Category Archives: Understanding pain

29Oct/12
The brain changes in pain

The brain changes

The nervous system is plastic meaning that it changes and moulds according to the stimuli presented. Norman Doidge wrote about the ‘brain that changes itself’ and we have seen over the past 10 years or so an increasing number of studies that show this in a range of conditions, some painful and others not. Our ability to change and adapt have been a vital characteristics for our survival and to learn new skills. The same principles apply when we think about rehabilitation and treatment of painful conditions. We need to tap into these properties and stimulate the brain and other body systems (e.g. immune system, neuroendocrine) so that we are creators of health manifesting physically through normal movement, function and optimal performance.

Here are some examples of studies that have shown brain changes using functional MRI. You will note the variety that includes rheumatoid arthritis, osteoarthritis, pain, chronic pelvic pain, schizophrenia and fibromyalgia. This has serious implications for treatment in that we need brain focused therapies as well as those that target the tissues and end-organs. This includes the absolute need to explain pain and symptoms from a neuroscience perspective.

Arthritis Rheum. 2012 Feb;64(2):371-9. doi: 10.1002/art.33326.

Structural changes of the brain in rheumatoid arthritis.

Wartolowska K, Hough MG, Jenkinson M, Andersson J, Wordsworth BP, Tracey I.

Abstract

OBJECTIVE: To investigate whether structural changes are present in the cortical and subcortical gray matter of the brains of patients with rheumatoid arthritis (RA).

METHODS: We used two surface-based style morphometry analysis programs and a voxel-based style analysis program to compare high-resolution structural magnetic resonance imaging data obtained for 31 RA patients and 25 age- and sex-matched healthy control subjects.

RESULTS: We observed an increase in gray matter content in the basal ganglia of RA patients, mainly in the nucleus accumbens and caudate nucleus. There were no differences in the cortical gray matter. Moreover, patients had a smaller intracranial volume.

CONCLUSION: Our results suggest that RA is associated with changes in the subcortical gray matter rather than with cortical gray matter atrophy. Since the basal ganglia play an important role in motor control as well as in pain processing and in modulating behavior in response to aversive stimuli, we suggest that these changes may result from altered motor control or prolonged pain processing. The differences in brain volume may reflect either generalized atrophy or differences in brain development.

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Am J Psychiatry. 2002 Feb;159(2):244-50.

Volume changes in gray matter in patients with schizophrenia.

Hulshoff Pol HE, Schnack HG, Bertens MG, van Haren NE, van der Tweel I, Staal WG, Baaré WF, Kahn RS.

Abstract

OBJECTIVE: Schizophrenia is generally characterized by a progressive decline in functioning. Although structural brain abnormalities, particularly decrements in gray matter volume, are considered important to the pathology of schizophrenia, it is not resolved whether the brain abnormalities become more prominent over time.

METHOD: Magnetic resonance brain images from 159 patients with schizophrenia and 158 healthy comparison subjects between 16 and 70 years of age were compared. Using linear regression analysis, the authors analyzed the relationship between the volumes of the total brain, gray and white matter, cerebellum, and lateral and third ventricles with patient age.

RESULTS: Total brain (-2.2%), cerebral gray matter (-3.3%), prefrontal gray matter (-4.4%), and prefrontal white matter (-3.5%) volumes were smaller, and lateral (27%) and third (30%) ventricle and peripheral CSF (11%) volumes were larger in schizophrenia patients. A significant group-by-age interaction for gray matter volume was found, as shown by a steeper regression slope between age and gray matter volume in patients (-3.43 ml/year) than in healthy comparison subjects (-2.74 ml/year).

CONCLUSIONS: The smaller brains of the patients with schizophrenia can be explained by decreases in gray matter volume. Moreover, the finding that the smaller gray matter volume was more pronounced in older patients with schizophrenia may suggest progressive loss of cerebral gray matter in schizophrenia patients.

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Psychosom Med. 2009 Jun;71(5):566-73. Epub 2009 May 4.

Decreased gray matter volumes in the cingulo-frontal cortex and the amygdala in patients with fibromyalgia.

Burgmer M, Gaubitz M, Konrad C, Wrenger M, Hilgart S, Heuft G, Pfleiderer B.

Abstract

OBJECTIVE: Studies in fibromyalgia syndrome with functional neuroimaging support the hypothesis of central pain augmentation. To determine whether structural changes in areas of the pain system are additional preconditions for the central sensitization in fibromyalgia we performed voxel based morphometry in patients with fibromyalgia and healthy controls.

METHODS: We performed 3 Tesla magnetic resonance imaging of the brain in 14 patients with fibromyalgia and 14 healthy controls. Regional differences of the segmented and normalized gray matter volumes in brain areas of the pain system between both groups were determined. In those areas in which patients structurally differed from healthy controls, the correlation of disease-related factors with gray matter volumes was analyzed.

