“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.

Outcomes of ME/CFS following infectious mononucleosis: seven-year follow-up of a prospective study

Abstract:

Background: Many individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) report experiencing an infectious illness prior to disease onset. Approximately 30% of cases are linked to Epstein–Barr virus (EBV) infection resulting in Infectious Mononucleosis (IM).

Methods: We examined the progression of ME/CFS following IM among a cohort of college students who were recruited before they developed the infection. This sample represented a socioeconomically and ethnically diverse population of young adults who were monitored over a 7-year period. Assessments of health status, psychological functioning, and blood biomarkers were conducted at four time points: (1) baseline, when participants were healthy and at least 6 weeks from IM onset; (2) within 6 weeks of IM diagnosis; (3) 6 months post-IM, when participants had either recovered or met criteria for ME/CFS; and (4) the 7-year follow-up.

Results: At follow-up, 81% of participants who had initially presented with severe ME/CFS continued to fulfill diagnostic criteria. In contrast, only about one-third of those with moderate or lingering symptoms at 6 months still had ME/CFS 7 years later.

Conclusion: These findings indicate that ME/CFS following IM tends to persist over the long term, particularly among those whose illness was more severe at onset.

Source: Jason LA, Furst J, Worth R and Katz BZ (2026) Outcomes of ME/CFS following infectious mononucleosis: seven-year follow-up of a prospective study. Front. Med. 13:1676628. doi: 10.3389/fmed.2026.1676628 https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2026.1676628/full (Full text)

The relevance of headache as an onset symptom in COVID-19: a network analysis of data from the LONG-COVID-EXP-CM multicentre study

To the Editor,

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus primary affects the respiratory system; however, a multiorganic affection is evident. Neurological symptoms are frequent at the acute- and post-acute phases after infection [1]. Headache is a neurological symptom experienced as a COVID-19-onset symptom associated with a more benign course of the disease [2]; however, it has been also associated with a higher prevalence of post-COVID headache [3].

During the acute COVID-19 phase, headache often co-exists with other neurological symptoms, e.g., anosmia or ageusia [4]. The presence of anosmia as an onset symptom is also associated with lower mortality rate and a less severe disease, although it seems that patients with anosmia and ageusia represent a different group than those with headache [5]. In this letter, we applied a network analysis to determine the relevance of COVID-19-onset symptoms, including headache, as well as pre-existing medical co-morbidities in a sample of previously hospitalised COVID-19 patients.

The LONG-COVID-EXP-CM is a multicentre cohort study including individuals with a diagnosis of SARS-CoV-2 infection by RT-PCR technique and/or radiological findings hospitalised during the first wave of the pandemic in five hospitals of Madrid (Spain). Among all patients hospitalised during the first wave, a sample of 400 from each hospital was randomly selected. The Ethics Committee of all the hospitals approved the study (HCSC20/495E, HSO25112020, HUFA20/126, HUIL/092-20, HUF/EC1517). Verbal informed consent was obtained from participants for the use of their data in this analysis. Demographic data, pre-existing medical comorbidities, COVID-19 symptoms at hospital admission, days at hospital, and intensive care unit (ICU) admission were collected from hospital records.

The network included 28 nodes linked by edges weighted by partial correlation coefficients. The dataset as well as the related two vectors specifying the type (“g” for Gaussian, “p” for Poisson, “c” for categorical) and the number of levels (or categories) for each variable is provided. The mgm was estimated for order = 2 to only take pairwise interactions into account, using least absolute shrinkage and selection operator (LASSO, ℓ1-regularisation) that seeks to maximise specificity (to include as few false positives as possible) with rule = “AND” (which specifies whether the two estimates for an edge are combined with an “AND” or an “OR” rule). Since not all nodes in a network are equally important, centrality was assessed by calculating strength centrality (defined as the sum of weights of edges), betweenness centrality (defined as the total number of shortest paths that pass through the target node, moderated by the total number of shortest paths existing between any couple of nodes in the graph) and closeness centrality (defined as the inverse sum of the distances of shortest of the target node from all other nodes in the network).

