CND - Further Organic Abnormalities in CFIDS PDF

9/8/2017 CND: Further Organic Abnormalities in CFIDS
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Further Organic Abnormalities in CFIDS
Tests of orthostatic intolerance shed light on cause and severity of symptoms
Joan S. Livingston, The Update, Mass. CFIDS Association, Summer 2000, 13(2)
When Dr. David S. Bell last addressed members of the Mass. CFIDS Association, he
reported on a fairly astonishing finding: his discovery, along with Syracuse
endocrinologist Dr. David Streeten, that a majority of Bell's chronic fatigue syndrome
patients had "extraordinarily" low circulating blood volume (a combination of plasma and
the red blood cells via which the plasma delivers oxygen throughout the body). While his
average patients ran about 70 percent of normal, several PWCs had only half the blood
volume of a healthy person, an amount so low that it would ordinarily cause shock and
prove fatal in a car accident. (See Winter 199798 Update for details on that study.)
From pain to brain fog

Bell hypothesized at that time that the low blood volume could help account for the
prevalence of "orthostatic intolerance" worsened symptoms, from pain to "brain fog"
among PWCs, because the limited amount of blood would tend to pool in the legs and
feet, that common feeling of unbearable gravity and of wearing lead boots, with a
corresponding drop in the amount of blood available to the brain. Other researchers'
work has added to the evidence that this is a core problem in CFIDS, including reduced
cerebral blood flow on SPECT scans, while some, like the Johns Hopkins group, have
demonstrated neurally mediated hypotension on tilttable testing (changes in posture).
Dr. Bell's Definition of "Fatigue"

Bell defines CFIDS symptoms as falling into four major clusters: socalled fatigue;
neurological problems (balance, cognition, paresthesias, etc.); pain ("which can be
anywherea lot of patients have skin pain, for example, and their doctor already thinks
they're a fruitcake, so it's one of those symptoms the patient won't even mention to the
doctor"); and multiple sensitivities.
In a disease whose formal name is (still) chronic fatigue syndrome, it's thought
provoking that Bell disdains the word "fatigue" as a "very inappropriate term for what
patients experience. It's not really fatigue at all, which is defined as a normal recovery
state from exertion, and that is precisely what does NOT happen in this illness. It's the
limiting of activity that defines this illness. Anybody who works a 20hour day will be
fatigued, but they'll recover from itit's not the same thing. A typical CFS patient might
function on a minimal level (housework, minor errands) for a total of 3 or 4 hours a day.
They may say they're fatigued, but what's really restricting their activity may be pain, like
headache, tremulousness, or weaknessa sense that they are on the verge of collapse.
That is not "fatigue" as we commonly think of it."
When the renowned Lyndonville, NY, clinician and researcher returned to the Boston
area this May, he had further research results to disclose regarding the implications of
low circulating blood volume (but no answers yetsorryon how to fix the problems
identified). Streeten and he had conducted tests of orthostatic intolerance (hypotension,
tachycardia, and other inappropriate physiological responses to standing) in 20 of Bell's
patients, simply by tracking their blood pressure and pulse while lying and then
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standing. Like the test in which they measured blood volume, the protocol for this one
was simple, requiring no special equipment like tilt tables (except time: at 40 minutes
per patient, you may have trouble selling your doctor especially HMOs on doing this
test. But, since it may document a disabling condition for Social Security, it's worth
fighting for.)
Who You Calling a Wimp?

