has the ability to put the cortex to "sleep": to slow or stop the information it feeds to the cortex and to send those neurons the instruction to stop processing. This is what happens when we go to sleep. This thalamo-cortical-thalamo circuit is where proprioceptive information could be blocked or disrupted. The TPJ may be a critical place to get into that circuit and mess with it.

And no, I didn’t think Ehrsson’s glove experiment that you linked to was more similar to anecdotally reported OBEs, and I think that answers some of your questions. Instead I meant Ehrsson’s OBE experiment that I had linked to.

To explain, I had originally linked to Ehrsson’s OBE experiment as good reason to question Blanke’s OBE experiment since it is a repeatable experiment and unlike Blanke’s, involves healthy people. Another reason was because it may not involve TPJ disturbance. Further, it also is more similar to anecdotal descriptions of OBEs than the experience in Blanke’s case. I raised it again here because it involves virtual sensations, suggesting involvement in this seemingly better OBE experiment of more, rather than less, sensation.
Blankes' is repeatable, in principle, though no one would allow such an invasive procedure under other circumstances. The Ehrrson demonstration is of gravity-bound autoscopy, not an OBE with floating near the ceiling. The Blanke OBE definitely sounds more like the average anecdotal report than the Ehrrson one. Also, I hope it is clear by now that I am not asserting the OBE consists exclusively of the lack of proprioception. The "more sensations" are obviously there, but they are supplied by hallucination: there are no cameras showing you a view of yourself from the outside, no one simultaneously touching you and your virtual image with a stick. That demonstration tells us that proprioception can be fooled: over-ridden by conflicting information from other senses. It doesn't begin to explain why someone should suddenly not feel located in their body or why they have a clear view of themselves from the outside in the absence of a camera set up.

I get the feeling you are attaching to the "healthy" part of the Ehrrson demonstration, as if it's a forgone conclusion that all spontaneous OBE experiencers are neurologically perfectly sound. The full body lab illusion in healthy people requires an elaborate technological set up to create autoscopy. What is creating the autoscopy in the spontaneous OBE? Clearly it is some kind of hallucination, and, as such, pathological: something isn't working right. The notion of a perfectly "healthy" spontaneous OBE doesn't really make sense.
 
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fuzzyfelt

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Re: Telepathy in dreamstate

I've just read more of the earlier parts of this thread and see the Ehrsson OBE experiment had been mentioned before me, sorry to be repetitive, but I'm now left with little time to reply fully to the previous post.

I was interested in clearer data shedding any light on various reasonable doubts.

as if it's a forgone conclusion that all spontaneous OBE experiencers are neurologically perfectly sound..
Odd it was felt that I’d leapt to that conclusion, despite being mindful of not doing so, and conversely the statement-

Clearly it is some kind of hallucination, and, as such, pathological
discounts the already mentioned toxicological anecdotal exceptions. General population surveys also suggest anecdotal cases without relationship to specific pathology.
 
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Oliver Sacks said:
Although Colman, in 1894, wrote specifically about "Hallucinations in the Sane, associated with local organic diease of the sensory organs, etc.," the impression has long remained both in the popular mind and among physicians, too, that "hallucinations" means psychosis - or gross organic disease of the brain. The reluctance to observe the common phenomenon of "hallucinations in the sane" before the 1970's was perhaps influenced by the fact that there was no theory of how such hallucinations could occur untill 1967, when Jerzy Konorski, a Polish neuropsychologist, devoted several pages of his Integrative Activity of the Brain to the "physiological basis of hallucinations". Konorski inverted the question "Why do hallucinations occur?" to "Why do hallucinations not occur all the time? What constrains them?" He conceived a dynamic system which, he wrote, "can generate perceptions, images, and hallucinations...the mechanism producing hallucinations is built into our brains, but it can be thrown into operation only in some exceptional conditions." Konorski brought together evidence - weak in the 1960's but overwhelming now - that there are not only afferent connections going from the sense organs to the brain, but "retro" connections going in the other direction. Such retro connections may be sparse compared to the afferent connections, and may not be activated under normal circumstances. But they provide , Konorski felt, the essential anatomical and physiological means by which hallucinations can be generated. What, then, normally prevents this from happening? The crucial factor, Konorski suggested, is the sensory input from ears, eyes, and other sense organs, which normally inhibits any backflow of activity from the haighest parts of the cortex to the periphery. But if there is a crucial deficiency of input from the sense organs this will facilitate a backfow, producing hallucinations phisiologically and subjectively indistinguishable from perceptions. (There is normally no such reduction of input in conditions of silence or darkness, beause "off-units" fire up and produce continuous activity.)

Konorski's theory provided a simple and beautiful explanation for what soon came to be called "release" hallucinations associated with de-afferentation." Such an explanation now seems obvious, almost tautological - but it required originality and audacity to propose it in the 1960's.

There is now good evidence from brain-imaging studies to support Konorski's idea. In 2000 Michael Griffiths published a detailed and pineering report on the neural basis of musical hallucinations; he was able to show, using PET scans, that musical hallucinations were associated with a widespread activation of the same beural networks that are normally activated during the perception of actual music.
-Musicophilia

pp 82-84
 

fuzzyfelt

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Re: Telepathy in dreamstate

Thanks, that was interesting too, although I wonder about a number of things including what overwhelming evidence is referred to aside from Griffiths’ 2000 report. Or, regarding that report, does it support Konorski’s idea in any way other than via activation of the same neural networks as activated during actual perception? Another wonder is, is there any difference between the workings of the brain during hallucination and such workings during sleep? For example, http://www.celiagreen.com/charlesmccreery/dreams-and-psychosis.pdf
 
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Thanks, that was interesting too, although I wonder about a number of things including what overwhelming evidence is referred to aside from Griffiths’ 2000 report.
The "overwhelming evidence" was for the existence of the "retro-connections". Sacks doesn't cite any sources for this. I assume it is so accepted he didn't feel the need to: that's the impression his wording has on me, anyway.

The Griffiths study was not called "overwhelming evidence", merely "good evidence". I take it from the context that the Griffiths' study is cited as one example of a pleurality of such studies (perhaps because it was the first?): "There is now good evidence from brain-imaging studies to support Konorski's idea."

Or, regarding that report, does it support Konorski’s idea in any way other than via activation of the same neural networks as activated during actual perception?
I am not sure what else you feel needs to be supported. The existence of "retro-connections" is, apparently, not in doubt, having been previously confirmed from other sources, according to Sacks' mention of "overwhelming evidence".

