Unique research at The University of Queensland could revolutionise the treatment of pain relief - thanks to a humble sea snail.
Dr Jenny Ekberg, a Research Fellow with UQ's School of Biomedical Sciences, has studied a toxin produced by a marine snail found on the Great Barrier Reef, which has the ability to precisely target chronic pain without severe side-effects.
"Chronic pain can be caused by an initial injury that affects the nerves, or conditions such as diabetes and arthritis," Dr Ekberg said.
"The problem with current drugs, such as morphine, is that they sometimes offer only marginal relief and come coupled with lots of problems with tolerance and side-effects.
"Our research show that a natural product, a conotoxin from the marine snail Conus marmoreus, produces pain relief without apparent side-effects in animal models of chronic pain."
The study, done with colleagues Professor David Adams in the School of Biomedical Sciences, Dr Richard Lewis at UQ's Institute for Molecular Bioscience and Professor Mac Christie at the University of Sydney, was recently published in the Proceedings of the National Academy of Sciences.
Dr Ekberg said with approximately one in five Australians will suffer from chronic pain at some point in their life the potential benefit of this research could be enormous.
She said sufferers of chronic pain can have the added problem of being diagnosed with no reason for the pain.
"The patient experiences severe pain because their nerve cells that are responsible for pain transmission are overactive," she said.
"This is primarily due to abnormal activity of voltage-gated sodium channels in the nerve cells.
"Conventional drugs, such as local anaesthetics, block all types of sodium channels, causing severe side-effects.
"Our toxin only blocks a specific channel - the first time a toxin like this has been shown to work - therefore providing pain relief without severe side-effects."
Dr Ekberg said it would be a number of years before such a treatment would be commercially available.
Originally from Sweden, Dr Ekberg came to UQ to complete her Honours in Biomedical Sciences and stayed to complete a PhD, from which this research stemmed, under the supervision of Professor David Adams and Associate Professor Phil Poronnik.
Dr Ekberg said she has since remained at UQ because of a combination of high-class research and a wonderful environment.
For further information please go to:
The University of Queensland, Brisbane Australia
Source:
UQ News Online
April 16, 2007
Gene Mutation Which Prevents Carriers From Feeling Pain Discovered By Cambridge Led Team
Researchers have discovered a gene mutation which prevents the otherwise healthy carriers from sensing pain, after studying three related families with a rare genetic disorder in northern Pakistan.
The research, published in the journal Nature, provides insight into the mechanics of pain and could lead to the development of more effective pain treatments.
The carriers of the very rare genetic mutation are unable to perceive any form of pain but have otherwise completely normal sensory functions. The initial case study was a ten-year-old street performer in Pakistan with the genetic mutation. His inability to feel pain enabled him to place knives through his arms and walk on burning coals. (The young boy died before his fourteenth birthday from injures sustained after jumping off a roof.)
The scientists subsequently studied six individuals with the genetic mutation from three related families, all originating from northern Pakistan. The six relatives had not experienced pain at any time in their lives. Detailed neurological examinations revealed that there was no evidence of motor or sensory disease, and that they could perceive a number of sensations (including touch, warm and cold temperature, tickle and pressure).
As pain is a survival mechanism which enables organisms to minimise damage to tissues, they had all sustained a variety of injuries, including injuries to their lips and/or tongue from biting themselves when young.
By studying these individuals, the scientists were able to determine that a mutation in the gene SCN9A causes a loss of function in the voltage-gated sodium channel it encodes (subunit Nav1.7). Sodium channels are proteins which excite neurons, and though the precise function of Nav1.7 is unclear, as part of a sodium channel it would play a role in exciting sensory neurons.
Dr Geoffrey Woods, from the Department of Medical Genetics and the University of Cambridge Institute for Medical Research (CIMR), said, “This paper shows that rare diseases can still be of great importance, because of the insights they give into biological and developmental processes".
Dr John Wood, from University College London, said, “The work of Geoff Woods and his team has provided us with an exciting new target for pain killing drugs - potentially this is as important as the identification of the morphine receptors. It is fascinating that this same gene, when mutated to encode a hyperactive channel, has also been found to contribute to ongoing pain in some heritable human disorders”.
As individuals with mutations in the gene SCN9A are otherwise healthy, the scientists are hopeful that the development of drugs that prevent Nav1.7 from functioning could be used as new and potentially safer pain medications.
###
The collaborative study, spearheaded by academics at the University of Cambridge, included researchers from a number of Pakistani and UK institutions (including University College London) and was funded in part by the Wellcome Trust.
Contact: Genevieve Maul
University of Cambridge
The research, published in the journal Nature, provides insight into the mechanics of pain and could lead to the development of more effective pain treatments.
The carriers of the very rare genetic mutation are unable to perceive any form of pain but have otherwise completely normal sensory functions. The initial case study was a ten-year-old street performer in Pakistan with the genetic mutation. His inability to feel pain enabled him to place knives through his arms and walk on burning coals. (The young boy died before his fourteenth birthday from injures sustained after jumping off a roof.)
The scientists subsequently studied six individuals with the genetic mutation from three related families, all originating from northern Pakistan. The six relatives had not experienced pain at any time in their lives. Detailed neurological examinations revealed that there was no evidence of motor or sensory disease, and that they could perceive a number of sensations (including touch, warm and cold temperature, tickle and pressure).
As pain is a survival mechanism which enables organisms to minimise damage to tissues, they had all sustained a variety of injuries, including injuries to their lips and/or tongue from biting themselves when young.
By studying these individuals, the scientists were able to determine that a mutation in the gene SCN9A causes a loss of function in the voltage-gated sodium channel it encodes (subunit Nav1.7). Sodium channels are proteins which excite neurons, and though the precise function of Nav1.7 is unclear, as part of a sodium channel it would play a role in exciting sensory neurons.
Dr Geoffrey Woods, from the Department of Medical Genetics and the University of Cambridge Institute for Medical Research (CIMR), said, “This paper shows that rare diseases can still be of great importance, because of the insights they give into biological and developmental processes".
