Tag Archives: chronic pain

11Feb/12

Manual therapy, pain and the immune system

As a physiotherapist I frequently use my hands to treat the joints and tissues. It comes with the territory, everyone expects hands-on therapy and it does helps to reduce tension and pain. Most likely, the pain relief from joint mobilisation is due to descending mechanisms that include those that are powered by serotonin and noradrenaline (see here). This is very useful to know as it tells us about the effects of passively moving joints and importantly permits wise selection of techniques to target the pain mechanisms. Building on the knowledge base, two very recent studies have identified some extremely interesting results.

Firstly, Martins et al. (2011) found that ankle joint mobilisation reduced pain in a neuropathic pain model in rats along with seeing the regeneration of nerve tissue and inhibition of glial cell activation (a blog will be coming soon that discusses the immune system in pain states) in the dorsal horn of the spinal cord. Secondly, Crane et al. (2012) looked at how massage helps reduce the pain of exercise-induced muscle damage in young males. Taking muscle biopsies they found that massaged subjects demonstrated attenuation of proinflammatory cytokines, key players in sensitisation. It was also noted that massage had no effect upon metabolites such as lactate – see below.

More research into the mechanisms that underpin the effects of hands-on therapy is needed despite the advancements in our understanding. The ability to focus treatment upon this understanding can only develop our effectiveness in treating pain. I am very optimistic about the movement forwards in pain and basic science, and how this can be applied  in our thinking with individual patients. The language is changing with the words ‘treatment’ being used rather than ‘management’, the latter of which can imply that one has reached their limit of improvement. This is exciting and more importantly, realistic when one considers therapies such as the graded motor imagery. We do not have treatments that work for all pains but we do have brains and body systems that are flexible, dynamic and can change if given the opportunity, the right stimulation within the right context on the background of good understanding. It is our duty to keep this rolling onwards and thinking hard about how to best use the findings such as those highlighted in this blog.

Pain. 2011 Nov;152(11):2653-61. Epub 2011 Sep 8.

Ankle joint mobilization reduces axonotmesis-induced neuropathic pain and glial activation in the spinal cord and enhances nerve regeneration in rats.

Martins DF, Mazzardo-Martins L, Gadotti VM, Nascimento FP, Lima DA, Speckhann B, Favretto GA, Bobinski F, Cargnin-Ferreira E, Bressan E, Dutra RC, Calixto JB, Santos AR.

Source

Laboratório de Neurobiologia da Dor e Inflamação, Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário, Trindade, Florianópolis, SC, Brazil.

Abstract

An important issue in physical rehabilitation is how to protect from or to reduce the effects of peripheral nerve injury. In the present study, we examined whether ankle joint mobilization (AJM) would reduce neuropathic pain and enhance motor functional recovery after nerve injury. In the axonotmesis model, AJM during 15 sessions every other day was conducted in rats. Mechanical and thermal hyperalgesia and motor performance deficit were measured for 5 weeks. After 5 weeks, we performed morphological analysis and quantified the immunoreactivity for CD11b/c and glial fibrillary acidic protein (GFAP), markers of glial activation, in the lumbar spinal cord. Mechanical and thermal hyperalgesia and motor performance deficit were found in the Crush+Anesthesia (Anes) group (P<0.001), which was significantly decreased after AJM (P<0.001). In the morphological analysis, the Crush+Anes group presented reduced myelin sheath thickness (P<0.05), but the AJM group presented enhanced myelin sheath thickness (P<0.05). Peripheral nerve injury increased the immunoreactivity for CD11b/c and GFAP in the spinal cord (P<0.05), and AJM markedly reduced CD11b/c and GFAP immunoreactivity (P<0.01). These results show that AJM in rats produces an antihyperalgesic effect and peripheral nerve regeneration through the inhibition of glial activation in the dorsal horn of the spinal cord. These findings suggest new approaches for physical rehabilitation to protect from or reduce the effects of nerve injury.

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Sci Transl Med. 2012 Feb 1;4(119):119ra13.

Massage therapy attenuates inflammatory signaling after exercise-induced muscle damage.

Crane JD, Ogborn DI, Cupido C, Melov S, Hubbard A, Bourgeois JM, Tarnopolsky MA.