RESULTS: Patients presented a decrease in gray matter volume in the prefrontal cortex, the amygdala, and the anterior cingulate cortex (ACC). The duration of pain or functional pain disability did not correlate with gray matter volumes. A trend of inverse correlation of gray matter volume reduction in the ACC with the duration of pain medication intake has been detected.

CONCLUSIONS: Our results suggest that structural changes in the pain system are associated with fibromyalgia. As disease factors do not correlate with reduced gray matter volume in areas of the cingulo-frontal cortex and the amygdala in patients, one possible interpretation is that volume reductions might be a precondition for central sensitization in fibromyalgia.

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Brain. 2008 Dec;131(Pt 12):3222-31. Epub 2008 Sep 26.

Working memory performance is correlated with local brain morphology in the medial frontal and anterior cingulate cortex in fibromyalgia patients: structural correlates of pain-cognition interaction.

Luerding R, Weigand T, Bogdahn U, Schmidt-Wilcke T.

Abstract

Fibromyalgia (FM) is a disorder of unknown aetiology, characterized by chronic widespread pain, stiffness and sleep disturbances. In addition, patients frequently complain of memory and attention deficits. Accumulating evidence suggests that FM is associated with CNS dysfunction and with an altered brain morphology. However, few studies have specifically investigated neuropsychological issues in patients suffering from FM. We therefore sought to determine whether neuropsychological deficits found in FM patients may be correlated with changes in local brain morphology specifically in the frontal, temporal or cingulate cortices. Twenty FM patients underwent extensive testing for potential neuropsychological deficits, which demonstrated significantly reduced working memory and impaired non-verbal long-term memory (limited to free recall condition) in comparison with normative data from age- and education-matched control groups. Voxel-based morphometry (VBM) was used to evaluate for potential correlations between test results and local brain morphology. Performance on non-verbal working memory was positively correlated with grey matter values in the left dorsolateral prefrontal cortex, whereas performance on verbal working memory (digit backward) was positively correlated with grey matter values in the supplementary motor cortex. On the other hand, pain scores were negatively correlated with grey matter values in the medial frontal gyrus. White matter analyses revealed comparable correlations for verbal working memory and pain scores in the medial frontal and prefrontal cortex and in the anterior cingulate cortex. Our data suggest that, in addition to chronic pain, FM patients suffer from neurocognitive deficits that correlate with local brain morphology in the frontal lobe and anterior cingulate gyrus, which may be interpreted to indicate structural correlates of pain-cognition interaction.

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Pain. 2012 May;153(5):1006-14. Epub 2012 Mar 2.

Changes in regional gray matter volume in women with chronic pelvic pain: a voxel-based morphometry study.

As-Sanie S, Harris RE, Napadow V, Kim J, Neshewat G, Kairys A, Williams D, Clauw DJ, Schmidt-Wilcke T.

Abstract

Chronic pelvic pain (CPP) is a highly prevalent pain condition, estimated to affect 15%-20% of women in the United States. Endometriosis is often associated with CPP, however, other factors, such as preexisting or concomitant changes of the central pain system, might contribute to the development of chronic pain. We applied voxel-based morphometry to determine whether women with CPP with and without endometriosis display changes in brain morphology in regions known to be involved in pain processing. Four subgroups of women participated: 17 with endometriosis and CPP, 15 with endometriosis without CPP, 6 with CPP without endometriosis, and 23 healthy controls. All patients with endometriosis and/or CPP were surgically confirmed. Relative to controls, women with endometriosis-associated CPP displayed decreased gray matter volume in brain regions involved in pain perception, including the left thalamus, left cingulate gyrus, right putamen, and right insula. Women with CPP without endometriosis also showed decreases in gray matter volume in the left thalamus. Such decreases were not observed in patients with endometriosis who had no CPP. We conclude that CPP is associated with changes in regional gray matter volume within the central pain system. Although endometriosis may be an important risk factor for the development of CPP, acting as a cyclic source of peripheral nociceptive input, our data support the notion that changes in the central pain system also play an important role in the development of chronic pain, regardless of the presence of endometriosis.

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Arthritis Rheum. 2010 Oct;62(10):2930-40.

Thalamic atrophy associated with painful osteoarthritis of the hip is reversible after arthroplasty: a longitudinal voxel-based morphometric study.

Gwilym SE, Filippini N, Douaud G, Carr AJ, Tracey I.

Abstract

OBJECTIVE: Voxel-based morphometry (VBM) is a method of assessing brain gray matter volume that has previously been applied to various chronic pain conditions. From this previous work, it appears that chronic pain is associated with altered brain morphology. The present study was undertaken to assess these potential alterations in patients with painful hip osteoarthritis (OA).

METHODS: We studied 16 patients with unilateral right-sided hip pain, before and 9 months after hip arthroplasty. This enabled comparison of gray matter volume in patients with chronic musculoskeletal pain versus healthy controls, as well as identification of any changes in volume following alleviation of pain (after surgery). Assessment involved self-completion questionnaires to assess pain, function, and psychosocial variables, and magnetic resonance imaging scanning of the brain for VBM analysis.

