Cognitive behavioural therapy for adults with dissociative seizures (CODES): a ... multicentre, randomised controlled trial (2020) Goldstein, Chalder

CODEs study group
ProfLaura HGoldsteinPhDaEmily JRobinsonMScbgJohn D CMellersMRCPsychhProfJonStonePhDiProfAlanCarsonMDiProfMarkusReuberPhDjNickMedfordPhDhProfPaulMcCronePhDcJoannaMurrayBAdProfMark PRichardsonPhDeIzabelaPileckaPhDaCaroleEastwoodMScaProfMicheleMoorePhDkIrisMosweuMSccIainPerdueMPhilaProfSabineLandauPhDb* ProfTrudieChalderPhDf*

https://www.sciencedirect.com/science/article/pii/S2215036620301280

 

These were all subjective outcomes, while the primary outcome (how many seizures patients had) is a lot less subjective. The secondary outcomes:

 

Ah, I see the latest edition of copy-paste research journal is up. Very expensive copy-paste. It would be measured in lives if anyone bothered to check but no one does so I guess it's all fun and games doing the same things over and over again with no results but arguing otherwise because reasons.

Quacks. Just pure quackery.

 

You guys... she’s gonna get knighted soon (kidding, sarcastic tone)

 

Merged thread

New Lancet publication from Trudie Chalder and crew.

This is perhaps rather long but I think important background information for the ME world.

Not specific to ME; however, as dissociative seizures are poorly understood and have been psychologised a great deal, it is interesting to compare how poorly the model of CBT fared here. Sometimes IAPT have tried to include DS under MUS. The last list of IAPT MUS's I saw it had dropped off the list. Probably because someone objected loudly

Here is the paper:
https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(20)30128-0/fulltext?fbclid=IwAR1eZLXCsM61_bzgxwpqXlNf81QvoUKS6H0ISdPIJnhSsD-iLWh2KPyOZxQ

CBT did not reduce the patient recorded and reported number of seizures - the primary outcome. The trial very modestly improved a few psychosocial measures - but that could be placebo given the nature of the study - clinician's can't be blinded to what they are doing - neither are the patients.

What stands out for me was how ineffective it was at reducing the initial modest levels of distress these patients have. Plus, the very high level of physical disability - which were also unaffected by the intervention. No mention about that in the paper. The researchers seem blind to this.

I've worked with many patients with epilepsy via my clinic at The Brain Charity in Liverpool and DS came up fairly frequently. Many patients with diagnosed epilepsy also have some DS's. Patients tend to see them as physical. They and 'do and don't' buy into the psychological explanation - it causes cognitive dissonance and they tend to put this aside and try and cope. It's quite marmite. I have helped people to mange and cope with them. People were generally quite stable medically when I'd see them so this is perhaps a different patients cohort to those seen in neurology clinics earlier on in the process. If there was PTSD/trauma reaction then I'd happy work on that with the patient, if they felt it was relevant, but I'd not suspect that this would reduce seizures or frequent - that might be nice if it happened (as in less stress as a trigger) but I'd not 'sell' it that way.

The CBT of model of DS is “Adapted specifically for patients with DS, the intervention was based on models of fear-avoidance 4,5”

Isn’t everything is TC et al’s world ‘fear avoidance’. We have seen this before!

And here are those references - check out the dates:

4 Lang PJ. Fear reduction and fear behaviour: problems in treating a construct. In: Shilen JM, ed. Research in Psychotherapy (Vol III). Washington DC: American Psychological Association; 1968.

5 Mowrer OH. Learning theory and behaviour. New York: Wiley; 1960.

From the main paper – on average the levels of anxiety and low mood (GAD7 & PHQ9) (Table 2) are modest and pretty low overall and remain unchanged over the intervention. Does not suggest this is a distress / psychologically driven condition. pwPTSD or depression score near the maximum on these two forms - pretty much universally. If I was referred modest/low distressed patients with trauma I'd suspect they were functioning emotionally pretty well..... so I'd be querying the diagnosis.

