Stephen Ralph on Psychiatry, Behçet's, ME/CFS and Misdiagnosis

The achilles heel of liaison psychiatry

Stephen Ralph DCR(D) Retired.

30th March 2013

Hello there,

In recent years I have been considering the reliability of the whole “CFS/ME” diagnostic process.

From personal experience I have encountered numerous doctors who failed to possess the detailed specialist knowledge they needed to make a diagnosis of Behçet’s disease at both GP and specialist level.

From personal experience I have learned that standard blood tests or even CT/MRI scans or indeed other diagnostic tests such as endoscopy can and do fail to detect a complex clinical disease present in a patient.

I have no doubt that there is a diagnostic black hole between the insufficient knowledge of the doctor and pathologies that are not detectable by the basic tests they choose to request which produce negative results they then choose to rely on.

The diagnoses of “CFS/ME” and now Somatic Symptom Disorder have in my view been deployed by liaison psychiatry to exploit that black hole.

Once a diagnosis has been made, that diagnosis is presumed to be accurate by subsequent doctors but in reality there is no standard of diagnosis from one doctor to another which means that the whole diagnostic system – especially for complex clinical presentations – is a total lottery.

The system to challenge a given diagnosis has not been changed in decades.

In the UK a patient has a right to ask for a 2nd opinion but there is no guarantee that the doctor who gives a 2nd opinion will have sufficient knowledge to correctly assess a complex clinical presentation where the usual round of simple tests come back negative.

And, having been given a first opinion of “CFS/ME”; the doctor who considers that patient for a 2nd opinion already has a subjective view of what could be wrong with that patient because they have been re-referred by a GP who will give a medical history that may lean towards a CFS/ME diagnosis because the GP has insufficient knowledge to write an accurate 2nd opinion referral listing all the relevant symptoms that could add up to a rare disease such as Behçet’s disease.

In my own case as an example, my GP had no appreciation that my episode of Epididymitis was relevant to a possible case of Behçet’s and so this issue was not referred to when I was sent to another out of area doctor who formed that 2nd opinion.

With regards to “CFS/ME” a GP or a psychiatrist or a general rheumatologist will give the patient a diagnosis based upon the repeated reporting of a set of “invisible” symptoms over a period of months.

At present, “invisible” symptoms are being ascribed as “medically unexplained” or as a sign of somatisation.

The doctors who make these diagnoses are not specialists in rare and complex diseases such as Behçet’s disease where there is a significant crossover of “invisible” symptoms.

In the case of Behçet’s disease the bulk of Behçet’s research is focused upon those who show all the physical signs yet the majority of those who have Behçet’s do not have to show those physical signs and indeed patients with Behçet’s may show few or no visible symptoms at an outpatient examination.

There is in fact a research black hole representing the majority of Behçet’s patients who do not have all the obvious signs of the disease which in turn misinforms those who rely upon such research to inform them about other potential cases.

In short, the diagnostic system presently in place is stacked heavily against the patient.

Having thought about this for a considerable period of time I have come to the conclusion that the pyramid built by liaison psychiatry that fuels their involvement in “CFS/ME” revolves around a simple foundation assumption that a “CFS/ME” diagnosis handed to a patient must be the correct diagnosis.

If a GP or a psychiatrist carries out tests in conjunction with an immunologist or a rheumatologist; a set of negative test results is all that GP/psychiatrist/rheumatologist needs to give a “CFS/ME” diagnosis.

If that diagnosis has been handed to a patient by doctors who have little or no knowledge of complex sero-negative clinical presentations relating to rare medical diseases then there is a significant risk that the diagnosis he or she is giving their patient is in fact the wrong diagnosis.

As people reading this will know, I was subjected to a medical misdiagnosis by a number of doctor’s including GP’s and specialists.

The number of doctors involved went into double figures over a period of 12 years in total.

Over that period, my many individual symptoms were wrongly ascribed to conditions other than Behçet’s disease but in the end when all those symptoms were put together and compared to the correct diagnostic criteria for Behçet’s disease; a doctor finally looked at the evidence and came to the conclusion that I had been misdiagnosed and that I did in fact have Behçet’s disease.

In recent months I have asked pretty well all the liaison psychiatrists in the UK if they have encountered cases of Behçet’s disease passing through their out-patient clinics and none of them has replied that they had.

Professor Sir Simon Wessely for example told me that he was no Behçet’s specialist and that he would have to phone a colleague who was. Professor Wessely did not know if he had seen cases of Behçet’s pass through his clinic wrongly diagnosed as “CFS/ME”.

I recently e.mailed Professor Wessely to ask him about the outcome of his enquiries that were aided by one of his medical students but in spite of a rapid reply to my previous sequence of e.mails; Professor Sir Simon Wessely has not replied to my query regarding his findings.

I sincerely believe that I have homed in upon the Achilles heel of liaison psychiatry and their dominance of “medically unexplained” CFS/ME or indeed their latest diagnosis of Somatic Symptom Disorder.

It is my view from the evidence that liaison psychiatry; by providing doctors with the diagnostic option of CFS/ME and SSD have been responsible for the dumbing down of the clinical diagnostic process within our NHS and indeed around the world.

It is my view from the evidence that liaison psychiatry has made the potential for medical misdiagnosis acceptable practice within the medical profession as a whole.

Instead of considering rare sero-negative auto-immune disease explanations for cases of what end up as CFS/ME, a doctor now has an easy pathway to give a benign diagnosis of CFS/ME on the grounds that their set of negative test results together with a certain set of “invisible” symptoms means that the condition they are looking at is “medically unexplained” or an example of somatised symptom disorder.

Once medically misdiagnosed, the patient is disqualified from being in receipt of medications and therapies that would have been prescribed had that patient been correctly diagnosed in the first instance.

Disqualification of access to treatment will lead to that patient suffering considerably yet the doctors concerned will not recognise the severity of that patients suffering because that suffering will be put into the wrong context by that medical misdiagnosis.

