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Lots of news outlets have been carring this story in the last 24 hours: Undamaged nerve fibres cause ongoing pain not damaged
New research shows that it is undamaged nerve fibres that cause ongoing spontaneous pain, not those that are injured.
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These unexpected findings, by Dr Laiche Djouhri, Professor Sally Lawson and colleagues from the University of Bristol, UK, are reported in the Journal of Neuroscience today [25 January, 2006].
Previous research into ongoing chronic pain has tended to focus on the damaged nerve fibres after injury or disease and overlooked the intact fibres. This new understanding may help pharmaceutical companies formulate novel pain killers.
Professor Lawson said: "The cause of this ongoing pain and why it arises spontaneously was not understood before. Now that we know the type of nerve fibres involved, and especially that it is the undamaged fibres that cause this pain, we can examine them to find out what causes them to continually send impulses to the brain. This should help in the search for new analgesics that are effective for controlling ongoing pain."
Ongoing pain is a burning or sharp stabbing/shooting pain that can occur spontaneously after nerve injury. Unlike 'evoked' pain caused, for example, by hitting your thumb with a hammer, ongoing pain is particularly difficult to live with because it is often impossible to treat with currently available pain killers.
Djouhri and Lawson show that the nerve cells responsible are 'nociceptors' or damage detectors. There are thousands of these nerves cells, each of which has a very long, fine nerve fibre emerging from it. These fibres run within nerves and connect the skin or other tissues to the spinal cord.
When activated through damage or disease, these nerve fibres fire electrical impulses that travel along the fibre from the site of injury to the spinal cord, from where information is sent to the brain. The faster the undamaged fine fibres fire, the stronger the ongoing pain becomes.
Dr Djouhri added: "The cause of this firing appears to be inflammation within the nerves or tissues, caused by dying or degeneration of the injured nerve fibres within the same nerve."
The mechanism described by Djouhri and Lawson occurs following nerve injury and in nerve and tissue inflammation. Further research is now needed to establish how generally this mechanism may contribute to ongoing pain associated with a wide variety of diseases such as back pain or shingles.
This is a nice piece of research with a finding that gives some hope. Being married to a chronic pain sufferer and seeing more than a far share of them in my clinic, its good to see this sort of progress.
Nerve damage found in chronic regional pain syndrome
Press release from ScienceDaily Study Finds Nerve Damage In Previously Mysterious Chronic Pain Syndrome
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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
Press release from Reuters: Pain patients often suffer in silence
Fri Feb 24, 2006 01:29 PM ET
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NEW YORK (Reuters Health) - More than 20 percent of patients with chronic pain do not seek physician care for their pain, according to a report.
"We need to get over what for many people appeared to be the 'don't ask, don't tell' mentality about chronic pain," Dr. Barbara P. Yawn from Olmsted Medical Center, Rochester, Minnesota told Reuters Health.
Among 3575 individuals who responded to a mailed questionnaire, 2302 reported having chronic pain and 2221 answered relevant questions. The investigators found that 497 of these patients (22.4 percent) said that they had not informed their doctors about their pain.
Of these silent pain sufferers, 70.6 percent had moderate or severe pain, 48.9 percent had pain for eight days or more per month, and 40.6 percent met both of these criteria.
About one quarter of them reported at least moderate interference with general activity and sleep, the results indicate. Vocal pain sufferers were more likely to report interference with general activity and sleep.
The survey showed that 78.9 percent of the silent sufferers used over-the-counter pain medications (compared with 56.3 percent of vocal sufferers), but only 5 percent used prescribed pain medications (compared with 35.2 percent of vocal sufferers).
Silent sufferers made fewer health care visits per year than their vocal counterparts (5.2 vs 8.6), the report indicates.
Educational and employment status had little impact on whether patients were silent or vocal about their pain. Men were more likely to be silent than women, the investigators say, and younger patients were more likely to be silent than older patients.