Another wonder is, is there any difference between the workings of the brain during hallucination and such workings during sleep? For example, http://www.celiagreen.com/charlesmccreery/dreams-and-psychosis.pdf
Sacks is speaking specifically about "release" hallucinations here, in reference to the concept of "hallucinations in the sane". I haven't read your link but from the "dreams-and-psychosis" in the address I assume it discusses "hallucinations in the insane", which Sacks isn't addressing here.
 

fuzzyfelt

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Re: Telepathy in dreamstate

I am not sure what else you feel needs to be supported. The existence of "retro-connections" is, apparently, not in doubt, having been previously confirmed from other sources, according to Sacks' mention of "overwhelming evidence".
Ok, thanks.

Sacks is speaking specifically about "release" hallucinations here, in reference to the concept of "hallucinations in the sane". I haven't read your link but from the "dreams-and-psychosis" in the address I assume it discusses "hallucinations in the insane", which Sacks isn't addressing here.
Do only psychotic people dream? :)
 

fuzzyfelt

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Re: Telepathy in dreamstate

I haven't read your link but from the "dreams-and-psychosis" in the address I assume it discusses "hallucinations in the insane", which Sacks isn't addressing here.
A look at the link (Charles McCreery, DPhil Formerly lecturer in Experimental Psychology, Magdalen College, Oxford, 2008,) should explain why I was alluding that the paper was not just about psychotic hallucinations, nor possibly at all, according to Sach's definition of psychotic.

To answer – a proposal linking dream and psychosis attendant hallucinations encompasses all who dream, psychotic or not. This is different to your assumption that it would only discuss psychotic people.

To elaborate, under a heading about Hallucinatory Episodes in the Sane, OBEs are discussed as a microcosm. For example,

‘ As Irwin (1985) points out, these experiences seem to occur in conditions either of
extremely low or extremely high cortical arousal.’

Interestingly, it also offers an alternative view to Sachs' definition ‘psychosis - or gross organic disease of the brain’, instead putting forward a case that although there may be some underlying organic lability,

‘the behavioural, affective and cognitive symptomatology may indeed be seen as functional on the present view, since they are only the observable by-products of a disorder of function’,

hence if the assumption that it only involved psychotic people according to Sachs' definition of psychotic and thus was not applicable, such an assumption could also be faulty.

I could ask my question differently, however - how does this ‘release’ hallucination differ from other hallucinations to be a sub-set of all hallucinations, or are you suggesting all hallucinations are 'release' hallucinations?
 
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A look at the link (Charles McCreery, DPhil Formerly lecturer in Experimental Psychology, Magdalen College, Oxford, 2008,) should explain why I was alluding that the paper was not just about psychotic hallucinations, nor possibly at all, according to Sach's definition of psychotic.

To answer – a proposal linking dream and psychosis attendant hallucinations encompasses all who dream, psychotic or not. This is different to your assumption that it would only discuss psychotic people.

To elaborate, under a heading about Hallucinatory Episodes in the Sane, OBEs are discussed as a microcosm. For example,

‘ As Irwin (1985) points out, these experiences seem to occur in conditions either of
extremely low or extremely high cortical arousal.’

Interestingly, it also offers an alternative view to Sachs' definition ‘psychosis - or gross organic disease of the brain’, instead putting forward a case that although there may be some underlying organic lability,

‘the behavioural, affective and cognitive symptomatology may indeed be seen as functional on the present view, since they are only the observable by-products of a disorder of function’,

hence if the assumption that it only involved psychotic people according to Sachs' definition of psychotic, (that is, on organic rather than functional grounds), and thus was not applicable, such an assumption could also be faulty.

I could ask my question differently, however - how does this ‘release’ hallucination differ from other hallucinations to be a sub-set of them, or are you suggesting all hallucinations are 'release' hallucinations?
If you are questioning why Sacks seems to be fusing psychosis with gross organic disease of the brain, then so do I. I tend to think it was an error in syntax on his part, that the thought he meant to express was "Hallucination is associated in people's minds with psychosis, or, gross organic disease of the brain." His main drift, clear from the context, is that there is a stigma associated with hallucination: hallucination = crazy, or, brain damaged, therefore the subject of hallucinations in people who don't fit the criteria of "crazy" or "brain damaged" was neglected for a long time because no one had any good ideas how a "sane" person might hallucinate.

"Hallucinations in the sane" are those cases where the person has full insight that the hallucination is not real, or is easily persuaded they are not real. There is no delusional system supporting the reality of the hallucination. Charles Bonnet Syndrome is often cited as the classic example of this:

Usually people with CBS are aware that their hallucinations, although vivid, are not real. CBS hallucinations only affect sight and do not involve hearing things or any other sensations. People with CBS do not develop complicated non-medical explanations about the cause of their hallucinations (sometimes called ‘delusions’). If you think you are having Charles Bonnet syndrome hallucinations, tell your GP about them. You may find it useful to take a copy of this webpage along with you to show to your doctor.
http://www.rnib.org.uk/xpedio/groups/public/documents/PublicWebsite/public_rnib003641.hcsp

Likewise the many cases of people he mentions who hear music playing when there is no music playing are not psychotic: they quickly figure out it is not real and, like Charles Bonnet sufferers, worry that they are going crazy. That worry, obviously, demonstrates that they aren't crazy: they have insight into the fact they're hallucinating.

The guy in your link is proposing that psychosis is a kind of dreaming resulting from either hypo- or hyper-arousal. To the extent he explains the OBE as a brief, sudden episode of the same thing in a person who is otherwise sane, he is, never the less, explaining the OBE as a brief, sudden psychotic episode. In his short side excursion into hallucinations in the sane, he is pretty much saying they're briefly insane.

In Charles Bonnet and other release hallucinations there is no overall delusional or psychotic mechanism believed to be at work. The mechanism Sacks reports from Konorski accounts fully for it.

As for the OBE being caused by extremely low or extremely high cortical arousal: this simply throws the explanation back to a simple partial seizure. (Your author doesn't seem to be aware that a solid connection has been made between OBE's and simple partial seizures, and he doesn't see this vector.) Seizures are most likely to occur during sleep, or, during episodes of high stress, emotional or physical. This is why, when being given an EEG, people are instructed for some of the time to relax as deeply as possible, and then, later, they are instructed to breath deeply and quickly, as if exerting themselves:

During the Procedure

An EEG may be performed on an outpatient basis or as part of your stay in a hospital. Procedures may vary depending on your condition and your physician's practices.