I have known a case of Behçet’s disease where a patient was wrongly diagnosed as having “CFS/ME” for more than a decade and only had that misdiagnosis overturned when they suffered ocular micro-embolisms that caused permanent blindness in one eye and partial blindness in the other eye.

Away from Behçet’s we know of patients who suffered “diagnostic overshadowing” that lead to the late diagnosis of cancer and a rare heart condition.

The symptoms of cancer and the complex heart pathology were fatal in both situations and in both examples, the symptoms of neurological cancer and the heart pathology were almost certainly wrongly ascribed to the “invisible” symptoms of “CFS/ME”.

As far as the medical profession is concerned, a medical misdiagnosis or a medically missed diagnosis are considered as being “unfortunate”.

For the patient, a medical misdiagnosis or a medically missed diagnosis have profound and serious consequences and outcomes.

None of the doctors involved in making or perpetuating a medical misdiagnosis are subsequently held to account for what they have done to those patients.

In my own case, once I had been re-diagnosed I was treated as though I had simply failed back to the bottom of the pack.

There was no process of clinical education in that no investigation took place and no doctor involved was alerted to their poor clinical opinions that lead to me being medically misdiagnosed.

In short, it is my view that the clinical diagnostic process is in fact seriously flawed.

Patient’s are at risk from the medical profession at GP and specialist level.

In particular patients are at risk from an insufficient level of expertise used to make a complex diagnosis based on negative test results and a history of “invisible” physical symptoms.

Patients who present with a history of “invisible” symptoms and a set of negative routine test results are no longer referred to a super-specialist for the objective consideration of a set of relatively rare sero-negative medical diseases.

Instead, patients are given a benign diagnosis of “CFS/ME”; a diagnosis that by virtue of its own “somatisation” description – created by liaison psychiatry - is then incredibly hard or indeed impossible to overcome.

The present system seriously needs to be challenged and changed so that the patient has a fairer chance of being correctly diagnosed in the first instance and not medically misdiagnosed by inadequately qualified members of the medical profession.

The question is – how do we go about making a powerful effective challenge that effects such a change?

If we do nothing then nothing will change.

The medical profession have proven themselves happy to maintain the status quo.

As far as liaison psychiatry is concerned, it is imperative that the present system of a flawed diagnostic process stays exactly the same as it is today.

As far as immunology or rheumatology are concerned, they surely do not want their out-patient departments packed with patients who have discovered that they have been medically misdiagnosed.

A flawed diagnostic process fuels the creation of a base of “heterogeneous” patients who are subsequently involved in Cognitive Behavioural Therapy (CBT) or Graded Exercise Therapy (GET).

Those diagnosed as having “CFS/ME” are fodder for the exclusive “closed shop” self reinforcing research carried out by liaison psychiatry and no other parts of the medical profession.

One could argue that a totally unknown number of patients who are presently medically misdiagnosed with “CFS/ME” are in fact adding credence to the views of liaison psychiatry because a misdiagnosed patient will have a set of self perpetuating and untreated disabling symptoms (fueled by an unrecognised disease process) that the patient is unable to “cast off” or rid themselves of from a course of CBT or GET.

Those patients will reliably keep on reporting “somatised” “invisible” symptoms not because they have any mental impairment but because an auto-immune disease is producing those symptoms.

Such an unknown number of medically misdiagnosed patients can be accused by liaison psychiatry of being so neurotic or so somatised that they are unable to be “cured” by CBT.

Such misdiagnosed patients will be readily available year upon year for future “peer reviewed” research studies that go to reinforcing the validity of Somatised Symptom Disorder or “CFS/ME” using medically misdiagnosed patients to helpfully legitimise those artificial mental health labels.

Such misdiagnosed patients become – in the eyes of liaison psychiatry – desperately in need of even more psychiatric interventions and their sincere professional “help”.

Such patients become so firmly shunted into the somatisation cul-de-sac that they may never have their real diagnosis established unless they suffer a loss of sight or a pulmonary embolism or another “visible” crisis event such as a brain tumour or a fatal heart condition.

However, a pyramid can be reduced to rubble if the foundations are seen and recognised to be rotten.

Once it is realised that the pyramid is built on rotten foundations then when those foundations are condemned and removed, that pyramid will be reduced to rubble.

Sincerely,

Stephen Ralph DCR(D) Retired (diagnostic radiography)

See also…

http://www.meactionuk.org.uk/systemic-vasculitis-and-myalgic-encephalomyelitis.htm

Will "THE" cause of ME/CFS ever be found?

Whenever I read someone writing that they are looking for "the" one cause of ME/CFS, or that even "the" one cause of ME/CFS might have been pinned down, I know that the person writing has no clue about ME/CFS.

If you take at random two persons with ME/CFS – regardless of how strict your diagnostic criteria are – chances are high that their similar diseases are caused by different things. One person's body might be tormented by an food-induced autoimmunity, the other person's body might fail to recuperate from an infection.

So I do not think that one single cause of ME/CFS will ever be found, but instead the many different causes of ME/CFS in different people will be found – one by one.

Maybe Lipkin has a fast-track to finding the most prevalent causes of ME/CFS, but he will not find a silver-bullet to solve ME/CFS, once and for all.

Giving idle talk about "THE" cause of ME/CFS (and presenting it like a silver bullet) is not giving hope, it is spreading BS.

Someone giving the impression that there might be one single cause of ME/CFS is a either a charlatan, a quack or a idiotic know-nothing bullshitter.

ME/CFS? Don't spend money on tests.

I just recently read about a ME/CFS patient being robbed 2500 (!) British Pounds by one of our resident ME/CFS quacks. The patient went to Belgium for a short visit, and got one blood drawing for 2500 GBPs.

Oh my, oh my, oh my.

