Specialistpainphysio

CRPS Blog

2011-07-25T05:04:00.000-07:00

There are now two blogs to follow:

www.specialistpainphysio/blog for general infomation about pain, research, neuroscience and clinic updates

www.crpsuk.com dedicated to CRPS and developing awareness and understanding

New blog location

2011-04-03T02:01:00.000-07:00

The Specialist Pain Physio Blog is now on the website at www.specialistpainphysio.com

Come and join in and see links to others interested in neuroscience, psychology and other sciences that we can use to help people understand and deal with their pain.

Happy Mother's Day!

Relationship of Common Pain Conditions in Mothers and Children

2010-11-14T02:53:00.003-08:00

Check out this website I found at journals.lww.com

Posted via email from Specialist Pain Physio

Effects of Acupuncture at Sanyinjiao (SP6) on Prostaglandin Levels in Primary Dysmenorrhea Patients

2010-11-14T02:53:00.001-08:00

Check out this website I found at pdfs.journals.lww.com

Posted via email from Specialist Pain Physio

Play with your kid, for their mental health's sake

2010-11-09T01:12:00.001-08:00

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...

Posted via email from Specialist Pain Physio

Chronic Pain: A Disease in its Own Right

2010-11-09T01:07:00.001-08:00

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.

via sciencebasedmedicine.org

I am always interested in reading and hearing about individual's experiences. This could be a worthwhile insight.

Posted via email from Specialist Pain Physio

Central sensitisation

2010-11-03T09:19:00.000-07:00

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.

Glial activation in the rostroventromedial medulla promotes descending facilitation to mediate inflammatory hypersensitivity

2010-11-03T04:01:00.000-07:00

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

Dysfunction of endogenous pain inhibition during exercise with painful muscles in patients with shoulder myalgia & fibromyalgia

2010-11-03T02:31:00.000-07:00

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.

New Specialist Pain Physio Website

2010-11-02T04:46:00.001-07:00

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

The human glucocorticoid receptor: molecular basis of biologic function

2010-10-20T05:30:00.000-07:00

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

Stress & disorders of the stress system

2010-10-20T05:26:00.001-07:00

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

Neuroendocrinology of post-traumatic stress disorder

2010-10-20T05:21:00.000-07:00

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

Positve mood & thinking - the benefits

2010-10-17T01:14:00.000-07:00

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

Using langauge in rehabilitation

2010-10-15T01:09:00.000-07:00

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

The Pain Neuromatrix

2010-10-14T07:43:00.001-07:00

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)

Pain Medication

2010-10-04T05:32:00.001-07:00

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.

Post-surgical inflammatory neuropathy

2010-09-30T01:19:00.000-07:00

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.

How to be happy

2010-09-28T15:09:00.001-07:00

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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 information

Since 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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Posted via email from Specialist Pain Physio

How old do you feel?

2010-09-28T05:05:00.000-07:00

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

2010-09-28T05:03:00.001-07:00

Check out this website I found at pdfs.journals.lww.com

Useful measures to identify factors that can affect outcomes: FABQ-PA & PCS

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How injured nerves grow themselves back

2010-09-28T05:02:00.001-07:00

via sciencedaily.com

Good new information about how injured nerves grow back, in particular identifying Schwann cell and fibroblast activity and inter-communication.

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Mindfulness meditation may ease fatigue, depression in multiple sclerosis

2010-09-28T04:51:00.001-07:00

via sciencedaily.com

More evidence for mindfulness.

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Pain Physio Tweeting

2010-09-27T02:01:00.000-07:00

PAINPHYSIO ON TWITTER

http://twitter.com/painphysio

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

2010-09-27T01:50:00.001-07:00

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.

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Emotional and Neuropsychological Profiles of Children With Complex Regional Pain Syndrome Type-I in an Inpatient Rehabilitation Setting

2010-09-27T01:47:00.001-07:00

Check out this website I found at pdfs.journals.lww.com

Expected findings from clinical experience, good to quantify.

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Avatar therapy: From couch to cyberspace

2010-09-27T01:44:00.001-07:00

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Continue reading page |1 |2

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.net

I 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

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The Development of Sensory Hypoesthesia After Whiplash Injury

2010-09-27T01:43:00.001-07:00

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

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Spinal cord

2010-09-22T01:43:00.000-07:00

My 2-year old daughter painted a spinal cord for me yesterday. Never too early to start biology! (Actually it is a butterfly)

What's in a name? The words behind thought

2010-09-21T13:32:00.001-07:00

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 ...

via feeds.newscientist.com

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.

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Heart disease-depression 'danger'

2010-09-16T06:41:00.001-07:00

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.

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Aerobic exercise relieves insomnia

2010-09-16T06:02:00.001-07:00

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.

Posted via email from Specialist Pain Physio

Royal Mail celebrates British medical and scientific breakthroughs

2010-09-16T05:37:00.001-07:00

via feedproxy.google.com

I've never been a stamp collector, but if I was, these would be a definite feature!

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Interleukin-6 Levels in Tension Headache Patients

2010-09-16T05:33:00.001-07:00

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.

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Religion causes a chronic biasing of visual attention

2010-09-16T03:32:00.001-07:00

via feedproxy.google.com

Perhaps any life philosophy that we hold will have the same impact, not just a particular region.

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Fart sniffer to hunt for life on Mars

2010-09-16T03:29:00.001-07:00

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 billion

The 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!

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The Importance of Neuron Diversity

2010-09-09T07:38:00.001-07:00

via thebeautifulbrain.com

Interesting findings

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Learning tricks

2010-09-09T06:35:00.001-07:00

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 determined
In 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.

via feedproxy.google.com

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.

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Judgement and Experience

2010-09-09T05:03:00.001-07:00

Judgement and Experience
Saturday August 21, 2010

About 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

#1 · karen

22 August 2010

Hello. Very interesting, and in my experience true. The desire to judge comes from a (false) belief of mine that somehow this judgment will keep me safe. It is a limiting habit and one that I must stay mindful of. Warmly,Karen

#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?

<< Having more than one name

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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Mice Show Heritable Desire For Exercise

2010-09-09T05:00:00.001-07:00

via rss.sciam.com

You can blame the genes! Great! Exercising is a behaviour determined by your belief about what it is and what it does. Identifying the barriers to exercising and of course adherence is important.

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Pain

2010-09-09T04:56:00.001-07:00

Post a Comment

via neurokuz.blogspot.com

I like this blog comment. Simple.

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Transdural motor cortex stimulation reverses neuropathic pain in rats: A profile of neuronal activation

2010-09-06T10:56:00.001-07:00

via sciencedirect.com

Posted via email from Specialist Pain Physio

Stress resilience returns with feeling for rhythm

2010-09-01T10:56:00.001-07:00

via sciencedaily.com

Providing accurate information about stress and the links with pain (mind-body) via the SNS and immune systems is a fundamental part of the treatment programme. It is about perception of threat. The task in hand is the task in hand. How is it perceived? This will judge the response. Why zebras don't get ulcers is a classic book as a great start point.

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Mindfulness meditation increases well-being in adolescent boys, study finds

2010-09-01T10:50:00.001-07:00

via sciencedaily.com

Mindfulness is gaining exposure as a really useful mode of working. Remaining in a state of non-judgment certainly gives you clarity, the presence of the now and removes feelings of discomfort associated with dwelling in the past or future. In terms of pain, observing and not judging or giving value to the sensation can be a valuable skill to lessen the impact.

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A Randomized Controlled Trial Comparing Manipulation With Mobilization for Recent Onset Neck Pain

2010-09-01T10:46:00.001-07:00

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via archives-pmr.org

Phew! There I was thinking for a minute that I would have to start manipulating necks! No chance. You just cannot really know if that neck is safe to 'click'

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Top 7 immunology papers - The Scientist - Magazine of the Life Sciences

2010-08-24T13:18:00.001-07:00

Check out this website I found at the-scientist.com

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CBC News - Health - Brain wiring key to quick decisions: study

2010-08-24T13:17:00.001-07:00

The ability to make quick decisions when they are needed depends on whether your brain connections are the neural equivalent of broadband or dial-up, an international study shows.

In a Proceedings of the National Academy of Sciences paper released online Tuesday, an international team shows flexibility in decision-making is dependent on structural features of the brain.

'As you get older, the bandwidth gets slower and slower.'— Scott Brown

Quick decisions tend to be error-prone while relatively slower contemplation tends to produce more accuracy, says one Australian research team member, Scott Brown, an associate professor at the University of Newcastle's cognition laboratory.