Bell and other clinicians, including Dr. Nancy Klimas, have long commented on their
patients' (reported and observed) intolerance to being in an upright position, while they
may feel "pretty good" while lying down. "When they get up," Bell said, "suddenly they
have a lot of symptoms, so I suspected that what we call "fatigue" in chronic fatigue
syndrome is really orthostatic intolerance. A patient might lie down for three hours and
feel pretty okay, then get up for just 10 or 15 minutes before they're forced to lie down
again to restore some blood flow to the brain."
Considering their blood volume and orthostatic intolerance, Bell's patients would be
expected to have trouble during the 30minute standing portion of his most recent
testing. ["Fortunately, the nurse in our office, Paula, is very good about predicting when
someone's about to go downand obviously it's better to terminate the test than have
patients hit the floor."] In addition, Bell stated, patients with CFIDS are widely assumed
"to be 'wimps' they're lazy, they're malingerers, right? But they'd say, 'I will push myself
through this test, I can do it.' They might be swaying in absolute agony, but they'd finish.
The normal controls, by contrast, were the wimps! After 20 minutes or so they'd say, 'I'm
exhausted. Can you bring me a chair?'" Bell noted that his patients were presumably so
used to "pushing to get something done that they often pushed themselves close to the
point of passing out", that the sensations they experienced during the test were nothing
new to them.
Hard Data

Consistent with Bell's longheld assumptions, virtually all of his patients (18 or 19 of 20)
showed abnormalities when standing, hard data that could be helpful in diagnosis, that
generally correlated with disease severity, and that could prove a powerful new tool in
fighting for disability benefits. Quantifiable and reproducible, not subjective, not "of
exclusion".
The new findings are particularly meaningful in bucking conventional notions of CFIDS
as a disease of selfreported, possibly overstated symptoms. And no one, physician or
Social Security judge, can reasonably provide an "AIYH" (all in your head) explanation
to a patient with some of the specific physiological abnormalities itemized below, like a
"pulse pressure" so low that no doctor can even read your pulse or dub as "within
normal limits" a standing blood pressure so low it indicates circulatory shock.
Physical Anomalies

As an introduction to his most recent findings, Bell shared his observations about the
wealth of already existing data on physical anomalies in CFIDS for those clinicians who
have been willing to <look> and do more than a rote physical exam and standard blood
test. "The abnormalities in this illness are numerous and striking," Dr. Bell observed.
Even before the last few years' research began pinpointing increasingly more
aberrations in virtually every body system, he says, "I was always quite annoyed when
doctors would say you can't find anything wrong on laboratory evaluations or physical
exam. <It's just not true.> Among other things, findings are very, very interesting."
Findings include increased CD8+ activated Tcells (generally a sigh of active viral
infection), low natural killer cell (NKC) function, and elevated circulating immune
complexes. Unfortunately, few doctors other than researchers are inclined to order up
such esoterica as immune system tests even when faced with a patient whose
symptoms are as severe as those found in CFIDS.
"It's always been said that this is an illness of exclusion, that everything must be ruled
out before the diagnosis of chronic fatigue syndrome can be made," Bell noted. "<That>
is not true. The pattern of symptoms is unique: <there is no other illness in general
medical practice that looks like this one.>" At first, he observed, the fluctuating
symptoms may be baffling to the patient and doctor alike: "Not only do they fluctuate
over the course of a single day, but also over the longer term. One week your sore
throat is so bad you're about to have your tonsils out, then the next week your worst
symptom is irritable bowel and you're off to see the gastroenterologist. It's only over a
period of time that the characteristic pattern emerges and the diagnosis becomes
evident."
Sleep dysfunction

Another nearuniversal symptom is sleep dysfunction. "Sleeplab studies in fibromyalgia
and chronic fatigue syndrome show an amazing array if abnormal findings. Virtually
everyone with these conditions has significant deviations from normal stages although
different laboratories interpret the sleep data differently. I had one patient who didn't
sleep for three days, and the lab report came back reading 'NORMAL STUDY; patient
did not sleep for three days."
Another notable irregularity to test for is "brain fog," though that can be problematic
(because most doctors don't have pre and postillness IQ scores to compare): "If you
give patients a basic cognitive test, they usually do pretty well," Dr. Bell said. "More
sophisticated tests will identify the cognitive problems specific to this illness. But on a
simpler level, you can also give one cognitive test while the patient is lying down
[enjoying maximum blood flow to the brain], and one while the patient is standing. The
difference between the two scores is often extraordinary.
"When doctors say that the physical exam is normal, that's also inaccurate," Bell
continued. "Virtually all patients will have abnormalities on physical exam [such as
lymphnode tenderness or swelling, flushing rash, abdominal pain, etc.], but on average
the patient will look pretty healthy. What the doctor is thinking is that the physical exam
is not abnormal enough to explain why someone says they can be up only two hours a
day. The degree of reported activity restriction is so dramatic physicians frequently just
don't believe it's possible."
But an understanding of low blood volume and severe orthostatic intolerance makes the
degree of activity restriction more than "possible": it makes it hard to believe patients
function as well as they do, because, as the data now suggest, many PWCs may
function in a continuous state of hypotension, tachycardia, and/or other posturerelated
abnormalities.
The Five Basic Working Theories

