UK Research Collaborative Conference in Newcastle: 13th - 14th October

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Sidereal

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Jonathan Edwards said:
I am not sure about two bit philosophising but I am a bit concerned about how the model would actually work in the context of the background he cites from people like Libet and Haggard. Models involving 'predictive coding' are very fashionable and almost certainly valid but he seems to be suggesting prediction or 'belief' of a rather different sort and I cannot quite see how it would fit in.
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More details in this paper he's written:

A Bayesian account of ‘hysteria’

This article provides a neurobiological account of symptoms that have been called ‘hysterical’, ‘psychogenic’ or ‘medically unexplained’, which we will call functional motor and sensory symptoms. We use a neurobiologically informed model of hierarchical Bayesian inference in the brain to explain functional motor and sensory symptoms in terms of perception and action arising from inference based on prior beliefs and sensory information. This explanation exploits the key balance between prior beliefs and sensory evidence that is mediated by (body focused) attention, symptom expectations, physical and emotional experiences and beliefs about illness. Crucially, this furnishes an explanation at three different levels: (i) underlying neuromodulatory (synaptic) mechanisms; (ii) cognitive and experiential processes (attention and attribution of agency); and (iii) formal computations that underlie perceptual inference (representation of uncertainty or precision). Our explanation involves primary and secondary failures of inference; the primary failure is the (autonomous) emergence of a percept or belief that is held with undue certainty (precision) following top-down attentional modulation of synaptic gain. This belief can constitute a sensory percept (or its absence) or induce movement (or its absence). The secondary failure of inference is when the ensuing percept (and any somatosensory consequences) is falsely inferred to be a symptom to explain why its content was not predicted by the source of attentional modulation. This account accommodates several fundamental observations about functional motor and sensory symptoms, including: (i) their induction and maintenance by attention; (ii) their modification by expectation, prior experience and cultural beliefs and (iii) their involuntary and symptomatic nature.
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Hutan

Hutan

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That article by Mark Edwards that @Sidereal posted above wouldn't win a prize for plain English. But my reading of it is that Edwards believes people find what they expect. So someone expects to have tremors, and then they do. And then they have to rationalise this by believing they have a disease that causes tremors.

First, there will be false perceptual inference as top-down prior beliefs overwhelm bottom-up sensory evidence from lower levels. Second, higher levels now have to explain the emergence of the belief, leading to a misattribution of agency in the sense that top-down attentional processes induced the belief but did not predict its content.
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Sort of like UK ME/CFS researchers expecting to find deluded stupid patients who leap to conclusions about their so-called 'symptoms' - and voila, there they all are! And, now that they are there, those researchers have to write papers with big words to explain why they are there.

Still spluttering into my muesli.
 
snowathlete

snowathlete

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The newly announced study looks to me like the researcher was encouraged in from outside to study ME/CFS. This sort of study would be the sort of study you'd expect to appear. As the biological evidence stacks up, the BPS message is manovered to appear less obviously psychological, fresher, cleverer, grantable.

Nowadays, with the biological research being much better than several years ago, with progress being made by sheer force of will, hard work by dedicated scientists, advocates and fundraisers, this sort of study no longer causes me great concern in terms of potential damage; instead, now I just see what a complete and utter waste it is. It's another chapter in the appaling history of our disease, as boring as the last. The story remains the same.
 
Wildcat

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£600,000 from the Medical Research Council for Dr Mark Edward's study ....
 
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Large Donner

Large Donner

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Jonathan Edwards said:
My impression is that he is not studying ME patients but people with functional neurological disorders - presumably of the sort he specialises in. I am familiar with this sort of problem but I would not associate it with ME.
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Well there are many problems with that. The main being all one has to do IS associate "it" with ME.

Can you explain how one objectively proves a functional neurological disorder regardless of ME?

Can you explain how one objectively proves that someone has "recovered from a functional neurological disorder" and not something else if during a "treatment process" they improve or fully recover?

Are "functional neurological disorders" prone to confirmation bias when diagnosing?

In order to reach a diagnosis of functional neurological disorder does every known test to man have to be carried out or is it down to the selection or lack of selection of tests carried out by the active physician?

If one doctor believes someone has a functional neurological disorder particularly if he claims to "specialise in that label", and another doctor shows objective tests results and diagnoses something else which doctor is correct?

If someone doesn't recover from a "functional neurological disorder" after being in receipt of the recommended treatment is it because they haven't done the treatment correctly? Therefore are they now even more "functionally neurologically disordered"?

Lastly is medical science in a place to state that it can objectively diagnose everything there is to diagnose therefore leaving the category of functional neurological disorder for people with no current objective diagnosis. What was the date and time in history that this position was reached? Where was this decision published if it exists?

When are people within the medical profession actually going to speak out and give an obvious critique of the flaws in such concepts as "functional neurological disorders, conversion disorders etc.

What do so called academics do in the Q and A section of a talk on functional neurological disorders by a "specialist", do they not see the obvious flaws, have they not seen how problematic such rhetoric is time and time again in medicine?

