Mind/Brain and ME theorising

[Jonathan Edwards]

Yes, sorry, it was unfair. Especially since you are one of the few people that is really listening to us. I suppose the frustration of it all, seeing yet more research efforts going in what I think is the same old backwards direction. I'm also acutely aware of how patients' concerns have been silenced by casting them as somehow simply personally "uncomfortable" with a psychogenic interpretation.

And maybe I did only speak for myself - maybe some of us here on PR are worried about words like "belief"?



I think we really do agree on this. To me, this is the very reason we refer to these as "levels of description". But we're not there yet - if ever - and we need to be aware of the dangers of incorrect translation.



If you're talking about the psychogenic movement disorder/Bayesian stuff, then Edwards talks about various levels of "belief". The patients form a powerful and very conscious belief that they have a movement disorder (when they in fact don't, or at least not any more), but this belief becomes a self-fulfilling prophecy because it operates to shape their movements at pre-conscious level. There's no role in the model for childhood trauma. But there needs to be psychopathology for the powerful belief to be formed/maintained: depression, anxiety, an intense focus on bodily symptoms (and/or too much time spent on forums like this one ).



To cut through some of the terminological confusion, we could instead put the focus on causation. In your example, the question is: is the problem caused or significantly exacerbated by a maladaptive response from the hypothalamus? To the extent that changing its response could significantly improve the condition and/or its major symptoms (without intervening at the level of autoantibodies)?

Or is the hypothalamus responding normally and the root cause is the autoantibodies themselves? To the extent that only changing the latter will lead to real improvement?

My worry with the Edwards/Harrison thing is if they study the first type of question without looking at the second (which seems likely given what has been reported), they will end up with an incorrect causal model - a maladaptive brain response model - when the real problem is way further downstream.

And I agree with all of that too. We seem to be doing well.

 

[Jonathan Edwards]

Just to be clear, you're not saying that Feynman is wrong at the quantum level, are you?
Feynman is very likely correct where he states:
.....It has always been known that making observations affects a phenomenon, but the point is that the effect cannot be disregarded or minimized or decreased arbitrarily by rearranging the apparatus.....
(emphasis added)
The Delft University experiment published just last week seems pretty close to making it a certainty now:

Loophole-free Bell inequality violation using electron spins separated by 1.3 kilometres

(There appears to be an additional experiment still to be done to try and close a final potential loophole, as noted in this layperson's summary of the study here:

Sorry, Einstein. Quantum Study Suggests ‘Spooky Action’ Is Real.)

This is a bit off the mind brain topic but deep down it may be important even to that so let's carry on.

Feynman was probably never wrong about the predictions and the mathematical structure in practice. But I think he was wrong about the deeper level, or as Leibniz would call it meta-physics - the level of knowing exactly what you mean when you say something like 'affects'. There is also a major trend to discard the 'perturbation' interpretation of QM, which dates back to Bohr, within physics because it does give rise to absurdities, but other members of the physics fraternity happily carry on with that sort of talk. It has no relevance to whether or not you can re-confirm the Aspect experiments and yet again show QM is consistent. That is true whichever way you look at things meta-physically, but the idea that an observation affects a phenomenon hides within it a pernicious error about causation - which may be the same error that leads to arguments between psychiatrists and PWME deep down.

The error is that you cannot say that making an observation affects a phenomenon because the observation IS the phenomenon. There may be two issues here. Firstly, the idea that an observation affects a phenomenon is linked to the idea that the 'thing' being measured must have been a certain way just before it was measured to be measured like that - to measure a quantum system as being in a certain state must mean that it was in that state just before you measured it. But it seems that the system would have no way of knowing that it should be in the sort of state that a particular sort of measurement measures, rather than a state that another sort of measurement would measure. It all gets spooky.

But if like Leibniz you take seriously the idea that a quantum system is indivisible then there is no state that the system is in just before a measurement because the system cannot be divided into different states at different times. The measurement is an intrinsic part of a single indivisible dynamic connection. It does not do anything to the connection, it is what the end of that connection is.

The other issue, or angle, has to do with our naive idea of choice. Bohr thought he could choose to measure one way rather than another and so affect the quantum system. But physics has no room for a concept of choice, things just follow rules. So we cannot say that the quantum system was happily going along this way and then Bohr suddenly said 'aha' I will switch the measurement to the other axis and the poor quantum system finds it is 'affected' by Bohr measuring it a way that is not the way it was going to be measured - because history tells us that it was in fact going to be measured the way Bohr switched it to. Nobody can ever change the way a quantum system is by 'changing to another measurement' because the previous sort of measurement was never going to happen anyway.

