Tag Archives: physiotherapy

25Mar/14
physiospot

Beyond the biomedical model of pain – an interview with Richmond Stace

physiospotRecently I was interviewed by Rachael from Physiopedia and Physiospot. We discussed some of the areas I feel are important in tackling the problem of pain, in particular chronic pain.

Click here for the interview

Primarily the topic focus was the psychosocial aspects of pain, an area that has provoked increasing interest. The word is often used but I find in practice that the social or societal influences upon pain are rarely included in a treatment programme. The most obvious example is the way in which a couple live and interact and how this impacts upon pain. Culture and gender both play a significant role in how pain is perceived, experienced and treated.

Of course the psychosocial elements are not in isolation to the physical and in fact I would argue that they are as biological as movement or nociception. All our experiences are constructed by the brain and involve neuronal activity driven by chemicals.

The understanding of pain sciences has moved on dramatically over the past 5-10 years but sadly the management trails behind, held back by old fashioned thinking and views based on out-dated thinking. We have an obligation to reconceptualise the way we deal with pain because the information exists and there are vast numbers of people who need to know that they can both control and change their pain.

Specialist Pain Physio Clinics in London for chronic pain, pain and injury

20Jul/13

Creating the right conditions to move forward

3 key points

1. Nothing happens in isolation.

2. We are designed to change, grow and develop.

3. Nothing is permanent.

Bearing these fundamental points in mind, we seek to create and then cultivate the right conditions so that we may move forward in life. In terms of rehabilitation, we also look to create the conditions to achieve wellness that manifests in an ability to perform at home, at work and on the field of play.

Nothing happens in isolation: we are on a continuous pathway with an underpinning genetic make up that is sculpted by our experiences and environment (epigenetics). So when we experience a pain or an injury, the immediate physiological and behavioural responses that so affect the pain perception, will be determined by what we know and by what our brain knows (we do not know all the things that our brain knows. Or our nose knows). When designing and implementing a training programme for a painful condition, this is an important principle as the patient will have a story leading to the point when they exercise that will determine the response including what they have done physically, how they are feeling and what they are thinking. Anticipation and expectation must be addressed.

We are designed to change: neuroplasticity is a feature of the neuroimmune system that allows us to learn and change. However, the mindset around this is key. We must understand the we can change and have a belief that it is possible in order to behave in a way that will promote forward movement in life. This must be addressed in any rehabilitation programme and indeed it may be that thinking needs to be ‘rehabilitated’ as well.

Nothing is permanent: the concept of impermanence comes from Buddhism. Nothing is permanent, even pain and other symptoms. They change as does our thinking, emotional state and body sense. We may not think it does and particularly in suffering on-going pain. However, the intensity, quality, location and nature of pain changes regularly and this is because the neuroimmune system is dynamic, ever-responding to the internal and external environments. This is why the context of the situation is so key in pain. We must think about this in rehabilitation: the context of the training.

In summary, the natural processes within the body are simply designed for us. To maximise their potential we must create the right conditions for these processes to act and this means considering the physical, cognitive and emotional dimensions of the pain experience and how they interact. A single leg squat is a single leg squat, but what is the person thinking about the single leg squat, have they done it before, will the brain consider it to be safe, where are they doing it, when are they doing it……..the list of considerations goes on. Lets consider them.

For further information about our treatment and training programmes or to book your first session, call us on 07932 689081

05Nov/12
Endometriosis & melatonin | Women and pain series

Women and pain | Part 1

‘As many as 50 million American women live with one or more neglected and poorly understood chronic pain conditions’ 

Generally I see more female patients than male. This observation supports the view that chronic pain is more prevalent in women than in men for some conditions – see the International Association for the Study of Pain fact sheet here. There are some ideas as to why this may be, including the role of the sex hormones and psychosocial factors such as emotion, coping strategies and roles in life. Additionally, experimental studies have shown that women have lower pain thresholds (this is a physiological reading) and tolerance to a range of pain stimuli when compared to men although this does not clarify that women actually feel more pain – see here. Pain is a subjective experience of course, and modulated by many factors.

