44 5.1.22
as when they fi rst arrived. When I meet patients
with chronic pain in the E.R., they narrate their
years of suff ering, and I respond with remedies
that I know — and they know that I know —
they’ve tried before with no success. This is
when I feel the most futility as a physician.
Figuring out chronic pain can be mystifying
for doctors. In M.R.I. studies of people’s spines,
disc herniations have been found in half of those
subjects who nevertheless report feeling no
pain. Age- related degenerative fi ndings also
show little correlation with symptoms. Some
patients with knee osteo arthritis continue to
have pain after joint- replacement surgery. While
chronic pain may fl ummox the usual scans and
tests, the condition is very much real, causing
immeasurable suff ering.
We have, at least, come to recognize that acute
pain resulting from damage to tissues is not the
same as chronic pain, which is now considered
a distinct disease. How we came to this under-
standing can be traced back to a serendipitous
experiment in London in the early 1980s. Before
then, scientists knew that the brain has some
control over pain, but that insight was mostly
confi ned to the situations described by Patrick
Wall’s and Ronald Melzack’s gate- control theory,
which helps explain why, say, a person running
from a house on fi re may not realize that she
sprained her ankle until she is a safe distance
away. The brain, so intent on escaping the fi re,
shuts the gate, blocking pain signals coming up
the spinal cord from the ankle. ‘‘You could close
the gate,’’ says Cliff ord Woolf, a neuro biology
professor at Harvard Medical School who
worked in Wall’s lab, but ‘‘essentially there was
nothing about the opposite possibility — which
is that the brain, independent of the periphery,
could be a generator of pain.’’
Woolf was conducting his own experiment
in Wall’s lab, applying painful stimuli to rats’
hind legs. The animals developed large ‘‘fi elds’’
of pain that could easily be activated months
later with a light tap or gentle warmth, even
in spots that weren’t being touched directly.
‘‘I was changing the function of the nervous
system, such that its properties were altered,’’
Woolf says. ‘‘Pain was not simply a measure of
some peripheral pathology,’’ he concluded; it
‘‘could also be the consequence of abnormal
amplifi cation within the nervous system — this
was the phenomenon of central sensitization.’’
Before this discovery, he says, ‘‘the feeling was
always pain is a symptom that refl ects a dis-
ease, and now we know that pain often is a
consequence of a disease state of the nervous
system itself.’’ Some ailments, like rheumatoid
arthritis, can exhibit both peripheral pathology
and central sensitization. Others, like fi bro-
myalgia, characterized by pain throughout the
body, are considered solely a problem of the
central nervous system itself.
A better grasp of how chronic pain changes
the central nervous system has emerged sinceWoolf’s experiment. A. Vania Ap karian’s pain
lab at Northwestern University found that when
back pain persists, the activity in the brain shifts
from the sensory and motor regions to the
areas associated with emotion, which include
the amygdala and the hippocampus. ‘‘It’s now44 5.1.22