on October 29th, 2014 2 Comments
How can you treat a disease when you don’t know what causes it? Such a mystery disease is chronic fatigue syndrome, which not so long ago was written off by many physicians as a psychiatric phenomenon because they just couldn’t figure out what else might be behind it. No one was even able to identify an anatomical or physiological “signature” of the disorder that could distinguish it from any number of medical lookalikes.
“If you don’t understand the disease, you’re throwing darts blindfolded,” Stanford neuroradiologist Mike Zeineh, MD, PhD, told me about a week ago. Zeineh is working to rip that blindfold from CFS researchers’ eyes.
From a release I wrote about some breaking CFS research by Zeineh and his colleagues:
CFS affects between 1 million and 4 million individuals in the United States and millions more worldwide. Coming up with a more precise number of cases is tough because it’s difficult to actually diagnose the disease. While all CFS patients share a common symptom — crushing, unremitting fatigue that persists for six months or longer — the additional symptoms can vary from one patient to the next, and they often overlap with those of other conditions.
A study just published in Radiology may help to resolve those ambiguities. Comparing brain images of 15 CFS patients with those from 14 age- and sex-matched healthy volunteers with no history of fatigue or other conditions causing similar symptoms, Zeineh and his colleagues found distinct differences between the brains of patients with CFS and those of healthy people.
The 15 patients were chosen from a group of 200 people with CFS whom Stanford infectious-disease expert Jose Montoya, MD, has been following for several years in an effort to identify the syndrome’s underlying mechanisms and speed the search for treatments. (Montoya is a co-author of the new study.)
In particular, the CFS patients’ brains had less overall white matter (cable-like brain infrastructure devoted to carrying signals rather than processing information), aberrant structure in a portion of a white-matter tract called the right arcuate fasciculus, and thickened gray matter (that’s the data-crunching apparatus of the brain) in the two places where the right arcuate fasciculus originates and terminates.
Exactly what all this means is not clear yet, but it’s unlikely to be spurious. Montoya is excited about the discovery. “In addition to potentially providing the CFS-specific diagnostic biomarker we’ve been desperately seeking for decades, these findings hold the promise of identifying the area or areas of the brain where the disease has hijacked the central nervous system,” he told me.
No, not a cure yet. But a well-aimed ray of light that can guide long-befuddled CFS dart-throwers in their quest to score a bullseye.
Previously: Unbroken: A chronic-fatigue patient’s long road to recovery, Deciphering the puzzle of chronic-fatigue syndrome and Unraveling the mystery of chronic-fatigue syndrome
Photo by Kai Schreiber