This is not how a proper differential diagnosis is done. A differential diagnosis rather follows a "rinse and repeat" pattern:

1. First, the doctor needs to get an overview of symptoms.
2. The she/he needs to consider the symptoms and think about what it might be, or might not be.
3. The doctor should then have list of a few diseases that could be it.
4. On that basis it may make sense to order one or the other test – it makes most definitely no sense to order tests for thousands of Dollars/Euros/Pounds
5. Taking into account the test-results and the symptoms, the doctor gets a preliminary diagnosis, based on which treatment can be chosen.
6. If there are signs that the diagnosis is not the correct one, some (or all) of the steps above need to be repeated.

A diagnosis based on a short consult and expensive tests is not worth the paper on which it is printed! Every symptom could be important.

I for an example did not put enough value into my skin symptoms. Turns out the aphthous ulcers I had (together with other skin symptoms) are a key sign for Behçet's – and there is no blood test (or otherwise) for Behçet's. The only thing a doctor can do is carefully make note of all the symptoms, and knowing to look up the diagnosis of Behçet's.

Blood tests alone are a waste of money, especially if a doctor orders lots of them.

If you have ME/CFS, don't spend large amounts of money on tests – you need the money, I'm certain.

If your doctor wants to extract $$$$$ from you for diagnosis, tests or treatments: Change your doctor. Even if he claims that the tests or the treatments are a bargain. Especially if he wants thousands of bucks from you for tests and claims it is a bargain. And especially if he does the tests in an lab that is closely associated with her/him.

My advise: If a doctor sees you as a walking ATM, then change this doctor, because she/he is bad for you and your health.

There are some tests that might be called for, e.g. tests for hypothyroidism, BUT THE WORTHWHILE TESTS ARE PAID FOR BY THE INSURANCE. There are some test that might be "interesting" (like the NK-cell function test), but they do nothing to help you get "more legit" as a patient, or to choose a better therapy.

And just because someone is "Anti-CBT" or "Anti-GET", that does not mean he knows what he does.

Behçet's Disease can look like CFS

Info Video by the American Behçet's Disease Association

It all sounds so familiar. Crippling chronic fatigue, friends saying "you are faking", doctors don't now what's wrong. So people are relieved and almost happy when they finally – after years in most cases – get a proper diagnose that explains their symptoms.

Differential between Behçet's and ME/CFS is needed

Some of the symptoms of Behçet’s:

• Unpredictability: impossible to predict onset or clearing-up of symptoms, onset of symptoms sudden, difficulties in keeping to arrangements, appointments, working, affairs, managing household, family, social activities, hobbies
• Arthritis: reduced mobility or complete immobility, pain.
• Oral ulcers: pain,diet restricted to soft or liquid food, inability to eat at all, inability to talk, dribbling, dehydration, malnutrition.
• Genital ulcers: immobility, sex-life affected, embarrassment, suspicion, urinary retention, pain.
• Visual level: fear of onset of blindness, handicapping according to level of impairment and ability to adapt, pain.
• Skin: disfiguring and embarrassing skin lesions, easy bruising, poor slow healing, pain.
• Gastro-intestinal: wind, diarrhoea (with blood and mucus) or constipation, severe abdominal pain. Mimics inflammatory bowel diseases, irritable bowel syndrome. Stomach ulcers, ulcers in gullet. Risk of perforated ulcer. Dehydration, malnutrition
• Thrombophlebitis: immobility, pain.
• Thrombosis: immobility, pain. Risk of embolism.
• Ears: hearing loss, tinnitus, vertigo
• Chest: wheezing, breathlessness, haemorrhages, haemoptysis, pleurisy, pain.
• Cardio-vascular: breathlessness, haemorrhages, dysrhythmias, pericarditis, valve problems, pain. Risk of ruptured aneurysms.
• Neurological: paralysis, strokes (CVAs), transient ischemic attacks (TIAs), memory & concentration impairment, seizures, migraine-type or meningitis-type headaches, double vision, incontinence, impotence, strange sensations, motor impairment ranging from mild clumsiness to vegetative states, personality changes, psychoses.
• Fatigue: profound persistent exhaustion affecting all activity.
• Feverishness: effects like having ‘flu, night sweats, bizarre sense of feeling cold or warm.

(Remember no patient has all symptoms! See below for the diagnostic criteria for Behçet’s.)

I marked those who I think are the most prominent overlap with ME/CFS. One can see that there is some kind of overlap (not including some of the neurological and gastro-intestinal symptoms that doubtlessly some of the ME/CFS patients have as well)

If some of primary symptoms of Behçet’s (oral ulcers, eye inflammation) are not pronounced (or in rare cases even oral ulcers can be absent), then it is easy to misdiagnose Behçet’s as ME/CFS.

Again, this shows how utterly important a proper differential diagnosis is in cases of suspected ME/CFS. There are many known diseases out there that can look to the untrained eye like another case of ME/CFS.

Of course there are newer and older diagnostic criteria. These are the newer (and probably better) 2006 ICBD criteria:

Add points for every symptom:

• Oral aphthosis ("mouth ulcers"): 1 point
• Skin lesions (e.g. acne): 1 point
• Vascular lesions: 1 point
• Positive pathergy test: 1 point
• Genital aphthosis ("genital ulcers"): 2 points
• Eye lesions: 2 point

3 points or more? It is most likely Behçet's.

And what are the older diagnostic guidelines for Behçet's?