Source

Department of Kinesiology, McMaster University, Hamilton, Ontario L8S 4L8, Canada.

Abstract

Massage therapy is commonly used during physical rehabilitation of skeletal muscle to ameliorate pain and promote recovery from injury. Although there is evidence that massage may relieve pain in injured muscle, how massage affects cellular function remains unknown. To assess the effects of massage, we administered either massage therapy or no treatment to separate quadriceps of 11 young male participants after exercise-induced muscle damage. Muscle biopsies were acquired from the quadriceps (vastus lateralis) at baseline, immediately after 10 min of massage treatment, and after a 2.5-hour period of recovery. We found that massage activated the mechanotransduction signaling pathways focal adhesion kinase (FAK) and extracellular signal-regulated kinase 1/2 (ERK1/2), potentiated mitochondrial biogenesis signaling [nuclear peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α)], and mitigated the rise in nuclear factor κB (NFκB) (p65) nuclear accumulation caused by exercise-induced muscle trauma. Moreover, despite having no effect on muscle metabolites (glycogen, lactate), massage attenuated the production of the inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) and reduced heat shock protein 27 (HSP27) phosphorylation, thereby mitigating cellular stress resulting from myofiber injury. In summary, when administered to skeletal muscle that has been acutely damaged through exercise, massage therapy appears to be clinically beneficial by reducing inflammation and promoting mitochondrial biogenesis.

03Feb/12

Chronic pain in sport – Specialist Clinic in London

Chronic pain is a real problem in the sporting world. The effects of not being able to participate are far reaching, especially when sport is your profession. There are a huge numbers of clinics offering treatments to deal with pain and injury and in many cases the problem improves. However, there are those who do not progress successfully, resulting in on-going pain, failed attempts to return to playing and varied responses to tissue-based treatment (manual therapy, injections, surgery etc). Understanding more about pain and how your body (brain) continues to protect itself is a really useful start point in moving forwards if you have become stuck. We know that gaining knowledge about the problem can actually improve a clinical test and the pain threshold.

When we injure ourselves playing sport the healing process begins immediately. Chemicals released by the tissues and the immune system are active locally, sealing off the area, dealing with the damaged tissue and setting the stage for rebuilding and repair. The pain asscociated with this phase is expected, normal and unpleasant. It is the unpleasantness that drives you to behave in a protective manner, for example limp, seek advice and treatment. Again, that is normal. Sometimes we can injure ourselves and not know that we have damaged the tissues. There are many stories of this happening when survival or something else is more important. This is because pain is a brain (not mind or ‘in the head’) experience 100% of the time. The brain perceives a threat and then protects the body. If no threat is perceived or it is more important to escape or finish the cup final, the brain is quite capable of releasing chemicals (perhaps 30 times more powerful than morphine) to provide natural pain relief. We know that pain is a brain experience because of phantom limb pain, a terrible situation when pain is felt in a limb that no longer exists. The reason is that we actually ‘feel’ or ‘sense’ our bodies via our virtual body that is mapped out in the brain. This has been mapped out by some clever scientists and in more recent years studies intensely using functional MRI scans of the brain.

Unfortunately, the brain can continue to protect the body with pain and altered movement beyond the time that is really useful. Changes in the properties of the neurons in the central nervous system (central sensitisation) mean that stimuli that are normally innocuous now trigger a painful response as can those outside of the affected area. One way to think about this functionality is that the gain or volume has been turned up, and we know that much of this amplification occurs in the spinal cord, involving both neurons and the immune system. Neurogenic inflammation can also be a feature, where the C-fibres release inflammatory chemicals into the tissues that they supply. On the basis that the brain is really interested in inflammation, even a small inflammatory response can evoke protective measures. Changes in the responsiveness of the ‘danger’ system as briefly described, underpin much of the persisting sensitivity. Altered perception is a further common description, either in the sense that the area is not controlled well or feels somewhat different – see here.

