Case Study – American ME and CFS Society

“The Poison Ivy Treatment” – An Intriguing CFS Case Study by Dr. Bell

by Dr. David S Bell, MD, FAAP*
February 2, 2011

This ME/CFS patient case history is one of 10 that Dr. David Bell included in his book Faces of CFS – Case Histories of Chronic Fatigue Syndrome, published in August, 2000.* Each case illustrates a different aspect of the illness that he observed in managing patients affected by the ‘Lyndonville Outbreak’ in New York, and none remains more fresh or intriguing than this one.

Reprinted with the kind permission of ProHealth: 2/2/11

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“This minor test is one of hundreds that prove to me that CFS is real and can be studied.” – David S Bell

I had been treating patients in my Lyndonville clinic for 10 years when, one day, I happened to pick up the chart of a patient whose name was unfamiliar to me. He was awaiting me in my examining room.

I quickly learned that Edwin Maxwell was the man who owned the beautiful farm on the Stillwell road. I had admired this farm every time I passed it on my way to the nearby hospital. The old barns were always maintained with care. I had come to expect an orderly procession of snowdrops, tulips and lilies on tended patches of lawn every spring and summer. I could see that a lovely stream ran through the rear of the property, which looked like a European forest – tidy, but natural, as wonderfully wild as anything could be and still be called a farm.

I also knew whoever tended this farm had a certain mysterious wisdom. If hay had just been cut on the Maxwell farm on a summer day, you could count on three sunny days to follow. Even the weather seemed to respect this farmer; his sixth sense was more reliable than any TV forecast.

I observed, as well, that there was no rush, no great urgency, to this farmer’s life. He tended his fields with patience, as if he knew that the earth would unfold its crops the way life unfolds its secrets – all in due time.

I liked the 45-year-old Edwin Maxwell immediately. He began our conversation by letting me know he was Dr. Wilson’s patient and would remain Dr. Wilson’s patient. He wanted to talk to me about this new disease I was studying, however, because he knew something about it.

He allowed as how he had every intention of paying for his visit, but he wanted me to understand that he was there to tell me something about CFS, not to be treated.

I settled back in my chair and waited. By then – the autumn of 1988 – there had been so much publicity about CFS that literally hundreds of people, some of them writing to me or calling me from the four corners of the earth, had already offered me their theories about what was causing CFS.

These theories of causation ranged from discarded plutonium at the nearby West Valley nuclear processing plant, to PCB’s in the salmon of Lake Ontario, to yeast in the intestinal tracts of sufferers. Then, as now, I listened to every one of these ideas with honest interest.

I continue to believe that, someday, someone would come up with the correct answer. Nevertheless, even then, these theories were growing pretty thin, sometimes bordering on the weird.

Edwin continued by stating that he, too, suffered from the disease I was studying. He was not looking for confirmation from me; in fact, his expression brooked no argument. He explained that he had been comparing notes on his symptoms with a number of his friends and neighbors who had CFS and were my patients.

I confess I was surprised: Most people with CFS show up in my clinic in a state of perplexed misery, wondering if I can tell them what is causing their joint pain and headaches and exhaustion. Edwin, in contrast, seemed to have a rare intellectual grasp on the disease.

When I tentatively asked him to tell me about his symptoms, he explained that the fatigue was the worst.

Three years before, he said, he could lift six, maybe seven, wagons of hay bales if he had to, and feed them onto the conveyor belt to the barn loft. He could plow and roll 17 acres of land in one day. Had for years – until three years ago. He added that he suffered from scratchy, sore throats. He had muscle pain, but he also pointed out that there was no reason, at his age, to have muscle pain. Hell, his father was still baling hay at 70.

He reported with obvious chagrin that he needed to wear sunglasses while he worked, even though he had always disliked sun glasses; they were something city people took to the beach.

So Edwin Maxwell could have CFS, I mused. Okay – now what? I waited.

“This spring,” Edwin said, “I had a lot of fields to plant in a short time.” He was choosing his words carefully. “The winters are okay, because it’s easy to cut the days down and get the extra rest. But not in the spring. There is so much to be done after the geese leave.”

Lyndonville happens to be on the migration pathway of Canadian geese. These great birds descend on the land for four to six weeks in the early spring, and when the fields begin to dry out from the winter snow, the geese head across the lake toward Canada. It is a time of great excitement in Lyndonville. The days begin lengthening in earnest now, and the geese are incredibly noisy.
You don’t even mind being woken at five in the morning by two thousand geese in the back cornfield. They leave when the ground begins to dry, the beginning of the plowing season.

“I remembered that the spring before,” Edwin continued, “I got poison ivy on my arm while cutting some brush in the back of the house. The poison ivy was nasty, but I noticed that the fatigue was better.

“I didn’t think much more about it. Then, this spring, just before plowing, I decided to pull up some poison ivy roots and rub them on my arms. Afterward, the itching was horrible, but my fatigue got better for about two full weeks. I could work just like before I got this disease, and I got all my planting done in time. But I noticed that as the poison ivy wore off, the fatigue came back.”

Edwin Maxwell was a careful observer of not only nature, but of himself, I realized. He asked for nothing in return. He was imparting some information to me, in case I was interested.

I was interested. New concepts about CFS either fit, or they did not fit, based on the selective “principles” I have developed over years of observation, principles framed by my experience. I realized immediately I had just heard a new “principle.”

Edwin’s revelation meant that the fatigue in CFS was not fixed; it could be variable. It could come and go, and was just a symptom; perhaps not even a necessary symptom. Theoretically, you could have CFS without being tired!

Consider the implications: if you were shot, or had a broken bone, little would be changed if you also acquired poison ivy; neither would exposure to the weed impact on your tuberculosis or your depression or your radiation sickness.

Poison ivy was an allergic response generated by the immune system, and localized at the point of exposure. Edwin was suggesting that this immune response – a sharp blip in the day to day functioning of the immune system, resulting from exposure to an allergen – might somehow diminish the fatigue in so-called “chronic fatigue syndrome.”

I had already discovered that among my CFS patients who were children, particularly, at least half had early childhood histories of either asthma, or allergies to various common substances.

I knew that there were a number of papers already published in the medical literature connecting CFS to medical histories of “atopic” illness, also known as allergies. A history of allergies appeared to be a risk factor for acquiring CFS. In fact, it was one of my established “principles” of the disease that a complex, if poorly understood, relationship existed between having CFS and allergies.

Yet, Edwin was telling me that if you applied an allergen to a small patch of an arm – if you localized an allergic response, in other words – you could make the fatigue in CFS go away while the allergic response lasted.

It didn’t really matter to me whether this held true for anyone else in the world. If it was true for one person with CFS, then it provided an hypothesis that could be tested in other CFS patients. The key was to learn whether this phenomenon represented a fundamental physiologic mechanism of the disease, or was just an interesting fluke.

If consistently true of all CFS sufferers, then any theory of the cause of CFS would have to hold an explanation as to why a poison ivy attack gave Edwin Maxwell an energy boost.

Sometimes when you think a great deal about something, you get so used to your own thoughts that they begin to seem dull. It takes someone else’s ideas to wake you up again. Edwin watched me as I struggled mentally to fit these new pieces of the puzzle together. He could see that I was taking his comments seriously.

I was ready to accept that fatigue need not be present for someone to have CFS.

I knew several people who lived in families where one member or more was thoroughly debilitated with full-blown CFS, and who suffered from severe intellectual problems along with other symptoms highly suggestive of CFS, even though they lacked the accompanying exhaustion. In fact, they had no more
than ordinary fatigue.

Could you jettison fatigue from the definition of the disease? I think you could, although this view would be unlikely to be published in a medical journal, especially since, even today, members of the scientific establishment are unwilling to agree that any of the symptoms of CFS are “real” and not psychiatric in origin. To persuade this same community that you can have what they call “chronic fatigue syndrome” without having “fatigue” would be next to impossible.

Nevertheless, the variability of fatigue – the idea that some people could have the disease without being tired – had become for me a defining principle. In truth, if this principle proved true, then the margins of CFS would begin to blur with the margins of attention deficit disorder (ADD), and other learning disabilities, especially in children. That was the population in which I most commonly saw patients with all the symptoms of CFS, minus one: fatigue.

Edwin Maxwell’s story got me thinking more intensively about the cause of the fatigue in CFS. I was intrigued that a natural substance, one manufactured by the body, called interleukin, might be the culprit.

While it may seem naive to look for a single substance responsible for fatigue, it did not seem a hopeless task. Scientists have been experimenting with one type of interleukin, interleukin-2 (or IL-2), as a therapy for several kinds of cancer. What researchers inevitably find, however, is that it doesn’t take very much IL-2 to induce symptoms in cancer patients that are almost as bad as the cancer.

Amidst the numerous side effects that include confusion and mood changes, IL-2 also causes profound fatigue when it is administered as a drug therapy.

Some months before Edwin Maxwell’s visit to my clinic, I had published a scientific paper with a collaborator, internal medicine specialist Paul Cheney, in which we reported that children and adults with CFS had startlingly high levels of the receptor molecule for IL-2. These levels were so high that it implied that the chemical IL-2 could be causing the fatigue and other symptoms of the disease.(1)

I realized that Edwin – if he was willing – could help me test my nascent theory that measuring IL-2 levels might be a way to quantitate the fatigue in CFS in a laboratory. He was willing.

I told him we would take blood samples from him when he was exhausted and measure IL-2 receptor. Then, we would apply poison ivy to his arm and wait until the fatigue improved. When the poison ivy kicked in and the fatigue went away, we would draw more blood. I suggested we do this three times, to be sure of our results.

Edwin liked my idea. It made sense to him. One sunny afternoon at the end of July that summer, I drew blood from Edwin’s arm during a “normal” period when the farmer’s exhaustion was pretty severe. I asked him to maintain a kind of symptom severity journal, as well, which required him to rate the severity of fatigue and 11 other symptoms on a scale of one to ten, with ten being the worst.

After I drew his blood, Edwin himself rubbed poison ivy on his arm. A week later I met him in the emergency room where they kept a camera and photographed the rash on his arms. A few days later, Edwin’s fatigue had subsided substantially, and I drew another sample of blood. We waited for the good effects of the poison ivy to wear off. Then we repeated the entire process.

We did not get to the third trial because by then Edwin had begun to dread the effects of the poison ivy as much as he had grown to dread the fatigue. He begged off, and I respectfully complied with his wishes. I already thought him very brave to offer himself up to medical science as he had done.

Also, the emergency ward staff was beginning to look at me in a funny way because I kept photographing the poison ivy someone was giving himself. Ah, science……

Ours was never anything more than an informal experiment, one that ended somewhat prematurely, but its results were provocative.

Just as Edwin had reported, his fatigue, as well as his other symptoms, were diminished when he was suffering from acute poison ivy. Somehow, this classic allergic response mitigated his most debilitating symptoms: fatigue, compromised intellectual capabilities, and physical pain.

However, the results failed to confirm beyond all doubt my theory about the relationship between IL-2 levels in the blood and fatigue. The results did suggest that fatigue severity was not just a coincidence, the normal ups and downs of CFS symptoms. It was intriguing to speculate that this relationship could even be someday turned into an effective treatment of the symptoms.

Unfortunately, the options are not that good. Edwin preferred the regular CFS symptoms to severe poison ivy symptoms. Maybe it’s not such a great treatment.

Medical science is cumbersome. Hints, such as the hints produced by this experiment, cannot be published in medical journals without real proof. And to conduct a proper experiment takes a great deal of time, money and paperwork, all of which are in short supply for the clinician. But the most frustrating part is the inability of clinicians to communicate to those able to do real experiments that CFS is real and must be taken seriously.

Two weeks ago I attended a neurology conference and CFS was dismissed by the lecturer as a minor psychosomatic nuisance for which there were no tests. The real problem is that academics and governmental public health personnel refuse to put aside their biases and look for the proofs. They seem content to criticize experiments like Edwin’s as incomplete. And of course they are correct.

But Edwin’s poison ivy treatment was over 10 years ago [now more than 20], and still nothing has come from it. This minor test is one of hundreds that prove to me that CFS is real and can be studied. From a scientific perspective, the relationship between the debilitating symptoms of CFS and allergic response is fascinating. I have been naive to think that it would be fascinating for others.

The misperception that CFS is psychosomatic comes only from scientists’ inability to look beyond their psychosomatic biases and look for the proofs.

Edwin doesn’t care, and in this respect he is unique. He gets on with his life, tends the springtime garden with care, manages to get the hay in every summer. He is able to accept the presence of symptoms as he accepts hail which damages the apple crop. And he is lucky, his symptoms are relatively mild and he can ration his time. If he worked in a factory assembly line with rigid hours, he would not be as lucky.

I rarely see Edwin now. Sometimes, while driving by his beautiful farm on the Stillwell road on my way to the hospital, I wave to him in the flower bed, or when he is putting the tractor into the barn. He is busy getting on with the business at hand, he doesn’t have time to feel sick.

– Dr. David S Bell, MD, Lyndonville, New York, August 15, 2000
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1. Citation: “Interleukin-2 and the Chronic Fatigue Syndrome,” Annals of Internal Medicine, Feb 15, 1989, by Paul R. Cheney, MD, PhD; Susan E. Dorman; David S. Bell, MD.

* This article is excerpted with kind permission from Dr. Bell’s classic book Faces of CFS – Case Histories of Chronic Fatigue Syndrome; © David S Bell, MD, 2000.

“The November Factor”: Dr. Bell on ME/CFS & the Flu that Isn’t Flu

by Dr. David S Bell, MD, FAAP*
March 30, 2011

This ME/CFS patient case history is excerpted from Dr. Bell’s book Faces of CFS – Case Histories of Chronic Fatigue Syndrome, published in August, 2000. Each case illustrates a different aspect of the illness that he has studied in patients affected by the ‘Lyndonville Outbreak’ over the years.

Reprinted with the kind permission of ProHealth: 3/30/11

THE NOVEMBER FACTOR

If robbery is taking without permission, CFS could be the greatest thief of all.

Certainly much has been stolen – the energy to go to work, to play with your children; the ability to enjoy reading a book; the luxury of a refreshing sleep. And, like true, great crimes, the victim sometimes does not even realize that a robbery has been committed.

It is as if the thief in a department store steals the surveillance camera along with the jewelry. The thief of CFS steals not only energy, it may rob the victim of the ability to perceive loss. And the mechanism is simple: Energy is quietly replaced with guilt.

Because the victim feels guilty about experiencing fatigue, the robbery goes unreported. Is it any wonder that this is a controversial illness?

The gift of human nature is the perception of who and what we are. We see ourselves either accurately or inaccurately dependent upon personality and the myriad of factors we call life. We see and feel, relating these experiences to our image of who we think we are. Because fatigue is something to be ashamed of in our society, it may go unreported.

The thief makes off with the priceless essence of our life and replaces it with a plaster statue of guilt. CFS becomes a thief of identity as well as activity. It is possible to say “I am an athlete,” or “’I am a devoted parent.”