1. International Study Group strict research level guidelines for diagnosis

Must have:

• mouth ulcers (any shape,size or number at least 3 times in any 12 months)

Along with 2 out of the next 4 ‘hallmark’ symptoms:

• genital ulcers (including anal ulcers and spots in the genital region and swollen testicles or epididymitis in men)
• skin lesions (papulo-pustules, folliculitis, erythema nodosum, acne in post-adolescents not on corticosteroids)
• eye inflammation (iritis, uveitis, retinal vasculitis, cells in the vitreous)
• pathergy reaction (papule >2 mm diameter, 24-48 hrs or more after needle-prick)

2. Practical clinical guidelines for patients not included in research cohorts

Must have:

• mouth ulcers

Along with 1 out of the 4 ‘hallmark’ symptoms above

Along with 2 of the following symptoms:

• arthritis/arthralgia
• nervous system symptoms
• stomach and/or bowel inflammation
• deep vein thrombosis
• superficial thrombophlebitis
• cardiovascular problems
• inflammatory problems in chest and lungs
• problems with hearing and/or balance
• extreme exhaustion
• changes of personality, psychoses
• any other member of the family with a diagnosis of Behçet’s disease

3. 'Suspected' or 'possible' diagnosis

Usually given when someone does not have mouth ulcers or has mouth ulcers but does not have 1 of the 4 'hallmark' symptoms but has other symptoms and signs of inflammation and other causes for these have been ruled out.

Care must be taken for a differential between ME/CFS and Behçet's. As with all diagnostic criteria:

• someone who meets some set of diagnostic criteria for a disease, does not necessarily have the disease – and could have another disease instead
• and someone who barely meets the criteria may actually have the disease (see "suspected diagnosis" above)

regardless of whether it is Behçet's, ME/CFS or any other disease.

Psychiatric conditions in Behçet’s

Psychiatric conditions in Behçet’s

Psychiatric conditions occur only very rarely in Behçet’s syndrome, when parts of the brain which look after emotion and thought are affected by the meningoencephalitis noted above. Occasionally patients may present with hallucinations, and abnormal thoughts such as paranoia, and difficulty thinking and remembering. This is most uncommon and normally settles down well with the correct treatment.

Separate to this is the syndrome of fatigue, anxiety and depression which can also cause thinking and memory problems, but which is not related to a problem within the brain. This, in contrast, is very much more common, not just in Behçet’s syndrome but in most chronic and difficult conditions. This is not surprising, but some Doctors, even GPs, fail to recognise this and I have found that this is frustrating to patients. It has been shown that patients with Behçet’s syndrome show higher ratings on depression and anxiety scores, and that these scores vary with the severity of the underlying illness. So-called fibromyalgia symptoms (aches and pains with tiredness) also correlate with how the Behçet’s is behaving, but it is also true that the symptoms of anxiety and depression can make the Behçet’s feel worse when it is not actually in relapse. So it is a very complicated problem. Fatigue management and a positive outlook to the disease are best. Avoidance of overtiredness and planning of the day, to allow rest before and after an activity, work well, and most find that fatigue improves and memory becomes more efficient. It’s easy for Doctors to prescribe and hard for the patients to do!

Could it be Behçet’s?

Interesting question: Do I have Behçet’s?

With my old diet I had all these following symptoms, (almost) enough to meet the diagnostic criteria for Behçet’s:

• Minor aphthous ulceration [every couple of months in the mouth]
• Pseudofolliculitis [maybe a very very slight, but my follicles were always red]
• Papulopustular lesions [sometimes some]
• Acneiform nodules [not sure, I thought it was acne]
• Extreme exhaustion [Wouldn't call it "extreme", but yes I am quite fatigued]
• Nervous system symptoms [do muscle twitches and migraines count?]

(I am not sure if I might have had a very slight iritis, an inflammation of the iris. My eyecolor changed from green-brown – with brown "patches" – to a more uniform green with slight brown. And the blood veins in the white of my eye got less visible.)

These are the symptoms I had on my old diet, some of which I still have. And some of the symptoms return when I leave the path of the Paleo Diet and venture into my old diet (mainly when I eat pasteurized milk products or when I eat eggs).

And every symptom counts. I really paid not much attention to the aphthous ulcers in my mouth. They came and went again, I could live with them and they were the least of my problems – and why concern myself or even a doctor with such a small thing?

I fear I need go again on my old diet to provoke these symptoms. But not at the moment.

At the moment I am too tired to write more – but is interesting the things one finds.

Stephen Ralph on Behçet’s, ME/CFS and Misdiagnosis by Psychologists (2)

See part 1 here.

Permission to Repost

Hello there,

In the background during my absence from campaigning, I have been plugging away at trying to get individuals of influence aware of the associations between the invisible symptom set of ME and the invisible symptom set of Behçet’s syndrome.

I was recently told by one doctor dealing with “CFS” that he could only find 11 research papers on Behçet’s syndrome and that one of those was in German.

This doctor then proceeded to give me all the classic stereotypical presentations of Behçet’s syndrome including patients having clusters of mouth ulcers, genital ulcers, eye involvement in the form of uveitis.

And together with this I discussed the fact that the HLA B51 blood test that can show positive for a case of Behçet’s is more often than not negative for a patient who has Behçet’s.

I then pointed out the following which will become crucially important in the coming months.

If you take a look at this link.... http://bit.ly/V5tLAe you will see the various levels of symptom certainty needed to make a diagnosis of Behçet's Syndrome.

The certainty level exists for the purposes of clinical research which means that anyone who participates in clinical research will have the top level of certainty diagnosis and many of the easily visible and detectable signs of Behçet’s disease.

However, you will also see on that web page that it is still viable to have Behçet’s disease without all the obvious classic signs.

Even if you do not have those classic signs, you can still be diagnosed as having Behçet’s syndrome.

The fact is that nobody appears to have carried out any research into the other end of the scale…. The end of the scale where patients who can have Behçet’s have hardly any or indeed no visible signs that would be observable by a specialist at an out-patient appointment.

…

Stephen Ralph on Behçet’s, ME/CFS and Misdiagnosis by Psychologists (1)

See part 2 here.

Permission to Repost

Dear Reader,

As some of you reading this will know, I was dragged into the world of Myalgic Encephalomyelitis and Chronic Fatigue Syndrome way back in 1996/1997. At around this time I jointly set up MEActionUK and the companion website www.meactionuk.org.uk

At that time I had been a practicing diagnostic Radiographer at a busy district general hospital in Dorset.