Generally, an EEG procedure follows this process:

1. You will be asked to relax in a reclining chair or lie on a bed.

2. Between 8 and 20 electrodes will be attached to your scalp with a special paste, or a cap containing the electrodes will be used.

3. You will be asked to close your eyes, relax, and be still.

4. Once the recording begins you will need to remain still throughout the test. You may be monitored through a window in an adjoining room to observe any movements that can cause an inaccurate reading, such as swallowing or blinking. The recording may be stopped periodically to let you rest or reposition yourself.

5. After the initial recording performed at rest, you may be tested with various stimuli to produce activity that does not show up while you are resting. For example, you may be asked to breathe deeply and rapidly for three minutes, or you may be exposed to a bright light.
 
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Re: Telepathy in dreamstate

I know telepathy works in a dream state as it has happened to me many years ago. I will tell more if any one is interested.
 

fuzzyfelt

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Re: Telepathy in dreamstate

The Out-Of-Body experience has been demonstrated to be a neurological phenomenon, a temporary failure, or blocking of, the sense of proprioception coupled with a release hallucination.
So most of this sentence and further posts relating 'release' hallucinations with 'retro' connections to OBEs etc., is no longer applicable, but is applicable in other cases involving the ‘sane’-

In Charles Bonnet and other release hallucinations there is no overall delusional or psychotic mechanism believed to be at work. The mechanism Sacks reports from Konorski accounts fully for it.
'Konorski brought together evidence - weak in the 1960's but overwhelming now - that there are not only afferent connections going from the sense organs to the brain, but "retro" connections going in the other direction. Such retro connections may be sparse compared to the afferent connections, and may not be activated under normal circumstances. But they provide , Konorski felt, the essential anatomical and physiological means by which hallucinations can be generated. What, then, normally prevents this from happening? The crucial factor, Konorski suggested, is the sensory input from ears, eyes, and other sense organs, which normally inhibits any backflow of activity from the haighest parts of the cortex to the periphery. But if there is a crucial deficiency of input from the sense organs this will facilitate a backfow, producing hallucinations phisiologically and subjectively indistinguishable from perceptions. (There is normally no such reduction of input in conditions of silence or darkness, beause "off-units" fire up and produce continuous activity.)

Konorski's theory provided a simple and beautiful explanation for what soon came to be called "release" hallucinations associated with de-afferentation." Such an explanation now seems obvious, almost tautological - but it required originality and audacity to propose it in the 1960's.’ -Musicophilia
http://www.americanscientist.org/bookshelf/pub/musical-maladies

'Konorski's thesis is that hallucinations are caused by connections going from the sensory regions of the brain to the sense organs (so-called "retro" or "descending" connections). He hypothesizes that hallucinations are normally inhibited by sensory experiences but that when sensory stimulation falls below a certain level, the "retro" fibers act on the sense organs to produce "virtual" experiences that are as vivid as real ones.

Sacks swallows this theory whole, stating that although evidence of such connections was scant in the 1960s, it is now overwhelming. In fact, the descending connections of the auditory system to the cochlea were well known even in the 1960s. However, the existence of retro connections cannot validate a particular theory about their function.

The explanation that a deficiency of input from the sense organs will facilitate a backflow "now seems obvious, almost tautological," Sacks says. But Konorski's schema is light-years away from being self-evident. It fails to explain why hallucinations can occur without any strong sensory deprivation. Nor does it shed any light on why the brain, which already possesses the hallucinatory material, needs to send extremely detailed hallucinatory scenes to the retina or cochlea, where they must be precisely reconstituted into a "real" sensory experience and returned to the sensory cortices. After all, the brain could produce the vivid images itself, as it does in the case of phantom limb sensations.'

And although simple partial seizures are difficult to diagnose, it is stated that because of evidence contrary to the original explanation of OBEs

this simply throws the explanation back to a simple partial seizure.
The Out-Of-Body experience has been demonstrated to be a neurological phenomenon, a temporary failure, or blocking of, the sense of proprioception coupled with a release hallucination. It's been known for decades that it commonly happens to some people diagnosed with seizures, and also to some people who suffer from Migraines, and it was specifically located to an area on the temporo-parietal junction a couple years ago when it was induced in a woman with epilepsy who was about to undergo epilepsy surgery.
And in another post-
No, it is mentioned as the specific location where OBE's were triggered by stimulation with an electrode.
So, ‘it’ here is not an OBE but the trigger of OBEs that was specifically located. Maybe it would have been helpful if there was some mention of ‘ trigger’ somewhere in that post (24).

Believers in the authenticity of the OBE are generally upset to find out there's any sort of coherent neurological explanation for it, it seems, and rush to form a sort of "callous" of rationalizations around this information, to prevent disillusionment I suppose, the main one offered being that these pathological and induced OBE's don't necessarily rule out the possibility of 'authentic' OBE's.
It doesn’t follow that believers would want to question this because it doesn’t explain enough, for, just as religions may accommodate both a meeting of gametes to trigger life and also mystery of life, so too may believers accommodate both a trigger of OBEs whilst maintaining supernatural facets of them.

However, given that: the patient was already diagnosed with a history of chronic seizures which could cause OBEs; the patient may have unusual damage resulting from siezures; anaesthetics or surgery or other trauma may also cause OBEs; the OBE the epileptic patient described varied from typical OBE reports and involved other hallucinations atypical of reported OBEs; little knowledge is shown here to explain how these various areas of the brain affect each other; at least two possibly exclusive factors, high and low cortical arousal, sensation and lack of sensation, may be associated with OBE causation; that Ehrsson’s OBE induction via virtual sensation may or may not involve the TPJ area, so too other information which is possibly related, like phantom limbs, toxins, changed brain structure in practitioners of meditation (Roepstorff 2009), etc.; and finally given how little is shown here to be known about hallucinations and their ambiguous nature (like the difference between OBEs, psychotic hallucinations and naturally occurring dreams), all sorts of permutations with a range of alternative possibilities may be allowed.

These could include ideas that the trigger in question is not a trigger but coincides with other circumstances; or, as mentioned, that which was triggered was like an OBE, or artificial OBE, unrelated to otherwise reported OBEs; that the trigger itself is only a trigger in exceptional circumstances and not necessarily a trigger for non-seizure or damaged patients; it is one of various triggers; or that this ‘trigger’ is not entirely a trigger, but a contributing factor toward triggering, either only in exceptional circumstances or not.

All of which allow reasonable doubts that this is

the specific location where OBE's were triggered by stimulation with an electrode.
in all cases, along with other ideas contained in post 24.
 