I realise this may be very confusing but my take on it is that it boils down to the fact that it is really the universe that makes a measurement and the universe always turns out to measure the way it was going to measure (because that is a truism) and so there is no 'affecting' going on, just the universe evolving through indivisible dynamic connections.

Or put very simply there is no such thing as free will in the sense that most people think of it - as Spinoza pointed out.

 

[Jonathan Edwards]

The view was not a lot different in the 90s, but Edelman considered that it was not individual neurons but small clusters of neurons that operated in a block, or group.

I note your suspicion of the invocation of individual neurons in function, Alex, which almost everyone has shared for the last 40 years. However, both Koch and Barlow have pointed out in the last 10 years that the technical reasons for being suspicious turn out not to stand up. So we are probably left with intuitive resistance. The question is what basis is there for such suspicion then?

In my Dutch auction analogy I would agree that we are probably dealing with an auction house with a hundred auctioneers all running auctions at the same time and traders running constantly from room to room to partake in different auctions according to the schedule on the programme. Lateral inhibition is local and there will be many domains of operation, which maybe shift in their boundaries and overlap.

However, I do not think that Edelman would suggest that the basic process of bidding was done by cells operating in a block. I see that as incompatible with the basic tenets of cell-level electrophysiology. Cell A will fire when the input to cell A is of a certain intensity or pattern. Cell A does not fire in response to inputs to cell B - that would be a sort of internal telepathy. I see neurobiologists and neuropsychologists presenting seminars every week who clearly think it is legitimate to think that neurons 'operate in blocks' in some causal chain. But there is no physiological basis for that. There are certainly correlations between cell activities and at each stage outputs from many cells become the many inputs to many other cells, but there cannot be any 'block causation' that is not based in each cell operating separately according to electrodynamic rules.

The thing that interests me is that if one takes an uncompromising view of this, as one should, then it is pretty difficult to avoid the conclusion that experience is determined individually in each cell and never 'combined' with that of other cells. But then I have only found about half a dozen people worldwide who seem to be able to accommodate that thought - one of whom is an academic neurologist in Miami who came to the same conclusion as I did, independently, in 2001 and who agrees on a whole lot of complex ramifications that are beyond this conversation (probably).

 

[Marco]

The thing that interests me is that if one takes an uncompromising view of this, as one should, then it is pretty difficult to avoid the conclusion that experience is determined individually in each cell and never 'combined' with that of other cells. But then I have only found about half a dozen people worldwide who seem to be able to accommodate that thought - one of whom is an academic neurologist in Miami who came to the same conclusion as I did, independently, in 2001 and who agrees on a whole lot of complex ramifications that are beyond this conversation (probably).

Mmm, Struggling with that one but not necessarily for the usual reasons. For argument's sake let's say it's somewhat analogous to the random creation of unique B cells that will lock on to a very specific pattern. In that way the binary switching of a single neuron makes sense although I still find the idea profligate (but not a problem for the immune system apparently). It's hard to conceive how a single neuron can encode the full richness of an experience but we can also propose that once the pattern is recognised, that single event can then link to other associated neurons or clusters of.

Problems with this that I can see is if these neurons are 'programmed' to match a very specific, unique pattern then how do they specify in advance which other neurons they in turn trigger. It also assumes (to me) that there is an 'objective reality) out there that presents a pattern to match whereas most cognitive science suggests that reality is a construct.

'Intuitively' it still seems more likely to me that experiences are constructed from a range of inputs in a combinatory fashion which I would think would be a more flexible and economic system?

 

[Jonathan Edwards]

It's hard to conceive how a single neuron can encode the full richness of an experience

No sweat in conceiving that. Estimates of the number of binary degrees of freedom needed to encode a conscious experience go from 50 to 50,000 maybe - let's guess 5,000. Many neurons have 10,000 inputs, which are probably better than binary. Just about right. And we would not want any redundant profligacy...!

I will come back to the other bit after supper.

 

[Marco]

No sweat in conceiving that.

I will come back to the other bit after supper.

Bon appétit!

I'm off to bed soon.

 

[Marco]

No sweat in conceiving that. Estimates of the number of binary degrees of freedom needed to encode a conscious experience go from 50 to 50,000 maybe - let's guess 5,000. Many neurons have 10,000 inputs, which are probably better than binary. Just about right. And we would not want any redundant profligacy...!

OK - I'll accept that. Presumably what this represents then is the instantaneous experience - like a single frame from web-cam? What then is the output from the neuron - a single indivisible 'experience' or there as many outputs as inputs. How does it relate to memory?