During the three years of my training and subsequently over the period of practice I extensively covered human anatomy, physiology, pathology, patient care and hospital practice as well as radiographic photography, equipment and radiation physics.

Some of our lectures mirrored those of medical students.

We were familiar with “Gray’s Anatomy” for the sort of detail we needed to cover.

Although optional, I attended an autopsy during my training to enable me to appreciate the internal anatomy that we had been studying for many months.

I also observed open heart valve replacement surgery – the anaesthetist let me stand where he usually stood so I could see what was where and how the surgery proceeded.

Our education and my subsequent career was comprehensive until I was forced to retire due to ill health.

Over the 10 years of my education and career in diagnostic radiography, it was drummed into me that there was an overriding importance within my profession to provide the best quality radiography possible to enable the doctor to form the correct diagnosis with thanks to the information presented to the radiologist (a doctor specialising in reading x-ray’s and performing x-ray examinations) or indeed any generic doctor or even medical students examining our work in a busy A&E.

If our work wasn’t to the highest of standards then we understood that there was a sliding scale of risk that a radiologist or non-specialist doctor could draw the wrong conclusions – missing a pathology from poor radiographic technique and then forming the wrong diagnostic opinions about what they were looking at.

…

Post-Mono can look like CFS - An Follow-Up

A follow-up to this:

Chronic fatigue syndrome following infections in adolescents

Katz BZ, Jason LA.

Abstract

PURPOSE OF REVIEW:
To review the recent epidemiology, pathophysiology, and treatment of postinfectious chronic fatigue syndrome (CFS) in adolescents.

RECENT FINDINGS:
Thirteen percent of adolescents (mainly women) met the criteria for CFS 6 months following infectious mononucleosis; the figure was 7% at 12 months and 4% at 24 months.

Peak work capacity, activity level, orthostatic intolerance, salivary cortisol, and natural killer cell number and function were similar between adolescents with CFS following infectious mononucleosis and recovered controls.

Autonomic system, oxygen consumption, peak oxygen pulse, psychological and cytokine network differences were documented between those who recovered and those who did not.

SUMMARY:
The prognosis of CFS is better in adolescents than in adults.

Activity level, exercise tolerance, and orthostatic testing could not distinguish patients with CFS from adolescents who have recovered from infectious mononucleosis (controls), while certain cytokine network analyses, life stress factors, and autonomic symptoms could.

Via Adrienne Dellwo

… Looking at post-mono adolescents, researchers found it was mainly the girls who continued to have symptoms long term.

Many of those who fit the ME/CFS diagnostic criteria early on no longer did at follow up.

Here's at look at how the length of time post-infection effected the diagnostic rate:

6 months: 13%
12 months: 7%
24 months: 4%

Researchers say the following factors distinguished those with ME/CFS from kids who'd fully recovered:
- Certain cytokine network test results
- Oxygen consumption, at rest and during exercise
- Life stress factors (such as those caused by long-term illness)
- Symptoms of autonomic nervous system dysfunction

They did not find significant differences in activity level, exercise tolerance or orthostatic testing.
…

Post-Mono can look like CFS

CFIDS in 2009: Post-Mono CFS in Teen Girls

Ben Z. Katz, M.D., of Northwestern University has just published results from a study of teens who were followed for two years after the onset of acute infection with Epstein-Barr virus (mononucleosis). The article is published in the July 2009 issue of Pediatrics. Criteria for CFS were met by 13 percent of adolescents at 6 months after acute infection. Seven percent remained ill at 12 months, and 4 percent met CFS criteria at 24 months. With time, most adolescents recovered. Only 2 adolescents with CFS at 24 months seemed to have recovered or had an explanation for CFS at 12 months, but then were reclassified as having CFS at 24 months.

All 13 adolescents who had CFS 24 months after onset of mononucleosis were girls. Compared with those who did not have CFS at 24 months, they reported greater fatigue severity at 12 months. Corticosteroid treatment during the acute phase of mononucleosis was not associated with an increased risk for the development of CFS.

This study was funded by NIH and its principal investigator is Renee Taylor, PhD, at University of Illinois-Chicago. Dr. Katz and Dr. Taylor are also collaborating with Association-funded researcher Gordon Broderick, PhD, who is studying the same patient group to understand differences between those who recovered from mono and those who remained ill at various time points. Read more about the Association's study at http://www.cfids.org/cfidslink/2009/030402.pdf.

An article about the study was circulated by Reuters and can be read at http://www.vancouversun.com/health/Mono+linked+chronic+fatigue+syndrome+teens/1817020/story.html.

Medscape News also reported on the publication at http://www.medscape.com/viewarticle/705653. You can also find continuing education courses about CFS on Medscape to share with your healthcare professional, including the one sponsored by the CFIDS Association of America that has attracted more than 243,000 page views since it went live in October 2008. The CFS course is located at http://cme.medscape.com/viewprogram/17442.

Journal citation: “Chronic fatigue syndrome after infectious mononucleosis in adolescents.” Katz BZ, Shiraishi Y, Mears CJ, Binns HJ, Taylor R. Department of Pediatrics, Division of Infectious Diseases, Northwestern University Feinberg School of Medicine and Children's Memorial Hospital, Chicago, Illinois 60614, USA. Pediatrics. 2009 Jul;124(1):189-93.

CFS Facts – ME/CFS Misdiagnosis on a grand scale?

I found a interesting blog on ME/CFS, a blog which I haven't stumbled up before: "CFS Facts"

[Update] I have seen the blog before, but I discarded it for the amount of BS, mainly the lickspittle Mikovits-friendly content… [/Update]

This is from their latest blog-post:

Misdiagnosis on a grand scale?

