Check out this website I found at journals.lww.com
Sunday, 14 November 2010
Tuesday, 9 November 2010
Play with your kid, for their mental health's sake
via sciencedaily.com
Clearly there is a huge role for parents in their child's development blended with the genetic and epigenetic influences as the recent New Scientist feature suggests: http://www.newscientist.com/article/mg20827852.500-epigenetics-can-take-us-to...
Chronic Pain: A Disease in its Own Right
Melanie Thernstrom has written a superb book based on a historical, philosophical, and scientific review of pain: The Pain Chronicles: Cures, Myths, Mysteries, Prayers, Diaries, Brain Scans, Healing, and the Science of Suffering. Herself a victim of chronic pain, she brings a personal perspective to the subject and also includes informative vignettes of doctors and patients she encountered at the many pain clinics she visited in her investigations. She shows that medical treatment of pain is suboptimal because most doctors have not yet incorporated recent scientific discoveries into their thinking, discoveries indicating that chronic pain is a disease in its own right, a state of pathological pain sensitivity.
Chronic pain often outlives its original causes, worsens over time, and takes on a puzzling life of its own… there is increasing evidence that over time, untreated pain eventually rewrites the central nervous system, causing pathological changes to the brain and spinal cord, and that these in turn cause greater pain. Even more disturbingly, recent evidence suggests that prolonged pain actually damages parts of the brain, including those involved in cognition.
Sometimes the original problem creates new ones as the patient distorts posture and avoids exercise in an attempt to reduce the pain. In chronic pain, the protective mechanism of avoidance becomes maladaptive. Muscles atrophy from disuse and new sources of pain develop. Jerome Groopman, MD, in The Anatomy of Hope, told how he conquered years of chronic back pain by realizing that his pain was not a warning to avoid further damage but a false message that he could refuse to listen to; with exercise and physical therapy he rebuilt his muscles and became pain-free.
Dr. John Sarno believes that chronic musculoskeletal pain is a manifestation of “tension myositis syndrome” due to repressed negative emotions. He recommends renouncing all treatments, accepting that pain is only in the mind, and resuming normal activities. I don’t accept his psychosomatic premise, but there is a grain of truth in his method. If patients can re-frame their thinking and resume normal activities despite the pain, they are more likely to improve than if they maintain the self-image of a sick, disabled victim.
Distraction is effective in removing the awareness of pain. Thernstrom tells us that as she got better,
I wasn’t aware of being in pain all the time, but whenever I thought about whether I had pain, I always did. There were pain-free moments owing to my being preoccupied — happily or unhappily — with something else, but I was never able to “catch” a pain-free moment and enjoy it, which meant that, in some sense, I was always in pain.
Pain perception in the brain involves two different pain systems: one of pain perception and one of pain modulation. Acute injuries always hurt more later as the modulation effects diminish and the brain releases neurotransmitters into the spinal cord that amplify incoming signals and augment pain. This serves the adaptive purpose of enabling flight at first and then enforcing rest. It is possible to induce complete analgesia in humans and animals by electrically stimulating pain-modulating areas of the brain. Various cognitive and affective states activate the two systems, especially attention and expectation. Simply asking patients to think about their pain activates the pain-perception circuits. Anticipation of a placebo effect causes the pain-modulating release of endorphins in the brain.
One medication requires the placebo effect for all of its effectiveness. An intriguing 1995 clinical trial proved an analgesic called proglumide to be a more effective pain reliever than a placebo when both groups were told they were being given an exciting new painkiller. But then subjects were slipped proglumide without their knowledge, thus ensuring they had no placebo effect, they felt no relief at all. None.
It turns out proglumide enhances the endorphin response by blocking cholecystokinin receptors. Thernstrom speculates that drugs could be designed to enhance or create a placebo effect. Hmm… what would medical ethicists have to say about that? For that matter, how can a treatment still be called a placebo if it is shown to have the effect of producing endorphins in the brain?
