In 2006, I
staggered into a
room. The previous week, my legs seemed stuck
to the floor, and I strained mightily to lift them.
I couldn’t tell whether my muscles were suddenly too
weak to raise my feet, or whether the signal to move
was getting lost as it traveled from my brain to my legs.
Whatever was happening, I needed help.
The neurologist’s diagnosis: chronic fatigue syndrome.
After I recovered from my incredulity — fatigue? — I
asked him about tests, treatments and specialists. He had
nothing to suggest. For him, chronic fatigue syndrome
meant, “I can’t help you.”
Such experiences are nearly universal among the
1 million patients with chronic fatigue syndrome in
America. Far more than just being tired constantly,
they also suffer from neurological problems, an inability
to regulate blood pressure when standing, worsened
symptoms after exercise and immune problems. Rest
doesn’t help, and the illness is more debilitating than
heart failure or multiple sclerosis.
Nevertheless, CFS (called myalgic encephalomyelitis
internationally and often abbreviated ME/CFS)
has received little research funding — $5 million
a year compared with more than $100 million for
multiple sclerosis, a similar disease. There is no simple
diagnostic test for the illness, and as a result, doctors
are often skeptical it’s real and serious, despite
substantial and growing evidence for
biological abnormalities in patients.
There are signs of change,
however. In February, the Institute
of Medicine, a private nonprofit
group that advises the government
on health issues, released an authoritative report on
ME/CFS, exhorting doctors to take it seriously. It also
developed new diagnosis criteria and recommended a
new name, contending that the name chronic fatigue
syndrome is misleading and trivializing.
A few weeks later, Ian Lipkin and Mady Hornig,
physician-scientists at the Columbia University
Mailman School of Public Health, published the largest
study of the immune systems of ME/CFS patients yet,
with 298 patients and 348 healthy controls. It showed
immune systems of relatively newly ill patients were
revved up, like they’d just detected a new infection.
But the immune systems of patients who’d been sick
for more than three years appeared exhausted — a
distinction never seen before.
“We see it not only as a way to help with differential
diagnosis,” Hornig says, “but also to perhaps open up
avenues for treatment.” The pattern of immune changes
might distinguish ME/CFS patients from those with
other diseases, eventually leading to a blood test to
diagnose the illness.
And in July, Øystein Fluge and Olav Mella of the
University of Bergen in Norway published a small study
bolstering evidence that the cancer drug rituximab can
treat ME/CFS, in which about two-thirds of patients
benefited notably. Rituximab kills off B cells, a type of
immune cell implicated in some autoimmune conditions.
These new developments are just the beginning
in unraveling the disease, and patients and
researchers alike agree that more funding is
essential to developing tests and treatments.
Patients like me certainly hope it’s coming.