RESULTS: Significant differences in brain gray matter volume between healthy controls and patients with painful hip arthritis were seen. Specifically, areas of the thalamus in patients with chronic OA pain exhibited decreased gray matter volume. Furthermore, when these preoperative changes were compared with the brain morphology of the patients 9 months after surgery, the areas of reduced thalamic gray matter volume were found to have “reversed” to levels seen in healthy controls.

CONCLUSION: Our findings confirm that gray matter volume decreases within the left thalamus in the presence of chronic pain and disability in patients with hip OA. The results also show that these thalamic volume changes reverse after hip arthroplasty and are associated with decreased pain and increased function. These findings have potential implications with regard to optimizing the timing of orthopedic interventions such as arthroplasty

29Oct/12
Chronic pain

Pain: perception, expectation, meaning – it’s all important

I regularly scour the literature for the latest studies that look at pain mechanisms. Firstly I am fascinated by the science and philosophy of pain, both personally as it is so intrical to life and living, and because I need to understand the current thinking in pain to be effective as a clinician–one day I will post a picture of my study that is largely held together by books, journals and papers. Secondly, and related to the first reason, is because we simply must maintain a contemporary perspective and keep up to date with the rapidly developing knowledge base that crosses basic sciences, neuroscience, cognitive sciences and other fields that together can provide explnantion for the complex experience that is pain.

Ulrike Bingel has done some fascinating work and here are some of the abstracts with my brief comments following:

 

Neurogastroenterol Motil. 2012 Oct;24(10):935-e462. doi: 10.1111/j.1365-2982.2012.01968.x. Epub 2012 Jul 2.

Perceived treatment group affects behavioral and neural responses to visceral pain in a deceptive placebo study.

Kotsis V, Benson S, Bingel U, Forsting M, Schedlowski M, Gizewski ER, Elsenbruch S.

Abstract

To assess effects of perceived treatment (i.e. drug vs placebo) on behavioral and neural responses to rectal pain stimuli delivered in a deceptive placebo condition. Methods  This fMRI study analyzed the behavioral and neural responses during expectation-mediated placebo analgesia in a rectal pain model. In N = 36 healthy subjects, the blood oxygen level-dependent (BOLD) response during cued anticipation and painful stimulation was measured after participants were informed that they had a 50% chance of receiving either a potent analgesic drug or an inert substance (i.e., double-blind administration). In reality, all received placebo. We compared responses in subjects who retrospectively indicated that they received the drug and those who believed to have received placebo. Key Results  55.6% (N = 20) of subjects believed that they had received a placebo, whereas 36.1% (N = 13) believed that they had received a potent analgesic drug. Subjects who were uncertain (8.3%, N = 3) were excluded. Rectal pain-induced discomfort was significantly lower in the perceived drug treatment group (P < 0.05), along with significantly reduced activation of the insular, the posterior and anterior cingulate cortices during pain anticipation, and of the anterior cingulate cortex during pain (all P < 0.05 in regions-of-interest analyses).

Conclusions & Inferences

Perceived treatment constitutes an important aspect in placebo analgesia. A more refined understanding of individual treatment expectations and perceived treatment allocation has multiple implications for the design and interpretation of clinical trials and experimental studies on placebo and nocebo effects.

RS: The way in which we interact (therapist/doctor and patient) alongside the expectations that are brought along to the session need due consideration. This includes the language used to educate and explain pain and symptoms, the way in which it is delivered, the context and environment where the delivery takes place and preceeding events such as previous consultations and the journey to the appointment.

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Curr Biol. 2012 Jun 5;22(11):1019-22. doi: 10.1016/j.cub.2012.04.006. Epub 2012 May 17.

Attention modulates spinal cord responses to pain.

Sprenger C, Eippert F, Finsterbusch J, Bingel U, Rose M, Büchel C.

Abstract

Reduced pain perception while being distracted from pain is an everyday example of how cognitive processes can interfere with pain perception. Previous neuroimaging studies showed distraction-related modulations of pain-driven activations in various cortical and subcortical brain regions, but the precise neuronal mechanism underlying this phenomenon is unclear. Using high-resolution functional magnetic resonance imaging of the human cervical spinal cord in combination with thermal pain stimulation and a well-established working memory task, we demonstrate that this phenomenon relies on an inhibition of incoming pain signals in the spinal cord. Neuronal responses to painful stimulation in the dorsal horn of the corresponding spinal segment were significantly reduced under high working memory load compared to low working memory load. At the individual level, reductions of neuronal responses in the spinal cord predicted behavioral pain reductions. In a subsequent behavioral experiment, using the opioid antagonist naloxone in a double-blind crossover design with the same paradigm, we demonstrate a substantial contribution of endogenous opioids to this mechanism. Taken together, our results show that the reduced pain experience during mental distraction is related to a spinal process and involves opioid neurotransmission.