As the problem persists, so thinking and beliefs about the pain and injury can become increasingly negative. Unfortunately this can lead to behaviours that do not promote progression. Avoidance of activities, fear of movement, hypervigilance to signals from the body and catastrophising about the pain are all common features, all of which require addressing with both pain education and positive experiences to develop confidence and deeper understanding. An improvement in the pain level is a great way of starting this process, hence the importance of a tool box of therapies and strategies that target the pain mechanism(s) identified in the assessment.

Experience and plenty of scientific data describe the integration of body, brain and mind. This can no longer be ignored. It is fact. The contemporary biobehavioural approach to chronic and complex pain addresses the pain mechanisms, issues around the problem and the influencing factors in a biopsychosocial sense:

  • Biology: e.g./ physiology of pain, body systems involved in protection, tissue health
  • Psychology: e.g./ fears, anxiety, beliefs about the pain, thinking processes, outlook, coping, past experiences
  • Social: e.g./ work effects, effect upon the family, socialising, role of significant others (spouse, family), financial considerations

Specialist Clinic in London and Surrey for chronic pain and injury in sport – call 07518 445493

Chronic pain and injury requires an all-encompassing biobehavioural approach. Although the end aims can be different, the structure and themes within the treatment programme are similar to those that tackle any chronic pain issue. Bringing these principles into the sports arena, we can incorporate traditional models of care and advance beyond the tissue-based strategies to a way of working that addresses the source of the problem alongside the influencing factors that are slowing or even preventing recovery.

If you as a player are struggling to move forwards or have a player on your team who is not recovering or failing to respond as expected to treatment, we would be very pleased to help you. Call 07518 445 493 or email [email protected] for further infomartion about the clinics:

The Specialist Pain Physio Clinics work closely with the very best Consultants and can organise investigations such as MRI scans and x-rays with reports rapidly, an on-site at the New Malden Diagnostic Centre, 9 Harley Street and in Chelsea.

01Feb/12

Can’t get over that skiing injury?

To the skier, the thought of watching friends and family clumping off in their boots towards the lift whilst sitting with a leg up, packed with ice and the daily paper, is intensely frustrating. Injuries happen. In many cases with the right early treatment, perhaps surgery and definitely a thorough rehabilitation programme, the symptoms resolve and the leg works again, good as new. However, there are a number of cases when this does not follow suit and the pain and limitations continue. There are reasons for this occurrence and they extend beyond the health of the tissues that almost always go through a healing process.

There are some complex mechanisms at play in the nervous and immune systems that are really useful when we first have an injury. This of course includes pain that is part of the way the brain defends the body when we damage ourselves. The way in which we go about protecting and treating ourselves is driven in part by the pain that motivates these actions: rest, seek advice or take analgesia. That is what pain really is, a motivator to take action to promote healing and survival. In the early stages of having injured tissues, often ligaments at the knee, this is really useful and important. Briefly, the damaged tissues release chemicals that sensitise the local nerve endings, stimulating a volley of danger signals to be sent to the spinal cord. Here, secondary neurons send this information to the brain for scrutiny. On deeming there to be a threat, the brain engages protective responses including pain, changes in movement and healing. Sometimes we can injure our tissues and the brain decides that something else is more important, perhaps escaping from the mountain, and will send signals down to the spinal cord to interfere with those coming from the tissues. The end result is the feeling of no pain and therefore you can take yourself to safety. Then it can start hurting. All in all, the responses will vary as will our ability to cope.

The early bombardment of the spinal cord and brain with danger signals that can also be influenced by the context of the injury, e.g. really scary, leads to changes in the properties of the neurons in the spinal cord. This means that subsequent signals can be amplified. It also means that normal signals (e.g. light touch) can start to provoke a painful response as can areas not directly involved. In the latter case one can find that the area of pain grows (click here). The on-going activity in the nervous system and other systems such as the immune system, endocrine system and autonomic system underpin the experience of persisting pain and protection, including altered movement that is so important to normalise.

In the case that the problem persists, the treatment is different. The tissues are addressed as one would expect with manual therapy, massage and other local treatments. However, alongside these traditional techniques are a range of strategies and treatments that are based upon the latest pain sciences that target the changes aforementioned and others. These strategies target the mechanisms at play and at source reduce the threat and hence the pain, normalise motor control and sensation of the affected area and restore function so that there can be a progression back to pre-injury activities.

