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Study finds nerve damage in previously
mysterious chronic pain syndrome
Reduction in small-fiber nerves may
underlie complex regional pain syndrome-I (reflex sympathetic dystrophy)
BOSTON - January 30, 2006 - Researchers at Massachusetts
General Hospital (MGH) have found the first evidence of a physical
abnormality underlying the chronic pain condition called reflex
sympathetic dystrophy or complex regional pain syndrome-I (CRPS-I).
In the February issue of the journal Pain, they describe
finding that skin affected by CRPS-I pain appears to have lost some
small-fiber nerve endings, a change characteristic of other neuropathic
pain syndromes.
"This sort of small-fiber degeneration has been found in every
nerve pain condition ever studied, including postherpetic neuralgia
and neuropathies associated with diabetes and HIV infection,"
says Anne Louise Oaklander, MD, PhD, director of the MGH
Nerve Injury Unit, who led the study. "The nerve damage
in those conditions has been much more severe, which may be why
it's been so hard to detect CRPS-I-related nerve damage."
Complex regional pain syndrome is the current name for a baffling
condition first described in the 19th century in which some patients
are left with severe chronic pain and other symptoms - swelling,
excess sweating, change in skin color and temperature - after what
may be a fairly minor injury. The fact that patients' pain severity
is out of proportion to the original injury is a hallmark of the
syndrome, and has led many to doubt whether patients' symptoms are
caused by physical damage or by a psychological disorder. Pain not
associated with a known nerve injury has been called CRPS-I, while
symptoms following damage to a major nerve has been called CRPS-II.
Because small-fiber nerve endings transmit pain messages and control
skin color and temperature and because damage to those fibers is
associated with other painful disorders, the MGH research team hypothesized
that those fibers might also be involved with CRPS-I. To investigate
their theory they studied 18 CRPS-I patients and 7 control patients
with similar chronic symptoms known to be caused by arthritis. Small
skin biopsies were taken under anesthesia from the most painful
area, from a pain-free area on the same limb and from a corresponding
unaffected area on the other side of the body.
The skin biopsies showed that, the density of small-fiber nerve
endings in CRPS-I patients was reduced from 25 to 30 percent in
the affected areas compared with unaffected areas. No nerve losses
were seen in samples from the control participants, suggesting that
the damage was specific to CRPS-I, not to pain in general. Tests
of sensory function performed in the same areas found that a light
touch or slight heat was more likely to be perceived as painful
in the affected areas of CRPS-I patients than in the unaffected
areas, also indicating abnormal neural function.
"The fact that CRPS-I now has an identified cause takes it
out of the realm of so-called 'psychosomatic illness.' One of the
great frustrations facing CRPS-I patients has been the lack of an
explanation for their symptoms. Many people are skeptical of their
motivations, and some physicians are reluctant to prescribe pain
medications when the cause of pain is unknown," says Oaklander.
"Our results suggest that CRPS-I patients should be evaluated
by neurologists who specialize in nerve injury and be treated with
medications or procedures that have proven effective for other nerve-injury
pain syndromes." She adds that the next research steps should
investigate why some people are left with CRPS after injuries that
do not cause long-term problems for most patients, determine the
best way of diagnosing the syndrome and evaluate potential treatments.
"Investigations that identify the causes of disease are only
possible if patients are willing to come to the lab and allow researchers
to study them," she adds. "We are tremendously grateful
to these CRPS patients, whose willingness to let us study them -
despite their chronic pain - allowed us to make an important step
in helping those who suffer from this condition." Oaklander
is an assistant professor of Anaesthesia and Neurology at Harvard
Medical School.
The study was supported by grants from The Mayday Fund, the National
Institute for Neurological Disorders and Stroke, and the American
Federation for Aging Research. Coauthors are Julia Rissmiller, Lisa
Gelman, Li Zheng, MD, PhD; Yuchiao Chang, PhD; and Ralph Gott, all
of the MGH.
Massachusetts General Hospital, established in 1811, is the original
and largest teaching hospital of Harvard Medical School. The MGH
conducts the largest hospital-based research program in the United
States, with an annual research budget of nearly $500 million and
major research centers in AIDS, cardiovascular research, cancer,
cutaneous biology, medical imaging, neurodegenerative disorders,
transplantation biology and photomedicine. In 1994, MGH and Brigham
and Women's Hospital joined to form Partners HealthCare System,
an integrated health care delivery system comprising the two academic
medical centers, specialty and community hospitals, a network of
physician groups, and nonacute and home health services.
Media Contact: Sue
McGreevey, MGH Public Affairs
Physician Referral Service: 1-800-388-4644
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