Dr Bell noted that five basic theories of the illness have been set forth over time and
remain current subjects of research:
Persistent infection (by a single agent)

"This theory is beginning to slip because it's just not felt by most researchers to be the
most promising candidate; the problem is that we haven't found a single agent in this
illness but in fact many pathogens." Just the same, the search is still on, as the recent
interest in HHV6 demonstrates.
Agentinduced immune dysregulation (i.e., a pathogen creates an initial infection that
causes the immune system to malfunction even after the infection may have cleared);
"This has been the best candidate over the past five years because the disease so often
begins with a sudden onset, theoretically leading to an upregulation of the immune
system and other longterm immune abnormalities."
Primary sleep disorder

While common in CFIDS, it doesn't account for enough of the symptomatology.
Mitochondrial abnormality

Like sleep disorders, this is probably also just one piece of the puzzle, despite ongoing
research in this area.
Autonomic nervous system injury or dysfunction (e.g., orthostatic hypotension)
Consisting of the parasympathetic and sympathetic nervous systems, the autonomic
nervous system (ANS) is responsible for controlling dozens of functions, such as the
functioning of the adrenals and other glands, and involuntary bodily functions like
breathing, pulse, and blood pressure. The ANS is the reason you keep breathing while
asleep and your heart keeps pumping, as well as why your system goes into overdrive
and why you sweat more when you're nervous.
The ANS is the root of orthostatic problems, and the inappropriate release of many
chemicals; its dysfunction may explain a range of CFIDS symptoms. (For a full
description of the parasympathetic and sympathetic nervous systems, see a good
medical dictionary, like Taber's.)
Feigning irritation with this kaleidoscope of changing theories, Bell said, "As a clinician,
you don't usually have to read much to keep up with what's going on." (His was a
pediatric practice in a rural community before a CFIDS cluster epidemic struck young
and old there in the 1980s.) "Sore throats haven't changed in 20 years. You give baby
shots, that kind of thing."
With the Lyndonville outbreak, he suddenly had more on his mind than baby shots.
"With the first two theories, I had to lean about all the intricacies of the immune system,
about cytokines, about natural killer cells, the workings of one pathogen after the next.
As soon as I had the immune system pretty well mastered, no one seemed to be talking
about it anymore; people were talking about mitochondrial function [energy production
at the cellular level]. So I read up on all that, and now we're not talking about
mitochondria much anymore.
"Most recently the emphasis has been on the autonomic nervous system, which
absolutely <nobody> understands." In this Bell is being a little disingenuous, as he has
been one of the pioneers in researching the role of ANS dysfunction in this illness.
A Word About Depression

"There is one piece of good news in this list of five theories, and that's the fact that you
don't see psychiatric disease there. That theory has largely fallen out of favor.
Psychiatric illness is serious and devastating, but there'' very effective treatment for it;
by contrast, there is still no good treatment for chronic fatigue syndrome.
"Having said that, I want to emphasize that, at some point in their disease, many CFIDS
patients <will> become depressed. At least 60 percent of my patients have had periods
of severe depression. This can take the form of despair that is truly lifethreatening, and
there may come a time for any individual patient when there is a role for counseling in
their lives. I would hope everyone would be open to this when feelings of despair
become overwhelming, and recognize that seeking help does not mean their disease is
primarily psychological, but instead that counseling can play a valuable role in coping
with any chronic physical illness."
Decrease In Circulating Blood Volume

