A new science of emotion: implications for functional neurological disorder, 2022, Jungilligens, Perez et al

Abstract
Functional neurological disorder (FND) reflects impairments in brain networks leading to distressing motor, sensory, and/or cognitive symptoms that demonstrate positive clinical signs on examination incongruent with other conditions. A central issue in historical and contemporary formulations of FND has been the mechanistic and etiological role of emotions. However, the debate has mostly omitted fundamental questions about the nature of emotions in the first place.

In this perspective article, we first outline a set of relevant working principles of the brain (e.g., allostasis, predictive processing, interoception, and affect), followed by a focused review of the theory of constructed emotion to introduce a new understanding of what emotions are. Building on this theoretical framework, we formulate how altered emotion category construction can be an integral component of the pathophysiology of FND and related functional somatic symptoms. In doing so, we address several themes for the FND field including: 1) how energy regulation and the process of emotion category construction relate to symptom generation, including revisiting alexithymia, “panic attack without panic”, dissociation, insecure attachment, and the influential role of life experiences; 2) re-interpret select neurobiological research findings in FND cohorts through the lens of the theory of constructed emotion to illustrate its potential mechanistic relevance; and 3) discuss therapeutic implications. While we continue to support that FND is mechanistically and etiologically heterogenous, consideration of how the theory of constructed emotion relates to the generation and maintenance of functional neurological and functional somatic symptoms offers an integrated viewpoint that cuts across neurology, psychiatry, psychology, and cognitive-affective neuroscience.

Paywall, https://academic.oup.com/brain/advance-article-abstract/doi/10.1093/brain/awac204/6599028

 

Dare I ask what constitutes related functional somatic symptoms? Perez seems to publish literature more prolifically than anyone I’ve encountered. “Flooding the zone” is often an effective strategy. Produce so much drivel that it’s impossible to rebut every insipid, pseudo scientific argument.

Also, it seems like a considerable percentage of posts under the “recent posts” tab belongs to FND articles. It’s a testament to how fast this cancer is growing

 

Random bullshit does tend to cut across loads of stuff.

 

I can PM a PDF. It is long and I don't think I can post it on open thread?

It is drivel on steroids, on more steroids. It could win the all time prize for Pseuds Corner.

 

Perez was also involved in a series of articles (discussed in threads here) describing current practice/good practice in treating FND in relation to the various professions allied to medicine. These articles present a whole set of interventions and clinical management strategies as well established and widely endorsed by health services internationally, without addressing the complete lack of any research under pinning.

He seems to be putting a lot of energy into developing a literature based on the assumption that FND is a valid diagnostic category that is a generally accepted and well understood concept, whilst avoiding addressing the unevidenced beliefs it is based on.

 

The irony for me I that I think that there are illnesses (quite different from ME) that justify a term like FND but if people like the are involved I see that a a very powerful reason not to have the category.

 

What gets me is that there are plenty of people out there who could do with good research into how they could stop their emotions ruining their lives.

Things like OCD, social anxiety, panic attacks, depression are horrible to live with but instead of helping them they keep putting out papers like this.

The awful thing is that no one understands the word salad but there are so many published it looks there must be a solid basis to them.

 

Several of these authors are on Twitter, by the way.

https://twitter.com/jungjoha
https://twitter.com/popkirov
https://twitter.com/LFeldmanBarrett

The latter of which was on a podcast to talk about “theory of constructed emotion.”
https://whyy.org/episodes/range-of-emotion/

 

>“panic attack without panic”

Will this be the new go-to explanation to handwave symptoms of dysautonomia? As in: "POTS? Nah, you just experience silent panic attacks upon standing up." Reminds me of slow onset schizophrenia.

 

.......anything goes. I was once diagnosed with atypical depression - depression without feeling depressed.

 

I'm laughing - thanks --- OK that may not be appropriate.

 

There's already anxiety without anxiety so it was a natural development.

And yeah like oldtimer said there's also depression without depression. And deconditioning without deconditioning. Basically words don't matter in BPSland.

 

20 or so years ago my then GP told me, when she asserted I was suffering from depression but I said I wasn't depressed, that in her opinion I was, and that I was not qualified to know, if I was depressed, or not.

