Dr. Bell Finds Dramatic Abnormalities in CFIDS - Part 2 of 2
by Joan S. Livingston
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[Dr. David S.] Bell and [Dr. David H.] Streeten obtained their most recent, detailed findings about ANS [autonomic nervous system] dysfunction through "a very simple test, one that can be performed anywhere, using only a blood-pressure cuff." The patient lies down quietly for 10 minutes while a nurse takes his or her pulse and blood pressure (BP) several times; then the patient is asked to stand quietly for 30 minutes while the same measurements are taken.
Bell pointed out that when a normal person stands up, the pulse may or may not rise slightly at first; the blood pressure usually remains stable (a graph of the systolic and diastolic numbers is notable for its constancy-a "band" that stays the same size); and the pulse pressure remains constant.
Despite the fact that their pulses and BPs were "pretty normal" while lying down, study participants consistently displayed orthostatic irregularities-last-ditch efforts to force blood to the brain-which were categorized into five basic patterns or subgroups. Many patients, however, actually had more than one of the following abnormalities:
A fall in systolic (upper) BP of 20 mmHg (millimeters of mercury) or more.
A fall in diastolic (lower) BP of 10 mmHg or more. Dr. Bell notes, "This seems to be the least common abnormality in the CFS [Chronic Fatigue Syndrome] patients I have tested. The body will put out adrenaline and other chemicals as a result of decreased blood circulation, which narrows the blood vessels further."
A rise in diastolic BP to 98 mmHg or more. Explains Bell, "The lower number of the BP often reflects systemic resistance, and while standing many CFS patients seem to 'raise' this lower number up in an attempt to push blood to the brain."
An increase in heart rate of 28 beats per minute (bpm) OR a pulse of more than 110-120 bpm. Also known as POTS for postural orthostatic tachycardia syndrome, this was a very common finding even among patients with other severe deviations.
A fall in pulse pressure-the difference between systolic and diastolic-to 18 mmHg or lower (vs. the 40-point difference in a "normal" BP of 120/80, for example). Dr. Bell explains, "Usually, when the pulse pressure falls much below 20, you can't even read the person's pulse. When it falls this low, the patient is in a state of circulatory shock."
In the most recent edition of his publication, The Lyndonville News, Bell wrote briefly about a woman with systolic hypotension: "One patient had a normal BP lying down (100/60) but it fell to 60/0 on standing. No wonder she was unable to remain upright-a blood pressure that low is really unable to circulate blood. In any ICU [intensive care unit] they would panic seeing a blood pressure like that. And yet she was turned down for disability because she was considered a hypochondriac." Her case was not unusual in Bell's study or in his clinical practice.
Among the chemicals released by the ANS are cortisol, dopamine, epinephrine (adrenaline), and norepinephrine (very similar to epinephrine but with somewhat less effect on the heart). Dr. Bell suggested that most of these chemicals are probably involved in CFIDS [Chronic Fatigue and Immune Dysfunction Syndrome] -especially when released inappropriately, causing further vasoconstriction in those furnace pipes. He cited a recent article regarding norepinephrine (released by the adrenal gland), which noted a relationship between orthostatic intolerance and "norepinephrine transport." Bell suggested that "a physiological mishandling of norepinephrine" may play a role in CFIDS.
Monitoring "hyperadrenergic" (norepinephrine-related) orthostatic problems, Bell predicted, is likely to prove a helpful measure in the future. "Norepinephrine is the best method the body has for getting blood to the brain, to get that mental clarity of the fight-or-flight response," he noted. "But in CFS it seems to get kicked in inappropriately. Half the patients I've tested have an abnormality on testing. I think we'll soon see testing of such things as plasma norepinephrine when patients are experiencing orthostatic symptoms.
"[Norepinephrine is] good for getting blood to the brain but it's counterproductive in CFIDS-it probably causes further vasoconstriction, it raises pulse, it causes panicky symptoms and makes you feel tremulous, it causes exhaustion and forgetfulness, and it can cause poor sleep later." Many CFIDS patients can relate to that frazzled, revving-on-empty feeling.
While Bell and Streeten have yielded further insights into the body's different responses to low circulating blood volume, there are no answers yet about how best to treat the five subgroups they identified. Perhaps one group will turn out to comprise the "Florinef responders"; in the past Bell has seemed bedeviled by the fact that the drug has worked so well for some PWCs but not others (relatively few of his own patients have shown improvement on it).
While there is still nothing as simple as a swab strep-throat culture for diagnosing CFIDS, the subgrouping may be a step in that direction, as well as toward determining the optimum treatment for each subgroup. "The reason I'm excited about this [most recent study] is that it provides a method to subgroup patients and perhaps to find the different mechanisms behind each abnormality," Bell said. With these mechanisms more fully understood, advances in therapies should follow.
Previous - Part 1
Copyright © 2000, Joan S. Livingston
Posted with permission from the author.
This article was originally posted at chronicfatigue.about.com in July 2000.
Note: Dr. David H. Streeten died September of 2000. His research and understanding of Orthostatic Intolerance (OI) will always be greatly appreciated.
Information in brackets has been added.
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