Can Telepathy Occur During Dreams and OBEs?

[NeoDevin]

One cannot prove that there are no genuine OBEs. We can show evidence that OBEs can induced and explained using conventional science. We can also cite the lack of evidence to support other explanations for OBEs.

And then we simply apply Occam's Razor to shave away the "other explanations" for OBE's, and conclude that there are no "genuine" OBE's. Once cannot prove that there are no genuine OBE's in the same sense that one cannot prove that there is no sasquatch, yeti, loch ness monster, aliens visiting earth, secret "new world order", fairies, dragons, dodo birds alive today, leprechauns, and/or mermaids.

We have a perfectly reasonable explanation, based on well established scientific principles, which reasonably explains all the claims of OBE's. Without any further evidence (which you admitted we don't have in posts #4, #16, and #17), there is no reason to consider any "other explanations".

Why has this thread lasted this long? This thread should have been locked after the first post or at least after Zz's response.

 

[Ivan Seeking]

And then we simply apply Occam's Razor to shave away the "other explanations" for OBE's, and conclude that there are no "genuine" OBE's.

Occams razor is a rule of thumb, not a scientific principle that can be used to draw conclusions.

 

[NeoDevin]

Occams razor is a rule of thumb, not a scientific principle that can be used to draw conclusions.

Well in that case you can't disprove that it is actually invisible faeries holding us down and keeping the planets in orbit.

 

[Ivan Seeking]

Well in that case you can't disprove that it is actually invisible faeries holding us down and keeping the planets in orbit.

Correct. We can only cite evidence to the contrary, and the lack of evidence to support the assertion.

Long ago it was believed that the angels pushed the planets along on their celestial spheres. Then Newton came along and rotated the positions of the angels by ninety degrees.

 

[NeoDevin]

Correct. We can only cite evidence to the contrary, and the lack of evidence to support the assertion.

So you would contend that genuine OBE's are as worthy of consideration as invisible faeries holding things down? I can live with that.

 

[Ivan Seeking]

So you would contend that genuine OBE's are as worthy of consideration as invisible faeries holding things down? I can live with that.

We have anecdotal evidence for OBE's, but as far as I know, we don't even have anecdotal evidence for fairies. So, no, they are not the same. The question in my mind is whether we have compelling anecdotal evidence for any claims of OBEs.

This almost seems like a religion to you [and many others here]. Why? Why are you determined to have a definite opinion?

 

[Ivan Seeking]

The assertion of invisible fairies was designed to not be falsifiable. If a person really believes that they experience genuine OBEs, then they could be tested and the claim confirmed [evidence presented to support the claim] or falsified [the person is not able to provide information about a remote location as claimed]. But, like fairies, we could never prove that there are no genuine OBEs even if no one claimed to experience them. We can reduce - generalize - the claim to one that can't be falsified.

 

[NeoDevin]

http://www.youtube.com/watch?v=RFO6ZhUW38w"

 

[zoobyshoe]

I'm lost here, with this and discussions of phantom limbs etc., are you still discussing TPJ disturbance?

Ivan is comparing the OBE to other sorts of hallucinations, the hallucination of a sound, for example, or the hallucination of something in the visual field, saying that the ability to induce such an hallucination does not disprove real sounds or real visual experiences. His train of reasoning is: just because there can be a false OBE doesn't mean there are no real experiences of this sensation. I am pointing out the flaw in that train of reasoning, which is that the proprioceptive failure that is required for an OBE is not a stimulation of a sensation, it is the failure of a sensation: the failure of proprioception to give you internal information about your body. When you have no feel for where your limbs are in relation to each other, no feel for your body position as a whole, it is a situation of sensory deprivation. And it is from sensory deprivation that hallucinations easily arise. Failure of proprioception is not the hallucination of something that isn't there, it's the inability to sense something that is there. It is analogous to blindness or deafness.

Phantoms limbs and their opposite (the inability to sense the position of a limb which is still there) are further examples of the importance of proprioception, and the sensory and cognitive confusions that result when it is disturbed. The inability to feel the position of a limb results in a massive crisis of self-image, and emotional and cognitive disownership of the limb. By extension, during the OBE where complete sense of body ownership is lost, you often have people hallucinating the sight of themselves from outside.

 

[zoobyshoe]

Occams razor is a rule of thumb, not a scientific principle that can be used to draw conclusions.

In Principia Mathematica Newton laid out some "Rules of Reasoning" which are essentially a restatement of Occam's Razor:

RULE 1

We are to admit no more causes of natural things, than such as are both true and sufficient to explain their appearances.

RULE II

Therefore to the same natural effects we must, as far as possible, assign the same causes.

RULE III

The qualities of bodies, which admit neither intension nor remission of degrees, and which are found to belong to all bodies within reach of our experiments, are to be esteemed the universal qualities of all bodies whatsoever.