Accepting the possibility also accepts the possibility that an experience is very local. I wonder is there any evidence to from neurology to support this. We're obviously dealing in a much finer scale than even the post meticulous techniques are likely to detect but if experiences are indeed localised then they may aggregate temporally or thematically (or other).

The previous owner of our house had suffered a stroke and had lost any French he'd acquired which may have related to a certain (probably extended) time period but more likely reflects damage on a larger scale to something like Broca's area. Loss of recent memory while retaining distant ones is common but probably just reflects non-localised impairment in laying down new memory. There are frequent (psychological/neurological) reports of amnesia relating to a specific episode (stress related or a boxer not remembering a fight post concussion).

I wonder are there any reports of episode losses following surgery or very localised stroke etc (assuming experiences are 'stored' temporally?

 

[Jonathan Edwards]

Problems with this that I can see is if these neurons are 'programmed' to match a very specific, unique pattern then how do they specify in advance which other neurons they in turn trigger. It also assumes (to me) that there is an 'objective reality) out there that presents a pattern to match whereas most cognitive science suggests that reality is a construct.

'Intuitively' it still seems more likely to me that experiences are constructed from a range of inputs in a combinatory fashion which I would think would be a more flexible and economic system?

OK - I'll accept that. Presumably what this represents then is the instantaneous experience - like a single frame from web-cam? What then is the output from the neuron - a single indivisible 'experience' or there as many outputs as inputs. How does it relate to memory?

Accepting the possibility also accepts the possibility that an experience is very local. I wonder is there any evidence to from neurology to support this. We're obviously dealing in a much finer scale than even the post meticulous techniques are likely to detect but if experiences are indeed localised then they may aggregate temporally or thematically (or other).

The previous owner of our house had suffered a stroke and had lost any French he'd acquired which may have related to a certain (probably extended) time period but more likely reflects damage on a larger scale to something like Broca's area. Loss of recent memory while retaining distant ones is common but probably just reflects non-localised impairment in laying down new memory. There are frequent (psychological/neurological) reports of amnesia relating to a specific episode (stress related or a boxer not remembering a fight post concussion).

I wonder are there any reports of episode losses following surgery or very localised stroke etc (assuming experiences are 'stored' temporally?

Sorry, I never got back after supper.

The idea that I share with Arnold Trehub and some others is that you have a store of randomly tuned cells ready to be 'tagged' to new patterns of sensory input or conceived ideas. When the relevant input arrives the cell is assigned to it and further tuned to make it even more specific. Also, there is a reinforcement of connections, including feedback, being used at the time that allows the newly tagged cell to be linked in to cells tagged to words or other symbols and motor output patterns. This allows a sort of 'reverse causation' that I suspect is fundamental to brain function. Arnold talks of 'autaptic cells' - whose output is designed to re-stimulate the input that generates that output. The connection diagrams get a bit hairy.

I am suggesting that there is an objective reality of dynamic or causal connections out there - events if you like. We tend to represent that as 'things' but usefully so because we endow these things with ideas of tendency or disposition that co-vary usefully with the mathematical patterns of outside dynamic connections. That sounds a bit jargony but it means that what we experience is constructed within but it usefully mirrors real causal patterns outside.

The model I envisage does indeed generate experiences combinatorially from inputs - and yes these are the instantaneous frames on the webcam. But some of those combinations get 'captured' by autaptic cells that can re-run them in response to triggers like names or parts of the content.

The output from experiencing cells would be more or less binary fire or not fire (although timing may add to that). However, since there will be 10,000 cells all receiving a pattern of ons and offs in their 10,000 inputs and all responding in different ways - varying in sensitivity and specificity - then at each step in the process you still have meaning encoded in 10,000 signals. At each step the meaning changes in level of abstraction but with the autaptic cells working you do not lose the early levels if you want to keep them ticking over.

The evidence from neurology that experience is local is simply that integration of signals is always entirely local to individual cells. Without integration there is no physical explanation of how you get combination of elements in the experience. This evidence is so basic and obvious that everyone forgets it. They forget it because clinical evidence indicates that experience is widely distributed over the cortex. The false argument is to assume that this is AN experience being distributed rather than lots of local ones being distributed.

The memory issue is interesting. My wife lost her recent memory back for about five years after several courses of ECT but over the next year or two most of it came back. We remember very little from twenty years back but what we do remember seems very durable. Amnesia for very recent events is easy to explain on the basis of short term reinforcement being fragile but that does not explain some of the things you mention. It is worth a lot of thought I think, but I am not sure it impacts on my model of experience because I am not suggesting that you need to move away from conventional models of memory. I am just suggesting that you use standard models but place experience where the physics seems to need to put it.