Our editorial in the most recent Breakthrough magazine (Autumn 2012) seems to have stuck a chord, so the text is now available on our website http://www.meresearch.org.uk/information/publications/misdiagnosis.html

The key point – that many people referred from primary care with a diagnosis of ME/CFS are found to have another, treatable condition when assessed at a specialist clinic – might not surprise patients themselves, since many have already questioned their own diagnosis and/or have had difficulties with the "patient-GP encounter" (for the patient view see http://www.ingentaconnect.com/content/rmp/qpc/2009/00000017/00000004/art00004 and for the GP view http://www.biomedcentral.com/1471-2296/6/49 ). Yet, the accumulating evidence of misdiagnosis on such a scale should be astonishing to healthcare professionals, and ought to greatly concern the NHS as an institution. Something is far wrong, and it needs to be fixed.

* * *
I've said the same thing. Some doctors will never diagnose CFS, no matter what; they'll call it depression even when there are symptoms reported that aren't seen in depression. Other doctors will diagnose CFS in any patient who's tired, regardless of the reason.

Dr. Bell has noted that fully half of people initially diagnosed with hypochondria are eventually diagnosed with something very real that matches the symptoms they complained of all along.

Trust the patient!

Narcolepsy

…
Narcolepsy is as common as MS, or Parkinson's disease, but only 25 percent, or one in four, of people with the disorder have been diagnosed. Of the estimated 200,000 Americans with narcolepsy, only 50,000 have been identified.
…

Individuals do not always readily bring up their symptoms with their health care providers, and begin to see symptoms as their personal norm, because the onset is often gradual. They believe that their problems will be seen as psychological in nature and fear that their concerns might be misunderstood or will not be taken seriously.

Their concerns are not unfounded. Many people with narcolepsy were misdiagnosed with psychiatric problems or told sleepiness was due to the effect of an unrelated medication. On average they had to see five physicians before being diagnosed with narcolepsy.

The mean length of time between the onset of symptoms and the diagnosis of narcolepsy is 15 years.

“…the reality is that many clinicians are unable to identify and diagnose narcolepsy, and patients end up losing their jobs, relationships, and other important elements of their lives instead of receiving the treatment they need."

(Word Document)

It all sounds so familiar.

Sleep Apnea

NHLBI on: What Is Sleep Apnea?

Obviously, one big difference in the case presented above is tiredness in sleep apnea versus fatigue in ME/CFS.

What's interesting is that he thought he might have depressions.

The other interesting thing he said was: "Now that I am feeling better [with treatment] I am coming home from work with energy still."

I guess the presentation of cases is a continuum (especially considering the different types of apnea and the unknown causes of apnea) and that therefore some bona fide apnea cases may be misdiagnosed as ME/CFS.

I think sleep apnea is one of the many other conditions that need to be considered as differential diagnosis to ME/CFS. As sleep apnea more often affects men and ME/CFS more often affects women, this should be taken into consideration when trying to make a differential diagnosis.

Toni Bernhard on ME/CFS

If Chronic Fatigue Syndrome is, indeed, several discrete illnesses, until they are isolated from each other and studied individually, little progress will be made in finding effective treatments or cures.
…

Because those of us with a CFS diagnosis are lumped into one group, when we read about CFS-diagnosed person being cured by a treatment, we rush out and spend hundreds, sometimes thousands of dollars on it, only to be terribly let down and possibly further harmed. Since writing How to Be Sick, I’ve lost count of the number of cures that well-intentioned people have suggested to me. But there’s no reason to believe that these cures would be effective for my particular constellation of symptoms.

If Chronic Fatigue Syndrome is several discrete illnesses, it makes sense that some people will be helped by a particular treatment, while others will not. It’s finally dawned on me that it doesn’t make sense to spend money on a treatment just because it helped or cured another person, when the two of us are unlikely to even have the same illness.

IgM and IgG Seronegative Q Fever: A Hypothesis for Veterans? Medically Unexplained Chronic Multi-symptom Illnesses.

Immunoglobulin M and Immunoglobulin G Seronegative Q Fever: A Hypothesis for Veterans? Medically Unexplained Chronic Multi-symptom Illnesses.

Chagaris MJ, Smith RC, Goldstein AL.

J Spec Oper Med. 2012 Spring;12(1):37-48.

Abstract
We present Q fever as a credible hypothesis for Gulf War Veterans Illnesses (GWVIs) and as a possible etiology for prevalent symptomologies affecting currently serving servicemembers.

Q fever is caused by the bacteria Coxiella burnetii, which is endemic throughout the Middle East. Q fever may manifest in many forms of widely varying and often inconstant symptoms. Due to false-negative interpretations in current and past diagnostic testing, Q fever has not received appropriate consideration as a possible causative agent for medically unexplained veterans illnesses.

Review of current literature invites us to consider that a form of Q fever involving an incomplete immune response is a potential cause of these debilitating illnesses.

We hypothesize C. burnetii infection coincidental to exposures suppressing antibody-specific immune response results in infection mediated by immunoglobulin D (IgD). Literature indicates that successful treatment for this form of Q fever requires the concurrent administration of doxycycline and hydroxychloroquine.

Well, it is a hypothesis – without any evidence, it seems.

Usually at the acute phase of an infection you get an IgM titer increase, and after the acute phase the IgM titers level off. And an IgG titer increase follows that, usually persistent for life, even when the pathogen is long gone ("Adaptive Immune System"). So it is intruging that IgD titers might be raised and not IgM or IgG – but where is the evidence?

Because, I've seen this before and I bloody hate it: These f*cking "out of the blue" hypothesis without any evidence. Stupid quacks who write things like "Oh, CFS could be an allergy to an pathogen" without any shroud of evidence for their quack hypothesis. Is it too much to ask that they do some minimal testing for their hypothesis and supply at least some results – before publishing?

"The phenomenon of 'chronic Lyme'; an observational study."

The phenomenon of 'chronic Lyme'; an observational study.
Ljøstad U, Mygland A.