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So most of this sentence and further posts relating 'release' hallucinations with 'retro' connections to OBEs etc., is no longer applicable, but is applicable in other cases involving the ‘sane’-





http://www.americanscientist.org/bookshelf/pub/musical-maladies

'Konorski's thesis is that hallucinations are caused by connections going from the sensory regions of the brain to the sense organs (so-called "retro" or "descending" connections). He hypothesizes that hallucinations are normally inhibited by sensory experiences but that when sensory stimulation falls below a certain level, the "retro" fibers act on the sense organs to produce "virtual" experiences that are as vivid as real ones.

Sacks swallows this theory whole, stating that although evidence of such connections was scant in the 1960s, it is now overwhelming. In fact, the descending connections of the auditory system to the cochlea were well known even in the 1960s. However, the existence of retro connections cannot validate a particular theory about their function.

The explanation that a deficiency of input from the sense organs will facilitate a backflow "now seems obvious, almost tautological," Sacks says. But Konorski's schema is light-years away from being self-evident. It fails to explain why hallucinations can occur without any strong sensory deprivation. Nor does it shed any light on why the brain, which already possesses the hallucinatory material, needs to send extremely detailed hallucinatory scenes to the retina or cochlea, where they must be precisely reconstituted into a "real" sensory experience and returned to the sensory cortices. After all, the brain could produce the vivid images itself, as it does in the case of phantom limb sensations.'

And although simple partial seizures are difficult to diagnose, it is stated that because of evidence contrary to the original explanation of OBEs





And in another post-

So, ‘it’ here is not an OBE but the trigger of OBEs that was specifically located. Maybe it would have been helpful if there was some mention of ‘ trigger’ somewhere in that post (24).



It doesn’t follow that believers would want to question this because it doesn’t explain enough, for, just as religions may accommodate both a meeting of gametes to trigger life and also mystery of life, so too may believers accommodate both a trigger of OBEs whilst maintaining supernatural facets of them.

However, given that: the patient was already diagnosed with a history of chronic seizures which could cause OBEs; the patient may have unusual damage resulting from siezures; anaesthetics or surgery or other trauma may also cause OBEs; the OBE the epileptic patient described varied from typical OBE reports and involved other hallucinations atypical of reported OBEs; little knowledge is shown here to explain how these various areas of the brain affect each other; at least two possibly exclusive factors, high and low cortical arousal, sensation and lack of sensation, may be associated with OBE causation; that Ehrsson’s OBE induction via virtual sensation may or may not involve the TPJ area, so too other information which is possibly related, like phantom limbs, toxins, changed brain structure in practitioners of meditation (Roepstorff 2009), etc.; and finally given how little is shown here to be known about hallucinations and their ambiguous nature (like the difference between OBEs, psychotic hallucinations and naturally occurring dreams), all sorts of permutations with a range of alternative possibilities may be allowed.

These could include ideas that the trigger in question is not a trigger but coincides with other circumstances; or, as mentioned, that which was triggered was like an OBE, or artificial OBE, unrelated to otherwise reported OBEs; that the trigger itself is only a trigger in exceptional circumstances and not necessarily a trigger for non-seizure or damaged patients; it is one of various triggers; or that this ‘trigger’ is not entirely a trigger, but a contributing factor toward triggering, either only in exceptional circumstances or not.

All of which allow reasonable doubts that this is

in all cases, along with other ideas contained in post 24.
So, you're saying you believe in a "real" OBE.
 

fuzzyfelt

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Re: Telepathy in dreamstate

I didn't mention another possibility, that everything about triggers and OBEs is fictitious.
I'm interested in factual information.
 
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I didn't mention another possibility, that everything about triggers and OBEs is fictitious.
I'm interested in factual information.
Direct question: do you believe in "real" OBE's?
 

Ivan Seeking

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Re: Telepathy in dreamstate

That has nothing to do with the discussion. He is saying that you have not represented the facts accurately.
 
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So most of this sentence and further posts relating 'release' hallucinations with 'retro' connections to OBEs etc., is no longer applicable, but is applicable in other cases involving the ‘sane’-
I'm not sure what this means.
http://www.americanscientist.org/bookshelf/pub/musical-maladies

'Konorski's thesis is that hallucinations are caused by connections going from the sensory regions of the brain to the sense organs (so-called "retro" or "descending" connections). He hypothesizes that hallucinations are normally inhibited by sensory experiences but that when sensory stimulation falls below a certain level, the "retro" fibers act on the sense organs to produce "virtual" experiences that are as vivid as real ones.

Sacks swallows this theory whole, stating that although evidence of such connections was scant in the 1960s, it is now overwhelming. In fact, the descending connections of the auditory system to the cochlea were well known even in the 1960s. However, the existence of retro connections cannot validate a particular theory about their function.

The explanation that a deficiency of input from the sense organs will facilitate a backflow "now seems obvious, almost tautological," Sacks says. But Konorski's schema is light-years away from being self-evident. It fails to explain why hallucinations can occur without any strong sensory deprivation. Nor does it shed any light on why the brain, which already possesses the hallucinatory material, needs to send extremely detailed hallucinatory scenes to the retina or cochlea, where they must be precisely reconstituted into a "real" sensory experience and returned to the sensory cortices. After all, the brain could produce the vivid images itself, as it does in the case of phantom limb sensations.'
Weinberger seems not to understand Konorski is describing "release hallucinations", that he is attempting to explain "hallucinations in the sane", not hallucinations in general, and faults him for not explaining other hallucinations, in particular hallucinations in the absence of sensory deprivation. On the other hand I think his taking issue with the need for "retro" connections in this kind of hallucination is a good point. Given Phantom Limbs, why would this Konorski mechanism be necessary? I looked on Amazon for Konorski's book and it is $170.00, so I'm not about to buy it to find out. Perhaps Sacks will hear about Weinberger's criticism and address it somewhere at some point.



And although simple partial seizures are difficult to diagnose, it is stated that because of evidence contrary to the original explanation of OBEs

Originally Posted by zoobyshoe

this simply throws the explanation back to a simple partial seizure.

Originally Posted by zoobyshoe

The Out-Of-Body experience has been demonstrated to be a neurological phenomenon, a temporary failure, or blocking of, the sense of proprioception coupled with a release hallucination. It's been known for decades that it commonly happens to some people diagnosed with seizures, and also to some people who suffer from Migraines, and it was specifically located to an area on the temporo-parietal junction a couple years ago when it was induced in a woman with epilepsy who was about to undergo epilepsy surgery.