This trade-off between speed and accuracy means people need to be able to switch between the fast risky and slower cautious modes of decision-making, as required.

But, says Brown, little is known about the neurology underpinning this flexibility.

Broadband or dial-up?

In their study, Brown and colleagues, which included researchers from the United Kingdom, Germany and the Netherlands, examined what brain mechanisms underpin decision-making flexibility.

They found it was determined by the "purely physical measurement" of the thickness of the connections between the brain's cortex and the striatum of the basal ganglia.

He says the results are the equivalent of brain communication being reliant on a broadband connection or still using dial-up.

"The underlying finding that a purely physical measurement could predict behaviour is very surprising," he says.

Brown says the team has not determined what causes one person's connections to be thicker than another's.

"It could be that it is the 'use it or lose it'" phenomenon, he says.

However, in a paper still under review, Brown says, the team has also shown the connection thins with age.

"As you get older, the bandwidth gets slower and slower," he says.

MRI scans measure fibre thickness

For the study, participants were placed in an MRI scanner and the researchers measured the thickness of "fibres" that carry inputs from the cortex to the basal ganglia.

Brown says the technology allows researchers to "track millimetre by millimetre which direction fibres in the grey matter are travelling," and determine the number (or thickness) of fibres connecting one region to another.

These measurements were done when the participants were not making decisions. They were also required to undertake a series of tasks that required them to make decisions either quickly or slowly.

They found those with the stronger connections in the brain were more able to move flexibly between a fast response and a more accurate slow response.

The study was based on only nine participants, however, the researchers used a previous independent study, which had included MRI scans, to verify their findings.

'Train the brain'

Brown says their work could help in tracking cognitive decline in aging.

"People who have a disease of aging often have their symptoms exacerbated by the slowing that comes with aging," he says.

"If you can understand the slowing, we might be able to separate the effects and better understand what is happening."

He says there is a view that older people are slow and cautious because they choose to be so.

However, these latest findings would suggest that as brain connections thin, the person is "stuck in a regime where response is always slow and cautious."

In current work, Brown says they are trying to force older participants to be faster at decision-making.

"We are seeing if you can train the brain to use these tracks more efficiently," he says.

© Australian Broadcasting Corporation, 2010

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Keeping Your Prefrontal Cortex Online: Neuroplasticity, Stress and Meditation

2010-08-24T08:02:00.003-07:00

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Keeping Your Prefrontal Cortex Online: Neuroplasticity, Stress and Meditation

2010-08-24T08:02:00.001-07:00

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The multi-tasking myth

2010-08-23T13:56:00.003-07:00

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Pregabalin and Transcutaneous Electrical Nerve Stimulation for Postherpetic Neuralgia Treatment

2010-08-23T13:56:00.001-07:00

Check out this website I found at journals.lww.com

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Oxytocin: It’s a Mom and Pop Thing

2010-08-23T13:55:00.001-07:00

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Illusions of bodily awareness adapted for the pub

2010-08-23T13:54:00.001-07:00

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Autism Might Slow Brain's Ability to Integrate Input From Multiple Senses

2010-08-23T13:52:00.001-07:00

August 21, 2010 | 10 comments

Autism Might Slow Brain's Ability to Integrate Input From Multiple Senses

A new study found that kids with autism were slower to integrate stimuli from different senses, providing possible explanations for behavioral differences

By Katherine Harmon

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Changes in Pain Perception and Descending Inhibitory Controls Start at Middle Age in Healthy Adults

2010-08-23T13:51:00.001-07:00

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Physiotherapy after surgery: The best solution for shoulder problems, Swedish study finds

2010-08-23T13:01:00.001-07:00

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Delayed chronic fatigue syndrome paper to be published

2010-08-23T12:58:00.001-07:00

Cross posted from Nature's The Great Beyond blog.

A highly anticipated paper linking viral infection with chronic fatigue syndrome will at last see the light.

The paper, to be published online later today by Proceedings of the National Academy of Sciences USA (PNAS), is the first to back up a previous report that chronic fatigue syndrome may be linked to infection by a virus called XMRV (see ‘Virus linked to chronic fatigue syndrome’). Chronic fatigue patients and their advocates embraced the findings as a long-sought clue to the cause of the mysterious ailment, but several research teams have since tried and failed to reproduce this link.

The PNAS paper was originally accepted for publication on 27 May. But on 4 June, the authors, who work for the US National Institutes of Health and the US Food and Drug Administration, asked to delay publication while they considered conflicting results from a second paper authored by other government researchers. (For more see ‘Chronic fatigue findings were held back’.) That second paper appeared in the journal Retrovirology on 2 July, but there was still no sign of the first.

Read the rest of the post on The Great Beyond. Or for more background information, check out Nature Medicine’s timeline of the XMRV controversy.

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A little adversity bodes well for those with chronic back pain, study suggests

2010-08-06T12:52:00.001-07:00

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Quantification of the Effects of Transcutaneous Electrical Nerve Stimulation With Functional Magnetic Resonance Imaging: A Double-Blind Randomized Placebo-Controlled Study

2010-08-06T12:50:00.001-07:00

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Pain Physiology Education Improves Pain Beliefs in Patients With Chronic Fatigue Syndrome Compared With Pacing and Self-Management Education: A Double-Blind Randomized Controlled Trial

2010-08-06T12:49:00.001-07:00

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Good to see some further evidence supporting the use of pain education. Clearly understanding pain helps to reduce anxiety and fear in relation.

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Fear-Avoidance and Endurance-related Responses to Pain: New Models of Behaviour and Their Consequences For Clinical Practice

2010-08-03T06:56:00.001-07:00

Check out this website I found at pdfs.journals.lww.com

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Exercise and caloric restriction rejuvenate synapses in lab mice

2010-08-03T06:55:00.001-07:00

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Looking at ways of motivating people to undertake exercise, the 'brain effects' could be a seller. Working at the belief level is clearly important in changing behaviours which is after all what exercise is, a behaviour.

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When memory-related region of brain is damaged, other areas compensate, study finds

2010-08-03T05:04:00.001-07:00

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More evidence of a plastic brain

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Why Do We Have Ten Fingers?

2010-08-03T05:03:00.001-07:00

In How Many Limbs Should Humans Have? I described my Limb Law, an empirical law I discovered which relates how long an animal’s limbs are to how many limbs it has. This law is explained by virtue of animals having evolved a limb design that minimizes the amount of needed materials to reach out into the world (see links to my academic work in the previous piece).

To see the Limb Law in action, go to my web site where you can play with an animal’s limb length and watch how the optimal number of limbs changes. Roughly speaking, the animal designs you can create in this program are the ones we find on Earth (…among radially-directed-limbed animals).

The Limb Law applies to more than just animal legs. By “limbs” I refer to any appendages that reach out, and so the hypothesis applies to hands as well, but where a hand’s “limbs” are its digits.

The only thing we must keep in mind in order to apply the Limb Law to hands is that hands are not free-range animals, but are, rather, connected to an animal. Hands have digits pointing away from the arm that connects to the hand, and so have only about half of the digits one would expect if the hand were roaming the world on its own.

In light of this fingers-are-the-hand’s-limbs observation, in this piece I’d like to ask…

Why do we have ten fingers?

In addition to being fundamentally interesting, this question also has deep implications for why we use a base-10 number system (rather than a base-2 or base-8 system, each which would arguably be better).

How can the Limb Law tell us how many fingers we should have, given that it only tells us the relationship between limb length and number of limbs?

Because hands like ours have plausible constraints on how long their fingers should be. Hands must close, i.e., their fingers must be able to reach back over the palm and cover it up. And that simple requirement is enough to enable us to predict roughly how many fingers we should have.

Recall that the Limb Law was that the number of limbs, N≈2π/k, where k was the “limb ratio,” k = L/(L+R), where L is limb length and R the radius of the body.

The demand that finger length be approximately the diameter of the palm means that the finger length should be about twice the palm’s “radius”. So, L≈2R. It follows that k ≈L/[L + (L/2)] = 2/3. And, plugging in k=2/3 into the equation for the number of limbs, N, we have N≈2π/ (2/3) = 3*π ≈ 9.42.

That is, given that fingers must be roughly as long as the diameter of one’s palm, then there should be about 9.42 fingers poking out from the circumference of the palm.

But remember that palms aren’t animals living freely on their own, but are attached to arms, and thus we expect palms to have digits on only about one half of their circumference. So, 9.42 is twice what we should expect for the number of fingers. Divide 9.42 by 2 and we have 4.78 fingers per hand. Or, about five.

Could it be that your run-of-the-mill alien would also have ten fingers, and thus get saddled with base-10?

