Using an Emergency Room Properly

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Last Updated: 20 November 2015 20 November 2015

In today's world, so many people do not have medical insurance that when things get bad they go to the Emergency Room (ER) of a hospital.

As a Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) patient, going to an ER should be the last thing you do rather than the first. For a serious accident, broken bones or body parts that aren't where they should be, definitely head to an ER. Know that you will be there for hours and if you need to eat (i.e. diabetics) bring something with you, if possible.

There are some things you should know first: ER's triage, treat and transfer.

They do not do follow-ups and do not deal with chronic long-term issues. They are trained in solving a problem, not in preventing one. Some patients who repeatedly end up there become "frequent fliers" at the ER.

The doctors and nurses have special training in trauma which means they stabilize and then send you out; either to be admitted, or released to home or another facility. The physicians hardly ever see the patients after the ER so when an ME/CFS patient walks through the door, in the majority of cases the medical staff doesn't know what to do with or for ME/CFS.

It is imperative that you, the patient, have a clear idea of what you need from this visit and stick with it. If your foot is broken, get it set. Having Orthostatic Intolerance has nothing to do with the broken foot.

If you are running a high fever and haven't slept in 4 days, they should know you have a faulty immune system. Do not go in expecting an answer to ME/CFS. Instead, try to find a primary care physician with whom you can work. This is easier said than done but we don't want patients unrealistically setting expectations that can not be met.

There is a time and place for an ER visit and it is for emergencies.

According to the American College of Emergency Physicians Foundation (ACEP) at www. Emergencycareforyou.org the following are the reasons to go to an Emergency Room:

 

Good Reasons to Go to an Emergency Room:

Bad Reasons to Go to an Emergency Room:

Loss of consciousness. Signs of heart attack that last two minutes or more. These include: pressure, fullness, squeezing or pain in the center of the chest; tightness, burning, or aching under the breastbone; chest pain with lightheadedness. Signs of a stroke, including: sudden weakness or numbness of the face, arm or leg on one side of the body; sudden dimness or loss of vision, particularly in one eye; loss of speech, or trouble talking or understanding speech; sudden, severe headaches with no known cause; unexplained dizziness, unsteadiness or sudden falls, especially when accompanied by any other stroke symptoms. Severe shortness of breath. Bleeding that does not stop after 10 minutes of direct pressure. Sudden, severe pain. Poisoning (Note: If possible, call your local poison control center first and ask for immediate home treatment advice-certain poisons should be vomited as soon as possible while others should be diluted with water as soon as possible. Such preliminary home treatment could save your life.) A severe or worsening reaction to an insect bite or sting, or to a medication, especially if breathing is difficult. A major injury, such as a head trauma. Unexplained stupor, drowsiness or disorientation. Coughing up or vomiting blood. Severe or persistent vomiting. Suicidal or homicidal feelings.

Earache. Minor cuts where bleeding is controlled. A minor dog or animal bite where bleeding is controlled (but see your doctor-a rabies shot may be necessary). A broken bone (call your doctor to see if he/she can treat you the same day, if not- or if bone is showing, limb is deformed-go to the ER). A sprain. A sunburn or minor burn from cooking. An insect sting or delayed swelling from a sting (if there is breathing difficulty, go to the ER). A skin rash. Fever (if there is a convulsion, go to the ER). Sexually-transmitted diseases. Colds and cough, sore throat, flu.

Dr. Klimas Speaks to MassCFIDS on Cutting-Edge Developments - June 1999

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Last Updated: 02 December 2015 02 December 2015

by Ken Casanova

June 27, 1999

On June 27, 1999, Dr. Nancy Klimas, an internationally respected Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) researcher and clinician, and a member of the federal CFS Coordinating Committee, presented a thorough review of the latest scientific information on CFS research and treatment. At the end of her lecture the Massachusetts CFIDS/ME & FM Association presented Dr. Klimas with a substantial donation for her work. This donation would not have been possible without the support of our members and contributors.

Dr. Klimas emphasized that ME/CFS patients have good reason to be hopeful since ME/CFS research has advanced in these last few years as a result of more research funding. Dr. Klimas stressed that the political and advocacy work of patient organi­zations are a key to obtaining future research funds. Political pressure pushes the federal government to provide the ME/CFS research funds critical to future progress. (Since this lecture, Dr. Klimas has received an NIH CFIDS Research Center grant.)

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ME/CFS and overlapping illnesses

Dr. Klimas outlined the progress that has been made in properly classifying ME/CFS patients under the very broad 1994 case definition. Researchers have found that there are a variety of illness subgroups under the defini­tion's large umbrella that probably include many patients who do not have ME/CFS.

Dr. Klimas said that the two symptom criteria that are most characteristic of ME/CFS are post­-exertional malaise and unrefreshed sleep. Thus she questions whether a person really has ME/CFS in the absence of these symptoms.

Dr. Klimas next compared ME/CFS and fibromyalgia (FM). While many ME/CFS patients have FM and many FM patients have ME/CFS, there are a "vast majority" of FM patients who do not have ME/CFS. Therefore, while ME/CFS and FM are somewhat overlapping illnesses, they are not the same illness.

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ME/CFS disease process

Dr. Klimas next turned to an in-depth discussion of the pathophysiology of the ME/CFS illness process. First, she presented a general model of the stages of the disease process.

The model indicates that ME/CFS is triggered, in a genetically susceptible person, by an infection or some other event. Next, in response to the trigger, the immune, endocrine, and neuroendocrine systems are mobilized. However, these systems remain activated or in a state of imbalance.

According to this theory, ME/CFS is not a dis­ease involving an ongoing infection or contin­uous triggering process. Instead, ME/CFS is the body's prolonged response to the original triggering events. This prolonged neuroim­mune and endocrine activation then sets up the cascade of physiological events to follow.

Possible genetic predisposition

As of 1999, there has been only one study (Keller et al.) that assessed genetic factors in ME/CFS. The results showed that ME/CFS has at least one component that runs 4 to 6-fold higher than normal controls for three gene types (HLA DR haploytypes: DR4, DR3, and DQ3)—which happen to be the same three gene types that are associated with juvenile rheumatism, arthritis, juvenile diabetes and ­Sjogren's Syndrome. These are genes that are connected with immune regulation—thus there might be an autoimmune piece to ME/CFS, since these other illnesses are autoimmune in nature.

ME/CFS triggers

Sixty to 80% of ME/CFS patients can date their illness onset to an acute viral-like illness or infection. (However, only 18% of fibromyalgia patients report having an infection just prior to becoming ill.) There is clear documentation that a percentage of patients developed ME/CFS after contracting an Epstein-Barr virus (EBV) or a cytomegalovirus (CMV) infection. However, instead of recovering, the patients remained sick.

