From The Nets -- Discussions of the Johns-Hopkins "Tilt-Table Test" Regarding CFS

Area: alt.med.cfs
Date: 03-19-95
From: Marjorie_J_Panditji@ccm.jf.intel.com
To: All
Subj: Lancet article on tilt test


Jesse Lemisch wrote:

Does anyone have, or have an idea about how to get hold of: Peter Rowe, et. al., "Is Neurally Mediated Hypotension an Unrecognized Cause of Chronic Fatigue?" Lancet, March 11, 1995. 345:623-624.

Jesse, thanks for being my straight man! :-)

You can get a free copy of the of the article mentioned above by calling the following number:

(410) 821-7253

You will get a person, not a recording. I called today (Sunday) and I was surprised to find out that they staff this number even on weekends.


Area: alt.med.cfs
Date: 03-11-95
From: David Rice
To: All
Subj: MED: Hopkins Study


After reviewing the posts last night, there appears to be a lot of misinformation regarding the Hopkins study. Researchers discovered a link between a cardiac condidtion known as neurally mediated hypotension (aka vasodepressor syncope) and chronic fatigue. Neurally mediated hypotension generally involves a mis-regulated blood flow and blood pressure which can lead to recurrent fainting. The new study however indicates that a number of individuals have this condition without any symptoms of actually fainting.

They believe there is a strong genetic component with respect to mediated hypotension and that the onset of CFS has been triggered by some type of viral infection. Peter Behan, a professor of neurology at the University of Glasgow stated that the European medical community has known about this problem for some time and in Germany, doctors generally blame CFS on this type of low blood pressure. Behan believes that the actual onset of neurally mediated hypotension can occur as the result of brain cell damages, triggered by some sort of trauma or viral infection.

The AP reported that "normally when standing, heart rate rises a bit -- about 10 to 15 percent -- helping pump blood from the toes to the head. In some people this compensatory system fails. The result is a dramatic drop in blood pressure after standing for some time, even just ten minutes..."

The point is regardless of your actual blood pressure, be it high, low, or normal, the key is whether the compensatory system described above fails. LOW BLOOD PRESSURE PER SE DOES NOT CAUSE CFS.

The University team used a specialized tilt table in testing the patients. Generally these types of tables are available at major medical centers and it is the cardiologists who are familiar with the testing technique. However, Dr. Rowe, from John Hopkins University, believes for the time being it will be an uproad battle convincing your cardiologist to give you the test unless he or she is a true believer that CFS is a real disease.


Area: alt.med.fibromyalgia
Date: 03-11-95
From: Nyeda@uwec.edu
To: All
Subj: Re: Is low blood pressure a cause or result of CFS?


Ann LeBlanc writes:

Can the results be interpreted to mean that low blood pressure causes or accommodates CFS (and maybe FM)? Is the cure as simple as raising our blood pressures? (And, if so, why didn't my FM lessen during the brief period about 1.5 yrs ago when my blood pressure was way up, at about 110/75? My normal readings are about 90/60 or 95/70.)

FWIW, until about 10 years ago my blood pressure was always *very* low and FMS/CFS pain was... how does one measure it? Minimal I guess. Last 10 years it has been high for me, normal for most folks, and I've increasingly gotten worse.

I think it is *very* unlikely that low BP causes either CFS or FMS. I have had plenty of patients whose BP was higher when they were doing worse. In fact, I'd say this is the rule rather than the exception.

A new theory is worth considering only if it explains the available data better than any other theory. Moldofsky's sleep-cytokine theory (see the FAQ) remains the one to beat. It neatly explains all of the major features of FMS, including the symptom complex and relationship to sleep and exercise. It is the only theory for which a human model exists -- selective stage 4 sleep deprivation in normal volunteers for 5 days induces temporary FMS complete with tender points.

All the alternatives have significant problems. St. Amand's theory about calcium deposits for example is not supported by the finding of such deposits in biopsies of tender points, fails to account for the relationship of FMS to sleep and exercise or explain any of the other associated symptoms other than pain, and is not yet supported by any studies showing that guaifenesin actually works. Even if guaifenesen is shown to work, the offered explanation seems less likely than that it simply treats nasal congestion which may disrupt sleep or has some as yet undiscovered effect on cytokines.

The idea that FMS is a muscle disorder is seriously weakened by the observation that some tender points are not over muscles (the one over the medial joint line of the knee) and the more recent finding that changes in ATP levels and other metabolic findings in muscles of patients with FMS can be caused simply by disuse. The idea that FMS and CFS are caused by some as yet unidentified infectious agent remains plausible and not inconsistent with Moldofsky's theory but so far there are no good candidates, and an infectious etiology doesn't very well explain how these disorders are sometimes triggered by injuries.