When CFS has crept out the back door with energy and hope in a burlap sack, these statements are no longer possible.

It makes no difference whether they were accurate to start with. Even if a fantasy, they were a real fantasy for us. With CFS, even fantasies and dreams are stolen. It is like the movie The Dark Crystal, where the small victims are placed in an evil machine that sucks out their ‘vital essence’. CFS is the thief of the ‘vital essence’.

CFS will do to medicine what quantum mechanics has done to physics. The laws, once considered inviolable, are turned on their head.

Just as we were comfortable with the simplistic notions of physics before relativity, doctors are comfortable with the simple notions of medicine now. It really makes little difference that these notions are incorrect, except to those who are not helped by modern medicine.

When CFS becomes accepted and understood, the simplistic mechanisms will be replaced by theories that are able to explain what is now considered subtle. And, of course, with this understanding will come effective treatments – not just those to improve the symptoms of CFS – but those that will revolutionize medicine.

An example of an illness assumed to be straightforward but is, in fact, bewildering, is the ‘flu.’

A person will say, “I was well until a year ago February when I got the flu.” Or “In the months before I got sick I kept getting the flu.” Or “My immunity must be low because I have had the flu three times this winter.” And of course, when the doctor has no idea of what may be causing your symptoms, comes the standard, “I think it is the flu.”

The longer I study medicine the less I understand about the flu.

Jason Ewing was in his mid-thirties, and apart from being a little overweight, appeared like many up-and-coming executives who trooped into the company offices in the morning, brief case swinging at his right side. He had a promising career until two years ago when he developed a typical case of the flu. Actually, as with many persons with CFS, there was one minor difference. This flu had more-than-usual exhaustion associated with it.

It is a detail frequently overlooked, and it has always been difficult to tell whether there really was more exhaustion with this first flu or whether now, two years later, the fatigue is remembered more prominently.

But at the time Jason took time from work and returned, still not feeling well, a week later. He had not even bothered to see his doctor during the illness because ‘it was just the flu.’ Two weeks later he had crept almost to the point of recovery, and paid it little attention. He was at work when the flu came back a second time.

Jason noted with clarity that this second flu episode was identical to the first.

Not just a similar illness, but the same illness. And now we are getting into strange territory. If a person gets a cold, we assume runny nose, cough, sore throat. But, like ice cream, colds come in many varieties – hundreds in fact – and they are all slightly different.

For example, one cold starts off with a scratchy throat, swollen glands, a little nausea and intense sneezing which lasts a day. But this cold is not the same as that of the neighbor down the street, sore throat and headache but no sneezing. We can call them both colds, but the pattern of symptoms is slightly different, and indeed with viral studies we can see that the initiating virus is also different. But what Jason noticed was that whatever the first virus had been, the second one felt exactly the same.

It would be hard to describe the specific combination of 20 symptoms that made up this particular ‘flu’. It would be like trying to describe an unknown ice cream flavor. In the ice cream store drooling Mocha Vanilla from the corner of your mouth, you say, “that’s it.” And it was a second one. It was separate from the first because he had recovered, implying that his body’s immune mechanism had conquered the first invader. He had returned to work and nearly forgotten about the flu three weeks before.

He went to the doctor and described the course and symptoms, and the exact similarity of the second course to the first. His doctor said that he could not get the same ‘flu’ twice, and that it must be a coincidence that the two were similar.

Jason nodded agreement; they had just made a pact to accept a statement, clothed in the language of science, that was obviously wrong.

There are many viruses that cause the illness we call the common cold. In fact the viruses that cause colds are of several different groups. Flu viruses are a little different, but sometimes it is difficult to say by the symptoms if something is a cold or the flu, because they overlap so much.

In general a cold is mild, one or two days of feeling crummy, and the flu is a week. The flu can be dangerous to older people because they develop secondary infections. And there is a vaccine to cover many of the strains of flu that appear during a given winter. There is the ‘Warsaw’ flu, the ‘Beijing’ flu, the ‘Moscow’ flu. It always seemed to me as a medical student that the different strains of flu were named for communist cities as if they were deliberate attempts at biologic warfare.

Each flu strain is distinct. If you had the ‘Hong Kong’ flu once, you would develop antibodies to this particular viral strain and recover. Then, because of blood cells called memory T-cells, you would remember this strain and not get it again, except in the rare instance after decades when the memory T cells become a little senile. That is why, in general, we get chicken pox or measles once in childhood and then do not get these illnesses again when our children have them.

It is difficult to measure or determine the specific strain of virus during an infection. The government will look for new strains in order to include them into the flu vaccine, but because they take several weeks and are costly they are not routinely done during a flu infection. You go to the doctor and he or she says “You have the flu. Please pay at the front desk.” (As an aside, have you ever noticed that the first ten visits for CFS are said to be due to a virus, and the next ten are said to be due to depression?)

So therefore it is not likely that Jason had the same flu twice in a row. And all of this would not have made any difference if everything got better and resolved.

Jason didn’t care much about T-cells and strain variation. Unfortunately, as he was recovering from this second bout he had a third, again with identical symptoms. There was a very particular set of discomforts that made up this flu and a particular malaise, and it came back full force.

He was treated with antibiotics – maybe it was a sinus infection – and again recovered, only to get it again a fourth time.

Over the next six months the process kept repeating with one significant trend. The episodes of this “flu” began coming closer and closer together and the recovery period shortened.

Six months after the initial episode, they were no longer separate bouts, but a constant illness with the symptoms of abdominal pain, flu-like aching, sore throat, joint pain, headache, blurry vision, trouble concentrating, and, of course, exhaustion.

Instead of being 35 and playing piggy-back with his children, Jason had CFS.

Jason’s six-month onset was not the most common for CFS, but then, again, there are many types of onset in this illness.

Jason’s particular onset, however, raises several important questions:

• Is the illness due to a flu-like virus?

• Is CFS due to an unusual virus that plays hide and seek for the first six months?

• Or does CFS have nothing to do with a virus at all?

Can flu-like symptoms be due to something other than an infection with a tiny microbe? The first time this question ever occurred to me was while I was an intern, working 36-hour shifts in the intensive care nursery. After being up all night and struggling to remember where I parked my car, I would notice that my lymph gland felt swollen and that I was coming down with the ‘flu.’ But after a coma-like sleep I would be recovered and ready to hit the next 36-hour shift.

Another of life’s ironies: They have now made it illegal for interns to work those hours because they would prescribe the wrong medications, put IV fluids in the wrong patients, and make other mistakes due to fatigue. But when a person is disabled with CFS and is constantly in that exhausted state, no one believes them, particularly the former interns.

The most common type of onset in CFS is the “acute onset” flu-like illness that does not resolve.

Yet even in this more frequent type, there are parallels with Jason’s flu. In the acute onset, there is a flu-like event, which after five days or so begins to resolve, just as one would expect with the flu. But after the initial resolution, almost to good health, the symptoms come crashing back and do not disappear again.

This implies that the illness is a little uncertain, it wavers a little at the beginning as if trying to make up its mind. “Shall I come down on Mrs. Peterson or not?” If this is so, it had a really hard time deciding about Jason.

A second unusual detail common to the onset of CFS is the severity of the fatigue during the initial episode of the apparent flu. Again, difficult to differentiate in retrospect, but in the initial illness, the fatigue seemed to be more severe than usual.

When I observed the outbreak in Lyndonville, I felt that this was one detail which set this flu apart from all the others. In fact I felt that you could even guess which people were destined to not get better – although I never hinted that at the time.

The belief I held was that there was a unique infection which caused CFS.

What is it about the flu that causes the symptoms that everyone knows only too well? The conventional explanation is that with an infection, viral or otherwise, chemical mediators designed to fight the infection are released into the blood stream. And it is the presence of these immune substances that actually cause the symptoms.

Part of the evidence for this is that when these substances are infused into healthy people they feel rotten, as if they had the flu. The flu virus and many other viral, and bacterial agents stimulate the production of these normal chemicals, which causes the symptoms. When the body’s immune mechanism destroys the infecting virus or bacteria the production of these immune mediators shuts down with a return to good health.

With Jason, the onset had begun as a typical viral infection followed by repeat episodes or relapses until a continuous illness developed. His course of CFS was then typical: There were good days and bad days, but no days without exhaustion, brain fog, and muscle and joint pain.

There were the usual problems with diagnosis, many specialists consulted, tests run. After 15 months the
diagnosis of CFS was made.

The time when the flu-like events coalesced into a continuous illness was around March of 1995. By summertime the symptoms followed a daily ritual that varied little.

• He would have four or five hours of up-and-around activity, headaches every other day, and so on.

• When he had a bad week, his activity would drop down to two to three hours a day and he would feel more ill.

• On a good week, sometimes coinciding with sunshine and a warm breeze off the lake, the activity could go as high as six good hours a day.

Summer eased on into fall, and into November.

Jason had a severe relapse in November, and felt the same as at the onset of his illness. Exactly the same.

His symptoms worsened to the degree that he was confined to bed for two weeks. He saw his physician who, predictably enough, said he had a virus and to take plenty of fluids and aspirin. On the next visit he was given an antibiotic just to be on the safe side. The flavor of this virus was the same flavor that had started his illness nearly two years earlier.

In this detail, Jason is not unique. CFS is an illness of relapses and remissions, and when patients describe relapses, they describe very similar events to those which occurred in their onset. It is not uncommon to hear, “It was like it was beginning all over again.”

It is because of this observation that the theory of a persistent infection, one that does not resolve, has been a steady thread through the tapestry documenting the history of CFS.

Viral and bacterial candidates come and go, but the proof has been hard to come by.

A second characteristic of Jason’s relapse that seems typical of CFS was its occurrence in November. In our office we call it the “November Factor.” For some reason, people with CFS get sick or sicker in late fall, and our telephone rings off the hook. I believe there is some connection between the unusual onset type and the worsening which occurs in November.

One possible explanation is that the patient has caught another bug. Kids are back in school, a perfect breeding ground for bugs of all sizes. They bring these bugs home, particularly this year’s variety and share them with their parents. The relapse is due to a worsening caused by an intercurrent infection, probably viral. This explanation implies that the relapses, and possibly the onset, are random, due to any old virus.

A second possible explanation is that summer is over and winter is setting in. Many persons with CFS feel better in the summer, perhaps because there is less stress, and more time sitting around on the porch in the warm August air. For young persons and schoolteachers, summer is a time of unsustained activity. That is, instead of eight straight hours of work, school or study, it is an hour here, a couple of hours there with rest in between. Therefore starting back to a day with eight straight hours of work or school can precipitate a relapse.

In this theory, the November factor is the resumption of sustained upright activity after a stress-free, relaxing summer. This possibility implies that a critical amount of sustained activity initiates a relapse, a common experience for persons with CFS.

A third possibility has to do with sunlight. Upstate New York, next to Lake Ontario, undergoes a change in November. The days become short with sunset at 4:45 PM by mid December. Worse yet, water vapor from the lake creates a perpetual cloud bank that drifts over Lyndonville and lingers for the next four months. Mid day is gray, bleak and cold, and all sensible adults have left for Florida.

Perhaps the lack of sunlight alters the brain’s melatonin and the addition of seasonal affective disorder is the November factor. Nearly everyone around here is depressed all winter, a fact that the chamber of commerce leaves out of the brochures. Our great joy in winter is a good nor’easter storm which blows the clouds up to Toronto and gives us several wonderful days of sunlight in which we can shovel snow. My lack of enthusiasm for winter here is more than compensated for by the arrival of the geese in the spring and the following months of cherry and apple blossoms that blanket the county.

There are other possibilities. With the coming of cold and bleak weather in November, people go into their homes, shut the windows, add plastic sheeting to help insulate the windows and begin breathing more carbon monoxide. Carbon monoxide, despite being a deadly poison, is very interesting. It can cause a flu-like illness and prolonged neurologic symptoms very similar to CFS.

Oxygen makes many persons with CFS feel better, at least temporarily. Experiments with hyperbaric chamber treatments, where oxygen is pushed into tissues at high concentrations, have shown improvement in patients with CFS. High altitude sickness also shares many of the symptoms of CFS, again due to decreased oxygen availability to brain cells.

Could it be that the flu-like event is not due to an elusive virus at all, but instead to decreased oxygen availability to the cells? [Note: In 2007, Dr. Bell published Cellular Hypoxia in Neuro-Immune Fatigue – a book laying out his hypothesis that ME/CFS and FM may involve a dysregulation of cellular metabolism leading to the inability of the cells’ mitochondria to utilize oxygen normally.]

Medical science is amazing. The technological advances are astounding. We can rescue one pound preemie babies and transplant hearts, livers, and fingers. We can diagnose retroviruses and have made great strides in treating AIDS. Few pediatricians can boast of seeing measles epidemics, and chicken pox will not be seen by the next generation of doctors. But try to explain something as simple as the flu.

Jason did well for the most part. The one time he got really sick was when I tried to treat him with fludrocortisone.

He got the same flavor flu-like event, initiating the relapse. It was not as severe this time, and it was not in November. He has been the only person treated with this medication who has had a relapse, but it again raises the question of whether the flu-like symptoms are due to infection or an entirely different mechanism. We stopped the medication, left him alone for two weeks and the relapse ended, albeit slowly.

It has now been almost five years since Jason began his journey, and he has improved slowly and steadily. He is up to eight hours of daily activity, and while the symptoms persist, Jason feels grateful that the crushing flu-like malaise has passed.

– Dr. David S Bell, MD, Lyndonville, New York, August 15, 2000

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This article is excerpted with kind permission from Dr. Bell’s classic book Faces of CFS – Case Histories of Chronic Fatigue Syndrome; © David S Bell, MD, 2000.

“The Fruitcake Factor”: Dr. Bell on the Neurologic Nature of ME/CFS

by Dr. David S Bell, MD, FAAP*

This ME/CFS patient case history is one of 10 that Dr. David Bell included in his book Faces of CFS – Case Histories of Chronic Fatigue Syndrome, published in August, 2000. Each case illustrates a different aspect of the illness that he has studied in patients affected by the ‘Lyndonville Outbreak’ over the years.

Reprinted with the kind permission of Prohealth: 3/2/11

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THE FRUITCAKE FACTOR

“Neurologic symptoms appear to me to be the most direct window into the heart of this illness; they both define and explain CFS.” – David S Bell

When I was a child, I lay in a field one sunny day, puzzling over something that was brand new. Staring at the sky, I noticed what seemed to be an object of unknown identity hovering in my left field of vision. When I turned my head in its direction, however, it seemed to slide away and disappear. I realized I could also see a similar strange shape in my right field of vision. If I directed my gaze ever so slightly away, it might remain still for a moment, delicately balanced, but it slid away, too, when I turned my head to focus on it. They were shy, transparent objects, and they were not really in the sky. I studied the problem for an hour or so, then I fell asleep.

During my medical training, I learned that these curious objects are called “floaters” by neurologists and eye specialists. They are white cells that have collected in the anterior chamber of the eye. Almost everyone will notice them from time to time.