Two thousand (n = 2000) patients were randomly selected and invited to participate. A total of 1969 (age:61 ± 16 years, 46.4% women) were included. The most common symptoms at hospital admission were fever (74.6%), dyspnoea (31.5%), myalgia (30.7%) and cough (27.9%). The network identified one group of variables grouping all COVID-19-onset symptoms at hospitalisation, and a second one grouping all pre-existing medical co-morbidities (Fig. 1). Multiple positive correlations between the variables in each group were found. The highest correlation (ρρ:5.87) in the medical co-morbidity group was between asthma (node 9) and rheumatological diseases (node 13). Within the COVID-19-onset symptoms group, headache (node 20) had several high correlations with fever (node 16, ρρ:5.981), dyspnoea (node 17, ρρ:5.617), anosmia (node 22, ρρ:5.2276 and ageusia (node 23, ρρ:4.660). No correlations between both groups of variables were seen. In the group of COVID-19-onset symptoms, headache was the node showing the highest strength centrality, highest betweenness centrality and highest closeness centrality (node 20, Fig. 2).

Read the rest of this article HERE.

Source: Fernández-de-las-Peñas, C., Varol, U., Gómez-Mayordomo, V. et al. The relevance of headache as an onset symptom in COVID-19: a network analysis of data from the LONG-COVID-EXP-CM multicentre study. Acta Neurol Belg (2022). https://doi.org/10.1007/s13760-022-01998-x  https://link.springer.com/article/10.1007/s13760-022-01998-x (Full text)

Onset Patterns of Chronic Fatigue Syndrome and Myalgic Encephalomyelitis: A Mixed Method Approach

Abstract:

The onset of Chronic fatigue syndrome (CFS) and Myalgic Encephalomyelitis (ME) is considered a key area of inquiry. Case criteria for ME and CFS and much of the academic literature suggest that patients typically experience one of two possible onset patterns: sudden or gradual. The current study provided an in-depth investigation of ME and CFS onset in order to provide insight into early symptoms, onset duration, and the progression of functional disability. We collected qualitative descriptive data to gain a rich description of illness onset from the patients’ point of view.

Overall, qualitative findings revealed detailed descriptions of ME and CFS onset experiences. Major themes that emerged from the data included: onset/illness progression patterns, illness causes, methods of adapting and coping, hardworking and active lives prior to onset, healthy lives prior to onset, prior health problems, comorbid health conditions, emotional responses to onset, exertional effects, the illness as life limiting, stress, traumatic experiences, lack of support, support, and treatment limitations. A closer examination of the onset/illness progression patterns that emerged from the data provided evidence that individuals with ME and CFS experience complex onset patterns.

Furthermore, the study findings suggest that the method of categorizing individuals into sudden versus gradual onset groups fails to capture the more nuanced and varied onset experiences. Prospective research studies that capture the onset period as it is developing could lead to improvements in the way we define and assess ME and CFS onset, and may also lead to methods for early detection, prevention, and individualized treatment approaches.

Source: Meredyth Anne Evans & Leonard A. Jason. Onset Patterns of Chronic Fatigue Syndrome and Myalgic Encephalomyelitis: A Mixed Method Approach. Res Chron Dis (2018) 2(1), 001–0030 (Full article)

Chronic fatigue syndrome versus sudden onset myalgic encephalomyelitis

Abstract:

A revised sudden onset case definition for Myalgic Encephalomyelitis (ME) has been developed (Jason, Damrongvachiraphan, et al., 2012 ) based on past case definitions. In a prior study, Jason, Brown, and colleagues ( 2012 ) compared patients recruited using the 1994 case definition of chronic fatigue syndrome (CFS) to contrast those meeting criteria for the revised ME criteria.

They found that this revised ME case definition identified patients with more functional impairments and physical, mental, and cognitive problems than those meeting the CFS criteria. The study by Jason, Brown, et al. ( 2012 ) only selected individuals who first met the CFS criteria, and it only relied on one Chicago-based data set. The current study replicated this comparison with two distinct data sets with different case ascertainment methods. Results indicate that the ME criteria identified a group of patients with more functional disabilities as well as more severe post-exertional malaise symptoms.