A campaign for women’s pain | Chronic pain in women (2010) report

It is not uncommon for a female patient to tell me about her back pain and continue the narrative towards other body areas that hurt and cause problems. This may include pelvic pain, migraine, headache, irritable bowel syndrome, chronic knee pain, widespread sensitivity and gynaecological problems (including dysmenorrhoea, endometriosis and difficulty conceiving). These seemingly varied conditions are typically looked after by a range of medical and surgical disciplines: gynaecology, neurology, rheumatology, gastroenterology and orthopaedics. More recent science and thinking has started to join the dots on these problems, offering new insight into the underpinning mechanisms and more importantly approaches that can affect all the conditions in a positive way. This is certainly my thinking on this hugely significant matter.

Reconceptualising pain

Undoubtedly pain is complex. This is particularly the case when pain persists, disrupting and impacting upon life. Reconceptualising pain according to modern neuroscience is making a real difference to how we think and treat pain – see this video. Briefly, thinking of pain as an output from the brain as a result of a complex interaction of circumstance, biology, thought, emotion and memory begins to give an insight into the workings of the brain and body. Pain is individual, it is in the ‘now’ but so coloured by the past and what it may mean to the individual. The context or situation in which the pain arises is so very important. We talk about pain from the brain but of course we really feel it in our physical bodies, but the location is where the brain is projecting the sensation – see this video.

Neuroscience has shown us that the danger signals from the body tissues are significantly modulated by the brain before the end output is experienced. Factors that influence the messages include attention, expectation and the circustance in which the individual finds herself. We have powerful mechanisms that can both facilitate and inhibit the flow of these signals and these reside within the brain and brain stem. For this reason we must consider the person’s situation, their expectations, hopes, goals, past experiences and current difficulties, and how these can affect their current pain.

Stress & emotion

Any hugely emotive issue within someone’s life can impact enormously upon pain and sensitivity. This can be the stress of a situation including caring for a relative, losing someone close, work related issues and divorce. The problem of conception certainly features in a number of cases that I see, causing stress and turmoil for both partners but clearly in different ways. Fertility receives a great deal of attention in the media and there are a many clinics offering treatment and therapies, in effect raising awareness and attention levels towards the problem. The pain caused by difficulties having children can manifest physically through the stress that is created by the situation. Thoughts, feeling and emotions are nerve impulses in the brain like any other and will trigger physical responses including tension. Stress physiology affects all body systems, for example the gastrointestinal system (e.g./ irritable bowel), nervous system (e.g. headaches, back pain) and the immune system (e.g. repeated infections).

Lifestyle

Lifestyle factors play a significant role in persisting pain. Modern technology and habits that we form easily may not be helpful when we have a sensitive nervous system. For example, sedentary work, the light from computer screens, pressures at work, limited exercise, poor diet, binge drinking and smoking to name but a few. All are toxic in some way as can be our own thinking about ourselves. When we have a thought, and we have thousands each day, and we pay attention, becoming absorbed in the process, the brain reacts as if we are actually in that situation. Consequently we have physical and emotional responses that can be repeated over and over when we dwell on the same thinking. This is rumination and is likely due to ‘hyper-connectivity’ between certain brain areas – see here. We can challenge this in several ways including by changing our thinking and using mindfulness, both of which will alter brain activity and dampen these responses. It does take practice but the benefits are attainable for everyone.

In summary, the underlying factors that must be addressed are individual and both physical and psychological. Pain is complex and personal, potentially affecting many different areas of life. How we live our lives, what we think and how we feel are all highly relevant in the problem of pain as borne out of sensible thinking and the neuroscience of pain. Understanding the pain, learning strategies to reduce the impact, receiving treatment that targets the underlying mechanisms, making healthy changes to lifestyle and developing good habits alongside the contemporary brain based therapies can make a huge difference and provide a route forwards.

For information on our ‘join the dots’ treatment programmes for chronic pain, contact us here or call 07932 689081

 

11Jul/12

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

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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.

Abstract

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.

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

Classification and genetics of dystonia.

de Carvalho Aguiar PM, Ozelius LJ.

Abstract

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.

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

Pathophysiology of dystonia: a neuronal model.

Vitek JL.

Abstract

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.

28May/12

Specialist Pain Physio Clinics | Temple, London

The Specialist Pain Physio clinic based at Positive Heath Strategies in Temple is located just on the edge of the City and Fleet Street. Sitting just back from the River Thames, the office is a short stroll away from a magnificent view of London.

