Category Archives: Treatments

Pain is a whole person experience

CRPS Research Update | October 2014 #CRPS

Physiotherapy LondonWelcome to the Complex Regional Pain Syndrome Research Update for October, a summary of the latest studies. 

If you are suffering with CRPS, I am here to show you how you can move forward — come and visit the CRPS clinic page here.

Spinal cord stimulation for complex regional pain syndrome type 1 with dystonia: a case report and discussion of the literature.
Voet C1, le Polain de Waroux B2, Forget P2, Deumens R3, Masquelier E4.

Complex Regional Pain Syndrome type 1 (CRPS-1) is a debilitating chronic pain disorder, the physiopathology of which can lead to dystonia associated with changes in the autonomic, central and peripheral nervous system. An interdisciplinary approach (pharmacological, interventional and psychological therapies in conjunction with a rehabilitation pathway) is central to progress towards pain reduction and restoration of function.
This case report aims to stimulate reflection and development of mechanism-based therapeutic strategies concerning CRPS associated with dystonia.
A 31 year old female CRPS-1 patient presented with dystonia of the right foot following ligamentoplasty for chronic ankle instability. She did not have a satisfactory response to the usual therapies. Multiple anesthetic blocks (popliteal, epidural and intrathecal) were not associated with significant anesthesia and analgesia. Mobilization of the foot by a physiotherapist was not possible. A multidisciplinary approach with psychological support, physiotherapy and spinal cord stimulation (SCS) brought pain relief, rehabilitation and improvement in the quality of life.
The present case report demonstrates the occurrence of multilevel (peripheral and central) pathological modifications in the nervous system of a CRPS-1 patient with dystonia. This conclusion is based on the patient’s pain being resistant to anesthetic blocks at different levels and the favourable, at least initially, response to SCS. The importance of the bio-psycho-social model is also suggested, permitting behavioural change

RS: With CRPS we absolutely need to consider ‘multilevel’ modifications and adaptations within the nervous system but also how all the other systems that have a role in protecting us are functioning. This often manifests as habitual thinking and activities that maintain protection. Realising these habits, automatic by the nature of being a habit, and making changes with specific training creates new patterns of activity that head towards health.


Longstanding Complex Regional Pain Syndrome is associated with activating autoantibodies against α-1a adrenoceptors.
Dubuis E1, Thompson V2, Leite MI3, Blaes F4, Maihöfner C5, Greensmith D6, Vincent A7, Shenker N8, Kuttikat A9, Leuwer M10, Goebel A11.

Complex Regional Pain Syndrome (CRPS) is a limb-confined post-traumatic pain syndrome with sympathetic features. The cause is unknown, but the results of a randomized crossover trial on low-dose IVIG treatment point to a possible autoimmune mechanism. We tested purified serum immunoglobulin G (IgG) from patients with longstanding CRPS for evidence of antibodies interacting with autonomic receptors on adult primary cardiomyocytes, comparing with control IgG from healthy and disease controls, and related the results to the clinical response to treatment with low-dose intravenous immunoglobulins (IvIG). We simultaneously recorded both single cell contractions and intracellular calcium handling in an electrical field. Ten of 18 CRPS preparations and only 1/57 control preparations (p<0.0001) increased the sensitivity of the myocytes to the electric field and this effect was abrogated by pre-incubation with alpha1a receptor blockers. By contrast, effects on baseline calcium were blocked by pre-incubation with atropine. Interestingly, serum-IgG preparations from all four CRPS patients who had responded to low-dose IVIG with meaningful pain relief were effective in these assays, although 4/8 of the non-responders were also active. To see if there were antibodies to the alpha1a receptor, CRPS-IgG was applied to alpha 1a receptor transfected rat1-fibroblast cells. The CRPS serum IgG induced calcium flux, and FACS showed that there was serum IgG binding to the cells. The results suggest that patients with longstanding CRPS have serum antibodies to alpha 1a receptors, and that measurement of these antibodies may be useful in the diagnosis and management of the patients.


A CRPS-IgG-transfer-trauma model reproducing inflammatory and positive sensory signs associated with complex regional pain syndrome.
Tékus V1, Hajna Z1, Borbély É1, Markovics A1, Bagoly T1, Szolcsányi J2, Thompson V3, Kemény Á1, Helyes Z2, Goebel A4.