Dr John Wood, from University College London, said, “The work of Geoff Woods and his team has provided us with an exciting new target for pain killing drugs - potentially this is as important as the identification of the morphine receptors. It is fascinating that this same gene, when mutated to encode a hyperactive channel, has also been found to contribute to ongoing pain in some heritable human disorders”.
As individuals with mutations in the gene SCN9A are otherwise healthy, the scientists are hopeful that the development of drugs that prevent Nav1.7 from functioning could be used as new and potentially safer pain medications.
###
The collaborative study, spearheaded by academics at the University of Cambridge, included researchers from a number of Pakistani and UK institutions (including University College London) and was funded in part by the Wellcome Trust.
Contact: Genevieve Maul
University of Cambridge
Genetic Mechanism Helps Explain Chronic Pain Disorders
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.
Other researchers were Dr. Inna Tchivileva, a postdoctoral research associate within the Center for Neurosensory Disorders; Kathryn Satterfield, a former research assistant within the center; Dr. Olex Korchynskyi, a former postdoctoral research associate within the UNC-Chapel Hill School of Medicine's Thurston Arthritis Research Center; Dr. Sergei S. Makarov, a former associate professor at the Center for Neurosensory Disorders and the Thurston center and now president and chief executive officer of Attagene Inc.; and Dr. Svetlana A. Shabalina, a staff scientist with the National Center for Biotechnology Information.
Funding was provided by the National Institute of Dental and Craniofacial Research, National Institute of Child Health and Human Development and National Institute of Neurological Disorders and Stroke, all components of the National Institutes of Health. Additional support came from the Intramural Research Program of the National Center for Biotechnology Information.
Other Center for Neurosensory Disorders research initiatives are currently under way that further explore the genetic basis of pain: One seven-study, a $19-million National Institute of Dental and Craniofacial Research-funded agreement involving multiple institutions and based at the center, will follow 3,200 health individuals and 200 who have facial pain. Titled OPPERA (Orofacial Pain: Prospective Evaluation and Risk Assessment), the study is designed to identify both environmental and genetic factors that increase an individual's susceptibility to TMJD and other chronic pain conditions.
University of North Carolina at Chapel Hill
210 Pittsboro St. Campus Box 6210
Chapel Hill, NC 27514
United States
http://www.unc.edu/
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.
Other researchers were Dr. Inna Tchivileva, a postdoctoral research associate within the Center for Neurosensory Disorders; Kathryn Satterfield, a former research assistant within the center; Dr. Olex Korchynskyi, a former postdoctoral research associate within the UNC-Chapel Hill School of Medicine's Thurston Arthritis Research Center; Dr. Sergei S. Makarov, a former associate professor at the Center for Neurosensory Disorders and the Thurston center and now president and chief executive officer of Attagene Inc.; and Dr. Svetlana A. Shabalina, a staff scientist with the National Center for Biotechnology Information.
Funding was provided by the National Institute of Dental and Craniofacial Research, National Institute of Child Health and Human Development and National Institute of Neurological Disorders and Stroke, all components of the National Institutes of Health. Additional support came from the Intramural Research Program of the National Center for Biotechnology Information.
Other Center for Neurosensory Disorders research initiatives are currently under way that further explore the genetic basis of pain: One seven-study, a $19-million National Institute of Dental and Craniofacial Research-funded agreement involving multiple institutions and based at the center, will follow 3,200 health individuals and 200 who have facial pain. Titled OPPERA (Orofacial Pain: Prospective Evaluation and Risk Assessment), the study is designed to identify both environmental and genetic factors that increase an individual's susceptibility to TMJD and other chronic pain conditions.
University of North Carolina at Chapel Hill
210 Pittsboro St. Campus Box 6210
Chapel Hill, NC 27514
United States
http://www.unc.edu/
Psychological Treatments Improve Outcomes For Back Pain Sufferers
Psychological interventions for chronic low back pain are effective, a new review of studies has found. Not only do these approaches improve psychological outcomes such as depression and health-related quality of life, they also reduce patients’ experience of pain.
“Because this analysis was both more inclusive and more conservative than previous reviews, we have the best evidence to date that these interventions are helpful,” said psychologist and review lead author Robert Kerns, Ph.D., of the VA Connecticut Healthcare System.
The review, part of a new article series, appears in the January issue of the journal Health Psychology. Each evidence-based review centers on a specific psychological assessment or treatment conducted in the context of a physical disease process or risk reduction effort.
To evaluate the effects of psychological interventions on pain-related outcomes, Kerns and his team gathered data from 22 randomized trials published between 1982 and 2003. Trials were limited to adults with nonmalignant low back pain that had persisted for at least three months. However, most patients had been living with pain for much longer. The average duration was seven and a half years.
The studies were not limited to any one psychological approach. Included in the review were behavioral and cognitive-behavioral techniques; self-regulatory techniques such as hypnosis, biofeedback, and relaxation; and supportive counseling.
The review reports on 12 pain-related outcomes, including pain intensity, pain interference, depression, health care use, disability and health-related quality of life.
In the broadest analysis, psychological interventions alone or as part of a multidisciplinary approach proved to be superior to waiting lists or standard treatments on the entire range of pain-related outcomes.
When the researchers analyzed specific outcomes, they found that the largest and most consistent effect was a reduction in pain intensity.
This was somewhat surprising, Kerns said, because when psychologists first began developing interventions for chronic pain several decades ago, the goal was not to reduce pain but to help patients live with their pain more successfully.
“However, a growing body of knowledge suggests that these interventions are actually having a primary effect on people’s experience of pain,” he said.
The review found that psychological interventions also yielded improvements in health-related quality of life, work-related disability, interference of pain with daily living and depression.
Not all treatments were equally effective. Cognitive-behavioral and self-regulatory treatments seemed to yield the greatest effects, particularly when compared to waiting list control groups. Multidisciplinary approaches that included a psychological component also stood out on some measures, reducing pain interference and work-related disability when compared to other active treatments.
