By David Tuller, DrPH
For decades, Kumar & Clark’s Clinical Medicine has been a standard textbook for medical education around the world. Last month, Elsevier pubished the 11th edition. The miniscule section on what it calls “chronic fatigue syndrome/myalgic encephalopathy” is pathetic. This section is in a chapter called “General Hospital Psychiatry,” promotes “psychological symptoms” as a core component of the illness, and recommends the fraudulent PACE trial as “further reading.”
(The authors offer no explanation for their decision to use “encephalopathy” rather than the much more widely accepted term “encephalomyelitis.”)
Patient advocates have had concerns about this matter for a while. A petition “to request updating of the description of ME/CFS in Kumar and Clark’s Clinical Medicine textbook,” based on the 10th edition, was posted on change.org more than a year ago. It has racked up more than 10,000 signers. (An article on the ME Association website provides more details.)
Elsevier responded last February, noting that “the book’s editors are aware of the petition, and of the strength of feeling held by many ME/CFS patients and their friends and family members about the way the condition has traditionally been approached within the medical profession.”
In its response, Elsevier further noted that, for the upcoming version, “the editors have worked with the specialist chapter authors to produce content which addresses the concerns of patient groups, whilst being based on the range of published literature and contemporary treatment approaches within the field.”
Yeah, right.
The 11th edition does feature some modest changes corresponding to some of the requested changes. It now includes a mention of “ME”–albeit the wrong ME. It drops graded exercise therapy (GET) as a recommendation—yet it highlights the PACE trial as a reliable source of information, even though that piece of crap purported to prove that GET was effective. Etc.
In the new edition, the discussion of CFS/ME appears in a section of the General Hospital Psychiatry chapter headed “Medically Unexplained Symptoms and Functional Neurological Disorder.” In the text, these two groups are lumped together as MUS/FND, with general observations intended to apply to any clinical entity falling within the parameters of these categories. (In reality, FND is a subset of MUS.)
One paragraph is focused solely on CFS/ME, identified as one of several kinds of MUS. Here it is:
“Although several studies have demonstrated abnormalities in endocrine, neurological, and immunological parameters in patients with CFS, understanding of potential biological mechanisms underlying the condition remains poor. Historical approaches that have suggested that the disorder is ‘all in the mind’ are unhelpful and stigmatizing, and prevent the development of a beneficial therapeutic relationship between doctors and patients. A more helpful approach acknowledges the presence of both physical and psychological symptoms, with no assumptions about the underlying aetiology.”
This paragraph is full of misrepresentations. There are obviously far more than “several” studies demonstrating “abnormalities” in multiple domains. (What these studies ultimately mean is another discussion.) As far as “historical approaches,” it is ironic that the textbook suggests the “all in the mind” approach is a relic of the past even as it touts the PACE trial and embeds the illness within the chapter on “general hospital psychiatry.”
Finally, it would be nice if “no assumptions” were made about the underlying etiology. But that is obviously not what has happened with this illness.
The presumption of the biopsychosocial fantatics has always been that CFS, as they call it, was solely caused by unhelpful illness beliefs, which led to sedentary behavior, which led to deconditioning, and on and on. The two interventions—graded exercise therapy and cognitive behavior therapy—were presented as addressing these concerns and therefore potentially curative.
Whatever has been claimed more recently, the only role in this schema for “bio” was the notion that a viral infection could trigger the entire cycle. Beyond that initial event, the perpetuation of symptoms was said to arise solely from problematic and dysfunctional patterns of thought and behavior.
In any event, no one reasonably disputes, or has ever reasonably disputed, that patients experience “psychological symptoms.” I mean, why wouldn’t they feel depressed and distressed and anxious, given that they have a complex illness that no one seems to understand? The issue is not whether they experience such symptoms but whether psychological and associated behavioral factors are the root cause of their illness. This paragraph reads as if that debate were non-existent.
The subsequent sections are headlined “clinical approach to MUS/FND,” “communication of a diagnosis of MUS/FND,” and “approaches to treatment.” Not surprisingly, given the bias inherent in this chapter, there is no mention of the updated 2021 guidelines for ME/CFS from the National Institute for Health and Care Excellence, which rescinded recommendations for GET as well as for cognitive behavior therapy presented as anything other than supportive. Instead, these paragraphs in the textbook are full of biopsychosocial blah blah, like this:
“Delivering and explaining a positive diagnosis of MUS/FND is the stepping stone towards a successful management plan that may include guided self-help, CBT and input by several other members of a multidisciplinary team (e.g. physiotherapy or speech and language therapy, depending on the nature of the FND symptoms). Recovery depends on positive patient engagement with the process.”
