Mar. 19, 2013 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."
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 comorbidity -- 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 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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