According to Dennis Turk, Ph.D., a professor of anesthesiology and pain research at the University of Washington in Seattle, patients with chronic pain sometimes fail to recognize the value of psychological treatments because they’ve been set up to expect a cure.
“Even the latest and greatest treatments don’t cure people with chronic pain,” he said. “Psychological interventions are not cures, but they do reduce pain and improve function and they are important components in the treatment of people with chronic pain.”
Turk added that psychological interventions are also cost-effective when compared to other treatments for chronic low back pain a key finding, considering that estimates for treatment-related costs range from $20 billion to $80 billion a year in the United States.
“Surgery, opioids, nerve blocks, spinal cord stimulators, implantable drug delivery systems every one of those particular alternatives is much more expensive and has poorer or at best equal outcomes compared to rehabilitation programs that include psychological components,” said Turk. “The paradox is that, despite data on the effectiveness of psychological interventions, insurers are less willing to pay for them.”
Getting the word out that these treatments are effective and cost-effective is a challenge that psychologists will have to tackle head-on, Kerns said.
“We need to specifically target health care system administrators and third-party payers to try to engage them in a more productive dialogue about the importance of these interventions,” he said. “We continue to have a huge, very costly problem in our society, but we have an intervention that is effective, and we need to do a better job of creating access to these services.”
“Evidence-based Treatment Reviews” is a new series initiated within Health Psychology, an official journal of the American Psychological Association. This series of articles is intended to inform health psychology practice, add to teaching and mentoring resources, and inspire further evidence-based research and questions.
Hoffman BM, et al. Meta-analysis of psychological interventions for chronic low back pain. Health Psychology 26 (1), 2007.
Health Behavior News Service
Center for the Advancement of Health 2000 Florida Ave. NW, Ste 210
Washington, DC 20009
United States
http://www.hbns.org
“Because this analysis was both more inclusive and more conservative than previous reviews, we have the best evidence to date that these interventions are helpful,” said psychologist and review lead author Robert Kerns, Ph.D., of the VA Connecticut Healthcare System.
The review, part of a new article series, appears in the January issue of the journal Health Psychology. Each evidence-based review centers on a specific psychological assessment or treatment conducted in the context of a physical disease process or risk reduction effort.
To evaluate the effects of psychological interventions on pain-related outcomes, Kerns and his team gathered data from 22 randomized trials published between 1982 and 2003. Trials were limited to adults with nonmalignant low back pain that had persisted for at least three months. However, most patients had been living with pain for much longer. The average duration was seven and a half years.
The studies were not limited to any one psychological approach. Included in the review were behavioral and cognitive-behavioral techniques; self-regulatory techniques such as hypnosis, biofeedback, and relaxation; and supportive counseling.
The review reports on 12 pain-related outcomes, including pain intensity, pain interference, depression, health care use, disability and health-related quality of life.
In the broadest analysis, psychological interventions alone or as part of a multidisciplinary approach proved to be superior to waiting lists or standard treatments on the entire range of pain-related outcomes.
When the researchers analyzed specific outcomes, they found that the largest and most consistent effect was a reduction in pain intensity.
This was somewhat surprising, Kerns said, because when psychologists first began developing interventions for chronic pain several decades ago, the goal was not to reduce pain but to help patients live with their pain more successfully.
“However, a growing body of knowledge suggests that these interventions are actually having a primary effect on people’s experience of pain,” he said.
The review found that psychological interventions also yielded improvements in health-related quality of life, work-related disability, interference of pain with daily living and depression.
Not all treatments were equally effective. Cognitive-behavioral and self-regulatory treatments seemed to yield the greatest effects, particularly when compared to waiting list control groups. Multidisciplinary approaches that included a psychological component also stood out on some measures, reducing pain interference and work-related disability when compared to other active treatments.
According to Dennis Turk, Ph.D., a professor of anesthesiology and pain research at the University of Washington in Seattle, patients with chronic pain sometimes fail to recognize the value of psychological treatments because they’ve been set up to expect a cure.
“Even the latest and greatest treatments don’t cure people with chronic pain,” he said. “Psychological interventions are not cures, but they do reduce pain and improve function and they are important components in the treatment of people with chronic pain.”
Turk added that psychological interventions are also cost-effective when compared to other treatments for chronic low back pain a key finding, considering that estimates for treatment-related costs range from $20 billion to $80 billion a year in the United States.
“Surgery, opioids, nerve blocks, spinal cord stimulators, implantable drug delivery systems every one of those particular alternatives is much more expensive and has poorer or at best equal outcomes compared to rehabilitation programs that include psychological components,” said Turk. “The paradox is that, despite data on the effectiveness of psychological interventions, insurers are less willing to pay for them.”
Getting the word out that these treatments are effective and cost-effective is a challenge that psychologists will have to tackle head-on, Kerns said.
“We need to specifically target health care system administrators and third-party payers to try to engage them in a more productive dialogue about the importance of these interventions,” he said. “We continue to have a huge, very costly problem in our society, but we have an intervention that is effective, and we need to do a better job of creating access to these services.”
“Evidence-based Treatment Reviews” is a new series initiated within Health Psychology, an official journal of the American Psychological Association. This series of articles is intended to inform health psychology practice, add to teaching and mentoring resources, and inspire further evidence-based research and questions.
Hoffman BM, et al. Meta-analysis of psychological interventions for chronic low back pain. Health Psychology 26 (1), 2007.
Health Behavior News Service
Center for the Advancement of Health 2000 Florida Ave. NW, Ste 210
Washington, DC 20009
United States
http://www.hbns.org
Premature Babies Probably Feel And Are Aware Of Pain
Although it is wellknown that premature babies react to pain, it has not been known to what extent they are aware of pain and uncomfortable procedures. Therefore premature infants have not always received sufficient analgesia. Now, however, the grounds for this have been seriously undermined by a new doctoral thesis from Karolinska Institutet (KI) in Sweden. New measurement techniques show that even premature babies display all the signs of a conscious experience of pain.