=====

There was a healthy discussion when this was posted at Science20.com, and it is worth repeating one exchange here. Here is the comment, followed by my reply…

We have a maximum of 5 digits per limb, because ancient ancestors of all subsequent quadrupeds settled on 5 digits per limb, after initially starting out with a higher number (7 or 8 digits per limb – see for example, http://www.dinosaurjungle.com/prehistoric_animals_acanthostega.php ).

My reply…

The fact that number of digits has tended to only fall among tetrapods (from polydactylous to pentadactylous and lower in many cases) could mean there is some kind of (genetic or developmental) difficulty in adding digits, as you suggest. But abnormal polydactyly is fairly common in vertebrates (including humans), and often has a hereditary component. On this basis it would seem that adding a digit is possible. And, evolution can take more creative approaches as well, like the Giant Panda extra pseudo-digit you mentioned.

Rather than supposing that there is some kind of difficulty in adding digits, or some kind of upper limit of five, an alternative hypothesis is that the original polydactylous tetrapod had simply “too many” digits for most hand designs relevant for terrestrial environments, and that tetrapods ever since have been disproportionately losing digits to fill in vacant spots in design space, with only the occasional added digit. That is, the tendency for digit loss over time may be due to adaptive selection pressures, not a no-adding-digits constraint.

So, I’m not convinced that developmental / genetic constraints force a five digit maximum.

Also, I’m of course not suggesting that prior “evolutionary stages are planning ahead for the number of fingers humans would need in millions of years time.”

And, at any rate, all this is beside the point. Let’s suppose that some kind of historical accident were to force exactly five digits on all progeny of an animal, and that some of those progeny became primates with our hand design. Is it true that it is a historical accident that we have five fingers, in this thought experiment? Not quite. Being stuck with five digits would have constrained the kinds of hand (and body) designs possible for this animal’s progeny. Some hand designs, and animal designs, would then be out of reach to this lineage. The hand designs within reach for such a lineage would be ones which work really well with five digits. …and one such hand design is the “grasper” one where the digit length is of similar length to the palm diameter, very roughly our hand. The question is whether our hand/digit design is optimal in some hypothesized sense. My suggestion is that our 5 digits and our digit-length-to-palm ratio are “designed for one another” (because that relationship is consistent with cheap reaching-out wiring costs). My suggestion is an engineering hypothesis, not a historical hypothesis. If five-ness was historically fixed, then what historically evolved was the length of the digits to become a proper grasping hand. To put it another way, if our long ago ancestors had, say, three fingers, and could not add new ones, then primates would probably not have evolved in the first place, because the hand would have led the lineage down new design paths.

=====

This first appeared on May 17, 2010, as a feature at Science 2.0

=============

Mark Changizi is Professor of Human Cognition at 2AI, and the author of The Vision Revolution (Benbella Books) and the upcoming book Harnessed (Benbella Books).

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The purpose of the Law

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Women attracted to men in red, research shows

2010-08-03T05:01:00.001-07:00

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What do we do about placebo?

2010-07-29T08:45:00.001-07:00

Body in Mind recently featured a piece on the ‘Moral Dilemma of Offering a Known Placebo’ in which Neil O’Connell talks about how the ‘placebo effect … in part rests on the effects of expectation, belief in the treatment and possibly a re-evaluation by the patient of their symptoms’. He was referring to treatments like acupuncture, electrotherapy and so on, and calls them ‘magic kisses’ because they work in a similar fashion to the ‘Mummy will kiss it better’ treatment I’ve given to my kids when they were younger. The dilemma lies in the fact that placebo is simply an inert, inactive ‘intervention’ given as if it was active - inevitably requiring deception on the part of the practitioner, and what this can do to things like trust and informed choice by the patient.
So much of what we do as clinicians, particularly physical and occupational therapies, has a limited evidence base. At the same time, some of the ‘active ingredients’ that have been identified in ‘placebo’ are the very things we are taught to develop – like active listening, instilling positive expectations, helping people re-evaluate their situation. It’s incredibly difficult to disentangle the ‘active’ from the inactive components of the treatment.
Like Neil, I have concerns about encouraging, even inadvertently, any belief in a mystical, magical ingredient – chi anyone? I also have concerns about any intervention that suggests the need for an ongoing relationship with a clinician – six-weekly ‘adjustments’ sir? Or interventions that leave the power (or locus of control to be pedantic) with a gadget or device or substance that someone else needs to operate – three monthly infusions madam?
Dan Moerman’s view of health interventions suggests that every treatment inevitably contains culturally-based elements. These are the result of an interaction between the person seeking treatment, the social environment in which they live, the treatment setting, the ritual associated with the treatment process, and the interpersonal relationship with the practitioner – everything we do in any healthcare encounter will influence the ‘healing’ or ‘meaning response’ of the patient.
Along with the placebo effect (meaning response), we sometimes forget the nocebo effect – the ill effects that people develop as a result of receiving an inactive treatment. Take a look at any of the randomised, double-blinded, placebo controlled studies, and in a good one, you’ll see listed all the side effects that people developed when receiving the active treatment – and if you look carefully, you’ll also see the side effects that people developed when receiving the inactive treatment. It’s entirely likely that along with our very effective, evidence-based treatments, some people will also either fail to respond, or will develop side effects that negate the positive effects of the intervention.
So what on earth do we do about this placebo thing?
Putting my ‘patient’ hat on for a moment, and remember that we are ALL patients at some point in our lives, I know that I want honesty from the practitioner I’m seeing. I want to choose whether I have a certain treatment – or not. And I want to know my options. I’d like to be told about both the side effects and the hopefully positive effects of the treatment. I want to know the evidence-base for the treatments I get (and if I don’t get told, you can bet, like many of our patients, I’ll be onto the internet and into the journals quick as a flash to find out!)
I don’t want to have a long-term relationship with a practitioner who will want to see me every six weeks or three months, and I don’t want chi (or woo). I’m not into magic, superstition or intuition.
I’m inevitably going bring all my socially-shaped judgements and beliefs and prejudices into the treatment setting, and I know this is going to influence the outcome.
I’m likely to decide on a particular practitioner on the basis of word of mouth (reputation), what I’ve read from the literature (call that advertising if you will), and I’ll probably decide to return (or not) depending on his or her interpersonal skills – and because I too am influenced by the superficial – I’ll probably be influenced by the decor in his or her rooms and the cost of the treatment!
You see, we’re all influenced by these meaning responses.
So… what to do about placebo? I, like Neil, hope that as the evidence accumulates, I will throw out the treatments that don’t have solid support from well-constructed RCT’s. I will be mindful of my reputation and hope to have one that means I’m recognised by my adherence to an evidence-based approach to pain management. I also hope I’ll always focus on helping people to help themselves, so I don’t inadvertently foster dependence on me. I won’t be incorporating woo, chi or crystals (at least, not on the basis of current evidence!) I won’t be using gadgets except as part of helping someone develop their own skills. If I ask someone to come back after a bit of a break, it will be only to review how they’re going with their own goals, and to help them re-jig their plan for the future.
And I will try to recognise that some people will come to see me and will not ‘get better’ – not because of my approach, but because they have come into treatment with their own beliefs and expectations, their own ‘meaning response’ might interfere with what I’m doing. Above all, I hope I’ll be honest about what I’m doing and be prepared to change my approach on the basis of science.
That darned placebo – whatever do we do about it? Learn more I hope!
Moerman DE (2002). The meaning response and the ethics of avoiding placebos. Evaluation & the health professions, 25 (4), 399-409 PMID: 12449083
Moerman, D., (2003). Doctors and patients: The role of clinicians in the placebo effect. Advances in Mind-Body Medicine. Vol.19(1), pp. 14-22.
Moerman, D., (2003). “Placebo” versus “meaning”: The case for a change in our use of language. Prevention & Treatment. Vol.6(1), pp. No Pagination Specified

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Filed under Chronic pain, Clinical reasoning, health, pain, psychology, research, therapy · Tagged with health, healthcare, Chronic pain, therapy, biopsychosocial, pain management, Clinical reasoning, treatment, occupational therapy, physiotherapy, psychology, placebo, self management, meaning response

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Comments
9 Responses to “What do we do about placebo?”

MM says:

July 29, 2010 at 10:56 am

It appears your approach to providing a placebo treatment is to place yourself in the shoes of the patient, and then provide service in conformity with your own expectations. And you appear to be typical of doctors: trained to make decisions as scientists, disdainful of superstition, and desirous to personally weigh the possible consequences of various courses of action.

While you and I may not like woo, many patients clearly do. Some people look to doctors or other experts not for information and choices, but answers.