RS: Nervous system activity takes place on a spectrum. the peripheral nerves at one end, the spinal cord in the middle and the brain on top. Ascending and descending mechanisms are key players in the overall perception of pain which is why we can distract ourselves and feel less pain for example, or indeed by re-evaluating the meaning of our pain, we can use parts of our brain to facilitate the flow of messages down to the spinal cord to influence danger signals coming up from the tissues. In central sensitisation though, we can see facilitation of the flow of danger signals, this being one of the mechanism based features of chronic and persisting pain.

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J Neurosci. 2010 Dec 1;30(48):16324-31.

Anterior insula integrates information about salience into perceptual decisions about pain.

Wiech K, Lin CS, Brodersen KH, Bingel U, Ploner M, Tracey I.

Abstract

The decision as to whether a sensation is perceived as painful does not only depend on sensory input but also on the significance of the stimulus. Here, we show that the degree to which an impending stimulus is interpreted as threatening biases perceptual decisions about pain and that this bias toward pain manifests before stimulus encounter. Using functional magnetic resonance imaging we investigated the neural mechanisms underlying the influence of an experimental manipulation of threat on the perception of laser stimuli as painful. In a near-threshold pain detection paradigm, physically identical stimuli were applied under the participants’ assumption that the stimulation is entirely safe (low threat) or potentially harmful (high threat). As hypothesized, significantly more stimuli were rated as painful in the high threat condition. This context-dependent classification of a stimulus as painful was predicted by the prestimulus signal level in the anterior insula, suggesting that this structure integrates information about the significance of a stimulus into the decision about pain. The anticipation of pain increased the prestimulus functional connectivity between the anterior insula and the midcingulate cortex (MCC), a region that was significantly more active during stimulation the more a participant was biased to rate the stimulation as painful under high threat. These findings provide evidence that the anterior insula and MCC as a “salience network” integrate information about the significance of an impending stimulation into perceptual decision-making in the context of pain.

RS: The anticipation and expectation of pain play a role in the end perception of pain, this study illustrating the connectivity within important brain regions known to be active in pain. Salience is key. The meaning that we give to the pain plays such a significant role in the threat level: how dangerous is this? Really? The brain has to answer this question biologically and on concluding that there is a problem, pain is an output in response. An amazing device that protects us and is vital for survival.

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Sci Transl Med. 2011 Feb 16;3(70):70ra14.

The effect of treatment expectation on drug efficacy: imaging the analgesic benefit of the opioid remifentanil.

Bingel U, Wanigasekera V, Wiech K, Ni Mhuircheartaigh R, Lee MC, Ploner M, Tracey I.

Abstract

Evidence from behavioral and self-reported data suggests that the patients’ beliefs and expectations can shape both therapeutic and adverse effects of any given drug. We investigated how divergent expectancies alter the analgesic efficacy of a potent opioid in healthy volunteers by using brain imaging. The effect of a fixed concentration of the μ-opioid agonist remifentanil on constant heat pain was assessed under three experimental conditions using a within-subject design: with no expectation of analgesia, with expectancy of a positive analgesic effect, and with negative expectancy of analgesia (that is, expectation of hyperalgesia or exacerbation of pain). We used functional magnetic resonance imaging to record brain activity to corroborate the effects of expectations on the analgesic efficacy of the opioid and to elucidate the underlying neural mechanisms. Positive treatment expectancy substantially enhanced (doubled) the analgesic benefit of remifentanil. In contrast, negative treatment expectancy abolished remifentanil analgesia. These subjective effects were substantiated by significant changes in the neural activity in brain regions involved with the coding of pain intensity. The positive expectancy effects were associated with activity in the endogenous pain modulatory system, and the negative expectancy effects with activity in the hippocampus. On the basis of subjective and objective evidence, we contend that an individual’s expectation of a drug’s effect critically influences its therapeutic efficacy and that regulatory brain mechanisms differ as a function of expectancy. We propose that it may be necessary to integrate patients’ beliefs and expectations into drug treatment regimes alongside traditional considerations in order to optimize treatment outcomes.

RS: Again this emphasises the point that we must address belief systems and expectations that patients bring along as an integral part of who they are as an individual. What we observe and what the patient experiences are key factors that require ‘marrying’ in order to target this interface with education, strategies, training and treatment. But, it has to make sense to the patient and fit with their belief system. In many cases this may require shifts in thinking to promote healthier behaviours and habits for moving forwards.

07Apr/12

Tackling chronic pain – it’s like learning a new language..and unlearning an old

Tackling chronic pain is a challenge. Undoubtedly our understanding of pain, the role of the nervous system and other body systems, has advanced to permit a reconceptualisation of the experience and how we can approach it. The knowledge that there is a form of conditioning and learning that goes on, means that we can switch our thinking to address these mechanisms. Clearly a change in reasoning was and continues to be required to be more effective in dealing with persisting pain.