And in another post-
Originally Posted by zoobyshoe

No, it is mentioned as the specific location where OBE's were triggered by stimulation with an electrode.

So, ‘it’ here is not an OBE but the trigger of OBEs that was specifically located. Maybe it would have been helpful if there was some mention of ‘ trigger’ somewhere in that post (24).
I can't tell what you're saying here. Your original sentence before the quotes was never completed. Likewise it's clear you frequently have difficulty making out the intent of my sentences. I have explained this but I'll repeat: the reason I did not specifically characterize the tpj as the place where the OBE could be triggered, saying instead merely that they had been "located" to that area, is that my intent was simply to point out it was neurological.

It doesn’t follow that believers would want to question this because it doesn’t explain enough, for, just as religions may accommodate both a meeting of gametes to trigger life and also mystery of life, so too may believers accommodate both a trigger of OBEs whilst maintaining supernatural facets of them.
I think this is a straw man. I did not say they questioned it because it did not explain enough.
However, given that: the patient was already diagnosed with a history of chronic seizures which could cause OBEs; the patient may have unusual damage resulting from siezures; anaesthetics or surgery or other trauma may also cause OBEs;
This is the point: the OBE was easy to trigger in this patient because she was epileptic. This was not her normal seizure, but because she was epileptic she had hyperexitable neurons. The OBE happened incidentally to their search for her seizure focus, they were not looking for it or expecting it.

Could the same thing be triggered in a non-epileptic at this spot? Almost certainly, but it would require more voltage and would not be allowed because it could leave them vulnerable to spontaneous seizures once the neurons here had been "kindled".
the OBE the epileptic patient described varied from typical OBE reports and involved other hallucinations atypical of reported OBEs;
The haptic hallucinations were not typical, yes. In other respects it was much more like the typical OBE than the Ehrrson demonstration.
little knowledge is shown here to explain how these various areas of the brain affect each other
What various areas? How much knowledge would satisfy you?
at least two possibly exclusive factors, high and low cortical arousal, sensation and lack of sensation, may be associated with OBE causation;
How are they exclusive? As I pointed out earlier one can lead to the other: seizures can be followed by paralysis, and subdued cortical activity can lead to seizures. Likewise, the spreading cortical depression of migraine aura is preceded by a slow wave of neuronal hyperactivity. The depression that follows can then spawn another wave of hyperactivity. To the extent your linked paper ascribes hallucination to a dream state caused by either hypo- or hyper- activity it is also, apparently unknown to that author, proposing the circumstances from which seizures and migraine aurae arise. In other words, it isn't providing an air tight case for the dream mechanism of OBE at all, but points back at seizures instead.

The dream mechanism has the misfortune of ascribing the OBE to a brief period of psychosis. Even if we stipulate that is the cause, you couldn't call it an "hallucination in the sane" anymore. Your promise about that paper was that it had something relevant to say about hallucinations in the sane. Instead, I wasted my time reading up to that part only to find out it was actually saying sane people sometimes lapse into brief psychosis.

[However, given that:]... Ehrsson’s OBE induction via virtual sensation may or may not involve the TPJ area, so too other information which is possibly related, like phantom limbs, toxins, changed brain structure in practitioners of meditation (Roepstorff 2009), etc.;
I don't see a complete thought here.
and finally given how little is shown here to be known about hallucinations and their ambiguous nature (like the difference between OBEs, psychotic hallucinations and naturally occurring dreams), all sorts of permutations with a range of alternative possibilities may be allowed.
No, it's not "anything goes". Certain kinds of hallucinations are associated with certain causes. The OBE is known to be a simple partial seizure. There may be other related mechanisms for it (Migraine aura) , or some experience similar enough to it to be casually described as an OBE, but that one, at least, has been positively identified. Infrequently and by itself a simple-partial seizure is harmless. The danger is that if a person finds themselves to be frequently having spontaneous OBE's they could also be having more serious seizures for which they have amnesia (complex partial seizures) and should be checked out. The notion we can just throw out any "alternative", and one is as good as another is not correct.

These could include ideas that the trigger in question is not a trigger but coincides with other circumstances; or, as mentioned, that which was triggered was like an OBE, or artificial OBE, unrelated to otherwise reported OBEs; that the trigger itself is only a trigger in exceptional circumstances and not necessarily a trigger for non-seizure or damaged patients; it is one of various triggers; or that this ‘trigger’ is not entirely a trigger, but a contributing factor toward triggering, either only in exceptional circumstances or not.
This paragraph is pretty silly.

All of which allow reasonable doubts that this is

Originally Posted by zoobyshoe

the specific location where OBE's were triggered by stimulation with an electrode.

in all cases, along with other ideas contained in post 24.
All the cases linking the OBE to the tpj in seizures pretty much sews up the case that it is an essential area to this phenomenon. That doesn't limit the experience to that area, the activity is almost certainly spreading out from there, just based on the fact seizure activity usually does spread out into adjacent areas, and sometimes to remote areas. In any event, stimulation of the brain areas of epileptics by electrode is how Wilder Penfield mapped out many areas of the cortex and created his famous "homunculus". From this we got further proof that brain areas are dedicated. The homunculus is not in dispute: the brain areas of epileptics perform the same tasks as those of non-epileptics. People who deviate from the normal map are rare. The right temporo-parietal junction is clearly important for creating the sense we are located in our bodies. That's fascinating. Who knew we even needed such a sense?

If you read all these books by Sacks, Ramachandran, Penfield, and Klawans you find they are packed full of cases of unbelievable neurological experiences you never imagined existed. In 95% of these cases no one questions that they are neurological, despite the fact none has been fully explained. It is only when you get to the small percentage of experiences that have become attached in people's minds to the paranormal or mystical that people suddenly start trying to pick the neurological explanations apart. No one ever seems to come out of the woodwork and argue that hemi-neglect after stroke has a mystical significance. No one seems interested in asserting that the "shuffling gait" of Parkinson's sufferers is the characteristic walk of the Ascendent Masters of the Third Level of Sainthood and Uppity Consciousness, or some such. Malfunction is accepted as malfunction, and the neurological explanation is not doubted EXCEPT when it has become attached to a notion people don't want to relinquish. Obviously people must have been suffering these seizures going back to prehistoric times, and the experience was taken at face value: the 'spirit or 'mind' was assumed to be able to leave the body, because that what it seemed like.
 
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Re: Telepathy in dreamstate

That has nothing to do with the discussion.
It does, of course, and addressing it could prevent tedious, sentence by sentence argument of things that are not the real issue.