I have decided that floaters are very like CFS since, whenever you try to look directly at them, they skitter off to the periphery and then disappear. If you pretend not to really look at them, they may hold still just long enough for you to get some sense of their shape and size. Certainly, the illness I study in Lyndonville is like that. The harder you look at a specific aspect of CFS, the more whole disease slides off to one periphery or another, hiding itself just beyond your line of sight.

Let me give you an example. Nearly 80% of people suffering from CFS will have joint pain at some point in their disease, and many will have it as a chronic symptom. Yet, this pain is by no means a true arthritis.

When these painful joints are subjected to X-rays, the image looks normal; there is no joint damage or deterioration. I am able to rule out rheumatoid arthritis, a more severe disease than the common osteoarthritis, in CFS patients, as well, because the blood tests used to diagnose rheumatoid arthritis are negative.

I have noticed that the typical rheumatologist seeing a CFS patient may end up – as I did once as a child studying curious objects in the sky – falling asleep before the patient even comes to the end of his symptom list. Whatever the root cause of CFS, joint pain is some distance away from it.

Still, there are a few symptoms a doctor notices in CFS sufferers that I believe are crucial to understanding the disease.

Amanda Lewis was nearly 40 when I first saw her, and she had been ill with CFS for years. She had all the typical symptoms: unending fatigue, joint and muscle aches, headaches, trouble concentrating.

As her years of illness wore on, she had learned ways to cope with these unpleasant sensations, but there were a whole category of symptoms, which came under the heading of “neurologic,” from which she rarely found relief or escape, nor could she hide them from others.

• Lights hurt her eyes, and certain high pitched noises caused her to experience pain just behind her ears.

• Sometimes her fingers hurt when she touched objects.

• Amanda also described a burning sensation in her arms, as if they were in flames, and occasional episodes of either numbness, or tingling, in her arms.

• On occasion, she would also experience tremors in her upper arms, which would shake and begin to rise involuntarily. If Amanda had lost consciousness at such times, one could say she was suffering a seizure, but these were not true seizures because she was fully conscious throughout the ordeal.

• Amanda discovered, too, that on occasion her arm and hand muscles were so weak objects like empty coffee cups would just slip out of her hand.

Most distressing to her, Amanda’s intellectual capabilities seemed to have been shattered.

Sometimes she got lost – in her house. When she cooked, she sat by the oven until her food was ready in order to make sure she remembered to turn off the burners. She was utterly helpless when it came to managing two simple tasks simultaneously; she simply lacked the ability to concentrate.

She felt her brain’s gears had gone rusty.

I was hardly the first doctor Amanda had consulted. Among those few doctors who took her complaints seriously, a few had suggested her intellectual difficulties were the natural result of aging, a worrisome suggestion, as she was young.

In addition, although all the symptoms she described to these doctors could be huddled together under the umbrella of neurologic disease, they had been unable to find evidence of muscle wasting or atrophy, nor had they been able to measure any abnormal degree of weakness, using standard neurological tests. (They did detect a slight tremor in her arms and hands, however.)

In addition, Amanda failed what’s known in medicine as the Romberg test, named after its inventor. When she stood in a relaxed stance with her arms outstretched, she wobbled and usually fell backward and to the right.

When Amanda came to see me and described these problems, I decided to test her reflexes.

Everyone who has ever had a physical exam remembers the doctor tapping a rubber hammer on their knee, and watching their lower leg jerk forward. That’s a normal reflex.

When doctors test reflexes, they are checking a “reflex arc,” a nerve circuit or pathway that travels from a tendon in the leg to the spinal cord and back to the leg muscles. Diseases that interfere with the nerves of the leg will suppress that reflex to kick your doctor in the groin.

I was startled when I tapped Amanda’s kneecap tendon. She didn’t kick me – her whole body shook.- In fact, she almost jumped off the table. I then tested her vibratory sense with a tuning fork, the ability of her leg nerves to detect vibration. Her reaction was more muted, but similar to the first response by being exaggerated. It seemed to me as if Amanda was very much like a set mousetrap that was ready to trip given the tiniest nudge. I think this was the first time I was worried about hurting someone by tapping a tendon with a rubber hammer.

• I sent Amanda to a specialist, a neurologist. His diagnosis: Huntington’s chorea, a fatal disease of the central nervous system. Amanda was hardly cheered by the news, and I was dubious because her tremor was unlike the jerking motions of “chorea.”

• I arranged for another neurologist to see her in an effort to get a second opinion. The second neurologist suggested that Amanda might have multiple sclerosis, but seemed unwilling to test his own hypothesis by conducting the standard diagnostic tests for the disease.

• A third neurologist insisted that all of Amanda’s symptoms could be ascribed to depression. He prescribed antidepressants.

When I asked him, in a telephone conversation afterward, about Amanda’s remarkable response to tendon tapping, he assured me that her response was phony. Nobody jumps off the table when you tap their reflexes, he noted with a degree of confidence I found chilling.

I realized he was telegraphing to me some basic information he believed I needed to know: Amanda was a fruitcake. Amanda’s exaggerated reflex response became “the fruitcake factor.”

Neurologic symptoms appear to me to be the most direct window into the heart of this illness; they both define and explain CFS.

The reluctance of neurologists to be interested in CFS mystifies me. Perhaps it is too difficult; perhaps it is because they prefer the classic symptoms of seizure, isolated headache, and the shaking of Parkinson’s disease.

CFS is a unique blend of numerous neurologic symptoms, none of which are well understood today.

• The fatigue (not tiredness) must be generated somewhere in the primitive midbrain;

• The sleep center is nearby and clearly does not work correctly.

• Cognitive problems, pain, and headache are clearly neurologic.

• Even the immune system problems of CFS may be neurologic as we know that brain injured patients display immune system abnormalities.

But right now it is too complicated. Physicians can be very interested and scientific when it regards any other organ of the body, but the thing that sits atop the shoulders remains the “black box” of medicine and is largely ignored.

I have no problem with not understanding the exact mechanism of the symptoms of CFS. I was never good in the two week neuroanatomy class in medical school. I do have a problem with the lack of respect given patients with poorly understood neurologic disease.

Science has created a false aura of mastery, and if there is an area where mastery does not apply, it is an area to be disregarded, ignored, and even ridiculed. And this injury by the medical profession and society hurt almost as much as the symptoms of CFS.

I routinely see patients with CFS who are disappointed when an MRI scan does not find a nice big brain tumor. At least that is real. Ultimately, the neurologic symptoms of CFS will gain a foothold in the thinking of neurologists and garner respect. The brain is the Rodney Dangerfield of medicine.

It was a colleague who first described to me a possible mechanism for the fruitcake factor in CFS. Paradoxically, this symptom is prominent in only a small minority CFS sufferers, always the most severely ill; it may even be the medical marker for the degree of severity.

When I look for it, however, I can see traces of it, or at least very subtle myoclonus, in up to half of all patients.

And here I will reveal my hunch: The fruitcake factor not only represents a fundamental process of the disease, it probably exists in every patient to some degree, however minor, and expresses itself as pain.

Amanda’s violent reaction to tendon tapping was a manifestation of what doctors call “myoclonus.” Neurologists define myoclonus as a sudden and generalized jerking contraction of the muscles. You may have noticed your sleeping partner in the early stages of sleep either jump or jerk, sometimes kicking you quite fiercely without once offering an admission of guilt or regret.

So called “sleep myoclonus” is sometimes violent enough to wake you just as you’re falling asleep. Sleep myoclonus is perfectly normal, but – with few exceptions – it is the only kind of myoclonus that is normal.

Sadly, although myoclonus is a markedly abnormal finding, it is also the ultimate humiliation for the patient with CFS. Although this finding may be one of the most important signs of neurologic disease during any clinical exam, doctors most typically dismiss it as “hysterical” when they are examining CFS sufferers. What they mean by this is that the patient is going for dramatic effect.

In my view, this is like calling an epileptic patient a drama queen when he has a seizure.

Epilepsy is not due to “evil humors,” as seventeenth century healers once decreed, and the fruitcake factor – myoclonus – is not hypochondria.

Of course, muscle tension can cause the tendon reflex to be increased, and anxiety certainly increases muscle tension. But an abnormal reflex due to mere muscle tension would never cause someone to jump off the examining table.

This response is due to the fact that the reflex travels up the spinal cord, not just the isolated arc back down the leg.

Anxiety could not possibly explain Amanda’s reaction. Some experts on the subject consider myoclonus to be a form of epilepsy, because it originates in the brain. But whether myoclonus is a seizure or not, in a sane world, the neurologists Amanda visited should have recognized her abnormal response to their sensory stimulation for what it was: a highly abnormal neurologic sign.

Amanda had seen three neurologists over a one month period. She has been told:

• That she will either die soon, maybe in a while,

• And that she was a fruitcake and will probably never die.

She is in a bit of a dilemma; and I, as her doctor, am also in a bit of a spot. As primary care physicians, we suggest specialty examinations to offer patients the “real doctors”, who will solve their problem, perhaps verifying an opinion to instill confidence. However, as a first line clinician, one who sees the patients who walk off the street, I am now in a bad spot. I admit to bafflement at this juncture.

My patient was diagnosed with Huntington’s chorea, but if the neurologist who announced that dramatic news had really believed his own diagnosis, he should have conducted additional tests to confirm the diagnosis, as well as offered genetic counseling, since the disease is passed from generation to generation within families.

My patient was then diagnosed with multiple sclerosis, but if the neurologist who rendered that diagnosis had really believed Amanda had MS, he should have offered to perform the standard tests that MS experts use to confirm the presence of the disease, and told Amanda about some of the new MS drugs on the market, which are considered most effective when prescribed early in the disease.

My patient was then diagnosed as an hysteric, but if that doctor really believed his diagnosis, he should have written me a collegial letter explaining his theory about Amanda’s myoclonus response.

I guess few self-respecting neurologists, especially if they thought she was seriously ill, would call Amanda’s disease by its absurdly trivial and unscientific name: ‘chronic fatigue syndrome’.

As it turns out, this name not only debases the patient who suffers from it, this name also seems to chip away at the self-esteem of the doctor, especially if he is a highly paid specialist with a reputation to protect. I suspect that’s why people suffering from CFS are showered with myriad vaguely outlined diagnoses, or no diagnosis at all, despite having prominent abnormalities during examinations and on a number of lab tests.

Very few medical schools teach young doctors about this illness, and as medical students move into specialty training, their opportunities to learn about CFS from senior doctors who have actually studied the disease become even more rare. Publishing scientific papers about CFS has become so difficult in the last decade, a group of researchers decided in 1995 to establish a journal specifically for the disease, one that would afford clinicians and scientists a forum in which to report on developments in the field. [The Journal of Chronic Fatigue Syndrome, now discontinued, but succeeded by the Bulletin of the IACFS/ME.]

I sat down with Amanda in my office soon after the third specialist rendered his opinion. We had been offered a less than appealing choice by these men, all of whom were well respected: Either Amanda was going to die, or she was a great actress.

I suggested to Amanda that rather than arbitrarily choosing one of these diagnoses out of a hat, or choosing the one we liked best, that we throw them all out.

• I told her that her central nervous system symptoms were part of a disease that none of these highly regarded specialists really knew anything about.

• I told her she had CFS.

Over the next few years, that diagnosis has proven correct. Her symptoms abated somewhat except for a marked worsening when we tried a mild stimulant drug because of the fatigue. At that time the myoclonus became worse, but, fortunately quieted down when the drug was stopped.

She has not gone on to develop Huntington’s chorea nor has she developed the typical findings of MS. The symptoms persist; she has good years and bad years. So that means that she has either CFS or is a consistent fruitcake.

How do you go about diagnosing someone as a fruitcake; what, exactly, are the diagnostic markers?

Actually, while I know that many of my colleagues consider my patients fruitcakes, I am not really sure what a fruitcake is, exactly. It is a sweet pastry filled with nuts. Neurosis was defined by Carl Sandberg as the denial of legitimate suffering, and therefore most of my patients are surely neurotic as hell. But fruitcakes?

It turns out there is a diagnostic test for the diagnosis of fruitcake: time.

I have now known Amanda for several years. I have seen her during crises and during relatively good times, and the symptoms and signs persist. I have shared her sadness and anger – normal, healthy emotions that anyone should have. And as time passed I have come to admire her courage to get by despite the illness and the society’s contempt. And I respect her wishes not to be referred for further neurologic opinions.

– Dr. David S Bell, MD, Lyndonville, New York, August 15, 2000
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This article is excerpted with kind permission from Dr. Bell’s classic book Faces of CFS – Case Histories of Chronic Fatigue Syndrome; © David S Bell, MD, 2000,

“Maggie’s Panic”: When Fibromyalgia & ME/CFS Symptoms Gang Up

Reprinted with the kind permission of ProHealth: April 13, 2011

This case history of a patient with CFS and fibromyalgia, plus panic attacks fueled by the autonomic dysfunction that is common with both, is excerpted from Dr. Bell’s book Faces of CFS – Case Histories of Chronic Fatigue Syndrome,* published in August, 2000. “Maggie’s Panic” illustrates one aspect of the illness he has studied in patients affected by the ‘Lyndonville Outbreak’ over the years.

MAGGIE’S PANIC

I do not think a hidden neurosis or other psychiatric condition was lurking in Maggie’s subconscious. Her panic was organic in nature; it came on as a result of physiologic, not psychiatric, factors.

Maggie came into my office about two years ago. By then, she had been ill with chronic fatigue syndrome (CFS) for ten years. She was fairly classic for the disease: joint and muscle pain; night sweats; a headache that would not end; severe fatigue. Despite the latter, she could barely sleep at night.

Naturally, the doctors she had seen in the past were unable to explain the strange combination of symptoms that seemed to possess her like some demon from a haunted past. Maggie, in fact, had been to so many doctors, including two psychiatrists, that she had lost count.

Doctors grow suspicious when patients tell them they already have seen several doctors for the same problems; they assume such patients are looking for a medical opinion they like, as opposed to a medical diagnosis. This is called, in the trade, “doctor shopping.” Maggie knew she had been typecast as a shopper, but she was searching for a diagnosis that made sense.

The symptoms that distressed Maggie the most had to do with her heart.

If she took a walk, she developed chest pain and become short of breath. Once, she told me, after taking a very long walk, she had seen a doctor the next day. She looked ragged, as if she run a marathon and come in last. Her resting pulse was too fast – 110 beats per minute. She told the doctor that she was afraid she was having a heart attack, but the doctor surprised her with a diagnosis of panic attack, instead. Panic disorder has long been viewed as a bona fide condition in which the patient experiences panic at inappropriate times.

Chest pain and shortness of breath were just part of Maggie’s ‘heart’ symptoms, however.

• She often had episodes when her heart would race. Her heartbeat wasn’t merely rapid, it felt as if her heart was flopping around in her chest, as if she had drunk a gallon of coffee, but she had given up caffeine years ago.

• Her face would flush and her palms would sweat.

• Her lips would quiver, her hands would tremble, and one of her eyelids would twitch.