The last sentence is classic in how it appears to lay the blame squarely on patients for failure to attain “recovery.” In this framing, if the treatment doesn’t work, the fault is clearly due to the patient’s “negative” engagement rather than to an inappropriate clinical approach.
I hope the petition to Elsevier gets a reboot based on this awful update.
**********
*As a side-note, the MUS/FND section claims that FND accounts for half of new neurology consultants. This is a ridiculous and untrue claim. The most ardent FND experts have regularly stated that 16% of new neurology consultations involve FND. And that figure itself was an exaggeration. The study used as the source actually found that 5.5% of new outpatient neurology patients were diagnosed with conversion disorder symptoms–i.e. FND, per later nomenclature–as several colleagues and I have pointed out in a published letter. I know of no subsequent research that has found a 50% rate among new neurology consultations.
‘Yeah Right’ seems to cover it.
If my illness was psychological I would never have been ill.
Elsevier needs to hang its head in shame. What a load of utter garbage!
Many thanks for shining a light on this, David. Inherent bias compromising patient safety in such a widely read medical textbook is hugely concerning.
More and more I find that I’m having to regularly remind myself that some medics are good people.
I’d be interested to know if the MUS/FND section is new to this edition and whether the FND prevalence claim is too. (With regard to the latter, perhaps that’s what a self-fulfilling prophecy has caused by hyping of FND prevalence leading to doctors seeing everywhere they look? Was any reference given for that? I assume not. ) I imagine that FND sufferers won’t be too impressed by their illness being housed in the psychiatry chapter when leading FND proponents insist that FND is not in the patient’s head and that psychiatric/psychological issues are not a cause and only a risk factor/ of relevance to some patients. Has there been any protest from that direction, I wonder?
If recovery starts with patient engagement, how come so many people with FND are being diagnosed and discharged and/or are experiencing badly delivered diagnoses? This is a backwards step from the editors.
CT – I will post this in the FND Hub I’m in when I can and it’ll be interesting to see what the reaction is there although many of the members are short of spoons too. In my albeit limited experience the FND Society themselves are not great at patient engagement (I did not request a ‘moderated’ conversation with anyone so I have no idea why Prof Carson thought I had) but you might be interested to know that Stone is now saying that the term ‘functional’ is still being used because it’s the ‘least offensive’ term available.
I wonder what the authors of the FND is a Feminist Issue paper think about this. Not one of them bothered to answer the relatively simple questions I posed in my initial rapid response to their paper and my second response didn’t get published. Likewise Stone silenced himself when I told him that women with rare conditions are being misdiagnosed with FND on the basis that they don’t have Parkinson’s (poor clinical reasoning) and then told that questioning the FND diagnosis proves that it’s the right diagnosis. It doesn’t.
PJM – I suspect that ‘functional’ has become an extremely offensive term to very many people because is has meant them being neglected or shown the door to reduce healthcare spending. My guess is that repeatedly stressing the cost of ‘functional’ patients to healthcare services or the draining effect they have on them in introductions to papers about ‘functional’ illness likely didn’t help with that.
Follow the money. Who benefits from M.E. sufferers being denied benefits and being classified as psychosomatic?
I would add:
Other patients obviously need to decide for themselves which doctors (if any) they’re content to put their faith in, but I wouldn’t trust doctors who don’t correct paper/s they’ve authored or co-authored that have been clearly shown to need correcting because, to me, that’s putting their reputations and/or careers ahead of medical accuracy and patient safety and if doctors can do that in one area of their work then I suspect they could do it in another. I suppose at the end of the day we all need medical services and are limited in choice so have to hope or pray that our doctors aren’t driven by self-interest, but if anyone suggested ‘functional’ illness to me again I’d be out of the door like a shot, even if it meant receiving no care for that issue. ‘Functional’ isn’t just offensive to me, it’s also highly dangerous in my book.