I often use the analogy of learning a language with patients. Most people at some stage have had to go through this process, with some more natural than others at developing the skill. Equally, the thought of learning a musical instrument provokes a similar comparison. What is needed? Understanding, time, motivation and practice are certainly necessary ingredients. We also require adequate rest and sleep to cement the changes in brain function that occurs as a result of its plasticity.

So what has been learned in chronic pain?

We can divide this into biological responses and behaviours that we purposely adopt. The brain learns to produce pain and becomes very good in some cases, creating the experience even when it is not required–recalling that pain is an output from the brain in response to a perceived threat based upon the danger (nociceptive) signals received from the body via the spinal cord; the caveat being that nociceptive signals and the act of nociception is neither needed nor necessary for the brain to create pain. Equally, nociception can be ticking on but without the brain producing the conscious experience of pain. This means that as soon as the brain is sure we are under threat, it will protect us with pain and concurrent responses. These include changes in movement, activity in the endocrine system (hormones) and the immune system that pervades our body as a second nervous system.

‘..pain cannot exist out of consciousness. In contrast, but often erroneously considered analogous, nociception can exist outside of consciousness. In fact, nociception can occur without the brain–high-threshold peripheral afferents and their spinal projections can be activated in the absence of brain activity. Indeed, tactile perception, pain and other bodily feelings can be thought of as outputs of the brain that are based on an informed interpretation of the information coming from one’s body.’ Taken from Moseley & Flor (2012)

The way we respond to pain is individual and learned from previous experiences. Clearly it is both useful and vital to learn that an oven is hot and a pin is sharp. Acute pain is an incredible device and one of the body’s responses to perceived danger. In persisting pain states, arguably the pain is not useful or promoting adaptive behaviours. Although, when the tissues are not as healthy as they may be, the peripheral nervous system is sensitive and movement is not normal, perhaps some level of pain is useful as a motivator to develop healthier tissues. Undoubtedly though, in many cases of chronic pain, the intensity and impact far outweighs any benefit. The incredible sensitivity, robust and lengthy responses to normal activities cause utter havoc and enormous distress such as in the case of complex regional pain syndrome.

Approaching the problem of chronic pain requires a 360 view on the individual. Understanding pain mechanisms, limitations, social impact and influential factors are all important in the planning of a treatment programme. In addition, as argued here, considering chronic pain as a learned response on different levels is a useful way of conceptualising the problem in terms of understanding how the situation has evolved and how it must be tackled.

RS

12Feb/12
Tackling pain

Pain Mechanisms – what underpins our pain?

Understanding pain mechanisms is the key to effective treatment. The mechanisms that have been studied, written about in science journals and discussed with patients include nociceptive pain, inflammatory pain, neuropathic pain and central sensitisation. Elucidating which are playing a role in the patient’s experience allows the doctor to prescribe the right medication and the modern physical therapist to address the issues of pain in a biopsychosocial manner. I will now clarify the latter point.

In taking a detailed history, observing patterns of movement and protection, assessing the state of the nervous system and health of the body systems, understanding behaviours and the beliefs behind them and learning of the influences upon the individual’s pain experience, one can know about the likely pain mechanisms underpinning the experience. From here the treatment strategies can be chosen to target these mechanisms. For example, top-down approaches for central sensitisation focus on the change in the properties of the central nervous system. The interventions themselves are observant of the amplification that occurs in the spinal cord and higher centres and would seek to dampen the responses with input to the brain that is perceived as normal or non-threatening. This could include sensory stimulation or movements outside of the receptive field, education to reduce fear of movement or imagery to name but a few. Inflammatory pain can also be treated with a top-down approach but local tissue based strategies would also be used. Just to note that the separation of the ‘top end’ (brain and spinal cord) from ‘bottom end’ (tissues) is really a false dichotomy as all conscious experiences are from the brain including what we see and what we feel.

Stephen McMahon and David Bennett, both experts in the field of pain science from King’s College London, produced a poster that describes these mechanisms – click here to visit the page in Nature Reviews Neuroscience. This is what they say about it:

Pain is an unpleasant sensation resulting from the intricate interplay between sensory and cognitive mechanisms. Chronic pain, resulting from disease or injury, affects nearly every fifth person in the Western world, constituting an enormous burden for the individual and society. Sensitization of pain signalling systems is a key feature of chronic pain and results in normally non-painful stimuli eliciting pain. Such sensory changes can occur not just at the sites of injury, but in surrounding normal tissues. This and other observations suggest that sensitization occurs within the CNS as well as within nociceptor terminals. Here we consider the consequences of noxious stimulus applied to our unfortunate builder’s hand, from sensory transduction to pain perception. We describe the structural and functional elements present at different levels of the nociceptive system, as well as some of the changes occurring in chronic pain states. Although our poster highlights a flow of information from the periphery to the CNS, it should be noted that higher brain centres exert both inhibitory and facilitatory controls on lower ones. The challenge for the next decade will be to effectively translate this knowledge into the development of novel analgesic agents for better pain relief.

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.