More from Table 2 - These patients are physically really debilitated (SF-12 score around 40 pre and post – out of max score of 100). My PTSD patients (non-injurious ones) are not physically disabled at all. My panic/agoraphobia patients are well physically usually. What’s with the v low physical functioning? That’s completely missed.

From the supplementary information: CBT for DS is supposed to be similar to that for CBT for panic / trauma along with assuming the patients are dissociating during an attack – i.e. a coping mechanism along with avoidance re previous trauma. OK, well I treat all of that using trauma focused CBT and I get a high recovery rate and there is a good evidence base for this. My patients will start of scoring high/max on PHQ9 / GAD7 and end up low/close to zero by the end. So, why doesn’t CBT work in DS? Suggests strongly to me that the model is wrong. There is no voice in this work for the patients experience of the therapy. That could be illuminating.

Also, having read what is covered in therapy (pages 7 and 8 of the supplementary info) it is NOT close to CBT for panic or trauma at all. There is no psychoeducation re fight, flight, freeze response (FFF) and adrenaline/cortisol reaction etc and normalisation of this response – a big part of CBT for panic. Along with the importance of examining and reframing the cognitive processes of the impeding catastrophe that is usually predicted by panic patients in response to benign bodily symptoms of the FFF response- i.e. "I'm going to die / have a heart attack / faint / cause a scene" and so forth. Here we have something else: Relaxation, breathing techniques and distraction is used/taught in CBT for DS – but these are by definition cognitive and behavioural avoidance strategies…… Duh – you could not make it up if you tried. The CBT potentially taught them how to be more avoidant! There was little exploration of previous traumas. When it is there, there is no structured approach to working on the narrative / meaning and the updating of trauma narrative / meaning so that they can move on from their trauma (if relevant – it is assumed to be relevant though – psychometrics don’t suggest severe impact of trauma). In summary, during CBT – patients experience training in how to carry on avoiding upsetting feelings and thinking. Words fail me.

75% compliance is pretty low – i.e. attended 9 out of 12 sessions or more. I'd expect 90% or more for such a brief intervention if patients were engaged - and that's not the patients fault - it suggests there was a significant group that did not buy into this.

From the supplementary material: “CBT specifically focuses on reducing DS and arousal and emotional/behavioural avoidance, enabling people to reengage in activities of everyday life.” How did they assess this post intervention? I can’t see how they did this. In PTSD the PTSD cognitions questionnaire can be a helpful measure. A shift in thinking about how people respond to trauma symptoms goes hand in hand with reduced distress and patient recovery. How come nothing like that was used here to evaluate if the patients actually are less avoidant post CBT? Partly because I fear that their CBT intervention taught them to be more behaviourally and cognitively avoidant – good grief.

Psychiatric assessment at 3 months - process – structured? No mention of using the SCID. Reads more like a bit of a chat rather than robust process. It needed to be robust. Otherwise this is meaningless.

Use of self complete Mini-International Neuropsychiatric Interview (MINI) (no match for a clinician administered SCID) and Standardised Assessment of Personality-abbreviated Scale (SAPAS-SR) for maladaptive personality traits. Pretty much anyone who was irritable, annoyed, upset, distressed or traumatised after developing poorly understood debilitating condition will score 'positive' on this rubbish scale (e.g. > 3):

You’ll get my drift when you read the 8 Q’s:
https://www.nhshighland.scot.nhs.uk/Services/Documents/Personality disorder service/3 Assessment/SAPAS.pdf

This is a questionnaire that at best should lead into a discussion as to how relevant a positive response is – and being impulsive, irritable, a bit of a worrier, need to depend on others, and so forth could all be raised when developing a distressing medical condition…….. that needs separating out otherwise it’s going to provide a high number of false positives/misleading data. But it helps to bolster the view that DS are a problem caused by patients dodgy coping / personality. Lovely.

