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Answers to general questions about CFS, etc., as published in the Lyndonville
News:
From the August 2010 Lyndonville News:
Question: Oh, and my vertigo story has taken an interesting turn. Last week I saw a new doctor who was filling in for my family physician. He suspected I have migraine-associated-vertigo and gave me a Maxalt in his office. Within twenty minutes my nausea was gone and most of my balance was restored. It felt like a miracle. He also gave me a referral to a neurologist to talk about preventative medications. I've been struggling with bouts of vertigo since 1995, so this is good news.
Comment: There is an old paper establishing the link between vertigo, CFS, and migraine (Ash-Bernal R, Wall C, Komaroff A, Bell D, Oas J, Payman R, et al. Vestibular function tests anomalies in patients with chronic fatigue syndrome. Acta Otolaryngol. 1995;115:9-17.) It is quite reasonable to try migraine meds in this situation.
Question: I have had several episodes of shingles but my doctor will not test them, but suggests the vaccine.
Comment: I feel that repeated episodes of shingles do occur in CFS and may be related to reduced number or function of natural killer cells. I do not know how CFS patients respond to the vaccine for shingles. But here is what I would do.
a) ask for a referral to an infectious disease specialist
b) without being arrogant, ask during the visit if he or she would be willing to follow you if XMRV turns out to be the cause of CFS. If the specialist says no, then you have not lost anything. If the specialist says yes, then you wait. But wait respectfully and patiently.
c) See the specialist regularly so he or she can get to know you. Maybe when the time is right a treatment will be offered. If XMRV turns out to be the cause of CFS, the infectious disease specialists will embrace it and lead in the treatment efforts.
Question: In the Dubbo study, a percentage of persons developed CFS after Epstein-Barr virus, Ross River virus or Q fever. They must have saved blood from those who came down with CFS and those who did not. Test the blood for XMRV. If this virus is present in the subjects who came down with CFS, but not present in the blood of those people who had regular illnesses and quickly recovered, we would have the answer as to whether XMRV "causes" CFS.
Answer: Excellent question. I would hope that the CDC and the Australian government are doing exactly this.
Question: There were many questions about getting tested for XMRV.
Answer: I am reluctant to suggest to anyone that they spend big bucks for a commercial test now. We do not know if a particular test is accurate, and even if it is accurate we do not know what it means, and even if we did know what it meant we would not know what to do with it. I would be patient. Answers will start flowing soon, so stay tuned.
Question: I was fascinated by the clinical notes in the last issue of the Lyndonville News. The comment regarding the 2 types of CFS is the sort of observation that could seem obvious to clinicians, while still being overlooked in empirical research, and even obscuring many studies' results. As a side-note, I've read a lot of scientific CFS literature since being diagnosed myself, and I haven't come across anything as thought-provoking as your Faces of CFS. I wonder if many CFS researchers are skeptical about case-studies because they may seem non-scientific; however, such detail, I think, is very productive.
What particularly interested me about the notion of a frazzled subtype is the potential role of epinephrine in CFS. Some recent studies have found propranolol useful in treating CFS and FM. This treatment struck me as a little counter-intuitive; that is, what doctor would be cruel enough to deny adrenaline to patients who can't get out of bed? If propranolol ends up being very useful, you can see why it might have been overlooked.
But I think there are a couple of general and specific connections between epinephrine and CFS symptoms, which play out in the literature on propranolol. Propranolol's effect on POTS is well-documented, but the drug probably also boosts immune functioning, reduces inflammation in certain circumstances, regulates sense and pain perception, eases digestion (particularly of carbs), and increases the threshold for exertion. Epinephrine's negative effect in these areas could fuel a self-reinforcing cycle, like Pall's NO/ONOO cycle. Moreover, anecdotal risk factors for CFS, like long-term exercise and type A personality, probably involve increased epinephrine.
Lastly, it's also curious to think about propranolol in terms of all the obtuse research that favors psychological treatment. This is because epinephrine can be consciously controlled to a small degree by, for instance, self-awareness and breathing slowly. However, if the long-term benefits of psychological treatments ultimately lie in teaching patients to control epinephrine release, then propranolol would be much more effective.
