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
Wednesday, 20 October 2010
The human glucocorticoid receptor: molecular basis of biologic function
Abstract:
The characterization of the subfamily of steroid hormone receptors has enhanced our understanding of how a set of hormonally derived lipophilic ligands controls cellular and molecular functions to influence development and help achieve homeostasis. The glucocorticoid receptor (GR), the first member of this subfamily, is a ubiquitously expressed intracellular protein, which functions as a ligand-dependent transcription factor that regulates the expression of glucocorticoid-responsive genes. The effector domains of the GR mediate transcriptional activation by recruiting coregulatory multi-subunit complexes that remodel chromatin, target initiation sites, and stabilize the RNA-polymerase II machinery for repeated rounds of transcription of target genes. This review summarizes the basic aspects of the structure and actions of the human (h) GR, and the molecular basis of its biologic functions.
Steroids (2010), 75(1):1-12
The characterization of the subfamily of steroid hormone receptors has enhanced our understanding of how a set of hormonally derived lipophilic ligands controls cellular and molecular functions to influence development and help achieve homeostasis. The glucocorticoid receptor (GR), the first member of this subfamily, is a ubiquitously expressed intracellular protein, which functions as a ligand-dependent transcription factor that regulates the expression of glucocorticoid-responsive genes. The effector domains of the GR mediate transcriptional activation by recruiting coregulatory multi-subunit complexes that remodel chromatin, target initiation sites, and stabilize the RNA-polymerase II machinery for repeated rounds of transcription of target genes. This review summarizes the basic aspects of the structure and actions of the human (h) GR, and the molecular basis of its biologic functions.
Steroids (2010), 75(1):1-12
Stress & disorders of the stress system
Chrousos (2009). An excellent article; abstract below:
All organisms must maintain a complex dynamic equilibrium, or homeostasis, which is constantly challenged by internal or external adverse forces termed stressors. Stress occurs when homeostasis is threatened or perceived to be so; homeostasis is re-established by various physiological and behavioral adaptive responses. Neuroendocrine hormones have major roles in the regulation of both basal homeostasis and responses to threats, and are involved in the pathogenesis of diseases characterized by dyshomeostasis or cacostasis. The stress response is mediated by the stress system, partly located in the central nervous system and partly in peripheral organs. The central, greatly interconnected effectors of this system include the hypothalamic hormones arginine vasopressin, corticotropin-releasing hormone and pro-opiomelanocortin-derived peptides, and the locus ceruleus and autonomic norepinephrine centers in the brainstem. Targets of these effectors include the executive and/or cognitive, reward and fear systems, the wake-sleep centers of the brain, the growth, reproductive and thyroid hormone axes, and the gastrointestinal, cardiorespiratory, metabolic, and immune systems. Optimal basal activity and responsiveness of the stress system is essential for a sense of well-being, successful performance of tasks, and appropriate social interactions. By contrast, excessive or inadequate basal activity and responsiveness of this system might impair development, growth and body composition, and lead to a host of behavioral and somatic pathological conditions. Nat Rev Endocrinol 5(7):374-81
All organisms must maintain a complex dynamic equilibrium, or homeostasis, which is constantly challenged by internal or external adverse forces termed stressors. Stress occurs when homeostasis is threatened or perceived to be so; homeostasis is re-established by various physiological and behavioral adaptive responses. Neuroendocrine hormones have major roles in the regulation of both basal homeostasis and responses to threats, and are involved in the pathogenesis of diseases characterized by dyshomeostasis or cacostasis. The stress response is mediated by the stress system, partly located in the central nervous system and partly in peripheral organs. The central, greatly interconnected effectors of this system include the hypothalamic hormones arginine vasopressin, corticotropin-releasing hormone and pro-opiomelanocortin-derived peptides, and the locus ceruleus and autonomic norepinephrine centers in the brainstem. Targets of these effectors include the executive and/or cognitive, reward and fear systems, the wake-sleep centers of the brain, the growth, reproductive and thyroid hormone axes, and the gastrointestinal, cardiorespiratory, metabolic, and immune systems. Optimal basal activity and responsiveness of the stress system is essential for a sense of well-being, successful performance of tasks, and appropriate social interactions. By contrast, excessive or inadequate basal activity and responsiveness of this system might impair development, growth and body composition, and lead to a host of behavioral and somatic pathological conditions. Nat Rev Endocrinol 5(7):374-81
Neuroendocrinology of post-traumatic stress disorder
Pervanidou & Chrousos (2010)
Abstract: Dysregulation of the stress system, including the hypothalamic-pituitary-adrenal (HPA) axis and the locus caeruleus/norepinephrine-sympathetic nervous system (SNS), is involved in the pathophysiology of post-traumatic stress disorder (PTSD), an anxiety disorder that develops after exposure to traumatic life events. Neuroendocrine studies in individuals with PTSD have demonstrated elevated basal cerebrospinal fluid corticotropin-releasing hormone concentrations and contradictory results from peripheral measurements, exhibiting low 24 hours excretion of urinary free cortisol, low or normal circulating cortisol levels or even high plasma cortisol levels. The direction of HPA axis activity (hyper-/or hypo-activation), as evidenced by peripheral cortisol measures, may depend on variables such as genetic vulnerability and epigenetic changes, age and developmental stage of the individual, type and chronicity of trauma, co-morbid depression or other psychopathology, alcohol or other drug abuse and time since the traumatic experience. On the other hand, peripheral biomarkers of the SNS activity are more consistent, showing increased 24h urinary or plasma catecholamines in PTSD patients compared to control individuals. Chronically disturbed hormones in PTSD may contribute to brain changes and further emotional and behavior symptoms and disorders, as well as to an increased cardiometabolic risk. Prog Brain Res. 182:149-60
Abstract: Dysregulation of the stress system, including the hypothalamic-pituitary-adrenal (HPA) axis and the locus caeruleus/norepinephrine-sympathetic nervous system (SNS), is involved in the pathophysiology of post-traumatic stress disorder (PTSD), an anxiety disorder that develops after exposure to traumatic life events. Neuroendocrine studies in individuals with PTSD have demonstrated elevated basal cerebrospinal fluid corticotropin-releasing hormone concentrations and contradictory results from peripheral measurements, exhibiting low 24 hours excretion of urinary free cortisol, low or normal circulating cortisol levels or even high plasma cortisol levels. The direction of HPA axis activity (hyper-/or hypo-activation), as evidenced by peripheral cortisol measures, may depend on variables such as genetic vulnerability and epigenetic changes, age and developmental stage of the individual, type and chronicity of trauma, co-morbid depression or other psychopathology, alcohol or other drug abuse and time since the traumatic experience. On the other hand, peripheral biomarkers of the SNS activity are more consistent, showing increased 24h urinary or plasma catecholamines in PTSD patients compared to control individuals. Chronically disturbed hormones in PTSD may contribute to brain changes and further emotional and behavior symptoms and disorders, as well as to an increased cardiometabolic risk. Prog Brain Res. 182:149-60
Sunday, 17 October 2010
Positve mood & thinking - the benefits
Ask most people and of course they would agree that positive thinking is going to make life better. Asking people how often they spend time in a positive mood can be an interesting self-reflective exercise. It all seems quite obvious really, but it does seem that in many cases negative thinking and rumination prevails. An increasingly popular method of dealing with this way of living is the Buddhist approach of mindfulness. Maintaining awareness of the present moment without judgement is the essence of this practice underpinned by regular meditation. The argument is that we spend far too much time pondering on the past (it's too late, nothing can be done about that) or the future (that has not happened yet) and not enough in appreciating the now. The mind is blamed for taking us off into past events or into scenarios that have not even occurred (e.g. the argument that you are going to have with the boss). How about reducing this mind activity?