For further information please contact the clinic: 07518 445493

18Jan/12

Contemporary understanding of factors in joint pain

Recent research has identified biological reasons for joint pain in arthritis:

  • Interleukin-6, a pro-inflammatory cytokine released both locally at the joint and in the spinal cord, consequently plays a role in the widespread nature of the pain via its role in central sensitisation.
  • Sprouting of sensory and sympathetic fibres at the joint may well have a role in sensitisation
  • Angiogenesis, the growth of new blood vessels, at the joint, perhaps having a role in inflammation

Some of this may sound familiar. IL-6 is known to play a role in the spinal cord following nerve injury, sprouting of the sympathetic fibres at the DRG and in tendinopathy, and angiogenesis also seen in tendinopathy. All are clearly responses by the body and are involved in pain–remembering that pain is a brain experience 100% of the time of course.

Spinal interleukin-6 is an amplifier of arthritic pain (Vazquez et al. 2011)

Objective.

Significant joint pain is usually widespread beyond the afflicted joint which results from the sensitization of nociceptive neurons in the central nervous system (central sensitization). In the present study we explored (a) whether the proinflammatory cytokine interleukin-6 (IL-6) in the joint induces central sensitization, (b) whether joint inflammation causes IL-6 release in the spinal cord, and (c) whether spinal IL-6 contributes to central sensitization.

Methods.

In anesthetized rats electrophysiological recordings were made from spinal cord neurons with sensory input from the knee joint. Neuronal responses to mechanical stimulation of the knee and the leg were monitored. IL-6 and its soluble receptor sIL-6R were applied to the knee joint or the spinal cord. Spinal release of IL-6 was measured by ELISA. Sgp130 which neutralizes IL-6/sIL-6R was spinally applied during development of joint inflammation or during established inflammation.

Results.

A single injection of IL-6/sIL-6R into the knee joint as well as spinal application of IL-6/sIL-6R significantly increased the responses of spinal neurons to mechanical stimulation of the knee and ankle joint, i.e. induced central sensitization. Spinally applied sgp130 attenuated this IL-6 effect. Development of knee inflammation caused spinal release of IL-6. Spinal application of spg130 attenuated the development of inflammation-evoked central sensitization but did not reverse it.

Conclusions.

Not only IL-6 in the joint is involved in the generation of joint pain but also IL-6 which is released in the spinal cord. Spinal IL-6 contributes to central sensitization and thus promotes the widespread hyperalgesia in the course of joint disease.

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Neuroplasticity of sensory and sympathetic nerve fibers in the painful arthritic joint (Ghilardi et al. 2011)

Objective.

Many forms of arthritis are accompanied by significant chronic joint pain. Here we studied whether there is significant sprouting of sensory and sympathetic nerve fibers in the painful arthritic knee joint and whether nerve growth factor (NGF) drives this pathological reorganization.

Methods.

A painful arthritic knee joint was produced by injection of complete Freund’s adjuvant (CFA) into the knee joint of young adult mice. CFA-injected mice were then treated systemically with vehicle or anti-NGF antibody. Pain behaviors were assessed and at 28 days following the initial CFA injection, the knee joints were processed for immunohistochemistry using antibodies raised against calcitonin gene-related peptide (CGRP; sensory nerve fibers), neurofilament 200 kDa (NF200; sensory nerve fibers), growth associated protein-43 (GAP43; sprouted nerve fibers), tyrosine hydroxylase (TH; sympathetic nerve fibers), CD31 (endothelial cells) or CD68 (monocytes/macrophages).

Results.

In CFA-injected mice, but not vehicle-injected mice, there was a significant increase in the density of CD68+ macrophages, CD31+ blood vessels, CGRP+, NF200+, GAP43+, and TH+ nerve fibers in the synovium as well as joint pain-related behaviors. Administration of anti-NGF reduced these pain-related behaviors and the ectopic sprouting of nerve fibers, but had no significant effect on the increase in density of CD31+ blood vessels or CD68+ macrophages.

Conclusions.

Ectopic sprouting of sensory and sympathetic nerve fibers occurs in the painful arthritic joint and may be involved in the generation and maintenance of arthritic pain.