“58% had SAPAS-SR scores suggestive of maladaptive personality traits” – now that’s pretty leading – if this is turned around it can be said that 42% of the patients had no hint of personality issues – that’s a big chunk of people. Personality disorders are notoriously controversial and are often a consequence of trauma – so complex PTSD would perhaps be a more useful ‘label’ (if one is needed) for the majority of the time – context is all here. And they used a self-report form of this questionnaire (see above) so there is massive scope for misunderstanding / misinterpretation of what is being assessed / asked about and for positive result where no ‘problems’ exist. Personality disorder is usually a lazy psychiatric diagnosis which does not tell much about how a person ended up where they have done (personality wise). i.e. it is not in context or that meaningful for the patient – stigmatising (minimises the impact of trauma and social context and places the ‘disorder’ within the person) rather than being helpful. Again this was not well assessed (and this needs to be). Raised scores on the SAPAS-SR could easily be a consequence of developing distressing condition. Or in part due to deprivation. Or lots of things like autism or brain injury or just being a human. Not to mention the upset as a result of breaches of trust in medical circumstances.

Use of multiple self competed forms - GAD, PHQ, WSAS, Visual analogue scales, CORE, PHQ-15, Global impression of improvement, SF-12, etc. All these subjective measures are open to bias.

DS diagnosis versus epilepsy:
Video EEG? Limitations of EEG? My understanding is that EEG measures electrical activity over the scalp. This is then interpreted as being a measure of brain activity. However, I can’t see how this this assesses deep brain activity away from the surface? My question for my neurology colleagues is: Is it not possible DS are deeper brain disruption as opposed to whole brain disruption in epilepsy? Is that even possible? Frontal lobe epilepsy is often missed by EEG..... I wonder if anyone can comment here?

Me thinks that overall: DS patients have not been well assessed or understood and largely psychiatrised / psychologised. More work is, I think, needed here to actually understand the phenomenon. For example, frontal lobe epilepsy is often missed by EEG…... So, in summery – epilepsy remains a clinical diagnosis – so uncertainty is everywhere. And when that’s present in spades – it therefore must be the patient that is the ‘problem’. It’s a bit weak this tired argument and I suspect lacks much face validity.

From Mellers (2004) (one of the co-authors of the CBT trial) (https://pmj.bmj.com/content/postgradmedj/81/958/498.full.pdf):

“According to Chadwick50 the EEG is “one of the most abused investigations in clinical medicine and is unquestionably responsible for great human suffering”. While a single routine EEG may be normal in some 30% of patients with epilepsy (the false negative rate falls to around 15%, or even less in patients with repeated studies or sleep recordings51) Chadwick was highlighting the problem of false positives. Anything up to 15% of the normal population may have a “non-specific” abnormality noted on EEG. There is clearly a danger both that an EEG may be “over reported”, especially if the request form sent to the electrophysiologist expresses no doubt about the diagnosis, and also that such non-specific abnormalities might be misunderstood by inexperienced clinicians as backing a diagnosis of epilepsy when they do no such thing. This problem is compounded by the fact that such non-specific abnormalities (principally a slow background rhythm) are more common in patients with DS than in healthy volunteers52 and in patients with borderline personality disorder,53 which is common in patients with DS (see below). It should be noted, however, that rigorously defined specific “epileptiform” abnormalities (generalised spikes or polyspike and slow wave abnormalities) are very rare (about 3 in 1000) in healthy people.54,55 The EEG is just one factor that must be weighed up in making a diagnosis of epilepsy that ultimately rests on clinical judgement.” So in summary – plenty room for misdiagnosis / misunderstanding…. Sounding familiar?

So in summary:

• The outcome failed because CBT model they used had no impact on the mechanism causing DS.
• And the intervention failed because it didn’t even target the trauma / panic / dissociation.

This is frustrating and a lost opportunity.

In the commentary by Perez (Harvard):
https://www.thelancet.com/pdfs/journals/lanpsy/PIIS2215-0366(20)30143-7.pdf

"The first question is whether seizure frequency should be the preferred primary outcome measure in clinical trials for dissociative seizures."

