Functional neurological disorder: new subtypes and shared mechanisms, 2022, Hallett, Dworetzky, Stone et al

[Arnie Pye]

The only things I took away were, ensure I don't have something else like untreated hypothyroidism, and consider diet.

From a UK perspective ...

Be aware that diagnosis of hypothyroidism is usually restricted to just diagnosing Primary Hypothyroidism (PH). Other forms of hypothyroidism are rarely tested for and rarely treated because doctors are trained that such other forms are rare and thus belong in the "zebra" category which is often ignored. Also note that if a patient has PH they can still be missed for many years because doctors seem to rarely think of it - I don't know why.

Also testing and dose levels are usually determined by TSH alone these days because "TSH is the gold standard marker for thyroid disease" and setting doses for treatment. And - "If the TSH is in range then the thyroid hormone levels must be okay so we don't have to test them". This is nonsense and leaves many people struggling for years without treatment.

TSH is produced by the pituitary. But doctors think pituitary problems are vanishingly rare so can again be ignored. There are oodles of thyroid forums on the web if it interests you.

 

[SNT Gatchaman]

Just having a look at this older thread as I was reviewing previous comments on predictive coding.

The author of this fawning dross is Richard Kanaan. Not surprisingly, he and Wessely are old cronies.

That paper was the commentary article on the thread's main paper. Here's a few quotes —

But, functional neurological disorder is still exceptional in one way: its classic symptoms are largely overt, as are their inconsistencies. These overt and inconsistent symptoms might explain why functional neurological disorder was more reviled than other unexplained syndromes in the past: whereas an individual with unexplained fatigue might appear to a critical eye to be exaggerating, an individual with functional disorder might appear to be feigning. This inconsistency is also why researchers have had to go to such efforts to explain functional neurological disorder, developing new psychological models (eg, dissociation or conversion) for the apparent division in conscious control. These reasons are also why functional neurological disorder was always classified separately from other somatoform disorders.

So, expanding the syndrome of functional neurological disorder makes it less exceptional, and reveals how much it resembles other unexplained syndromes. Dizziness and brain fog, which Hallett and colleagues propose including, are undoubtedly common symptoms in functional neurological disorder, but they are also among the most common symptoms of all unexplained syndromes. Once it is acknowledged that pain and fatigue are also common, important, and (plausibly) neurological symptoms in functional neurological disorder, then the overlap with unexplained syndromes such as chronic fatigue syndrome will be such that people could question whether they are really one and the same.

The biopsychosocial model of functional neurological disorder that Hallett and colleagues propose is fundamentally generic to unexplained syndromes.

Even the positive signs that Hallett and colleagues consider characteristic are found in other unexplained syndromes.

The acceptance of a biopsychosocial model in functional neurological disorder has given hope for broader acceptance of such models in medicine, perhaps even to the extent that functional neurological disorder would no longer be considered unexplained. However, by contrast, other unexplained syndromes (eg, chronic fatigue syndrome) offer a warning: their biopsychosocial model has been rejected by patient groups with such ferocity that it has become dangerous to endorse it.

The closing sentence referencing Courage for sound science wins John Maddox prize (2012, Nature)

 

[SNT Gatchaman]

I was reviewing some of these previous comments on predictive coding

as far as I could see Edwards's 'model' would predict the opposite of what he said. It is all very hand-waving because nobody actually has any evidence for this predictive coding stuff

It is funny that their model of "predictive coding" works backwards to how predictive coding works in other fields.

The predictive coding theory of Hohwy, Friston and others says that what we experience is what the brain calculates to be the difference between what it expects to sense and what comes in from sense organs.

If this is applied to 'false beliefs 'about e.g. pain or fatigue then the story doesn't seem to work. The brain is supposed now to predict pain, despite there being nothing wrong. The sense organs should send in no signal. So the brain should perceive minus pain. Or for fatigue it should experience boundless energy.

And of course this is another example of what I bang on about. You need two explanations for a disease of regulation. You need an explanation of normal regulation and a completely different explanation of why that does not apply in a disease.