Research shows us that positive moods increase our visual attention aiding the collection of information about the world around us, improves creativity, social skills, ability to deal with criticism, our verbal reasoning and problem-solving ability. Practicing postive thinking regualarly seems to build our resilience and ability to gain benefit. There is likely to be a genetic disposition (accounting for around 50% of the variability) but we also have the ability to change through learning and adaptation.
It is likely that personality type will affect the way in which you create your positive mood. Therefore trying different methods is best. Some ideas to change your mood for the better include challenging your negative thoughts (cognitive restructuring), meditation and developing relationships with family and friends.
Those suffering pain often present with a negative mindset that is understandable. Working to restructure the beliefs and thoughts and subsequently how the pain is interpreted is an excellent way of improving control. At Specialist Pain Physio we work closely with patients to lessen the impact of pain and suffering with techniques that increase positivity for the aforementioned reasons. Additionally it has a good effect upon the immune system that is very much involved in pain. It takes time and effort as part of the treatment and rehabilitation programme for pain, chronic pain & injury.
Reading
Be Happy, Dan Jones. New Scientist 25th Sept 2010
Research shows us that positive moods increase our visual attention aiding the collection of information about the world around us, improves creativity, social skills, ability to deal with criticism, our verbal reasoning and problem-solving ability. Practicing postive thinking regualarly seems to build our resilience and ability to gain benefit. There is likely to be a genetic disposition (accounting for around 50% of the variability) but we also have the ability to change through learning and adaptation.
It is likely that personality type will affect the way in which you create your positive mood. Therefore trying different methods is best. Some ideas to change your mood for the better include challenging your negative thoughts (cognitive restructuring), meditation and developing relationships with family and friends.
Those suffering pain often present with a negative mindset that is understandable. Working to restructure the beliefs and thoughts and subsequently how the pain is interpreted is an excellent way of improving control. At Specialist Pain Physio we work closely with patients to lessen the impact of pain and suffering with techniques that increase positivity for the aforementioned reasons. Additionally it has a good effect upon the immune system that is very much involved in pain. It takes time and effort as part of the treatment and rehabilitation programme for pain, chronic pain & injury.
Reading
Be Happy, Dan Jones. New Scientist 25th Sept 2010
Friday, 15 October 2010
Using langauge in rehabilitation
One of the most interesting aspects to keeping an on current science is the application of the findings to the rehabilitation process. A recent article in the New Scientist by David Robson discussed the effects of language upon perception. It seems that the words we use have an impact upon what we see. The example used describes words related to up and down movements such as 'climb' and 'drip' have an impact upon the eye's sensitivity to vertical motion. This is based upon the work of Gabriella Vigliocco at UCL who found that individuals were more likely to determine the direction of moving dots when accompanied by a verb that described the movement.
Robson suggests that words prime the visual system, further evidenced by a studies that show when we hear a word we are more able to find obscured images and letters. Creating a mental image from the word may allow us to identify the object more rapidly. It seems that the sounds could also be important and further enhance our perception.
Clearly there is a huge integration and scrutiny of the massive input of information from within and around us to create our sense of self. Many people have spoken about this including Melzack who describes the sentient hub and Bud Craig who discusses interoception. Our representation is known to be altered with pain and injury as demonstrated in many fMRI studies but also from descriptions that patients give of their experience of their body. For example, joints feel 'out of place' and hands feel bigger ('sausage fingers'). Lorimer Moseley has done some interesting work where he asked individuals with chronic low back pain to draw their perception of their trunk and spine. The results demonstrated altered awareness and quite distorted images.
I see a role for perceptual tasks within a rehabilitation programme and most definitely in a multimodal sense. Working with our mental representation of the body whilst performing motor control exercises seems to enhance the quality of the movement. We know about graded motor imagery and imagined movements and how this can be really effective as part of a programme of care for complex regional pain syndrome (CRPS). Applying these principles to altered perception of body shape, size and position with mental imagery is an interesting application and potentially reconfiguring the neuromatrix. Adding language and sounds to the process may enhance this process on the basis that any additional and 'normal' input can reduce the threat value and restore function. Clearly this need to be studied appropriately to discover whether the idea is tangible, however in the meantime, if the individual's perception of their body and its motion can be enhanced with a few simple words, it is a simple application.
The Voice of Reason. Robson, D. New Scientist 4th September 2010
Robson suggests that words prime the visual system, further evidenced by a studies that show when we hear a word we are more able to find obscured images and letters. Creating a mental image from the word may allow us to identify the object more rapidly. It seems that the sounds could also be important and further enhance our perception.