Most doctors, if not all, would diagnose what I have just described as panic disorder.

But Maggie also suffered from a constellation of symptoms that were diametrically opposed; in fact, they were remarkably akin to the state of being comatose.

• She was exhausted to the point of being unable to walk. She showered seated on a lawn chair because she could not stand, for instance; she slept on the couch in her living room because she was unable, at times, to climb the stairs to her bedroom.

• Another coma-like symptom had to do with the way her intellect was dulled. While driving, she sometimes couldn’t remember whether green meant stop or go. Nor could she recall the names of members of her family, or remember a seven digit telephone number – even if it happened to be her own. She found the dialogue on afternoon soap operas incredibly confusing, like a foreign language. Everyone spoke so fast!

• Her body felt leaden, and curiously toxic; she felt a certain kinship with Chernobyl’s radiation sickness victims.

• Her bowels couldn’t decide between coma or panic; they alternated between constipation and diarrhea.

In truth, her entire body couldn’t decide whether it was in a panic or a coma.

At night, when she awoke drenched in sweat, her heart pounding, it was as if panic was awakening her from her coma. There seemed to be no middle ground. Her doctors told her all these symptoms were ‘due to stress.’ To one such doctor, Maggie commented that, aside from the fact that she had lost her job and her husband, that she was bankrupt, and that she was often too weak to climb the stairs of her house, she really had no stress at all.

Our bodies respond to stressful events with the release of adrenaline from the adrenal glands. Adrenaline activates the body’s primal “fight or flight” response. It is a natural stimulant, resulting in a sudden rush of energy to deal with the crisis at hand. Panic is appropriate in times of danger, and adrenaline will give someone the strength to run, if that’s the best choice, or fight. A cave man confronted by a saber tooth tiger might choose to run; the student faced with final exams might choose to knuckle down and study.

Of course, after the adrenaline rush, we are left exhausted and weak, but the crisis is over and with a little rest we are good as new. This, in fact, is the key difference between panic disorder and CFS. Patients who have panic disorder may have relatively normal activity and energy when there is no panic. CFS patients never achieve a normal level of activity, no matter how much they rest or what measures they take to relieve stress. Take a person with CFS and put them on a sunny beach for a day, and their fatigue will not go away, nor will their panic-like symptoms.

Doctors and researchers have long experienced difficulty differentiating CFS [or the dysregulated autonomics of fibromyalgia (1,2,3)] from simple anxiety.

It is true that many persons with CFS experience anxiety. But because CFS patients tend not to have obvious, diagnosable psychiatric illnesses, I suspect that when panic occurs in CFS patients, the cause is physiological, not psychiatric. Whatever else this disease does to the human brain, it includes agitation in its repertoire.

That first time I evaluated Maggie, I realized her medical history was consistent with both CFS and panic disorder, however. In fact, if I were to follow the strict guidelines that the government has laid down regarding CFS, I would not diagnose Maggie with CFS. That’s because research criteria in use today are designed to create a homogeneous population of CFS patients for research purposes.

From clinical experience, however, Maggie’s tender lymph nodes, sore throat, endless headache, and intellectual difficulties were not consistent with a diagnosis of panic disorder. From a clinical point of view the most accurate diagnosis I could render for Maggie was both panic disorder and CFS.

Maggie didn’t really care about the label; she wanted to get at the basis of her symptoms.

Together, we decided to try some of the newer tests for CFS, tests involving the autonomic nervous system. In particular, we would look at the blood vessels and the heart’s ability to pump blood throughout the body. By the time I met Maggie, I had already learned that many CFS patients had low levels of circulating blood in their bodies, an abnormality sometimes accompanied by pulse and blood pressure changes when standing.

The medical term used for this is “orthostatic intolerance,” meaning, simply enough, a worsening of symptoms when in the upright position.

In many medical illnesses, the patient will feel ill regardless of whether he or she is lying down or standing up. With CFS, patients will say, “I feel so exhausted I have to lie down.” For 15 years, nearly every patient with CFS has said this sentence, and I, as well as most other doctors, have misinterpreted it. No wonder this illness is so poorly understood. People should not be tired from standing up for 15 minutes.

We have concentrated on the word “exhausted,” but the key words are, in fact, “lie down.”

The terms “fatigue” or “exhausted” don’t even really describe the unpleasant sensation experienced. “Collapse” is more accurate. What the patient with CFS is really saying is “If I don’t lie down, I am going to collapse.” Medically, the appropriate term is “pre-syncopal,” meaning the state which occurs prior to fainting.

Maggie agreed to allow me to test her orthostatic tolerance, her ability to function during quiet standing.

During a physical exam, she had two abnormalities:

• Fibromyalgia tender points in her muscles

• And difficulty maintaining her balance standing with her eyes closed, a common finding in patients with CFS.

The practical expression of this finding is that patients with CFS are frequently unable to stand for periods in a hot shower. The heat of the water in the shower makes standing more difficult than normal, and often patients will have to go to bed after a simple shower. Sometimes, persons with CFS will put a chair in the shower even though they may be able to walk around the kitchen for ten minutes. A curious, but important detail that Maggie related, implying that heat somehow worsened the process.

The first test we did was very simple, a test of concentration done on two different days, once while standing for 15 minutes and once after lying down for the same length of time.

One of the most prominent symptoms of CFS is the cognitive impairment. Patients will have difficulty with confusion, short term memory, doing simple calculations, and remembering names or telephone numbers. Sometimes this is so severe that concern is raised about dementia or senility. The hardest thing for a patient with CFS is “double tasking.”

My son has amazing powers of concentration. He can be in his room doing his homework, listening to rock-and-roll music while the TV, without sound, shows a football game. I made many vain attempts to inform him that it is not possible to do his homework that way, but his grades were good, and studying this way seemed to do little harm. He was able to “multiple task,” just like I do when I talk on the car phone, drive, and find a quarter for the toll booth, all at the same time. For my son, he probably used 80% of his brain studying, 19% enjoying the music, and 1% watching the football game. Most shows on TV, the sitcoms, can be enjoyed with even less dedicated brain function.

Double tasking is one of the first things to go in CFS.

The test we gave to Maggie was the coding test of the WISC, a standard intelligence test. In this test, a series of simple codes are made for numbers between 0 and 9, the code printed at the top of the page. The test involves finding, or remembering, the codes for a list of numbers, and scoring is done by adding up the correct coding accomplished in two minutes. It is an annoying little test.

After lying down, Maggie did the test, getting 55 right in two minutes, a normal amount. A week later we repeated the test after standing, and she was able to get only 40 correct, a 20% drop. We have been testing this with healthy persons, and found that, in general, they do as well standing as after lying down.

Maggie’s cognitive problems are related to the position she is in before the test. When horizontal, she does well; after standing, she is dull as a melon. This correlates to another curious detail often found in the history taking of someone with CFS – they read lying down. Most healthy persons prefer to read sitting up.

We measured Maggie’s circulating blood volume at a nearby hospital, and like 80% of our CFS patients, she was low, or as she would later say, “down a quart.”

This finding seems to mesh with the difficulty standing; gravity makes it difficult for blood to get up to the brain, and if the circulating blood volume is low, it should affect brain blood flow. And the mechanism of CFS may be that simple: decreased blood flow to the brain. We don’t know if animals can get CFS, but if they do, giraffes would be in big trouble.

The next test was the most exciting for me, the most unpleasant for Maggie. We call it “orthostatic testing” and it can be done in any doctors office.

It is a simple test, perfected by Dr. David Streeten (4), and described in Andrea Thompson’s case. The patient lies down for 10 minutes during which the pulse and blood pressure are taken. Then during a half hour of quiet standing the pulse and blood pressure are measures every five minutes along with observations of what the patient is experiencing.

Maggie’s blood pressure and pulse were normal while lying down, and she was feeling relatively well – it was a good day for her. We measured the amount of adrenaline in her blood while lying down and it came back at 350, a normal level. The first ten minutes standing were not bad for Maggie, although she started feeling tired. Then she described pain in her legs, lightheadedness, and spiraling fatigue. Her palms were sweaty, and I saw her grow visibly pale. Most significantly of all, she became agitated, and, eventually, she became panicked.

The pulse and blood pressure measurements began to change. When Maggie said she could no longer stand, we terminated the test, I did not want her to pass out on the floor. Her pulse had risen to 140 beats per minute, 80 more than when she had started, and her blood pressure had skyrocketed, almost to levels that could cause a stroke.

As soon as Maggie lay down, we drew a second blood sample to measure her adrenaline again. I also gave her an infusion of saline water. Normally, saline is the last thing you want to give someone with high blood pressure, but I already knew Maggie had abnormally low circulating blood volume.

The elevation of her blood pressure had to be due to a constriction of the blood vessels, a compensation mechanism that would help circulate the blood to her brain. The fast pulse reflected the same problem: Her autonomic nervous system was trying to make her heart beat faster in order to circulate blood.

While standing, Maggie began to fall apart because her brain was deprived of blood.

A healthy person has several compensatory mechanisms that automatically keep blood flowing to the brain indefinitely. Maggie might look healthy to a casual observer, and the private disability company she had paid into for many years prior to becoming ill said that she was just fine.

But imagine Maggie trying to work an eight hour day when she had such dramatic changes in pulse and blood pressure after just 20 minutes standing. I would definitely not want her to be my bank teller trying to make change after standing for two hours.

Maggie’s compensatory mechanisms were impaired. All but one, that is: adrenaline production.

The body produces adrenaline to compensate for impaired blood flow to the brain. In fact, it is one of the body’s most effective ways of improving circulation, which is why it is called the “fight or flight” mechanism.

Perhaps the most significant finding we made that day had to do with Maggie’s adrenaline. Her adrenaline level had risen to 1450, way above normal, when she had been forced to stand for 20 minutes. Maggie’s body was pumping out adrenaline like mad just to compensate for the crisis of quiet standing.

Adrenaline has one drawback: It causes anxiety.

I believe now that Maggie’s panic was simply due to elevation of her adrenaline levels in an attempt to compensate for impaired blood flow to the brain. I do not think a hidden neurosis or other psychiatric condition was lurking in her subconscious. Her panic was organic in nature; it came on as a result of physiologic, not psychiatric, factors. Panic is appropriate during a crisis, but not during quiet standing.

The surge of adrenaline has several drawbacks. First, it doesn’t work very well. If it had, Maggie would feel wonderful, like the burst of energy after having a cup of coffee in the morning after a good night’s rest. It may be that the adrenaline keeps her up longer, but the price is fatigue. A healthy person will notice that after a crisis, a near car accident for example, the surge of adrenaline is followed by profound exhaustion. Chronic stress will leave a person drained and tired, but recovery occurs quickly once the stress is removed and good rest is supplied.

Maggie’s fatigue is due to a combination of decreased blood flow to the brain and the surge of adrenaline her body produces to attempt to remedy the problem.

Suddenly, there were several medical diagnoses I could give Maggie.

Technically speaking, she had chronic fatigue syndrome, fibromyalgia pain and tender points, idiopathic hypovolemia (decreased blood volume), postural orthostatic tachycardia, orthostatic narrowing of the pulse pressure, orthostatic diastolic hypertension, and hyperadrenergic orthostatic intolerance.

Maggie was not displeased; literally overnight, she had gone from being a hypochondriac to having seven medical diagnoses.

Research into blood volume and brain blood flow is in its infancy. Nevertheless, while we are still in the dark as to what initiates these problems, breaking CFS down into its many parts may allow us to develop specific diagnostic tests for the disease.

Moreover, Maggie’s testing results inspire theoretical treatment options. If we could somehow increase blood flow to the brain and deliver more oxygen to brain tissue, the symptoms of impending collapse should improve. The need for the adrenaline surge would be removed, so the postadrenaline exhaustion would also disappear. In concept, that is.

The co-existence in CFS patients of simultaneous coma and panic symptoms is no longer paradoxical.

Doctors and researchers who assume panic disorder is caused by psychiatric problems exclusively have been looking at the phenomenon in an overly simplistic way. The same chemical mediators that are present in emotionally stressful situations are also the same chemical mediators that help circulate the blood. A test would be to find a way to improve the blood circulation in the brain.

We started with a drug to expand her blood volume, and Maggie’s response to treatment made me so excited that my socks started rolling up and down all by themselves.

Peter Rowe and his colleagues at Johns Hopkins made an important discovery in 1996 after discovering that patients with CFS would faint when tilted upright on a tilt table. They treated their patients with a drug called fludrocortisone (Florinef™), which works by increasing salt and water retention by the body, thus raising blood volume.

I had tried Florinef in many of my patients, and it improved their symptoms about one-third to one-half the time. In my experience, adolescents and those with milder illness responded best to this treatment. The drug helped Maggie: her rapid pulse slowed down, her sleep improved, and she felt slightly more energy. Her panic nearly disappeared.

The concept that a presumably psychiatric symptom – panic – would be helped by a drug which increases circulating blood volume is hard to believe. But it happened to Maggie. Her panic was clearly caused by CFS and its concomitant blood volume deficits, not the other way around. I was encouraged by these changes, but my socks had not yet started rolling, the surprise was yet to come.

Maggie and I talked almost every day during this trial, and we decided to push the therapy a little further by adding salt tablets, hopefully to augment the response.

Two days after adding salt tablets, Maggie returned to “normal.”

At first, I didn’t know what Maggie meant by “normal.” Did she feel a bit better? No, she was reporting complete recovery, normal for the first time in ten years. It was as sudden as a switch being thrown; she described her transformation as “awakening from a dream.” Her thinking was crystal clear. She walked for two miles that first day, smelling the flowers of spring. The whole feeling of illness, the malaise, was gone.

Unfortunately, her recovery was brief. Thirty-six hours later, she began slipping back to her former state, minus the panic, and she has remained in that particular jail cell since then.

We have tried 20 different treatments, raising and lowering doses of this and that, but she has not regained her freedom. In retrospect, the memory of 36 hours of freedom remains a cruel reminder of how nice it feels to be healthy.

The importance of Maggie’s experience to me is a confirmation of a long held belief that CFS is a reversible state, even after ten years.

Not just treatable by reducing some of the symptoms, but reversible. Her return to health was short lived, but it occurred. If she had permanent damage to her brain, I do not think the 36 hours would have been possible.

What is so frustrating is the fact that this state could not be maintained, even though we tried treatments that pushed so much blood into her brain that her skull was ready to explode. Maggie has been a good sport about all of this. Each treatment attempt was discussed in detail and she was eager to take the steps.

While disappointed that we have not been successfuI I see the problem a little differently now. By expanding blood volume it is possible to make some improvements, but not all the time. Even with Maggie’s dramatic 36 hours, the response cannot be maintained even if the blood volume is returned to normal or even elevated levels.

The problem must be in the blood vessels themselves. They must be constricted so tight in the brain that little blood gets through. Perhaps it is one of the hormones that constricts blood vessels. Perhaps an infection of the blood vessels. Perhaps it is an excessive sensitivity of the blood vessels to adrenaline.