Department of Neurology, Sørlandet Hospital, Kristiansand, Norway Institute of Clinical Medicine, University of Bergen, Bergen, Norway Department of Habilitation, Sørlandet Hospital, Kristiansand, Norway

Abstract

Purposes:
To chart clinical, laboratory, and psychometric profiles in patients who attribute their complaints to chronic Lyme disease.

Methods:
We assessed the patients by clinical examination, laboratory tests, and questionnaires measuring fatigue, depression, anxiety, health-related quality of life, hypochondriasis, and illness perceptions.

Results:
We found no evidence of ongoing Borrelia burgdorferi (Bb) infection in any of the 29 included patients using current diagnostic guidelines and an extended array of tests.

Eight (28%) had other well-defined illnesses.

Twenty-one (72%) had symptoms of unknown cause, of those six met the suggested criteria for post-Lyme disease syndrome.

Fourteen (48%) had presence of anti-Bb antibodies.

The patients had more fatigue and poorer health-related quality of life as compared to normative data, but were not more depressed, anxious, or hypochondriacal.

Their beliefs about the illness were characterized by negative expectations.

Conclusion:
Our patients, who all attributed their symptoms to chronic Lyme disease, were heterogeneous.

None had evidences of persistent Bb infection, but whether current diagnostic criteria are functional in patients with longstanding complaints is controversial.

Other well-defined illnesses or sequelae from earlier Lyme disease were probable as main explanatory factor in some cases.

The patients were not more depressed, anxious, or hypochondriacal than the normal population, but they had poorer health-related quality of life, more fatigue, and negative expectations about their illness.

Unforutnatly only the abstract is available. The other "well-defined illnesses" would be interesting to collect.

And about half(!) of the patients who were seen by these doctors supposedly with "chronic Lyme" did actually not have anti-bodies against Borrelia Burgdorferi - and none had evidences of persistent infection! There are certainly some Quacks out there diagnosing people with "Chronic Lyme". And only "six met the suggested criteria for post-Lyme disease syndrome".

NIAID on Chronic Lyme and long-term Antibiotic use

NIAID on Chronic Lyme:

The first clinical trial, which included two studies conducted at multiple research sites, provided no evidence that extended antibiotic treatment is beneficial (New Engl J Med 345: 85-92, 2001). In those studies, physicians examined long-term antibiotic therapy in patients with a well-documented history of previous Lyme disease, but who reported persistent pain, fatigue, impaired cognitive function, or unexplained numbness. Patients were treated with 30 days of an intravenous antibiotic followed by 60 days of treatment with an oral antibiotic.

These studies did reinforce the evidence that patients reporting PLDS symptoms have a severe impairment in overall physical health and quality of life. However, prolonged antibiotic therapy showed no benefit when compared with groups who received placebo.

In another study, published in 2003, researchers examined the effect of 28 days of intravenous antibiotic compared with placebo in 55 patients reporting persistent, severe fatigue at least 6 months following treatment for laboratory-diagnosed Lyme disease. Patients were assessed for improvements in self-reported fatigue and cognitive function (Neurology 60: 1923-30, 2003).

In that study, people receiving antibiotics did report a greater improvement in fatigue than those on placebo. However, no benefit to cognitive function was observed. In addition, six of the study participants had serious adverse events associated with intravenous antibiotic use, and four patients required hospitalization. Overall, the study authors concluded that additional antibiotic therapy for PLDS was not supported by the evidence.

More recently, a study supported by the National Institute of Neurological Disorders and Stroke (NINDS), also a part of the National Institutes of Health, again showed that long-term antibiotic use for Lyme disease is not an effective strategy for cognitive improvement (Neurology 70(13): 992-1003, 2008). Researchers compared clinical improvement following 10 weeks of intravenous ceftriaxone versus intravenous placebo. The patients were treated for Lyme disease and presented with objective memory impairment tests. In a complicated statistical model, the ceftriaxone group showed a slightly greater improvement at 12 weeks, but at 24 weeks, both the ceftriaxone and the placebo groups had improved similarly from baseline. In addition, adverse effects attributed to intravenous ceftriaxone occurred in 26 percent of patients. The authors concluded that because of the limited duration of the cognitive improvement and the risks involved, 10 weeks of intravenous ceftriaxone was not an effective strategy for cognitive improvement in these patients, and more durable and safer treatment strategies are still needed.

To recap:

• The people are ill 
• Long-term antibiotics do most certainly not cure
• Long-term antibiotics have dangers
• Diagnose is done through "a well-documented history of previous Lyme disease"

As far as I am concerned, there is no evidence that "Chronic Lyme" or "post-Lyme disease syndrome" (PLDS) is anything else then just another pathogen that can cause CF(S) or PVFS.

"Multiple Chemical Sensitivity (MCS): A Spurious Diagnosis"

Stephen Barrett, M.D. at Quackwatch on Multiple Chemical Sensitivity ("MCS"):

…
Psychologist Herman Staudenmayer, Ph.D., of Denver, Colorado, has treated "MCS" patients for more than 30 years. He believes that although some people are very sensitive to various microorganisms, noxious chemicals, and common foods, there is no scientific evidence that an immunologic basis exists for generalized allergy to environmental substances. During the 1990s, like Rea, Staudenmayer and his colleague—the late John C. Selner, M.D. (an allergist)—used an environmental chamber to test sensitivity to airborne chemicals. However, they rejected clinical ecology theories and practices. Using well-designed double-blind tests, they demonstrated that "universal reactors" may develop multiple symptoms in response to the testing process without being allergic to any of the individual substances administered. One of their reports describes how they used an environmental chamber to evaluate 20 patients with multiple symptoms attributed to chemical hypersensitivity. These patients believed that they were reactive or hypersensitive to low-level exposure to many chemicals. Some had previously been evaluated and managed by clinical ecologists and diagnosed with "MCS." During nonblinded tests, these patients consistently reported symptoms they had associated with exposure at work, at home, or elsewhere. The environmental chamber enabled the patients to encounter measured amounts of purified air, compressed gasses, and air containing specific chemical concentrations, without knowing which situation was which. None of the patients demonstrated a response pattern implicating the chemicals supposedly responsible for their symptoms. Eighteen reported no symptoms at least once when the suspect chemical was present. Fifteen reported symptoms at least once when the suspect chemical was absent [10]. In other words, patients reacted to their feelings and beliefs about the test, rather than to the substance in question [11].