Clearly there is a huge integration and scrutiny of the massive input of information from within and around us to create our sense of self. Many people have spoken about this including Melzack who describes the sentient hub and Bud Craig who discusses interoception. Our representation is known to be altered with pain and injury as demonstrated in many fMRI studies but also from descriptions that patients give of their experience of their body. For example, joints feel 'out of place' and hands feel bigger ('sausage fingers'). Lorimer Moseley has done some interesting work where he asked individuals with chronic low back pain to draw their perception of their trunk and spine. The results demonstrated altered awareness and quite distorted images.
I see a role for perceptual tasks within a rehabilitation programme and most definitely in a multimodal sense. Working with our mental representation of the body whilst performing motor control exercises seems to enhance the quality of the movement. We know about graded motor imagery and imagined movements and how this can be really effective as part of a programme of care for complex regional pain syndrome (CRPS). Applying these principles to altered perception of body shape, size and position with mental imagery is an interesting application and potentially reconfiguring the neuromatrix. Adding language and sounds to the process may enhance this process on the basis that any additional and 'normal' input can reduce the threat value and restore function. Clearly this need to be studied appropriately to discover whether the idea is tangible, however in the meantime, if the individual's perception of their body and its motion can be enhanced with a few simple words, it is a simple application.
The Voice of Reason. Robson, D. New Scientist 4th September 2010
Thursday, 14 October 2010
The Pain Neuromatrix
The pain neuromatrix was a concept that came from Ron Melzack who partnered Pat Wall in developing our understanding of pain in a modern sense. Moving on from the Pain Gate Theory, Melzack described a widespread distribution of neurons (brain cells) that imprint a 'neurosignature' upon nerve impulse patterns that pass through the matrix. The neurosignature creates our experience of self including movement and pain. We have an overall neurosignature for our sense of self and subsets of patterns that give us unique experiences such as pain, warmth and other qualities that are produced by these modules.
Melzack (2004) describes four components of this concept including the 'body self' where we have the experience of ourselves as a result of the unification of information from the body, the processing and synthesis of the signature, the sentient neural hub that converts the processes into awareness and the subsequent action to achieve the desired goal. In terms of pain as an output from the brain, this would be the end result of an activation of the pain neuromatrix with a characteristic signature, the pain signature. Pain is part of a multi system response to a perceived threat. There are many inputs to the brain that can trigger the pain neuromatrix including movement, thoughts, emotions, touch, memories, fear and visual stimuli to name but a few. The reason that these stimuli can trigger a pain response is in essence due to a perceived threat but also due to the fact that the widespread neurones that make up the pain matrix are involved in all of the aforementioned activities but are also part of the pain neuromatrix.
The neuromatrix model provides an excellent explanation for higher level parallel processing of information and the output that occurs as a smooth mechanism creating our conscious experience. Melzack points out that the matrix is genetically determined and moulded by sensory input. This makes sense as we continue to learn as we have new experiences, the nervous system being incredibly plastic (Doidge, 2007). Describing this to patients allows them to understand why there are so many influences upon the pain that they suffer, even if they are unaware of the exact stimulus. In many cases of chronic pain the patient describes an increase in symptoms despite no change in their daily routine. The neuromatrix allows us to look at some of the possible reasons for a flare-up and give reassurance that they have done no 'damage' in the case that there has been no further injury. Empowering the individual with the knowledge that hurt does not mean harm can be extremely useful in many cases.
Evolution of the neuromatrix theory of pain. The Prithvi Raj Lecture: Presented at the Third World Congress of World Institute of Pain, Barcelona 2004. Pain Practice, 5(2), 85-94
The brain that changes itself. Doidge, N. (2007)
Melzack (2004) describes four components of this concept including the 'body self' where we have the experience of ourselves as a result of the unification of information from the body, the processing and synthesis of the signature, the sentient neural hub that converts the processes into awareness and the subsequent action to achieve the desired goal. In terms of pain as an output from the brain, this would be the end result of an activation of the pain neuromatrix with a characteristic signature, the pain signature. Pain is part of a multi system response to a perceived threat. There are many inputs to the brain that can trigger the pain neuromatrix including movement, thoughts, emotions, touch, memories, fear and visual stimuli to name but a few. The reason that these stimuli can trigger a pain response is in essence due to a perceived threat but also due to the fact that the widespread neurones that make up the pain matrix are involved in all of the aforementioned activities but are also part of the pain neuromatrix.
The neuromatrix model provides an excellent explanation for higher level parallel processing of information and the output that occurs as a smooth mechanism creating our conscious experience. Melzack points out that the matrix is genetically determined and moulded by sensory input. This makes sense as we continue to learn as we have new experiences, the nervous system being incredibly plastic (Doidge, 2007). Describing this to patients allows them to understand why there are so many influences upon the pain that they suffer, even if they are unaware of the exact stimulus. In many cases of chronic pain the patient describes an increase in symptoms despite no change in their daily routine. The neuromatrix allows us to look at some of the possible reasons for a flare-up and give reassurance that they have done no 'damage' in the case that there has been no further injury. Empowering the individual with the knowledge that hurt does not mean harm can be extremely useful in many cases.
Evolution of the neuromatrix theory of pain. The Prithvi Raj Lecture: Presented at the Third World Congress of World Institute of Pain, Barcelona 2004. Pain Practice, 5(2), 85-94
The brain that changes itself. Doidge, N. (2007)
Monday, 4 October 2010
Pain Medication
Below are some of the common medications that can be prescribed by your doctor or consultant
Paracetemol
This is a simple analgesic that can be beneficial for mild pain. Widely available and safe within prescribed doseages, paracetemol probably works by indirectly inhibiting enzymes known as cyclooxygenases (COX-1 & COX-2). In addition to analgesic effects, there is the well-known antipyretic action (reduces temperature).
NSAIDs (Non-steroidal anti-inflammatory drugs), e.g. neurofen, ibuprofen, diclofenac
Commonly prescribed for inflammatory pain, NSAIDs are active in the inhibition of the COX exnzymes. This has been demonstrated scientifically with both COX-1 and COX-2 enzymes although many anti-inflammatories are not able to be selective and hence inhibit both. This is the reason for the well-documented side-effects such as gastric irritation and renal failure. Your doctor will advise you on the use of these drugs according to your current medical condition.