For many years, doctors have assumed that foetuses, premature babies and fully developed new-born babies do not have the cerebral cortical functions required to feel pain. Babies’ reactions to potentially painful stimuli have been explained away as unconscious reflexes, and so doctors have felt it justified to withhold painkillers during surgery and the like so as to avoid adverse reactions.
The doctoral thesis by Italian-Swedish researcher Marco Bartocci now shows that the brains of premature babies are far more developed than previously thought. His studies using infrared spectroscopy, carried out at the Astrid Lindgren Children’s Hospital in Stockholm, Sweden, show that pain signals from a pin prick are processed in the cerebral cortex of premature babies in the same way as in adults. This means that all known pre-conditions for the conscience experience of pain are present, even though this still does not provide any conclusive evidence that they actually undergo a subjective painful experience.
The results of the processing of painful stimuli have been published in the scientific journal Pain and have been cited in a news article in Nature. They are expected to have a major impact on pain-relief management for new-born babies as well as on approaches to child development in general. Public defence of doctoral thesis will be held on December 8. Professor Michael Wweindling from the University of Liverpool, UK is the external examiner.
Thesis: Brain functional near infrared spectroscopy in human infants: cerebral cortical haemodynamics coupled to neuronal activation in response to sensory stimulation , Department of Women and Child Health, Karolinska Institutet.
Karolinska Institutet is one of the leading medical universities in Europe. Through research, education and information, Karolinska Institutet contributes to improving human health. Each year, the Nobel Assembly at Karolinska Institutet awards the Nobel Prize in Physiology or Medicine.
http://diss.kib.ki.se/2006/91-7357-034-6
For many years, doctors have assumed that foetuses, premature babies and fully developed new-born babies do not have the cerebral cortical functions required to feel pain. Babies’ reactions to potentially painful stimuli have been explained away as unconscious reflexes, and so doctors have felt it justified to withhold painkillers during surgery and the like so as to avoid adverse reactions.
The doctoral thesis by Italian-Swedish researcher Marco Bartocci now shows that the brains of premature babies are far more developed than previously thought. His studies using infrared spectroscopy, carried out at the Astrid Lindgren Children’s Hospital in Stockholm, Sweden, show that pain signals from a pin prick are processed in the cerebral cortex of premature babies in the same way as in adults. This means that all known pre-conditions for the conscience experience of pain are present, even though this still does not provide any conclusive evidence that they actually undergo a subjective painful experience.
The results of the processing of painful stimuli have been published in the scientific journal Pain and have been cited in a news article in Nature. They are expected to have a major impact on pain-relief management for new-born babies as well as on approaches to child development in general. Public defence of doctoral thesis will be held on December 8. Professor Michael Wweindling from the University of Liverpool, UK is the external examiner.
Thesis: Brain functional near infrared spectroscopy in human infants: cerebral cortical haemodynamics coupled to neuronal activation in response to sensory stimulation , Department of Women and Child Health, Karolinska Institutet.
Karolinska Institutet is one of the leading medical universities in Europe. Through research, education and information, Karolinska Institutet contributes to improving human health. Each year, the Nobel Assembly at Karolinska Institutet awards the Nobel Prize in Physiology or Medicine.
http://diss.kib.ki.se/2006/91-7357-034-6
A Protein Essential For Touch Sensation - First Evidence For A Touch Receptor Gene In Mammals
The skin is the largest sensory organ in humans. The sensory innervation of the skin allows us to perceive touch and pain. Now, Christiane Wetzel, a researcher in the laboratory of Professor Gary Lewin at the Max DelbrГјck Center for Molecular Medicine (MDC) Berlin-Buch, Germany, and her colleagues have deciphered the function of a molecule necessary for the conversion of mechanical stimuli into neural impulses. They have demonstrated that this molecule, a protein called SLP3, is essential for the detection and discrimination of fine tactile stimuli. This study provides the first evidence for a touch receptor gene in mammals and shows that molecules may in the future prove to be important therapeutic targets for the control of chronic pain. The findings of Christiane Wetzel and Professor Lewin were published in Nature online (DOI: 10.1038/nature05394).
Christiane Wetzel could show that mice lacking SLP3 are unable to distinguish normally between finely structured surfaces. This serious sensory deficit could be traced to the fact that around one third of the mechanoreceptors in the skin of SLP3 mutant mice fail to respond to any mechanical stimulation.
Although the sensation of touch is not usually associated with pain this situation is dramatically altered after injury to nerve. Thus many people with such injuries suffer from chronic pain in which even light brush stimuli can provoke intense pain.
This type of pain, called neuropathic pain, can be modelled in animals and mice lacking SLP3 show virtually no touch-evoked pain when confronted with such a lesion. This data further indicates that by targeting molecules involved in the detection of touch one could achieve a novel way to control neuropathic pain a clinical condition for which few effective treatment options are available.
Touch and pain are detected by sensory neurons which are located in the dorsal root ganglia (DRG) and their “working end” is in the skin attached to the cell body by a long process called the axon. Mechanical stimuli of the skin (brush or pressure) activates the “working end” of the sensory receptor and initiates an electrical signal that is relayed to the spinal cord and brain.
The sensory receptor must then convert a mechanical signal into an electrical signal and this process is called sensory mechanotransduction. It is this process of sensory mechanotransduction, that is very poorly understood in mammals. It is thought that mechanical stimuli are converted into electrical events by specialized ion channels, these channels can be opened when the membrane is physically indented, leading to an increased flow of charged ions into the cell to produce an electrical signal.
In this study the activity of such ion channels was measured in response to extremely small indentation stimuli (nanometer range). It was found that in many sensory neurons SLP3 was required for the function of such mechanosensitive channels.
This study is the very first to show any protein that is directly involved in the detection of touch in mammals. Many genes have been shown to be necessary for mechanosensation in simpler organisms like worms and flies. The SLP3 protein is also very closely related to such a necessary mechanotransduction protein in worms called MEC-2. This study therefore provides the first evidence for a touch receptor gene in mammals and shows that molecules may in the future prove to be important therapeutic targets for the control of chronic pain.