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Contributions of angiogenesis to inflammation, joint damage, and pain in a rat model of osteoarthritis (Ashraf et al. 2011)

Objective

To determine the contributions of angiogenesis to inflammation, joint damage, and pain behavior in a rat meniscal transection model of osteoarthritis (OA).

Methods

OA was induced in male Lewis rats (n = 8 per group) by meniscal transection. Animals were orally dosed with dexamethasone (0.1 mg/kg/day), indomethacin (2 mg/kg/day), or the specific angiogenesis inhibitor PPI-2458 (5 mg/kg every other day). Controls consisted of naive and vehicle-treated rats. Synovial inflammation was measured as the macrophage fractional area (expressed as the percentage), thickness of the synovial lining, and joint swelling. Synovial angiogenesis was measured using the endothelial cell proliferation index and vascular density. Channels positive for vessels at the osteochondral junction were assessed (osteochondral angiogenesis). Medial tibial plateaus were assessed for chondropathy, osteophytosis, and channels crossing the osteochondral junction. Pain behavior was measured as weight-bearing asymmetry.

Results

Dexamethasone and indomethacin each reduced pain behavior, synovial inflammation, and synovial angiogenesis 35 days after meniscal transection. Dexamethasone reduced, but indomethacin had no significant effect on, the total joint damage score. PPI-2458 treatment reduced synovial and osteochondral angiogenesis, synovial inflammation, joint damage, and pain behavior.

Conclusion

Our findings indicate that synovial inflammation and joint damage are closely associated with pain behavior in the meniscal transection model of OA. Inhibition of angiogenesis may reduce pain behavior both by reducing synovitis and by preventing structural change. Targeting angiogenesis could therefore prove useful in reducing pain and structural damage in OA.

19Dec/11

Healthy tissues in 1-2-3

The simple fact is that our tissues need movement to be healthy. By tissues I am referring to muscles, tendons, ligaments, bones, fascia and skin. This does not need to be extreme movement but it must be regular and purposeful. Even without pathology, pain or an injury it is vital that the tissues are moved consistently throughout the day. It is likely that if you are recovering from a pain state, this movement will need to be ‘little and often’ to follow the principle of ‘motion is lotion’. I love this phrase. It was coined by the NOI Group guys and I use it frequently. At the moment I a considering some other phrases with similar meanings. If anyone has any suggestions please do comment below.

There are many types of movement from simple stretching to walking and more structured exercise such as yoga.  For convenience I talk to patients about the ‘themes’ of the treatment programme. In relation to movement there are three themes 1-2-3: specific exercises to re-train normal movement and control of movement, general exercise and the self-care strategies to be used throughout the day.

The specific exercises could include re-learning to walk normally, to re-establish normal control of the ankle or to concurrently develop confidence such as in bending forwards in cases of back pain. Normal control of movement is a fundamental part of recovery. When the information from the tissues to the brain is accurate, there is a clear view on what is happening, menaing that the next movement is efficient and so on.

General exercise is important for our health in body and mind. As well as reducing risk of a number of diseases, our brains benefit hugely from regular exercise. We release chemicals such as serotonin that make us feel good, endorphins that ease pain and BDNF that works like a miracle grow for brain cells. Gradually increasing exercise levels is a part of the treatment programme for all of these reasons.

Regularly punctuating static positions with movement nourishes the tissues and the brain’s representation of the body. The tissues will tighten and stiffen when they remain in one position for a long period of time, and more so when there is pathology or pain. Often there is already overactivity in the muscular system when we are in pain as part of the way the brain defends the body. This overactivity leads to muscle soreness that can be eased with consistent movement.

These three simple measure are behaviours. Behaviours are based on our belief system and therefore we need to understand why it is so important to move and re-establish normal control of movement as part of recovering from an injury or pain state. This includes tackling any issues around fear of movement and hypervigilance towards painful stimuli from the body. Our treatment programmes address these factors comprehensively, employing the biopsychosocial model of care and the latest neuroscience based knowledge of pain.

Email [email protected] for more information about our treatment programmes or to book an appointment.