COX-1 is expressed constitutvely and gives rise to prostaglandins which have a a role in normal cell function. COX-2 is expressed when an inflammatory process is underway to produce more prostanoids. Inhibiting the prostaglandin activity by the use of NSAIDs means that normal physiology is affected and therefore the adverse effects can be experienced.
Prostaglandins are metabolised from arachidonic acid by the COX enzymes following tissue damage. NSAIDs act by inhibiting these enzymes and therefore inhibit prostaglandin production. Prostaglandins have the ability to sensitise nerve endings by altering the membrane excitability, therefore the nerve becomes more likely to send 'danger' signals to the spinal cord. There are other breakdown products that have this action, but prostaglandins are one of the best understood. Following sensitisation, pripheral nerves become more respondant to mechanical, chemical and thermal stimuli, hence the reason for pain when we press on or near injured tissue (mechanical), why it is painful to take a shower with sunburn (temperature) and why exercise can be painful (release of acids, i.e. chemical).
Opioids (e.g. morphine, tramadol, codeine, dihydrocodeine, pethidine)
Opioids have been studied in detail over the last 30 years and now we have a great deal of knowledge about how they work and how they affect the nervous system. The discovery of the opioid receptor (like a lock that a specific key would fit, the key being the opiate drug and the lock being the receptor) and where these receptors are situtated. Knowing that there are receptors in the brain for example, means that we can explain the feelings of drowsiness and cognitive impairment (ability to concentrate).
Once an opiate has bound upon a receptor, it inhibits several channels that cross the nerve membrane (calcium and potassium) because it is linked to these channels. The channels allow for the passing of specific ions which alter the excitability of the nerve (i.e. become more excited and sensitive with a change in the balance of flow of these ions). There are further effects within the cell that reduce excitability of the nerve (inhibition of several pathways of activity that lead to increased excitability; cAMP & MAP kinase cascades).
Anticonvulsants (e.g. carbamazepine, gabapentin, pregabalin)
Anticonvulsants are used to treat neuropathic pain (see page on pain types) that is underpinned by changes in nerve excitability. This is as a result of an alteration in the channel (sodium & calcium) expression upon the nerve membrane (see opioids for brief explanation of channels) that is similar to changes that occur in epilepsy (this does not mean that you have epilepsy just because there are some similarities in channel changes).
Gabapentin decreases the on going firing of signals that are generated through sodium channel activity, inhibits calcium channels and acts with the NMDA receptor. The end result is reduced excitability and less signalling to the spinal cord from the periphery.
Carbamazepine is related to tricyclic antidepressants. It inhibits noradrenaline and has an effect upon sodium channels therefore has inhibitory effects by reducing spontaneous nerve activity (a feature of neuropathic pain) and promoting descending inhibition (signals descend from higher levels, brain & brain stem, to inhibit ascending danger signals).
Pregabalin has a similar action to gabapentin. It has been shown to be effective in diabetic neuropathy and postherpetic neuralgia.
Antidepressants (e.g. tricyclics, SSRIs; amitriptyline, fluoxetine, citalopram, paroxetine)
Antidepressants have been discovered to provide pain relief by activating the descending pain-inhibiting system (brain stem to spinal cord). This includes an endorphin release link between the periaqueductal gray (PAG) and the raphe nucleus and a serotonergic link between the raphe nucleus and the dorsal horn of the spinal cord. There is also a noradrenaline pathway from the locus coeruleus to the spinal cord. The most effective drugs appear to be those that have a combined effect upon both the serotonergic and noradrenaline pathways.
Antidepressants are effective in the treatment of neuropathic pain, relieving the stabbing and steady pains. There are side-effects that can be experienced. Your doctor should tell you about the dosage and how the drug is best taken.
Thursday, 30 September 2010
Post-surgical inflammatory neuropathy
Post-surgical inflammatory neuropathy has been studied by these authors as they felt that other mechanisms maybe at play other than the usual mechanical factors (stretch, compression, contusion, transection). They analysed the clinical features, nerve conduction, imaging and biopsy of the nerves demonstrating some interesting findings indicative of an inflammatory-immune response. For example, Staff et al. (2010) found increased nerve size, abnormal biopsy (increased epineural perivascular lymphocyte inflammation, microvasculitis, ischaemic nerve injury and axon degeneration). Those treated with immunotherapy showed good improvements in pain and nerve function supporting the notion of an immune response.
Typically this kind of neuropathy is found remote to the surgical site and presents at a median time of 2 days (0-30 range). This does not fully explain a presentation that occurs on the same limb.
Overall this study suggests that the inflammatory-immune response is not uncommon and should be considered as a mechanism to guide treatment. The authors also point out that it may be difficult to distinguish between a mechanical cause and an inflammatory cause and therefore a biopsy would be required to confirm. Of course there could be concurrent mechanisms that we know occur in LBP.
Typically this kind of neuropathy is found remote to the surgical site and presents at a median time of 2 days (0-30 range). This does not fully explain a presentation that occurs on the same limb.
Overall this study suggests that the inflammatory-immune response is not uncommon and should be considered as a mechanism to guide treatment. The authors also point out that it may be difficult to distinguish between a mechanical cause and an inflammatory cause and therefore a biopsy would be required to confirm. Of course there could be concurrent mechanisms that we know occur in LBP.
Tuesday, 28 September 2010
How to be happy
Editorial: Don't get too happy
It's good for your health, it makes you smarter – and our brains are hard-wired for it. New Scientist counts our reasons to be cheerful
DOOM and gloom are the order of the day across most of the western world. Economies are faltering, the cost of living is going up and many people's real income is falling. For some, unemployment is a reality now or in the near future. If the pursuit of happiness is supposed to be one of our goals, prospects appear bleak.
Take a closer look, and it isn't that simple. In fact, economic hard times have little impact on how happy most people feel. Indeed, it would appear that we humans are built to experience happiness, and understanding why is helping us work out what enhances our feelings of well-being. It even points to ways we can adapt to cope with the hardships the recession may bring, and keep smiling whatever happens.