The aetiology of complex regional pain syndrome (CRPS), a highly painful, usually post-traumatic condition affecting the limbs, is unknown, but recent results have suggested an autoimmune contribution. To confirm a role for pathogenic autoantibodies, we established a passive-transfer trauma model. Prior to undergoing incision of hind limb plantar skin and muscle, mice were injected either with serum IgG obtained from chronic CRPS patients or matched healthy volunteers, or with saline. Unilateral hind limb plantar skin and muscle incision was performed to induce typical, mild tissue injury. Mechanical hyperalgesia, paw swelling, heat and cold sensitivity, weight-bearing ability, locomotor activity, motor coordination, paw temperature, and body weight were investigated for 8days. After sacrifice, proinflammatory sensory neuropeptides and cytokines were measured in paw tissues. CRPS patient IgG treatment significantly increased hind limb mechanical hyperalgesia and oedema in the incised paw compared with IgG from healthy subjects or saline. Plantar incision induced a remarkable elevation of substance P immunoreactivity on day 8, which was significantly increased by CRPS-IgG. In this IgG-transfer-trauma model for CRPS, serum IgG from chronic CRPS patients induced clinical and laboratory features resembling the human disease. These results support the hypothesis that autoantibodies may contribute to the pathophysiology of CRPS, and that autoantibody-removing therapies may be effective treatments for long-standing CRPS.

RS – as ever we must consider the role of the immune system but in the light of other systems as no system works in isolation to the others. There is vast interaction between the immune system, nervous system, endocrine system and autonomic nervous system to the point where I believe we are a single system interpreting and responding. One response maybe pain as part of protection and our systems become very good at protecting us — this is not to suggest that our systems and ‘me’ are separate entities. Whole person is the only way we can sensibly think about this.

Local Anesthetic Sympathectomy Restores fMRI Cortical Maps in CRPS I after Upper Extremity Stellate Blockade: A Prospective Case Study.
Stude P, Enax-Krumova EK1, Lenz M, Lissek S, Nicolas V, Peters S, Westermann A, Tegenthoff M, Maier C.

Patients with complex regional pain syndrome type I (CRPS I) show a cortical reorganization with contralateral shrinkage of cortical maps in S1. The relevance of pain and disuse for the development and the maintenance of this shrinkage is unclear.
Aim of the study was to assess whether short-term pain relief induces changes in the cortical representation of the affected hand in patients with CRPS type I.
Case series analysis of prospectively collected data.
We enrolled a case series of 5 consecutive patients with CRPS type I (disease duration 3 – 36 months) of the non-dominant upper-limb and previously diagnosed sympathetically maintained pain (SMP) by reduction of the pain intensity of more than > 30% after prior diagnostic sympathetic block. We performed fMRI for analysis of the cortical representation of the affected hand immediately before as well as one hour after isolated sympathetic block of the stellate ganglion on the affected side.
Wilcoxon-Test, paired t-test, P < 0.05.
Pain decrease after isolated sympathetic block (pain intensity on the numerical rating scale (0 – 10) before block: 6.8 ± 1.9, afterwards: 3.8 ± 1.3) was accompanied by an increase in the blood oxygenation level dependent (BOLD) response of cortical representational maps only of the affected hand which had been reduced before the block, despite the fact that clinical and neurophysiological assessment revealed no changes in the sensorimotor function.
The interpretation of the present results is partly limited due to the small number of included patients and the missing control group with placebo injection.
The association between recovery of the cortical representation and pain relief supports the hypothesis that pain could be a relevant factor for changes of somatosensory cortical maps in CRPS, and that these are rapidly reversible

RS – we are either in pain or not in pain. If our focus is elsewhere and we are not experiencing pain, then we are not in pain. Whilst this may sound obvious, many people tell me that they are in pain all of the time. When I ask about times that they feel no pain, an oft given answer is that the pain is hidden at times when they do not feel it. Pain cannot hide. It is on-off, binary. At any given moment, we are either in pain or not in pain. Every moment changes and hence pain can change in a moment — referring to the rapidly reversible change in maps in this article; and why wouldn’t we have the ability to rapidly adapt? I believe we can change and it happens in a moment — our thinking, actions and experiences. Consider how we can be happy in a moment, and sad in a moment. Happiness is a feeling, pain is a feeling. Both have a purpose, to motivate us to do something or think in a particular way. There is a desperate need to change the globe’s thinking on pain, this being my main purpose. In doing so, we can alleviate a vast amount of suffering from pain, narrowing it down the pain that we need for survival and eliminating the pain that persists for no good reason.