Answer: A very interesting set of questions. First of all, adrenalin (epinephrine and/or norepinephrine) is very involved in the illness, particularly the frazzled subtype. It can be measured after simple standing, and when it is over 600 it is considered abnormal (Hyper-adrenergic). It is my observation that treating patients with this type with any medication (coffee, stimulants, midodrine) which increases adrenalin, they get worse.
Secondly, I don’t think beta blockers such as propranolol do very much good. The hyperadrenergic response is a response – it is trying to improve a sad state of affairs, and when it is blocked, patients don’t seem to feel much better. Their chest pain goes away, though. CT scans of the adrenals show that they are small, thus the name “adrenal fatigue”, probably because they have been squeezed for so long.
Question: It was Volume 2, Number 3: July 2005, The Presence of Cerebral Atrophy in CFS, Cognitive Symptoms of CFS, Abnormal Cerebral Perfusion in CFS.
I have CFS/FMS/MPS. I am very sick, with no good medical care… But what is really hurting tonight is that article. My tests are showing diffuse brain shrinkage and I have gotten sicker and sicker the past 3 years. I first got FMS in 1994. Anyway that article has me feeling hopeless, because my brain isn't working anymore and I'm getting worse and worse and have no $ to get good help. I feel really hopeless after reading that article. I am alone, family not close - alone and scared. Is there any hope?Attempted Answer: The periods of despair that persons with this illness experience are beyond description. I apologize for the article of cerebral atrophy and progressive cognitive difficulties, but unfortunately they are true findings for some with the illness. I apologize for rubbing salt into the wounds. When will the medical providers begin to approach this illness with compassion? I don’t know. Is there any hope? Absolutely yes. And it is not a false hope. I remain convinced that the problems with this illness are reversible, and someday we will find them.
Question: Dear Dr. Bell, This is the first time I've ever heard about the origins of CFIDS. My question, to me, is simple. How does a debilitating medical condition appear from nowhere? I consider myself a reasonable person. I am 59 years young and have been suffering from Fibromyalgia for the last 10 years…diagnosed in the last year. If something is that time specific and geographic specific then logically it must be causal.
Answer: Good question and I have no idea of the answer. It seems to strike out of nowhere. I have a number of professional athletes as patients and they were in the peak of health when they got sick. But where does a strep throat come from? Before we understood about germs we considered “evil humors” as the cause. Someday we will understand exactly the genetic predispositions, the triggering factors and the reasons the illness is sustained. Now we are stuck with the “evil humors” equivalent.
Question: Hi Dr.Bell, If the new study at Stanford confirms the first one, will you be ready to prescribe it? This seems to be the best news on ME/CFS I've ever heard. Do you agree?Answer: A very exciting development, and the group at Stanford is working as hard and as fast as they can. Until we get some answers from their next round of studies we have to sit and wait. But I agree it is the best news I have heard in many years.
Question...on people who develop CFIDS as a result of inoculation. I had one flu shot in my life, became terribly ill within 48 hours with what felt like flu. And it was the flu that never went away, eventually dx'd as CFIDS. From my years on online support groups, I know there are many more people who have reported the same occurrence.
Answer: There is no doubt that inoculations can set off the process. These shots are designed to stimulate the immune system in a way that can prevent a future infection with something like a strain of the flu virus. Therefore it is just like getting that particular flu virus strain and thus can set off the process. The vaccine that I have seen causing the greatest problem is the Hepatitis B. Maybe that is a coincidence, but...
Question: Neither genetic susceptibility nor increased psychological stress answer this question (about increased incidence) to my satisfaction. That leads me to believe either there's a new pathogen about—or an old one acting in atypical fashion, or that the toxic overload in the environment has reached a critical mass, damaging either the brain, the immune system or both. I can't think of any other explanations. I'd love to be corrected if I'm wrong.Answer: Because it has been ignored for so long, we really do not know if there is an increased incidence of this illness. If there is, I like the idea of a two hit process. It would go like this. Hit #1 would be silent, either with an infectious agent, a new agent, or a toxin. By itself it does not do anything but sets the stage for hit #2 which would be the standard infection. Because of the silent first hit, the second hit causes ME/CFS. It would make a good science fiction/horror movie.
Question: I have several questions that have plagued me for years; I’m hoping that you can provide the answer.
1. I have always been amazed at the similarities between CFS and BSE and Scrapie. I am curious to know if you have ever found a person with CFS among the vegan/vegetarian population?