I want to summarise for myself, which I hope may also be useful for other later readers of this thread. If I'm following correctly the proposals are —

The brain is constantly predicting the environment. It may do this for all sensory inputs but this is theoretical and we don't have evidence for this beyond established things like being too fast for eg visual nerve conduction velocities. Allowing the ability to predict a ball's motion and move a hand to catch it faster than the time taken to receive/process/send the totality of visual/audio/motor signals.



The prediction is checked and if the real input signals are within satisfactory error, the model simply remains as "truth". If the input signals are out-of-error-bounds, the model is discarded and updated. So that is a mechanism of regulation claimed for the normal situation.

But BPS says "your model's totes out of whack my dude", making the prediction wrong (because "false beliefs") and that's why you are expecting pain, fatigue, whatever.

But as Jo says the real inputs are claimed to be zero pain, zero fatigue (because they say there's nothing actually biologically wrong in the periphery to give a positive signal). So the above mechanism should be invoked, the model refreshed with the bottom line result of "akshully no pain, fatigue" (or even minus pain, fatigue).

But BPS are claiming that the outcome is still pain and fatigue, as initially predicted and the model is ignoring the actual inputs. So the update mechanism is not invoked. So now two things are wrong: initial model parameters (I hurt / will experience fatigue); and no error-correction.

So we're left with (as Jo says) a requirement for how this works normally, but also how it now fails / is inverted in illness. In which case "false beliefs" or indeed any psychological inputs are irrelevant, because the mechanism of creating and updating the model is broken. (Which if true sounds like there might be a structural problem...)

If the model-error-correction mechanism is indeed broken, as per the above requirement, you could fix it by simply telling yourself "no pain", "no fatigue" and the model would just stick with it. (This is LP/CBT/GET/ANS rewire etc). Lots of credulous people are very keen on the idea of brain retraining - why aren't they all fixed just by convincing themselves "no pain"?

It can't be that the brain retraining also repairs the model-error-correction bug, as again the problem would be fixed regardless of the person's prior ideas. Or you would now need yet another failure mode where

initial_model = "no pain" + zero sensory input => "pain".

In other words you might need a third explanation for why these mechanisms don't apply in failed cure.

I hope I've got the broad strokes right.

 

[Jonathan Edwards]

The brain is constantly predicting the environment. It may do this for all sensory inputs but this is theoretical and we don't have evidence for this beyond established things like being too fast for eg visual nerve conduction velocities. Allowing the ability to predict a ball's motion and move a hand to catch it faster than the time taken to receive/process/send the totality of visual/audio/motor signals.

I think that analysis is a misunderstanding. Predictive coding has nothing to do with explaining how we do things 'too fast'. That is an argument about the role of conscious percepts, which occur too late to explain what the brain does in action. The nerve pathways are fast enough. It is just that the conscious aspect that we like to think is the cause of our 'free will' in practice cannot be. Our will works at a lower level of processing.

 

[Jonathan Edwards]

I hope I've got the broad strokes right.

Yes, the hypothesised bad prediction should give the opposite result on a comparison and update model.

In fact the whole predictive coding thing is pretty rubbish because it muddles up all sorts of different neural computational processes. The main predictive coding aspect is oculomotor. Our visual perception is entirely interpreted in the context of what they muscles are doing. Things being still is what we see if the retinal input is shifting in synch with our muscles moving the eyes. But even for visual perception there are other aspects that are not using predictive coding. For hearing it is all different at different stages. The blanket concept of predictive coding is just wrong. Herring a clap of thunder is not about your prediction of no clap of thunder being adjusted, you hear a clap of thunder!

But if predictive coding were involved, which it could be, its role in perceiving fatigue when all is well would be opposite.

It is quite intriguing how often one sees biomedical scientists making such basic mistakes in their theories. Which is why I query so many things around PoTS and salt intake etc. The theories don't actually predict what they think they predict. I have always been fascinated by these disconnects. The best one is the theory that in nephrotic syndrome the oedema is due to low oncotic pressure. But it cannot be because it occurs within hours of onset, long before plasma protein levels fall. It must be due to capillary or venular permeability changes.