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Signals From Brain Aid the Spread and Persistence of Pain, Discovery Reveals |
 Treatments for pain at the site of an injury may not always be good
enough, according to a novel study by University
of Maryland (UM) scientists reported March 20 in The Journal of Neuroscience. The
study results could change conventional thinking about pain management,
they say.
Several days after a painful event, signals from the central nervous
system (CNS) spread the pain to distant sites away from the injury, as
demonstrated in extensive tests in laboratory animals, says lead author
of the study Ronald Dubner, PhD, DDS,
of the UM School of Dentistry
in Baltimore.
"The increased pain sensitivity continues even though signals from the
site of injury have been blocked with a painkiller," says Dubner, who
is a professor in the School's Department of Neural and Pain Sciences.
"The pain signals from the central nervous system persist for months
and may be an underlying cause of the transition of acute pain to
chronic pain in humans."
Video: Dubner tells more on discovery
of protective pain signaling switch. Click here.
Based on these and other findings at the University and elsewhere, says
Dubner, pain scientists and clinicians now need "a transformation in
thinking" about how persistent or chronic pain may work, because the
spread of the pain may involve mechanisms in the CNS.
New classes of pain medications could emerge from the discovery. The
report is the latest in a trend of scientific discoveries in animal and
human studies of co-morbidity--the experience of pain in one part of the
body that is associated with pain in another. The discoveries
underscore an expanded role for CNS receptors that signal pain. For
example, hip arthritis can often result in the perception of pain
coming from the leg, explains Dubner.
In another example, other researchers in the School's Department of
Neural and Pain Sciences recently developed an animal model that sheds
some light on the simultaneous occurrence of temporomandibular
disorders (TMD) and irritable bowel syndrome (IBS). More than 60
percent of women who suffer TMD also report symptoms of IBS.
"We are studying how pain is processed in the nervous system," says
Dubner. "What our report means is that initially after the injury, the
pain is related predominantly to signals going to the brain from the
site of injury. Then, because of the switch to central nervous system
processing, there is increased sensitivity that persists at sites where
there is no injury, even though the signals coming from the site of the
injury have been blocked."
Dubner and co-researchers in the UM schools of dentistry and medicine
found in their study that a few days after an injury, the
neurotransmitter serotonin was being released from the brain stem and
affected receptors either in the spinal cord or in its counterpart in
the trigeminal system, which provides nerve signals from the face and
mouth.
"At that point, the pain is being maintained by this central nervous
system mechanism and not from the signals coming from the injury site.
It is another protective mechanism that is the nervous system response
telling you that the injury has not healed," says Dubner. The finding
that serotonin can act at receptors that result in hypersensitivity to
pain as well as at receptors that suppress pain may explain its
previous limited usefulness as an analgesic.
The five-year study is a collaboration among Dubner; Masamichi Okubo,
PhD; Ke Ren, PhD, MD; Wei Guo, MD; and Feng Wei, PhD, MD, at the School
of Dentistry; and Alberto Castro, PhD, and Asaf Keller, PhD, at the UM School of Medicine. The
study resulted from a National Institutes of Health-funded
collaboration between the dental and medical school researchers.
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| Posting Date: 03/19/2013 |
| Contact Name: Steve Berberich |
| Contact Phone: 410-706-0023 |
| Contact Email: sberb001@umaryland.edu |
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