"I think we need to reassure our patients (probably by example) that we will listen to concerns about chronic pain and take those concerns seriously," Yawn said, and "that we do have alternatives to the 'stronger' pain medications that can cause side effects and have the potential for addiction."
"I think it is important to determine if the chronic pain is interfering with work, play, or sleep and if it is, try to help," Yawn commented. "We also need to know when patients are able to deal with the pain on their own and don't need us--but I would prefer they have the confidence to ask us when it is interfering with activities they want to do."
Pain is a disease unto itself.Before,it was only seen as a symptom of a condition.Now,pain is a coverable,payable diagnosis(for Medicare and non Medicare payors-as a matter of fact,here in NewYork Medicare it can be coupled with onychomycosis and when this occurs,Medicare WILL pay for debridement of toenails.)In addition to that,now there are pain management specialists to help patients with their pain issues.
Science Daily are reporting: Researchers Identify Potential Targets For New Pain Therapies
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Studying mice, pain researchers at Washington University School of Medicine in St. Louis have identified two key components in the pain cascade that may provide targets for more effective analgesic drugs with potentially fewer side effects.
Dorsal horn neurons (shown here in green) have different firing patterns in wild-type mice, which fire less frequently, from those bred without Kv4.2 potassium channels, which fire more often in response to a potentially painful stimulus. (Image courtesy of Washington University School of Medicine)A team led by Robert W. Gereau IV, Ph.D., associate professor of anesthesiology, reports in the April 6 issue of the journal Neuron the identification of a potassium channel that plays a crucial role in what scientists call pain plasticity, the ability of molecules in the spinal cord to amplify or diminish the response to a painful stimulus.
Electrical activity in neurons is produced by subtle changes in the cell's potassium concentration. To maintain correct amounts of potassium, cells are equipped with proteins that poke through the cell membrane like small pores. The proteins are called ion channels or potassium channels, and they create tiny sieves through which potassium can flow from the inside to the outside of the cell.
"The potassium channel we are studying is called Kv4.2," says Gereau, who also is chief of the basic research division of the Washington University Pain Center. "Through a series of experiments, we've been able to determine that Kv4.2 decreases transmission through the pain pathway. It helps regulate the ability of pain-transmitting neurons to transmit their signals to the brain."
We sense pain through primary sensory neurons with nerve endings in the skin, the joints, internal organs or muscles. Those nerve cells interpret signals indicating tissue injury or potential injury and transmit these signals to a part of the spinal cord called the dorsal horn. Pain-transmission neurons in the dorsal horn receive those messages and transmit their own pain signals to the brain.
The signals from neurons in the dorsal horn can be either damped down or enhanced, depending upon many factors, according to Gereau. That's the plasticity that makes some things hurt more than others, even though the painful stimulus itself might not change.
"Say you pinch your finger," Gereau says. "It might not feel painful because even though you activate some of these pain-sensing neurons, that pain signal doesn't just pass through the spinal cord to the brain. Active potassium channels in the spinal cord neurons may inhibit their firing."
On the other hand if a person has a sunburn, a light touch that would not normally cause pain may suddenly hurt a great deal. In that case, the potassium channels in dorsal horn neurons are less active, and they can't interfere with the transmission of pain signals to the brain.
The researchers tested the role of Kv4.2 in damping down the pain response by studying knockout mice that had no Kv4.2 gene. The mice were bred so that some pups in a litter were knockout mice while others were normal, wild-type mice with the gene. Knockout mice withdrew their paws from a heat source or mechanical stimulus more quickly than their wild-type siblings.
The scientists also looked at dorsal horn neurons in culture from both wild-type and knockout mice and found that the neurons from the knockout mice fired more readily than neurons from wild-type mice.
"That's because the inhibitory Kv4.2 channel was gone in the knockout mice," Gereau says. "It's hard to say that these mice somehow sense pain more intensely, but their thresholds for withdrawal from heat and touch are much lower than their brothers and sisters that are genetically normal."