 

Source: Jason LA, Evans M, Brown A, Sunnquist M, Newton JL. Chronic fatigue syndrome versus sudden onset myalgic encephalomyelitis. J Prev Interv Community. 2015;43(1):62-77. doi: 10.1080/10852352.2014.973233. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295655/ (Full article)

 

Search for Borna disease virus in Danish fibromyalgia patients

Abstract:

OBJECTIVE: The purpose of this study was to look for Borna disease virus (BDV) in 18 patients with acute onset of fibromyalgia (FMS) following a “flu-like” episode. BDV is a neurotropic RNA virus affecting horses and sheep. Infections in animals have been reported to cause immune mediated disease characterized by abnormalities in behavior. A possible link between BDV and neuropsychiatric diseases in man has been described, and lately a connection to chronic fatigue syndrome (CFS) has been suggested.

METHODS: A BDV-specific nested PCR (RT-PCR) was performed on serum and spinal fluid.

RESULTS: The BDV genome was not detected in any of the FMS cases.

CONCLUSION: Although BDV was not demonstrated in spinal fluid or serum from the tested patients with FMS, we believe that it is important to report our results, since FMS can exhibit many manifestations in common with CFS. Possible reasons for the discrepant findings are discussed.

 

Source: Wittrup IH, Christensen LS, Jensen B, Danneskiold-Samsee B, Bliddal H, Wiik A. Search for Borna disease virus in Danish fibromyalgia patients. Scand J Rheumatol. 2000;29(6):387-90. http://www.ncbi.nlm.nih.gov/pubmed/11132208

 

Longitudinal analysis of symptoms reported by patients with chronic fatigue syndrome

Abstract:

PURPOSE: To determine the effect of chronic fatigue syndrome (CFS) illness duration and onset type on the likelihood of reporting a symptom during successive follow-up periods.

METHODS: In 1997, a two-phase RDD survey in Wichita, Kansas, was conducted to estimate the prevalence of CFS. Phase I identified 56,154 respondents 18-69 years of age and screened for severe fatigue, extreme tiredness or exhaustion lasting for 1 month or longer. In phase II an equal number of fatigued (n = 7,176) and randomly selected non-fatigued subjects were asked about 8 CFS and 13 non-CFS symptoms, as well as the presence of specific medical and psychiatric conditions. Eligible respondents were clinically evaluated to establish CFS diagnosis. Phase II respondents were re-contacted at 12- (n = 4,331) and 24-months (n = 4,266) for additional follow-up and diagnosis. In this study we considered symptoms reported as being present most of the time during each successive observation period. Generalized estimating equations were used to model symptoms over time and to address study questions. Such a model accounts for correlations among repeated symptoms for each subject. We used an auto-regressive structure for the correlation matrix, assuming the correlations between each pair of repeated symptoms should decrease as the time between symptoms increased.

RESULTS: There were 74 CFS patients who had been ill for 1 to 20 years (median = 6.3 years). Among these, 46 reported gradual and 28 reported sudden onset. Symptoms fluctuated over the course of illness. However, only stomach pain (non-CFS symptom) was more likely to be reported as duration of illness increased (p < 0.05). There was no association between onset type and the likelihood of reporting a symptom during an interview, except that chills and severe headaches were more likely to be reported by sudden cases.

CONCLUSIONS: The likelihood of expressing CFS and non-CFS symptom “most of the time” is the same across years of illness. More analyses are warranted to consider expression of symptoms for >/=6 months and severe symptoms.

 

Source: Nisenbaum R, Jones A, Jones J, Reeves W. Longitudinal analysis of symptoms reported by patients with chronic fatigue syndrome. Ann Epidemiol. 2000 Oct 1;10(7):458. http://www.ncbi.nlm.nih.gov/pubmed/11018368

 

Idiopathic chronic fatigue and chronic fatigue syndrome: a comparison of two case-definitions

Abstract:

The aim of the study was to compare the signs and symptoms of individuals meeting two different definitions of chronic fatigue syndrome (CFS). Ninety-four patients fitting the eligibility criteria for idiopathic fatigue were enrolled into the study. Of the 94 patients, 48 met the 1988 definition of CFS, 20 the 1994 (but not the 1988) definition of CFS, and 26 met neither definition.