One thing that is clear is that once life's basics are paid for, the power of money to bring happiness is limited. In fact, it can be positively harmful to our sense of well-being. Jordi Quoidbach of the University of Liège, Belgium, and colleagues recently asked a group of people to taste a piece of chocolate in their laboratory. They found that the wealthier members of the group spent less time savouring the experience, and reported enjoying the chocolate less than the subjects who weren't so well off. The same was also true of one group in a separate experiment. This time, half the people had been primed with images of money before they tasted the chocolate. These participants enjoyed the tasting less than a group who had not seen the images, suggesting that just the thought of money is enough to stem our enjoyment of life's simple pleasures (Psychological Science, vol 21, p 759).
So just what is it that makes us happy? Happiness can take the form of many different positive emotions (See "Happiness is..."), and some hints of what makes us happy may come from work that questions why these emotions first evolved. The answer isn't as obvious as it is in the case of negative emotions. These are clearly beneficial in the rough and tumble of survival: anger readies us to fight an opponent, fear makes us run away from danger, and disgust steers us away from contaminated foods and other sources of infection. Although there is no shortage of evidence that feelings of pleasure - obtained by finding a tasty meal or a sexy mate, for example - are important in rewarding and consolidating beneficial behaviours, it is harder to explain how the more diffuse positive emotions such as awe, hope or gratitude evolved.
This troubled psychologist Barbara Fredrickson of the University of North Carolina at Chapel Hill, so she started looking for evolutionary benefits that pleasure might confer. "I thought there must be more to it than this," she recalls.
Fredrickson's "broaden and build" theory proposes that happiness and similar positive states of mind improve our cognitive capacities while we are in safe situations, allowing us to build resources around us for the long term. That's in marked contrast to the effects of negative emotions like fear, which focus our attention so we can deal with short-term problems. "Positive feelings change the way our brains work and expand the boundaries of experience, allowing us to take in more information and see the big picture," Fredrickson argues.
Positive feelings change the way our brains work, allowing us to take in more informationSince she proposed it in 1998 in the Review of General Psychology (vol 2, p 300), her theory has gathered a wealth of experimental support. Eye-tracking and brain-imaging experiments, for example, have revealed that positive moods increase and broaden the scope of visual attention, helping the brain gather more information.
A happy solution
Feeling good has also been shown to improve people's creativity and ability to solve problems. In one experiment, subjects were shown a video of comedy bloopers to lighten their mood, before being presented with a practical problem involving a box of matches, a box of tacks and a candle. They were told to attach the candle to a pinboard in such a way that wax didn't drip on the floor (the solution is to use the matchbox as a plinth for the candle). The experimenters found that people who had viewed the comedy clips were more likely to solve the problem than controls who saw a mathematics documentary intended to put them in a more neutral mood (Journal of Personality and Social Psychology, vol 52, p 1122).
Other experiments have found that a good mood improves people's verbal reasoning skills (Proceedings of the National Academy of Sciences, vol 104, p 383). And various studies have shown that when people are in a good mood, their social skills improve: they become more gregarious and trusting of others, and deal more constructively with criticism.
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Optimistic Twaddle?
Tue Sep 28 21:29:48 BST 2010 by Cannonfodderson
Here we have some 'cheer up your not dead yet' kind of optimistic nonsense and yet there's another article on your website saying there's only 5 billion years till the end of the Universe.
Optimism ? I'm not too happy about that
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How old do you feel?
We all know of people who look fantastic ‘for their age’. How do some individuals achieve this status whilst others feel twice their age? There are a number of physical and psychological factors that affect the process of ageing such as general health and wellbeing, disease and our own perception of our age. It is this latter point that we shall focus upon with a growing body of scientific literature identifying the very real physiological links between thoughts, beliefs and the physical body.
Beliefs are grooved through our upbringing and molded by experience. Behaviours are driven by our beliefs and therefore the choices we make depend upon what we believe to be ‘true’. The importance of this in terms of ageing is that if we believe that we are ‘old’, ‘past it’ or ‘getting on a bit’, then typically the way that we go about our business will reflect this attitude. This of course includes our outward appearance to the world. Believing that you are ‘old’ may lead to the choice of clothing that supports this belief rather than considering an outfit that enhances your positive features and gives you a sense of femininity, glamour or sexiness.
Age can be noted in three ways, chronologically, physiologically and psychologically. Chronological age is the actual number of years that you have been alive, physiological age is the age of your organs and tissues and psychological age is your own perception of your age. The former is clearly unchangeable, however physiological and psychological ages vary according to our health. For example, smoking, drinking and a lack of exercise will have a detrimental effect upon our organs and tissues and hence the physiological ages of these structures. Interestingly, psychological age has an effect upon the physiology of the body as proven by a famous study completed in 1979. In placing individuals in a 1950s environment their measurable health parameters changed for the better, including eyesight. These individuals became ‘younger’ by manipulating the environment to alter their perception of the era.
So what does this mean? Essentially we can affect our health by feeling younger, changing our thought patterns and our beliefs. This is really very exciting as there are practical ways of becoming healthier and enjoying life to the full by changing our thinking and perception of ourselves. A makeover and styling session that optimises your look will have a significant impact upon your perception of who you are including how old you feel. Combining this with an exercise programme and healthy diet and you can really feel and look different. We know that exercise makes your brain fitter and more capable of concentrating, learning, remembering, reverses some of the effects of ageing by promoting the growth of new brain cells and improves mood. There’s no time like the present to ‘grow younger’.
See NHJ Style website: click here
Clinical Investigation of Pain-related Fear and Pain Catastrophizing for Patients With Low Back Pain
Check out this website I found at pdfs.journals.lww.com
Useful measures to identify factors that can affect outcomes: FABQ-PA & PCS
How injured nerves grow themselves back
via sciencedaily.com
Good new information about how injured nerves grow back, in particular identifying Schwann cell and fibroblast activity and inter-communication.