So, the research community might move towards smudging the issue and moving towards using more subjective outcome measures – which is not helpful as this will be biased by what you expect the patients to learn / understand during therapy. And as such a trial cannot be blinded to the clinicians undertaking the therapy it ideally needs to involve an objective, primary, real world relevant outcome measure - seizure frequency. That much the CBT research world should have learned from PACE.

His second question re 'one size fits all' is important:

What Perez is saying is that there needs to be subgrouping – and I agree here, for example:

• e.g. DS plus PTSD – identify and treat that (there is a good solid evidence base for trauma therapy) and does that have an effect on DS frequency? That does need to be studied.
• Ditto panic disorder
• Ditto personality disorder (if that is necessary? They probably largely come under PTSD when examined via SCID).
• DS patients with low levels of distress. Now that’s a bit more tricky but necessary as overall these patients are not highly distressed. This will form quite a large group of DS patients.
• DS and the impact of physical therapy – does activity trigger a DS? I wonder if that has ever been studied? Objectively measured would be ideal. I’ve not looked. Their levels of physical disability are really high. Why? What other symptoms do they have? Pain? PEM? It’s absent from the literature but patients talk about it on forums and in responses to online articles.

Studying those might be helpful. If that work is done well with independent assessors pre and post, uses SCID and appropriate psychometrics pre and post interventions using the evidence based model and dose of CBT and so forth it might reveal a lot.

From Perez: "In my opinion, CBT remains an effective treatment for dissociative seizures. I have witnessed how some patients with dissociative seizures can benefit greatly from a CBT approach that equips the patient with new psychotherapeutic tools, which in certain individuals can lead to robust and sustained clinical improvement." Me thinks that is called eminence based medicine. We can't role out ineffective CBT to everyone without knowing the subgroup of patients this does work in - if at all - based on what a chap at Harvard says so. As a psychologist I suspect his view is impacted by his selective recall of one to two patients who improved a lot - but were they cured? Were they largely PTSD anyway? Were these few patients misdiagnosed? CBT can help with tolls to cope well - but that was not what this trial was about. And it failed in that endeavour too - no real world, significant reduction in distress.

Joan Crawford
Counselling Psychologist
UK

 

Yes, but it can, I think, and for sleep patterns it should be well known (I should check it out again though!), say from here: Thalamic dual control of sleep and wakefulness. Gent et al 2018.

I currently cannot remember well what I knew, but this short article with new insights I found interesting: Thalamic control of functional cortical connectivity. Nakajima and Halassa 2017

I think such questions are very helpful, even if they could not be answered by now.

I havn´t delved into DS, but it seems that they are compared, by psychiatrists at least, with classical seizures, and should therefore be comparable. But meanwhile I doubt that there has been made any halfway reasonable attempt to assess the situation in terms of whats going on in the brain, although many isolated detail is already known, so there is no obstacle to think about it.

In epileptic seizures there is too much action potential cummulating in unstructured firing of large amounts of nerve cells. In DS we see a kind of ticks with any repetition in movements or whatever, wasn´t it? The thesis then is that this (amount of somehow unstructured ?? action potential) can be influenced by CBT, and hopefully may lead to further success when be able to somehow better understand adverse experiences asf. which "obviously" underlie these seizures. (And sometimes it sounds even as there would be hope for classical seizures.)

More plausible though is that some structure, probably in the thalamus or in addition in the basal ganglia, has come out of proper function, and induces these "seizures" by firing in an isolated circuit. This might or may have been triggered by adverse experiences or whatever, but the question is, if not such a structure is too autonomous as that it could be simply reversed by a "counter experience". A further question is, if there is not a predisposition which makes people vulnerable to any experiences which rather are not that adverse or whatever. And finally it simply could be without any detectable experience, belief, or whatever.

I guess thalamus and basal ganglia will be shown to be key in many not already understood conditions, including all the variety with unspecific symptoms.