Answer: I have never systematically looked for lifetime vegans with ME/CFS. You question is really about the possibility that the illness may be a prion disease. To my knowledge no one has looked at this in any detail. I would be interested to hear from any reader who has any information about this. The known prion diseases are neurologic illnesses that are fatal. It may be that there are variations not yet understood that are not fatal.
2. Have you ever found CFS to exist in people or their children who are monogamous and have had only one sexual partner?
Answer: The question is whether ME/CFS can be transmitted sexually. The question cannot be answered because we do not know the specific agent that has initiated ME/CFS in a specific individual. It is likely that some known sexually transmitted illnesses can initiate ME/CFS. (Remember, the illness is more often a post-infectious phenomenon rather than due to a specific infection) However ME/CFS clearly may occur in persons who have never had sexual exposure. One “outbreak” many years ago occurred in a convent.
Question: Can you tell me if orthostatic intolerance causes breathlessness on standing and is there any mechanism through which diazepam could help this?
Answer: Good question. Orthostatic intolerance certainly causes breathlessness, and this symptom is often mistaken for asthma in patients with ME/CFS. One easy way to tell the difference is that the asthma medicines do not work. The cause of the breathlessness is probably a reduction in blood flow through the heart and lungs, but this may be different for every “type“ of CFS. I have definitely noticed benzodiazepines (Valium® or Xanax®) help this symptom but do not know why. The usual answer is that it reduces the respiratory rate by reducing anxiety, and the reduced respiratory rate improves carbon dioxide balance. But I have my doubts that this is correct. It is related to the observation that patients with ME/CFS cannot hold their breath as long as healthy people. This was first noted by Dr. Paul Cheney, but I have never been happy with the explanations I have heard to attempt to explain it.
Question: In your last newsletter you wrote about two research studies. One found that 53.3% of CFS patients tested positive for a certain autoantibody...my fear is that this study, as in so many studies that you read about, will be dismissed because it does not provide a marker for CFS. It seems to me that when they find positive results like this, then the thing to do is to find other people with the same positive test and group them together and call that one disease. I have never seen this done. My question is: why?Answer: Thanks for the question. And it pinpoints the current dilemma that the CFS research community finds itself in. How can we break ME/CFS/FM down into meaningful groupings? Lets take this example: There are fifty persons with fever, cough, and abnormal chest x-ray. There are numerous germs measured in these fifty persons, including viruses, bacteria, and other organisms. In an attempt to determine what to call this illness, many studies have been done, and it turns out that of the fifty, forty were born in New York state. Aside from being somewhat unlucky for them, does this detail have any importance, or help in defining this disease? The answer to this question is that the fifty persons have pneumonia, and the detail that some were born in New York state is irrelevant.
But subgrouping is exactly what we are trying to do with CFS. There are several potential subgroups that come to mind: 1) acute vs gradual onset; 2) severe neurologic symptoms vs milder neuro symptoms; 3) presence of “viral” type symptoms (sore throat and lymph node pain) vs absence of “viral” symptoms; presence of markers such as RNAse-L and so on. The problem is that when we look at specific groups, instead of nice crisp groups, the edges begin to blur.
Take the separation of CFS from fibromyalgia (FM) for example. In the early eighties they were considered two distinct illnesses. FM was seen by the rheumatologists and CFS was seen by the infectious disease specialists. But when the studies started coming in, the Epstein-Barr virus titers did not help to separate them into different groups, nor did the immunology, nor even the symptom pattern as it all crossed the lines. Now it seems that both the pain of FM and the exhaustion of CFS are due to the autonomic nervous system. One of the reasons that the work of Dr. Spence and colleagues is so valuable is that they may have come across a clear physiologic difference between FM and CFS. We will return to this point in later editions of the newsletter.
In the study referred to in the question, it would be wonderful if discrete subtypes of ME/CFS/FM evolved from autoantibody tests. But this will require several studies with different laboratories for confirmation. In the past, this confirmation has not come. Epstein-Barr virus antibodies, for example, may be as irrelevant as being born in New York state. But who knows? Maybe autoantibodies will be the needed break. Time will tell.
Disclaimer Any medical advice that is presented in the Lyndonville News is generic and for general informational purposes only. ME/CFS/FM is an extremely complex illness and specific advice may not be appropriate for an individual with this illness. Therefore, should you be interested or wish to pursue any of the ideas presented here, please discuss them with your personal physician.
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