In Australia, Dr. Andrew Lloyd has undertaken a large prospective study to identify ME/CFS triggers by looking at patients who get EBV; Q Fever or Ross River viral infections. The latter two illnesses have chronic courses similar to mononucleosis. At onset of their ill­nesses, Dr. Lloyd is doing a comprehensive bat­tery of immunological tests, and then is follow­ing the subjects over time to see what factors could predict patients' failure to recover. Early findings indicate that those subjects with decreased cell-mediated immunity are most likely to have ongoing, persistent symptoms. Cell-mediated immunity is tested by delayed hypersensitivity skin test­ing. The test consists of an intradermal injection under the skin and is similar to TB, candida, and other allergy testing.

One hypothesis that might explain these findings, according to Dr. Klimas, is that many ME/CFS patients may have an underlying immune abnormality that impedes normal recovery from infections. Dr. Klimas stressed that, as a matter of treatment, it is more important to focus on the "mediators"—the chemicals produced by the neuroimmune and endocrine systems in response to the trig­gers—because these chemicals can be changed as opposed to invariants such as genetics or triggering events.

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Immune system involvement

She showed a chart presenting the two different immune response processes (or cascades) that occur following various infections.

The chart showed that the immune sys­tem has two subsystems: TH-l and TH-2. Each is designed to activate according to the type of microorganism or antigen involved. The TH-2 system responds particularly against bacteria and parasites. The system's cytokine patterns activate B-cells to make antibodies. However, if there are too many B-cells, then autoantibodies may be produced, that can trigger autoimmune diseases, or profound allergic reactions. The inflammatory cytokines, such as IL-10 linked to the TH-2 response, are found to be closely linked to ME/CFS.

In ME/CFS the immune response appears to be shifted improperly and persistently to the TH-2 system. The TH-l pattern produces Natural Killer (NK) cells and cytotoxic T-cells that help to clear viruses. The TH-l system is not function­ing well. One form of therapy would be to try to shift the overworking TH-2 response to an improved TH-l response. Dr. Klimas is exploring treatments that would accomplish this shift.

Immune system dysregulation

The evidence, according to Dr. Klimas, is substantial and irrefutable. Hundreds of scientific articles have been published, nationally and internationally, confirming evidence of immune activation, natural killer cell dysfunction, TH-2 cytokine patterns, and the poor functioning of the TH-l system.

Dr. Klimas summarized some of the evidence.

1. Immune dysregulation in ME/CFS:

A. Up-regulation of macrophages

B. CD-4 cell activation, CD-8 activation

C. TH-2 shift, B-cell derived illness (allergy)

D. TH-l-dependent poor function, NK-cell dysfunction

E.  Pro-inflammatory cytokine release

2. Evidence of chronic immune activation

A. Activation markers on cells

B Products of activated cells (cytokines, etc.)

C. Enzyme systems of up-regulation (e.g., interferon, 2,5a-RNaseL activity)

D. Messenger RNA up-regulation of cell products (cytokines)

Dr. Klimas particularly noted the dramatic up-regulation of the anti-viral enzyme systems. The work of Dr. Suhadolnik on the 2,5a-RNaseL pathway in ME/CFS has shown that the cells and the enzymes are so activated that the reaction, instead of taking 1-2 minutes to digest a viral protein, occurs almost instantly, in as few as 3 seconds.

Dr. Klimas praised Dr. Suhadolnik's research. His Ampligen research findings have been confirmed by four other studies. And not only has he been able to discover enzyme system diagnostic markers for ME/CFS, he has even been able to correlate these markers to the severity of illness. Dr. Suhadolnik included other illness subgroups in his research, but found that ME/CFS subjects have the highest level of activation in the antiviral RNaseL pathway ever reported in the medical literature. Fortunately, he has recently received NIH research funding to continue his groundbreaking work.

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Viral persistence: reactivation of HHV-6

In concluding her discussion on the role of the immune system in ME/CFS, Dr. Klimas reviewed the recent work of Dr. Konstance Knox, who has shown that the Human Herpes Virus 6 (HHV-6) is periodically reactivated in some ME/CFS patients. The work is especially intriguing, since many patients and a number of ME/CFS researchers have suspected that a major component of ME/CFS involves chronic viral persistence.

Dr. Knox and her team conducted a significant study involving 4 sites with a total number of 368 subjects. Thirty-five percent of the ME/CFS subjects expressed the HHV­-6 virus in their serum while no HHV-6 virus was found in the control group. While this finding was signifi­cant, it really did not demonstrate expression of this virus as a funda­mental key to the ill­ness, since two-thirds of ME/CFS patients did not show expression.

An interesting discovery was when 26 ME/CFS patients, who had first tested negative were re-tested, they were then found to have reacti­vated virus. The testing technique in the study involved the direct identification of the virus itself, rather than antibodies to it. These results may be significant in identifying a char­acteristic of the disease process, since periodic reactivation of HHV-6 may occur in more than 37% of ME/CFS patients.

Dr. Knox and her colleagues then did a smaller study of 35 subjects with ME/CFS who had neurological problems. They looked for HHV-6 in the patients' central nervous systems and found the virus actively expressing in 7 patients. Therefore, at least in some patients, the virus is getting into the brain. According to Dr. Klimas, the virus has the propensity to go into the tiny little ves­sels in the brain that supply blood and cause inflammatory reactions. In ME/CFS patients, abnormalities in PET, MRI, and SPECT scans often show decreased blood perfusion. This decreased perfusion may be caused by local inflammatory responses caused by HHV-6. Interestingly, Drs. Ablashi, Krueger, and Knox found no active expression of the HHV-7 or HHV-8 virus in ME/CFS patients.

Other Herpes Viruses

The Herpes family of viruses may play a role in the pathophysiology of ME/CFS. Dr. Klimas already cited EBV (HHV-3) and cytomegalovirus (CMV or HHV-4) as known triggers for ME/CFS. The viruses in this family are generally latent viruses. An individual usually is first infected in childhood or adolescence. At this age, the initial infection is usually quickly overcome by the immune system, but the virus itself manages to "hideout" in some part of the body's tissues, becoming inactive or "latent".

For instance, HHV-6 hides out in natural killer cells. Dr. Klimas theorized about HHV-6 and ME/CFS: why would someone at age 20, 30, or 40 begin to express a virus that should be latent? Something must have happened immunologically to allow the virus to reactivate. She recalled Dr. Lloyd's hypothesis that people can get infections which then persist if the immune system is already not performing properly.

If HHV-6 were active in some ME/CFS patients, would the virus be contagious? Dr. Klimas said she has not found anything in the secretions of ME/CFS patients that is infectious or contagious, including HHV-6, EBV, or any­thing else.

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HPA-Axis dysregulation: hormones

Dr. Klimas emphasized that it is incorrect to separate the immune, endocrine, and nervous systems. In fact, all three form one complex system where the component parts interact with intricate feedback loops.

A major portion of the hormonal or endocrine system is the hypothalamic-pituitary-adrenal (HPA) axis. The hypothalamus and the pituitary glands are in the brain, while the adrenal glands sit atop the kidneys.

The hypothalamus is the master gland; it tells the pituitary when a particular hormone is needed. The pituitary, in turn, sends signals to the adrenals and other glands. The problem in ME/CFS is that activity of the hypothalamus is blunted and hormone-producing signals are not produced properly.