 

Thanks for that when I get a chance I'll look it up Do you happen to come from a medical / neurology background per chance?

that's good to know. I suspect by comparing those currently labelled DS and epileptic the mind-set of 'real' and 'not real' seizures has developed and taken root for a long time. Which has perhaps hobbled the other possibility of epileptic seizures and 'other brain dysregulation NOS' So, I suspect this has been poorly researched as it has been left largely to the psychoanalysts / psychodynamic practitioners to continue Freud's work (i.e. anything medicine doesn't understand is all in yer head / stress / catastrophisation etc) Sigh.

I'd picked this up about classical seizures when I read in the past about DS. I could find no evidence in the literature that reducing stress via psychotherapy reduced the frequency of classic type epileptic seizures. There is a possibility as many pw Epilepsy will cite stressors including psychological stress as aggravators/triggers but tbh when I've worked with pw Epilepsy there has been such a wide range of issues that they want to cover it's not been a focus. Nor do I think that this would have much face validity.

Bw
Joan Crawford
Counselling Psychologist

 

No, I haven´t, instead I have a philosophical and carpendrical background, and this combination makes that I am interested in nerves with all their axons. If I may say this, the carpendry has given me a good idea, to put up nerves (their connections rather) again (which implicates that there has happened a breakdown from two or even three trigger events).

Yes, this obviously has happened, and still happens. I may have expressed myself here a bit unclear though, I mean there is already many detail in general known, which should allow for guesses on issues and specific issues, e.g. on DS. Admittedly it might be still difficult, and might be expansive. It is probably easier just to stick to psychodynamics. And this way it may even be somehow hidden that the consequences can be a disaster for patients.

No, the whole approach has not much face validity, already not in other somehow softer diseases, which might be not due to an inert failure but only to a sever dysregulation.

It is not that everybody would be upset by trials based on psychological interventions, they only must be honest, including and especially when there is not much face validity. It is also much better to say to a patient: "Sorry, we don´t know." than to convey that the patient in fact doesn´t face their problems (which is especially laughable (and can also be offend, sadly) when you suffer on and on with pain and have to deal with operative inabilities to do anything for your very own life´s sake).

I ever wondered why there hasn´t been any attempts to identify specific traits when it comes to investigate specific diseases which are presumably psychologically driven. This is not treating it appropriately, right? So it doesn´t surprise me that there is no specific focus in pwE, and more likely is that the stressors are due to a perception which is already altered by the upcoming seizure.

 

Thanks for your input.

I'll try and work out the system for quotes etc. I hope this works

This for sure is the problem. Why so hard to admin and say within medicine? Causes so much trouble :-(

Bw
Joan

 

DS may have slipped from the mus category because it is a poster child for Functional Neurological Disorders. No longer medically unexplained because it is now explained as FND. They call it NES, non epileptic seizures and NEAD nonepileptic attack disorder and it is mixed in with things like irritable bowel syndrome and interstitial cystitis in research into FND. They will have, say, 60 patients with a mixture of these problems lumped in together as subjects.

Jon Stone worked with Michael Sharpe on the first research done in Edinburgh but has now blossomed on his own. He sees his research as proving that FND, blatantly described as the new name for conversion disorder, the modern name for hysteria on research papers, is a real disease category which can be demonstrated by physical signs. The problem is that all the research is designed to "prove" the diagnosis rather than seek the biological facts.

The answer to it all, from seizures to diarrhoea is .... CBT.

I get very angry and fearful. Any sign for neurological disease can now be passed off as FND -which is classified as a mental disorder - and there is no hope of research into the true problems.

 

I've been doing a bit more background reading and I found this positive and informative website:

https://fndhope.org

From the CODES trial paper I was struck by how highly physically debilitated and disabled the participants were. It made me think about what other symptoms they might be experiencing and whether this had been studied / distilled out?

I was struck when I looked at the symptoms list here: https://fndhope.org/fnd-guide/symptoms/ just how widespread a host of debilitating symptoms they have. So, it's not only DS and increased distress: it's way more than that.