Potassium channels in dorsal horn neurons are regulated by a molecule called extracellular signal-related kinase (ERK). Past research has demonstrated that if ERK activity is inhibited, much of the spinal cord's sensitivity to pain can be diminished. But scientists haven't really known what ERK was doing.
In this study, the research team looked for targets that might interact with ERK, and the potassium channel Kv4.2 happened to be one of those potential targets. They studied dorsal horn neurons from mice to clarify the relationship between ERK and Kv4.2.
"When an injury occurs, there is a massive barrage of activity in pain-sensing neurons, and as those neurons fire, that causes neurochemical changes in dorsal horn neurons," Gereau explains. "Those neurochemical changes activate the ERK pathway. One of the things ERK does is modify Kv4.2, so it can't inhibit the firing of dorsal horn neurons as efficiently as it normally does. Because Kv4.2 can't do that, more pain signals get sent to the brain."....
This is an interesting breakthrough.Potassium channels are something I never much gave thought to.Now that I am reading this,I can see why 2 people with the same injury will have different tolerances for pain.
Medical News Today are reporting: Genetic Mechanism Helps Explain Chronic Pain Disorders
27 Dec 2006
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Researchers at the University of North Carolina at Chapel Hill have discovered that commonly occurring variations of a gene trigger a domino effect in chronic pain disorders. The finding might lead to more effective treatments for temporomandibular joint disorder (TMJD) and other chronic pain conditions.
Catechol-O-methyltransferase (COMT), an enzyme that metabolizes neurotransmitters such as epinephrine, norepinephrine and dopamine and that has been implicated in the modulation of persistent pain, as well as cognition and mood, is regulated by a gene, also called COMT. Previous UNC-led research showed that common genetic variants of this gene are associated with increased pain sensitivity and the likelihood of developing TMJD.
Now, the researchers have discovered that specific variants of the COMT gene can dramatically affect the secondary structure of corresponding messenger RNA - which, in turn, leads to alterations in the amount of enzyme crucial for regulating pain processing. The discovery is published in the Dec. 22 issue of Science.
"TMJD is a complex pain condition that is frequently associated with other pain conditions such as fibromyalgia syndrome, chronic headaches and irritable bowel syndrome," said Dr. William Maixner, director of the Center for Neurosensory Disorders in UNC's School of Dentistry and a study co-author.
"This study has identified a new genetic mechanism that influences an individual's susceptibility to develop chronic pain conditions such as TMJD," Maixner said.
The study was conducted to understand the mechanism by which the identified genetic variants influence enzymatic activity and, ultimately, biological functions such as pain transmission. The researchers found that three major variants of COMT show significant differences in how they code for the secondary structure of messenger RNA, or mRNA. The differences lead to dramatic alterations in protein expression, which substantially influences pain sensitivity in humans.
These findings are clinically important because pain conditions resulting from low COMT activity or elevated catecholamine levels are likely to be susceptible to treatment with pharmacological agents that block beta 2- and beta 3-adrenergic receptors, which mediate COMT-dependent pain signaling, or that control mRNA secondary structure.
"Elucidating the genetic mechanisms that mediate pain perception will provide new insights into how chronic pain develops and will ultimately contribute to the identification of unique markers for diagnosing clinical pain conditions, as well as provide novel targets for the development of effective individualized therapeutics for TMJD and related conditions," said Dr. Andrea Nackley Neely, a research assistant professor in the Center for Neurosensory Disorders and the study's lead author.
"These data have broad medical and evolutionary implications regarding the analysis of variants common in the human population," Nackley Neely said. "It is believed that variants leading to altered protein structure have the strongest impact on gene function. However, this study demonstrates that combinations of common genetic variants that influence mRNA secondary structure may have even stronger effects and, thus, represent another key factor responsible for disease onset and progression."
"This study provides additional evidence of a genetic, molecular and physiological basis for pain perception and human pain conditions and should help to remove the stigma associated with conditions such as TMJD and fibromyalgia," said Dr. Luda Diatchenko, an associate professor in the center and the study's chief investigator.
Important new insight into chronic pain
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