Discussion in 'Health News and Research unrelated to ME/CFS' started by Andy, Oct 23, 2020.
Sci hub, https://sci-hub.se/10.1136/bmj.m3745
- Previously, FND was always considered to be a consequence of adverse life events such as recent stress or childhood experience. Newer models take account of motor physiology and predictive coding theories. Growing evidence supports the notion that in FND the early pre-conscious phases of motor planning are corrupted by a combination of abnormal involuntary brain-generated predictions about bodily states and interference from more emotionally orientated brain networks such as the limbic system and amygdala. For example, signs such as tubular visual field loss (see infographic) can be explained by considering the brain as a largely “predictive” organ which makes and tests predictions about the body rather than constructing perceptions from scratch. In FND it is thought that the brain prioritises excessively strong predictions based on what the brain expects to “see” (such as “tunnel vision”) or be able to do (leg weakness) over the actual incoming sensory input.
Such models acknowledge that previous adverse experiences are a risk factor for the development of FND, but they also explain how symptoms are formed, allow for symptom development in patients who have not had adverse experiences, and help explain why symptoms are
often triggered by minor physical trauma or pathophysiological events such as migraine or panic attacks. These models challenge outdated ones that are dependent on a dualistic separation of mind and brain. They present FND as a disorder of a dynamic, plastic brain that constantly modifies its structure and function through interactions with the environment and its interoceptive relationship with the body.
Summary in the article:
What you need to know
Functional neurological disorder (FND) is associated with considerable distress and disability. The symptoms are not faked
Diagnose FND positively on the basis of typical clinical features. It is not a diagnosis of exclusion
FND can be diagnosed and treated in presence of comorbid, pathophysiologically defined disease
Psychological stressors are important risk factors but are neither necessary nor sufficient for the diagnosis
Not a good advert for neurology, is it? The are saying they have no clue what's wrong with most of their patients, and that in fact "we have no clue" is the second commonest outcome of a visit to the neurologist (presume after Alzheimer's).
Last time I looked, there was no special trick to diagnosing FND, it is a placeholder word which means "no diagnosis". It is literally saying you have no clue. Perhaps one needs to be a specialist to before they can achieve the appropriate level of cluelessness.
It´s not necessarly a placeholder.
It could be a dysfuntion of nerves indeed, e.g. a reitertion of wrong patterns where though all algorithms function as they should, induced e.g. by way too much of otherwise normal actions, of e.g. this or that nutrition, e.g. through a viruses.
This contradicts those papers that have come out recently which flatly state that FND is the new name for conversion disorder or hysteria.
Their brain findings may be approaching a truth but they treat it all with CBT! If the theory of emotional problems was true this would work but it doesn't.
I find it truly frightening this sort of diagram. It is all lies which are designed to look scientific but then science is throw out the window with the usual "if you wanted to get better you would" Like there being no need for psychological distress but that it because they believe that psychological distress is being expressed by the bodily symptoms.
It takes everything wrong in the brain into account but then ignores it all for superficial unscientific 19th century ideas.
Complete gibberish. Plus most papers say it straight up that it is the rebranded concept of hysteria, I guess they truly expect us to be too stupid to read papers, it's not as if they are difficult to read, most of the substance is just poor rhetoric at a high school level.
And even if that argument were serious, it's clearly not, this is just typical rebranding of the same crap, it would completely invalidate everything the field has done for the past century because everything is based entirely on the notions of hysteria and whatever the hell conversion disorder is supposed to be.
Speaks very poorly of the complete lack of genuine oversight and accountability in medicine. And I'm getting pretty sick of this crap about the duality of mind and whatever, their quack predecessors were saying the exact same thing a full century ago. It's nothing but a thought-terminating cliché.
Actually what you describe IS a placeholder. It "might be" is not a scientific fact. Sure it might, most of these patients probably do have a not as yet understood neurological disorder. However until the science is done its an hypothesis, and the label is a placeholder for a real diagnosis.
This is a common problem, and is definitely a problem with the CFS diagnosis. Its a placeholder till we understand what a patient has a lot better. Indeed even SEID and ME are placeholders. That does not mean the patients do not have real physiological conditions, only that we do not yet fully understand them. ME in particular seems to bridge many disciplines, from genetics and epigenetics, to metabolism, neurology, immunology and exercise physiology. The label is a placeholder in ME, the advances are being made within and between various disciplines used to study ME. The label may vanish once we have a good understanding and diagnostic tests.
I think FND will vanish once we have a good understanding and diagnostic tests.
Agree with @alex3619. It could be a lot of things. Its unlikely to be even a single coherent thing. And yea, saying it might be wrong algorithms, poor nutrition viruses, etc., is another way of saying that the cause right now is anyone's guess. We don't use that sort of language to explain Parkinson's, Alzheimers, any other neurological disorder for which we have a clue. We reserve this language for when we have no clue.
Its important for us here at this forum not to buy the "algorithms" stuff. This is a another (very tricksy) way of saying that these people have false beliefs - at some level - that are perpetuating their symptoms. Their predictive coding model is built on a number of false assumptions. Its main function, from what I can see, is to distract readers from the fact that its is built on the notion that FND isn't a "disease" at all but rather a set of maladaptive learning patterns that can be reversed through therapy.