Modern treatment of painful conditions requires a comprehensive approach that addresses the reasons for pain, the influences upon pain, past experiences of pain and lifestyle factors. Employing science-based therapies that range from hands-on techniques to cognitive and brain focused strategies, we aim to reduce symptoms, increase activity levels and maximise quality of life.
We see individuals who reside locally and those who travel from around the UK and beyond, either referred by their specialist or self-referring for treatment. Common reasons for consultation and treatment include back pain, neck pain, complex regional pain syndrome (CRPS), recurring/persisting sports injuries, tendinopathy, fibromyalgia, repetitive strain injury (RSI), medically unexplained symptoms (pain yet no demonstrable pathology or injury), whiplash injury (whiplash associated disorder), rheumatological complaints and arthritis.
If you are suffering pain, persisting pain or are finding it difficult to return to normal activities, come and see us in London and Surrey. Other sites for the clinics are Chelsea, Temple and New Malden in Surrey.
T 07518 445493
04Apr/12

Reconceptualising pain for better treatment – a revolution? A revelation?

Traditionally pain is understood to be an unpleasant experience in the body where a problem exists, and is something to be got rid of as quickly as possible. The so-called ‘biomedical model’ considers which structures require treatment or surgery, stopping at the tissues as the cause of pain. This paradigm has been challenged over the years and rightly so in the light of recent research. Many studies have revealed the underlying physiology within the nervous system, and in particular the brain, and the role of other body systems such as the immune system and endocrine system (hormones) in pain. Understanding that pain is a normal response to a perceived threat has helped mould new treatments and ways of dealing with pain.

The most pertinent discovery and emergent shift in thinking came when it was realised that pain is a brain experience. This came via studies of the brain but also by looking at why phantom limb pain exists and how people present with a range of injuries and such varied levels of reported pain. There are many stories of people suffering severe physical injury yet experience little or no pain at the time.

Pain relief

The fact that we know pain is a brain experience has helped us to understand the many influences upon the pain, especially one’s emotional state. For instance, we know that the danger signals that are sent by the body to the brain via the spinal cord, travel to the emotional centres of the brain to try and give some meaning to the pain. These signals reach the brain and receive scrutiny to work out the level of threat, and this can vary enormously depending upon a range of factors. On activating a widespread group of neurons termed the ’pain matrix’, the output from the brain, a response, can be the pain experience. Knowing that there are many parts of the brain involved has meant that there are now a range of approaches that can tackle the problem of pain.

We are now far more optimistic about treating pain. This is not just with medication, which does have a role when used wisely, but with a range of contemporary treatments, strategies and techniques that address the underpinning mechanisms at a tissue level, spinal cord level and a brain level alongside beliefs, attitudes and behaviours that can be moulded to change the pain. The term used to describe the contemporary approach to pain is ’biopsychosocial’, implying a role for the overlapping biological, psychological and social factors that must be addressed.

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.

For appointments at one of the clinics please call 07518 445493

  • 9 Harley Street
  • The Chelsea Consulting Rooms
  • Temple
  • New Malden Diagnostic Centre
12Mar/12

Football Injury Blog @Footymatters

Footy Matters

I am really excited to be writing a regular blog on the Footy Matters website looking at injuries in football.

Injury Time with Richmond Stace

About Footy Matters

Footy Matters is an online football magazine like no other. We’ll be bringing you sharp commentary on the latest football news, providing unique insight, views and opinions away from the mainstream.

Our aim is to inform and educate with well researched and well written content you won’t find in the crowded football blog-osphere and that is tailor-made for the thinking football fan.

Footy Matters is your place to share, discuss and debate every aspect of the beautiful game.

Thinking Football

The Thinking Football ethos is Footy Matters’ approach to everything we write. We’re not interested in Wags, Heat magazine gossip or what players wear or drive – for us it’s all about the game.

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You can follow Footy Matters on Twitter @footymatters

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.

21Jan/12

Central sensitisation is more common than you may think

Clifford Woolf recently said this about central sensitisation:

Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.

And Latremolier

Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations. PERSPECTIVE: In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors.

In essence we are talking about changes within the central nervous system that underpin the widespread, unpredictable and varied nature of persisting pain.