18Jan/12

Pain – some things you may not have realised

Pain is multidimensional. Pain is 100% produced by the brain in response to a perceived threat. The brain allocates a location using the cortical maps, hence why we feel pain in our backs or knees. The brain tries to make sense of the situation, scrutinising what is going on on the basis of past experience (learning) and comparing to the information being received from ALL body systems. This is the reason for the term ‘multisystem output’ as a way of describing what is happening when we are in pain.

The most obvious reason why the pain worsens is that we move, exercise or sit for too long. All of these activities are ‘physical’, asking the tissues to take the strain either rapidly or gradually. On reaching a certain level of strain, lower than normal in cases of sensitivity, nerves start sending danger signals to the spinal cord. From the spinal cord messages are relayed to the brain, still on the subject of danger. Theses are not pain signals. It is only when the brain interprets the information as threatening that the experience of pain is produced – an output from the brain. This is typical in acute situations when the injury or problem is new. The pain is vital, useful and motivates action.

A key point to understand is that the brain does not actually need the tissues to produce pain. Think about phantom limb pain. There is no limb. There are no tissues. But it hurts. It seriously hurts in may cases. So, there are other ‘triggers’ for pain besides actually moving or asking the tissues (muscles, tendons, ligaments, bones etc) to take the strain. Common ‘non-tissue’ circumstances that can amplify pain include stress, circadian rhythms, menstrual cycle, fatigue and thoughts. I think that to take this on board is an enlightening experience. To understand that your pain can be as a result of other reasons besides what you are doing physically can help to explain why it hurts at times when you have not done anything differently and you really cannot comprehend why the pain has increased.

A further influential player in our experiences is vision. I’m really interested in this as the process of ‘seeing’ is much aligned to the way pain is experienced. Information is received by the brain via the optic nerve. The brain must make sense of this data and create a credible outcome, again very much using past experience to judge the present. We still see a bird in his cage despite slender lines dividing his body (the struts of the cage). We don’t see ‘slices’ of a bird. Also consider optical illusions. A great deal of work has been done looking at the use of vision for therapeutic effect, i.e. the graded motor imagery programme. Clearly the mirror box is creating the illusion that the affected side is moving and appearing to be normal. Imagined movements requires us to ‘see’ and feel movement although we are keeping very still. The premotor cortex is very active during these imagined movements, and this part of the brain is involved in the production of pain.

What we are seeing is deemed to be an illusion in some quarters. We all have different experiences and backgrounds. Our beliefs about life and ourselves vary. This will influence what we ‘see’. If you have just watched a scary movie and then go outside into the dark to put the rubbish out, a shadow could be ‘seen’ as something more dangerous than if you have just laughed at a comedy show. Also consider when we see someone injure themselves, again on TV or watching sport. We often wince, grab our corresponding body part or take some other defensive action. Our brains are interpreting someone else’s danger and imprinting this onto our experience, perhaps as a way of helping us to learn that it is dangerous to be in their situation. This is likely due to the mirror neuron network and that when we watch someone else move or position themselves, our virtual body that exists in the brain mimics that position. There are also aspects of empathy in sharing someone’s pain. But, if that position is ‘threatening’ to our brain, we will hurt.

What do we do about that? We use strategies to desensitise and habituate, similar to dealing with any fear. The modern way of tackling pain states, especially those that persist, is using a biobehavioral approach. This means that as well as addressing tissue health with movement and treatment, we must concurrently target the brain and other systems that are involved in the pain experience, e.g. immune, endocrine. It is called ‘top-down’ – ‘bottom-up’. Top-down referring to the brain and our beliefs, understanding, thoughts, how the brain is controlling movement and protecting us; bottom-up signifying the need to nourish the tissues with movement. These exist on a spectrum and both are addressed in a contemporary biopsychosocial treatment programme – see www.specialistpainphysio.com/treatment

Below are some interesting abstracts in relation to this blog:

Pain. 2010 Feb;148(2):268-74. Epub 2009 Dec 11.

Pain sensation evoked by observing injury in others.

Osborn J, Derbyshire SW.

Source

School of Psychology, University of Birmingham, Edgbaston, UK.

Abstract

Observing someone else in pain produces a shared emotional experience that predominantly activates brain areas processing the emotional component of pain. Occasionally, however, sensory areas are also activated and there are anecdotal reports of people sharing both the somatic and emotional components of someone else’s pain. Here we presented a series of images or short clips depicting noxious events to a large group of normal controls. Approximately one-third of this sample reported an actual noxious somatic experience in response to one or more of the images or clips. Ten of these pain responders were subsequently recruited and matched with 10 non-responders to take part in an fMRI study. The subjects were scanned while observing static images of noxious events. In contrast with emotional images not containing noxious events the responders activated emotional and sensory brain regions associated with pain while the non-responders activated very little. These findings provide convincing evidence that some people can readily experience both the emotional and sensory components of pain during observation of other’s pain resulting in a shared physical pain experience.

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J Cogn Neurosci. 2007 Jan;19(1):42-58.