David A. Nye MD (nyeda@uwec.edu) * Midelfort Clinic, Eau Claire, WI


Area: alt.med.cfs
Date: 03-19-95
From: Marjorie_J_Panditji@ccm.jf.intel.com
To: All
Subj: MED: Another tilt-table test experience


Now that the first John Hopkins research paper has been published, I've been told it is okay to share my personal experiences about the tilt-table test. Some of you have gotten private email from me, but I have been waiting for permission before sharing with the whole CFS list.

Standard disclaimer: I am not a doctor. These are just my personal experiences. I have not fully digested the research so please forgive me for any inaccuracies. I've posted a separate message on how to get reprints of the Lancet article.

Since this mail is so long, I'll give you an executive summary here! :-) I took the tilt table test on Jan 10. I tested positive for neurally mediated hypotension, also known as vasodepressor syncope. I have been undergoing treatment for 2 months and I have had very positive results.

I want to mention that you do *not* have to have low blood pressure to have this condition. Your resting blood pressure can be high or low. The issue is whether your blood pressure *drops* in response to the adrenaline released when you stand for more than a couple minutes. There is a miscommunication between your brain and your heart. Also, the standard test for orthostatic hypotension (comparing you blood pressure and heart rate while lying, sitting, and standing) will not catch this problem. Earlier I sent some private email suggesting this test, but the interview in CFS-NEWS issue #45 shows that I was incorrect.

First, some background: My symptoms started with lightheadedness in Jan. 1990. It progressed to extreme fatigue, rapid heartbeat, shortness of breath, and heat intolerance. In 1990-1991, I had a complete remission for about 8-10 months. In the summer of 1991, the initial symptoms came back (with increased intensity), along with new symptoms of muscle pain, muscle twitching, migraines, tingling/numbness, night sweats, and more. Since my lowest point of fall/winter 1991, I've been functional but never close to my pre-illness normal.

I have never been formally diagnosed with CFS. I have had several doctors mention it as a possibility, but I never quite fit the CDC criteria. I never had low grade fevers. I rarely had swollen glands and sore throats. I never thought I had brain fog. I had trouble thinking while I was standing up, but I thought that was just because I was tired while standing. I now know that this was because standing triggered this response.

I ran the gamut of doctors and tests, as have many others in this group. I never came up with an effective treatment. I did eventually improve, but I was never able to say what actually helped or if I just got better spontaneously. Still, even during periods when I was "better" I was prone to random up and down days that were impossible to predict.

Late last year, a friend from high school told me about a research study at John Hopkins. She urged me to fill in the form and try to get in the study. After I did, one of the doctors was kind enough to call me at home. He said that based upon my answers to the questionnaire I really should have this test done. I must say that I was pleasantly surprised with his caring enough to call me at home. I live in Oregon, so I decided to try to find a doctor here who would do the test rather than fly to Baltimore, Maryland.

I talked with several local doctors about having the tilt table test done. Some of you may remember one doctor I visited in November (who shall remain nameless) who told me to forget about all this and just come in for a checkup once a year. This doctor said something like, "They will probably never find what you have, and even if they do find it, they probably won't be able to treat it." I vented on this list (Acceptance vs. giving up) and persevered in spite of this opinion. After my neurologist and primary care physician both agreed that the test was worth taking, I finally got a referral.

On Jan. 10th, 1995, five years after I went to a doctor with my initial symptoms, I tested positive on this tilt table test. Believe me, folks, if you test positive, you *know* it! I have never passed out before. It is pretty unnerving, to say the least. They told me afterwards that I was thrashing around which is probably why I never completely blacked out. I guess it was survival instinct ("No, I don't want my body in that position, thank you!"). I don't remember exactly what I said or did. I was sort of semi-conscious. The weird thing is, if you have never passed out, you don't know that the really awful feeling you are having is the same feeling you get before you pass out. Now, I know. [ both :-) and :-( ]

Since this is already so long, I'll post another message describing the tilt table test in more detail.

The doctor prescribed Florinef (fludrocorticone acetate). This drug helps your body to retain sodium in the kidneys. This is commonly prescribed for people with Addison's disease. We have been working on adjusting the dosage. I started at 1/2 tablet and have worked up to a full tablet per day. Other drugs commonly prescribed are beta blockers, which block the response to adrenaline. I have not yet tried any of these.

I also drink more water and eat more salt. I loved Sarah's image of unscrewing the salt shaker and pouring it over her food! As a vegetarian, I wasn't getting my daily sodium via Big Macs and french fries. :-) I was way below the average in sodium intake. None of the stuff I commonly eat has any salt! My resting blood pressure is low. Even with the treatment it is still on the low side. If your resting blood pressure is high and you also have this condition, you might not want to add salt to your diet.

