The Lyndonville Journal:

The Relationship Between Neurally Mediated Hypotension and CFS

David S. Bell, MD, FAAP

Published in Lyndonville News, July 1999

In my opinion, the paper by Bou-Holaigh, Peter Rowe and Hugh Calkins in 1994 was the biggest leap forward for CFS in many years. In this paper they connect CFS with neurally mediated hypotension (NMH) and suggest florinef™ as a treatment. A question submitted by a patient and friend asked: what specifically is the relationship?

CFS is not NMH, but NMH is certainly a part of CFS. NMH means that through neurally mediated pathways, hypotension (a drop in blood pressure) will occur. Now, in its simple form, this constitutes a simple faint. A young lady, standing in choir practice faints because of a drop in the blood pressure and subsequently blood flow to the brain. A soldier, standing at attention on a hot summer day will faint. Perfectly healthy persons, otherwise, and both have NMH. The difference between NMH and CFS is that in NMH a person will have a drop in blood pressure at certain times but will feel just fine all the rest of the time. CFS patients will get dizzy, lightheaded and have orthostatic intolerance, but will feel rotten all the time. This is the central unanswered question between the two.

There is no doubt that orthostatic intolerance is a central part of CFS, and the inability to maintain an upright position (orthostatic intolerance) is the fatigue experienced by those CFS persons. In our office we routinely do orthostatic testing by standing a patient next to the wall, monitor pulse and blood pressure, a sort of "poor-man's tilt table test". Then we stand back and watch them get very sick and keel over in a faint. Interestingly, normal young persons will stand for fifteen minutes, feel OK then become clammy, dizzy and faint. Persons with CFS go through stages of agony. First is increased fatigue, yawning, getting wobbly, then headaches and pain worsen, and then faint. The pulse pressure (the difference between the upper and lower numbers of the blood pressure) is different in CFS than in healthy fainters, I think. It is an area we are currently exploring.

The orthostatic intolerance is probably due to inadequate blood flow to the brain while in the upright position. I suspect that it is a continuous process rather than an "event" as is the typical NMH. In CFS the decreased blood flow is due to some regulatory mechanism that gets stuck on a "low-flow" setting. Why is unknown.

The florinef™ treatment suggested in the 1994 paper will expand circulating blood volume and is helpful is some patients. In a future article I will detail how many it has helped in my practice, who it works for and who it doesn't. Tales for another day.

As many of you may have guessed, it is not pleasant for CFS patients to undergo tilt table testing or our poor man's version. Recovery from the test is helped by an infusion of normal saline after the test. I am not sure whether it is important in the diagnosis, but abnormalities have been found in all 12 of the most recent orthostatic tests we have performed. There are five categories of abnormalities:

1. Orthostatic systolic hypotension: fall in systolic blood pressure of 20 mm Hg or more.
2. Orthostatic diastolic hypotension: fall in diastolic BP of 10 mm Hg or more.
3. Orthostatic diastolic hypertension: rise in diastolic BP to 98 mm Hg or higher.
4. Orthostatic narrowing of pulse pressure: fall in pulse pressure to 18 mm Hg or lower.
5. Orthostatic postural tachycardia: increase in heart rate of 28 bpm or to greater than 110 b/min.

Normal responses of pulse and blood pressure to prolonged standing are as follows:

1. Normal systolic BP: recumbent: 100-142; Standing (4 min): 94-141; Orthostatic change: -19 to +11
2. Normal diastolic BP: recumbent: 55-90; Standing : 61-97; Orthostatic change: -9 to +22
3. Normal Pulse: recumbent: 54-96; Standing : 62-108; Orthostatic change: -6 to +27.

Reference: Streeten DHP. Orthostatic disorders of the circulation. New York: Plenum, 1987:116.

The most common abnormalities we are seeing are postural orthostatic tachycardia, orthostatic narrowing of pulse pressure, and orthostatic systolic hypotension. What we would like to do is to see the pattern of abnormalities on orthostatic testing and try to determine if they represent subgroups of CFS and specifically if they respond to different medications. Hopefully more on that in a few months.

The relationship between NMH and CFS is like the relationship between migraine and CFS. It is there, actually most of the time. But by itself does not fully explain the manifestations of the illness. It is a little piece of the clinical expression of the illness, but an important one, and may turn out to be the most important one. The reason I feel it is so important is that when florinef™ works, it reduces all the symptoms, not just lightheadedness or near fainting episodes. Therefore there must be a fundamental mechanism within NMH that is important to CFS.

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