In 1999, the American Health Foundation's Environmental Health and Safety Council reached a similar conclusion. After reviewing the evidence for various alleged mechanisms though which odor-bearing chemicals might cause MCS symptoms, the council concluded:

In no case was there persuasive evidence that any olfactory mechanism involving fragrance underlies either induction of a sensitized state or the triggering of MCS symptoms. Fragrances and other odorants could, however, be associated with symptoms as claimed by MCS symptomatics, because they are recognizable stimuli, but fragrance has not been demonstrated to be causal in the usual sense. [12]

A more recent study tested whether "MCS" patients could reliably distinguish between airborne solvents and placebo and whether there were significant differences in measurable biological and neuropsychological parameters between solvent and placebo exposures. During the study, 20 MCS patients and 17 controls underwent six sessions in a challenge chamber in which they were exposed to solvent fumes and clean air in random order. Neither the patients nor the experimentors knew which exposures were which at the time they took place. No differences accuracy in identifying chemical exposure were found between the two groups. Nor was cognitive performance influenced by solvent exposure or different between the groups. Nor was there any difference between the groups in serum cortisol levels measured before and after exposures [13].

So probably no MCS, but other illnesses.

So what about the symptoms? They are interesting:

… The complaints associated with these labels include depression, irritability, mood swings, inability to concentrate or think clearly, poor memory, fatigue, drowsiness, diarrhea, constipation, dizziness, mental exhaustion (also called "brain fog" or "brain fag"), lightheadedness, sneezing, runny or stuffy nose, wheezing, itching eyes and nose, skin rashes, headache, chest pain, muscle and joint pain, urinary frequency, pounding heart, muscle incoordination, swelling of various parts of the body, upset stomach, tingling of the fingers and toes, and psychotic experiences associated with schizophrenia.

Well, some of it sounds like from ME/CFS, Fibromyalgia and POTS…

William J. Rea, M.D., who says he has treated more than 20,000 environmentally ill patients, states that they "may manifest any symptom in the textbook of medicine."

Oh my. If someone can diagnose literally anyone with MCS for having "any symptom in the textbook of medicine", then MCS is a worthless diagnose. And most certainly one will miss many other diagnoses, of real illnesses and diseases.

"40% of CFS patients seen by the Newcastle Service could in fact be diagnosed with other conditions"

Breakthrough magazine Autumn 2011

The correct diagnosis
Are we getting better at diagnosing ME/CFS?

At present, there are many ways of diagnosing ME, CFS, CFIDS, CFS/ME and ME/CFS – and just listing these acronyms illustrates the confusion that besets the field. Yet each new definition delivers only a “diagnosis of exclusion” of other conditions, based on clusters of vaguely defined symptoms shared with other illnesses. How valid a diagnosis of ME/CFS really is depends critically on the rigour of the initial clinical assessment, and the efforts expended to exclude other treatable conditions that might be causing the collection of symptoms.

The clinical guideline produced by the UK’s National Institute for Health and Clinical Excellence (NICE) in 2007 came up with its own variant of diagnostic criteria for “CFS/ ME” – new, unexplained, persistent/recurrent fatigue with a post-exercise component plus one or more of a range of common symptoms such as difficulty with sleeping, muscle and/or joint pain and headaches. …

The most important finding was that 103 (40%) of patients seen by the Newcastle Service could in fact be diagnosed with other conditions. As the Figure opposite shows, the most common alternative diagnosis in these patients was fatigue associated with a chronic disease (47% of all alternative diagnoses …). The next common alternative diagnosis was primary sleep disorder (20%), including 8 patients with obstructive sleep apnoea and 12 with another primary sleep disorder – an important finding since sleep disorders form a significant and potentially treatable diagnostic group. Furthermore, 15% of all alternative diagnoses were psychological/psychiatric illnesses (most commonly, depression, anxiety and post-traumatic stress disorder); 13% were “unexplained” but not ME/CFS (5.2% of total referrals); and 4% were cardiovascular disorders (vasovagal syncope in patients with fatigue symptoms, who also had a history of episodes of loss of consciousness, with the diagnosis made after a reproduction of symptoms in head-up tilt testing). [Other conditions included metabolic syndrome and coeliac disease.]

Prof. Newton’s results concur with those from two smaller service audits (Dundee 1993; Newcastle 2007), and reiterate that a significant minority of UK patients referred from primary care with a diagnosis of ME/ CFS can receive alternative, exclusionary diagnoses if investigated at a specialist clinic. And they illustrate that in the absence of a full clinical assessment (which most patients in the community have either never undergone, or last had many years ago), the diagnosis of ME/CFS can easily become a stopping-off point for clinically complex patients with a variety of different illnesses.

This problem is encountered not only in the UK. A fascinating commentary in 2008 in Minnesota Medicine (available online) described the difficulties experienced at a clinic in the USA for patients with fatigue, exercise intolerance and weakness (i.e., patients very like ME/CFS patients in the UK). After reporting on three paediatric cases (all of whom received serious, new diagnoses), the authors commented that, “a thoughtful and thorough physical exam can sometimes reveal otherwise hidden diagnoses”. Commentaries like this, and investigations like this one at Newcastle, certainly raise the question of which treatable diagnoses might be uncovered if all patients currently parked in the ME/CFS diagnostic layby were examined intensively at a specialist Centre of Excellence by thoughtful and thorough physicians.

The ideal would be for ME/CFS or the subtypes within to be diagnosed objectively with criteria based on clinical or laboratory measurements. …

Amen to the last.