09Dec/11

Mindfulness

Mindfulness has grown in popularity over recent years, and for good reason. Those who regularly practice mindful meditation and mindfulness on a day-to-day basis will tell you about their clarity of thought, their sense of ease and their good physical health. The practice is recommended by NICE for depression as well as the frequent teaching of mindfulness as a way to deal with pain.

At the clinic, I encourage mindful practice to help the individual be released from the pull of negative and unhelpful thinking about pain. We all have thoughts. This is the action of the mind and is a normal process. Automatic thoughts pop into our head and trigger emotional and physical responses–think about a waxy, yellow lemon resting upon a plate; you take a knife and cut into the rind, releasing the citrus odour as you divide the lemon in two, the pieces rolling away from the blade; you further cut the two halves into quarter segments, each time triggering a small burst of juice into the air around; imagine taking one segment and gently placing it into the front of your mouth; what are you experiencing? Thoughts change our physiology because our brains respond to thinking or imagining, just as if we are present. This is why it can hurt when we watch someone else move their body in a way that would be painful for us.

Automatic thoughts are just that. How we respond next we can decide. By being observant of our thoughts we can avoid following an automatic thought with another thought and another that lead to persisting physiological responses and emotions that are unpleasant and unhelpful. In particular those thougths that often recur and create unease and anxiety. They are simply thoughts. They are not us and they are not reality. They are just thoughts. But, they can be powerful unless we can find a way to be observant, non-judgmental, aware and present. That ‘way’ can be mindfulness.

Here are some great people talking about mindfulness and meditation

 

There has been and continues to be a great deal of work looking at mindfulness and how it may work. The Oxford Mindfulness Centre (OMC) undertakes research and provides training.
‘The OMC Team does ground-breaking clinical and neuroscience research on mindfulness. It assesses the efficacy of different forms of mindfulness practice for different types of problem, and is building up a peer-reviewed body of knowledge about what forms of mindfulness intervention best suits which type of person.’
A list of the OMC publications is available here

For further information on our use of mindfulness for pain, please email [email protected]

09Dec/11

Top 3 recommended books

These three titles I frequently recommend to patients to help develop the necessary deeper understanding of pain, stress and the role of the mind in physical health. They are all extremely well written and designed to educate to promote change towards more healthy behaviours. This sits exactly with my approach to physiotherapy for painful conditions that are complex, chronic or often both.

Painful Yarns by Lorimer Moseley

‘Moseley is pain management’s answer to James Herriot. This book capture that illusive ability to both educate and entertain’. Dr Micheal Thacker, Pain Sciences Program, Kings College London

‘I love a good story…..but the best thing was that when the stories were compared to how pain works, it made sense’. Dimos, lorry driver with chronic back pain

Available from NOIgroup 01904 737919

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Why zebras don’t get ulcers by Robert Sapolsky


Now in a third edition, Robert M. Sapolsky’s acclaimed and successful Why Zebras Don’t Get Ulcers features new chapters on how stress affects sleep and addiction, as well as new insights into anxiety and personality disorder and the impact of spirituality on managing stress. As Sapolsky explains, most of us do not lie awake at night worrying about whether we have leprosy or malaria. Instead, the diseases we fear – and the ones that plague us now – are illnesses brought on by the slow accumulation of damage, such as heart disease and cancer. When we worry or experience stress, our body turns on the same physiological responses that an animal’s does, but we do not resolve conflict in the same way – through fighting or fleeing. Over time, this activation of a stress response makes us literally sick. Combining cutting-edge research with a healthy dose of good humour and practical advice, Why Zebras Don’t Get Ulcers explains how prolonged stress causes or intensifies a range of physical and mental afflictions, including depression, ulcers, colitis, heart disease, and more. It also provides essential guidance to controlling our stress responses. This new edition promises to be the most comprehensive and engaging one yet.