CRPS Clinics | London & New Malden

CRPS – the narrative holds the clues |#CRPS

CRPS Clinics | London & New MaldenThe story told by the patient with CRPS provides insight into their suffering, characterised and brought to life by their chosen language, body posturing, body language, and changing facial expressions. The priming for a condition frequently arises months or years before from an illness, a stressful event, a previous injury or painful event. The way in which the body systems respond to the prior challenge creates a learning experience so that when the body is faced with another similar threat, the responses swiftly kick in. In CRPS this can be with absolute gusto as the level of protection reaches the stratosphere in many cases.

One of the common problems in CRPS is an altered sense of the body, particularly where the condition manifests but this can extend to that whole side of the body. Careful testing of movement precision and sensation identifies these changes as does questioning about clumsiness and the feel of the body. The feel of the body has a substrate in at least the sensory cortex — neurons + immune cells and their neurotransmitters and cytokines.

On questioning, people will volunteer that the limb feels detached, as if it does not belong to them, the sense of size changes and that it does not do what they demand. This is vital information as this identifies a key feature of CRPS (and other pain problems) that must be addressed with understanding and specific training. It is highly unlikely that pain will improve until body sense and precision improves.

So, as a patient you should always explain this feeling, strange (and scary) as it may appear, and as a clinician you should always ask.

London CRPS clinic with Richmond Stace — call now to book your first appointment 07932 689081

Massage for pain and chronic pain in London

5 reasons why I use manual therapy for cases of persisting pain

Some will argue that manual therapy — joint and/or soft tissue techniques — has no role in chronic pain. I disagree. Why?

(In no particular order)

1. Touch is normal and it is something that we do when we care.
2. Hands on treatment is expected when you visit a physiotherapist or physical therapist.
3. Stimulation in the area of the body that hurts can feel good. If it causes little or no pain, the brain is happy and interpreting the stimulus (touch, pressure, movement) as being safe. More of that please! A great way to desensitise and for the experience of pleasure in the affected area.
4. Change the brain’s output by addressing the area with therapy that feels good — that’s the output feeling good, along with reflexive reduction in protection.
5. What do you do if you bang your elbow? Rub it. In chronic pain, you may need to think about how and when to rub it, but nonetheless, rubbing it needs. Combine rubbing with visual feedback and there you have a pain relieving strategy.

Chronic pain treatment programmes

You’ve had an intervention for pain – what is next?

Chronic pain treatment programmesMany people with persisting and chronic pain elect to have an intervention for pain relief. This can include steroid injections, facet joint injections, nerve root blocks, epidurals, denervations and sympathetic blocks to name but a few. These procedures are usually administered by a pain consultant (a doctor who specialises in pain management), an orthopaedic surgeon, a radiologist or a rheumatologist.

Undoubtedly, the interventions can afford pain relief but of course the results do tend to vary from person to person. Ideally, the procedure forms part of a multidimensional treatment programme that aims to reduce symptoms, increase activity levels and improve quality of life in the patient’s eyes.

So, what happens next?

In some cases nothing and in others patients are advised to reactivate with the help of a physiotherapist. In the former scenario, the expectation is that the procedure will solve the problem, the pain will ease and life returns to normal. Unfortunately there is an error with this thinking as in the vast majority of cases this leaves the patient with a host of unanswered questions: how much should I do? Can I do this or that? Is it safe? etc etc. If the pain persists in any shape or form, this increases the threat value of these questions. They must be answered with practical solutions.

Undoubtedly to follow a comprehensive programme that addresses the physical and cognitive dimensions of pain is desirable. The intensity and length of a programme will vary from person to person, but as a minimum, the patient should know what they can do and how they can do it as a way of moving forward.

Within the programme there are fundamental issues that must be tackled. For example, in many cases of persisting pain, the way in which movement is controlled has changed as has body perception. This has to be retrained and there are specific ways of achieving this goal. We know that these mechanisms play a role in sensitivity and hence need to be targeted.