He is saying that you have not represented the facts accurately.
No, he/she was saying my case was weak.
 

Ivan Seeking

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Re: Telepathy in dreamstate

It does, of course, and addressing it could prevent tedious, sentence by sentence argument of things that are not the real issue.
No, it doesn't. Personal beliefs have nothing to do with the evidence.

No, he/she was saying my case was weak.
I will let FF respond. I only care that you don't try to make this personal.
 

fuzzyfelt

Gold Member
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Re: Telepathy in dreamstate

I'm not sure what this means.
I'll make it a question. You wrote that OBEs were a neurological phenomenon, a blockage... coupled with release hallucinations, and are you now saying that this isn't the case?

Weinberger seems not to understand Konorski is describing "release hallucinations", that he is attempting to explain "hallucinations in the sane", not hallucinations in general, and faults him for not explaining other hallucinations, in particular hallucinations in the absence of sensory deprivation. On the other hand I think his taking issue with the need for "retro" connections in this kind of hallucination is a good point. Given Phantom Limbs, why would this Konorski mechanism be necessary? I looked on Amazon for Konorski's book and it is $170.00, so I'm not about to buy it to find out. Perhaps Sacks will hear about Weinberger's criticism and address it somewhere at some point.
Yes, I had been wondering about their superfluous nature as well as evidence of function. I don’t really see how this idea makes much sense. Also I feel any wish to link sensory deprivation and release hallucinations only to sanity and extra noise and different hallucinations only to psychosis is not supported here. Is such a link supported?

I can't tell what you're saying here. Your original sentence before the quotes was never completed. Likewise it's clear you frequently have difficulty making out the intent of my sentences. I have explained this but I'll repeat: the reason I did not specifically characterize the tpj as the place where the OBE could be triggered, saying instead merely that they had been "located" to that area, is that my intent was simply to point out it was neurological.
My sentence was completed by the quote, but the intention is fair enough.

I think this is a straw man. I did not say they questioned it because it did not explain enough.
No straw man, the words in the sentence following the word 'because' was part of my explanation, not any addition of words to your position.

This is the point: the OBE was easy to trigger in this patient because she was epileptic. This was not her normal seizure, but because she was epileptic she had hyperexitable neurons. The OBE happened incidentally to their search for her seizure focus, they were not looking for it or expecting it.


Could the same thing be triggered in a non-epileptic at this spot? Almost certainly, but it would require more voltage and would not be allowed because it could leave them vulnerable to spontaneous seizures once the neurons here had been "kindled".

That there is an understandable reason for the experiment to be limited doesn’t change that fact that it is limited.

The haptic hallucinations were not typical, yes. In other respects it was much more like the typical OBE than the Ehrrson demonstration.

Agreed other hallucinations involved were not typical and, again, it varied in other respects from typical OBE reports.

What various areas? How much knowledge would satisfy you?
Accurate information and relevant facts.

How are they exclusive? As I pointed out earlier one can lead to the other: seizures can be followed by paralysis, and subdued cortical activity can lead to seizures. Likewise, the spreading cortical depression of migraine aura is preceded by a slow wave of neuronal hyperactivity. The depression that follows can then spawn another wave of hyperactivity. To the extent your linked paper ascribes hallucination to a dream state caused by either hypo- or hyper- activity it is also, apparently unknown to that author, proposing the circumstances from which seizures and migraine aurae arise. In other words, it isn't providing
an air tight case for the dream mechanism of OBE at all, but points back at seizures instead.


My words were ‘possibly exclusive’. The paper offers two complimentary possibilities.

Failure of proprioception is not the hallucination of something that isn’t there, it’s the inability to sense something that is there
states a possibly exclusive course.

Certainly states may change.

I'm not in any position to speak for the author, but there was no mention of any air-tight case.

The dream mechanism has the misfortune of ascribing the OBE to a brief period of psychosis. Even if we stipulate that is the cause, you couldn't call it an "hallucination in the sane" anymore. Your promise about that paper was that it had something relevant to say about hallucinations in the sane. Instead, I wasted my time reading up to that part only to find out it was actually saying sane people sometimes lapse into brief psychosis.

Then also included in this criterion of psychosis is sleep with attendant hallucinational dreams. Recalling that McCreery was discussing functional dis-order, sleep - something that happens routinely in all humans, and considered beneficial isn’t considered dis-order, but natural order. The bigger picture here is that he is not discussing sanity and insanity as mutually exclusive, but that there are varying degrees that is something more like a continuum across the population. Also interesting is an idea that unusual experiences and cognitive disorganisation are linked with academic achievement and creativity (Nettle 2006) and problem solving and adapting (Jackson 1997) so that degrees may be beneficial.

I don't see a complete thought here.

The explanation given for OBEs may not accommodate additional information.

No, it's not "anything goes". Certain kinds of hallucinations are associated with certain causes. The OBE is known to be a simple partial seizure. There may be other related mechanisms for it (Migraine aura) , or some experience similar enough to it to be casually described as an OBE, but that one, at least, has been positively identified. Infrequently and by itself a simple-partial seizure is harmless. The danger is that if a person finds themselves to be frequently having spontaneous OBE's they could also be having more serious seizures for which they have amnesia (complex partial seizures) and should be checked out. The notion we can just throw out any "alternative", and one is as good as another is not correct.

I see the misunderstanding, I was not expanding on the little knowledge shown of hallucinations, I meant here that given all these problems with the statements in post 24that there were a range of alternative explanations to those stated.

This paragraph is pretty silly.


It is pedantic, sure, and I could have left a range of alternatives that I spoke of above to be guessed at, but thought it might be helpful to suggest what these may be. Given how misunderstood my language has been, it would seem to have actually been not so silly.

All the cases linking the OBE to the tpj in seizures pretty much sews up the case that it is an essential area to this phenomenon. That doesn't limit the experience to that area, the activity is almost certainly spreading out from there, just based on the fact seizure activity usually does spread out into adjacent areas, and sometimes to remote areas. In any event, stimulation of the brain areas of epileptics by electrode is how Wilder Penfield mapped out many areas of the cortex and created his famous "homunculus". From this we got further proof that brain areas are dedicated. The homunculus is not in dispute: the brain areas of epileptics perform the same tasks as those of non-epileptics. People who deviate from the normal map are rare. The right temporo-parietal junction is clearly important for creating the sense we are located in our bodies. That's fascinating. Who knew we even needed such a sense?

That is a fairer explanation.