###
*A stomatin-domain protein essential for touch sensation in the mouse
Christiane Wetzel1, Jing Hu1,5, Dieter Riethmacher2,5, Anne Benckendorff1,5, Lena Harder1, Andreas Eilers1, Rabih Moshourab1, Alexey Kozlenkov1, Dominika Labuz3,Ombretta Caspani3, Bettina Erdmann4, Halina Machelska3, Paul A. Heppenstall1,3, and Gary R. Lewin1
1 Growth Factors and Regeneration Group, Max-Delbrück Center for Molecular Medicine and Charité Universitätsmedizin Berlin, Robert-Rössle-Str. 10, Berlin-Buch D-13125 Germany.
2 Zentrum für Molekulare Neurobiologie, Universität Hamburg, Falkenried 94, 20251 Hamburg, Germany.
3 Klinik für Anaesthesiologie und Operative Intensivmedizin, Charité Universitätsmedizin Berlin, Campus Benjamin Franklin,Hindenburgdamm 30, D-12200 Berlin, Germany.
4 Electronmicroscopy, Max-DelbrückCenter for Molecular Medicine, Robert-Rössle-Str. 10, Berlin-Buch D-13125 Germany.
5 These authors made an equal contribution.
Contact:
Barbara Bachtler
Max DelbrГјck Center for Molecular Medicine (MDC) Berlin-Buch
Robert-Rössle-Straße 10; 13125 Berlin; Germany
details here
For further information please go to:
Max DelbrГјck Center for Molecular Medicine
Christiane Wetzel could show that mice lacking SLP3 are unable to distinguish normally between finely structured surfaces. This serious sensory deficit could be traced to the fact that around one third of the mechanoreceptors in the skin of SLP3 mutant mice fail to respond to any mechanical stimulation.
Although the sensation of touch is not usually associated with pain this situation is dramatically altered after injury to nerve. Thus many people with such injuries suffer from chronic pain in which even light brush stimuli can provoke intense pain.
This type of pain, called neuropathic pain, can be modelled in animals and mice lacking SLP3 show virtually no touch-evoked pain when confronted with such a lesion. This data further indicates that by targeting molecules involved in the detection of touch one could achieve a novel way to control neuropathic pain a clinical condition for which few effective treatment options are available.
Touch and pain are detected by sensory neurons which are located in the dorsal root ganglia (DRG) and their “working end” is in the skin attached to the cell body by a long process called the axon. Mechanical stimuli of the skin (brush or pressure) activates the “working end” of the sensory receptor and initiates an electrical signal that is relayed to the spinal cord and brain.
The sensory receptor must then convert a mechanical signal into an electrical signal and this process is called sensory mechanotransduction. It is this process of sensory mechanotransduction, that is very poorly understood in mammals. It is thought that mechanical stimuli are converted into electrical events by specialized ion channels, these channels can be opened when the membrane is physically indented, leading to an increased flow of charged ions into the cell to produce an electrical signal.
In this study the activity of such ion channels was measured in response to extremely small indentation stimuli (nanometer range). It was found that in many sensory neurons SLP3 was required for the function of such mechanosensitive channels.
This study is the very first to show any protein that is directly involved in the detection of touch in mammals. Many genes have been shown to be necessary for mechanosensation in simpler organisms like worms and flies. The SLP3 protein is also very closely related to such a necessary mechanotransduction protein in worms called MEC-2. This study therefore provides the first evidence for a touch receptor gene in mammals and shows that molecules may in the future prove to be important therapeutic targets for the control of chronic pain.
###
*A stomatin-domain protein essential for touch sensation in the mouse
Christiane Wetzel1, Jing Hu1,5, Dieter Riethmacher2,5, Anne Benckendorff1,5, Lena Harder1, Andreas Eilers1, Rabih Moshourab1, Alexey Kozlenkov1, Dominika Labuz3,Ombretta Caspani3, Bettina Erdmann4, Halina Machelska3, Paul A. Heppenstall1,3, and Gary R. Lewin1
1 Growth Factors and Regeneration Group, Max-Delbrück Center for Molecular Medicine and Charité Universitätsmedizin Berlin, Robert-Rössle-Str. 10, Berlin-Buch D-13125 Germany.
2 Zentrum für Molekulare Neurobiologie, Universität Hamburg, Falkenried 94, 20251 Hamburg, Germany.
3 Klinik für Anaesthesiologie und Operative Intensivmedizin, Charité Universitätsmedizin Berlin, Campus Benjamin Franklin,Hindenburgdamm 30, D-12200 Berlin, Germany.
4 Electronmicroscopy, Max-DelbrückCenter for Molecular Medicine, Robert-Rössle-Str. 10, Berlin-Buch D-13125 Germany.
5 These authors made an equal contribution.
Contact:
Barbara Bachtler
Max DelbrГјck Center for Molecular Medicine (MDC) Berlin-Buch
Robert-Rössle-Straße 10; 13125 Berlin; Germany
details here
For further information please go to:
Max DelbrГјck Center for Molecular Medicine
Mutations Can't Go All The Way In Paget Disease
Paget disease is a bone disease that results in enlarged bones and causes bone pain, arthritis, deformities, and fractures. It mostly affects individuals over the age of 40 and has a hereditary component. One gene that is mutated in approximately one third of patients with hereditary Padget disease is p62 (sequestosome 1). However, it has not been clear whether mutations (such as the common p62P392L mutation) in this gene actually cause Paget disease.
In a study appearing online in advance of publication in the January print issue of the Journal of Clinical Investigation, Noriyoshi Kurihara and colleagues from the VA Pittsburgh Healthcare System show that expression of the p62P392L mutation causes abnormal development of human bone cells in vitro and mouse bone cells in vivo but does not cause a Padget-like disease in mice. Specifically, expression of p62P392L in the precursors of human bone cells known as osteoclasts (the cells that destroy bone) caused them to be more responsive to factors that drive osteoclast development. Similarly, expression of p62P392L in osteoclast-lineage cells in mice resulted in increased numbers of osteoclasts. Although increased numbers of osteoclasts is a feature of Paget disease, it is not the full range of characteristics. This study therefore suggests that although mutations in p62 predispose an individual to developing Paget disease, other factors are required for the full development of Paget disease.