Concurrent with physical training is the absolute need to create the right mindset and deal with any associated fears of movement. This may include working upon resilience, motivation and coping so that the training outcomes are optimised.

In summary, the understandable use of pain interventions should be part of a multidimensional treatment and training programme that tackles the physical, cognitive and emotional aspects of the pain problem.


Treatment is not in a vacuum | the patient experience and the healthcare approach

A phrase I often use with patients is ‘nothing happens in isolation’. This concept is about priming and how the neuroimmune system is set at the time of an intervention as this will affect the outcome. The question to ask is ‘how is this system likely to respond to the treatment I am about to employ based on what I hear from the patient and what I can see?’ 

How will this system respond to the treatment I am about to give?

This is the same for any healthcare practitioner whether it be a physiotherapist about to mobilise a joint or ask a patient to perform a movement, a doctor prescribing a drug or administering an injection.

The key factors that are somewhat controllable are the environment in which the treatment is taking place and the approach of the practitioner. Both of these can be created to optimise the patient experience and hence the effect of the therapy. We must also consider prior experiences and expectations of the patient. Here are two scenarios to illustrate.

1. A patient arrives at the clinic and discovers that there is a delay. There is no explanation given when they are directed to their seat. Naturally the patient is a little anxious about the forthcoming injection. They sit in a waiting room that is plastered with posters and leaflets about various health matters. And there is a pile of old magazines. Dogeared. Twenty minutes later the patient is called to Room 5 by an electric sign. They tap on the door and a gruff response permits entrance. There is no eye contact, no smile and no invitation to sit down because the practitioner is looking at the computer.

How would this prime a neuroimmune system? What would an aroused and threatened system do? Will it be readily acceptant of a needle? May the musculoskeletal tighten in response?

2. A patient arrives at the clinic and is greeted warmly by the reception team. On taking a seat the patient notices the artwork on the wall. The healthcare professional emerges smiling from his room and invites the patient to enter, welcoming them to take a seat and be comfortable.

What might this do to a threatened neuroimmune system (threatened because the patient has been thinking about the injection and is slightly anxious)?

Whilst it is always easy in theory to create scenarios, it is quite feasible to employ an approach that considers the influential factors upon the patient experience. In essence they do not want to be there, they do not want to have to have treatment but they must for the sake of their health. The neuroimmune system is on alert because of the actual health issue and also because of the experience of visiting the professional. We can certainly impact upon this in a positive way by thinking about our interface with the patient, use techniques to reduce anxiety and construct an environment that is conducive to better outcomes. Nothing happens in isolation. 

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Rehabilitation of thinking – A key element in maximising performance

The rehabilitation journey following an injury must be traveled with full commitment and completed. Usually when we talk about rehabilitation, it is the exercises that are focused upon: the movement, the task, the goal and how much to do. Nothing wrong with this of course as the training parameters are important to understand the effects of the exercise and how to subsequently progress. An aspect that is vital, yet less frequently mentioned, is the thinking both behind the activity and that of the individual undertaking the training.

Each exercise must have a meaning that needs to be explained. Full understanding of how, when and why the particular task is being undertaken is vital for full engagement, both physically and cognitively. In addition we have to consider the context of the exercise including the time of the day, the environment, the mood of the participant, level of discomfort, general health factors and other variables. Being aware of these influences and how they affect performance permits accurate assessment of the outcomes and where to focus upon for future improvement. In essence it is a learning process similar to that of learning a language or a musical instrument. Feedback plays a key role via the trainer correcting movement verbally and physically, and other means including exercising in front of a mirror.

The thinking of the participant before engaging in the exercise, during and afterwards will have an impact on success and hence learning. We can call this his or her mindset. Carol Dweck talks about a fixed mindset which describes a thought pattern underpinned by inflexible beliefs: it is how it is, this is my lot, change does not happen etc. Clearly this thinking can limit success and progression. A growth mindset on the other hand, is characterised by a belief that we can learn, change and grow. This mindset is one I encourage and seek to nurture as part of moving forwards following an injury or in progressing with a painful condition. In essence we are designed to change and adapt to our environment and circumstances. Given the right opportunity, input, motivation and timeline, we can evolve and develop healthier notions and actions for life both physically and in thought.