If you read all these books by Sacks, Ramachandran, Penfield, and Klawans you find they are packed full of cases of unbelievable neurological experiences you never imagined existed. In 95% of these cases no one questions that they are neurological, despite the fact none has been fully explained. It is only when you get to the small percentage of experiences that have become attached in people's minds to the paranormal or mystical that people suddenly start trying to pick the neurological explanations apart. No one ever seems to come out of the woodwork and argue that hemi-neglect after stroke has a mystical significance. No one seems interested in asserting that the "shuffling gait" of Parkinson's sufferers is the characteristic walk of the Ascendent Masters of the Third Level of Sainthood and Uppity Consciousness, or some such. Malfunction is accepted as malfunction, and the neurological explanation is not doubted EXCEPT when it has become attached to a notion people don't want to relinquish. Obviously people must have been suffering these seizures going back to prehistoric times, and the experience was taken at face value: the 'spirit or 'mind' was assumed to be able to leave the body, because that what it seemed like.


Certainly it would be difficult to question things that had not yet been imagined :)

I don’t know, but possibly it is that reports of OBEs in 15-25% of the general population (Irwin 1985- I think, I'll check it later) that makes them prone to some explanation.
 
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fuzzyfelt

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Re: Telepathy in dreamstate

Re the last reference, it is Irwin 1985, from 'Flight of the Mind'.

I think this has been argued on reasonable grounds and, as argued, any convictions or not is irrelevant and it would not be helpful to answer the direct question. If it matters at all where my interests lie, they are more especially concerned with physical theories about creativity and perception- only slightly related to the thread and I wouldn’t ask to discuss them here particularly. I have tried to understand the position of post 24, and argued that there reasonable questions remain.
 
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Re the last reference, it is Irwin 1985, from 'Flight of the Mind'.

I think this has been argued on reasonable grounds and, as argued, any convictions or not is irrelevant and it would not be helpful to answer the direct question. If it matters at all where my interests lie, they are more especially concerned with physical theories about creativity and perception- only slightly related to the thread and I wouldn’t ask to discuss them here particularly. I have tried to understand the position of post 24, and argued that there reasonable questions remain.
I am hard at work composing an answer to your last post!

You could start a thread in Medical Sciences on the topic you want to discuss. There have been some threads about things somewhat related to creativity such as synesthesia and problem solving in autistic savants. Maybe some others.
 

fuzzyfelt

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Re: Telepathy in dreamstate

No hurry, Zooby, I'll be away for a while. Look forward to it! Yes, thanks, I enjoy those threads often when they come up, and I'll think about what I'd like to discuss specifically.
 
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I see you're back.

I'll make it a question. You wrote that OBEs were a neurological phenomenon, a blockage... coupled with release hallucinations, and are you now saying that this isn't the case?
No, I haven’t changed my position. Weinberger has cast doubt on the mechanism proposed by Konorski for release hallucinations, but not on the phenomenon of release hallucinations.

Release hallucinations are those arising from sensory deprivation.

Here is how Sacks explains these kinds of hallucinations to a patient:

“Her hallucinations, I replied, were not psychotic, but neurological, so-called “release” hallucinations. Given her deafness, that auditory part of the brain, deprived of its usual input, had started to generate a spontaneous activity of its own, and this took the form of musical hallucinations, mostly musical memories from her earlier life. The brain needed to stay incessantly active, and if it was not getting its usual stimulation, whether auditory or visual, it would create its own stimulation in the form of hallucinations”

Musicophilia
p.57

That phenomenon isn’t disputed by Weinberger. He’s disputing the proposed mechanism, specifically the need for efferent connections. His argument was (paraphrasing): “Why do we need all this stuff about efferent connections when release hallucination happens without them in Phantom Limbs?”

Yes, I had been wondering about their superfluous nature as well as evidence of function. I don’t really see how this idea makes much sense.
Unfortunately, after I said that Weinberger seemed to have a good point, something important Ramachandran said about Phantom Limbs came back to me. I found it and reread it. Now I have reservations about Weinberger’s criticism. I can’t sort it out till I read Konorski, though. Sacks’ brief digest of what Konorski said may lack important points. God spoke to me recently in a telepathic dream state during a temporal lobe seizure and told me a copy of this book would soon come into my hands at a cheap price, so I'm holding out for that. In any case I hope it’s clear to you the phenomenon of release hallucinations is not being doubted by Weinberger, just the need for efferent connections in producing them. I get the feeling you do understand that, but I want to state it clearly.

Also I feel any wish to link sensory deprivation and release hallucinations only to sanity and extra noise and different hallucinations only to psychosis is not supported here. Is such a link supported?
I wasn‘t linking them like that. I only objected to the particular “noise and different hallucinations” you brought into the discussion, because they were specifically being asserted by that author as arising from his proposed mechanism for psychosis. My repeated pointing to the fact that Sacks and Konorski were explaining “hallucination in the sane” wasn’t intended to rule out “noise and other hallucinations” in the sane, it was to prevent ascribing any specifically psychosis-based hallucinations to the sane. You can’t ascribe psychosis to the sane, because then, of course, they aren’t sane.

Konorski is trying to explain a certain kind of hallucination in people who don’t really fit the criteria for psychosis. The notion there might be a continuum of sanity/insanity across the population is fine, but beside the point, because release hallucinations arise independently of a person’s place on that continuum. “Noise and other hallucinations” which aren’t stipulated as arising from psychosis are, it follows, allowed to be ascribed to the sane.

Repeating myself: “His main drift, clear from the context, is that there is a stigma associated with hallucination: hallucination = crazy, or, brain damaged, therefore the subject of hallucinations in people who don't fit the criteria of "crazy" or "brain damaged" was neglected for a long time because no one had any good ideas how a "sane" person might hallucinate.”

That there is an understandable reason for the experiment to be limited doesn’t change that fact that it is limited.
The fact it’s limited could mean all such experiences are limited. I explain below.
Agreed other hallucinations involved were not typical and, again, it varied in other respects from typical OBE reports.
It did, but I feel you are overemphasizing the differences and failing to appreciate the rather more important similarities.

I realized on reading this we have never established what you consider to be a typical OBE. Doing that would probably bring the discussion more to the point.