Why not provide treatment based on the patient’s preferences, not your own? You could provide each patient, prior to being diagnosed or treated, with information regarding the placebo effect and ask whether they would like placebo-like treatments to be incorporated where appropriate.

Recognizing the limits of medical understanding the and the real effects of placebo treatments doesn’t mean you need to take advantage of patients by seeing them three times a week. As noted in the Mind and Body article, you can suggest relatively inexpensive acts that are otherwise beneficial to a patient–taking a vitamin, eating green leafy vegetables, walking 30 min. a day–even if there is no evidence these acts will help the specific problem at issue.

Give patients information and let them decide–even on the issue of whether they should be given further information. The alternative may be that patients without adequate information will simply seek out expensive placebo treatments on their own.

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Ronny says:

July 29, 2010 at 12:06 pm

Placebo/nocebo is of no serious clinical value or significance, and lying to patients is never acceptable (perhaps with a tiny handful of short term exceptions, like when dealing with a parent who is strongly suspected of abusing their child, or patients who are tipping over into psychosis and need hospitalising).

(Of course, this effect should always be controlled for in formal studies. But beyond that, meh.)

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Bernadette Murray says:

July 29, 2010 at 2:30 pm

I chuckled when you admitted that the decor might play a role in your perception of a practitioner.
Seriously though, I really started thinking about the ethics of the nocebo effect particularly when I caught
myself mentally entertaining the thought of forwarding an email to a friend with graphic pictures of a particularly
ghastly outcome from a repetitive behavior. I did not take this action because of course this is manipulation –trying to influence my friend to stop a behavior that I have ever so helpfully identified as being inimical to her health and well-being. And that frankly –TRUTH now–I find irritating and annoying.

The stupidest use of nocebo IMHO are those chain-mail emails that have magical benefits if only one forwards to the certain stipulated number of recipients; otherwise if one breaks the chain, whamm-o the curse is upon thee.

Slightly more subtle, in the past I have had a doctor use the “if you do not take this medicine as prescribed, you
could die” exhortation. I would have preferred a candid tempered discussion of limits of knowledge about the consequences of not treating the condition. Since I did not die when I stopped the taking medication and my test results came back within normal ranges, I unfortunately came to harbor some cognitive beliefs about doctors in my early twenties such as “doctors lie and exaggerate to ensure patient compliance ” and “doctors always minimize how painful a procedure really is so you will agree that the benefit surely outweighs such modest discomfort.” ha!

I did not think doctors were EVIL or malicious. Seemed to me that they were rationalizing that the end justifies the mean (and they did not believe that they could present evidence to me and expect me to make a rational decision ) so they needed to employ some extreme emotional motivation.

Fortunately, I have had many more encounters and opportunities to interact with doctors and I realize that those human beings, many of whom have discarded the white coat and are willing to share evidence and discuss options, are not homogeneous in their orientations.

I have also come to realize that many alternative remedies are marketed in a weird kind of nocebo-fashion as non-existing illnesses are invoked so that the “remedies” can alleviate or cure them. ” A Toxic system filled with free radicals is the underlying cause of all illness….sip on acai juice while experiencing the health benefits of chelation therapy combined with a colonic.” Yup time to exorcize that demon “toxicity”

Coming back to what you are saying so well in your post: the problem with placebos is the Dumbo’s magic feather conundrum. Dumbo can fly without the feather, and we as patients actually generate our own neurotransmitters which modulate our own systems. I really like your emphasis on interacting with your patients so that they can fly on their own (metaphorically speaking of course ;-)

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Neil O'Connell says:

July 29, 2010 at 6:45 pm

Great post Bronnie (thanks for the mention) and I couldn’t agree more. I think patient choice is a difficult concept here because it is very difficult for patients to access or distinguish good health information. There is so much misdirection, anecdote and outright fraud out there and when you are in desperate need you become vulnerable to the peddlers of false hope. I guess it boils down to “keep what works, keep the care and dump the magic”.

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ian stevens says:

July 29, 2010 at 10:35 pm

Its a difficult issue, ethically prqctically and economically (for both private providers and patients) in many ways. However, positively if we can enhance meaning ,facilitate a persons own process of restitution and understand what may move a person towards this state than this has to be a good thing? Spaces and places where treament takes place for example have been studied by the Rheumatologist Esther Sternberg. Often complex cases of distress and disabilty are shunted into stark clnical rooms with rushed appointments (this was my experience of several pain clinics).
I fully endorse pain managment , enhancing self efficacy and minimising disability. However in Neils terms a few ‘kisses’ probably will not go amiss. A good narrative which looks at a patients journey dealing occupational therapy following an elbow fracture and secondary neurogenic pain is the Sociologist Ann Oakley’s Fracture. The response Ann obtained through the enhanced treatment effect cultivated by the acupuncturist (environment ,demenour , care ) was in stark contrast to the orthopaedic clinic . People often seek care, reasurance and an ‘individualised’ approach –this is often lacking in many protocol led clinics.
I disagree with the post that suggest placebo and nocebo are of no clinical importance. For many people nocebo is a feature of many health care interactions and according to Benedetti may have strong negative physiological consequencies. As biomechancial explanations of pain are dominant many people are told or interpret the results of tests,scans etc in often maladpative ways ….you have the spine of a 70 year old often leads to catastrophisation and disability for example.
I think for some people ‘chi’ used as a metaphorical explanation is not too bad… metaphors used wisely may indeed enchance meaning and downregulate threat. I suggest tai chi and use the principles all the time–it does not mean that I think chi,prana etc are ‘real’ but perhaps these metaphors may improve a persons self image /intereoception (especially if they learn to do things themself) .The danger perhaps is if these things are relied upon too much …..’Peddlars of false hope’ …yes a big problem and it is easy for those in the scientific medicla community to sit on a pedastal casting stones on CAM etc when many interventions offered by the medical profession offer little and in many cases are iatrogenic. I would have no problem suggesting certain ‘woo’ therapies offered by some caring people I know over and above an interventional pain clinc or rheumatology clinic for example . Allowing a stressed out person with often complex social issues a little respite seems fine in some circumstances . It may be a better use of resources than the mri/ct multiple health professional pharmacology route which tends to be a frequent occurrence.
Sometimes I just think we live in a overly medicalised culture and placebo treatments will just evolve to meet the demands of the population seeking care and attention!

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Yep!

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Brainstem, spinal cord images hidden in Michelangelo’s Sistine Chapel fresco

2010-07-29T08:44:00.001-07:00

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This is cool!

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Acupuncture Pseudoscience in the NEJM

2010-07-29T08:42:00.001-07:00

Here is the conclusion quoted from a recent New England Journal of Medicine (NEJM) review article on acupuncture for back pain:

As noted above, the most recent wellpowered clinical trials of acupuncture for chronic low back pain showed that sham acupuncture was as effective as real acupuncture. The simplest explanation of such findings is that the specific therapeutic effects of acupuncture, if present, are small, whereas its clinically relevant benefits are mostly attributable to contextual and psychosocial factors, such as patients’ beliefs and expectations, attention from the acupuncturist, and highly focused, spatially directed attention on the part of the patient.

Translation – acupuncture does not work. Why, then, are the same authors in the same paper recommending that acupuncture be used for chronic low back pain? This is the insanity of the bizarro world of CAM (complementary and alternative medicine).

Let’s break down their conclusions a bit. They have reviewed the clinical evidence, as I and others have done before, and found that when real acupuncture is compared to various forms of sham acupuncture (the acupuncture version of a placebo) there is no difference. As I have written many times before – it doesn’t matter where you stick the needles, or even if you stick the needles. Since acupuncture consists of sticking needles in acupuncture points, the only reasonable conclusion from this evidence is that there is no specific effect from acupuncture – acupuncture does not work.

The phrase, “contextual and psychosocial factors, such as patients’ beliefs and expectations, attention from the acupuncturist, and highly focused, spatially directed attention on the part of the patient.” is a fancy way of saying “placebo effects.” In other words, there are some non-specific subjective benefits to getting attention from a practitioner. There is this assumption, however, that these benefits are real and worthwhile. However, they are likely to be illusory – an artifact of observation and reporting, not a real improvement in the patient’s condition. In real science-based medicine, that is the underlying assumption – placebo effects are largely illusory – a variable to be controlled for.