So, how am I doing? Since I have started this treatment, I have not missed a single work day, nor have I had to call in late. Before, even though I only worked 25 hours a week, I used to take about 1-2 sick days a month. I also would take a couple mornings off and try to make up the hours later. Now, I am so predictable. I can make an appointment and be fairly sure I'll be feeling well enough to keep it. I even worked 40 hours one week (I took extra time off the following week) when we had a schedule crunch. It is nice to have more predictability in my life.

My friend who was in the research study is also feeling better. Her biggest problem was brain fog, not fatigue (just the opposite of me!). She is now attending college which was previously unthinkable. I should mention that she (and others) had quite a time finding the right dosage. She is cautiously optimistic, but waiting for a little more time to pass before relying on this treatment.

I still have a few symptoms. For example, after carrying grocery bags into the house, I get chest pains and lightheaded. I am going to investigate adding a beta blocker (to block the adrenaline response) to see whether that will help with the remaining symptoms.

I don't know how many people who have CFS will be helped by this research. For me it is at least part of the answer.


Area: Fidonet Chronic Fatigue Syndrome Echo
Date: 09-29-95
From: Deborah Shearer
Subj: Cfs Treatable....?


Crosspost:
Date: Tue, 26 Sep 1995
From: Roger Burns
Subject: WIRE: CFS is Potentially Treatable Say Hopkins Researchers

** CFS Newswire **

SOURCE: Johns Hopkins Children's Center, Office of Public Affairs
SUBJECT: CFS is Potentially Treatable Say Hopkins Researchers
AUTHOR: Press release text: Michele Fizzano, Office of Public Affairs
Introductory note: Roger Burns
COPYRIGHT: None


[INTRODUCTORY NOTE: The research described below is an extension of previous work published in the Lancet last March. What is new here is that (1) the current study focuses solely on CFS patients (the Lancet research studied seven fatigued adolescents, only four of whom had CFS), (2) the number of CFS patients in this study is 23, and (3) this major research from Johns Hopkins is being published in JAMA, which means that the average American M.D. will be reading positive, legitimizing news about CFS research for the first time in many years, since most MDs do not read the specialty journals where CFS research usually appears. -- Roger Burns, publisher of CFS-NEWS Electronic Newsletter.]


CFS is Potentially Treatable Say Hopkins Researchers

Patient Request Line: 410-821-7253

Embargoed until 4 p.m. EDT
Tuesday, September 26, 1995

Results of a new Johns Hopkins study show that chronic fatigue syndrome is strongly linked to a common and potentially treatable abnormality of blood pressure regulation.

The findings, reported in the Sept. 27 issue of The Journal of the American Medical Association link CFS with a blood pressure regulation disorder called neurally mediated hypotension and advance earlier work that drew similar conclusions among fatigued adolescents. Both studies found that symptoms such as exhaustion, exercise intolerance, muddled thinking, and dizziness cleared after neurally mediated hypotension was diagnosed and treated.

"This study is the first to demonstrate that the symptoms of CFS can be improved with treatment directed at neurally mediated hypotension," says Hugh Calkins, M.D., associate professor of medicine and electrophysiology. "Further research will help us define the basis of a link and a randomized, placebo-controlled study is still needed to confirm the favorable response to therapy that we observed."

In the Hopkins study, 22 of 23 patients (18 women, five men, median age 34 years) with CFS tested positive for neurally mediated hypotension. After treatment, nine patients reported full recovery from fatigue and seven others noted some improvement, say researchers.

Neurally mediated hypotension cannot be detected during a routine blood pressure or heart rate screening. Tilt testing, available in most hospitals and academic centers throughout the United States, is the only means of positive diagnosis.

Each patient in the Hopkins study underwent all or part of a head-up, three-stage tilt table test. The tilt table rests at a 7--degree angle to simulate standing for long periods -- a common trigger of neurally mediated hypotension (NMH). Heart rate and blood pressure were monitored throughout the test.

Of the 22 patients diagnosed with NMH, all experienced lightheadedness, nausea or fainting and a 25 mmHG decrease in systolic blood pressure without an associated increase in heart rate. All became tired and lethargic and remained so for several days after the test, suggesting that fatigue can become chronic if neurally mediated hypotension occurs frequently, says Calkins.

Sixteen of the 22 CFS patients who tested positive did so at the first stage of the tilt test, unlike four of 14 controls (10 women, 4 men, median age 36 years) who tested positive, at a much later point after a drug was administered to simulate high adrenaline levels. "The difference is that those with CFS generally had a drop in blood pressure more quickly and without artificial stimulation," explains Peter Rowe, M.D., the pediatrician who first made the link between the two disorders.

