I use Graded Motor Imagery commonly for a range of painful conditions including CRPS. In essence, GMI is brain training that targets mechanisms that we know are involved in ongoing pain states. Here is David Butler talking about GMI, mirrors and neuroscience.
Part 1
Part 2
Part 3
Part 4
Mirror Therapy
Neurodynamics and neuroscience
For more information about treatment of CRPS and other chronic and complex pain states, visit www.specialistpainphysio.com
Many readers will know about mirror box therapy for CRPS and other painful conditions. The Graded Motor Imagery Programme that we use at Specialist Pain Physio is sequential training that starts with laterality, progressing to imagined movements and then to mirror therapy. There is some really good data for the programme and CRPS but it can also be effective with other chronic pains. Interestingly we are now seeing components of GMI being used and written about in the popular press, most recently for Parkinson’s disease and arthritis.
Brain training for pain
A brief article in New Scientist describes the Parkinson’s research by David Linden at Cardiff University. 10 subjects were asked to think about movement for 45 minutes whilst they were having brain scans. Five of the subjects were given feedback that showed them how they were activating the brain and all were asked to practice the imagery at home. Two months later rigidity and tremor had reduced some 37% in the feedback group. The thinking is that there is cortical change underpinning this improved function that is feasible.
Mirror therapy for pain
At The Society for Neuroscience annual meeting 2011 a small study was performed with arthritis (OA & RA) patients used mirror therapy. Subjects observed the moving reflection of the researcher’s hand in the mirror whilst producing the same movement themselves with their hidden hand. After 1 minute it was noted that the subjects pain improved. This was reported in The Guardian today.
For details on our treatment programmes including imagery, mirror therapy, graded motor imagery and other neuroscience-based techniques, come and see our website at http://www.specialistpainphysio.com or call 07518 445491. Our clinics are based in London and Surrey http://www.specialistpainphysio.com/clinics
Readers will be familiar with the importance that I attach to the explanation of pain. The data on the benefits of understanding pain is good and growing. This includes a raised pain threshold and an increase in range of movement–the straight leg raise (SLR). The more we understand about the power of language and learning, the better will become our educational interventions, recently termed ‘information medicine” by David Butler at an Explain Pain weekend. I like that term because of the implication that we are administering medicine by the provision of information. This can be given in doses, like pills and manual therapy, titrated and adjusted to the individual need at that moment, seeking the best route forwards.
This short animation really struck a chord with me. The narrative is clear and raises important points that are understandable.
Here are a few papers looking at this fascinating a relevant area. Our sense of self is clearly affected in many pain states and in other situations when we are under threat. This is an area we address fully as part of our rehabilitation and treatment programmes for CRPS, other chronic pain states and injuries. The loss of a sense of self is underpinned by a range of physiological changes throughout the nervous system and must be re-trained for normal functioning.
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aExperimental Neuropsychology Research Unit, Monash University, Clayton, Victoria bSansom Institute for Health Research, University of South Australia, Adelaide, South Australia cNeuroscience Research Australia, Randwick, New South Wales, Australia.
Phantom pain is a frequent consequence of amputation or deafferentation. There are many possible contributing mechanisms, including stump-related pathology, spinal and cortical changes. Phantom limb pain is notoriously difficult to treat. Continued consideration of the factors associated with phantom pain and its treatment is of utmost importance, not only to advance the scientific knowledge about the experience of the body and neuropathic pain, but also fundamentally to promote efficacious pain management.
This review first discusses the mechanisms associated with phantom pain and summarizes the current treatments. The mechanisms underlying phantom pain primarily relate to peripheral/spinal dysfunction, and supraspinal and central plasticity in sensorimotor body representations. The most promising methods for managing phantom pain address the maladaptive changes at multiple levels of the neuraxis, for example, complementing pharmacological administration with physical, psychological or behavioural intervention. These supplementary techniques are even efficacious in isolation, perhaps by replacing the absent afferent signals from the amputated limb, thereby restoring disrupted bodily representations.
Ultimately, for optimal patient outcomes, treatments should be both symptom and mechanism targeted.
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Neuroscience Research Australia, Barker Street, Randwick, Sydney, NSW 2031, Australia.