At the 1998 AACFS conference in Cambridge, MA, Dr. Ted Dinan presented a preliminary but extraordinary piece of research in which CAT scans showed very shrunken adren­al glands in ME/CFS patients. In contrast, both depressed persons and healthy controls showed entirely normal-sized adrenals. Furthermore, the ME/CFS patients showed hypothalamic and pituitary dysfunction in addition to the shrunk­en adrenals.

The hypothalamus is also dysfunctional in fibromyalgia patients. Dr. Robert Bennett, a leading fibromyalgia researcher, was irked by critics of studies demonstrating organic deficits in FM. The constant criticism was that the studies were invariably too small, so he decided to respond.

In a study of 500 patients, Dr. Bennett demonstrated abnormal hypothalamic function. In a sub-sample he found that it was the hypothalamus, not the pituitary, which was not functioning properly.

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Dysfunction in the autonomic nervous system

The autonomic nervous system is divided into two segments: the sympathetic and parasympa­thetic systems. The sympathetic system mobi­lizes the flight or fight response; adrenalin is produced and blood is sent to the muscles and brain.

The parasympathetic system, on the other hand, puts the body into a state of relax­ation, allowing the body to recuperate and restore itself. Dr. Klimas stated that in ME/CFS patients the sympathetic and parasympathetic systems are not in proper balance with each other.

The regulation of blood pressure by these systems is often dysfunctional. The evidence for this has come from research at Johns Hopkins (Drs. Calkins, Rowe et al) and from the blood volume/cell studies by Drs. Bell and Streeten.

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Cognitive dysfunction

Dr. John LaManca et al. administered IQ tests to ME/CFS patients and to a control group four hours and 24 hours after treadmill testing. The ME/CFS patients experienced a cognitive loss four hours after treadmill, which continued to persist for 24 hours. Usually when cognitive testing is repeated, learning occurs and there is a gain in score. The control group had a good improvement in score while the ME/CFS patients had scores that went down as they relapsed fol­lowing the treadmill testing.

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Neurally-mediated hypotension in ME/CFS

Dr. Klimas gave a short description of this con­dition. Normally, when a person stands up much of the blood volume goes to the legs and feet. As a result, there is a very brief reduction of blood volume available to the heart; sensors in the heart respond by sending a sympathetic nerve signal to the brain calling for increased blood pressure and pulse. The brain sends the signal to provide increased blood flow, and within a couple of minutes, having obtained blood it needs, the heart should send a second message to the brain calling for a small parasympathetic response to reduce blood flow to prevent any overshooting or hypertensive response.

In ME/CFS, upon standing, everything happens properly until the final parasympa­thetic response. The parasympathetic response, instead of providing a small downward adjust­ment in blood pressure, is way overstated and you get a big blood pressure and pulse drop.

The blood pressure can go to 60/30 or under and the pulse to 40. Many doctors fail to diagnose this condition, because they ask if the patient actually has had instances of fainting. If the ME/CFS patient has been able to prevent actual fainting and answers no, then the doctor moves on. The doctor fails to ask if the patient has felt like fainting.

Blood volume and red blood cell mass

Similarly, Drs. Bell and Streeten found an intriguing set of abnormalities in their work on ME/CFS patients' blood volumes. They did sophisticated tests that tagged red blood cells to make a count of the entire number of RBCs in the body. At the same time, they measured the volume of blood plasma. Bell and Streeten found abnor­mal numbers both in plasma and RBCs.

If the number of red cells is much lower, then the cells have to try to deliver less oxygen much more quickly. This can result in tachycardia and other circulatory difficulties. If blood volume or plasma volume is low, then the blood goes to the feet and there is greater difficulty get­ting blood to the heart and head.

The kidneys control blood volume. They determine how much liquid goes out through the urine and how much stays in. The kidneys also make erythropoetin (EPO), a hor­mone that tells the bone marrow to make more red blood cells. The sympathetic nervous system is responsible for signaling the kidneys to retain or excrete liquid, thereby altering blood volume.

Dr. Klimas is doing a partially funded NIH study to determine if the sympathetic tone of kidneys is affected in ME/CFS, and if there is a therapeutic intervention She has commenced EPO clinical trials, by injection, to induce more red blood cell formation (in people with docu­mented low RBC). She hopes the trials will show efficacy of the treatment.

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Treatments 

Interventions for Low Blood Volume

If an ME/CFS patient  has low blood volume or neurally mediated hypotension (NMH), there are basical­ly two therapeutic approaches. The whole sys­tem can be visualized as a system of pipes and a pump. The first approach would be to fill up all the space in the pipes, so that the heart would not experience the temporary loss in volume. Water, salt and the drug Florinef would be the therapeutic means to increase the blood volume.

The alternate approach is to regulate the heart (pump). The cardiologist can give beta blockers, that make the heart beat at an even 60 beats per minute all the time. This allows the heart a little more time to fill between beats, so it more fully fills. But beta blockers can have the side effect of fatigue. Therefore the physician must balance the risk vs. the benefit of the therapy.

Dr. Klimas outlined her approach for increasing blood volume. First, over a two-week period, substantially increase the intake of water and salt, using salt tablets. She clearly warned that water should not be increased without also taking salt, since increased water by itself acts as a diuretic (you will pee out more fluid; in so doing, you will reduce blood volume and become sicker). Also, you must take proper amounts of water and salt. Too much salt can result in hypertension. Your blood pressure will go down when you stand up. If you overshoot, you will do so when you are lying down. The blood pressure must be moni­tored, both lying down and standing up.

In addition to water and salt a physician may prescribe Florinef. However, Florinef caus­es the body to lose potassium. Potassium loss can be serious. The result can be terrible fatigue, heart arrhythmias, or skeletal muscle malfunction and paralysis. You must have your doctor monitor your potassium levels regularly.

One aid for NMH is to elevate the head of your bed 30 degrees or higher. The elevation maintains a signal in your brain all night long that you're a little upright. This keeps the tone in the vessels a little tight all night, preventing a relaxation in the venous tone of the legs. As a result, when you rise in the morning, the blood supply is not pushed entirely into the legs and there is less of a drop in blood pressure.

A minimal and achievable exercise program

Again, in relation to blood pressure, the body's muscles help to control the tone of the blood vessels. For this reason and many others, it is very important to take care of the body's muscles. ME/CFS patients need to find ways to do even the most minimal exercise. Here is the approach recommended by Dr. Klimas.

To start, deter­mine how many minutes you have during a good part of your day to do minimal movement before you start to feel tired. This is the amount of time you will exercise at the beginning. There are two types of exercise: aerobic and strengthening.

Aerobic Exercise

Aerobic exercise consists of body movement that increases the heart rate, such as swimming, bicycling, even walking. Dr. Klimas highly rec­ommends swimming since the water compresses vascular space, thereby encouraging circulation throughout the body. Swimming also cools and prevents overheating.

Your goal is to prevent deconditioning. Start with your minimal, fixed amount of time and do the same exercise every day for two weeks. Don't try to advance the amount of time or push yourself for the first 2 weeks.

After two weeks, add 7 minutes of the exercise at a different time of day.