TITLE: Mutation of the sequestosome 1 (p62) gene increases osteoclastogenesis but does not induce Paget disease
###
JCI table of contents: Dec. 21, 2006
AUTHOR CONTACT:
Noriyoshi Kurihara
VA Pittsburgh Healthcare System and University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Contact: Karen Honey
Journal of Clinical Investigation
In a study appearing online in advance of publication in the January print issue of the Journal of Clinical Investigation, Noriyoshi Kurihara and colleagues from the VA Pittsburgh Healthcare System show that expression of the p62P392L mutation causes abnormal development of human bone cells in vitro and mouse bone cells in vivo but does not cause a Padget-like disease in mice. Specifically, expression of p62P392L in the precursors of human bone cells known as osteoclasts (the cells that destroy bone) caused them to be more responsive to factors that drive osteoclast development. Similarly, expression of p62P392L in osteoclast-lineage cells in mice resulted in increased numbers of osteoclasts. Although increased numbers of osteoclasts is a feature of Paget disease, it is not the full range of characteristics. This study therefore suggests that although mutations in p62 predispose an individual to developing Paget disease, other factors are required for the full development of Paget disease.
TITLE: Mutation of the sequestosome 1 (p62) gene increases osteoclastogenesis but does not induce Paget disease
###
JCI table of contents: Dec. 21, 2006
AUTHOR CONTACT:
Noriyoshi Kurihara
VA Pittsburgh Healthcare System and University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Contact: Karen Honey
Journal of Clinical Investigation
Pain Relief Effectiveness Down To Mind-Set?
Research by the Human Pain Research Group at The University of Manchester suggests that people's responses to placebo or "dummy" pain relief varies according to their way of thinking.
40 pain-free volunteers took part in an experiment funded by the Arthritis Research Campaign using an artificial pain stimulus, and were led to expect reduced pain after the application of a cream which was actually a placebo.
Lead researcher Alison Watson said: "Any medical treatment involves a placebo element; the psychological suggestion that it is going to work. So we theorised that a proportion of any treatment's effectiveness would relate to how much we wanted it to work, believed in it or trusted the person administering it.
"Doctors and nurses can transmit a lot of information about a treatment and its effectiveness through their words and gestures. We know that when people visit their preferred GP the treatment or advice they receive will be more effective than that given by a GP they prefer not to see. Similarly, red pills have been shown to be more effective than green ones; so we wanted to test whether all this was due to expectations of successful treatment and trust in the person giving it."
24 of the volunteers initially received a moderately painful heat stimulus to both arms. The placebo cream was then applied to the skin, but they were led to believe that the cream on one of their arms may be a local anaesthetic.
After the application of the cream, the intensity of the heat stimulus was turned down on one arm without informing the volunteer. Subsequently the intensity was returned to its previous level, but - in contrast to the 16 people in the control group - 67% of the treatment group continued to perceive the heat as less painful.
Alison said: "The expectation of pain relief leads to a release of endorphins, the brain's natural pain killers, which is likely to contribute to a sensation of reward and well-being.
"Interestingly, there was an exact split in the range of responses to the placebo; a third of people reporting a reduction in the pain intensity in the "treated" arm only, another third in both arms and the remainder's intensity-ratings not being influenced by the application of the cream. The different responses can be related to the different levels of pain relief the volunteers expected, which may have allowed their individual suggestibility to influence their assessment of the pain experience.
"Our findings suggest that different individuals may have different styles of placebo response, which is likely to affect how they respond to real treatments too. Understanding these differences could better inform the way doctors and nurses provide treatments in the future.
"It could also facilitate more effective clinical trial design, which could substantially reduce the costs of developing new pain killers for patients with conditions like cancer and arthritis.
"A further, exciting possibility is that we could develop talking and drug-based therapies to enhance people's response to placebos. The experimental methods we're using will allow us to test out such possibilities as a method of treating pain."
###
A copy of the full paper, published in the Elsevier journal Pain, is available upon request.
For further information
Mikaela Sitford:
Jo Nightingale:
The University of Manchester (http://www.manchester.ac.uk/) is the largest single-site higher education institution in the country, with 24 academic schools, over 5200 academic and research staff and around 36 000 students. It was awarded University of the Year by the Times Higher Educational Supplement in 2005 and The Sunday Times in 2006, and receives more undergraduate applications than any other UK university.
Its Faculty of Medical & Human Sciences (www.mhs.manchester.ac.uk) is one of the largest faculties of clinical and health sciences in Europe, with a research income of around ВЈ51 million (almost a third of the University's total research income). The School of Medicine http://www.mhs.manchester.ac.uk/) is the largest of its five Schools, encompasses five teaching hospitals and is closely linked to general hospitals and community practices across the North West of England.
The Arthritis Research Campaign (arc), founded in 1936, raises funds to promote medical research into the cause, treatment and cure of arthritic conditions: to educate medical students, doctors and allied healthcare professionals about arthritis and to provide information to people affected by arthritis and to the general public. arc is the only major medical research charity in the UK investigating arthritis in all its forms. Millions of pounds are provided every year for grants funding research, education and training.
Contact: Mikaela Sitford
University of Manchester
40 pain-free volunteers took part in an experiment funded by the Arthritis Research Campaign using an artificial pain stimulus, and were led to expect reduced pain after the application of a cream which was actually a placebo.
Lead researcher Alison Watson said: "Any medical treatment involves a placebo element; the psychological suggestion that it is going to work. So we theorised that a proportion of any treatment's effectiveness would relate to how much we wanted it to work, believed in it or trusted the person administering it.
"Doctors and nurses can transmit a lot of information about a treatment and its effectiveness through their words and gestures. We know that when people visit their preferred GP the treatment or advice they receive will be more effective than that given by a GP they prefer not to see. Similarly, red pills have been shown to be more effective than green ones; so we wanted to test whether all this was due to expectations of successful treatment and trust in the person giving it."