I just don't get how people like neurologists, virologists etc being in the position to have to navigate a minefield of possible tests to try to be as objective as possible and still know they may not have answers, can sit through such a talk on FND and not have alarm bells going of when all the "expert on FND" has to do is stand up and make pronouncements.

With 600k going to this study just how does this character plan to disprove his own theories when all that is required to "prove" them is pure statements.

I think we all know. I am afraid I saw this kind of thing coming, however whenever one tries to encourage critical thinking and to be aware of slights of hand quite often people involved with some of the the ME charities will accuse you of "being negative towards........".

Most recently it was people being accused of being negative towards British research. Its the same old game being played over and over again, with groups like AYME, AFME, Peter White, Esther Crawley etc etc. Who wouldn't be negative from the offset with people like them always invited in their droves?

Why oh why do we never learn to say it as it is about them when it comes to research projects that promise to be the breakthrough or the end of BPS crowd.

The science will never win out if we keep giving them invitations to Bio med research projects.

Its time we learned from the lessons of FIFA, the whole things needs cleared out top to bottom when it comes to the BPS crowd.
 
A

Aurator

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Wildcat said:
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£600,000 from the Medical Research Council for Dr Mark Edward's study ....
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This is a mockery, and it's hard not to feel we're fooling ourselves if we believe that the people who hold the purse strings have any intention of earnestly trying to get to the bottom of ME/CFS. Such a grotesquely inappropriate funding decision demonstrates that the MRC are content (perhaps determined) that ME/CFS remains relegated to the dustbin of medical diagnoses.
I'm prepared to be persuaded there's another point of view and ME/CFS as a biomedical entity is being taken seriously by the people who dish out the money, but the answer is going to have to be very very good.
 
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Sean

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This article provides a neurobiological account of symptoms that have been called ‘hysterical’, ‘psychogenic’ or ‘medically unexplained’, which we will call functional motor and sensory symptoms. We use a neurobiologically informed model of hierarchical Bayesian inference in the brain to explain functional motor and sensory symptoms in terms of perception and action arising from inference based on prior beliefs and sensory information. This explanation exploits the key balance between prior beliefs and sensory evidence that is mediated by (body focused) attention, symptom expectations, physical and emotional experiences and beliefs about illness. Crucially, this furnishes an explanation at three different levels: (i) underlying neuromodulatory (synaptic) mechanisms; (ii) cognitive and experiential processes (attention and attribution of agency); and (iii) formal computations that underlie perceptual inference (representation of uncertainty or precision). Our explanation involves primary and secondary failures of inference; the primary failure is the (autonomous) emergence of a percept or belief that is held with undue certainty (precision) following top-down attentional modulation of synaptic gain. This belief can constitute a sensory percept (or its absence) or induce movement (or its absence). The secondary failure of inference is when the ensuing percept (and any somatosensory consequences) is falsely inferred to be a symptom to explain why its content was not predicted by the source of attentional modulation. This account accommodates several fundamental observations about functional motor and sensory symptoms, including: (i) their induction and maintenance by attention; (ii) their modification by expectation, prior experience and cultural beliefs and (iii) their involuntary and symptomatic nature.
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I have read this several times, and I cannot see any fundamental difference between it and the model Wessely & co have been advocating for decades.

That certainly casts (at least part of) this conference in a different light. :grumpy:
 
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D

Dolphin

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SOC

SOC

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Sonya Chowdhury ‏@SonyaChowdhury 10h10 hours ago
Sonya Chowdhury Retweeted Russell Fleming

£600k from MRC but funding from others too.
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O...M...G... You mean that even more than 600,000 of funds that could have been spent on something useful is going to be wasted on this garbage? This makes me so sick. We have so little funding already, and such a huge sum was already wasted on PACE, it's enough to bring tears to my eyes. UK citizens should be up in arms at this continued incredible waste of government and/or donated funds. Frankly, the worldwide ME population would be better off if the UK just quit funding any so-called ME research at all. Better nothing than garbage we have to waste time, energy, and funds refuting.
 
Esther12

Esther12

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We can't say for sure it's garbage yet. It just smells of it.

Actually... I've been ground down by a decade of CFS research which ends up being even worse than it had sounded... this is going to be garbage.
 