But there has been recent controversy over the role of the placebo effect in ethical and evidence-based practice. This is, in my opinion, largely a back door attempt to justify CAM treatments that do not work. The claim is that placebo effects are real and useful. But a systematic review of the placebo effect in clinical trials concluded:

We did not find that placebo interventions have important clinical effects in general. However, in certain settings placebo interventions can influence patient-reported outcomes, especially pain and nausea, though it is difficult to distinguish patient-reported effects of placebo from biased reporting. The effect on pain varied, even among trials with low risk of bias, from negligible to clinically important. Variations in the effect of placebo were partly explained by variations in how trials were conducted and how patients were informed.

In other words – for any objective outcome, there is no important placebo effect. For outcomes that are subjectively reported by patients, there is a highly variable placebo effect. It is plausible that the expectation of benefit could result in the release of dopamine and endorphins and produce a physiological decrease in pain, for example, in a subset of people, and there is some evidence for this. But this is, at best, a transient symptomatic effect – not therapeutic.

Such effects are also non-specific – meaning they do not derive from the intervention itself, but from the therapeutic ritual surrounding the intervention. Even treatments that do not work may therefore provide these non-specific benefits. My opinion is that the non-specific benefits of the ritual of treatment should be combined with an actually effective treatment, not magic pretending to be medicine. There are many reasons for this. One is the ethics of patient autonomy and informed consent – giving a fake treatment to a patient violates the patient’s rights, in my opinion.

Further, there is potential downstream harm from convincing patients that fake magical treatments are effective, because of placebo effects. Then using obscure language to hide the fact that the treatment actually does not work. This distorts the public’s view of medicine, and of what works, and sets them up to be victims of fake treatments when their ailment is not subjective or self-limiting. In other words – refer them to an acupuncturists when they have back pain and they may rely upon acupuncture, or some other non-scientific intervention, when they have a more serious illness.

The authors of this article recommend:

He has specifically requested a referral for acupuncture, and we would suggest a course of 10 to 12 treatments over a period of 8 weeks from a licensed acupuncturist or a physician trained in medical acupuncture.

This contradicts their own conclusions. Why is training in acupuncture necessary? That training largely consists of identifying acupuncture points, knowing which points to use on an individual patient, and knowing the technique of needle insertion – but none of these things matter. The sham ritual is all that matters – you can literally fake it and get the same response. I bet a 10 minute video is all that is necessary. In fact I bet even that is not necessary – you could probably fake it well enough to get a maximum placebo effect without any prior demonstration.

What the authors of this article have done is something that is increasingly common in CAM (when it is trying to infiltrate academia and peer-reviewed journals like the NEJM) – reviewing the evidence, admitting that the CAM treatment does not work, then making an elaborate and misleading appeal to placebo effects, and ending with a recommendation to use the treatment that does not work. Specifically, they not only recommend using the treatment, but in its fullest magical form, complete with all the disproven claims (that is what “medical acupuncture” is). It’s a bait and switch con game, nothing more. Come for the placebo effect, then be treated with magical nonsense.

via theness.com

Acupuncture does have beneficial effects with some people. I have recently stuck some needles randomly about my knee that has been hurting intermittently for a year or so and it felt great afterwards (a case study of one!). We know that something happens but no-one knows exactly what. Stick needles anywhere and there's an effect. Well, the brain is probably going to do something in response to this tissue 'invasion' and maybe in certain cases it prioritises away from the pain hence the relief. Some talk about endogenous opioids, adenosine and DNIC. Perhaps they all have a role. Certainly expectation, belief and understanding will have a part to play as in any treatment. Modulation of pain is complex and the notion of local effects is out-dated. Multidimensional responses are more likely (Thacker & Gifford, 2002).

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Champagne fizzles out if served with a splash

2010-07-23T13:33:00.001-07:00

Not the best way to pour champagne.Carlos Alvarez / iStockphoto
If you want to enjoy champagne to the full, pour it out as you would a beer.

Sommeliers and connoisseurs may find the suggestion hard to swallow, but the evidence published in the Journal of Agricultural and Food Chemistry¹ seems irrefutable. Pouring champagne into a tilted glass helps it to retain the dissolved gas that is vital for the gustatory experience, say Gérard Liger-Belair and his colleagues at the University of Reims in France.

The French team compared the amount of dissolved carbon dioxide in a fresh flute of champagne poured the traditional way — splashing it into a vertical glass — with that after pouring along the inside of a tilted glass, as one does with beer to avoid giving it too much frothy 'head'. The researchers found that champagne served chilled (at 4 °C) contains about twice as much dissolved CO₂ using the beer-like method.

A typical 75-cubic-centimetre bottle of champagne contains five litres of dissolved CO₂. When uncorked, the release of pressure means that the liquid becomes supersaturated with the gas, which then begins to escape as bubbles. These contribute to the pleasure of drinking champagne in several ways: they give it a lively appearance, release aromas (the 'nose'), produce the stimulating oral sensation of collapsing bubbles, and create sharp tang owing to the conversion of CO₂ to carbonic acid inside the mouth.

"CO₂ has a strong effect on the sensory experience and flavour of champagne," says Susan Ebeler, an analytical chemist and oenologist at the University of California, Davis. "Flavour is a multisensory experience, including aroma, taste, colour, mouth-feel and even auditory cues. CO₂ can affect many of these senses."

Cold comfort
The slower a glass of bubbly releases its CO₂, the longer it remains vivacious. Yet it turns out that most CO₂ is lost not through bubbles bursting but by simple diffusion across the liquid surface. That is why flutes are used in the first place: the narrow neck reduces the surface area from which gas can escape.

Tilting the glass helps to keep more carbon dioxide in solution.Gérard Liger-Belair / American Chemical Society
Pouring has a big influence on the gas content, both because the 'tongue' of liquid falling from the bottle to the glass exposes a large surface area and because turbulence and entrapment of air bubbles as the liquid hits the glass can speed up diffusion of CO₂ out of solution.

The beer-pouring action should cut CO₂ loss on both counts: the column of flowing liquid is less exposed to air, and the gentler impact reduces turbulence. Liger-Belair and his colleagues have confirmed this, using a standard method for measuring dissolved CO₂ concentrations (based on the activity of the enzyme carbonic anhydrase, which reacts with carbonic acid), and using a method called thermography, which provides snapshots of CO₂ levels in air based on how strongly it absorbs infrared radiation.

The researchers also show that both to maximize CO₂ retention and to obtain the full benefits of the beer-pouring technique, the champagne must be chilled. When served at close to room temperature (18 °C), champagne served by the beer technique loses about two and a half times more CO₂ than when chilled — almost as much as it loses when served in the traditional way at room temperature.

Liger-Belair and his team show that increased gas loss from warm champagne is mostly a result of two factors. First, the colder liquid is more viscous, and so gas-leaking turbulence is dampened more quickly. Second, CO₂ molecules diffuse slowler in cold water, and so are unable to reach the surface as quickly.

Will champagne lovers be persuaded to alter their ways? "Champagne is a universe full of traditions," says Liger–Belair, who has worked as a consultant for the research department of Moët & Chandon. "But maybe champagne and science can mix to offer a better way of tasting," he says. He has at least one convert already. "Based on this paper, I probably will pour using the beer-like method now," says Ebeler.

References

Liger–Belair, G. et al. J. Agric. Food Chem. advance online publication doi:10.1021/jf101239w (2010).

via nature.com

Absolutely vital advice!

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Pregabalin and Transcutaneous Electrical Nerve Stimulation for Postherpetic Neuralgia Treatment

2010-07-23T13:31:00.001-07:00

Check out this website I found at pdfs.journals.lww.com

Perhaps this synergy will help other conditions that involve neuropathic pain, e.g. back pain that has a NP component. Understanding the TENS parameters will allow us to determine potential mechanisms and hence other ways of facilitating these processes and pathways.

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Serotonin cell discoveries mean rethink of depression

2010-07-22T14:25:00.001-07:00

IF YOU thought depression was caused by low serotonin levels, think again. It looks as if the brain chemistry of a depressed person is much more complex, with mounting evidence suggesting that too much serotonin in some brain regions is to blame.

If correct, it might explain some of the negative side-effects associated with selective serotonin re-uptake inhibitors (SSRIs), antidepressants like Prozac which increase the amount of the neurotransmitter serotonin in some parts of the brain.

The traditional view of depression was largely based on the observation that SSRIs boost mood- although why they do so is unknown. "Because antidepressants increase serotonin in some parts of the brain, people assumed that depression must be the result of low serotonin levels," says Christopher Lowry of the University of Boulder in Colorado. But the discovery of multiple types of serotonin-releasing neurons in the brain, along with high levels of serotonin recorded in people with depression, is prompting a rethink.

"What's more likely is that there are subgroups of serotonin neurons that are overactive in depressed patients, rather than underactive as we have all been assuming," says Lowry.