Available from Amazon here

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Mindfulness by Mark Williams & Danny Penman

‘If you want to free yourself from anxiety and stress, and feel truly at ease with yourself, then read this book.’ –Ruby Wax

‘You would do well to put yourself in the experienced hands of Mark Williams and Danny Penman, and give yourself over to their guidance and to the programme that they map out.’ –Jon Kabat-Zinn

‘Want a happier, more content life? I highly recommend the down-to-earth methods you*ll find in ‘Mindfulness’. Professor Mark Williams and Dr. Danny Penman have teamed up to give us scientifically grounded techniques we can apply in the midst of our everyday challenges and catastrophes’ –Daniel Goleman, Author of ‘Emotional Intelligence’

‘Peace can’t be achieved in the outside world unless we have peace on the inside. Mark Williams and Danny Penman’s book gives us this peace’ –Goldie Hawn

‘Want a happier, more content life? I highly recommend the down-to-earth methods you’ll find in ‘Mindfulness’. Professor Mark Williams and Dr. Danny Penman have teamed up to give us scientifically grounded techniques we can apply in the midst of our everyday challenges and catastrophes’ –Daniel Goleman, Author of ‘Emotional Intelligence’

Available from Amazon here

21Oct/11

Using neuroscience to understand and treat pain

I love neuroscience. It makes my job much easier despite being a hugely complex subject. Neuroscience research has cast light over some of the vast workings of our brains and helped to explain how we experience ourselves and the richness of life. An enormous topic, in this blog I am briefly going to outline the way in which I use contemporary neuroscience to understand pain and how we can use this knowledge to treat pain more effectively. This is not about the management of pain, it is the treatment of pain. Management of pain is old news.

Understanding pain is the first step towards changing the painful experience. Knowing how the brain and nervous system operate allows us to create therapies that target the biological mechanisms that underpin pain. Appreciation of the plastic ability of the nervous system from top to bottom–brain to periphery–provides us with the opportunity to ‘re-wire’, and therefore to alter the function of the system and make things feel better. Knowing the role of the other body systems when the brain is defending us, is equally important. The synergy of inputs from the immune system, endocrine system and autonomic nervous system provides the brain with infomration about our internal physiology that it must scrutinse and act upon in the most appropriate way. We call this action the brain’s ‘output’ which is the responses that it co-ordinates to promote health and survival.

Excellent data from contemporary research tells us that understanding pain increases the pain threshold (harder to trigger pain), reduces anxiety in relation to pain and enhances our ability to cope and deal with the pain. We know that movement can also improve after an education session. This is because the perceived threat is reduced by learning and understanding what is going on inside, and knowing what can be done. The vast majority of patients who come to the clinic do not know why their pain has persisted, what pain really is, how it is influenced and what they can do about it themselves. For me this is the start point. Explaining the neuroscience of pain. Facts that we know people can absorb, understand and apply to themselves in such a way that the brain changes and provides a different experience.

It is the brain that gives us our experience of ourselves and the world around us. This includes the sensory and emotional experience of pain. The brain receives information from the body via the peripheral nervous system that suggests there is a threat to the tissues (input). In response, the brain must decide whether this threat is genuine based upon what is happening at the time, the emotional state, past experience, the belief system, gender, genetics, health status, culture and other factors. In the case that the brain perceives a threat, the output will be pain. The Mature Organism Model developed by Louis Gifford describes this beautifully (see below).

Pain is a motivator. It grabs our attention in the area of the body that the brain feels is threatened based upon the danger signals it is receiving from the tissues via the spinal cord. The brain actually ascribes the location of the pain via the map of the body that exist in the sensory cortex. On feeling the pain, we take action. This is the reason for pain. It motivates us to move, seek help or rest. Pain is an incredible device that we have for survival and learning, necessary to navigate life and completely normal. The brain constructs the pain experience and associated symptoms in such a way that we have to take note and do something about it immediately.

29Sep/11

Mastering your rehabilitation – Part 1: why exercise & train?

When we sustain an injury or experience a painful condition, our movement changes. In the early stages this can be obvious, for example we would limp having sprained an ankle. Sometimes the limp, medically termed an ‘antalgic gait’, persists without the individual being aware. This is the same for other forms of guarding that is part of the body’s way of protecting itself. By tightening the affected area or posturing in a manner that withdraws, the body is changing the way that we work so that healing can proceed. Clearly this is very intelligent and useful. The problem lies with persisting guarding or protection that continues to operate.