The neural substrate of human empathy: effects of perspective-taking and cognitive appraisal.

Lamm C, Batson CD, Decety J.

Source

INSERM Unit 280, France.

Abstract

Whether observation of distress in others leads to empathic concern and altruistic motivation, or to personal distress and egoistic motivation, seems to depend upon the capacity for self-other differentiation and cognitive appraisal. In this experiment, behavioral measures and event-related functional magnetic resonance imaging were used to investigate the effects of perspective-taking and cognitive appraisal while participants observed the facial expression of pain resulting from medical treatment. Video clips showing the faces of patients were presented either with the instruction to imagine the feelings of the patient (“imagine other”) or to imagine oneself to be in the patient’s situation (“imagine self”). Cognitive appraisal was manipulated by providing information that the medical treatment had or had not been successful. Behavioral measures demonstrated that perspective-taking and treatment effectiveness instructions affected participants’ affective responses to the observed pain. Hemodynamic changes were detected in the insular cortices, anterior medial cingulate cortex (aMCC), amygdala, and in visual areas including the fusiform gyrus. Graded responses related to the perspective-taking instructions were observed in middle insula, aMCC, medial and lateral premotor areas, and selectively in left and right parietal cortices. Treatment effectiveness resulted in signal changes in the perigenual anterior cingulate cortex, in the ventromedial orbito-frontal cortex, in the right lateral middle frontal gyrus, and in the cerebellum. These findings support the view that humans’ responses to the pain of others can be modulated by cognitive and motivational processes, which influence whether observing a conspecific in need of help will result in empathic concern, an important instigator for helping behavior.

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Hum Brain Mapp. 2009 Oct;30(10):3227-37.

Empathic neural responses to others’ pain are modulated by emotional contexts.

Han S, Fan Y, Xu X, Qin J, Wu B, Wang X, Aglioti SM, Mao L.

Source

Department of Psychology, Peking University, Beijing 100871, People’s Republic of China. [email protected]

Abstract

Recent brain imaging studies indicate that empathy for pain relies upon both the affective and/or the sensorimotor nodes of the pain matrix, and empathic neural responses are modulated by stimulus reality, personal experience, and affective link with others. The current work investigated whether and how empathic neural responses are modulated by emotional contexts in which painful stimulations are perceived. Using functional magnetic resonance imaging (fMRI), we first showed that perceiving a painful stimulation (needle penetration) applied to a face with neutral expression induced activation in the anterior cingulate cortex (ACC) relative to nonpainful stimulation (Q-tip touch). However, when observation of the painful stimuli delivered to a neutral face was intermixed with observation of painful or happy faces, the ACC activity decreased while the activity in the face area of the secondary somatosensory cortex increased to the painful stimulation. Moreover, the secondary somatosensory activity associated with the painful stimulation decreased when the painful stimulation was applied to faces with happy and painful expressions. The findings suggest that observing painful stimuli in an emotional context weakens affective responses but increases sensory responses to perceived pain and implies possible interactions between the affective and sensory components of the pain matrix during empathy for pain.

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Neuron. 2007 Aug 2;55(3):377-91.

The cerebral signature for pain perception and its modulation.

Tracey I, Mantyh PW.

Source

Centre for Functional Magnetic Resonance Imaging of the Brain, Clinical Neurology and Nuffield Department of Anaesthetics, Oxford University, OX3 9DU Oxford, England, UK. [email protected]

Abstract

Our understanding of the neural correlates of pain perception in humans has increased significantly since the advent of neuroimaging. Relating neural activity changes to the varied pain experiences has led to an increased awareness of how factors (e.g., cognition, emotion, context, injury) can separately influence pain perception. Tying this body of knowledge in humans to work in animal models of pain provides an opportunity to determine common features that reliably contribute to pain perception and its modulation. One key system that underpins the ability to change pain intensity is the brainstem’s descending modulatory network with its pro- and antinociceptive components. We discuss not only the latest data describing the cerebral signature of pain and its modulation in humans, but also suggest that the brainstem plays a pivotal role in gating the degree of nociceptive transmission so that the resultant pain experienced is appropriate for the particular situation of the individual.

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Neuroimage. 2009 Sep;47(3):987-94. Epub 2009 May 28.

The influence of negative emotions on pain: behavioral effects and neural mechanisms.

Wiech K, Tracey I.

Source

Nuffield Department of Anaesthetics, University of Oxford, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK. [email protected]

Abstract

The idea that pain can lead to feelings of frustration, worry, anxiety and depression seems obvious, particularly if it is of a chronic nature. However, there is also evidence for the reverse causal relationship in which negative mood and emotion can lead to pain or exacerbate it. Here, we review findings from studies on the modulation of pain by experimentally induced mood changes and clinical mood disorders. We discuss possible neural mechanisms underlying this modulatory influence focusing on the periaqueductal grey (PAG), amygdala, anterior cingulate cortex (ACC) and anterior insula as key players in both, pain and affective processing.