Accurate information and relevant facts.
Hmmm. All neurological authors I’ve read explain that the way we learn what the brain does is to observe it when it fails. This discovery-by-deficit started with Paul Broca who noticed that people with injuries to the same place on the left hemisphere had the same language deficits, a fact from which he drew the right conclusion. Brain damage isn’t considered the only, or best, source of info, however. Penfield called Epilepsy “The Great Teacher, and I’m sure many agree that more has been learned about the brain from Epilepsy than from any other neurological disorder. (But every disorder contributes huge amounts to our understanding. ) Brain damage is often gross and can simultaneously affect several functions, while simple partial seizures tend to either emphasize or delete the functions of specific “circuits”. (J. Hughlings Jackson deduced the existence and layout of the motor strip in the 1800’s from the progression of seizure activity in his wife’s simple partial motor seizures, to name a famous example.) Broca's "right conclusion" has had to be refined and updated according to a more sophisticated understanding of the contributions of different areas to what we consider a single function, but his basic conclusion was right: this area of the brain is important for specific aspects of language.

The distortions a person experiences during these seizures at the TPJ represents the typical sort of information anyone has about what this area does when it‘s working properly (depending on how well you interpret the distortions). We, in this thread, probably have 70% of the information known about what this area does. Deeper understanding will require hypothesis and detective work by clever experimentalists like Ramachandran, Ehrrson, and others.

“How much knowledge would satisfy you?” is the important question. Statements like this: “and finally given how little is shown here to be known about hallucinations and their ambiguous nature (like the difference between OBEs, psychotic hallucinations and naturally occurring dreams), all sorts of permutations with a range of alternative possibilities may be allowed,” are symptomatic of a desire for a specific kind of answer to a specific kind of question. Approaching the subject with that kind of mental filter can result in missing all the information that actually is there.This happens often in the hard science forums here: “What is a photon?, “What is energy?” The questioner is expecting a certain kind of definite answer, but runs into the confusing fact that physicists don’t analyze things such that they can give an answer that is satisfying to the questioner at the level the question was asked. Unbeknownst to the questioner the question is naïve. “…how little is shown here to be known” could easily be changed to the opposite statement by someone who, like myself, is constantly surprised by how much they have recently figured out, and characterizing hallucinations as having an “ambiguous nature” about which little is known, simply demonstrates that your specific questions aren’t answerable at the level they’re asked. My level of curiosity about hallucinations would lead me to the opposite statement, that we actually know a great deal about hallucinations. If you know what the terms mean and imply, it's entirely possible to distinguish OBE's from psychotic hallucinations and naturally occuring dreams.

Then also included in this criterion of psychosis is sleep with attendant hallucinational dreams. Recalling that McCreery was discussing functional dis-order, sleep - something that happens routinely in all humans, and considered beneficial isn’t considered dis-order, but natural order. The bigger picture here is that he is not discussing sanity and insanity as mutually exclusive, but that there are varying degrees that is something more like a continuum across the population.
I’ve personally observed varying degrees of insanity across the population, yes.

On the subject of psychosis that paper was very interesting and I’m sure I would have had an enthusiastic reaction to it if that were what I was focused on at the moment. I’ll go back to it sometime and read it through carefully. The kind of sanity/insanity continuum you report he’s proposing doesn’t really have any applicability to “release” hallucinations; those caused by sensory deprivation. Does it have any applicability to OBE’s? I don’t think so because OBE’s are stereotyped experiences with the same features in evidence across large populations of individuals and cultures. Dreams are more obviously individual-specific and lack the relatively rigid stereotype format you see in OBE reports. The OBE is stereotyped because its content does not arise from “mind,” as dreams do, it arises from a glitch in neurological hardwiring common to all people. If you aren’t looking for a preconceived mystical explanation it’s evident that the OBE both arises from, and informs us of, the existence of a sensory/neural mechanism that evolved to tell us that we are located in our body in the first place. I, personally, was incredibly surprised to find out we even needed such a sense. Isn't it self-evident that we're located in our bodies? But no: it is not enough that things and phenomena exist for us to be aware of them: in all cases we need sensory/neural mechanisms to be aware of them.

This video is a brief look at one of the 6 known people in the world to have completely lost proprioception:

http://videos.howstuffworks.com/discovery/30683-one-step-beyond-loss-of-proprioception-video.htm

With decades of constant self-training, he manages to function pretty well. The scary part of the video is the brief glimpse of Charles Freed, another of the 6 with no proprioception, who is clearly incapacitated by it.

Also interesting is an idea that unusual experiences and cognitive disorganisation are linked with academic achievement and creativity (Nettle 2006) and problem solving and adapting (Jackson 1997) so that degrees may be beneficial.
Yes, see also: Townshend, Daltry, et al. 1969:

“Sickness will surely take the mind where minds can’t usually go.”

I see the misunderstanding, I was not expanding on the little knowledge shown of hallucinations, I meant here that given all these problems with the statements in post 24that there were a range of alternative explanations to those stated…
… It is pedantic, sure, and I could have left a range of alternatives that I spoke of above to be guessed at, but thought it might be helpful to suggest what these may be. Given how misunderstood my language has been, it would seem to have actually been not so silly.
I am not persuaded that post #24 has “all these problems”.

I think the range of alternatives has to be reigned in to what we know is possible and probable. What I meant earlier when I said all such experiences could be limited is that they could all be seizures. Since seizures are the only documented cause, we should suspect they are all seizures (hypersynchronous neuronal firing), first, and not start throwing other speculative causes around for the hell of it, and especially not to accommodate mystical notions that probably arose in an attempt to explain this kind of seizure in the first place. There should be a pretty good reason, something pointing directly at some other cause for us to suspect some other cause. (Migraine runs second in my mind, but I haven’t found any Migraine OBE descriptions that fit with total comfort: there are sensations of floating, of having no body, but not coupled with autoscopy.)

Certainly it would be difficult to question things that had not yet been imagined J
Um…good point.

However, things like Autism, Parkinson’s, Alzheimer’s, Tourette’s, Stroke, Amnesia, and Migraine are well known, but you don’t find people claiming they’re anything but neurological problems.

Explanations are questioned (doubted) when the questioner has a different belief about the cause already in mind.

fuzzyfelt said:
It doesn’t follow that believers would want to question this because it doesn’t explain enough, for, just as religions may accommodate both a meeting of gametes to trigger life and also mystery of life, so too may believers accommodate both a trigger of OBEs whilst maintaining supernatural facets of them.
I haven't exactly searched, but as far as I know but there’s no organized religion that asserts the OBE is any sort of religious phenomenon. It’s “authenticity” seems mostly to be claimed by armchair mystics and paranormal afficionados of eclectic lineage: a little yoga, a dash of zen, two parts Moody, a smattering of Swedenborg, etc. Lord Nelson declared his phantom limb was proof of the existence of the soul. No doubt many followers of organized religion would nod at that with approval, but it is not a tenet of any of those religions that this is the case.
 

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