In summary, rehabilitation is not about simply going through the motions of certain exercises. It is about taking the opportunity to grow and develop physically and cognitively. In many cases we have to address thinking that is affecting the rehabilitation process, for example, thoughts that would be of a fixed mindset. Working upon these with strategies can and often are as important as the physical activities for optimum outcome. Our comprehensive rehabilitation programmes encompass these details so that you can progress from pain to performance.


Cervical Dystonia | What can we do?

I see a number of cases of cervical dystonia (spasmodic torticollis) that features awkward posturing and movement of the head and neck. This can be painful and have consequences for normal activities. We rely upon being able to orientate ourselves to our environment by controlling our head and gaze direction and then responding appropriately.

Primary dystonia has no neurological or metabolic cause whereas secondary dystonia is attributable to outside factors such as physical trauma, exposure to certain medications and other neurological or metabolic diseases.

Here is a fact sheet from the National Institute of Neurological Disorders & Stroke

Common treatment of cervical dystonia includes botulinum toxin injections and physiotherapy.

Modern physiotherapy for cervical dystonia at the Specialist Pain Physio Clinics

In addition to the manual techniques that are used to help ease tension and the soreness associated with spasm and tightness in the muscles, we use strategies that target the motor centres in the brain where the signals are coming from. In other words, as well as treating the symptoms, we are focusing upon the mechanisms and causes of the muscles going into spasm. The Graded Motor Imagery programme provides a way of aiming to retrain movement by targeting the adaptations that have occured in the motor system. Initially this programme was devised for complex regional pain syndrome, but since then the training has been found to help those with a range of painful problems with associated movement issues.

Typically a treatment programme includes themes that aim to develop a deep understanding of the problem(s), nourish and mobilise the body tissues, improve motor control, body sense and awareness, manage posture, increase exercise an activity tolerance and ultimately improve quality of life. We call the approach biobehavioural because it is a comprehensive way of tackling the issues and influencing factors that are unique to the individual, addressing the physical signs and symptoms as much as the underpinning beliefs and lifestyle factors that impact.

Call for appointments: 07518 445493


Dr Marie-Helene Marion, a consultant neurologist specialising in the treatment of dystonia and movement disorders has a comprehensive blog here

Recent research papers

Behav Neurol. 2012 May 24.

Cervical dystonia: From pathophysiology to pharmacotherapy.

Patel S, Martino D.


Background: Dystonia is a chronic disorder characterised by an aberration in the control of movement. Sustained co-contraction of opposing agonist and antagonist muscles can cause repetitive and twisting movements, or abnormal postures. Cervical dystonia (CD), often referred to as spasmodic torticollis, is a type of focal dystonia involving the muscles of the neck and sometimes the shoulders. Methods: This systematic review collates the available evidence regarding the safety and efficacy of a range of treatments for CD, focusing on their effectiveness as shown by double-blinded, randomised controlled trials. Results: Our review suggests that botulinum toxin type A (BTA), botulinum toxin type B (BTB) and trihexyphenidyl are safe and efficacious treatments for CD. Evidence shows that botulinum toxin therapies are more reliable for symptomatic relief and have fewer adverse effects than trihexyphenidyl. When comparing BTA to BTB, both are found to have similar clinical benefits, with BTA possibly having a longer duration of action and a marginally better side effect profile. BTB is also safe and probably just as efficacious a treatment in those patients who are unresponsive or have become resistant to BTA.

Discussion: The current evidence shows that the pharmacological management of CD relies on BTA and BTB, two agents with established efficacy and tolerability profiles.


Lancet Neurol. 2002 Sep;1(5):316-25.

Classification and genetics of dystonia.

de Carvalho Aguiar PM, Ozelius LJ.


Dystonia is a syndrome characterised by sustained muscle contractions, producing twisting, repetitive, and patterned movements, or abnormal postures. The dystonic syndromes include a large group of diseases that have been classified into various aetiological categories, such as primary, dystonia-plus, heredodegenerative, and secondary. The diverse clinical features of these disorders are reflected in the traditional clinical classification based on age at onset, distribution of symptoms, and site of onset. However, with an increased awareness of the molecular and environmental causes, the classification schemes have changed to reflect different genetic forms of dystonia. To date, at least 13 dystonic syndromes have been distinguished on a genetic basis and their loci are referred to as DYT1 to DYT13. This review focuses on the molecular and phenotypic features of the hereditary dystonias, with emphasis on recent advances.