Patients with neurally mediated hypotension were treated with drugs commonly used to regulate blood pressure. While some of the drugs work by allowing the kidneys to retain more sodium, others block the body's response to adrenaline, a kick-starter of the blood pressure abnormality.

More than half of the patients experienced some improvement over time, but the researchers say that compliance with these drug therapies proved challenging.

"It takes a great deal of persistence from the patient and physician to find the right combination for each individual," says Rowe. Careful monitoring by a physician is required because the drugs pose a risk of serious side effects such as excessive elevation in blood pressure or depression. In addition, patients often need to change therapies three or four times over several months before noticing an improvement, he says.

Part of therapy also includes increased salt intake combined with increased fluid intake, but diet changes alone may not be effective for treating patients with CFS or neurally mediated hypotension, warn researchers. "We believe salt plays an important role in blood pressure regulation, but it appears to be most effective when used in conjunction with drug therapies," says pediatric cardiologist Issam Bou-Holaigah, M.D., lead author of the study.

Neurocardiogenic syncope, neurally mediated syncope, vasodepressor syncope, vasovagal syncope and neurally mediated hypotension are different names for the same disorder. The condition commonly occurs when the autonomic nervous system, which controls heart rate and blood pressure response, misinterprets what the body needs during periods of upright posture and sends a message to the heart to slow down and lower blood pressure. This is the opposite of what the body needs at such times, says Jean Kan, M.D., Helen B. Taussig Professor and director of the division of pediatric cardiology. Neurally mediated hypotension occurs typically after exercise, long periods of standing or exposure to warm environments. If the heart rate slows down at these times -- when heart rate and blood pressure should be increasing -- lightheadedness, fainting and headaches are common results.

In contrast to all that is known about neurally mediated hypotension, CFS remains poorly understood. It is estimated that nearly 25 percent of the population will develop prolonged fatigue at some point in their lives. Chronic fatigue syndrome is a related but less common and more severe condition with worldwide prevalence of up to three per 1,000 people. It is defined as a profound fatigue lasting at least six months, often beginning abruptly after an apparent viral infection, and not explained by known medical or psychiatric disorders. The fatigue often worsens after physical exertion and other symptoms include lightheadedness and blurry concentration (see attached definition from the CDC). Many medical professionals used to dismiss CFS as primarily psychiatric, but these results suggest that NMH may be the physical underpinning for symptoms in a large portion of patients, says Calkins.

Bou-Holaigah was partially funded by the Saudi Arabian Oil Co. (Saudi ARAMCO).


CFS/NMH REQUEST LINE

The Johns Hopkins Medical Institutions are pleased to assist those seeking more information about chronic fatigue syndrome and neurally mediated hypotension. Please help us help them by publishing the following telephone number - 410-821-7253. Callers can also request a copy of this press release, the JAMA article or an information sheet about an upcoming randomized-controlled trial in the Baltimore/Washington region.


Johns Hopkins Medical Institutions' news releases can be accessed on-line through the following services:

World Wide Web at http://infonet.welch.jhu.edu/news/news_releases

CompuServe in the SciNews-MedNews library of the Journalism Forum under file extension "JHM"; also in NASW Online in the same forum.

JHM1 toll-free Health Newsfeed BBS at 1-800-JHH-0046.

Quadnet: send e-mail to: scitech@quadnet.vyne.com. In the body of the body of the message type "info Quadnet".

To enroll in our direct e-mail news release service, call 410-955-6680.


DEFINITION: CHRONIC FATIGUE SYNDROME

As reported from the Centers for Disease Control and Prevention, The National Institutes of Health, and the International Chronic Fatigue Syndrome Study Group in the Annals of Internal Medicine, Volume 121, Number 12, December 15, 1994, page 956, "The Chronic Fatigue Syndrome: A Comprehensive Approach to Its Definition and Study."

"A case of chronic fatigue syndrome is defined by the presence of the following: 1) clinically evaluated, unexplained, persistent or relapsing chronic fatigue that is of new or definite onset (has not been lifelong); is not the result of ongoing exertion; is not substantially alleviated by rest; and results in substantial reduction of previous levels of occupational, educational, social or personal activities; and 2) the concurrent occurrence of four or more of the following symptoms, all of which must have persisted or recurred during six or more consecutive months of illness and must have not predated the fatigue; self-reported impairment in short-term memory or concentration severe enough to cause substantial reduction in previous levels of occupational, educational, social or personal activities; sore throat; tender cervical or axillary lymph nodes; muscle pain, multijoint pain without joint swelling or redness; headaches of a new type, pattern, or severity; unrefreshing sleep; and postexertional malaise lasting more than 24 hours."

Web page design by Bill Jackson, 1996.

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