CT and all – ‘functional’ forms part of the overarching vestibular disorders diagnostic Venn diagram, with ‘structural/cellular’ forming another and ‘psychiatric’ being the third. However we know from various papers that ‘functional’ still means ‘hysteria’ in the minds of some doctors and although hysteria (which doesn’t infer malingering, not that that is very helpful to patients unless they know this) is no longer in DSM, FND is. There are various different theories about why the term ‘functional’ was chosen, one being that it maps onto an understanding of modern imaging techniques, avoids a pointless conversation about brain and mind and is, apparently, ‘easily used with patients’. Yeah, right (again). When I read Stone’s Bare Essentials; functional symptoms in neurology paper I dubbed it ‘deliberately deceptive, dangerous dumbing-down double Speke’ and not much has changed (at the time I thought ‘hysteria’ was out of the picture for good) although I know some people/doctors find it a useful term. However I mentioned the term ‘functional’ to a lovely neurologist I met at a BC (Before Covid) Migraine Action meeting and he said ‘Ugh. Blame the patients, it’s cheaper’ and if you mention diagnostic odysseys to medical students with an interest in rare conditions they tend to roll their eyes and say ‘functional’, since they know that our odysseys can be derailed by this term, as they can when people are told that if they don’t accept a ‘conversion disorder’ diagnosis their primary care will be withdrawn. Stone is now saying that ‘functional’ is the least offensive term available which is hardly a ringing endorsement for continuing to use it.
Lumping everyone with M.E./CSF under the FND brolly smacks of empire building and is unlikely to empower patients to better health. Plus it could be highly detrimental to scientific research too, both for people with a current FND dx and for people with M.E. and many other conditions which can impair our vestibular/visual systems. It’s also another attempt to label a condition which mostly presents in women as being psychiatric which is every level of wrongness and probably several others I haven’t figured out yet.
And the ‘territorial claim’ commentary from Kanaan that accompanied the FND Subtypes paper is still making me shudder, metaphorically.
Let’s hope the editors see sense before too long and, as ever, many thanks to David for his impressive work in bringing all this to light and speaking truth to power.
I agree the textbook made significant errors, but not for the same reasons as you do. The textbook is indeed incorrect to lump MUS and FND together as “MUS/FND.” FND is classified separately as functional neurological symptom disorder in DSM-5 and dissociative neurological symptom disorder in ICD-11. MUS, on the other hand, refers to non-neurological symptom presentations (now categorized as bodily distress disorder in ICD-11 and somatic symptom disorder in DSM-5), such as fibromyalgia, IBS, interstitial cystitis, non-cardiac chest pain and yes, ME/CFS. As you mentioned, their claim that FND is 50% of neurology visits is incorrect. This seems to come from this conflation with MUS as the literature reports MUS makes up 25-50% of primary care visits. The conflation of MUS with FND has been addressed in the literature and the editors should correct this mistake: https://www.cambridge.org/core/journals/cns-spectrums/article/conceptual-field-of-medically-unexplained-symptoms-and-persistent-somatic-symptoms/EC7A7F21781AD242B88AC83FF92D556E.
Regarding ME/CFS, the textbook’s framing is not “biopsychosocial dogma”…it reflects the consensus in clinical medicine. The editors likely chose “encephalopathy” over “encephalomyelitis” because there is no evidence for ongoing CNS inflammation (“-itis”). The term “encephalomyelitis” is only preferred by patients because it makes the condition sound more serious (in their opinion), but it completely misrepresents the condition.
ME/CFS shares many of the same characteristics as other functional disorders (acute/subacute onset often after a physical or mental stressor, fluctuating symptoms often moment to moment or day to day, and disability level out of proportion to exam findings/pathology). Also, it is highly comorbid with them and responds to similar treatment frameworks. People who have recovered present the same as those who don’t and they almost always treat it as a functional disorder. Rejecting psychological and behavioral contributors because they’re seen as invalidating is itself very common in people with somatic symptom disorder.
If there was a disease process underlying ME/CFS it would have already been found. No matter the cause, organ damage/disease is quite easily identified with current tools – clinical exam, routine bloodwork, and diagnostic imaging. There is way too much emphasis placed on the findings in the biomedical research. They are often contradictory and unreplicated with very poor methodology. No findings are said to have clinical relevance because they often don’t make sense with the patient presentation. Perceiving clinicians as incompetent and malicious because they acknowledge the clear psychosocial factors that led to the development and maintenance of the condition is just a projection. Unfortunately the ME/CFS community is unlikely to see any progress until they can acknowledge that their symptoms are not signs of damage/disease, psychosocial factors are involved in their illness and functional disability, and that none of this is their fault and it is their responsibility to recover (with guidance and support of course!).
MUS: Dear lovely doctors, medical knowledge is incomplete, especially in conditions that mostly present in women and are #medically under researched symptoms #medically under funded symptoms. So it is understandable that you can’t explain them or explain why symptoms can fluctuate but that doesn’t mean we’re the cranks. Labelling us as heatsink patients is not OK either. See ‘MUS’ or ‘DEN’?