Mov Disord. 2002;17 Suppl 3:S49-62.

Pathophysiology of dystonia: a neuronal model.

Vitek JL.


Dystonia has commonly been thought to represent a disorder of basal ganglia function. Although long considered a hyperkinetic movement disorder, the evidence to support such a classification was based on the presence of excessive involuntary movement, not on physiological data. Only recently, with the return of surgical procedures using microelectrode guidance for the treatment of dystonia, has electrophysiological data demonstrated an alteration in mean discharge rate, somatosensory responsiveness and the pattern of neuronal activity in the basal ganglia thalamocortical motor circuit. Previous models of dystonia suggested that reduced mean discharge rates in the globus pallidus internus (GPi) led to unopposed increases in activity in the thalamocortical circuit that precipitated the development of involuntary movement associated with dystonia. This model has subsequently been modified given the clear improvement in dystonic symptoms following lesions in the GPi, a procedure that is associated with a further reduction in pallidal output. The improvement in dystonia following pallidal lesions is difficult to reconcile with the “rate” hypothesis for hypokinetic and hyperkinetic movement disorders and has led to the development of alternative models that, in addition to rate, incorporate changes in pattern, somatosensory responsiveness and degree of synchronization of neuronal activity. Present models of dystonia, however, must not only take these changes into account but must reconcile these changes with the reported changes in cortical excitability reported with transcranial magnetic stimulation, the changes in metabolic activity in cortical and subcortical structures documented by positron emission tomography (PET), and the alterations in spinal and brainstem reflexes. A model incorporating these changes together with the reported changes in neuronal activity in the basal ganglia and thalamus is presented.


The importance of the first minutes, hours and days of an injury

Sustaining an injury is commonplace in sport. What happens in the first few minutes, hours and days can play a big part in how well we recover. The injury needs to be diagnosed and understood, for example an ankle twisting beyond the normal range of movement that results in a sprained ligament. As important is our response to the injury, what action we take and what we think about it. This blog explores these points with the aim of clarifying good practice in the first instance of an injury.

Our response to an injury includes how we protect the area, how we communicate that we are injured and the thoughts going on in our head. All are influential. How we protect a new injury is often by holding it, perhaps rubbing the area, limping, applying a bandage or using a set of crutches. This is very useful as the healing process begins immediately and the tissues need this protection to enable this activity. Communicating our pain and injury is individual. Some will cry out, use a facial expression, raise an arm to call the bench for help and others will suppress the urge to call out or use other ways of minimising body language. However, it is often difficult to do this with the acute pain of a freshly sprained ligament or strained muscle. Finally, the thoughts running through our head will vary but could include ‘What have I done?’, ‘What does this mean to my career in football?’ or ‘Not again!’. These thoughts are really important as they will be the conscious reflection of our beliefs about the situation. Our beliefs in turn, drive behaviours and consequently what we do in our injured state. In essence, what we do early on can impact upon the course of the recovery.

In the early stages, having a good understanding of what has happened, what has been injured and the extent of the injury is important from a reassurance viewpoint. Often the responses of the body to an injury are normal yet unpleasant. We need to know what is normal and what may not be normal so that the latter can be dealt with effectively. We also like to know what it is that needs to be done. For these questions to be answered we make a prompt visit to a healthcare professional. Rapid pain relief helps to take a positive stance on managing the early stages and indeed, high levels of uncontrolled pain can lead to beliefs and behaviours that are unhelpful. This is a pertinent point that I would like to emphasise. Gaining a realistic and accurate view of the situation with a good management plan promotes adaptive behaviours and responses that means you are doing everything that you should to support the healing and recovery. Developing fears of movement, catastrophising about the pain and excessively worrying about the injury usually lead to persisting problems. Clearly the former is a better scenario.

In summary, we must think about the early stages of injury management and have a clear strategy. This must include a good explanation of the problem, relevant investigations if required, a management plan that works with the healing process and monitoring of any thinking that could impact upon one’s choices.

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.


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.


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.


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.


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.


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


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.