Tag Archives: Explain 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.

30Apr/12

Teaching old dogs new tricks

Not that I am calling anyone an ‘old dog’, ‘you can’t teach an old dog new tricks’  is a universally understood phrase implying that once we are set in our ways, change is impossible. This is simply not the case. I am referring to our ability to change our views, beliefs, behaviours and experience of life. Our brains are not, as previously thought, hard-wired. Behaviours, actions and activities that we ‘choose’, are based upon our belief system that are created and moulded by life experience. I say ‘choose’ as there is a debate as to whether we really have free will or not that is rather interesting. As we go through life, there is a huge amount of learning that is continuous and fundamental to our development and very existence. Pain is also part of our learning experience: you soon learn that it is hot to touch an oven when it is turned on.

We can learn all sorts of skills. We can develop and master these skills with practice in the case of playing a musical instrument or becoming a great sportsmen or sportswomen. This takes dedication and rehearsal, and as we improve our brain is changing. In fact, the brain is changing all the time. I frequently say to patients that both our brains have changed within this session from our conversation. We take on board new information and place this into our existing belief about ourselves and the World. It may make sense and we take it on board and adapt or we may see the new information as being too challenging or as holding no value, although this may change at a later date.

The brain changes, we can change

In terms of pain and in particular chronic pain, the brain and body has adapted to continue to protect itself and often vehemently in the face of a perceived threat. This is conditioning and learning. During this time we can also construct a set of beliefs that can be defensive: ‘I’d better not move as it hurts and this means I am damaging myself’. The reality is that in most cases of on-going pain, the problem lies not so much in the tissues, although they can be unfit, tight, boggy and inflamed, but in other body systems such as the nervous and immune systems. This statement alone is challenging and requires qualification in the clinic with high quality education and positive experiences if it is to be absorbed and taken on at a deeper level. Even when we take the message to heart we can slip at times, similar to the smoker who stops until a certain set of circumstances arise. The message then needs re-evaluation and re-integration. In pain we now talk about the messages of ‘pain from the brain’ (not the mind) and ‘hurt but not harm’. These too are challenging statements and thoughts but based upon current science.

So, we know that the brain creates the experience of pain as an ‘output’ in response to ‘input’ that can include danger signals from the tissues, thoughts, past experiences, genetic factors, emotional state and stress for example – see Lorimer Moseley talk about this here. To treat pain therefore, we must target the brain to a greater or lesser extent depending upon the circumstances – perhaps more tissue based in acute cases although I fundamentally believe that some form of tissue-based treatment is important in all cases including chronic pain – this for another discussion. The brain is plastic, meaning that we can mould and manipulate the structure and function of this incredible organ with the right stimulation. We also know about changes in the actual size of certain areas of the brain in pain (prefrontal cortex) and with learning (hippocampus).

Taking this on-board, we can design and implement treatments and strategies that conceptualise pain in its most modern sense and really tackle the ‘at source’ mechanisms and issues for improved perfomance and better living. Considering pain within a conditioning and learning paradigm, understanding that nerves that ‘fire together, wire together’ and that pain is one of the responses to danger amongst a number of other contemporary, science-based concepts, means that we are becoming increasingly effective in dealing with this significant and costly problem. We can then, teach an old dog new tricks by thinking the right way about pain and using treatment that promotes tissue health and movement that is only as good as the brain that controls it.

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

29Mar/12

It’s tight…it’s being protected

Tight as steel rope

Tightness in the muscle is a common complaint. Often part of a profile of symptoms following an injury and frequently a stand alone sense that persists, tightness and stiffness need addressing to normalise movement and control of movement. Normalising movement is a key part of desensitisation in that it is one less reason for the body to protect itself.

Tightness can be an expression of protection – what is being protected and why?

To address persisting tightness we must determine why and what is being protected. There could healing tissue, a pocket of inflammation or sensitivity to movement within the nervous system (mechanosensitivity). A detailed assessment of the problem, the preceding history and prior events reveal the nature and underpinning source(s), i.e. biological mechanisms. These mechanisms are then targeted with appropriate treatment and strategies.

Nerve | Blood supply

A common treatment method that we use is called neurodynamics. This is a range of hands-on techniques and movement-based exercises that nourish and mobilise the nervous system. Bearing in mind that our tissues will only be as healthy as the nerves that supply them (a general rule of thumb, but other factors are important including the immune system and endocrine system), it is very important that the nervous system be moving and its blood supply patent.

Tightness can be a sign of guarding. Guarding is protection orchestrated by the brain and can occur at a motor planning level. This means that before moving, the brain increases the activity of certain muscles as a way of protecting a body region for when movement actually occurs. A common example of guarding is in the case of back pain when the muscles remain ‘on’ as the spine is flexed forwards. These muscles should switch off and relax, however the fact that they remain active means that the movement is not normal. Addressing this is important for re-establishing motor control.

Local treatments are often used and can help in the short-term. However, these should be used as part of a rounded programme addressing the pain, symptoms, impact, limitations and other dimensions of the problem. Delving into the details and observing the sometimes subtle changes in movement and control of movement allows us to elucidate the reason(s) for protection and deal with persisting tightness.

22Mar/12
London Marathon - Tower Bridge

Training for the marathon – developing pain & injury

London Marathon - Tower Bridge

At this time of year, as the London Marathon nears, runners reaching new levels of training can start to develop aches and pains. Usually the pains are in the legs or feet and often begin as an annoyance but develop into a problem that means training has to stop.

The tissues are constantly breaking down and rebuilding. This is a carefully orchestrated process that is impacted upon by exercise. This is how we develop muscle bulk. However, we do need a period of adaptation that can be disrupted if there is inadequate rest. The balance tips towards tissue breakdown and inflammation triggers the development of sensitivity that if ignored can progress and become amplified. A good training programme should account for both rest periods and gradual progression of intensity.

A second issue is that of control of movement. On a day to day basis we can walk around, undertake normal activities, play sports and even run for certain distances with minor motor control issues. Motor control refers to the way in which our body is controlled by the brain with a feedback-feedforward system. The tissues send information to the brain so that there is a sense of position and awareness, allowing for the next movement to be made and corrected if necessary. The problem lies in the increasing distances, often never reached before, that can highlight these usually minor issues. Compensation and extra strain upon muscles and tendons that are trying to do the job of another can lead to tissue breakdown as explained previously. The sensitivity builds and training becomes difficult.

A full assessment of the affected area, body sense and the way in which movement is controlled will reveal factors that need addressing with treatment and specific exercises. This fits alongside a likely modification in the training programme that allows for the sensitivity to reduce before progressing once more. In some cases a scan or other investigations are recommend to determine the tissue nature of the problem.

If you are starting to develop consistent twinges that are worsening, pain that is affecting training or you are concerned, you should seek advice.

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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.

11Feb/12

Manual therapy, pain and the immune system

Pain relief

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