After anoth­er two weeks or so, you can begin to exercise a third time a day for another 7 minutes.

When you feel absolutely ready, you can increase the number of minutes in each period, but be flexi­ble. If you're having a relapse, don't make your­self worse by forcing yourself to stick to your schedule. But as soon as you feel better, get back to your program. By sticking with it, over time, you will improve physically. In six months, you may be able to exercise moderately for 15 minutes, two to three times per day. For many ME/CFS patients this is a rational goal that can be achieved without undue relapsing.

Strengthening with isometric or weightlifting exercise

A major problem for ME/CFS patients is the loss of muscle tone due to inactivity. Strengthening exercises are a very good way to maintain tone, and these exercises are not as difficult for the patient since they require less blood flow and oxygenation. Moreover, the exercises should only be done every other day.

To start take a one-pound can of soup and do repetitions (biceps curls) with one hand until your arm is a little tired, then stop. Remember how many repetitions you did.

Next, move on to the next muscle group and do the same thing. Rest the next day, since the rest allows the muscle to strengthen.

For the first week don't change the number of repetitions. You will need a book of weight exercises to teach you how to progress. Dr. Klimas recommends the FM Survivors Guide by Dr. Mark Pellegrino that outlines an excellent exercise program. [Editor's note: 2015 research at Marquetts Univeristy has shown that for older healthy people, such exercise has to be carried out slowly for the best results.]

Medications for compressing the vascular system

Besides exercise, the vascular system can be compressed using various medications. Many patients use caffeine or Sudafed. The problem is these substances can cause tachycardia.

Midodrine, a prescription medication, is a more specific vasoconstrictor, especially in the legs. It shunts blood to the head, but some patients can't tolerate it. Dr. Klimas said she has had good experience with it. It is best to start at very low doses. ME/CFS patients should divide the stan­dard dose by 4 or 10. Dr. Klimas starts patients at one half or quarter tablet the 1st day. If the patient does well, then she gives the same dose in the morning and at lunch. The next increase is to morning, lunch, and then mid-afternoon.

There is a timing issue involved in tak­ing Midodrine. Blood pressure shifts after meals, and the blood supply is then shunted to the gut. Therefore, it is best to take the med­ication before meals.

Don't take Midodrine before bed since it raises blood pressure 10-20 points.

If your blood pressure is normal lying down, you don't need this medication. If your pressure is too low when you are lying down, then Midodrine might help you.

Sleep disorder and ME/CFS

Dr. Klimas said that sleep was one of the most critical factors affecting the illness: "If you can't get sleep under control and help the patient get restorative sleep, you really can't help the patient make any substantial improve­ment with any real speed. Every effort must be made to help the patient get restorative sleep."

The problem of sleep best highlights the interactive involvement of the brain, hormonal, and immune systems in ME/CFS. If a person has a severe sleep disorder, his or her immune and hormonal systems may be severely out of bal­ance and dysfunctional.

Sleep sets the circadi­an rhythms of the immune and endocrine sys­tems. When normal sleep is disrupted, the diurnal patterns of cortisol and prolactin pro­duction are altered, as are the diurnal patterns of NK-cell function. Alpha-wave intrusion on sleep EEG also occurs.

Sleep Therapies

It is necessary to work to reestablish the body's circadian rhythm by reestablishing a regular sleep pattern. The goal is to set a bedtime for the same time each night, and then to fall asleep shortly after going to bed. Her idea is to create a conditioned response—to associate being in bed only with nighttime sleeping. If one is only in bed to sleep, then getting into bed is more likely to result in sleep. To establish this conditioned response, the ME/CFS patient must avoid using the bed for resting or reading during the day. Dr. Klimas says this approach will help you fall asleep at the same time each day. The approach may not help you stay asleep or help you obtain the proper restorative sleep.

If you do need medication, Klimas advises, "avoid using the short-acting hypnotics." These medications, like Ambien and Restoril, are designed to help you fall asleep. The problem is they don't help you stay asleep. Moreover, these medications trap people in the lighter alpha sleep.

ME/CFS patients need a drug to induce deeper sleep—stages 3 and 4. The drug also needs to last 8 hours so the per­son will remain asleep. Tricyclics in low doses, like Elavil and especially Doxepin, are very good choices. Doxepin has the added benefit of having antihistamine and anticholinergic prop­erties. It comes in a liquid so patients can control the dosage by adjusting it to just drops.

Dr. Klimas warned that ME/CFS patients must be careful in using the Selective Serotonin Reuptake Inhibitors (SSRIs) for sleep, i.e., the Prozac class. These drugs can be either sedating or activating. It is important to know which of these drugs sedate and in what doses.

Prozac is an acti­vating drug. If you take it in the morning, it will peak in the evening and then you won't be able to sleep. You should take it at night so it will acti­vate in the morning.

The new drug Serzone is used to improve stage 3 and stage 4 sleep. Klonopin can help with restless leg syndrome. Flexeril can be used to relax the muscles at night.

Treatment of Pain in ME/CFS

The effective treatment of pain has to be a high priority. Months and years of moderate and severe pain can take a serious toll physically and mentally. Most doctors rely on NSAIDs (nonsteroidal, anti-inflammatory drugs) like ibuprofen, which don't work very well with ME/CFS.

Tricyclics (Elavil, Doxepin) can help with pain thresholds so there is less perception of pain. Opiates, from codeine to morphine, are sometimes used to control pain. The use of opiates is controversial because of the fear of addiction.

Dr. Klimas, however, argued that because of the serious consequences of pain in ME/CFS, sometimes the use of opiates must be risked. She said, "I have never lost anyone to CFIDS/ME, but 1 have lost people to pain. The people who die of CFIDS/ME die from suicide, and typically people don't kill themselves unless there is a big pain piece to their illness."

She would argue vehemently that opiates have a role for some patients, though not a majority of patients. When serious pain control is needed, Dr. Klimas often prefers to use longer acting, low-dose morphine that lasts 12 hours or the new 24- hour type. Shorter-acting Percocet may be more addicting. New neurotransmitter analogs like Neurontin also have a role and are not addictive. She'll try these first.

Dr. Klimas also emphasized that it's essential to understand the interactions of the various medications the patient is taking. The interactions themselves could be causing symptoms and affecting the individual's sleep.

Other therapies: Self-help for cognitive symptoms

The prescription for cognitive dysfunction is: practice, practice, practice. There are many patients who become isolated and reduce their cognitive challenges. Do crossword puzzles, vol­unteer, go to a class, tutor, go to meetings, do something fun. Try not to sit by yourself at home all day. Listen to book tapes. Know your best time of day to do intellectually challenging work.

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Questions

Pregnancy and ME/CFS

Blood volume increases dramatically during pregnancy so most ME/CFs patients who are pregnant feel better. They often relapse after delivery, so sup­ports need to be in place. Dr. Klimas feels that breast-feeding is not a good idea. There is the exhaustion from having to get up at night, and there is also the potential of the baby's exposure to virus at too young an age.