Emma J Reinhold
British Journal of General Practice 2017; 67 (657): 156. DOI: https://doi.org/10.3399/bjgp17X690077 for further information.
It’s also well worth reading Dr Lisa Steen’s posthumous blog about the wilderness of MUS in the BMJ. I got to the part where she mentioned symptoms that are hard to explain and thought ‘oh no, here we go again’
Mr Grin will discover just how tunnel his vision is fairly soon.
So, if there was a disease process underlying migraine or bipolar disorder we would have found it by now?
And the fluctuation from moment to moment in narcolepsy/cataplexy excludes such a disease process? (Which of course it doesn’t because we know they are due to a deficiency of orexin.)
Bob Souhami pointed out the ‘functional’ is just a cover for ignorance.
I was Mike Clark’s registrar at Bart’s. How badly things have strayed from the promise of a medicine based on reliable evidence and clear thinking we had in the 1970s.
I’d say there are huge patient safety issues with ‘non-cardiac chest pain’ being categorized as a “functional somatic syndrome”/ “somatic symptom disorder”/”bodily distress disorder” . I’ve raised this issue before. In this 2020 paper -https://www.sciencedirect.com/science/article/pii/S1470211824033694 in a themed edition of a journal of the Royal College of Physicians where the theme was functional disorders, the authors appeared to conflate non-cardiac chest pain with cardiac syndrome X and non-specific chest pain. They seem to have been quite rightly ticked off by two cardiologists and a trainee in a letter to the journal’s editor –
https://www.sciencedirect.com/science/article/pii/S1470211824033591?via%3Dihub. This illustrates the problem of the MUS construct and, in my opinion, an unscientific view that because no biomedical/’organic’ cause has been found to date for a set of symptoms that one can’t exist and the cause must therefore be mind or brain related. As I understand it, patients with microvascular angina/INOCA – predominantly women – historically had their debilitating chest pain dismissed as psychosomatic/’functional’/non-specific chest pain/non-cardiac chest pain until a biomedical cause was found for it. It looks to me like some doctors failed to keep up to date such that they still thought that cardiac syndrome X was ‘functional’ / non-cardiac many years after a biological pathology had been established. Whose to know there aren’t other biomedical/’organic’ causes as yet undiscovered for other presentations of so-called non-cardiac chest pain? I think people are badly mistaken if they think that we are anywhere close to fully understanding the workings of the human body, or anything else in our universe for that matter.
Apologies for the error in my last comment. The paper I mentioned above was published in 2021, not 2020.
“If there was a disease process underlying ME/CFS it would have already been found.”
It has been found. Just because you are ignorant and won’t do basic research doesn’t mean the evidence doesn’t exist. We’ve known the immune system was dysfunctional since the 1980s and the findings have been replicated over and over through the years. Yet you, a physical therapist, want us to believe we can get better by just changing our attitude and doing some exercise. Apparently you know better than the immunologists that study the disease in labs around the world; maybe our T, B, and NK cells just have false illness beliefs and need to have a better attitude.
Next the physical therapist might try to tell us he can cure cancer too. Oh, you don’t think ME/CFS is on the level of cancer? Three studies (Levin 1998, Jason 2006, Chang 2012) show ME/CFS patients have elevated cancer risk and/or die from cancer considerably younger than the rest of the population.
But I’m not going to enumerate all of the evidence that ME/CFS is a disease of the body. That would take a book. There is so much out there, you should have found it by now, but since you haven’t, what does that say about you? Thanks for making yourself an example of the Dunning-Kruger effect.
CT – I appreciated your comments about the economic burden of FND/Conversion Disorder/Hysteria (or whatever they are calling it these days) and this was something I discussed with the admin of the old PPPD and Life group (which closed due to the high level of suicide ideation amongst some of the members) since there can be a huge cost – emotional and financial – involved with being a group admin and this has not been captured in the financial burden of FND papers. Neither have the costs involved with setting up and running the many charities/not for profits there are re FND so that needs addressing too. I did some work for Genetic Alliance UK on their hidden costs of rare conditions studies which were qualitative and quantitive so gave a much clearer overview of all this. What I’d also like to see from the FND Society is a deep dive into how costly it can be (in terms of time and money) to get a misdiagnosis of FND recorded officially.
Mr Grin – do you think doctors and other health care providers have a duty of candour to tell their patients/clients with FND that FND is in DSM? Is there any evidence to suggest that questioning the FND diagnosis proves that it’s the right diagnosis?