Monday, 27 September 2010
Pain Physio Tweeting
PAINPHYSIO ON TWITTER
Having dabbled lightly in social media, my interest in Twitter was first aroused by hearing Aggers and Bumble talk of ‘tweeting’ during a test match. Wondering what it was all about, I thought I would check out this phenomena and here we are some 450 tweets later. In fact, Twitter is a really good way of passing on information in a quick and ‘no-fuss’ way, either making a brief comment or linking to a page on the web. If you take a moment and click on link above you will be able to see that the vast proportion of the painphysio tweets relate to pain, science, health and medicine that is relevant to clients and health professionals.
Can't focus? Maybe it's the wrong time of month, finds estrogen study on attention and learning
via sciencedaily.com
Pain is influenced by hormone activity. Focus and concentration are affected by pain. It is good to think about these interrelations and how we can consider our treatments in response. If pain is amplified at certain times in the cycle and focus is a problem at particular points or when in pain, education can be tailored and exercise programmes prescribed accordingly.
Emotional and Neuropsychological Profiles of Children With Complex Regional Pain Syndrome Type-I in an Inpatient Rehabilitation Setting
Check out this website I found at pdfs.journals.lww.com
Expected findings from clinical experience, good to quantify.
Avatar therapy: From couch to cyberspace
Psychotherapy in a virtual world has its advantages – particularly if the real world is what you can't cope with
BY MY fourth interview, I'd developed a checklist to use before each meeting. For starters, I would make sure I had grown some hair. I'd also check that I was fully clothed - I had learned the hard way about that one. Only then would I teleport to the interview, hoping that this time my avatar wouldn't materialise in anyone's lap.
Welcome to Second Life, a virtual world with almost 20 million players globally, where the avatars - digital stand-ins for the players - create everything around them. Every cobbled street, every tree swaying in the wind, even the wind itself, is the product of someone's imagination.
For some users, though, this isn't merely a game. It is precisely this ability to construct and control a virtual environment that is creating a new branch of psychotherapy - avatar therapy - in which therapists interact with their clients avatar to avatar.
On the face of it, this might sound like a pale imitation of a real-life therapy session. Yet its proponents say avatar therapy has some unique advantages that take psychotherapy to the next level. In Second Life, therapy sessions are not confined to the therapist's virtual office; they can also involve role-play scenarios to allow the patient to practise their newly learned coping skills in virtual environments tailored to their needs. All the while the therapist gives real-time feedback, like a medically qualified Jiminy Cricket.
Launched in 2003, Second Life was one of the first virtual worlds known as massively multiplayer online games. It was designed not for fighting monsters, but for people to socialise and, increasingly, emulate real life. Musicians have concerts, artists display their work and scientists go to meetings. People work, learn and connect in these virtual worlds. So can they be used for healing too?
As a technophile, I love the idea; as a psychotherapist used to working the old-fashioned way, I had reservations. So I decided to meet some of the advocates of virtual therapy in their own domain, avatar to avatar, to see if they could address my concerns.
One of my first interviews was with Dick Dillon, a real-life psychotherapist with Preferred Family Healthcare, a Missouri-based non-profit organisation that also leads the field of virtual therapy. In Second Life, Dillon's avatar is a bald, square-jawed hunk with a passing resemblance to Bruce Willis. He took me through a typical therapy session.
Talking by voice chat or instant messaging, you and your therapist may decide it is time to revisit the site of a traumatic event - a car crash, say. But in real life it is too far away, or perhaps you don't yet feel happy driving. No problem: your therapist builds, or "rezzes", the scene in a matter of minutes. Soon you are driving on a familiar road, with a steep bend similar to the one that you lost control on in the rain. As you approach the turn, your anxiety increases and your breaths become faster.
The therapist coaches you, reminding you of symptom-management techniques. If it all becomes too much, they zap you instantly back into the office.
According to Dillon, this set-up lets the therapist give real-time feedback while providing an experience that feels genuine, yet takes place in the safe environment of a simulation. The emotions are real. The rewards are real. Only the location is fake.
The emotions are real. The rewards are real. Only the location is fake"When the brain sees a 3D object in real life it converts it to a 2D object in the visual cortex," says Jeremy Bailenson, head of the Virtual Human Interaction Lab at Stanford University in California. Perhaps that's why a virtual scene can still provoke a strong psychological reaction, he says.
Phobia exposure
One of the first applications of avatar therapy was in treating social anxiety disorder, a crippling shyness that can confine people to their homes. James Herbert, head of the anxiety treatment and research programme at Drexel University in Philadelphia, Pennsylvania, was among the first wave of researchers to investigate avatar therapy. Encouragingly, clients generally rated the treatment highly, though there were exceptions. "Some patients and therapists reported frustration with not being able to see the individual's face," he says, and sometimes technical difficulties interrupted the sessions.
Avatar therapy has also helped people with phobias. In real life, the usual treatment is to gradually expose people to the source of their fear, but this can sometimes be difficult. An avatar therapist can introduce the phobia source while remaining in complete control, scaling the experience up or down according to the client's reaction.
In fact, many of the conditions treated by face-to-face talk therapy can also be treated virtually, including depression and anxiety. Avatar therapy is proving useful for more diverse conditions too, such as traumatic brain injury, schizophrenia and Asperger's syndrome. So far studies have shown similar success rates to traditional therapy for social anxiety (Cyberpsychology & Behavior, vol 8, p 76) and post-traumatic stress disorder (Cyberpsychology, Behavior, and Social Networking, vol 13, p 3). Dillon's team will soon publish a study showing its effectiveness in drug and alcohol addiction.
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Count Me In. . . World.