Vaccination

Dr. Klimas' advice is to get vaccinated if you can tolerate it. The medication Amantadine can treat half of the various influenza strains as well as prevent them. She gives patients Amantadine during the flu season.

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Who gets better?

Some studies say the younger the patient, the better the recovery. But Dr. Dedra Buchwald found that this is not true. A CDC study says chances for improvement are higher if the patient is ill less than 3 years. Buchwald's study says the duration of illness is not a predictor of prognosis.

Dr. Klimas did say, "What we really do know is that people who are depressed do worse than people who are not. Depression is treat­able. ME/CFS patients may be reluctant to get this part of the illness treated because of the stigma of depression. Half of ME/CFS patients do not have any depression. Those that do, most often have a secondary depression.

 

Can Blood Transfusions Cause ME/CFS?

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Last Updated: 01 December 2015 01 December 2015

From Sydney, Australia: One Research Team Says "Yes"

Belgium's Dr. Kenny De Meirleir explained to a long-time Dutch patient with ME/CFS that his RNase-L enzyme test showed a high level of viral activation consistent with Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS). "We now understand the im­munological basis of Chronic Fatigue Syndrome(CFS)," he said. "Because of your RNase-L test, it is certain that your illness has a viral basis."

Expressing his concern that ME/CFS might be contagious, the patient asked the doctor about the possibility of infecting others through casual contact. "I don't think so," Dr. De Meirleir answered. "But blood products can transmit it; we are sure of that. We have a rather large number of CFS patients who became ill immedi­ately after transfusion." 

If supported by subse­quent research, this hypothesis would obviously hold serious implications for public health.

Dr. De Meirleir shared the findings of his study on blood transfusions at the CFS Conference held in Sydney, Australia, this February. Bear in mind that these are the re­sults of a single study and that the numbers are fairly small. Just the same, because of the possible ramifications of this study, the abstract is reproduced here more or less in its entirety:

"We analyzed...1 ,210 consecutive patients... who visited our fatigue clinic at the Vrige Universiteit Brussel [Brussels, Bel­gium]. In this group, 752 patients fulfilled the [1994] CDC crite­ria for CFS. Of those patients, 34 (4.5%) have a common factor in their past medical history that immediately preceded the on­set of their CFS. These patients had received a blood transfu­sion a few days to a week prior to developing a 'flu­like' syndrome that later proved to be the acute onset of CFS. Another 8 patients also received a blood trans­fusion but their illness started at least two months later, so we cannot take these patients [into account] in our calculations.

"None of these post-transfusion patients devel­oped hepatitis C or other types of viral hepatitis. Some had antibodies (IgG) against CMV or EBV, but [when these antibodies developed] in time in relationship to the blood transfusion could not be determined. In 9 of 34 the LMW [low molecular weight] RNase-L test was performed; in all 9 patients, the [results were consistent with those seen] in viral disorders.

"These findings point towards a transmittable cause in this subset of CFS patients in which acute onset was temporally linked to blood transfusion. As viruses and possibly other micro-organisms seem to be able to trigger an acute onset of CFS, and [because] RNase-L dysfunction seems to be preferentially related to CFS, it comes as no real surprise that receivers of a blood transfusion, often being in a weakened status, [could potentially] develop CFS. We therefore would advise CFS patients not to be blood donors and, sec­ondly, [recommend] that the administration of blood transfusions... [should occur] only when strictly neces­sary and not as a standard procedure (e.g., as in after the delivery of a baby)."

(Abstract: "Blood Transfusion and Chronic Fatigue Syndrome," by K. De Meirleir, P. De Becker, and I. Campine, Human Physiology and Medicine, Vrige Uni­versiteit Brussel. Source: CPAR Digest, V.I #401)

A Conceptual Breakthrough? Dr. Bell Relates "Very Exciting" Findings on Possible Causes, Tests, Treatments for CFIDS Symptoms

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Last Updated: 07 November 2015 07 November 2015

by Joan Livingston

(Editor's note, 2008: This article is a report on a lecture by Dr. Bell and was written for the Massachusetts CFIDS/ME & FM Association newsletter The UDATE Winter 1997-1998. The report discusses Dr. Bell's and Dr. Streeten's finding of reduced plasma and red blood cell volume in the blood of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) patients. While Dr. Bell hypothesized at that time that these factors may be a primary cause of ME/CFS, more current research indicates that other physiological systems play a more important role in the causation of ME/CFS. However, many of the findings of Dr. Bell in this article continue to be current in 2008— these findings point to important physiological processes and symptoms found in the illness.)

(Editor's note, 2015: Many patients still have problems as described in this article, and may have improvement if they follow suggested treatments. However, the factors are not an important role in the causation of ME/CFS—more of a result of ME/CFS in many patients, according to current research.)

Introduction 

It may turn out to be more than just a whimsical metaphor. In describing their illness, many Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS) patients say they feel as if their life force has been sucked dry by a vampire. This subjective sensation may in fact be explained by a literal, objective ab­normality, according to Dr. David Bell. New, ex­ploratory research by Dr. Bell and his colleagues suggests that a majority of People with CFIDS (PWC) may have "extraordinarily" low circulating blood volume (note: not low blood pressure), and low red blood cell (RBC) mass (similarly, not anemia or other RBC counts routinely measured in basic blood tests).

While circulating blood volume, levels of plasma (the fluid, non-cellular portion of the blood), and RBC mass are rarely tested in the lab work most of us undergo during annual physicals, they are hardly esoteric measures. They can readily be gauged via standard—"not fancy, not controversial"—blood tests that have been in use for decades.

During a recent presentation to members of the Massachusetts CFIDS/ME & FM Association CFIDS, Dr. Bell—a renowned CFIDS/ME clinician and researcher based in Lyndonville, NY—described  "striking" blood abnormalities found in the patients he has studied, abnormalities that may go further than ­other, earlier documented anomalies in providing a strong theoretical basis for the constellation of symptoms, sensations, and disabilities inherent in CFIDS/ME. Not previously presented in the U.S., Bell's latest findings are scheduled for publication in the January Jour­nal of Chronic Fatigue Syndrome, in an article whose ­lead author is endocrinologist Dr. David Streeten of Syracuse, N.Y.

Piecing together the quilt 

The ramifications of Dr. Bell's theory? They could be far-reaching, encompassing a simple-to-obtain, possible diagnostic marker (finally!), a straightforward explanation for the crazy quilt of fluctuating symptoms experienced by patients (ditto!), a definitive end to the debate about whether CFIDS/ME is psychosomatic (ditto!), and—perhaps most meaningful to PWCs—implications for effective treatments to undo the blood abnormalities and hence resolve the panoply of debilitating CFIDS/ME symptoms (ditto, ditto, ditto!).

Until recently, Bell said, "Medical care for CFS has been abysmal. The basic underlying problem  has been the lack of physiological markers, which  has led to theory after theory about what's generating these symptoms. There's been almost nothing for physicians to work with. If doctors had a single marker like the visual-evoked response in MS, they'd say, 'Yes, I know what this is and what to do about it.' Instead, they've been bewildered by the pattern of CFS symptoms and often don't know how to deal with them."