24 of the volunteers initially received a moderately painful heat stimulus to both arms. The placebo cream was then applied to the skin, but they were led to believe that the cream on one of their arms may be a local anaesthetic.
After the application of the cream, the intensity of the heat stimulus was turned down on one arm without informing the volunteer. Subsequently the intensity was returned to its previous level, but - in contrast to the 16 people in the control group - 67% of the treatment group continued to perceive the heat as less painful.
Alison said: "The expectation of pain relief leads to a release of endorphins, the brain's natural pain killers, which is likely to contribute to a sensation of reward and well-being.
"Interestingly, there was an exact split in the range of responses to the placebo; a third of people reporting a reduction in the pain intensity in the "treated" arm only, another third in both arms and the remainder's intensity-ratings not being influenced by the application of the cream. The different responses can be related to the different levels of pain relief the volunteers expected, which may have allowed their individual suggestibility to influence their assessment of the pain experience.
"Our findings suggest that different individuals may have different styles of placebo response, which is likely to affect how they respond to real treatments too. Understanding these differences could better inform the way doctors and nurses provide treatments in the future.
"It could also facilitate more effective clinical trial design, which could substantially reduce the costs of developing new pain killers for patients with conditions like cancer and arthritis.
"A further, exciting possibility is that we could develop talking and drug-based therapies to enhance people's response to placebos. The experimental methods we're using will allow us to test out such possibilities as a method of treating pain."
###
A copy of the full paper, published in the Elsevier journal Pain, is available upon request.
For further information
Mikaela Sitford:
Jo Nightingale:
The University of Manchester (http://www.manchester.ac.uk/) is the largest single-site higher education institution in the country, with 24 academic schools, over 5200 academic and research staff and around 36 000 students. It was awarded University of the Year by the Times Higher Educational Supplement in 2005 and The Sunday Times in 2006, and receives more undergraduate applications than any other UK university.
Its Faculty of Medical & Human Sciences (www.mhs.manchester.ac.uk) is one of the largest faculties of clinical and health sciences in Europe, with a research income of around ВЈ51 million (almost a third of the University's total research income). The School of Medicine http://www.mhs.manchester.ac.uk/) is the largest of its five Schools, encompasses five teaching hospitals and is closely linked to general hospitals and community practices across the North West of England.
The Arthritis Research Campaign (arc), founded in 1936, raises funds to promote medical research into the cause, treatment and cure of arthritic conditions: to educate medical students, doctors and allied healthcare professionals about arthritis and to provide information to people affected by arthritis and to the general public. arc is the only major medical research charity in the UK investigating arthritis in all its forms. Millions of pounds are provided every year for grants funding research, education and training.
Contact: Mikaela Sitford
University of Manchester
Physical Therapists Can Help Relieve Pain
In light of proposed sterner warning labels for acetaminophen, aspirin, and ibuprofen by federal health officials, patients may wish to consider the benefits of physical therapist intervention for pain relief from certain conditions, according to the American Physical Therapy Association (APTA).
"Many people are looking for alternatives to the sole use of medication to deal with painful conditions," said APTA President R Scott Ward, PT, PhD. "Pain medication may help you get through periods of severe pain, but it won't always help you eliminate the underlying cause of some kinds of pain. For many individuals, it is the underlying causes such as poor posture and alignment, weak and/or inflexible muscles, or tight joint structures that actually exacerbate the painful condition," Ward explained. "A physical therapist will perform a complete musculoskeletal examination and design an individualized treatment program to reduce pain and improve function."
There are many types of pain and inflammation that can be reduced by physical therapist intervention. For example, chronic pain in the back, shoulder, or knee, or pain associated with certain degenerative diseases such as osteoarthritis, can be reduced with the appropriate combination of medication and exercise. "The physical therapist, in collaboration with the patient and the patient's physician, can help the patient manage his or her health over the long term," explained Ward.
For pain of a "mechanical" origin such as back, shoulder, or knee pain, physical therapist intervention may include therapeutic exercise, manual therapy, and functional training. "The goal of the physical therapist is to reduce pain, improve the ability to perform daily activities, and help the patient return to doing the things he or she likes to do," said Ward. "It is also true that patients may unknowingly contribute to their own pain, such as by exercising improperly or with poor posture, and physical therapists can identify and help to correct those behaviors." Ward added, "Through the use of home programs designed to fit the patient's needs, the physical therapist can efficiently progress the patient's rehabilitation and teach the patient how to prevent a recurrence of the original condition."
For osteoarthritis, a degenerative disease of the cartilage and bone, physical therapist intervention may include exercises for strength, flexibility, range of motion, and the use of devices designed to rest or support the joint, such as orthotics or splints.
Physical therapists, who treat nearly 1 million people every day, work with individuals to prevent the loss of mobility before it occurs by developing fitness- and wellness-oriented programs for healthier and more active lifestyles. Many insurance policies also cover post-rehabilitation gym programs. "Most people who desire a fitness plan are not athletes," Ward explained. "They are 'ordinary people' who exercise lightly to moderately. Many have a prior health condition, such as chronic low back pain, that can benefit greatly from physical therapist management focused on increasing muscle strength and endurance, restoring and improving range of motion in joints, increasing cardiovascular endurance, and decreasing muscle and joint pain." The physical therapist individualizes exercise programs based on functional limitations as a result of injury or illness.
For more information on physical therapy or to find a physical therapist near you, please visit http://www.apta.org/consumer.
The American Physical Therapy Association (http://www.apta.org) is a national professional organization representing more than 70,000 physical therapists, physical therapist assistants, and students. Its goal is to foster advancements in physical therapy practice, research, and education.
American Physical Therapy Association
http://www.apta.org
"Many people are looking for alternatives to the sole use of medication to deal with painful conditions," said APTA President R Scott Ward, PT, PhD. "Pain medication may help you get through periods of severe pain, but it won't always help you eliminate the underlying cause of some kinds of pain. For many individuals, it is the underlying causes such as poor posture and alignment, weak and/or inflexible muscles, or tight joint structures that actually exacerbate the painful condition," Ward explained. "A physical therapist will perform a complete musculoskeletal examination and design an individualized treatment program to reduce pain and improve function."