It's likely there are groups of serotonin neurons that are overactive, not underactive as assumed

One of the first clues that something might be amiss with the traditional theory came three years ago, when Murray Esler at the Baker Heart Research Institute in Melbourne, Australia, and colleagues found that the level of serotonin in the brains of people with panic disorder was four times higher than in healthy volunteers (Stress, DOI: 10.1080/10253890701300904), and in depressed people who were not receiving treatment it was two times higher than in volunteers (Archives of General Psychiatry, vol 65, p 38). They also showed that long-term use of SSRIs in people with depression and panic disorder seemed to decrease serotonin levels through an as yet unidentified mechanism.

Now, in studies of rats and mice, Lowry has found that there are multiple types of serotonin neurons that can be independently regulated. He presented his results at the Forum of European Neuroscience in Amsterdam, the Netherlands, last week.

This fits well with findings from other groups that there are two types of serotonin receptor in the amygdala, a brain region linked to emotion and anxiety: 5-HT2A receptors that inhibit anxiety, and 5-HT2C receptors that promote it. The roles of the receptors were identified by injecting drugs that either stimulated or inhibited each receptor and observing the animals' behavioural response.

Together, the findings might mean that while high levels of serotonin in some brain regions like the prefrontal cortex can lead to improved mood, high serotonin in other regions could have negative effects.

Evidence for this idea comes from Gina Forster at the University of South Dakota in Vermillion and colleagues, who injected a stress-related molecule into the brains of rats and found that it triggered two phases of serotonin release. An initial wave of serotonin appeared to increase fear-like behaviour in the rats, while a second wave decreased this behaviour, possibly because it activated a brain region called the medial prefrontal cortex, which is associated with calming of fears (Neuroscience, vol 141, p 1047).

The new findings have implications for how SSRI drugs work. In the long-term, SSRIs do tend to have a calming effect, although more research is needed to understand how they do this.

However, in the short-term some people taking SSRIs report feeling increased anxiety. This is "almost certainly due to the activation of one of these groups of serotonin neurons", says Lowry. The suicidal thoughts some people taking SSRIs claim to experience may also be linked to boosting serotonin, as suicide is thought to be associated with increased impulsivity. "It may be that certain types of SSRI are affecting these impulsivity circuits in the brain," says Lowry.

Learning more about these different groups of serotonin neurons could lead to better treatments for depression and anxiety disorders. "It might be possible to design very specific drugs that can turn on or off specific groups of neurons that are deregulated in anxiety or depression," says Lowry.

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Oh Pharmaceuticals. .

Thu Jul 22 18:48:44 BST 2010 by nigel

lol we've (kind of) known about this since 1997: http://www3.interscience.wiley.com/journal/119148194/abstract
-the intro's gives a good overview of how wavy the whole low-seretonin theory was 13 YEARS AGO
..but someone's gotta sell their SSRIs haha

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Structural brain alterations in patients with irritable bowel syndrome discovered

2010-07-22T14:24:00.003-07:00

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Brain training needed for IBS?

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Coffee perks up memory and balance in geriatric animals

2010-07-22T14:24:00.001-07:00

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This is great news, coffee may not be the stimulant we thought but it can help with memory!

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Flat-shoe pain? Blame the high heels, study says

2010-07-19T14:37:00.001-07:00

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'Cuddle chemical' eases symptoms of schizophrenia

2010-07-19T14:36:00.001-07:00

NASAL sprays containing the hormone oxytocin, nicknamed the "cuddle chemical" because it helps mothers bond with their babies, have helped people with schizophrenia.

Although the 15 participants used the sprays for three weeks only, most reported measurable improvements in their symptoms in this the first trial to test oxytocin in schizophrenia. "It's proof of concept that there's therapeutic potential here," says David Feifel at the University of California in San Diego, head of the team running the trial.

Most participants reported measurable improvements in the first ever trial to test oxytocin in schizophrenia

Each participant received oxytocin or a placebo for three weeks, then the opposite treatment for three weeks with a week break in between.

On the basis of two standard tests for schizophrenia, taken before and after each block of treatment, participants averaged improvements of around 8 per cent when taking the oxytocin compared with the placebo (Biological Psychiatry, DOI: 10.1016/j.biopsych.2010.04.039).

The effects didn't kick in until the final week, suggesting that it takes a while for the hormone to begin acting. "Standard antipsychotic drugs increase their efficacy several weeks later too, so oxytocin fits that profile," says Feifel.

Feifel thinks that oxytocin is dampening down the excessive production of the neurotransmitter dopamine, which can trigger schizophrenic symptoms such as hallucinations. He says the rationale for treating people came from his own team's studies showing that oxytocin could relieve a form of psychosis in mice, and research showing that people who sniffed nasal sprays of oxytocin became more trusting, which could ease paranoia symptoms in schizophrenia.

Feifel is seeking approval from the US National Institutes of Health for a larger trial testing oxytocin at a range of doses, and over a longer time.

"This work provides compelling data on the utility of oxytocin as a treatment for schizophrenia," says Heather Caldwell of Kent State University in Ohio, co-author of a study in 2008 showing that "knockout" mice unable to make oxytocin were more prone to a form of psychosis.

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Compelling?

Fri Jul 16 14:47:13 BST 2010 by Allan Brewer

Actually I wouldn't say "8% improvement" was "compelling data".

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Compelling?

Fri Jul 16 21:44:34 BST 2010 by allenallen

Yes, one wonders.... 8% fewer voices in their heads or were the voices 8% nicer in tone?

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The mind is the body - tumor suppression by enriched environment

2010-07-19T10:34:00.001-07:00

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This is a really nice piece of work providing mechanisms that could underpin the beneficial effects of an enriched environment. Understanding how we can create such environments for treatment and advising patients how to do so themselves to optimise their rehabilitation programmes that is so very important.

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Depression and dulled vision

2010-07-19T01:33:00.000-07:00

A group have found that those suffering depression have an altered contrast perception and therefore 'see' the world around them as duller. The team speculate that the neurotransmitters involved in vision may have an emotive function. Click here

Astrocytes & sleep

2010-07-19T01:28:00.000-07:00

As we find out more and more about the immune system and everyday function, it becomes pertinent that we develop a practical understanding of how we can work with this wonderful body system to benefit patients. This study looked at the way in which astrocytes influence neurons and how they affect sleep through action upon adenosine. Click here

Exercise and the brain

2010-07-13T06:29:00.000-07:00

As a physiotherapist with a background in neuroscience I am particularly interested in the effects of the exercises I prescribe upon the brain. Fortunately there is some excellent research that tells us about some of the responses and changes that occur in this wonderful organ when we engage in exercise. Understanding this can help us to make better decisions about being or becoming active and also to explain why we can feel different when we cannot exercise due to injury or another reason.

We know that exercise is important for cardiovascular health and reducing the risk of diseases such as diabetes, but less is commonly known about the beneficial effects upon the brain. In fact, knowing more about these responses could spur some individuals to taking on exercise or increasing activity levels.

Due to the release of certain neurotransmitters, neurotrophins and other factors in response to exercise, we see growth and repair of new brain cells (neurons), changes in neuron efficiency and the development of new blood vessels in the brain. What does this mean? It means that our mood is better, we can learn more effectively, reduce the effects of ageing, sharpen up our concentration levels, remember more and have an overall better experience of living. It’s a no brainer.

Mind your Immune System

2010-07-13T03:02:00.001-07:00

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Preventing CRPS after wrist fracture

2010-07-13T03:01:00.003-07:00

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NHS 'to undergo radical overhaul'

2010-07-13T03:01:00.001-07:00

By Nick Triggle
Health reporter, BBC News

Please turn on JavaScript. Media requires JavaScript to play.

Health Secretary Andrew Lansley: "GPs will lead a bottom up design of services"

The NHS in England is to undergo a major restructuring in one of the biggest shake-ups in its history, the government has announced.

Hospitals are to be moved out of the NHS to create a "vibrant" industry of social enterprises under the proposals.

And, as expected, GPs are to take charge of much of the budget.

The move will lead to the abolition of all 10 strategic health authorities and the 152 management bodies known as primary care trusts.

THE KEY CHANGES
Continue reading the main story

GPs - Asked to get together in groups to take on responsibility for spending much of the NHS budget

Hospitals - Encouraged to move outside the NHS to become "vibrant" industry of social enterprises

Patients - More information and choice, including ability to register with any GP they want to

Managers - Strategic health authorities and primary care trusts face the axe

The new structure will be held accountable by an independent NHS board which would be free from political interference, the government said.