Opioids relieve pain, but they are both under-used and over-used. If acute pain were better controlled, fewer patients would develop chronic pain. On the other hand, many chronic pain patients develop opioid-induced hyperalgesia, where their body becomes more sensitive to pain stimuli or even ordinary stimuli; they develop pain in parts of their bodies remote from the original injury site.
Caution is required. Relieving pain sometimes causes harm. A phase 3 study of tanezumab was recently halted by the FDA. Although the drug relieved the pain of osteoarthritis, it also resulted in more joint failure, presumably because there was more wear and tear on the joints when pain was absent.
The Pain Chronicles is a fascinating glimpse into the world of pain sufferers as well as a good overview of our current scientific knowledge. It suggests avenues of investigation that may vastly improve our management of pain. I highly recommend it to anyone who wants to know more about any aspect of the pain experience and the science.
I am always interested in reading and hearing about individual's experiences. This could be a worthwhile insight.
Wednesday, 3 November 2010
Central sensitisation
This new article by one of the most respected academics in pain is an excellent description of the current understanding of this most important concept. A pain mechanism appraoch to the treatment and management of pain seems to be the most sensible.
Woolf (2010)
Abstract
Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.
Woolf (2010)
Abstract
Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.
Glial activation in the rostroventromedial medulla promotes descending facilitation to mediate inflammatory hypersensitivity
Roberts et al. (2009), Eur J Neurosci
Abstract
Substantial evidence shows that activation of glial cells in the spinal cord may promote central sensitization and pain. Descending facilitation from the rostroventromedial medulla (RVM) is a critical component in the maintenance of chronic pain states, although the precise mechanisms through which facilitation maintains pain are unclear. Here, we investigated the possibility that glial activation in the RVM could promote descending facilitation from the RVM in states of inflammatory pain. Peripheral inflammation was induced with carrageenan injected into the hindpaws of male Sprague-Dawley rats, and behavioral responses to noxious thermal and light tactile stimuli were determined. Microinjection of the glial inhibitors minocycline or fluorocitrate, or of the p38 mitogen-activated protein kinase (MAPK) inhibitor SB 203580, produced a significant and time-related attenuation of behavioral hypersensitivity resulting from hindpaw inflammation. Carrageenan-induced inflammation increased immunolabeling for microglia and astrocytes in the RVM, as well as for phosphorylated p38 MAPK. Phosphorylated p38 MAPK was found in microglia and neurons of the RVM. Inflammation-induced microglial and astrocytic activation in the RVM were attenuated by RVM microinjection of the glial inhibitors. The data show that inflammatory pain is associated with glial activation in the RVM that probably participates in driving descending pain facilitation. These findings reveal a novel site of glial modulation of inflammatory pain.
There is huge scientific evidence for the role of the immune system in pain providing forward routes for new thinking in treatment
Abstract
Substantial evidence shows that activation of glial cells in the spinal cord may promote central sensitization and pain. Descending facilitation from the rostroventromedial medulla (RVM) is a critical component in the maintenance of chronic pain states, although the precise mechanisms through which facilitation maintains pain are unclear. Here, we investigated the possibility that glial activation in the RVM could promote descending facilitation from the RVM in states of inflammatory pain. Peripheral inflammation was induced with carrageenan injected into the hindpaws of male Sprague-Dawley rats, and behavioral responses to noxious thermal and light tactile stimuli were determined. Microinjection of the glial inhibitors minocycline or fluorocitrate, or of the p38 mitogen-activated protein kinase (MAPK) inhibitor SB 203580, produced a significant and time-related attenuation of behavioral hypersensitivity resulting from hindpaw inflammation. Carrageenan-induced inflammation increased immunolabeling for microglia and astrocytes in the RVM, as well as for phosphorylated p38 MAPK. Phosphorylated p38 MAPK was found in microglia and neurons of the RVM. Inflammation-induced microglial and astrocytic activation in the RVM were attenuated by RVM microinjection of the glial inhibitors. The data show that inflammatory pain is associated with glial activation in the RVM that probably participates in driving descending pain facilitation. These findings reveal a novel site of glial modulation of inflammatory pain.