 

We know that when the brain is co-ordinating a response to a threat, a number of systems are active. This includes the nervous system, the motor system, the immune system and the endocrine system (hormones). This is all part of a defence in and around the location that is perceived to be under threat. It is important to be able to move away from danger and then to limit movement, firstly to escape from the threat (e.g. withdraw your hand from a hot plate) and then to facilitate the natural process of healing by keeping the area relatively immobilised. Interestingly, at this point our beliefs about the pain and injury will determine how we behave and what action we take. If we are concerned that there is a great deal of damage and that movement will cause further injury, we will tend to keep the area very still, looking out for anything or anyone who may harm us. Over-vigilance can lead to over-protection and potentially lengthen the recovery process. This is one reason why seeking early advice and understanding your pain and injury is important, so that you can optimise your potential for recovery.

We have established that we move differently when we are injured and in pain. In more chronic cases, the changes in movement and control of movement can be quite subtle. An experienced physiotherapist will be able to detect these and other protective measures that are being taken. These must be dealt with, because if we are not moving properly, this is a reason for the body to keep on protecting itself through feedback and feed-forward mechanisms. Re-training movement normalises the flow of information to and from the tissues to the brain. Often this process needs enhancement or enrichment as the sensory flow and position sense (proprioception) is not efficient. Movement is vital for tissue and brain health, nourishing the tissues with oxygen and chemicals that stimulate health and growth.

To train normal movement is to learn. The body is learning to move effectively and this process is the same as learning a golf shot, a tennis stroke, a language or a musical instrument. Mastery. You are asking yourself to master normal movement. What does this take? Consistency, discipline, practice (and then some more practice), time, dedication, awareness and more. The second part of this blog will look at mastery as a concept that can help you understand the way in which you can achieve success with your rehabilitation.

26Sep/11

Dysmenorrhoea and Pain

Dysmenorrhoea and pain — You may wonder why I am writing about dysmenorrhoea. It is because in a number of cases that I see, there is co-existing dysmenorrhea and other functional pain syndromes. These include irritable bowel syndrome (IBS), migraine, chronic low back pain, pelvic pain, bladder pain and fibromyalgia. Traditionally all of these problems are managed by different specialists with their particular end-organ in mind—e.g./ IBS = gastroenterologist; migraine = neurologist; fibromyalgia = rheumatologist. The science however, tells us that these seemingly unrelated conditions can be underpinned by a common factor, central sensitisation. This is not a blog about dysmenorrhoea per se, but considers the problem in the light of recent scientific findings and how it co-exists with other conditions.

 

Central sensitisation is a state of the central nervous system (CNS)—the spinal cord and the brain. This state develops when the CNS is bombarded with danger signals from the tissues and organs.  It means that when information from the body tissues, organs and systems reaches the spinal cord, it is modified before heading up to the brain. The brain scrutinises this information and responds appropriately by telling the body to respond. If there is sensitisation, these responses are protective and that includes pain. Pain is part of a protective mechanism along with changes in movement, activity in the endocrine system, the autonomic nervous system and the immune system. Pain itself is a motivator. It motivates action because it is unpleasant, and provides an opportunity to learn—e.g./ do not touch because it is hot. This is very useful with a new injury but less helpful when the injury has healed or there is no sign of persisting pathology.

Understanding that central sensitisation plays a part in these conditions creates an opportunity to target the underlying mechanisms. This can be with medication that acts upon the CNS and with contemporary non-medical approaches that focus upon the spinal cord and brain such as imagery, sensorimotor training, mindfulness and relaxation. In this way, dysmenorrhoea can be treated in a similar fashion to a chronic pain condition although traditionally it is not considered to be such a problem. The recent work by Vincent et al. (2011) observed activity in the brains of women with dysmenorrhoea and found it to be similar to women with chronic pain, highlighting the importance of early and appropriate management.

The aforementioned study joins an increasing amount of research looking at the commonality of functional pain syndromes. We must therefore, be vigilant when we are assessing pain states and consider that the presenting problem maybe just part of the bigger picture. Recognising that central processing of signals from the body is altered in a number of conditions that appear to be diverse allows us to offer better care and hence improve quality of life.

* If you are suffering with undiagnosed pain, you should consult with your GP or a health professional.