D

Dolphin

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Is this the title of a grant? Or just a title he made up for a presentation to the CFS/ME Research Collaborative?

https://twitter.com/SonyaChowdhury/status/653966504732528640
Sonya Chowdhury ‏@SonyaChowdhury 11h11 hours ago
#CMRC2015 hearing about new MRC funded project
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CRNbEjGWwAA6eQx.jpg
 
S

Sidereal

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SOC said:
O...M...G... You mean that even more than 600,000 of funds that could have been spent on something useful is going to be wasted on this garbage? This makes me so sick. We have so little funding already, and such a huge sum was already wasted on PACE, it's enough to bring tears to my eyes. UK citizens should be up in arms at this continued incredible waste of government and/or donated funds. Frankly, the worldwide ME population would be better off if the UK just quit funding any so-called ME research at all. Better nothing than garbage we have to waste time, energy, and funds refuting.
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Agreed. What is happening in the UK is so depressing that I truly believe we would be better off with zero funding for this "research". I remember looking at the first batch of MRC grants they announced for "CFS/ME" a couple of years ago and it struck me as a bit of a scam designed to shut patients up who have been clamouring for funding for medical research, with some of the funding going to existing groups studying other diseases and disease models which are only tangentially related to ME - stuff about interferon alpha in hep C fatigue, Sjögren's fatigue etc. Now we get a big announcement about an almost one million dollar grant to study conversion disorder, with a 20-patient PEM neuroimaging sideshow tacked onto it. Yay. All clap now.

Sean said:
I have read this several times, and I cannot see any fundamental difference between it and the model Wessely & co have been advocating for decades.
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There really is no difference once you strip away the jargon and look at the essence of things. Both viewpoints boil down to there being nothing wrong with the body. The brain of a person with a personality disorder is generating false illness beliefs which are generating somatisation symptoms.

I've been watching this rhetorical repositioning of the psychogenic school for a while now. These days you can't get away with banal Freudian "explanations" like "child abuse caused her leg to go weak 30 years later!" (well, you can in a neurology clinic--this magical thinking is inflicted on patients on a daily basis--but it's considered a bit too simplistic and passé in the peer-reviewed literature) so you get 10,000-word word salads about Bayesian priors causing abnormal illness beliefs and thus generating symptoms.

Wessely cited approvingly in the Edwards paper I linked to a few posts up:

FMSS = functional motor and sensory symptoms

We wish to highlight here the notion of physical precipitating factors in the generation of FMSS, something highlighted by others, for example Reynolds (1869). It is notable that a physical precipitating event is commonly reported close to the onset of FMSS; and we believe that this provides an important explanation as to why particular FMSS develop. For example, viral infections commonly precede chronic fatigue syndrome or neurasthenia (Wessely et al., 1998), somatic symptoms associated with panic attacks are commonly reported prior to onset of non-epileptic seizures (Rusch et al., 2001) and physical injury to a limb (causing pain and immobilization) is commonly reported at the onset of fixed abnormal limb postures or limb paralysis (Schrag et al., 2004; Stone et al., 2009b, 2012a).

We suggest that salient sensory data arising from these precipitating events are afforded excessive precision (weight), and that this instantiates an abnormal prior belief at an intermediate level in the cortical hierarchy trying to explain or predict those sensations—and that abnormal belief or expectation is rendered resistant to extinction through the unusually high levels of precision (synaptic gain) enjoyed during its formation. For example, for sensory data from a triggering event signalling pain, the abnormal prior belief may reside in the insular cortex, an intermediate-level cortical level relevant to pain perception (Wiech et al., 2008). The excessive precision afforded to the novel sensory data could have a variety of causes in addition to the predisposing factors mentioned above, which include affective and cognitive biases and their interactions. Negative effects such as anxiety and depression themselves cause somatic symptoms, as well as increasing self-focused attention (Kolk et al., 2003) both through general arousal (Wegner and Giuliano, 1980) and ruminations (Vassend, 1989). In healthy subjects, Berna et al. (2010) demonstrated that inducing sadness increased the unpleasantness of painful stimuli with those experiencing the greatest unpleasantness showing the highest activations in the amygdala and inferior frontal gyrus.

Negative affect is very common in patients with personality disorders, who in turn are at a higher risk of developing FMSS (Binzer et al., 1997; Crimlisk et al., 1998). It has also been proposed that somatically focused attention occurs in the setting of traumatic events in order to avoid a potentially overwhelming affect (Brown, 2004). Indeed, patients with non-epileptic seizures—which have been associated in some patients with childhood sexual abuse (Sharpe and Faye, 2006)—commonly report somatic symptoms associated with panic attacks (palpitations, sweating, hyperventilation) at the onset of attacks, but fail to report associated affective symptoms (panic without panic). This process could produce physical symptoms that the patient interprets as being due to physical illness as he or she is not aware of the affective content of the panic episode. Somatic symptoms of panic occurring in conjunction with a physical trigger such as injury are also reported in patients who go on to develop functional weakness (Stone et al., 2012a). This might be an important mechanism that adds additional physical symptoms and arousal to a physical precipitant such as an injury, increasing the salience of the resultant sensory data and facilitating the formation and retention of an abnormal prior belief. A predisposition to learning, in the context of salient information, is due to the fact that precision in Bayes optimal schemes plays the role of a ‘learning rate’ in classical reinforcement learning schemes. This means a high level of precision promotes fast associative learning.
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See all those "predisposing", "precipitating" and "perpetuating" factors the Wessely school has been talking about in ME/CFS for decades? It's all in there (highlighted).
 
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