Meanwhile, responsibility for public health will be passed to local authorities.

In many ways, the plans outlined in a White Paper go further than expected. The coalition agreement had promised no top-down reorganisations.

But Health Secretary Andrew Lansley said he had decided to go further than first envisaged to rid the health service of "unnecessary" bureaucracy.

He said the proposals would be challenging and turn the NHS "upside down" but in doing so help reduce management costs by nearly a half within four years.

He added: "The government's ambition is for health outcomes - and quality services - that are among the best in the world."
'Experiment'
The GP move had long been championed by Mr Lansley - and in recent months the British Medical Association had indicated it was willing to work with him on the idea.

The plans mean GPs working in groups will be in charge of a vast collection of hospital, mental health and community services - although specialist services and dentistry will not fall under their remit.

ANALYSIS
Continue reading the main story
It had been clear for some time that Andrew Lansley was planning big changes.

But it is a mark of how far-reaching the White Paper actually is that many experts are still shocked by the scale of the proposals.

At a time when the NHS is having to find savings of up to £20bn by 2014, the proposals are being seen as a huge gamble for the service itself and the health secretary personally.

At the heart of the plans are GPs. They, Mr Lansley believes, are better placed than managers to make decisions about services.

Buffeted by years of criticism over what have been perceived as excessive pay rises, GPs now find themselves in the curious position of being given the keys to the NHS safe.

The question on everyone's lips now is: Can they spend it wisely?

Under the new system, the independent board will sit above as many as 500 consortiums of GPs to set standards and hold the groups to account.

Another key aspect of the changes involves giving patients more information and choice. To achieve this, a new body, HealthWatch, will be set up to compile data on performance, while GP boundaries will be abolished to allow patients to register with any doctor they want.

Mr Lansley also announced he expected all NHS trusts, which run hospitals and mental health units, to get foundation status by 2013.

He also said he would be relaxing the rules which cap the amount of income a trust can make outside the NHS, opening the door to them seeing more private patients.

He said this would allow them to innovate and widen the scope of what they did, but he also admitted it would mean those which were not financially viable could go under.

The government will now consult on its plans before rolling them out over the next three years.

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Shadow Health Secretary Andy Burnham: "reorganisation is last thing the NHS needs"

Professor Chris Ham, chief executive of the King's Fund think-tank, said: "It is a very radical programme. We have never seen anything like this since the inception of the NHS in 1948."

But he said the moves were not without risk, pointing out some GPs would not have the skills to manage the budget.

Shadow health secretary Andy Burnham went further, describing the changes as a "political experiment".

"It is a huge gamble with a NHS that is working well for patients."

There was a mixed reaction from NHS staff. Unison said the changes could lead to "chaos", but the BMA said they could benefit patients and it was looking forward to working with ministers.

Katherine Murphy, of the Patients Association, called for more clarity over how and what information would be provided to patients.

"We need more details," she added.

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Low vitamin D levels associated with cognitive decline

2010-07-13T03:00:00.003-07:00

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Vitamin D levels associated with Parkinson's disease risk

2010-07-13T03:00:00.001-07:00

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Early Alzheimer's identification method discovered

2010-07-12T03:09:00.001-07:00

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Antibody cuts brain damage in strokes

2010-07-12T03:08:00.001-07:00

THE discovery of an antibody that binds to certain brain receptors could reduce the side effects of a common stroke drug and buy additional time in which to use it.

The preferred treatment for ischaemic stroke, in which a blood clot cuts off the blood supply to brain tissue, is a drug called rtPA, which dissolves the clot. However, that drug has to be given within the first few of hours of a stroke, otherwise the risks of treatment outweigh the benefits. Dissolving the clot can lead to a sudden rise in blood pressure, increasing the chance that a blood vessel will rupture and bleed into the brain.

Only 5 to 10 per cent of people who suffer a stroke make it to hospital early enough to be treated with rtPA, says Denis Vivien of the University of Caen Basse-Normandie in France. The rest are given drugs that do not destroy the initial clot but reduce the chance of further clots forming.

One reason for a delay in administering rtPA is that a brain scan must be carried out to determine the nature of the stroke. People with haemorrhagic stroke, in which a blood vessel in the brain bursts, should not receive rtPA as it increases the risk of bleeding.

Now a startling discovery by Vivien has put a different perspective on this relatively simple picture: rtPA is actually released by brain cells. "This was completely unexpected," he says.

In small quantities, rtPA binds to brain-cell receptors for a chemical called NMDA. This triggers a short-lived influx of calcium, enhancing learning and memory. But damaged neurons release rtPA in large quantities, and this can cause neighbouring neurons to die. High levels of rtPA can also damage the blood-brain barrier, which may explain why the drug sometimes triggers dangerous bleeding.

Vivien has also developed an antibody that could overcome these problems. It stops rtPA from binding to the NMDA receptors, blocking its negative effects. When mice were injected with the antibody on its own or in combination with rtPA, the amount of brain damage resulting from a stroke was reduced by up to 70 per cent - both when the antibody was given immediately after the stroke and 6 hours later. Three months later, these mice also showed significantly less disability.

"With the antibody, we completely prevent the deleterious effect of rtPA and we can increase the time window during which it can be given," says Vivien, who presented his results at the Forum of European Neuroscience in Amsterdam, the Netherlands, this week. If the results are replicated in humans, this might mean that the antibody could be given on its own, even before a stroke sufferer reaches hospital. The antibody could also make it safer to administer rtPA for a much longer period, vastly increasing the number of people who could benefit from it.

What's more, because the antibody blocks the effects of the rtPA being released by damaged brain cells, the treatment might benefit people who have had a haemorrhagic stroke. "We can postulate that maybe all stroke patients could benefit," says Vivien, who is now working with a pharmaceutical company to take the antibody into clinical trials.

We suggest that maybe all stroke patients could benefit from receiving this antibody

Resting brain activity shows up damage

Studying brain activity at rest could help assess the extent of damage caused by strokes.

Imaging techniques can highlight large areas of damage, but disabilities seen in people who have had a stroke suggest that more brain regions have been affected than are picked up by scans.

To better pinpoint damage, Maurizio Corbetta of Washington University in St Louis, Missouri, used functional MRI to scan the brains of 23 stroke patients. He measured resting state activity in networks of neurons involved in controlling arm movements and directing visual attention. He then correlated these patterns with the extent of each person's disabilities.

Corbetta found that the coordination between these networks was disrupted in those who have had strokes compared to healthy individuals, even though the regions themselves showed no obvious structural damage.

"For the first time we can assess the damage to brain networks in areas that otherwise appear normal on a scan," says Corbetta, who presented his results at the Forum of European Neuroscience in Amsterdam, the Netherlands, this week. He now plans to see whether this activity can be used to predict how well people will recover from a stroke.

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"rtpa" Versus "tpa"

Thu Jul 08 16:35:52 BST 2010 by Eric Kvaalen

Most of the places in this article where it says rtPA it should say tPA, which stands for "tissue plasminogen activator". The r of "rtPA" stands for "recombinant", so this refers to tPAs which are made artificially using recombinant technology. In other words, rtPAs are "drugs", whereas tPA is the natural protein produced by our cells.

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Brain Re-training To Decrease Pain

2010-07-12T03:06:00.001-07:00

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What should we do about tennis elbow

2010-07-01T04:04:00.001-07:00

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Predictors of Adherence to Treatment in Women With Fibromyalgia

2010-06-30T05:41:00.005-07:00

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Management of Pediatric Patients With Complex Regional Pain Syndrome

2010-06-30T05:41:00.003-07:00

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Management of Pediatric Patients With Complex Regional Pain Syndrome

2010-06-30T05:41:00.001-07:00

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Sympathetic Dysfunction in Long-term Complex Regional Pain Syndrome

2010-06-30T05:38:00.001-07:00

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Evidence and Practice in the Self-Management of Low Back Pain: Findings From an Australian Internet-based Survey

2010-06-30T05:34:00.001-07:00

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Carpal Tunnel Syndrome. Part I: Effectiveness of Nonsurgical Treatments–A Systematic Review

2010-06-30T05:31:00.001-07:00

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Using unconventional therapies to troubleshoot the brain

2010-06-29T02:57:00.001-07:00

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Psychometric Properties of the Fear-Avoidance Beliefs Questionnaire and Tampa Scale of Kinesiophobia in Patients With Shoulder Pain

2010-06-29T02:51:00.001-07:00

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Charlie Rose Brain Series Episode Nine

2010-06-23T20:58:00.001-07:00

Charlie Rose Brain Series Episode Nine

with Jeffrey Lieberman, Elyn Saks, Kay Redfield Jamison, Eric Kandel, Helen Mayberg and Stephen Warren
in Science & Health part of Charlie Rose: The Brain Series
on Tuesday, June 22, 2010 * * * * --> * * * * *

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Opioid Endocrinopathy: A Clinical Problem in Patients With Chronic Pain and Long-term Oral Opioid Treatment

2010-06-23T20:55:00.003-07:00

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Don't get sick in July?

