- Last Updated: 07 November 2015 07 November 2015
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.
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."
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."
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."