When I am listening to a patient, observing their movements and performing a ‘multi-system’ examination, I am in part looking for the pain mechanisms at play, including central sensitisation. Several of my questions are: ‘what is going on here to create this experience for the person in front of me?’, ‘why are the nervous and other systems responding in such a way?’ and ‘what is influencing the behaviour of those systems?’. I really need to know what it is that is prolonging this protection and is it really worthwhile for the individual.

Suspecting that there is a component of central sensitisation at play in many cases of chronic pain that I see, it is pleasing to see a group looking at this closely and finding evidence to support this thinking:

J Bone Joint Surg Br. 2011 Apr;93(4):498-502.

Evidence that central sensitisation is present in patients with shoulder impingement syndrome and influences the outcome after surgery.

Gwilym SE, Oag HC, Tracey I, Carr AJ.

Source

Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX3 7LD, UK. [email protected]

Abstract

Impingement syndrome in the shoulder has generally been considered to be a clinical condition of mechanical origin. However, anomalies exist between the pathology in the subacromial space and the degree of pain experienced. These may be explained by variations in the processing of nociceptive inputs between different patients. We investigated the evidence for augmented pain transmission (central sensitisation) in patients with impingement, and the relationship between pre-operative central sensitisation and the outcomes following arthroscopic subacromial decompression. We recruited 17 patients with unilateral impingement of the shoulder and 17 age- and gender-matched controls, all of whom underwent quantitative sensory testing to detect thresholds for mechanical stimuli, distinctions between sharp and blunt punctate stimuli, and heat pain. Additionally Oxford shoulder scores to assess pain and function, and PainDETECT questionnaires to identify ‘neuropathic’ and referred symptoms were completed. Patients completed these questionnaires pre-operatively and three months post-operatively. A significant proportion of patients awaiting subacromial decompression had referred pain radiating down the arm and had significant hyperalgesia to punctate stimulus of the skin compared with controls (unpaired t-test, p < 0.0001). These are felt to represent peripheral manifestations of augmented central pain processing (central sensitisation). The presence of either hyperalgesia or referred pain pre-operatively resulted in a significantly worse outcome from decompression three months after surgery (unpaired t-test, p = 0.04 and p = 0.005, respectively). These observations confirm the presence of central sensitisation in a proportion of patients with shoulder pain associated with impingement. Also, if patients had relatively high levels of central sensitisation pre-operatively, as indicated by higher levels of punctate hyperalgesia and/or referred pain, the outcome three months after subacromial decompression was significantly worse.

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Treat the brain, treat the pain

Arthritis Rheum. 2009 Sep 15;61(9):1226-34.

Psychophysical and functional imaging evidence supporting the presence of central sensitization in a cohort of osteoarthritis patients.

Gwilym SE, Keltner JR, Warnaby CE, Carr AJ, Chizh B, Chessell I, Tracey I.

Source

University of Oxford, Oxford, UK. [email protected]

Abstract

OBJECTIVE:

The groin pain experienced by patients with hip osteoarthritis (OA) is often accompanied by areas of referred pain and changes in skin sensitivity. We aimed to identify the supraspinal influences that underlie these clinical manifestations that we consider indicative of possible central sensitization.

METHODS:

Twenty patients with hip OA awaiting joint replacement and displaying signs of referred pain were recruited into the study, together with age-matched controls. All subjects completed pain psychology questionnaires and underwent quantitative sensory testing (QST) in their area of referred pain. Twelve of 20 patients and their age- and sex-matched controls underwent functional magnetic resonance imaging (MRI) while the areas of referred pain were stimulated using cold stimuli (12 degrees C) and punctate stimuli (256 mN). The remaining 8 of 20 patients underwent punctate stimulation only.

RESULTS:

Patients were found to have significantly lower threshold perception to punctate stimuli and were hyperalgesic to the noxious punctate stimulus in their areas of referred pain. Functional brain imaging illustrated significantly greater activation in the brainstem of OA patients in response to punctate stimulation of their referred pain areas compared with healthy controls, and the magnitude of this activation positively correlated with the extent of neuropathic-like elements to the patient’s pain, as indicated by the PainDETECT score.

DISCUSSION:

Using psychophysical (QST) and brain imaging methods (functional MRI), we have identified increased activity with the periaqueductal grey matter associated with stimulation of the skin in referred pain areas of patients with hip OA. This offers a central target for analgesia aimed at improving the treatment of this largely peripheral disease.