Hopefully, this story will soon have a new and more encouraging ending. CFS is a devastating physiologic process that undermines the body’s energy and the brain’s cognitive ability, but I believe that full recovery will someday be possible.

We await the next step, the step that will make Maggie’s precious 36 hours stretch into days, months and years. There is so much to study in this illness, and so much to be gained. Science needs to recognize the importance of CFS, embrace its difficult paradoxes, and get to work.

• CFS is not an isolated, rare illness nor is it an illness behavior for lazy people.

• The consequences of this illness weigh heavily on not only the victim, but also on family, community and society.

• Its tentacles seem to reach across boundaries, blurring the lines between other neurological and immunological disorders.

CFS, and the patients who suffer from it, have a great deal to teach those of us who have made medicine our life. Once researchers unravel the physiologic mechanisms of this illness, the discoveries will help unravel basic mechanisms of unnumbered other diseases.

– Dr. David S Bell, MD, Lyndonville, New York, August 15, 2000

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* This article is excerpted with kind permission from Dr. Bell’s classic book Faces of CFS – Case Histories of Chronic Fatigue Syndrome; © David S Bell, MD, 2000.

“Arnie’s Story”: A Child’s CFS, Misdiagnosed as Munchausen’s by Proxy

Reprinted with the kind permission of ProHealth: 4/27/11

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ARNIE’S STORY

A chronic disease robs children of many things, but it should never destroy the life-affirming refuge children find in their home, as it did with a boy named Arnie… because everything about Arnie was typical of CFS – a disease his doctor did not believe existed.

Karl Friedrich Hieronymus Baron von Munchausen was a German “soldier, adventurer, and a teller of tales,” according to one description, who lived from 1720 to 1797. His fantastic lies about his daring and conquests were so notorious that their memory survives to this day as German lore.

Medical science has borrowed from this ancient character’s name to categorize the patient who engages in equivalently tall tales, all having to do with physical illness. When a parent or caretaker makes up bizarre tales concerning the health of their child, doctors call it Munchausen’s syndrome by proxy.

Sometimes the parent intentionally harms their child, by poisoning for example, to create the symptoms. Experts suggest the parent is motivated by a need for attention, and get it they eventually do, one way or another.

Although it was the Baron who proved himself capable of such outrageous falsehoods, women are more vulnerable than men to being suspected as having Munchausen’s syndrome. And women are suspected of Munchausen’s syndrome by proxy when doctors are unable to find a simple answer to a child’s ills.

This is because women typically take the dominant role in helping children through the maze of doctor’s visits, hospitalizations, and treatments when children fall chronically ill.

Every year, parents in this country and abroad face court hearings before judges and juries in which they are subsequently found guilty or innocent of intentionally harming their child due to Munchausen’s syndrome by proxy.

Depending on the circumstances, the prosecutor, representing the state, may add fraud to the charges. Usually, the mother’s psychological competence becomes an issue of enormous significance in such a trial. If a child has been judged to have Munchausen’s syndrome by proxy by a psychiatrist serving as the state’s expert witness, the mother may face the removal of her child from her household, usually into foster care, as well as criminal charges.

The notion of a mother deliberately hurting her child is difficult for most of us to comprehend. Nevertheless, for some years now, Munchausen’s syndrome by proxy has been accepted by the medical profession as bona fide, if somewhat baffling. And there is no question that it occurs. Hidden videotapes in hospital rooms show parents either injuring their children, or doing things that make it appear that a child is ill. What a world….

But, because this does occur, physicians have grown suspicious, particularly when confused by symptoms in the patient they treat.

With this in mind, imagine what might happen when a mother whose child suffers from an extremely complex, misunderstood – even overlooked – chronic disease, becomes an outspoken advocate for that child, struggling to explain her son’s illness to unsympathetic doctors and suspicious school officials.

Imagine the situation from the perspective of the sick child, who can barely articulate to his friends, much less to an attorney or a psychiatrist, what ails him. Imagine how, over time, these quiet struggles can escalate, thrusting mother and child into a firestorm of accusations by authorities of all stripes, as they attempt to salvage their dignity and even their right to remain a family.

A chronic disease robs children of many things, but it should never destroy the life-affirming refuge children find in their home, as it did with a boy named Arnie.

Arnie was ten when he experienced the onset of CFS, but for much of his brief life he had suffered a seemingly endless succession of colds, allergies, sore throats, stomach aches, and headaches.

The doctors his parents took him to see somehow failed to notice a pattern of minor infections that, in retrospect, strongly suggested Arnie may have had a medical problem for some time before the symptoms suddenly escalated.

Instead it was attributed to an over-anxious parent worried about trivial illnesses. In July, 1990, Arnie’s heightened level of exhaustion, hitting him hard after an intestinal flu, heralded the onset of full-blown CFS.

By the time school began that September, Arnie was too weak to stand and was confined to bed. His mother took him to see a pediatrician numerous times, but the doctor was unable to explain Arnie’s profound fatigue.

Months passed, a period during which Arnie failed to receive either a diagnosis, or an education. By law, school systems are required to provide home tutoring to students who are too sick to come to school, but school systems also require that the child carry a diagnosis before they hire a private tutor using state dollars. Arnie had no diagnosis.

The school year ended, and another began.

Arnie was still house-bound because of the exhaustion. In every respect, he was absolutely typical of a child with CFS.

• He suffered from sore throats, headaches, sensitivity to light and blurred vision, pain in his muscles, joints, and lymph nodes.

• His ability to learn was diminished because of difficulties with memory and attention.

• He could not remember what he had read.

• His attempts to exert himself physically uniformly resulted in relapse, or worsening of his fatigue.

Eventually, doctors ruled out thyroid disease, lupus, multiple sclerosis, rheumatoid arthritis, HIV disease and hepatitis.

Some of these doctors did find immune abnormalities that suggested that Arnie was suffering from an on-going viral infection.

But the doctors believed that the abnormalities failed to fit a pattern associated with any particular disease – at least, any disease with which they happened to be familiar.

• Neurological tests revealed that Arnie suffered from vertigo and lacked the kind of fine motor control in his hands that might be expected of a boy his age.

• Other tests of intellectual capability demonstrated that Arnie’s short term memory and concentration skills were impaired.

All in all, everything about Arnie – his long history of illness, his physical exam, his laboratory tests – were typical of CFS, a disease his doctor did not believe existed.

It was just eight months after Arnie had become severely ill, however, that his parents began arguing about whether or not he was really sick.

Arnie’s father sided with the child’s pediatrician and other specialists, who had suggested that there was nothing medically wrong with the boy. Arnie’s father was particularly tired of paying for medical exams that failed to provide definitive answers. He believed his son needed psychiatric care.

Arnie’s mother felt differently. She did not believe the doctors. Instead, she began to explore unconventional treatments for her son, embracing, for a time, the “fringe” medicine offered by “ecologists,” naturopaths, and acupuncturists, each of whom seemed confident they understood Arnie’s problems, yet each of whom had a different explanation for them.

Arnie’s father thought these alternative healers were a bunch of loonies.

In time, the boy found himself at the hub of an escalating battle between his parents.

Large conflicts and petty complaints that had smoldered for years between the two adults erupted in a war centered on their son. Naturally, the boy tried hard to feel better in order to bring an end to the war. When his illness continued, in spite of his best efforts, he became withdrawn. And when Arnie’s father moved out of the house, Arnie assumed he had caused the break up.

A child sees the world from a simplistic, egocentric point of view. By the age of ten, children are better able to assess the relationship between cause and effect than they were at five, but the tendency to believe in a magical connection between one’s own actions and unrelated events has yet to vanish entirely at Arnie’s age.

Arnie’s parents made a mistake, too. They were unable to separate their private conflicts from their son’s illness, leaving him caught in the crossfire. What followed was probably inevitable: a kind of chain reaction in which a sick child became a battleground, fought over not only by his parents, but by the local school system, and, eventually, the state of New York.

As far as Arnie’s pediatrician and his teachers were concerned, the issues were clear.

Arnie seemed to be incapacitated with a slew of mysterious symptoms, just as his parents were in the process of divorce. These authorities believed Arnie was suffering a kind of psychiatric meltdown because of his parents’ acrimony.

According to the law of the land, if parents are causing a child’s illness – whether psychiatric or medical – then the parents are guilty of child abuse. In such cases, the law decrees that the appropriate social institutions intervene on behalf of the child, even removing the child from the destructive environment if necessary. In Arnie’s case, the vultures were beginning to swarm.

The principal of his school made several visits to the boy’s house during the first year he was absent, acutely aware that neither his parents nor his doctors had been able to offer the school a diagnosis. Each time she visited, Arnie was in the living room, seated, and watching television. He did not look sick to her.

The principal assigned a truant officer to the case.

The officer saw Arnie in his back yard one spring day, resting in a lawn chair, sipping lemonade. Finally, the school filed a truancy petition with the local court in order to force Arnie to return to classes. In addition, the local social services department launched an investigation of Arnie’s parents to determine if they were guilty of child abuse.

At the court hearing on the matter of truancy, the judge listened to the attorney representing the school argue that Arnie had been absent without good cause.

Arnie’s mother, representing herself, told the judge about her son’s medical condition. She called it chronic fatigue syndrome. She also described the holistic-style therapy of vitamins and herbs and acupuncture she had embarked upon to cure her son.

In turn, the impassive judge inquired about the impending divorce, as well as the custody hearing. Arnie’s parents had begun arguing about which one of them would raise their son after the divorce.

Not surprisingly, the judge, who knew of CFS only as the rather flaky sounding “yuppie flu,” concluded the hearing by ordering a psychiatric evaluation of Arnie. He also ordered Arnie to return to school.

The next day, two things happened, both of which ended in disaster: Arnie went to school, and his mother hired an expensive attorney.

At school, Arnie found to his dismay that his old friends greeted him with poorly concealed contempt. They had heard the rumors: Arnie was faking it. On the second day, the gym teacher decided that Arnie could benefit from exercise; the teacher believed exercise would shake the boy out of his long “slump.”

On the morning of the third day of this new regime, Arnie discovered he was once again too weak to get out of bed.

In the meantime, the lawyer hired by his mother had obtained Arnie’s medical records and had read them closely, paying special attention to the variety of opinions from specialists suggesting Arnie’s problem was psychosomatic.

The attorney made a unilateral decision: Assuming the doctors were correct that family turmoil had caused Arnie’s psychiatric problem, she decided to put her energy into helping Arnie’s parents obtain their divorce.

At the court-ordered psychiatric evaluation, the doctor began by interviewing Arnie and his mother together. Arnie was dizzy, exhausted, and found it difficult to concentrate on the psychiatrist’s questions. His mother recognized her son’s distress, and consequently did most of the talking in order to help conserve his limited energy. Afterward, the psychiatrist asked to talk to Arnie without his mother present.

The exhausted child was slumped in his chair. It was flagrantly apparent to Arnie that the psychiatrist had believed very little his mother said, and, after her departure from the room, he became even more withdrawn, even hostile. He responded to the doctor’s queries in monosyllables. Finally, the psychiatrist talked to Arnie’s mother privately.

The woman tried to “explain” chronic fatigue syndrome to the psychiatrist, who eyed her warily.

Struggling to suppress her own feelings of despair, she spoke as enthusiastically as possible about the alternative medical treatments she was continuing to explore. She wanted the doctor to know just how hard she was trying to help her son get well. The psychiatrist concluded the interview eventually, leaving Arnie’s mother feeling uneasy.

Afterward, the doctor called her husband, who took the opportunity to tell the psychiatrist that his boy was fine. His wife was the sick one, he added.

A week later, the psychiatrist submitted his report to the court. At the end of a lengthy discussion, he unveiled his diagnosis: Munchausen’s syndrome by proxy.

Arnie ‘looked well’, the doctor had argued in his report.

In addition, Arnie was clearly depressed. He pointed out, too, that neither the boy’s father nor the boy’s doctors believed Arnie was medically ill, and that the child was at the center of a custody battle between divorcing parents. More critically, the psychiatrist noted, there existed an unusual degree of “enmeshment” between mother and son; Arnie’s mother had acted as his spokesperson during their interview.

Further, she had appeared enthusiastic, even cheerful. Clearly, she had created an environment of oppressive neediness that had driven Arnie to feign illness, and her subsequent “over-involvement” with her child’s illness stemmed from this deviant desire to be needed.

The judge ordered that Arnie be removed from his mother’s custody and placed in a foster home.

He ruled that the final determination of Arnie’s fate would be decided in the custody hearing. He also demanded, for a second time, that Arnie return to school and receive twice-weekly psychiatric counseling. In a small concession to the boy’s claim of illness, the judge ruled that Arnie could be excused from gym class.

One week later, Arnie swallowed a handful of aspirin and several sleeping pills he discovered in his foster mother’s medicine chest. He was admitted to a psychiatric hospital immediately afterward. Though it had never been Arnie’s specific intent, his suicide attempt had confirmed beyond all doubt the diagnosis of the court’s psychiatrist, school officials, and the judge who had presided over his truancy hearing: He suffered from a serious psychiatric illness.

Arnie’s incarceration and resulting isolation would have been considerably less had he robbed the corner grocery store.

• The psychiatric hospital administrators forbade his mother to visit him; after all, she had fostered the imaginary illness in her son, then encouraged his belief in it.

• Hospital doctors ordered him to submit to counseling sessions, sessions during which he found it hard to avoid confessing his depression. Such confessions only served to strengthen the prevailing view that his bizarre “illness” was psychiatric in origin.

• Arnie was given large daily doses of tricyclic antidepressant medications, a class of drugs that often increase fatigue in CFS sufferers. When Arnie complained that the drugs made him feel worse, staff at the hospital simply ignored the complaints.

• They further demanded that he participate in all the ward activities. Arnie followed the path of least resistance, dragging himself from project to project without comment, but he felt as if he was dying a slow death.

In short, Arnie was snared in a trap worthy of Franz Kafka’s imagination.

He would remain incarcerated and drugged until he was successfully rehabilitated, which chiefly meant renouncing his absurd belief that he was sick.

Doctors like to solve problems. They like to make people well. Nothing makes them happier. Sadly, when they fail, their universal fallback position amounts to blaming the patient for his or her own disease. Even when the evidence points in the opposite direction, doctors frequently come up with psychological diagnoses in the absence of clear answers.

Children may be the most vulnerable of all to such treatment. It’s hard for them to fight for their rights, or make the case for their own sanity. Pediatricians, when flummoxed by their small patients’ complaints, tend to cast a suspicious eye at the child’s home environment: If the parents are in distress, pediatricians are provided with a convenient explanation for mysterious symptoms in the child.

As a pediatrician, I recognize the legitimacy of including the status of a child’s home life in my differential diagnosis – the decision tree I work from as I search for the correct diagnosis. But I do not automatically exclude the possibility of medical illness in a child because his parents are on the verge of a divorce, or if a grandmother died.