Eighty percent, or the vast majority, of the patients in Bell and Streeten's first study (of
19 patients, versus the 20 in the more recent study), had a "marked, striking" decrease
in circulating blood volume. "One nice thing about that finding," Bell said wryly, "is that it
is a discrete physiological abnormality that cannot possibly be explained as
psychosomatic."
How severe were the abnormalities? As mentioned before, the average was 70 percent
of normal blood volume; still, "we have six people with only 50 percent of normal blood
volume and yet they are still walking around. It seems to be a different mechanism than
what happens to a healthy person [who loses that much blood] in a car accident."
In fact, the blood vessels in CFIDS seem to be constricted dramatically, and yet
attempts to restore normal blood volume (through use of Florinef, salt, saline injections,
transfusions) have met with only limited success so far. "All of the body's normal
mechanisms to restore blood [when it is lost in other ways] seem to be turned off." It is
as if the CFIDS body <wants> to have low blood volume and that its blood vessels want
to stay constricted. Bell likens the blood vessels to water pipes that are only half the
proper diameter you simply cannot make a metal pipe hold any more fluid than the
pipe is built to carry.
"When you tell people about these findings, their immediate question is, 'What
happened to the blood? Where did it go?' The answer is we don't know. It's not like the
patients bled out or are dehydrated although they do experience a lot of thirst." Turning
to the audience, Dr. Bell noted that his patients carry "buckets of fluid" with them at all
times an observation made by other clinicians. "How many people here also have
excessive thirst? Whoa look at all those hands!" It's as though some rudimentary alert
system is crying out for more fluid, but because of the vasoconstriction, it just gets
flushed away.
Straight Off The Presses: The Latest Findings

Bell and Streeten obtained their most recent and detailed findings about ANS
dysfunction in Bell's patients through a "very simple test, one that can be performed
anywhere, using only a blood pressure cuff" much like the 'poor man's tilttable test'
but I would argue it is more accurate because it reproduces exactly what happens to a
patient waiting in the checkout line at the supermarket."
The patient lies down quietly for 10 minutes while a nurse takes his or her pulse and
blood pressure (BP) several times. The patient is then asked to stand quietly for 30
minutes while the same measurements are taken.
The following <objective> abnormalities and the number of patients who actually
passed out while standing are compelling evidence for a disability case, Bell noted.
"Bank tellers will stand on their feet for 8 hours a day without much discomfort, and this
test will show definitively why a CFS patient may not be able to do that for 30 minutes.
You can hand this data to a disability judge and say, "Obviously, this person can't work
as a bank teller."
The Context

To put the study's findings in context, here is a quick review of the normal pulse and
blood pressure, drawn from Dr. Streeten's book on orthstatic hypotension.
Normal Systolic Blood Pressure (sBP; the higher number in a blood pressure
measurement):

Recumbent: 100142

Standing (after 4 minutes): 94141

Orthostatic change, if any: 19 to +11
Normal Diastolic Blood Pressure (dBP; the lower number in a blood pressure
measurement):
Recumbent: 5590


Normal Pulse Pressure (the difference between the systolic and diastolic pressures):
No known norms

Orthostatic change, if any: Difference narrows to 18 mmHg (millimeters of mercury) or
lower
Normal Pulse

Recumbent: 5496


Bell noted that when a normal person stands up, the pulse may or may not rise slightly;
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
(the difference between the sBP and dBP) remains constant, not surprising since the
systolic and diastolic remain steady.
Findings And Five Subgroups

The normal baselines just outlined proved to be significantly different from the five basic
patterns or subgroups Bell found in his study, despite the fact that his patient's pulses
and BPs were generally "pretty normal" while laying down.
Abnormalities in ANS function documented in virtually all of Bell's patients some of
whom had multiple severe abnormalities were as follows:
1. Orthostatic systolic hypotension:

A fall in the sBP of 20 mmHg or more. As with the other abnormalities, this presumably
reflects a desperate attempt by the body to boost blood circulation to the brain. This
phenomenon, like all five of the abnormalities, is probably most obvious to the laymen
with subgroup 4, Orthostatic postural tachycardia.
2. Orthostatic diastolic hypotension:

A fall in the dBP of 10 mmHg or more. "This seems to be the least common abnormality
in the CFS 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 still further."
3. Orthostatic diastolic hypertension:

A rise in dBP to 98 mmHg or more. "The diastolic 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."
4. Orthostatic postural tachycardia:

An increase in heart rate of 28 beats per minute (bpm) OR a pulse of more than 110120
bpm. "A healthy person's pulse will not change even if they stand up for an hour. You
need a steady pulse to circulate the blood."
5. Orthostatic narrowing of pulse pressure:

A fall in the pulse pressure to 18 mmHg or lower. "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.
Case Study

In his Mass. CFIDS lecture, Dr. Bell presented case examples, with details and
supporting slides, for each of the five abnormalities listed above. In one of the
examples, he presented a patient who actually had several of the five abnormalities,
falling into more than one subgroup, and was one of Bell's patients with only 50 percent
of normal circulating blood volume. Her resting BP was actually a little higher than
normal, at 160/100. As soon as she stood up, however, it dropped to 90/0 (!), before
flattening out at 70/60, the 10point pulse pressure that signifies "it's basically
impossible to read a pulse." Even without her other anomalies, at that pulse pressure
and that BP, she was in a shock state and could no longer remain standing. In the
meanwhile, her resting pulse had jumped from 80 to 120 as her ANS attempted to get
blood to her brain.
Her physiological abnormalities included systolic hypotension (sBP=70), a drop to zero
in her diastolic (dBP=0) immediately upon standing, and a narrowing of her pulse
pressure to 10 (70/60) from her resting BP of 160/100 (pulse pressure=60). With her
rise in pulse to the tachycardia figure of 120, she had a BP too low and a pulse too high
to circulate her blood.
Another Drop To Zero

In the most recent edition of his publication, the Lyndonville News (CFS
DSB@juno.com) Bell wrote briefly about another woman with systolic hypertension.
"One patient I follow had a normal BP while laying down (100/60) but it fell to 60/0 on
standing. No wonder she was unable to stand up a blood pressure that low is really
unable to circulate blood. In any ICU they would panic seeing a patient like that, and yet
she was turned down for disability because she was considered a "hypochondriac."
These two examples are certainly sensational. Of the five slides Dr. Bell showed as
examples of the five disparate patterns he and Streeten identified, he mentioned that
three of his patients whose data he used to illustrate three other disorders also had
tachycardia, so clearly some patients suffered from more than one form of orthostatic
intolerance (OI). Unfortunately, he did not enumerate precisely how many patients fit
into each of the five subgroups or several, or whether the slides he showed were
representative of the whole study sample or were chose because they illustrated the
most severe abnormalities. Nonetheless, this was an initial study and we can probably
expect more results and more details down the line.
Some Chemicals Behind BP, P, And OI: An Area For Future Research
Among the chemicals released by the ANS are cortisol, dopamine, epinephrine
(adrenaline), and norepinephrine (chemically very similar to epinephrine but with
somewhat less direct effect on the heart). Dr. Bell concluded his lecture by noting that
these chemicals probably play a role in CFIDS, especially when released
inappropriately, causing further vasoconstriction in those furnace pipes.
He favorably cited a recent article regarding norepinephrine, released by the adrenal
gland. Many PWCs have long felt that the adrenal gland plays some central role in their
illness, whether from underactvity, from longterm overuse, or from releasing too much
adrenaline, leaving them with that frazzled, running onempty feeling.
In the study Bell cited, researchers performed measurements of norepinephrine on a
twin subjects who have orthostatic intolerance as the result of a rare genetic defect,
both while the subjects were recumbent and while standing. The subjects, who suffered
from symptoms like rapid pulse, difficulty breathing, cognitive difficulties, and fainting
spells, had excessive blood levels of norepinephrine while standingbut their symptoms
were suggestive both of too much norepinephrine and of too little.
"It could be," Bell said, "that a physiological mishandling of norepinephrine
('norepinephrine transport'), for different reasons in CFIDS than in this exceedingly rare
genetic condition, plays a role in both conditions."
Testing for "hyperadrenergic" (norepinephrinerelated) orthostatic problems is likely to
prove a useful tool in the future, Bell predicted. "Norepinephrine is the best method the
body has for getting blood to the brain, to get that mental clarity of the fightorflight
response," he noted. "But in CFIDS 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 norepinephnne when patients are experiencing orthostatic symptoms.
It's good for getting blood to the brain but it's counterproductive in CFIDS as it probably
causes further vasoconstriction and raises the pulse. It causes panicky symptoms and
makes you feel tremulous, it causes exhaustion and forgetfulness, and it can cause
poor sleep later."
Speaking of chemicals, Bell added, in regard to CFIDS pain, that PWCs might suffer
from an inadequate supply of endorphins, the body's natural opiates. "Though there's no
good research on this, there's a fellow in our area who's a superb acupuncturist, and
what he's been doing with my patients has been knocking my socks off," Bell related. "I
think that somehow acupuncture may have a relationship to the autonomic nervous
system and centrally mediated pain."
While Bell and Streeten appear to have provided further insights into many of the body's
different responses to low circulating blood volume, especially blood to the brain, there
are no answers yet about how best to treat the five subgroups (and members of multiple
subgroups) they identified. Perhaps one will turn out to comprise the "Florinef
responders." In the past Bell has seemed bedeviled by the fact that the drug works 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 strepthroat 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, there should be advances in which therapies to use and which really
work over time. And the simple orthostatic testing should provide more reliable data on
treatment and responses than patients' comments on how they feel, since symptoms
remit and relapse over time.
The roles of orthostatic hypotension, orthostatic tachycardia, and subnormal erythrocyte
volume in the pathogenesis of the chronic fatigue syndrome.