Dr. Bell further noted that the Centers for Disease Control & Prevention's (CDC) current, ­symptom-based diagnostic criteria are highly problematic, causing "horrendous problems in disability claims, and patients being hassled by insurance companies, with a type of discrimination I think is really inexcusable;" the criteria also generate difficulty in diagnosing children, who may present with symptoms different from those of adults.

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Reviewing the key ME/CFS symptoms

To lay the foundation for his potentially groundbreak­ing theory, Dr. Bell began by outlining what he sees as the four major clusters of symptoms that any viable theory of CFIDS/ME etiology must explain: fatigue, neurological symptoms, pain, and multiple sensitivities.

Fatigue

Dr. Bell's first observation was that "fatigue" is a totally "inappropriate" word to describe the utter exhaustion and weakness experienced by PWCs. In common usage, it connotes a normal person's recovery from abnormal exertion, "like regaining energy after a busy day"—not the characteristic CFIDS/ME experience. He described CFIDS/ME fatigue as including asthenia (weakness), orthostatic intolerance (the inability to stand up or remain upright, rather than fatigue), and sensations of impending collapse—for example, a patient may walk out to her mailbox, and then feel so weak that she feels unable to walk back to the house. The latter may be "the most important [CFIDS-specific] of this first group of symptoms," he said.

Bell noted that, while post-exertion fatigue in CFIDS is not readily improved with rest, "Many patients will say that they feel okay if they just lie down all day—that life becomes tolerable with [consistent] rest." Standing up or even sitting up, by contrast, can trigger the fatigue, pain, and other symptoms.

Another unusual aspect of CFIDS/ME fatigue is that it often follows a relapsing-and-remitting pattern—not just day to day, but frequently also over the course of a single day. Many patients might be unable to function in the morning and evening, say, but have higher functioning level for a couple of hours during the afternoon, during which they can run errands or do light housework. On the other hand, some patients have a consistently low functioning level all day long, day after day and year after year: "It has always been my feeling that people with few fluctuations have the worst course [prognosis], while those who feel '20 percent' one day and ‘80%' the next have the greatest chance of recovery. This though, has never been formally documented," Dr. Bell noted.

Neurological symptoms 

While many patients have symptoms in virtually every body system, Dr. Bell feels that the combination of fatigue and the neurological problems, "which are very disruptive," are the principal factors in PWC's inability to work. This second category of symptoms includes the cognitive dysfunction—mental exhaustion, an inability to focus, poor short-term memory—as well as balance disturbances, paresthesias, myoclonus, and lightheadedness or dizziness.

Pain 

Often disabling, pain represents the third key CFIDS/ME symptom Dr. Bell said. "It can be of variable intensity, it may or may not parallel the severity of the illness, and it can be literally any place in the body," he observed, adding that many patients seek care from multiple doctors in their quest for relief: ­perhaps an Ear/Nose/Throat (ENT) for headaches, a neurologist for the muscle pain, a gastroenterologist for digestive problems. One consistent and suggestive characteristic of the pain is its laterality—painful lymph nodes, muscles, sore throat, etc., that occur on only one side of the body. This suggests to Dr. Bell that CFIDS is a disorder of pain modulation—"clearly a disorder in the brain"—rather than a problem in the affected organ systems.

Sensitivities 

The fourth problem category, multiple sensitivities, is extremely consequential in diagnosis, Dr. Bell stated. It is so common that "I feel there's something wrong with any theory [regarding the basis of CFIDS] that doesn't provide an explanation for these." Sixty to 70 percent of PWCs report sensitivities, he estimated—"an extraordinarily high percentage." The sensitivities from which patients suffer are many and motley: to light, noise, odor, alcohol, drugs, temperature, foods.

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Current theories of pathogenesis

The "Why" behind the "What"

After this symptom review, Dr. Bell proceeded to a theory review: a look at the most popular current the­ories about the cause and nature of CFIDS/ME, and their strengths and weaknesses in explaining the illness fully.

First Bell addressed the theory of persistent subclinical infection. Historically (especially in the early and mid-'80s), this was the most prevalent hy­pothesis; with reactivated Epstein-Barr virus com­monly considered the driving force behind the illness (which was, in fact, called chronic Epstein-Barr syn­drome at that time). Myriad other agents have been proposed since then, with Human Herpes Virus 6 still under active consideration, as well as other herpes ­family viruses, a "stealth" virus, a retrovirus, Cox­sackie virus, Chlamydia, and more—many more, as any issue of The UPDATE or The CFIDS Chronicle will demonstrate. Bell finds this theory unconvincing, since no single bodily area of infection and no single causative agent has yet been pinpointed, despite more than a decade of research. "This theory may be correct," he said, "but my hunch says otherwise."

Second is a related conjecture that CFIDS/ME results from agent-induced immune activation i.e., that some trigger (most likely a virus or bacterium) alters the immune system and keeps it habitually upreg­ulated, with the bulk of CFIDS/ME symptoms stemming from the immune abnormalities rather than the triggering agent. While this remains the most prominent the­ory at present, it suffers from one deficiency also em­bodied in the first: the failure to identify a single infectious or other agent in a majority of PWCs. Moreover—and more significant—says Dr. Bell, "The sickest people should, but don't, have the worst immune-system activation. The immune activation is there, but we haven't been able to explain why, and if it were closely linked to the cause [of CFIDS], the severity of the illness should parallel the severity of the immune activation."

(In a humorous aside, Dr. Bell noted that he once subscribed to this theory but no longer believes it's correct: "If anyone here was misfortunate enough to purchase my book [The Doctor's Guide to Chronic Fatigue Syndrome], this theory is the whole second half of the book. I now think it's all wrong and I want to apologize for having wasted your money. ")

Three other theories that Bell quickly dis­patched: abnormal adrenal function (it doesn't ac­count for enough of the CFIDS/ME symptomatology); mi­tochondrial disease ("hard to study and hard to mea­sure"); and the notion that CFIDS/ME is either psychoso­matic or a form of malingering ("an attitude which, fortunately, is beginning to disappear, especially in the last five years").

Having provided his opinion of these theories and their shortcomings, Dr. Bell introduced his new hypothesis—still in the initial stages and requiring more research, still not an answer for every patient he's studied, but intuitively logical, consistent with a lion's share of the CFIDS/ME symptoms just listed, and quite promising in terms of identifying treatments: neurocirculaton asthenia.

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Neurocirculatory Asthenia, or, the Vampire Chronicles

"Neurocirculatory asthenia" is a formidable-sounding term for the rather straightforward findings attendant upon Dr. Bell and Dr. Streeten's recent research. In plain English, it connotes a person's inability—arising from the brain—to maintain adequate, normal blood flow to all areas of the body ("one of the most primitive" human survival mechanisms).

Dr. Bell explained it in part by using post-polio syndrome as a model, because that disorder also stems from brain abnormalities (in this case, true brain injury). The syndrome is present in 91 percent of polio survivors, and despite the differences, it does entail chronic symptoms similar to those of CFIDS/ME, including fatigue and cognitive dysfunction (including trouble with concentration, memory, and word-finding).