 

[Marco]

Thanks Jonathan. Lots to think about but that all makes a lot more sense now seeing these various concepts in more concrete terms.

Sorry, I never got back after supper.

The idea that I share with Arnold Trehub and some others is that you have a store of randomly tuned cells ready to be 'tagged' to new patterns of sensory input or conceived ideas. When the relevant input arrives the cell is assigned to it and further tuned to make it even more specific. Also, there is a reinforcement of connections, including feedback, being used at the time that allows the newly tagged cell to be linked in to cells tagged to words or other symbols and motor output patterns. This allows a sort of 'reverse causation' that I suspect is fundamental to brain function. Arnold talks of 'autaptic cells' - whose output is designed to re-stimulate the input that generates that output. The connection diagrams get a bit hairy.


The model I envisage does indeed generate experiences combinatorially from inputs - and yes these are the instantaneous frames on the webcam. But some of those combinations get 'captured' by autaptic cells that can re-run them in response to triggers like names or parts of the content.

Now that's interesting and sounds like the sort of mechanism that could underlie conditions such as PTSD where the experiences may be strongly encoded at the time and constantly refreshed when confronted with associated cues.
Which brings up the issue of attention/salience which we normally think of as a higher order cognitive function but maybe it's driven from the bottom up.

Talking of which, I may be wrong but I sense what the other Edwards (can't remember his name - Mark?) is chasing is attentional mechanisms which are of course open to all sorts of interpretation.

 

[Marco]

Carrying on the PTSD theme (before I go strum my banjo), taking the stereotypical PTSD scenario (active service) it's usually assumed that some trigger (loud cracking sound etc) triggers associations that then bring back the traumatic memories and the events are 're-experienced'. Standard therapies often involve some sort of gradual exposure to trigger scenarios combined with something like rational-emotive therapy/CBT to gradually extinguish the fear via exposure and top down 're-interpretation' (which all sounds slightly familiar).

Using your schema, we may have an array of neurons tuned in a Fourier/Gausssian fashion to more or less match a particular experience, strongly encoded and readily refreshed (via the feedback mechanisms discussed). When a similar pattern (or association) occurs like a sudden loud noise this array could be triggered and refreshed well before any access to 'conscious' processes which may help explain why these disorders can be so resistant to treatment. Interestingly some recent PSTD treatment protocols have paired cogntive/exposure therapy with glutamatergic agents to reinforce the 'long term potentiation' of the adaptive memories.

 

[Cheshire]

I just came across this:

Medscape Medical News > Psychiatry
Confirmed: Neurologic, Psychiatric Disorders Distinct
A meta-analysis examining neuroimaging studies of neurologic and psychiatric disorders concludes that they are distinct illnesses.

Just seems to me that they just foundthere is a dicrease of grey matter in both categories, but they affect different part of the brain, any difference of nature.

In the light of M. Edwards future research, I'd be interested to have your insight about this (specially @Woolie since you are really knowledgeable about this and able to make things so clear)

 

[Woolie]

@Cheshire, I had to calm down a bit after reading this before I could write something reasonable!

These researchers looked at previously published studies that had reported brain grey matter volume losses (reduced thickness of the cortex) in various neurological and psychiatric disorders. They then recorded the locations of these decreases in the different disorders.

The neurological disorders included Alzheimers, Parkinsons, MS, and a whole lot of others, anything with a confirmed disease process. The psychiatric disorders include schizophrenia, bipolar disorder, depressive disorder, but also autism, ADHD, PTSD, even anorexia.

They averaged the results for the psychiatric and neurological disorders, and found were some similarities, but also some differences in the regions of grey matter loss in the two groups.

They concluded that neurological and psychiatric disorders constitute two separate classes of disorders (and, more by implication than outright statement, that there is good reason not to merge them into a single specialty).

Here's the main conclusion:

Although there were many similar brain regions affected across types of disorders, our meta-analytic techniques also showed differences between the two groups of disorders. The basal ganglia, insula, lateral and medial temporal cortex, and sensorimotor areas showed greater impairment in neurological disorders; whereas the medial frontal cortex, anterior and posterior cingulate, superior frontal gyrus and occipital cortex (bilateral lingual gyrus and left cuneus) showed greater impairment in psychiatric disorders. These structural differences between the two classes of disorders affected distinct functional networks, with the effect of neurological disorders evident in the sensorimotor and frontoparietal networks and the effect of psychiatric disorders evident in the visual and default mode networks.