Sat Sep 25 03:33:52 BST 2010 by Rick Schettino
http://futuretimes.netI really can't wait to see where all this is going. virtual worlds have not caught on as fast as I thought they would, but it's great for this kind of stuff. I'm a life coach and coach for people who want to be self-employed and I can certainly think of creative ways to incorporate SL into a session and I expect to be offering lectures in Second Life some day. Perhaps when I can get it on an iPad with a cam
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Interesting concept, may allow for 'conversations' that would not otherwise take place face to face. Cannot see this working for physical therapy....virtual massage & manipulation..mmm
The Development of Sensory Hypoesthesia After Whiplash Injury
Check out this website I found at journals.lww.com
Possibility to identify those at risk of poor recovery with these tests: vibration, electrical & heat stimuli, quite simple in the clinic
Wednesday, 22 September 2010
Spinal cord
My 2-year old daughter painted a spinal cord for me yesterday. Never too early to start biology! (Actually it is a butterfly)
Tuesday, 21 September 2010
What's in a name? The words behind thought
You think more words than you speak – perhaps because language really does shape the way we navigate the world
THERE I go again, talking to myself. Wherever I am, and whatever I'm doing, words bounce around my head in an incessant chatter. I am not alone in my internal babbling. Measuring the contents of people's minds is difficult, but it seems that up to 80 per cent of our mental experiences are verbal. Indeed, the extent of our interior monologue may vastly exceed the number of words we speak out loud. "On average, 70 per cent of our total verbal experience is in our head," estimates Lera Boroditsky of Stanford University in California. The sheer volume of unspoken words would suggest that language is more than just a tool for communicating with others. But what else could it be for?
One answer to that question is emerging: language helps ...
I found this article really interesting and potentially applicable in the clinic. Simply asking the patient to name the body part that they are about to move or exercise could enhance their perception. Increasing normal feedback is a rehabilitation aim, either verbally from the therapist or by vision via a mirror, but using the patient's own language maybe we can engage other higher processing systems top-down.
Thursday, 16 September 2010
Heart disease-depression 'danger'
via bbc.co.uk
This is a finding to be considered when discussing co-existing & past medical histories with patients. Physios are in a good position to identify risk factors when looking at the patient's health status.
Aerobic exercise relieves insomnia
via sciencedaily.com
Regular exercise has many benefits and here is one more. Reading John Ratey's book (Spark) gives a great overview of the advantages that include musculoskeletal health, cardiovascular health and the release of chemicals in the brain that nurture brain cells. This latter activity increases our capacity to learn, remember and feel good to name but a few benefits.
Royal Mail celebrates British medical and scientific breakthroughs
I've never been a stamp collector, but if I was, these would be a definite feature!
Interleukin-6 Levels in Tension Headache Patients
Check out this website I found at journals.lww.com
There is so much data supporting the role of the immune system in pain that we are obliged to consider this in our on-going education and reasoning as physiotherapists. We must understand the modern concepts and how we can influence the immune system in our approach and what we ask patients to do. We have an impact on the immune system at every interaction and of course this can be positive or negative.
Religion causes a chronic biasing of visual attention
Perhaps any life philosophy that we hold will have the same impact, not just a particular region.
Fart sniffer to hunt for life on Mars
IF THERE'S life on Mars, we might smell it before we see it. A chemical involved in bad breath and flatulence in humans could lead us to alien microbes on the Red Planet.
The sulphur-containing molecule methyl mercaptan is naturally produced in significant quantities on Earth only by microbes, including some that make their pungent presence known in the human body. NASA's next Mars rover is highly sensitive to the smelly chemical, which could betray the presence of Martian microbes, says Steven Vance of NASA's Jet Propulsion Laboratory in Pasadena, California.
The instrument in question is the Tunable Laser Spectrometer, which will fly on the Curiosity rover - set to land on Mars in 2012. TLS was designed to analyse the carbon isotopes in Mars's methane to search for signs that the gas has a biological origin. But the isotope tests might produce ambiguous results, so finding methyl mercaptan would help bolster the case for Martian microbes, Vance says. TLS should be able to detect the gas at concentrations below 100 parts per billion, according to his team's tests on a similar spectrometer (Planetary and Space Science, DOI: 10.1016/ j.pss.2010.08.023).
The rover should be able to detect the biomarker gas at concentrations below 100 parts per billionThe researchers are also planning to check TLS's sensitivity to other gases produced by terrestrial microbes, like ethane. "We're demonstrating its ability to look at additional biomarkers and hopefully that will help us in our search for life," Vance says.
Kenneth Nealson at the University of Southern California in Los Angeles, who was not involved in the study, says finding several potential indicators of life in the same place would make it a good target for follow-up missions. "I think you'd get pretty excited," he says. "You'd want to make sure that the next lander would spend time at that site."
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Nice work if you can get it!
Thursday, 9 September 2010
Learning tricks
Benedict Carey does a nice summary of what we do and don't know about different approaches to enhancing learning.
Take the notion that children have specific learning styles, that some are “visual learners” and others are auditory; some are “left-brain” students, others “right-brain.” In a recent review... in the journal Psychological Science in the Public Interest, a team of psychologists found almost zero support for such ideas...Ditto for teaching styles...Some excellent instructors caper in front of the blackboard like summer-theater Falstaffs; others are reserved to the point of shyness...the common threads between teachers who create a constructive learning atmosphere have not been determinedIn recent years, cognitive scientists have shown that a few simple techniques can reliably improve what matters most: how much a student learns from studying…For instance, instead of sticking to one study location, simply alternating the room where a person studies improves retention. So does studying distinct but related skills or concepts in one sitting, rather than focusing intensely on a single thing.
Varying the type of material studied in a single sitting — alternating, for example, among vocabulary, reading and speaking in a new language — seems to leave a deeper impression on the brain than does concentrating on just one skill at a time. Musicians have known this for years, and their practice sessions often include a mix of scales, musical pieces and rhythmic work. Many athletes, too, routinely mix their workouts with strength, speed and skill drills.
When the neural suitcase is packed carefully and gradually, it holds its contents for far, far longer. An hour of study tonight, an hour on the weekend, another session a week from now: such so-called spacing improves later recall…cognitive scientists see testing itself — or practice tests and quizzes — as a powerful tool of learning, rather than merely assessment. The process of retrieving an idea is not like pulling a book from a shelf; it seems to fundamentally alter the way the information is subsequently stored, making it far more accessible in the future.
None of ... these techniques — alternating study environments, mixing content, spacing study sessions, self-testing or all the above — will turn a grade-A slacker into a grade-A student. Motivation matters.