Streeten DH; Thomas D; Bell DS, Department of Medicine, State University of New York
Health Science Center, Syracuse 13210, USA.
Am J Med Sci 2000 Jul;320(1):18

CITATION IDS: PMID: 10910366 UI: 20365736
BACKGROUND: Orthostatic hypotension during upright tilt is an important physical
disorder in patients with chronic fatigue syndrome. We have tested its occurrence during
prolonged standing, whether it is correctable, and whether reduced circulating
erythrocyte volume is present.
METHODS: Fifteen patients were randomly selected from a large population of patients
with chronic fatigue syndrome, studied, and observed for several years (by DSB). Blood
pressure (BP) and heart rate (HR) measured with Dinamap every minute for 30 minutes
supine and 60 minutes standing were compared with these findings in 15 healthy age
and gendermatched control subjects and later during lower body compression with
military antishock trousers (MAST). Plasma catecholamines and circulating erythrocyte
and plasma volumes were also measured by isotopic dilution methods.
RESULTS: Abnormal findings in the patients included excessive orthostatic reductions
in systolic (P < 0.001) and diastolic BP (P < 0.001) and excessive orthostatic
tachycardia (P < 0.01), together with presyncopal symptoms in 11 of the 15 patients and
in none of the control subjects after standing for 60 min. Lower body compression with
the MAST restored all orthostatic measurements to normal and overcame presyncopal
symptoms within 10 min. Circulating erythrocyte but not plasma volumes were
subnormal in the 12 women (P < 0.01) and plasma norepinephrine concentration rose
excessively after standing for 10 min.
CONCLUSION: Delayed orthostatic hypotension and/or tachycardia caused by
excessive gravitational venous pooling, which is correctable with external lowerbody
compression, together with subnormal circulating erythrocyte volume, are very frequent,
although not invariably demonstrable, findings in moderate to severe chronic fatigue
syndrome. When present, they may be involved in its pathogenesis.
Related Information
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Activism Disability Pain About Melissa Kaplan

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