Jonathan Edwards – thank you. I hadn’t come across Bob Souhami’s writing before and now I have 🙂 As a person with familial Mal de Debarquement Syndrome/vestibular migraine (currently in remission, thank heavens) I am interested in the genetics involved, including between MdDS/migraine and connective tissue conditions. It’ll be interesting to see if there is a genetic/genomic factor involved with FND (maybe there already is and it’s been identified but I’ve missed the paper about it – there are so many of them.)
Professor Edwards – (It’s Dr. Grin by the way) Although we don’t know everything about the causes of migraine, bipolar, and narcolepsy, we’ve identified several underlying mechanisms which has led to several pharmacological treatments (CGRP receptor antagonists, triptans, sodium oxybate, mood stabilizers, etc.). Additionally the clinical presentations of these conditions make sense when we look at their underlying mechanisms and treatments. Many conditions have fluctuations in symptoms (narcolepsy with cataplexy as you mentioned) but symptom fluctuations in functional disorders present differently. We look for evidence of internal inconsistency, changes with attention, and preserved automaticity in functional disorders. As an expert in RA, I’m assuming you know that ME/CFS is very different from RA and other rheumatological diseases. Internal inconsistency is present in the symptomatology of ME/CFS. Some examples include reporting significant memory problems but able to remember all the things they can’t remember, not having enough energy to chew and swallow but can be on social media, and experiencing PEM from one physical/mental task it not another that clearly has a higher physical or cognitive demand. I’ve seen your responses to several topics on the science for ME forum, and you often seem to talk about ME/CFS as a functional disorder without saying the term and also denouncing the term and category. A good example is your comments on the Maeve thread where you perfectly described what happens with functional swallowing symptoms in FND without using those terms. I think we agree on more things than not.
CT – there are many causes of chest pain other than cardiac which can fall under GI, psych, MSK, etc. – that’s why differential diagnosis is important. Even us PTs learn how to do this in our training. For some people it is very clearly is not cardiac, like same pain reproduced with palpation to certain muscles or certain movements. The diagnosis of non-cardiac chest pain isn’t harmful or a patient safety issue – it’s very common. It does highlight the problem with the term “MUS” though because there is often a cause for the non-cardiac chest pain other- anxiety, acid reflux, muscle spasm etc and a diagnosis of “non-cardiac chest pain” or “medically unexplained chest pain” tells us nothing and does not inform treatment.
CCS – I’m very familiar with the historical and recent research on ME/CFS. I treat people with it and have read a lot on it. The disease process of ME/CFS has absolutely not been found. Many hypothesis have been proposed but so far minor biological differences have been found that cannot explain the clinical symptoms and several medication trials targeting proposed underlying mechanisms have failed when put to placebo. Those placebo trials actually show ~30% of people in placebo arm experienced long term improvement in symptoms. Your comment is a perfect example of what I talked about in my post – “want us to believe we can get better by just changing our attitude and doing some exercise”. I never said that and don’t think that. Functional disorders are real, serious, very disabling, not a persons fault or due to some character flaw, and are deserving of treatment.
PJM – Good question. I would not say providers have a duty to tell people with FND that it is in the DSM anymore than telling people with Alzheimer’s and other neurocognitive disorders, narcolepsy, obstructive sleep apnea, etc that their conditions are in the DSM. Do you think providers have a duty to tell patients with these other diagnoses that the diagnosis is in the DSM? If so, why? I think there is a lot of misunderstanding about the DSM. It is just one diagnostic manual. FND also has criteria in the ICD-10/11, and various subtypes have clinical criteria established in the literature (functional movement disorder, functional seizures, PPPD, and functional cognitive disorder). Personally I mention the DSM often when discussing the diagnosis with patients because there is nothing wrong with it and it’s not the only source used for diagnosis. There’s no evidence that questioning the diagnosis proves the diagnosis is correct. It’s common for people to question it because of outdated information, misinformation online, and internal biases, but that has no diagnostic value. People question many diagnoses all the time for various reasons.