Autopsies performed on people who did survive their infection with polio reveal lesions in the same areas of the brain believed to be affected in CFIDS/ME. "This model is not particularly encouraging in that damage caused to the brain by polio can be ­irreversible, which is worrisome. But I think that CFS symptoms are much more likely to be reversible," Bell ­said, because CFIDS/ME symptoms caused by poor blood ­flow to the brain can be reversed if normal blood flow is restored.

Tilt tables, tests, trousers

Bell next addressed the well-publicized Johns Hopkins study involving tilt-table testing, which led directly to his current research focus, for several reasons. Among other things, he knew that his patients had trouble maintaining a standing position (orthostatic hypotension). The Johns Hopkins researchers had identified a similar problem—abnormal heart-rate and blood-pressure responses upon changes in body position—but they hypothesized that the cause was neurally mediated hypotension (NMH), reflecting a derangement in the autonomic nervous system (ANS). Other researchers have attempted to substantiate the Johns Hopkins work but with different study methodologies and thus, different findings, so the work has yet to be replicated.

In his Massachusetts CFIDS/ME & FM Association presentation, Bell pointed out that NMH—from which 22 of the hand-picked 23 Hopkins PWCs suffered —is different from CFIDS/ME; also, it would not explain the full constellation of CFIDS/ME symptoms. As a result. Bell doesn't feel that NMH is the mechanism behind CFIDS/ME; just the same those findings led him to go down a similar road, if not the same road, in studying the cause of CFIDS/ME: "I find this was still a very exciting study and perhaps one of the most interesting directions we are pursu­ing."

One problem with the Hopkins study was that, of the participants, only about half responded favorably and dramatically to the anti-NMH drug Florinef and salt (some others improved on Procardia, a heart medication; others did not respond to any therapy or actually worsened). "The medications sometimes led to a complete resolution of symptoms. This led me to wonder, why did some people respond to the med­ications and other people don't?" Bell asked. As with so many other CFIDS/ME abnormalities—EBV titers, antinuclear antibodies, specific immune abnormalities—there seemed to be vast differences among people who presumably had the same illness.

Falling down

However, because of the potentially substantial ramifications of the NMH find­ings, Drs. Bell and Streeten conducted related research of their own on 19 severely ill patients. They mea­sured variables including blood pressure, blood volume, norepinephrine (a.k.a. adrenaline, the "stress hor­mone"), and cognitive functioning while their study subjects were lying down, sitting up, and standing for as long as they could tolerate (perhaps predictably, some PWCs simply fainted when asked to stand). While not all patients had abnormalities in norepinephrine, some had surprising reactions to changes in body positions: One patient's level "skyrocketed" upon standing and, after five minutes, so too did her pain—simply standing up stimulated all her CFIDS/ME symptoms. Bell and Streeten had her don "MAST trousers"—military anti-G-force pants that act as a blood-pressure cuff almost from head (upper chest) to toe, forcing blood up to the brain—and "her symptoms vanished immediately."

Pooling blood

While the stress-hormone findings were often provocative, what seemed to be the most meaningful data to emerge from the study concerned plasma volume, RBC mass, and total circulating blood volume. Most of the patients had "strikingly abnormal" circulating blood volume; 13 of 19 had both low plasma levels and low RBC mass. This was true despite normal blood pressure and normal hematocrits (a standard measure, the RBC-to-plasma ratio; it was presumably normal because the low RBC counts were proportionate to the low plasma levels). In addition, the blood that was present tended to pool in the extremities—particularly the legs—leaving even less blood in the brain for normal cerebral function. Based on these dramatic findings, Bell and Streeten are conducting further research in this area. "Low circulating blood volume," said Bell, "is, I think, the mechanism behind this illness."

The study subjects differed moderately in which blood variables were "off" and by how much, but 16 of 19, for example, had low RBC mass—a shortage of the cells that carry oxygen to the brain and elsewhere. Interestingly, just one subject had a normal, 100% RBC mass: she recovered and went back to work three months after the study. With this exception, the findings were quite consistent and re­markable. "Essentially," Dr. Bell observed, "all the patients had low circulating blood volume."

Feeling dead 

Besides the woman who re­covered, the participants had an average of 70 percent of normal circulating blood-volume levels. Some ac­tually had less than 50 percent of normal. "That's extraordinary. If you're in a car accident and you lose 50 percent of your blood volume, it's fatal," Dr. Bell noted. "You cannot survive such an acute loss of blood." (This finding puts a new spin on PWCs' common observation that they "feel dead"). 

Dr. Bell remarked that he'd assumed the aver­age PWC had been tested for everything—"They have medical files this thick"—but that this particular blood testing is non-routine and has simply been over­looked. It is simple to administer and undergo: you have blood drawn, chromium-51 is added to it, the blood is re-injected, and the volumes are tested two hours later. (Because it takes the body six weeks to clear itself of chromium, the test can be performed only that often.)

What else can affect blood volume? "Living at a high altitude, like the Himalayas, but even that doesn't affect blood volume much." The illness that seems most similar to CFIDS/ME in this respect, said Bell, is Addison's disease (adrenal insufficiency)—and it, too, causes asthenia, but cortisol treatment "makes it go away." (A possibly interesting side note is the CDC's finding, some time back, that PWC's fre­quently have low cortisol levels.)

If Bell and Streeten's theory proves correct, it might put an end to more than symptoms—it should silence the longstanding body-mind debate. "Nobody can say that a half-normal blood volume is psychosomatic," he noted. "Even if you're nuttier than a fruitcake, it will not affect your blood volume."

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Linking findings to symptoms

Just a glance back at the four symptom clusters enu­merated earlier will demonstrate how well Bell's new research findings account for CFIDS/ME abnormalities: blood pooling in the extremities, low body-wide blood volume, and resulting low blood flow to the brain have obvious implications for fatigue, neurology prob­lems, pain, and sensitivities. (Regarding alcohol intol­erance, for example, just imagine a PWC's blood alco­hol level after two drinks if the patient has 50 to 70 percent of normal blood volume! Likewise, the low volume could spur over-sensitivity to drugs, histamine, etc.). Even healthy people, Bell noted, are instructed to lie down after donating blood to the Red Cross, be­cause of the possibility of fainting and lightheadedness resulting from orthostatic hypotension.

Making sense of mish-mosh 

Given that some PWCs seemingly suffer only from low plasma levels and others only from low RBC mass, the mixed treat­ment results at Johns Hopkins begin to make sense: "The only thing that Florinef affects is blood volume," Bell noted. Therefore, the 50 percent of Florinef re­sponders may likely have been those with the lowest blood volumes, not with NMH per se. Bell noted that one of the Johns Hopkins subjects treated with Florinef went from a pre-medication functioning level of 20 to 40 percent, quickly recovered on Florinef, and then stayed at 100 percent for two full years, even af­ter discontinuing the drug. She later experienced a re­lapse, went back on Florinef, and recovered com­pletely in two weeks (she is now, not surprisingly, staying on Florinef!). "Such a rapid recovery is a re­markable finding and clearly not explained by chance but instead by the drug," Bell said.