2010-06-23T20:55:00.001-07:00

June is almost over. If you work in an academic medical center, as I do, that can mean only one thing.

The new interns are coming, and existing residents will soon be advancing to the next level. The joy! The excitement! The trepidation! And it's not all just the senior residents and the faculty feeling these emotions. It's the patients too. At least, it's the patients feeling the trepidation. The reason is the longstanding belief in academic medical centers, a belief that has diffused out of them and into "common wisdom," that you really, really don't want to get sick in July.

But is there any truth to this common wisdom, passed down from hoary emeritus faculty to professor to assistant professor to resident to medical student every year? Is there any truth to the belief commonly held by the public that care deteriorates in July? After all, this is something I've been taught as though it were fact ever since I first set trembling foot on the wards way back in 1986. So it must be true, right? Well, maybe. It turns out that a recent study published in the Journal of General Internal Medicine has tried once again to answer this question and come to a rather disturbing answer.

Imagine, if you will, that you want to determine whether there really is a "July effect," that quality of care really does plummet precipitously as common wisdom claims. How would you approach it? Mortality rates? That's actually fairly hard, because mortality rates fluctuate according to the time of year. For example, trauma admissions tend to spike in the summer. Well do I remember during my residency the fear of the fourth of July weekend, because it was usually the busiest trauma weekend of the year--and we had new residents to have to deal with it all. It was an attending's and senior resident's worst nightmare. In any case, if a hospital has an active trauma program it would naturally be expected that it would have more deaths during the summer regardless of resident status, quite simply because there is more trauma. Complication rates? That might also be a useful thing to look at, but that's actually not as easy as it seems either. How about comparing morbidity and mortality rates between teaching hospitals and community hospitals throughout the year and test whether mortality rates increase in academic hospitals relative to community hospitals. That won't work very well, either, mainly because there tends to be a huge difference in case mix and severity between academic institutions and community hospitals. Community hospitals tend to see more routine cases of lower severity than teaching hospitals do.

Yes, the probem in doing such studies is that it's not as straightforward as it seems. Choosing appropriate surrogate endpoints that indicate quality of care attributable to resident care is not easy. It's been tried in multiple studies, and the results have been conflicting. One reason is that existing quality metrics in medicine have not been sufficiently standardized and risk-adjusted to allow for reliable month-to-month comparisons on a large scale basis. In surgery, we are trying to develop such metrics in the form of the American College of Surgeons-National Surgical Quality Improvement Program (ACS-NSQIP), but these measures don't always apply to nonsurgical specialties and there are multiple competing measures of quality. It's true that we're getting much better at assessing quality than we used to be, but it's also true that we have a long way to go before we have a reliable, standardized, validated set of quality measures that can be applied over a large range of specialties.

That leaves investigators to pick and choose surrogates that suit their purposes, and that's exactly what the investigators of this most recent study, hailing from the University of Southern California and UCLA, have done. The surrogate that they chose is medication error-related deaths:

Inexperienced medical staff are often considered a possible source of medical errors.^1-6 One way to examine the relation-ship between inexperience and medical error is to study changes in the number of medical errors in July, when thousands begin medical residencies and fellowships.^1,7-11 This approach allows one to test the hypothesis that inexperienced residents are associated with increased medical errors^1,8,9,11-15--the so-called "July Effect."
Previous attempts to detect the July Effect have mostly failed,^1,8-17 perhaps because these studies examined small,^{8,10-13,15-17} non-geographically representative samples,^8-17 spanning a limited period,^11-16 although a study of anaesthesia trainees at one Australian hospital over a 5-year period did demonstrate an increase in the rate of undesirable events in February--the first month of their academic year.1 In contrast, our study examines a large, nationwide mortality dataset spanning 28 years. Unlike many other studies,18 we focus on fatal medication errors--an indicator of important medical mistakes. We use these errors to test the "New Resident Hypothesis"--the arrival of new medical residents in July is associated with increased fatal medication errors.

To test this hypothesis of the "July effect," the investigators examined the database of computerized United States death certificates from 1979 to 2006 containing the records of 62,338,584 deaths. The authors then looked for deaths for which a medication was listed as the primary cause of death. Their results are summarized below:

One thing that irritates me about this graph is that it does something I really, really hate in a graph. It cuts off the bottom, which, because the graph doesn't go to zero, makess the differences between the values seem a whole lot larger than they really are. That "July spike" plotted on this graph is an increase in the number of deaths due to medications over expected by maybe 7%, but it looks like a whole lot more. In fairness, though, the investigators analyzed: (1) only preventable adverse effects; (2) only medication errors (rather than combining several types of medical errors like medicinal and surgical); (3) only fatal medication errors; (4) only those medication errors coded as the primary cause of death (rather than medication errors coded as primary, secondary, and/or tertiary). Still, one always have to wonder about how the denominator is calculated; i.e., how the "expected" number of deaths for each month is calculated. Basically, the investigators used a simple least-squares regression analysis to estimate the "expected" number of deaths.

If this is where the investigators had stopped, I might not have been as annoyed by this study. Sure, it's questionable whether assuming that deaths due to medication errors are strongly correlated with new, inexperienced residents. After all, if there's one thing we're starting to appreciate more and more, it's that medication errors tend to be a system problem, rather than a problem of any single practitioner or group of practitioners. But the above graph does appear to show an anomaly in July.

Unfortunately the investigators did something that always disturbs me when I see it in a paper. They faced a problem. Death certificates didn't show whether the death occurred in a teaching hospital or not. So, in order to get at whether there was a correlation between a greater "July effect" and teaching hospitals, as would be expected, they looked at county-level data for hospital deaths due to medication errors. Then they determined whether each of these counties had at least one teaching hospital and estimated the percentage of the hospitals in each county that are teaching hospitals, the rationale being the higher the proportion of teaching hospitals in a county, the larger the July effect is likely to be. This is the graph they came up with:

Holy ecological fallacy, Batman! The investigators appear to be implying that a relationship found in group level data applies to individual level data; i.e., individual hospitals. it almost reminds me of a Geier study. In any case, why didn't surgical errors increase if the "July effect" exists? Wouldn't this be expected? I mean, we surgeons are totally awesome and all, but we're only human, too. If the July effect exists, I have no reason to believe that we would be immune to it.

The existence of a "July effect" is not implausible. After all, in late June and early July every year, we flood teaching hospitals with a new crop of young, eager, freshly minted doctors. I can feel the anticipation at my own institution right now. It's a veritable yearly rite that we go through in academia. Countering the likelihood of a "July effect" is the seasonally tightened anal sphincters of attendings and senior residents that lead them to keep a tight rein on these new residents--which is as it should be. In any case, this particular study is mildly suggestive, but hardly strong evidence for the existence of the "July effect." Personally, I find the previous study on this issue that I blogged about three years ago to be far more convincing; its results suggested a much more complex interplay of factors.

In the end, I have some serious problems with this study, not the least of which is the assumption that medication errors are correlated so strongly with inexperienced residents when we now know that they are far more a systems issue than they are due to any individual physicians or groups. There are many steps in the chain from a medication order all the way down to actually administering the medication to the patient where something can go wrong, and, in fact, these days the vast majority of the effort that goes into preventing medication errors is expended on putting systems in place that catch these errors before the medication ever makes it to the patient, either through computerized ordering systems that question orders with incorrect doses or medications, systems where pharmacists and then nurses check and double check the order, and then systems where the actual medication order is checked against the medication to be given using computerized bar code scanning systems. It's really a huge stretch to conclude that fatal medication errors are a good surrogate marker for quality of care attributable to the resident staff, the pontifications and bloviations of the authors to justify their choice in the Introduction and Discussion sections of this study notwithstanding. The other problem is the pooling of county level data into a heapin' helpin' of the ecological fallacy. Is there a July effect? I don't know. It wouldn't surprise me if there were. If the July effect does exist, however, this study is pretty thin gruel to support its existence and estimate its severity.

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New drugs to relieve cancer pain

2010-06-23T10:09:00.001-07:00

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Judgement and Experience

Judgement and ExperienceSaturday August 21, 2010

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Mice Show Heritable Desire For Exercise

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