Just as it is possible to have child with diabetes living within a family in turmoil, it is possible to have a child with CFS living within a family in turmoil. Family dysfunction has its own signature; it creates its own particular pattern of difficulties in children, and these problems are very different from the problems of CFS.

Demanding that a diagnosis of CFS may be made only in perfect families makes no sense at all.

In truth, family problems are common, and with the additional stress of a chronic illness in a family member, families can even fall apart. In my view, psychological diagnoses need to be made with the same specificity and accuracy as medical diagnoses. It is not enough to pull a psychological diagnosis out of your hat if you are stumped. It is necessary to be a good doctor. Of course, the attribution of the psyche to the cause of physical illness is hardly a new phenomenon, especially in children.

Autism is a severe neurologic disease of childhood, but for many years doctors ascribed autism to family dysfunction.

We now understand that autism has nothing to do with poor parenting; it is an organic disease.

Like medicine, psychiatry has a spotty history. Perhaps the most classic example of psychiatric miscalculation was the belief, in earlier centuries, that “shock,” – the dire condition we recognize today as the result of a dramatic loss of blood – was due to a “shock” to the emotions. Early psychiatric literature stated that the thready pulse, pale face, clammy hands, and drop in blood pressure – classic shock symptoms – are the result of an emotional shock, likely a reaction to the shock of the sight of blood.

During the American civil war, however, a doctor noted that this emotional condition called “shock” was quickly followed by death among soldiers who were mortally wounded on the battlefield. He reasoned and later proved that shock was a physiologic abnormality caused by blood loss. Imagine telling someone who has just been shot in the chest to snap out of their blues and pull themselves together.

I am not going to debate the legitimacy of Munchausen’s syndrome by proxy. It exists, a sad commentary on modern society. But the diagnosis of Munchausen’s is made by obtaining absolute proof of a parent inflicting conscious and active harm on their child. Frequently, hospital administrators who suspect a parent of Munchausen’s will install a videotape in the room of the young patient in order to acquire irrefutable evidence of a parent committing such harm.

In Arnie’s case, neither the court nor school officials bothered to offer proof of his mother’s intent to cause harm, or even actual harm, no doubt because they had no proof.

Their actions were based on conjecture.

Even putting aside medical arguments, common sense tells us that Arnie’s the activity limitation is not due to suggestions from his mother. Adolescents are known for being rebellious and not doing what their parents tell them to do. Sometimes I have a hard time getting my son to clean his room. How could a parent tell a child to be tired all the time and stay sitting in a chair?

Fatigue caused by Munchausen’s syndrome by proxy is a legitimate diagnosis only if the parent is secretly feeding their children barbiturates or poison, and this can be easily tested.

In my view, the mother’s so-called “enmeshment” in her son’s illness was an attempt to protect her child from the authorities in the school system, the legal system, and the medical establishment, who understood absolutely nothing about the disease from which he suffered. I believe she should have been guilty of child abuse if she had been indifferent to her son’s suffering.

It would be wonderful if I could report here that Arnie’s story is a singular one. Unfortunately, these events are becoming increasingly common as more and more children and adolescents fall ill with CFS.

The medical establishment and our federal health agencies are digging in their heels, so to speak, hewing with vigor to the mistaken belief that CFS is psychiatric in origin. As a result, more and more children who suffer from CFS are being diagnosed with Munchausen’s syndrome by proxy, and the courts are remanding them to foster homes.

Arnie’s attempted suicide attempt, under such conditions, is hardly uncommon, either. Too often, children with CFS who have been taken from their homes, told they are imagining their illness, and sent to live in strange homes with adults who refuse to acknowledge their symptoms and disability, find death to be a better option.

Like Arnie, these sick children frequently end up in psychiatric institutions, deprived of the comfort of the parent, or parents, who may be the only people who understand they are ill.

Failure to diagnose an illness is, in some circumstances, malpractice. Failure to properly diagnose Arnie resulted in a forced separation from his mother – his only advocate – and his subsequent suicide attempt and incarceration. For Arnie, failure to diagnose had serious consequences.

The existence of CFS has been confirmed by the National Institutes of Health and the Centers for Disease Control. There continues to be legitimate debate as to what causes the illness, but to deny its existence because of a collective failure to understand its cause is inexcusable.

The American Academy of Pediatrics has stated that at least one part of its mission is to act as advocates for children. On the contentious matter of CFS, which afflicts thousands of children and adolescents, however, the Academy has remained silent. I believe the Academy’s silence is equivalent to child abuse. Our court systems have an obligation to protect the young and the helpless. Our courts, however, take their advice from the medical profession.

There are many forms of child abuse: neglect, physical abuse, sexual abuse… I would like to suggest that the term “medical abuse” be used when children are directly hurt by apathy or ignorance of health care providers.

Not the ignorance expected prior to scientific discovery, but ignorance defined as refusal of accepted fact. We are not talking about a new religion here, CFS has been recognized and studied in this country for nearly 20 years [now 30].

In the villages of ancient Europe, citizens believed that hitching four widows to a plow and forcing them to labor through the night would ward off epidemics of plague and influenza. Some day, the current apathy, perhaps more accurately, the silence, that veils the existence of CFS, will be considered medical barbarism on a grand scale, and just as ridiculous as hitching widows to a plow.

Arnie is 19 years old now, and remains disabled by CFS.

His incarceration in the psychiatric institution lasted six months, after which he lived in foster care for another several years. He has reunited with his mother, and is at last receiving basic symptomatic care for his illness.

– Dr. David S Bell, MD, Lyndonville, New York, August 15, 2000
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* This article is excerpted with kind permission from Dr. Bell’s classic book Faces of CFS – Case Histories of Chronic Fatigue Syndrome; © David S Bell, MD, 2000.

“Anna’s Identity”: When Nobody Believes You’re Really Ill

This is the case history of a woman who suffered CFS symptoms since childhood but was never believed – until at age 35 doctors decided something ‘real’ was wrong. It is excerpted from Dr. Bell’s free e-book Faces of CFS – Case Histories of Chronic Fatigue Syndrome,* published in August, 2000. “Anna’s Identity” illustrates one aspect of cases he has followed since the mid-1980’s.

Reprinted with the kind permission of ProHealth: 9/14/11

ANNA’S IDENTITY

Where does self end and illness begin? When we are ill for years, or for a lifetime, what part of our personality is really our own, and what part has been shaped or even created by disease?

These questions are probably nowhere more pressing than in the realm of brain disease, in which the foundation of the personality – the physical brain itself – is under siege.

CFS, of course, presents a particularly difficult challenge to its sufferers because, unlike many brain diseases, CFS leaves the brain intact enough to sense its own difficulties. As a result, people who have CFS are forced to cope not only with unceasing physical pain and exhaustion, but with sorting out their real selves from the demon that has attacked their faculties as well as their body.

Adults have an advantage over children with CFS.

Adults have accrued years of personal history; they have a sense of who they are, a personality, against which they may compare their new, unwell selves. Everyone around them may be snickering and laughing, but the adult with CFS knows he or she is unwell, and that what is happening is anything but normal. Children, on the other hand, lack the requisite life experience and sense of self against which to measure a sudden development like CFS.

I am a pediatrician by training, and I have learned to see the world through the eyes of my youngest patients; I also frequently look into their eyes and see the adult world reflected there. I do not believe I am being disproportionate to state that, for children, CFS is among the very most difficult, if not the most difficult, disease to survive into adulthood.

Perhaps the greatest tragedy of CFS in children is that poorly informed adults ascribe a false identity to the child, and that false perception of self is carried by the child into adulthood.

CFS has robbed far too many children of their identities, or more precisely, has robbed them of the chance to develop an identity – to grow into themselves. In the case of at least one patient I know, however, a true perception of self has emerged, despite the odds, but it took 35 years.

I am speaking of Anna, who became ill with CFS when she was probably four or five years old.

We often remember of our childhood that which was wonderful and beautiful, but when there has been little joy, memories are dimmer. Anna’s memories are cloudy, but she recalls that by the time she was six or seven, she was unable to keep up with her playmates.

• She could not skip rope because her balance was poor and the slightest exertion left her breathless.

• The bright sunlight that poured onto the playground left her feeling blinded.

• She found herself on the sidelines, inexplicably exhausted. Other children seemed to shy away from her.

Anna went to school every day, but she felt sick all the time.

She found it difficult to learn skills like reading and math. It was humiliating. She couldn’t remember her multiplication tables. Everyone else could, but Anna couldn’t. Anna began to devise tricks to help her remember, tricks so complicated she could not have explained them to anyone. For example: eight times seven. Add a zero to a seven, subtract seven, then subtract another seven.

For Anna, visualization was easier than memorizing. She could see numbers in her mind, for instance, and in order to solve the problem, she would look at them. She knew she did not think like other children. The world was a very confusing place.

She had trouble following directions. Her teachers were harsh with her; they believed she was either deliberately ignoring them, or preoccupied with private thoughts. But Anna was simply puzzled and tired.

The simple noise of the classroom distracted and perplexed her. It made her ears hurt, too. She had trouble finding words to describe how she felt. She once told her teacher that her brain seemed to “ache” because of the noise, and her teacher dismissed it with a wave of her arm.

“Pooh,” she said, “everything seems to bother you.”

Perhaps Anna’s greatest humiliation was the way her one of her legs would jump without warning, hitting the desk, or even kicking toward the child sitting next to her. Her classmates would burst into laughter, and her teacher would inevitably become angry, scolding her for being disruptive. Anna had no control over these muscle spasms, but her teacher never believed that.

Eventually, Anna learned that if she rested the legs of her desk on top of her feet during class, the weight of the furniture would diminish the force of her jerking legs. The desk was heavy, and hurt her feet, but the technique worked.

Anna wondered why her muscles behaved unlike anyone else’s muscles, and why she was unable to memorize facts, and unable to remember what the
teacher said to the class from day to day. She wondered why she lacked the energy to run or play games. She struggled to hide these aspects of herself, her deficiencies, from the girls in her class, because like any child she desperately wanted friends.

Yet, even though Anna privately wondered every day what was wrong with her, no one believed Anna was sick.

She recalls that during her early adolescence, she was stricken with a remarkable number of sore throats, fevers, stomach aches, swollen glands, and headaches. As time passed, and she went from child to teenager, her doctor began voicing his opinion that Anna’s “illnesses” were an obvious cry for attention.

Occasionally, she was hospitalized while a teenager, but the tests ordered by her doctor rarely showed any abnormalities. Her doctor, and eventually, her own parents, began to exhibit increasing frustration.

By the time she was 15, no one believed Anna was sick.

• Her parents’ frustration turned to anger. They were poor people, and the medical bills caused by Anna’s frequent trips to the doctor were beginning to overwhelm their resources.

• Eventually, the doctor her parents took her to simply patted her on her head and told her she had a headache every day because she felt badly about doing poorly in school. The doctor told Anna she needed to stop “playing those games.”

Anna’s response to the anger and disbelief was hardly surprising: she learned not to complain.

She recognized that articulation of her sensations of illness only increased her isolation and actually invited ridicule. She vowed she would hide her symptoms and her feelings however she could from her family, her friends, and her teachers. She even learned to hide these things from herself.

In time, there were two Annas: the one who was sick, and the one who cleaned her room, performed her chores, and attended school every day just like everyone else her age.

• The first Anna would look at the second with a kind of astonishment; the second Anna was ashamed of the first.

• Neither of the Annas found any comfort at school or at home, but they got by.

By the time she became an adult, Anna had hidden her secrets for so long that she barely acknowledged them herself. In fact, by then, she had persuaded herself that her doctors had been right all along: if she had some dreadful illness, she reasoned, her doctors would have identified it, or she would have died.

She embraced fully what she had been told throughout her adolescence: She had made up her symptoms, although her reasons for having done so continued to remain mysterious to herself.

Anna finished high school, married, and began working as an aid in a nursing home. She also had four children. Most of the time, she could keep her secrets hidden, from her husband and children, and even from herself. She was not even being dishonest, because she was in agreement that all the sensations she felt – the weakness, the fatigue, the mental cloudiness – signified nothing at all. There really wasn’t anything wrong.

By then, the years of denial had worked their effect; her identity, her sense of herself, had been formed by the opinions of others. The part of her that felt and experienced was shut away from the part that reasoned. She was, she would tell herself, perfectly healthy, but in fact her identity was built on a foundation of silt, and had little to do with Anna’s true experience, the reality she lived day-to-day.

By the time she was in her early 30’s, Anna skills of self-deception and general deception were finely honed. She had become a master of covering up embarrassing intellectual gaffes with warm, genuine smiles that would put those around her at ease. No one could be expected to see through her smile to the memory loss, or the peculiar lapses in her speech, lapses in which she would jumble the order of her words in a sentence, or make bizarre mistakes in her choice of words.

She had learned to work despite her daily exhaustion and painful headaches. In fact, she felt weak all the time.

But if she had to help lift a patient at the nursing home, she found the strength, proving to herself and the other aids that she was as strong as any of them.

• Though she often experienced double vision, she never said a word about it to her co-workers.

• When she stood rapidly, she got lightheaded, and her hands and feet went numb.

• She developed a painful stomach condition – probably an ulcer, she decided. A doctor she consulted prescribed a drug for ulcers, but the pills did nothing to end the pain and Anna quit taking them.

She was disappointed in neither her doctor nor the drugs. Whatever the cause of this particular ailment, she reasoned, it was outside the doctor’s reach because, as she knew already, there was really nothing wrong with her. She could get by, she reasoned, just as she had always gotten by.

Of course, she never discussed these problems with her fellow workers in the nursing home, and no one around her ever suspected them.

One harsh, upstate New York winter after another passed. Anna acknowledged to herself a certain loneliness, familiar to her from earliest childhood. She had never quite rid herself of that. But her routines were well-established, her coping mechanisms firmly in place, her secrets tucked so deep inside that she barely thought of them.

Anna’s identity was a fragile construct, however, and vulnerable. One bitter day in March of 1988, it began to break up.

She suffered a seizure while working at the nursing home, an event witnessed by several people. She was taken to a local hospital. When the doctor informed Anna afterward that she had experienced a seizure, she found it extremely difficult to believe, despite the bite on her lip and the deep gash in her tongue.

In fact, she did not believe it – not really. After all, after a lifetime of feeling sick, this was the first doctor who had ever told her with any conviction that she actually was sick.

And so she fell back on the opinion of her condition that had been voiced by doctor after doctor from her earliest memories: she was just suffering from a little stress.

When the doctor prescribed medications for seizures, Anna nodded, as if accepting the diagnosis and the treatment. But she did not take the medication. Why should she? She knew there was nothing wrong. There never had been anything wrong.

For three decades, Anna had been able to secret away the ill woman she had been nearly all her life.

But things were starting to change. She continued to avoid the prescribed anti-seizure medication, and both her doctor and her husband insisted that she was having convulsions. Anna found their claims hard to believe. She was unconscious when these so-called seizures were reported to occur; how did she know they were really occurring?

It had been a life-long struggle, but Anna had achieved the ability to believe the medical profession, her parents, and her teachers, that nothing was wrong with her. Now her doctors and family were insisting something was wrong. In fact, her doctor arranged for her driver’s license to be revoked. Anna couldn’t even get to work.