So depression without being depressed has been a concept, in the NHS at least, for quite a while, not a new thing.

 

I had heard of this idea some time ago, and it is not necessarily as irrational as it might first sound. If you think of depression, particularly what used to be called endogenous depression, as a biomedical condition, then feeling depressed arises in this situation from the neurochemistry, and could be seen as the brain chemistry tricking the patient into thinking they are feeling depressed. In which case it is theoretically possible for an individual to have the depression biochemistry but not to misinterpret it as feeling depressed.

However, it is unlikely that such is intended in this situation.

 

Without having access to the article, I have the impression that it is still connected to the good old psychoanalytic theory explaining the conversion disorder (replaced by FND in DSM-5), obviously expressed with new words and " including "a bit of contemporary biosocial.

In short, from their psychological point of view, it is a somatization. The person, for example, suppresses emotions, internal conflicts deemed unbearable, which ends up producing physical (somatic) symptoms. The person detaches, dissociates himself unconsciously from an experience that is too painful to be able to integrate it (live it and accept it fully). Alexithymia is the difficulty in discerning and naming one's emotion of the moment, I grosso modo assume that the authors think that by helping the person to name his internal experience well, then to face it (bring it to consciousness), they will help reduce or even dissipate somatic symptoms.

 

I have read the article and I'm not sure I can be bothered to write up a detailed critique. But you are right, it is very much a modern rehash of the conversion disorder narrative.



(short version of critique: the authors invoke a series of conceptual jargon and apply it to FND without any direct empirical basis for any of the fundamental claims.

The first is the authors don't understand what the brain tries to predict and why - they seem to think that the brain tries to predict everything in great detail, despite a lack of an empirical basis in several cases which are simply assumed in the manuscript, or even a logical basis for that matter. Simply put, the brain only tries to predict in detail when real-time control is needed - motor control, control of the eyes, speech perception etc. Sensory inputs related to metabolism, pain, fatigue are not required to be in real time, nor is there any need to predict continuity - and we know there is no real time control, since effects on ventilatory drive and the autonomic nervous system always involve significant latency.

The authors seem to have no idea how the brain senses metabolic needs in the periphery and speculate about a meaningless all-encompassing predictive system of allostasis - which has already been falsified, if only they'd bothered to look. The cited model (Mark Edwards et al.) of predictive processing works backwards to normal predictive processing (Bayesian) models and has zero empirical basis for the claim that the brain decides to over focus on excessive precision of prediction (of noise), and therefore magically decide to increasingly rely on a predictive model and ignore afferent feedback. All of the claims of lower interoceptive accuracy are nonsense as they are based on studies of heart rate prediction which isn't actually a primary sense and most people are bad at it, and it is highly subject to various response biases.

They also make overreaching claims about hyperarousal based on weak and non-specific evidence such as heart rate variability, "muscle tension", comorbid PTSD etc. If they wish to claim this is a thing, then they first need a highly specific biomarker to confirm it.

Similarly with the claim that people with FND have a susceptibility to alexithymia and lack "emotional granularity", which (despite the lack of empirical basis) is in turn is hypothesised to be the basis of FND, due to a lack of "constructed emotion". Again, unless this is a highly specific factor (found in close to 100% of cases), it cannot be considered a primary factor.
Remember that afferents can be blocked pharmacologically, and thus the effect on interoception can be tested - yet very little FND research seems to embrace empirical methods like this.

I also strongly dislike how they try to reduce emotion down to bodily needs, rather than a complete system of human needs)

Side note, the original paper which they base their ideas is more interesting, if not for the fact that it also suffers from the same limitations (lack of empirical basis for many of the claims)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390700/ (open access)

Ignoring all of the speculative bullshit and going off on my own speculative tangent:
The central commonality to the 'functional' motor disorders is the existence of more than one motor control programmes (in terms of motor planning, generating the motor control impulse, the model of the motor function, and the afferent feedback - the key difference being the connectivity patterns between the two programmes).
I wonder therefore whether these conditions could actually be considered neurodevelopmental disorders, leading to disturbed functional connectivity - similar to autism for example. The underlying basis of the condition therefore would still be formed during childhood and perhaps there is room for childhood abuse exacerbating the condition.