In terms of modern physiotherapy I feel that we are teaching clients/patients new skills (physical and psychological) and providing the body with the opportunity to learn. The main principles outlined in this blog are applicable to the clinic:
1. alternating study environments, 2. mixing content, 3. spacing study sessions, 4.self-testing all with a healthy dose of motivation. Translated into the clinic perhaps we should think about: 1. changing treatment areas (rooms, gym etc), 2. using a range of interventions (although this means it becomes difficult to measure effectiveness of a particular intervention), 3. giving adequate time for the patient to absorb information, undertake exercise programme and develop self management skills between sessions, 4. experimentation, i.e. experiencing a particular task or movement that has been identified or prescribed successfully.
Judgement and Experience
Judgement and Experience
Saturday August 21, 2010About eighteen months ago, I wrote a post here about judgement and about the need to test judgements against the fine grain of experience. In that post, I quoted the story – a story that I have been fascinated by for a long time – about the friend of the painter Courbet who used to wake in a cold sweat crying “I want to judge! I want to judge!”
I’ve been thinking again about judgement, because I have been noticing whilst travelling that the mind does very curious things. This will not be news to anybody who a) has a mind and b) pays it any attention. But the particular thing that I have been noticing is the way, when I come across a new experience, I find myself succumbing to what could only be called a kind of restless hunger to pass judgement. So, for example, I arrive in a new town. Let us say Anyang in China (not the Anyang in Korea), where I am now. And as I come out of the railway station or the bus station, I find my mind doing the following. “Hmmm….” my mind says, “Looks a bit dowdy here. Not as good as the last place I was in. Oh look, there’s a person doing something unappealing. Just goes to show. I knew it. This town is rubbish. Aha, what’s this? Somebody has just pushed in front of me. Typical, eh? Looks like it’s going to be a grim couple of days.”
And immediately, poor old Anyang – or wherever I happen to be, because this is not a pattern that has anything to do with the objective qualities of a place – has been damned on the basis of rather faint evidence: one person doing something mildly unappealing, somebody else doing what anybody who doesn’t want to be crushed underfoot does when in a station in China, and… well, and that’s about it. Sometimes it goes the other way, and my mind says “Oh, look, this place is clearly great because I’ve just seen a cute cat by the station entrance.” Which is equally spurious stuff.
What is interesting here, I think – and what is interesting in the story about Courbet’s friend (as retold in an essay by Foucault, which is where I read it) – is the sheer hunger that we the mind has for casting judgement. It does this, more or less, of its own accord. It wakes up yelling “I want to judge! I want to judge!” Sometimes, at least, as time has gone on I have got better at ignoring its cries. Or better at putting its rapid judgements to one side, and leaving the door open for a bit more evidence to come in. Sometimes, however, I find myself succumbing.
I do still wonder what is going on here. Maybe it is a kind of attempt to control the future, or to deal with uncertainty. When you arrive somewhere new, the possibilities are wide open. The fact is, very often, you simply don’t know what a place holds, what it is like, what will happen. And the mind, poor little thing, doesn’t like not knowing. So perhaps this is why it spins webs of judgement over vast abysses of ignorance.
It is interesting to see the mind do these things, and to let it go about its business without taking its judgements too seriously. In the end, it gets fed up and stops, at least for a while. It is not that the faculty of judgement is not useful; but the proper exercise of judgement is very different from these curious little outbursts. And I’ve noticed that, if I don’t take these stories seriously, very soon they subside. Cities, and people too, are complex things. They cannot be easily summed up. Experience is constantly shifting and nuanced, hard to capture in judgements as simplistic as these. And when experience simply comes and goes without this layer of judging, it takes on a very different character, as the heat goes out of it. It just becomes that which happens.
Incidentally, I should say in the city’s defence – and if I have to come to some kind of provisional judgement – that Anyang has been a charming and fascinating place to spend a couple of days…
Image: thanks to Michael Kan on Flickr
#2 · Lilian Nattel
22 August 2010
This made me smile and chuckle. I think
it’s possible that quick judgment evolved
in a time when it could have been life-
saving to quickly assess a new environment.
It’s left-over from hunter-gatherer days.
Your post reminded me of my 2 trips to
China. I came here via Tasting Rhubarb and
so glad I did.#3 · Robert Ellis
22 August 2010
I find it creditable that you distinguish your ‘curious little outbursts’ from judgement in general. In general I think I’d want to argue that not using judgement is just as much of a problem as using it too readily: for example as a teacher of philosophy and critical thinking to 16-19 year olds, I find that learning always takes place when students are willing to exercise their judgement, even if crudely (as it can then be refined through challenging discussion), but if they don’t engage it at all and just greet a new argument or experience with blank indifference, I have much more of a sense of failure as a teacher. Your snap judgements about Anyang are the first indication that you are engaging with it (and thus to some extent, appreciating it). The refinements and the complexity can come later, but you need something to work with.
Of course the ‘curious little outbursts’ of judgement that you note also might be a bit of a problem if you were to take them too seriously. However, as a seasoned traveller, I’d be very surprised if you were in any real danger of doing so. I think you could take these stirrings of judgement much more positively and see them as crudely-formed clay.
#4 · Will
23 August 2010
Thanks for the comments folks. I’m not entirely sure that the snap judgements lie on a continuum with genuine judgement, however. I wonder if they are rather different processes. They certainly feel rather different, not just in extent but in kind. And certainly we do need to make judgements about this and that if we are to make any headway at all in the world.
But there is something different going on in this restless stamping of usually moral evaluations upon things.
#5 · Sabio Lantz
25 August 2010
“And the mind, poor little thing, doesn’t like not knowing”
—-> fantastic !#6 · star
4 September 2010
Wonderful example you provide of the way our minds seek to name and categorize everything. I like Richard Gombrich’s explanation that one of the reasons the Buddha used the metaphor of fire so often is because fire appears to be “appetitive” — it seeks fuel. Our minds are just like that, aren’t they? If I ever get my mind to settle down in meditation, I can feel the bubble of a thought “wanting” to arise, like a little pressure — it hasn’t got a shape yet, it’s just the desire to be thinking, to be doing — anything but just sitting silently! Surely this is a left over survival mechanism — the more quickly we can judge a situation, the less likely we are to get eaten by the bear?
via thinkbuddha.org
A nice piece on judgement. Of course being in a state of awareness in the present moment without judging is the basis of mindfulness.
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