Here's a nice analogy:

Aim: We wanted to show that fruit preferred by redheads (which includes oranges, apples, bananas strawberries, blackberries and pears) is a different colour, on average, to fruit preferred by blondes (which includes oranges, bananas, apples, kiwifruit and mangoes).

Results: We found, distinct differences in average fruit colour between these two fruit groups, with the redheads preferring, on average reddishy-orange fruit, and the blondes yellowy-green fruit.

Conclusion: There is a good basis for distinguishing between "redhead fruit" and "blonde fruit". These fruits should be be treated as separate kinds.

To be fair, they did make some attempt to address the but-these-fruit-are-all-different-colours problem (although not that convincing in my view, given the huge diversity within both groups):

Disorders within each class, either neurological or psychiatric, were more similar to each other in terms of neuroanatomical alterations than disorders belonging to different classes. In addition, psychiatric disorders were more dissimilar than neurological disorders, speaking of a more heterogeneous class.

You can get the full article here for free, if you feel moved to read it:
http://bjp.rcpsych.org/content/207/5/429

 

[Woolie]

PS Even if you get around the averaging problem (which is huge in my opinion), there's still a sort of weirdness to the conclusion. "Psychiatric and Neurological disorders are not the same".

Well, of course they're not the same! Who ever expected them to be? Different clinical features and probably different underlying processes (like, we needed all this hi-tech structural imaging to tell us this).

The difference is: one group is associated with a known disease process, and the other not. Individual diseases can even "change sides" once the process is known e.g., Alzheimers.

 

[Esther12]

Thought this may be of interest, but wasn't sure where to post it. Google suggested this thread.

http://www.functionalmovementdisorder.com/information/informational-podcasts/informational-podcast/

Podcast from a couple of years ago from Jon Stone and Mark Edwards on functional movement disorders. I haven't listened, because it started with Alan Carson pretending he understood the distracting controversies that cause such trouble around CFS and praising Wessely's Unity of Opposites propaganda/commentary... my deep emotional response led to an involuntary physical inability to continue listening. At least for now. May work up to it as part of a gradual rehabilitative process.

 

[worldbackwards]

May work my work up to it as part of a gradual rehabilitative process.

Prediction: you'll crash.

 

[Snowdrop]

Some really long posts so sorry if this isn't right on point but I found this:
http://disabilityintersections.com/2014/04/misunderstanding-the-mindbody-connection/
and thought it might be of interest.

 

[Woolie]

Some really long posts so sorry if this isn't right on point but I found this:
http://disabilityintersections.com/2014/04/misunderstanding-the-mindbody-connection/
and thought it might be of interest.

This really is a great article, @Snowdrop, so well written. A great find. Probably deserves its own thread.

I love how it throws the only "dualist" accusation of the psychobabblers back in their faces:

“You must be in pain because you have [depression/anxiety/BPD/other mental health disorder],” or “I’ve heard that [Fibromyalgia/CFS/CRPS] is a form of depression,” or “Are you sure that your illness is not just stress?” These comments might be well-meaning, but they all operate from a place of ignorance; just as crucially, they misunderstand and grossly oversimplify the mind-body connection.

The idea of certain pain and fatigue-based chronic illness as primarily psychological–the latter of which still continues to be championed by some high-profile people in the medical field, such as the British psychiatrist Simon Wessely–finds its roots in the concept and (still) high profile of somatoform disorders.
.... Some in the medical field, like the aforementioned “expert” Simon Wessely, believe that fibro, CFS and IBS are all the same thing, and that they are caused by unchecked mental illness on the part of the patient since these illnesses lack one unifying “cause.”

Its a short article, so I urge people to have a look themselves, the author deserves the traffic!

 

[Woolie]

Thought this may be of interest, but wasn't sure where to post it. Google suggested this thread.
http://www.functionalmovementdisorder.com/information/informational-podcasts/informational-podcast/

These guys really are hard to listen to - but thanks for posting Esther12, I love the punishment!

If wondering what to do with it, there's a thread here. Its old, but gets added to often (last week, in fact):

http://forums.phoenixrising.me/inde...a-psychogenic-movement-disorder.35315/page-11

 

[Snowdrop]

Thanks @Woolie

This subject has been of interest to me over the years. If you want to make a thread please do but for me I can't really enter into the discussion takes too much effort for me now.

Glad you enjoyed the article though and I hope other might find it interesting too.

When I found the article the Simon Wesseley name jumped out at me--conditioning?