RULE IV

In experimental philosophy we are to look upon propositions collected by general induction from phenomena as accurately or very nearly true, notwithstanding any contrary hypotheses that may be imagined, till such time as other phenomena occur, by which they may either be made more accurate, or liable to exceptions.

http://www.fordham.edu/halsall/mod/Newton-princ.html

 

[DaveC426913]

The thing about OBEs is that
1] we do have anecdotal evidence AND
2] there is some case for repeatability, reproducibility and falsifiability.

So it falls within the realm of scientific study.

 

[Whoeveryouare]

What Ivan Seeking says makes a lot of sense to me. It seems the only sensible approach. We can't hold a definite opinion on the basis of heresay evidence, we would have to verify it empirically. This means running an experiment and obtaining statistically significant and reproducible results.

Unfortunately in physics no such experiment is possible. In consciousness studies we can't even prove that people have in-body experiences. Elesewhere there is even a popular view by which bodies are illusory and OBE's the only kind of experience we can have.

Presumably Christians and those with similar beliefs have no choice but to believe in OBE's, (or is it because they do not believe in them that our bodies must come back to life at the Resurection?), but I'm quite sure that there's no way to demonstrate that they're possible or impossible. It seems to be just the 'other minds' problem in another guise.

I recently read Carlos Castenada's Tales of Power and would highly recommend to anyone looking into these things. His Don Juan, (who can shape-shift, teleport and other cool stuff as some Zen adepts are said to be able to do), gives the sorcerers explanation for our ability to act at times as if we are in Neo's Matrix. It would be because we are.

I think this would be the implication of OBE's, if such things are possible, but I can't see how their possiblity could ever be proved except by having one.

 

[NeoDevin]

Zooby, thanks for the reference.

Dave, then where are the studies?

 

[zoobyshoe]

Zooby, thanks for the reference.

You're welcome.

Dave, then where are the studies?

I just finished a book by V.S. Ramachandran, A Brief Tour of Human Consciousness in which he mentions that the drug Ketamine can produce OBE's. I googled "ketamine out of body experience" and got a few interesting links on the first page which you can do yourself if you're interested. This would be a relatively reliable way to produce the experience at will, however it doesn't seem to be a "clean" OBE: the person feels drugged and high, and it is mixed up in many cases with the travel through a tunnel experience of the "Near Death" experience. Ketamine was developed in the early 1960's and was used as a field anesthetic in Viet Nam for a while, but it was discontinued specifically because of this "OBE" side effect.
-------------------------------------------------------
In the same book Ramachandran mentions the following odd case that has an obvious bearing here:

"Shai Azoulai and I recently saw a patient with a right parieto-occipital tumor who constantly experienced a visual hallucination of a twin or doppelganger always about a foot to his left and front. The twin mimed his movements in perfect synchrony. When I irrigated his left ear canal with cold water (stimulating the vestibular system) the twin was seen to 'jump around' and 'shrink in size' to a midget. Here is yet another reminder of how tenuous our sense of being anchored to our body really is, even though we usually take it to be one of the axioms of our existence."

p.150

This irrigating the ear with cold water is a technique used in rural India to diagnose seizures since it will trigger a seizure in some epileptics. This is probably where Ramachandran picked it up. He mentions having tried it on a stroke patient who was paralyzed one one side but seemed unaware of that; to be hallucinating that the paralyzed side was working perfectly well. (This happens in some cases, this woman wasn't unique.) Irrigating the contralateral ear brought her to awareness of the paralysis, snapped her out of the hallucination for a time, but she later reverted. Perhaps he tried it here hoping it would make the man's doppelganger completely disappear, but he changed it to a midget instead.

 

[fuzzyfelt]

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. Another class of people who seem to report frequent OBE's is heavy pot smokers, I recently found out.

The "sensation" here is lack of sensation: the person's sense of proprioception is shut off or somehow disconnected from consciousness.

is comparing the OBE to other sorts of hallucinations, the hallucination of a sound, for example, or the hallucination of something in the visual field, saying that the ability to induce such an hallucination does not disprove real sounds or real visual experiences...

Phantoms limbs and their opposite (the inability to sense the position of a limb which is still there) are further examples of the importance of proprioception, and the sensory and cognitive confusions that result when it is disturbed.

The TPJ was mentioned as the specific location of proprioception, yet in the information you linked to about limbs (Ehrsson's virtual hand experiment) brain activity was mentioned as occurring in the premotor cortex.

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

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.

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.)

 

[zoobyshoe]

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]

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.

 

[zoobyshoe]

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.

 

[fuzzyfelt]

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.

 

[zoobyshoe]

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 until 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]

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

 

[zoobyshoe]

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]

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? :)

 

[zoobyshoe]

Do only psychotic people dream? :)

Meaning?

 

[fuzzyfelt]

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?

 

[zoobyshoe]

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.

 

[glondor]

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

 

[fuzzyfelt]

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.

 

[zoobyshoe]

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]

I didn't mention another possibility, that everything about triggers and OBEs is fictitious.
I'm interested in factual information.

 

[zoobyshoe]

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]

That has nothing to do with the discussion. He is saying that you have not represented the facts accurately.

 

[zoobyshoe]

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.

 

[zoobyshoe]

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]

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.