I suspect patients want the totality of their experiencing to be recognised and treated before they will consider themselves recovered / cured. This is what I'd thought when I've worked with a few folks with DS in my clinic at The Brain charity. I helped the to pace themselves and cope and mange their mood and debility. All helpful but not going to cure anyone.

So much more to all of this than DS. The focus on psychological trauma seems to be overdone massively. It's clear people develop DS / FND without a trauma history. Being inferred that your symptoms are largely psychological much in itself be stressful and distressing - traumatic. Especially if it makes zero sense to you. When pwME have experienced this they can feel as though it is an assault on their sense of self - which can be as traumatic as a physical assault. Really harmful.

Interesting research focus too: https://fndhope.org/fnd-research/researcher/

Research Priorities

FND Hope has surveyed FND patients to identify areas that are priorities for advancing research.
These include the following:

Treatments for FND, including

efficacy of such treatments,
tailoring of treatments to patient symptoms
post-treatment (long-term) efficacy
relapsing/remitting nature for some patients/symptoms
Outcome measures for FND Treatment
Neuroimaging
Biomarkers
Pharmaceutical treatments
All risk factors
Genetics/epigenetics

That kinda looks familiar

Notable absence of more "CBT away yer seizures" kinda research Seems clear that this is not what the patients want and is largely not helpful.

Bw
Joan Crawford
Counselling Psychologist

 

It is scary that this poor quality science has taken hold. I'm not surprised that you are angry. It's institutionalising and approving/prioritising one way of thinking that doesn't correlate to how patients see their experience. Hugely frustrating and upsetting. Please see my post above re FND hope. It seems clear that the movement of travel is away from unhelpful CBT approach to more biomedical based investigations and research. But that's going to take time.

In the meantime, arming ourselves with knowledge (patient and clinicians) and disputing the CBTers claims will do a lot of good. Sticking to good quality science is the way to solve / understand this (and ME). Objective primary outcome measures from clinical trials are a must. These must be relevant in the real world to patients and demonstrate object improvements e.g. return to work or equivalent, reduced social security benefits, improved exercise capacity, cognitive functioning and so forth. Perhaps there is a place for neuropsychological and QEEG testing too. Questionnaires have their place as secondary outcomes. And these need to show big improvements (large effect sizes) to demonstrate anything like healthy functioning. Not the small/modest/consistent ones in the Wessely school CBT trials to date for ME and DS. That should be expected given the unblinded nature of the trial methodology. That needs repeating a lot until it is understood by researchers, research funders and ethics committees etc.

Joan

 

LOL

https://twitter.com/user/status/1266145721473888256

 

I'm really not sure how people can seriously argue this is not a belief system given this is what makes it into published literature. What doesn't make it is even less credible and here we are literally discussing "I have witnessed".

Arguing that personal anecdotes should be considered more reliable than the experiment being discussed in the very paper that found the experiment to have null results as expected. There is no other field of science where this exists. In fact this is a literal feature of pseudoscience and belief systems.

And criticizing this as obvious bad science is twisted into being anti-science. Which is straight up bonkers.

"In my opinion", I can't get over the fact that this is promoted as credible science. Beyond absurd. Completely FUBAR.

 

it is the epitome of what Brian Hughes called "eminence-based science." If treatment should be based on Dr Perez personal opinion, there's not much need for studies.

 

Even though the Perez article is a commentary (on Goldstein et al.) and not a peer-reviewed article, one would hope that Lancet editors would not want this "In my opinion" stuff in their journal(s).

 

You'd have thought that a commentary would be peer reviewed? Am I being niave here? Just cos the chap is at Harvard doesn't mean he don't talk nonsense x

 

In my opinion kinda needs to be preceded by a lot of supportive data and evidence base. Not kinda like 'I think it is so because I believe it' Otherwise why consult a medical professional? Why not seek out the advice of a priest?
X

 

I'm totally with the amazeballs Baffles my head

Did no one at the lancet get the criticisms re PACE. What that passed them by?

X