Ah, @Mithriel, you're missing the "code"!
"no pathophysiological disease" means "psychiatric", which to these folks means "psychological".
"primarily from a disorder of nervous system functioning" means "psychiatric", which to these folks means "psychological".
I am pretty sure this is gobbledygook. This is not how the predictive coding theory works. The only paper on predictive coding I have seen is from Mark Edwards and I was pretty sure he had got it back to front there. It doesn't explain anything this way at all. It should produce the opposite.
I think the whole hypothesis is based around the "predictive coding" not working as it should.
But I note that a failure of predictive coding, would mean that either the feedback from the periphery is not correct, or is not being processed correctly, in addition to the feed-forward predictions being in error. Both errors have to be biased in the same direction, or predictive coding would correct the error.
Those who promote this theory have to explain why not only the peripheral proprioceptive signals are in error, but why limb-eye coordination is also being ignored as a feedback signal.
Of course they seem unable to provide a realistic model or (non-tautological) empirical observations of how this process is going wrong. There are necessarily limits on brain plasticity. The larger scale neuroanatomy for example, does not change, so large scale connectivity changes from other regions of the brain are not possible.
It is also a bold claim to state that motor force/positioning networks are influenced by "emotionally orientated brain networks" without direct evidence... They seem to be confusing different scales of brain function. Specifically confusing motivation (which certainly is influenced by emotion), with the motor control networks.
I actually think is much worse than that. They are using it backwards, it seems to me. Predictive coding has nothing to do with experiencing the predictions. You experience the deviation from predictions. There are mechanisms by which you can voluntarily elicit experiences such as colour which I think are understudies and potentially very significant but they are nothing to do with predictive coding. The idea that you experience tunnel vision because the brain 'predicts' that you will have tunnel vision seems to me bonkers.
I have got involved with the implications of the Friston and Hohwy type approaches as part of my work on phenomenal experience. The more I go into it the more it seems extremely flimsy and overblown. OK, we have known since Pat Merton wiggled his eyeball with forceps in the 1960s that you experience deviations from predictions based on both motor efferent copy signals and sensory inputs but beyond that seems to be mostly computer modelling with no relation to reality. It is all completely divorced from any theory of the site of experience. I have a paper coming out next month on where the site of experience is so I spend a lot of time thinking about this!
Why should this identification be necessary? Even if there would be a wrong algorithm, it doesn ´t say by any means that this would be caused by believes. Right, it could be, but this "could" says nothing.
A wrong (physiological) algorithm though, would be harder to cure compared to a wrong (physiological) pattern with rightly working algorithms. This direction hasn´t been investigated anyhow, and may well be complex, as could be seen from combinatorics.
Yes, that does seem absurd!
Its hard for me to explain what's wrong with the "algorithms" idea in a simple digestible way. Here are the problems:
1. It takes as its starting point the assumption that if there is no known disease, then the problem is a failure in learning. This is an argument from ignorance (not knowing the causes of something is taken as evidence for its being caused by your pet theory), it is the very same argument that has been used against PwMEs.
2. It misunderstands the function of error feedback in predictive coding models. In these models, error feedback (a mismatch between our prediction and our actual perception) is a key source of information that stimulates a person to learn, so that next time they encounter the same circumstances, they do not make the same error. In general, people do not deal with error feedback by imposing their own predictions onto reality. That would be stupid from an evolutionary point of view. We use it to learn how to better perceive reality. The idea that people induce their movement disorder to "bring it in line" with their belief - at some level - is just bizarre.
3. To deal with the fact that humans don't generally go around making stuff up to avoid error feedback, the authors appeal to "psychological variables". They propose that people possessing certain psychopathological characteristics may develop a belief that they have a movement disorder that is so powerful and important to their sense of identity that they will do anything to avoid having it disconfirmed. So they bring their movements into line with their belief. Those "psychological variables" include being anxious, depressed, introverted, hypochondriacal, etc. Note the powerful belief does not have to be at a conscious level. Poor dears may sincerely believe they have a genuine disease, which of course they do not, just bad learning.
4. Just like the other BPS models, there is no way of independently testing the hypothesis. There is nothing it doesn't predict. You might think, "hey, can't they just see whether those personality variables predict functional movement disorders?? Well, none of them do, but this doesn't seem to phase the authors at all. Its sounding a lot like the BPS stuff now, right?
5. The path to a cure is CBT, GET and physio to help "rewrite" the incorrect movement expectations. Is it sounding familiar yet?
An algorithm in general says, for any functional subunit: "If A comes, then I do B"
Now, if an virus would alter such an algorithm in any units inside our body, why should this be curable by CBT? Or GET??
Instead, with such a wrong algorithm in a nerve cell, GET may well induce damage to greater structures which depend on such algorithms.
Sorry, perhaps I wasn't clear. The "algorithms" view I was referring to above is in fact the predictive coding model of functional movement disorders that is described in the paper at the top of this thread.
One might even say it was old wine in new bottles.
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