Bell also spelled out how his findings could explain many of the signs and symptoms that have seemed like a random mish-mosh until now. To name just one: SPECT scans of PWCs frequently show "holes" in the brain; these represent areas of insufficient blood flow. (MRI abnormalities, too, could be the result of low blood volume.)

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Dr. Bell's hypothesis

One issue that remains unresolved is whether the severity of PWCs' symptoms are blood-volume depen­dent. Another—as with all newly documented abnormalities—is what causes the blood problems in the first place. "What is it that's keeping the volume low? Other body functions seem to be working ag­gressively to get the volume back up." Bell posited two different basic models, based on what is cause (trigger) and what is effect.

If low volume is what precipitates the other symptoms, "blood transfusions could correct the symptoms"; if the low volume is only secondary, an epiphenomenon, correcting it may be far more diffi­cult because the primary trigger will still be active.

Based on the study, Bell posits that there are two (or three, really) distinct groups of PWCs:

1. those with low RBC mass, who seem to have the worst course; and            .
2. those with low plasma volume, which is more likely to resolve with Florinef treatment.

(As already noted, most of the patients actually had both deficiencies.)

While PWCs are all too familiar with the Theory-of-the-Month Club, the work done by Dr. Bell and his colleagues should be easy to replicate (or re­fute) and ideally provide some definitive answers about the mechanism behind CFIDS, pointing the way toward meaningful tests and treatments. Finally, said Dr. Bell, "I hope this will help end the discussion about psychiatric causation." We vampire victims hope so, too.

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Question-and-Answer Session with Dr. Bell: Ex­cerpts

Q. Could the RBC count be treated, like anemia, with ­iron supplements?

A. No. These are totally different ab­normalities; blood volume in anemia is normal, with the RBC count disproportionately low.

 

Q. For those who can't tolerate it, is there any substi­tute for Florinef, like Prednisone?

A. No. While not a "miracle cure," this drug is unique in its effect on blood volume and ability to hold onto salt. Pred­nisone has only 1/50^th the salt retaining power of Florinef

 

Q. What about other therapies, given the distinction between low RBC patients and low plasma patients?

A. One other drug under study is Midodrine, an alpha ag­onist. "It has limited usefulness but seems good with the milder cases, and a number of my patients have had a marvelous response to it."

 

Q.  Can you talk about pregnancy?

A. It has long been observed that many women PWCs feel better—even "recovered"—during pregnancy, but the reason for this has been un­known. One explanation from the current study could be the rise in blood volume—an average of 33 percent­ that occurs during pregnancy.

 

Q. Can you talk about Dyspnea (shortness of breath) on exertion?

A. "Is it a central mechanism or something the lungs are just per­ceiving?"  Possibly, when circulating blood volume drops; the brain (oxygen-starved) may "read" this as shortness of breath, when in fact the lungs are not af­fected.

 

Q. What about food allergies?

A.  Bell noted that low blood vol­ume could be responsible for PWCs' apparent food al­lergies, "which you can't really prove." He noted that, after you eat, your blood pools in the gut—again, less cerebral blood flow, and "even a very small change can cause pronounced symptoms in the brain." (This, Bell said, "is why people take siestas after lunch in civilized countries." It appears that, among Florinef responders, food allergies "vanish" with the drug ther­apy. There may be other "pseudo allergy attacks" to other substances, because of the high amount of his­tamine in proportion to blood volume.)

 

Q. Any relationship to sleep disturbances?

A. Yes. "Our bodies have only one mechanism to get more blood to the brain, and that's to put out more norepinephrine—which can cause insomnia, tremulousness, the jitters"—the fight-or-flight response.

 

Q. Why do we drink so much fluid?

A. Many PWCs routinely carry bottles of liquid with them because of constant thirst—or is it the body's attempt to bring blood volume up to normal? Bell noted that drinking fluids will not help ("you'll just pee it out"). But IV treatments of vitamins or other fluids often do make people feel better, for a few hours or couple of days—not, presumably, because of the Vitamin C or other "medical" content but sim­ply because of the large quantity of transfused liquid (Just as the fatigue of Addison's disease is controlled with cortisol; people with diabetes—whose first symp­toms are generally thirst and tiredness—find that cor­recting their sugar levels with insulin corrects the thirst as well as the fatigue.)

 

Other quick points: PWCs may suffer from tachy­cardia and premature ventricular contractions (PVC) ("which are normal most of the time"); unlike most healthy people, PWCs feel the PVCs in the chest (a new theory has been proposed regarding the role of another heart disorder in CFIDS/ME, subclinical my­ocarditis) 

Bell has not been following progress on Ampligen: "Since that first study, I guess I'm not so enthusiastic about it as a long-term answer; the pa­tients I know didn't have any benefit from it"...

Yes, Reynaud's phenomenon (cold and loss of sensation in fingers, toes) does seem to be slightly increased in CFIDS/ME (sounds like another blood-volume-related symptom to us); similarly, Bell believes that notable facial pallor is one of the most characteristic signs of CFIDS/ME.

Dr. Cheney Warns Against Long-term Use of SSRIs and Stimulants

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Last Updated: 20 November 2015 20 November 2015

by Lucy Dechéne Ph.D.

The Massachusetts CFIDS/ME & FM Association Summer 2001 UPDATE

 

Dr. Cheney is warning patients and physicians against long-term use of SSRIs (Prozac, Zoloft, Paxil, etc.) and stimulants such as Ritalin and Provigil.

Both SSRIs and stimulants cause neurons to increase their firing. Taken over 10+ years or so, these medications can lead to the loss of brain cells, causing neurodegenerative disorders.

Many doctors have recently seen a sudden increase in patients with neurological symptoms and most have been on Prozac or a similar drug for about ten years. Dr. Cheney is seeing this in his own practice [although neuro­logical problems may be a natural result of ME/CFS after more than a decade. Most of the participants didn't use these medications (or at least weren't using them at the time of the study.)-L.D.]

Dr. Cheney recommends patients and physicians read the book Prozac Backlash: Overcoming the Dangers of Prozac, Zoloft, Paxil and Other Antidepressants by Joseph Glenmullen, M.D., a psychiatrist at the Harvard Medical School. ­Dr. Cheney explains that SSRIs are designed to stop the reuptake channel of serotonergic neurons from "vacuuming up" excess serotonin.

Often too much serotonin is left floating in the intersynaptic cleft between neurons. The only way the body can get rid of the excess serotonin is to oxidize it. Unfortunately, this turns into a toxic compound that, over time, kills both the sending and receiving neurons.

Dr. Cheney stated, "What starts out as an attempt to increase serotonin and reduce symptoms ends up with the destruc­tion of the serotonergic system itself. It takes about a decade, more in some, less in others."

[I will point out that the evidence that this occurs is still not definitive, it is only suggestive. However, patients should consider this possibili­ty when staying on such medications for a long time. A good article discussing the situation is "The Serotonin Surprise," Greenberg. (Discover July (2001): 64-69.)-L.D.]

(Source: Dr. Paul Cheney)