I know from personal experience that there are other causes of chest pain apart from cardiac ones. When visiting my GP once about a different issue, they happened to mention that any chest pain was a red flag that needed investigation. I told them that I had had chest pain with exercise a couple of times but I stressed that I didn’t believe that it was cardiac in origin. They referred me to a cardiologist – better safe than sorry I was told – who sent me for a heart scan and I was put on blood thinners as a precaution while waiting for that. I was also prescribed a proton pump inhibitor to protect my stomach which had played up for years. I firmly believe that I reacted adversely to one or both of those drugs because I experienced alarming neurological symptoms which went away when I stopped taking them. In relation to those neurological symptoms, I was seen first by a neurosurgeon and then by a neurologist. The consultant neurologist told me I had FND and directed me to the neurosymptoms.org website. When I finally had the heart scan – investigations can take a long time coming with the UK’s NHS – it showed that I had a hiatus hernia. That didn’t surprise me at all and it fitted perfectly with my symptoms. People may be aware that hiatus hernia has been dubbed “the great mimicker”. Was my GP wrong then to take the action they did? Was the cardiologist wrong to request the heart scan? I don’t believe so. I think they were both acting in my best interests. The person who was wrong in my book was the neurologist who attributed an adverse drug reaction to FND.
While my chest pain was found to be non-cardiac (as I thought all along), a few years ago I witnessed at close hand a patient being denied proper investigation for severe debilitating chest pain that was almost certainly cardiac in origin, and that denial of thorough investigation at the appropriate time not only caused them to suffer needlessly but also meant that their care was badly delayed for another serious health condition. So I maintain that labeling people with non-cardiac chest pain without proper investigation can be harmful and a patient safety issue, and I can imagine the distress caused to all those poor women with microvascular angina who, prior to a biological cause being found, had it put down to psychological problems by medics who perhaps believed that what they knew was all there was to know.
No, you are not “very” familiar with the research if you think ME/CFS is a functional disorder. There is no quality research that backs up your claim. There is substantial more research that contradicts your claim. You misrepresent the evidence, and advertise that you can treat CFS with physical therapy. That makes you a charlatan.
I’d add that I see no need for a label or diagnosis of “non-cardiac chest pain” in the field of cardiology. To my mind, patients should be thoroughly investigated to exclude known cardiac causes of their chest pain and then properly screened for other potential causes such as hiatus hernia, other GI problems, muscular issues etc. If an alternative cause is found then they can be dispatched to the relevant specialty for care. If no alternative cause is found then I think they should be described as having unexplained chest pain and remain under the care of the cardiologists with the diagnostic door left wide open. To label them with “non-cardiac chest pain” is to shut that diagnostic door and risk subjectivity in their medical management. The term medically unexplained symptoms (‘MUS’) has unfortunately been highjacked as a medical shorthand for ‘psychosomatic’ and wrongly used to convey that as a diagnosis. If it had not been then it could have been employed as a legitimate and worthwhile adjective (not diagnosis) for symptoms that were yet to be explained. Far from telling doctors nothing, it could have served to remind them that the diagnostic case hadn’t been closed and the patient was still suffering and in need of help. Then when medics with greater knowledge or diagnostic skills came by, or when research and medical knowledge moved on, those patients could have been the first to benefit.
Who are you to say that the immune system dysfunction present in ME/CFS could not explain its symptoms? I’m so glad we have a doctor of physical therapy here to explain how the immunologists are wrong. By that logic, SARS-CoV-2 shouldn’t cause serious disease either. It’s just a microscopic particle that’s not even alive. COVID-19 must be FND, doesn’t matter that it can be fatal, that’s immaterial. An unalive microscopic particle causing fatal disease? Mass hysteria I guess. There were people denying HIV/AIDS right as people were dying from it. It wasn’t a disease, but a punishment from god they said. If ME/CFS is an FND treatable by physical therapy, then homosexuality is a mental illness treatable by psychotherapy. One would think someone like you would be more open minded, but no. Just full of arrogance in peak form.
I would like to point out to the commenter above that if the conflation of MUS with FND (or FND with MUS) is wrong and the editors of the textbook being discussed in this blog need to correct an apparent claim (I haven’t seen it) that FND makes up half of neurology consultations/visits, then he may like to consider the very many papers (more than 50) by FND proponents that I’d say also need correcting for conflating FND (post the changes to its definition/diagnostic criteria) with MUS in a similar way by the papers’ authors citing the Stone et al 2010 paper that looked at prevalence of unexplained symptoms in neurology clinics (from before the FND criteria changes, see here -https://www.sciencedirect.com/science/article/abs/pii/S030384671000171X?via%3Dihub) to either evidence that FND cases (post the criteria changes) make up around 16% of new neurology consultations or that FND is second most common with respect to that, or both. If and when those papers are all corrected, then perhaps I could be persuaded to take FND proponents a little more seriously.