The seizures were exposing the sick side of Anna to herself. They could not be hidden away or covered up with a charming smile and a little joke. The turmoil in her mind was like a hurricane. If she accepted that the seizures were real, she risked opening the long-hidden conflicts about everything concerning her poor health.

In short, if the seizures were real, maybe everything else – the exhaustion, the mental fogginess, the numbness in her hands and feet, the pain, the forgetfulness, the endless headache – were real, too.

The bedrock foundations of her assumed identity began to erode. For the first time in years, Anna began to allow herself to acknowledge her physical sensations of fatigue and pain. She realized that she felt awful. But experiencing the pain and exhaustion somehow seemed better than pretending it wasn’t there. She answered one question that most people are unable to: Is it better to feel suffering than to feel nothing at all?

One day Anna saw a segment on television about CFS. Her mouth hung open as she heard about daily exhaustion, headaches, pain that no one would believe. It was Anna, not a doctor, who recognized at last that her symptoms were characteristic with CFS. In fact, with the exception of seizures, she was picture perfect for the symptom complex that defines the illness.

Anna read everything she could find on the subject. She felt as if she was waking up after lifetime spent cut off from her own feelings and perceptions.

She began to remember painful incidents from her childhood – how she had felt, and how she had learned to deny those sensations not only to those around her but to herself. They were disturbing memories, but Anna, by then 35, was at last beginning to experience her own reality and to recognize herself as she had always been. She was not the healthy, energetic woman she had pretended to be for so long; she was sick.

I met Anna during this period. We talked a lot about these matters in my clinic, and we talked over coffee sometimes in the Tiger’s Den Cafe down the street. We both recognized that her identity was in crisis, because she was having trouble distinguishing real illness from false illness.

After so many years of believing herself to be “falsely” ill, how could she turn around and be herself? In this, she had no experience.

The perception of pain and illness is very simple from a physiologic standpoint. Primitive animals feel pain in their nerve endings, and struggle to avoid it. Electric probes of one-celled creatures like amoebae show that even these tiniest of organisms feel pain. But advanced creatures, specifically human beings, have learned mechanisms for denying some of the basics of biology.

Nevertheless, our denial hardly changes the mechanical impulses of our nervous systems; our nerve endings continue to be stimulated, and send messages to our brain that are registered as pain or discomfort. Our denial merely creates an emotionally confused response to the pain, or health identity confusion.

Anna’s biggest problem, at 35, was her confusion over her health identity. Her confusion had logical origins, but her management of it – to deny her symptoms -put her at risk. She had lost what healthy people would call common sense. Her confusion had cost her the right to drive, and subsequently, her job. She could have controlled her seizures with medication, if only she had been able to believe they were real.

But because she had denied her illness for most of her life, she probably would have been hard pressed to believe she was injured if she had been run over by a truck.

As the years passed, Anna gradually began to learn how to feel. She said it was better to feel pain than to feel nothing at all. It was better to experience the reality of her life, in all its facets, than to deny all of its reality. After decades of pretending, she began to acknowledge to herself the truth of her own experiences, and the place of her identity within those experiences.

I marvel at Anna’s courage. She has been one of my teachers in life. And I wonder if I will ever find the same courage to explore the hidden parts of my own soul.

– David S Bell, MD, Aug 15, 2000
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* This article is excerpted with kind permission from Dr. Bell’s classic book Faces of CFS – Case Histories of Chronic Fatigue Syndrome; © David S Bell, MD, 2000. This information has not been evaluated by the FDA. It is general information only and is not meant to prevent, diagnose treat or cure any condition, illness or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and reviewing it in collaboration with your professional healthcare team.

“Andrea’s Revolver”: When ME/CFS Includes Pain

This case history of a CFS patient whose symptoms include chronic pain is excerpted from Dr. Bell’s book Faces of CFS – Case Histories of Chronic Fatigue Syndrome, published in August, 2000. “Andrea’s Revolver” illustrates one aspect of cases he has followed since the mid-1980s.

Reprinted here with the kind permission of ProHealth: 1/21/11

ANDREA’S REVOLVER

Pain is a common problem in CFS, but it is also symbolic of the enormous challenge this illness presents to doctors and to patients. Patients can’t prove it, and doctors usually fail to treat it.

Despite the fact that pain occupies nearly all of their working day, doctors have a very poor understanding of it. Although we now have in our arsenal good medicines to relieve pain, we nevertheless try to avoid prescribing them.

• When a person who has just shoveled the snow off a long driveway complains of back pain, his doctor is likely to prescribe the same pain medications you can readily buy at your local Seven-11.

• If the snow shoveler’s back pain doesn’t abate in a few weeks, then the doctor realizes the problem might be worse than suspected. He refers the patient to a back specialist, which gets rid of the problem – for the doctor.

Most practitioners tell patients who have unexplained pain to seek help elsewhere.

Doctors are, as a rule, genuinely concerned about doing harm to the patient. This concern merges with another worry: losing one’s medical license by prescribing too many narcotics.

By law in New York state, doctors are required to write prescriptions in triplicate for narcotics and other potentially addictive drugs, a category of pharmaceuticals that just happen to be the most effective drugs for pain. These triplicate prescriptions help insure that powerful drugs won’t be over-prescribed, but the law is both time consuming and expensive – a nuisance for busy doctors.

More importantly, we doctors secretly suspect that someone spends their days counting the number of prescriptions we write, and worry that we could lose our medical licenses if there are too many carbons in our waste bins.

Aspirin presents none of these anxieties for us.

We never get into trouble from state regulators for offering aspirin to our patients in pain. The great irony is that aspirin may be more likely to kill the patient by causing a bleeding ulcer. But, ignoring that, we urge our patients to try aspirin or acetaminophen or ibuprofen. And if all of these fail, we usually suggest another mild medication, preferably one that the patient has never heard of.

Cancer pain, of course, is dire, and it is hardly surprising that oncologists (doctors who care exclusively for cancer patients) tend to have the most sophisticated understanding of, and compassion for, pain. They also do the best job of treating pain. When a cancer patient complains of pain, for the most part, the doctor opens his medical chest and says, in effect, take what you need to help with your pain.

Three weeks ago I had a toothache.

Like most men, I find this difficult to confess: My toothache hurt. By Friday, two days after it began, my toothache really hurt. On Saturday, it was unbearable. As I hobbled around my house holding my jaw, I found myself thinking, as if silently reciting a mantra: So this is pain…. so this is pain.

A friend gave me some serious pain medication, the kind that requires a prescription written in triplicate, and I was able to fall asleep at last. Even with the narcotic, however, the weekend was horrible. On Monday, I underwent the most wonderful root canal and my pain vanished.

The experience was an important lesson for me. I was reminded of the vast gulf between the subjective complaints of the patient and the objective doctor who listens to these complaints, the difference between hearing about someone else’s pain, their toothache, and my own.

Most important, I was reminded of the gulf many CFS patients must navigate every day.

I was able to see the end of my pain, even when the pain was at its height. I knew that on Monday my dentist would help me, not only because I can afford a dentist and have always paid my bills on time, but because my dentist understood completely that my particular condition was a painful one, and he had been nicely trained to alleviate it.

I see patients with pain every day in my practice. Pain steals in under many guises: the twisted ankle, the stomach ulcer, the spread of a malignant tumor. I try to respond given my best estimation of the severity of the pain.

I have studied CFS for years, and I still am unsure precisely where CFS fits along the spectrum of pain.

• Some of my colleagues accept as bona fide the pain that often accompanies the disease, and try their best to relieve it with medication.

• Sadly, most of them tell their patients that CFS is a minor illness; they advise them to get used to the pain until either the pain or the illness goes away. They may suggest aspirin.

Despite the fact that pain can be a prominent and even disabling aspect of CFS, it is the rare CFS sufferer who receives adequate treatment for it.

Andrea Thompson had pain, pain that surpassed virtually anything that I had seen before in my practice.

By the time Andrea walked into my clinic, she had already seen over 30 doctors. Her story was typical of most of the CFS patients who end up in the village of Lyndonville: Each of the doctors she had consulted over the long years of her illness were mystified when she recounted her symptoms, inexcusable now that CFS has been studied in this country for so many years.

Some of them performed studies and offered a multitude of conflicting diagnoses, from the common thyroid disease, which causes fatigue, to the more arcane reflex sympathetic dystrophy, an extremely rare and famously painful nerve disease. All of these diagnoses were wrong, since Andrea had the other symptoms as well: sore throat, headache, numbness and tingling in her legs and arms, as well as a kind of intellectual fogginess that made her feel perpetually “out of it.”

As months turned into years, and her doctors found it increasingly difficult to support their original diagnoses given Andrea’s wide array of symptoms, several of them began to suspect Andrea was a junkie who wanted pain medication to get high.

Talking to Andrea for ten minutes displayed the absurdity of these suspicions. Con artists have a certain talent, but Andrea was hardly a con artist. She was in pain.

Andrea was 37 when I saw her for the first time. Before falling ill in 1988, she had worked as an executive in a brokerage firm in New York state. Her education had been top-notch, and she had a Masters degree in business administration. She was married, had three children, and a nice house in the suburbs. Andrea and her family had been living the American dream – even if they didn’t have a Beamer.

Two years after her symptoms began, Andrea’s husband was promoted and transferred to Boston. Andrea was looking forward to taking a few months off work to rest, and to settle into her new home in Boston, after which she planned to look for a new job.

Once the move was complete, however, Andrea seemed to fall apart completely. In the beginning, at a loss to explain the problem, she and her husband blamed her rapid decline on stress. Yet, the move had been relatively stress-free; her husband’s company paid for the packing and unpacking of their possessions, for example.

Andrea’s dominant and most crippling symptom was pain, though she was hard pressed to pin-point its source.

Pain seemed to migrate through her limbs and even her face. But there were other symptoms, too.

• She had migraine headaches that were impervious to medication.

• She became hypersensitive to light, and took to wearing sunglasses even when she was inside her house.

• Curiously, odors of any kind made her feel nauseous.

• Mere sound, too, was often too much to bear. Andrea was an avid R & B fan and had a large library of recordings dating to the 1940s, but she could barely tolerate even the softest music.

It was as if every sense she possessed was too finely wired for life on planet earth.

Her first encounter with a Boston doctor ended as badly as her numerous encounters with doctors in New York. Andrea hadn’t expected a miracle – she just wanted something to take away the pain. Wearing sunglasses and asking for pain medication at the same time apparently made a poor impression.

She downplayed her pain when she met with a second doctor, with the result that he gave her a complete physical exam, ordered several laboratory tests and an MRI scan of her brain and neck, and performed nerve conduction studies. The lab tests were normal, and he prescribed mild pain medications and suggested meditation

The drugs didn’t touch the pain she felt, however, and Andrea was unable to meditate while in so much pain. She soon gave up trying.

She found some relief when a dentist prescribed codeine after she complained of facial pain, but he denied her additional prescriptions for the drug on the grounds that she might develop an addiction to it.

Doctors at a famous Boston pain clinic prescribed exercise and antidepressants, two therapies that simply ended up causing more pain. After two agonizing weeks, Andrea checked out of the clinic.

She had always been an attractive woman, but now Andrea looked ragged. She pleaded with several Boston doctors for more powerful pain killers, but her need for pain relief was proportionate to the degree of skepticism she encountered.

In fact, by now, no one she consulted believed she was in pain at all.

Her life was little more than misery compounded by the skepticism of the medical establishment and her friends. Not surprisingly, she began to doubt her own sanity.

• She became disheveled; her weight plummeted to 89 pounds. She had begun to look like a junkie, even to herself.

• She felt as if she barely knew her children anymore; they spent much of their time in day-care facilities.

• Her once-loyal husband began to display frustration and skepticism about her condition.

And always the pain – pain that doctors refused to treat. Worst of all, pain with no end in sight.

One day, Andrea loaded her husband’s revolver and put it in her mouth.

To this day, she has no explanation for why she didn’t simply pull the trigger.

The following day, she entered a psychiatric unit of a Boston hospital, where she remained for three weeks. The psychiatrists talked to her about “relocation stress,” childhood traumas, and “displaced” anger.

Andrea felt she was the only person who saw the problem clearly: Get rid of the pain, she kept telling the psychiatrists, and she would be okay.

Finally, her pleas were heard.

The psychiatrists prescribed methadone, a synthetic form of morphine that is used to manage morphine addiction, but has the same pain-deadening effects as morphine. The drug worked. Slowly, Andrea began to reconstruct her life.

What was causing Andrea Thompson’s extraordinary pain?

Usually, pain is associated with tissue damage from injury. The pain sensation serves as a warning, preventing further damage to the victim. This sensation travels on nerve pathways from the injured tissue to the brain.

Sometimes, pain is due to damage in the pain receiving areas of the brain itself. In this case, the disease is to the actual pain processing centers, even though the body mistakenly interprets the sensation of pain as if it were coming from somewhere else.

Malignancies involving the thalamus, a part of the brain that helps to process sensory impulses, can cause this kind of pain. But Andrea Thompson had no malignancies, and the MRI scan I ordered of her brain proved to be normal.

A third cause of pain is known as “sympathetically mediated” pain – pain that derives from damage to the autonomic nervous system. The autonomic nervous system controls our breathing, body temperature, blood flow, and heart rate – all those functions we can’t control by sheer will; body functions we barely even notice.

One of the diseases associated with this kind of pain, “reflex sympathetic dystrophy,” was the nerve ailment proposed by at least one doctor as the cause of Andrea’s pain.

Usually, “RSD” is the a result of an injury to a leg or an arm, or even a single nerve in that extremity. What is most curious about RSD is that the pain may be delayed for months or years, long after the specific injury had healed.

RSD is often accompanied by changes in blood flow, sweating, and, curiously, atrophy of the fingers. In 1988, I heard Dr. Paul Cheney, who had studied CFS among Nevada patients, describe what he called the “disappearing fingerprints” of CFS sufferers. The surface of his patient’s fingertips had grown completely smooth, entirely lacking the normal, distinctive whorls.

Dr. Cheney, a true disease detective, even remanded a few of these patients to a police station to find out whether they could be fingerprinted, but their fingerprints left no distinctive pattern.

When I heard about this bizarre discovery, I wondered whether it was possible to experience RSD as a body-wide disease instead of one confined to an extremity.

Though it remains controversial, some doctors believe that sympathetically mediated pain can be eliminated by blocking the nerve pathways, or even severing the nerve itself. In truth, doctors argue about the causes – and the treatment – of sympathetically mediated pain every day. Some of my colleagues believe it to be a psychological condition, although new research suggests otherwise.

I began to learn about the relationship between CFS and another puzzling condition called orthostatic hypotension, a failure of the body to adequately pump blood while standing in the upright position, from Dr. Peter Rowe and colleagues at Johns Hopkins.

Soon afterward I began working with Dr. David Streeten, an endocrinologist who had worked extensively with “orthostatic intolerance” – the inability of the body to tolerate the upright position.