There are many types of pain and inflammation that can be reduced by physical therapist intervention. For example, chronic pain in the back, shoulder, or knee, or pain associated with certain degenerative diseases such as osteoarthritis, can be reduced with the appropriate combination of medication and exercise. "The physical therapist, in collaboration with the patient and the patient's physician, can help the patient manage his or her health over the long term," explained Ward.
For pain of a "mechanical" origin such as back, shoulder, or knee pain, physical therapist intervention may include therapeutic exercise, manual therapy, and functional training. "The goal of the physical therapist is to reduce pain, improve the ability to perform daily activities, and help the patient return to doing the things he or she likes to do," said Ward. "It is also true that patients may unknowingly contribute to their own pain, such as by exercising improperly or with poor posture, and physical therapists can identify and help to correct those behaviors." Ward added, "Through the use of home programs designed to fit the patient's needs, the physical therapist can efficiently progress the patient's rehabilitation and teach the patient how to prevent a recurrence of the original condition."
For osteoarthritis, a degenerative disease of the cartilage and bone, physical therapist intervention may include exercises for strength, flexibility, range of motion, and the use of devices designed to rest or support the joint, such as orthotics or splints.
Physical therapists, who treat nearly 1 million people every day, work with individuals to prevent the loss of mobility before it occurs by developing fitness- and wellness-oriented programs for healthier and more active lifestyles. Many insurance policies also cover post-rehabilitation gym programs. "Most people who desire a fitness plan are not athletes," Ward explained. "They are 'ordinary people' who exercise lightly to moderately. Many have a prior health condition, such as chronic low back pain, that can benefit greatly from physical therapist management focused on increasing muscle strength and endurance, restoring and improving range of motion in joints, increasing cardiovascular endurance, and decreasing muscle and joint pain." The physical therapist individualizes exercise programs based on functional limitations as a result of injury or illness.
For more information on physical therapy or to find a physical therapist near you, please visit http://www.apta.org/consumer.
The American Physical Therapy Association (http://www.apta.org) is a national professional organization representing more than 70,000 physical therapists, physical therapist assistants, and students. Its goal is to foster advancements in physical therapy practice, research, and education.
American Physical Therapy Association
http://www.apta.org
Is Workers' Comp Fair? Research Finds No Link Between Cash Settlements, Future Impairment
People who receive higher disability ratings for work-related back injuries don't necessarily fare worse over the long term than those who get lower ratings, a Saint Louis University study finds.
The study, which reinforced previous research showing blacks receive less treatment for their back pain than whites, was published online this month in the Journal of Pain. The new research is among the first to examine the relationship between Workers' Compensation settlements for back pain and long-term functional outcomes.
"A disability rating is supposed to reflect the amount of impairment a person has at the time that a case is closed. The presumption is that levels of impairment are stable and related to day-to-day levels of function. I was shocked that the associations between disability rating and subsequent levels of function weren't stronger," said Raymond Tait, Ph.D., professor of psychiatry at Saint Louis University School of Medicine.
Disability ratings also differed between African-Americans and Caucasians. According to Tait, those differences probably reflected differences in treatment: whites were four times more likely to have surgery than blacks. Thos who had surgery received larger settlements for their injuries, Tait said.
"While surgery inflated disability ratings, there appeared not relationship between surgery outcomes and how a person did thereafter," he said.
Tait and colleague John Chibnall, Ph.D., also a professor of psychiatry at Saint Lois University, looked at about 1,500 Missouri workers - 580 African-Americans and 892 Caucasians - whose Workers' Compensation claims for lower back pain were settled between Jan. 1, 2001 and June 1, 2002.
Researchers interviewed the employees 21 months after their settlements about how they were doing. They asked questions about pain intensity, general physical and mental health and whether they currently were working.
Tait and Chibnall said that their findings "raise questions about both the validity and the fairness of the current disability determination program. Disability settlements are designed to give people money toward a fresh start. Those settlements do not appear to reflect the residual levels of disability that people actually experience."
###
Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: cancer, liver disease, heart/lung disease, aging and brain disease, and infectious disease.
Contact: Nancy Solomon
Saint Louis University
The study, which reinforced previous research showing blacks receive less treatment for their back pain than whites, was published online this month in the Journal of Pain. The new research is among the first to examine the relationship between Workers' Compensation settlements for back pain and long-term functional outcomes.
"A disability rating is supposed to reflect the amount of impairment a person has at the time that a case is closed. The presumption is that levels of impairment are stable and related to day-to-day levels of function. I was shocked that the associations between disability rating and subsequent levels of function weren't stronger," said Raymond Tait, Ph.D., professor of psychiatry at Saint Louis University School of Medicine.
Disability ratings also differed between African-Americans and Caucasians. According to Tait, those differences probably reflected differences in treatment: whites were four times more likely to have surgery than blacks. Thos who had surgery received larger settlements for their injuries, Tait said.
"While surgery inflated disability ratings, there appeared not relationship between surgery outcomes and how a person did thereafter," he said.
Tait and colleague John Chibnall, Ph.D., also a professor of psychiatry at Saint Lois University, looked at about 1,500 Missouri workers - 580 African-Americans and 892 Caucasians - whose Workers' Compensation claims for lower back pain were settled between Jan. 1, 2001 and June 1, 2002.
Researchers interviewed the employees 21 months after their settlements about how they were doing. They asked questions about pain intensity, general physical and mental health and whether they currently were working.
Tait and Chibnall said that their findings "raise questions about both the validity and the fairness of the current disability determination program. Disability settlements are designed to give people money toward a fresh start. Those settlements do not appear to reflect the residual levels of disability that people actually experience."
###
Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: cancer, liver disease, heart/lung disease, aging and brain disease, and infectious disease.
Contact: Nancy Solomon
Saint Louis University
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