There is huge scientific evidence for the role of the immune system in pain providing forward routes for new thinking in treatment
Dysfunction of endogenous pain inhibition during exercise with painful muscles in patients with shoulder myalgia & fibromyalgia
Lannersten & Kosek
Pain 151 (2010) 77-86
The aim of this study was to investigate how exercise influenced endogenous pain modulation in healthy controls, shoulder myalgia patients and fibromyalgia (FM) patients. Twenty-one healthy subjects, 20 shoulder myalgia patients and 20 FM patients, all females, participated. They performed standardized static contractions, that is, outward shoulder rotation (m. infraspinatus) and knee extension (m. quadriceps). Pressure pain thresholds (PPTs) were determined bilaterally at m. infraspinatus and m. quadriceps. During contractions PPTs were assessed at the contracting muscle, the resting homologous contralateral muscle and contralaterally at a distant site (m. infraspinatus during contraction of m. quadriceps and vice versa). Myalgia patients had lower PPTs compared to healthy controls at m. infraspinatus bilaterally (p<0.01), but not at m. quadriceps. FM patients had lower PPTs at all sites compared to healthy controls (p<0.001) and myalgia patients (p<0.001). During contraction of m. infraspinatus PPTs increased compared to baseline at the end of contraction in healthy controls (all sites: p<0.003), but not in myalgia or FM patients. During contraction of m. quadriceps PPTs increased compared to baseline at the end of contraction in healthy controls (all sites: p<0.001) and myalgia patients (all sites: p<0.02), but not in FM patients. In conclusion, we found a normal activation of endogenous pain regulatory mechanisms in myalgia patients during contraction of the non-afflicted m. quadriceps, but a lack of pain inhibition during contraction of the painful m. infraspinatus. FM patients failed to activate their pain inhibitory mechanisms during all contractions.
This is an intreating study that suggests to exercise remote areas of the body can have beneficial effects for myalgia by having a pain relieving effect whereas in fibromyalgia this can aggravate if the intensity is too great. For the latter, a progressive programme built from an individualised baseline would be more beneficial.
Pain 151 (2010) 77-86
The aim of this study was to investigate how exercise influenced endogenous pain modulation in healthy controls, shoulder myalgia patients and fibromyalgia (FM) patients. Twenty-one healthy subjects, 20 shoulder myalgia patients and 20 FM patients, all females, participated. They performed standardized static contractions, that is, outward shoulder rotation (m. infraspinatus) and knee extension (m. quadriceps). Pressure pain thresholds (PPTs) were determined bilaterally at m. infraspinatus and m. quadriceps. During contractions PPTs were assessed at the contracting muscle, the resting homologous contralateral muscle and contralaterally at a distant site (m. infraspinatus during contraction of m. quadriceps and vice versa). Myalgia patients had lower PPTs compared to healthy controls at m. infraspinatus bilaterally (p<0.01), but not at m. quadriceps. FM patients had lower PPTs at all sites compared to healthy controls (p<0.001) and myalgia patients (p<0.001). During contraction of m. infraspinatus PPTs increased compared to baseline at the end of contraction in healthy controls (all sites: p<0.003), but not in myalgia or FM patients. During contraction of m. quadriceps PPTs increased compared to baseline at the end of contraction in healthy controls (all sites: p<0.001) and myalgia patients (all sites: p<0.02), but not in FM patients. In conclusion, we found a normal activation of endogenous pain regulatory mechanisms in myalgia patients during contraction of the non-afflicted m. quadriceps, but a lack of pain inhibition during contraction of the painful m. infraspinatus. FM patients failed to activate their pain inhibitory mechanisms during all contractions.
This is an intreating study that suggests to exercise remote areas of the body can have beneficial effects for myalgia by having a pain relieving effect whereas in fibromyalgia this can aggravate if the intensity is too great. For the latter, a progressive programme built from an individualised baseline would be more beneficial.
Tuesday, 2 November 2010
New Specialist Pain Physio Website
The new website for The Specialist Pain Physio Clinics is now live with information about our services, a regular blog, details about pain and the latest research.
www.specialistpainphysio.com
www.specialistpainphysio.com
Subscribe to:
Posts (Atom)