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Disclaimer: this blog is for informational purposes only. If you are concerned or unsure about your pain or condition, you must consult with your GP or a health professional.

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.

Move from your seat, or buy one of these!

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.

21Oct/11

Using neuroscience to understand and treat pain

Neuroscience to treat pain and injury

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.

Treat the brain and to reduce pain

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.

When we injure tissue there is a local release of inflammatory chemicals. These chemicals excite local nerves in the tissues called nociceptors. Normally, nociceptors are quiet but when they are stimulated by inflammation, these nerves send danger signals to the spinal cord where they meet secondary neurons. The early bombardment of signals into the spinal cord causes the secondary neurons to become excited. These cells then send danger signals up to the brain where the information is scrutinised. On the basis of this scrutiny, if the brain perceives a threat, pain will be allocated in the area of the body that is deemed to be in danger. The area of pain is allocated via the representation of the body in the brain (see previous blog here) in the sensory cortex, first mapped by Wilder Penfield and published in 1951. Therefore we know that actually there is no ‘muscle pain’ or ‘knee pain’ but rather pain as a brain experience, and not in the mind I hasten to add, that is detected in a body part or region according to the brain’s perception of threat. These are the body maps that the brain uses to know where information is coming from and to control movement.

This information is part of the neuroscience knowledge that can be used to help people understand their pain and to create therapies that treat pain. Future blogs will look at how we can change and nourish the nervous system to promote healthy tissues at one end of the spectrum with the brain end being targeted by deeper education and Graded Motor Imagery (GMI) for example–click here. The brain and the tissues are not separate, they affect each other in many ways, as do other body systems such as the immune and endocrine systems. Looking at healthy movement and functioning in a truly holistic and biopsychosocial manner with neuroscience underpinnings, provides us with an exciting route forwards in dealing with pain problems.
09Oct/11

Mastery (2): practice, practice and then….practice

Mastery is defined in the Oxford dictionary as:

  • comprehensive knowledge or skill in a particular subject or activity
  • control or superiority over someone or something

The concept of mastery is often applied to a musical instrument, golf, martial arts or a language. The word is rarely used in conjunction with the rehabilitation of an injury or a painful condition. It occurred to me that there are vast similarities between the principles and experience of training for a sport or a skill and the participation in a rehabilitation programme. The difference will be the end goals and the specific reason for the training. In the case of mastering a sport, it is about performance enhancement with greater skill and efficiency to achieve fewer shots or more accuracy for example. In rehabilitation the goal are pain relief, normal mobility, control of movement, restoration of strength, power and a return to daily activities (work, home, exercise).

End-stage rehabilitation

Undoubtedly the body has incredible mechanisms that heal injured tissue. Unfortunately there are many people who despite the healing process do continue to suffer painful symptoms. We see many cases of enduring and problematic pain at the clinic and set about the problem with a contemporary approach. This involves a range of treatment techniques and strategies including active rehabilitation or training. This training requires instruction, understanding, dedication, awareness, consistency, intention and practice. Just like learning a golf shot or the piano.

Setting up the principles of training (I will refer to the rehabilitation now as training) creates the right context and mindset. This includes pain/condition specific education so that the programme makes sense, the aims of the exercises, when to do them, how often and how to progress or moderate the intensity. In laying out the way forwards, the concept of mastery is introduced. What is it that needs mastery?

Mastering the mind

When we are in pain we change the way that we move. The longer the condition has been existing, the more the body and brain will have adapted alongside your thoughts and beliefs about the problem. The meaning that you give to the pain can also change with time and this is important. If the ‘meaning’ of the problem is significant, negative in nature and threatening to you as an organism (evolution speaking), the brain is more likely to protect you. This protection includes pain and altered movement, therefore perpetuating the cycle. This subject is for another day, important though it is, but dealing with negative thought patterns and unhelpful beliefs is fundamental, and requires restructuring. Returning to altered movement, this needs to be re-trained to reduce the guarding and protection. Of course this is one aspect of a treatment programme, but it is a great example to use when thinking about how you are going to master normal movement.

Mastering normal movement as mastering a language takes instruction, practice and dedication as mentioned. Often along the road we meet challenges and resistance both physically and mentally. One of those challenges is the plateau when it appears that nothing is happening or changing. The performance still seems to be the same, the outcomes like before. It is during this time that there is change occurring but it has not yet clearly manifest. Understanding that the plateau is an important part of the process and using the time as a chance to learn and an opportunity to create change. The nervous system is very plastic and adaptable according to the stimuli that it receives. In rehabilitation, the repeated stimulus of the right movements, in the right setting and mind set create such an opportunity.

To be good at any skill we must fully engage and spend the time with ourselves practice for the sake of practicing. Applying similar principles to rehabilitation in re-training normal movement, thoughts about movement and exercise and the functional skills of your chosen activity, provides a framework and a well trodden philosophical pathway to success. You will have your chosen goals that you will seek to achieve and on reaching them you will have further targets to attain. This is the journey.