The 1994 defined cases were more likely than 1988 defined cases, and non-syndromal individuals to be male, married, and high school educated. The 1994 cases were less likely than 1988 cases to present acute onset, self reported sore throat, mild fever lymphadenopathy, pharyngitis.

In conclusion, the 1994 criteria increased the number of patients classified as CFS; however, those who fit only the 1994 criteria were less likely to have an acute symptomatic onset and signs and symptoms suggestive of an infectious process.

 

Source: Arpino C, Carrieri MP, Valesini G, Pizzigallo E, Rovere P, Tirelli U, Conti F, Dialmi P, Barberio A, Rusconi N, Bosco O, Lazzarin A, Saracco A, Moro ML,Vlahov D. Idiopathic chronic fatigue and chronic fatigue syndrome: a comparison of two case-definitions. Ann Ist Super Sanita. 1999;35(3):435-41. http://www.ncbi.nlm.nih.gov/pubmed/10721210

 

A 56-Year-Old Woman With Chronic Fatigue Syndrome, 1 Year Later

In June 1997, at the Medicine Grand Rounds, Dr Anthony Komaroff discussed Ms H, an educator unable to work because of debilitating symptoms associated with a 2-year history of chronic fatigue. Her ailment, which began shortly after a flu-like illness, was marked primarily by weakness, fatigue, chronic insomnia, and depression that she felt was in response to her symptoms. In recent years she had felt somewhat less depressed, and wondered also if the disease might be slowly diminishing in its severity.

You can read the rest of this article here: http://jama.jamanetwork.com/article.aspx?articleid=187800

 

Source: Thomas L. Delbanco, MD; Jennifer Daley, MD; Erin E. Hartman, MS. A 56-Year-Old Woman With Chronic Fatigue Syndrome, 1 Year Later. JAMA. 1998;280(4):372. doi:10.1001/jama.280.4.372. http://jama.jamanetwork.com/article.aspx?articleid=187800

Course and outcome of chronic fatigue in children and adolescents

Abstract:

PURPOSE: To describe the epidemiology, symptoms, and psychosocial characteristics of children and adolescents evaluated in a chronic fatigue program and determine the course and outcome of the syndrome in these patients.

METHODS: During the summer of 1994, chart review was performed for the 58 patients evaluated between 1990 and 1994 and a telephone follow-up was conducted with 42 of the 58 families. Patients were predominantly female (71%) and white (94%), with 50% between the ages of 7 and 14 years and 50% between the ages of 15 and 21 years (mean age 14.6 years).

RESULTS: At time of presentation, 50% of patients had been fatigued for 1 to 6 months and 50% had been fatigued for 7 to 36 months. Sixty percent indicated the fatigue had begun with an acute illness and 60% had a history of allergies. Most commonly reported symptoms were fatigue (100%), headache (74%), sore throat (59%), abdominal pain (48%), fever (36%), and difficulties with concentration and/or memory (33%). Most patients had a worsening of school performance and a decrease in social activities. On follow-up, there was significant improvement in many patients during the summer after the first visit, with continued improvement in most patients during the second and third years. At time of the follow-up telephone call, 43% of families considered their child “cured” and 52% considered their child “improved,” whereas only 5% considered their child to be “the same.” Statistical analyses demonstrated no demographic or clinical factors that distinguished between those who did or did not participate in the follow-up study, or between those who did or did not do well on follow-up.

CONCLUSIONS: These data demonstrate that children and adolescents with chronic fatigue have a syndrome that is similar to that described in adults, but that the syndrome differs in several ways, most specifically, presentation earlier in the course of the illness and a more optimistic outcome.

 

Source: Krilov LR, Fisher M, Friedman SB, Reitman D, Mandel FS. Course and outcome of chronic fatigue in children and adolescents. Pediatrics. 1998 Aug;102(2 Pt 1):360-6. http://www.ncbi.nlm.nih.gov/pubmed/9685439