There are only a few truly great doctors who stand out from the thousands of ordinary ones; they are the true masters of medicine. [The late] David Streeten was one of these masters. He had both a brilliant scientific mind and the perception and intuition of a superb clinician. If I were 30 years younger and fresh from medical school, I would have become his intern and really learned medicine.

But working with a master has its drawbacks. When I sent my CFS patients to see him for a consultation, they returned to my clinic with the news that he was much nicer to them than I ever was.

I met Dr. Streeten for the first time in February 1994 when I accompanied Andrea Thompson to his offices in order to observe his evaluation of her first hand. Until this experience, I was under the mistaken perception that I understood CFS. Dr. Streeten proceeded to teach me some of the basics that I had overlooked for 15 years.

I had always viewed chronic fatigue as the result of the chemicals released by a viral infection, and had concentrated solely upon looking for the infection that might have caused the condition.

Now I was seeing what could be the mechanism, regardless of cause, which might be causing the symptoms to persist.

The myriad of symptoms revolving around exhaustion, weakness, lightheadedness, and inability to concentrate were likely due to the inability of the body to circulate blood to the brain when standing, or sometimes even sitting.

When the CFS patient is lying down, the symptoms are improved, although not gone entirely. The disability of CFS has to do with the fact that we spend our non-sleeping lives in the upright position.

Dr. Streeten utilized MAST trousers in his experiments. The acronym stands for Military AntiShock Trousers. These inflatable pants can be blown up like an inner tube in order to create a veritable body cast from the toes all the way to the mid-chest. When paramedics need to transfer trauma patients suffering from fractured legs, MAST trousers are very handy because they become an instant cast and compress the lower body.

Dr. Streeten performed a deceptively simple experiment with his patients.

He bid them don deflated MAST trousers, then asked them to stand next to a wall of his examining room. As they stood upright in these somewhat peculiar circumstances, he monitored the patient’s blood pressure and pulse. When the CFS patient would become ill during standing, he would inflate their MAST trousers.

Upon meeting Andrea, Dr. Streeten measured the amount of blood in circulating in Andrea’s body and discovered that the level was strikingly low. Next, he tested Andrea’s blood pressure and pulse for 10 minutes while she was lying down, and they were normal. Blood tests drawn at that time for adrenaline and other “catecholamines” were drawn and later shown to be normal.

Then Andrea stood quietly with the plastic MAST trousers around her body but not inflated. Then the problems began. Within minutes she began to feel ill, her pulse began to climb, and the pain began to grow. By 10 minutes of standing her speech was slurred and she appeared a little drunk, swaying back and forth and her feet began to look purple. Her blood pressure dropped and heart rate increased.

Then the pain really kicked in.

She was confused. All she could do was to say over and over, “The pain…the pain…” While still standing, a second sample of blood was drawn from the line in her arm, again tested for adrenaline.

At that point, while Andrea was still standing, Dr. Streeten inflated the MAST trousers, causing symmetrical pressure around her legs, thighs and abdomen. I had often seen Andrea in this state before, a state where she looked as if she had been on a binge for days. But my teeth nearly fell out when seven seconds later she straightened up and looked around and said with a clear voice, “What happened? The pain is gone.”

I was as astonished as Andrea. Even Dr. Streeten was surprised by the magnitude of this response. He hypothesized that the pressure on Andrea’s legs and abdomen by the MAST trousers had forced a more vigorous blood flow through Andrea’s brain, and that this increased blood flow stopped the pain.

Andrea wanted to buy a pair of MAST trousers for home use. (Later on we actually tried this, but it turns out to be impossible to walk around with these things on which sort of cancels out the purpose.)

Dr. Streeten was suitably impressed by Andrea’s case. He submitted his MAST trouser experiment on Andrea and about 20 other CFS patients to a scientific journal. The editors rejected the paper, initially, because the patient was not sufficiently “blinded” in this experiment. In the world of science, of course, it is optimum for patients in experiments to be ignorant of the researcher’s modus operandi.

My question to the journal editors is this: How could we sneak Andrea into a pair of MAST trousers without her finding out about it? I can think of only one way: Render her unconscious with a general anesthetic. The problem with that, of course, is that it is very difficult for people to describe their pain, or lack of it, while unconscious. Sometimes modern medicine is bewildering.

The temporary stoppage of Andrea’s pain in Dr. Streeten’s office that day offers up no simple explanations or conclusions, just theories.

One simplistic theory is that because Andrea had too little blood circulating in her body, her blood pressure dropped dramatically when she was forced to stand for any length of time. When her blood pressure dropped, so did the flow of blood to her brain, which houses the mechanism that mediates both the sensation of pain and blood flow: the autonomic nervous system.

By inflating Andrea’s MAST trousers, Streeten was able to rescue, so to speak, blood that was trapped in her legs, and send more to her brain.

Still, the theory has by no means been proven. In the time that has elapsed since Andrea’s visit with Dr. Streeten, however, it has become apparent to me and to other doctors who study CFS that problems with blood flow to the brain, and the regulator of that flow – the autonomic nervous system – is responsible for both the exhaustion and the migrating pain of the disease.

Of course, myriad questions remain. Might the cause of pain in CFS be a result of a decreased blood flow through the thalamus? Is there an inherent abnormality of the blood vessels that causes the decreased blood flow through the brain?

A different theory of CFS pain centers on hormones. Studies have demonstrated that a number of different hormones are in insufficient supply in CFS patients. One of these is called growth hormone. The pituitary gland of the brain produces this particular hormone, and besides its primary job of making children grow, it has numerous functions in the body.

Scientists have discovered that there is also a second hormone, called vasopressin, that is deficient in CFS patients.

This hormone is essential to regulate the concentration of water in the body, as well as to regulate the size, or diameter, of the blood vessels. I had already determined that Andrea had levels of vasopressin that were much too low to be considered normal. A deficiency of vasopressin could predictably cause excessive thirst as well as an insufficient supply of circulating blood in the body.

As things have turned out, many patients with CFS experience both of these problems.

And this is where the trail leads us to endorphins, hormones produced by healthy people that act as the natural pain killers for the body. Interestingly, vasopressin is a substance that reflects the production of the natural pain-killing endorphins.

Could it be that CFS patients have low levels of the endorphins, explaining in part, why they experience so much pain?

The fact remains: Regardless of why it exists, or what causes it, pain that is both intense and chronic is a daily fact of life for a great many patients who suffer from CFS.

I began testing CFS patients in my office for changes in pulse and blood pressure when they stand quietly, and found that the vast majority have abnormalities. This is the reason that people with CFS may look healthy to outsiders, but they are unable to stand at the check-out counter of the grocery store. In fact, on occasion, some of them faint, or come very close to fainting, presumably because they cannot maintain good blood flow to the brain.

One day, I showed the blood pressure graphs to one of my best friends, David Lieberman, a substance abuse counselor. I pointed out to him that in addition to their blood pressure abnormalities, these patients often experience a racing pulse. David made the observation that these physiological signs are picture identical to the body’s reaction during withdrawal from narcotics.

Could it be that CFS sufferers are in a constant state of ‘narcotic withdrawal’ because they fail to produce enough of the body’s natural pain killers, the endorphins?

I remember a patient with CFS that I had seen almost 15 years ago. This woman had taken doses of codeine three times a day, every day, for nearly 20 years. She told me it boosted her energy, and provided relief from her symptoms of muscle and joint pain, headache, and trouble thinking. Although she had never increased her dose, I privately suspected she was addicted to codeine.

To see if she was addicted, I asked her to stop taking codeine for a period of two months, and for reasons I will never understand, she actually agreed to do so upon my request. During those two months, her symptoms of pain and fatigue were prominent and troublesome, but she bravely stuck it out.

What fascinates me, in retrospect, is that after 20 years of taking codeine, this particular patient displayed absolutely no signs of withdrawal or even a craving for the drug. She never developed tolerance to codeine, where it would become ineffective without increasing the dose.

Could it be that for these 20 years she was replacing her own body’s deficient endorphins with daily codeine?

Many scientists would tend to dismiss this particular observation. The skeptics among them would probably assume that the woman was sneaking codeine on the side without my knowledge, and, frankly, I would be unable to prove otherwise, since I did not perform regular tests on this woman for the presence of codeine in her system. But, after years of practice, I believe that there is one factor in clinical medicine to which scientists rarely give credence: the bond of trust between doctor and patient. I tend to believe what my patients tell me. I may just be gullible.

Andrea has been taking methadone for four years now, and the synthetic morphine provides her with relief from her pain.

Curiously, she, too, has not required any increase in her dose, which typically occurs when people take drugs like morphine and methadone over the long haul. David Lieberman and I often talk about the possibility that CFS patients require narcotic drugs the way a diabetic needs insulin. The myriad symptoms of diabetes are caused, after all, by a deficiency of insulin, a natural substance that healthy people produce in adequate amounts.

I have wondered, as well, if blood volumes that are far too low are a clue to the cause of the major symptoms of CFS, particularly pain.

I frankly consider it embarrassing that so little research has been done on blood volume, blood flow, endorphins and other brain hormones in patients with CFS. If one tenth of the money that has been applied to psychological studies of people suffering from CFS had been used to study endorphins instead, we would have seen some progress in understanding this terrible disease.

One problem, of course, is that CFS continues to be so controversial throughout medicine that earnest investigators eager to study it are often stymied by the failure of government granting agencies to help.

This phenomenon is particularly unfortunate when one considers how many CFS patients are in pain each day. According to some researchers, more people in this country have CFS than all the people with AIDS, lung and breast cancer combined.

Currently, the disease is approximately 15 times more prevalent than paralytic polio was at the height of the polio epidemic of the late 1940s.

Research barriers have not only impeded my colleagues from understanding the disease, these barriers have prevented doctors from taking a hard look at the pain CFS patients experience, and from treating that pain appropriately.

Eventually, some patients just give up. The foundation of the Hippocratic oath is, “First, do no harm.”

By failing to treat her pain, doctors caused Andrea Thompson to spend half an hour with a loaded revolver in her mouth.

– Dr. David S Bell, MD, Lyndonville, New York, August 15, 2000
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* This article is excerpted with kind permission from Dr. Bell’s classic book Faces of CFS – Case Histories of Chronic Fatigue Syndrome; © David S Bell, MD, 2000. This information has not been evaluated by the FDA. It is general information only and is not meant to prevent, diagnose treat or cure any condition, illness or disease. It is very important that you make no change in your healthcare plan or health support regimen without researching and reviewing it in collaboration with your professional healthcare team.

Significant aggravation of pre-existing myalgic encephalomyelitis/chronic fatigue syndrome following proton beam therapy for sphenoid wing meningioma: case report

Abstract:

Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating multisystem disorder characterized by profound fatigue, post-exertional malaise (PEM), immune dysregulation, and mitochondrial dysfunction. While radiation exposure has been linked to fatigue syndromes with overlapping pathophysiology, no previous reports have described the effects of therapeutic radiation, including proton beam radiotherapy (PBRT), in patients with ME/CFS.

Case presentation: We report the case of a 46-year-old woman with a pre-existing, clinically confirmed diagnosis of ME/CFS (Bell score 60, ECOG 1), who underwent postoperative PBRT (50.4 Gy in 28 fractions) for a recurrent left sphenoid wing meningioma (CNS WHO grade 1). The tumor had been surgically resected but showed residual disease with early postoperative progression and close proximity to the left optic nerve, prompting the indication for adjuvant radiotherapy. The patient initially tolerated treatment well, with only mild acute worsening of pre-existing fatigue and transient corticosteroid-responsive symptoms. However, within weeks of completing radiotherapy, she developed progressive and severe worsening of fatigue, myalgia, vertigo, and hypersensitivity to sensory stimuli as well as cognitive decline. Over several months, she became completely bedridden (Bell score 0, ECOG 4) with persistent ME/CFS aggravation unresponsive to supportive measures persisting until the last known contact 20 months after radiation. Follow-up imaging showed stable postoperative findings without tumor progression or new structural brain lesions.

Discussion: This case illustrates a profound and irreversible deterioration of ME/CFS following PBRT, suggesting that radiation-induced mitochondrial dysfunction, oxidative stress, and chronic inflammatory activation may critically worsen pre-existing metabolic fragility. Despite the theoretical advantages of proton radiotherapy in reducing normal tissue exposure, its protective effects may be insufficient in patients with baseline mitochondrial malfunction.

Conclusion: This is, to our knowledge, the first reported case of severe and sustained ME/CFS exacerbation after radiotherapy. The case emphasizes the urgent need for risk stratification, tailored consent processes, and research in the field of radiotherapy tolerance in ME/CFS patients, as conventional expectations regarding side effects may not predict outcomes in this vulnerable population.

Source: Fischer C, Seidlitz A, Krause M. Significant aggravation of pre-existing myalgic encephalomyelitis/chronic fatigue syndrome following proton beam therapy for sphenoid wing meningioma: case report. Strahlenther Onkol. 2026 Jun 11. doi: 10.1007/s00066-026-02553-w. Epub ahead of print. PMID: 42277311. https://link.springer.com/article/10.1007/s00066-026-02553-w (Full text)

Severe Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Leading to Assisted Suicide in a Patient in Her Late 30s: A Case Report

Abstract:

A patient in her late 30s developed severe myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) following an Epstein-Barr virus infection. No distinct autoimmune or autoinflammatory disorder could be identified as the underlying cause of her symptoms, as the observed constellation of cytokine elevations (IL-2, IL-6, and IFN-γ) was not consistent with any known or established disease entity. Despite comprehensive multidisciplinary treatment over two years, including medical, psychological, and rehabilitative approaches, her condition deteriorated, and treatment-related hypersensitivities emerged. The severity and progressive nature of her symptoms, compounded by the absence of effective therapeutic options, ultimately led the patient to pursue assisted suicide.

Source: Opala D, Villiger E, Levenfus I. Severe Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Leading to Assisted Suicide in a Patient in Her Late 30s: A Case Report. Cureus. 2026 May 28;18(5):e109798. doi: 10.7759/cureus.109798. PMID: 42222634; PMCID: PMC13217520. https://pmc.ncbi.nlm.nih.gov/articles/PMC13217520/ (Full text)

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Successful Therapeutic Plasma Exchange Treatment After SARS-CoV-2 Infection-A Case Report

Abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex neuroimmunological disorder characterized by disabling symptoms that are often difficult to manage. More recently, in the context of SARS-CoV-2 infection, potential pathophysiological overlaps and disease modulation have been hypothesized. Our successful case highlights the need to investigate novel therapeutic approaches, including plasma exchange.

Source: Ciobanu G, Arn N. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Successful Therapeutic Plasma Exchange Treatment After SARS-CoV-2 Infection-A Case Report. Clin Case Rep. 2026 May 17;14:e72725. doi: 10.1002/ccr3.72725. PMID: 42158223; PMCID: PMC13180788. https://pmc.ncbi.nlm.nih.gov/articles/PMC13180788/ (Full text)