The sense of body ownership, knowledge that parts of our body ‘belong’ to us, is presumably developed using sensory information. Cutaneous signals seem ideal for this and can modify the sense of ownership. For example, an illusion of ownership over an artificial rubber hand can be induced by synchronously stroking both the subject’s hidden hand and a visible artificial hand. Like cutaneous signals, proprioceptive signals (e.g. frommuscle receptors) exclusively signal events occurring in the body, but the influence of proprioceptors on the sense of body ownership is not known. We developed a technique to generate an illusion of ownership over an artificial plastic finger, using movement at the proximal interphalangeal joint as the stimulus. We then examined this illusion in 20 subjects when their index finger was intact and when the cutaneous and joint afferents from the finger had been blocked by local anaesthesia of the digital nerves. Subjects still experienced an illusion of ownership, induced by movement, over the plastic finger when the digital nerves were blocked. This shows that local cutaneous signals are not essential for the illusion and that inputs arising proximally, presumably from receptors in muscles which move the finger, can influence the sense of body ownership. Contrary to other studies, we found no evidence that voluntary movements induce stronger illusions of body ownership than those induced by passive movement. It seems that the congruence of sensory stimuli ismore important to establish body ownership than the presence of multiple sensory signals.
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Macquarie Centre for Cognitive Science, Macquarie University, Sydney, NSW 2109, Australia. regine.zopf@maccs.mq.edu.au
Body ownership for an artificial hand and the perceived position of one’s own hand can be manipulated in the so-called rubber hand illusion. To induce this illusion, typically an artificial hand is placed next to the participant’s body and stroked in synchrony with the real hand, which is hidden from view. Our first aim was to test if the crossmodal congruency task could be used to obtain a measure for the strength of body ownership in the rubber hand illusion. In this speeded location discrimination task participants responded to tactile targets presented to their index or middle finger, while trying to ignore irrelevant visual distracters placed on the artificial hand either on the congruent finger or on the incongruent finger. The difference between performance on congruent and incongruent trials (crossmodal congruency effect, CCE) indicates the amount of multisensory interactions between tactile targets and visual distracters. In order to investigate if changes in body ownership influence the CCE, we manipulated ownership for an artificial hand by synchronous and asynchronous stroking before the crossmodal congruency task (blocked design) in Experiment 1 and during the crossmodal congruency task (interleaved trial-by-trial design) in Experiment 2. Modulations of the CCE by ownership for an artificial hand were apparent in the interleaved trial-by-trial design. These findings suggest that the CCE can be used as an objective measure for body ownership. Secondly, we tested the hypothesis that the lateral spatial distance between the real hand and artificial hand limits the rubber hand illusion. We found no lateral spatial limits for the rubber hand illusion created by synchronous stroking within reaching distances. In conclusion, the sense of ownership seems to be related to modulations of multisensory interactions possibly through peripersonal space mechanisms, and these modulations do not appear to be limited by an increase in distance between artificial hand and real hand.
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Department of Psychology, Royal Holloway, University of London, Egham, Surrey, UK. manos.tsakiris@rhul.ac.uk
Empirical research on the bodily self has only recently started to investigate how the link between a body and the experience of this body as mine is developed, maintained or disturbed. The Rubber Hand Illusion has been used as a model instance of the normal sense of embodiment to investigate the processes that underpin the experience of body-ownership. This review puts forward a neurocognitive model according to which body-ownership arises as an interaction between current multisensory input and internal models of the body. First, a pre-existing stored model of the body distinguishes between objects that may or may not be part of one’s body. Second, on-line anatomical and postural representations of the body modulate the integration of multisensory information that leads to the recalibration of visual and tactile coordinate systems. Third, the resulting referral of tactile sensation will give rise to the subjective experience of body-ownership. These processes involve a neural network comprised of the right temporoparietal junction which tests the incorporeability of the external object, the secondary somatosensory cortex which maintains an on-line representation of the body, the posterior parietal and ventral premotor cortices which code for the recalibration of the hand-centred coordinate systems, and the right posterior insula which underpins the subjective experience of body-ownership. The experience of body-ownership may represent a critical component of self-specificity as evidenced by the different ways in which multisensory integration in interaction with internal models of the body can actually manipulate important physical and psychological aspects of the self.
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Wellcome Department of Imaging Neuroscience, Institute of Neurology, University College London, London, UK. e.tsakiris@ucl.ac.uk
Body ownership refers to the special perceptual status of one’s own body, which makes bodily sensations seem unique to oneself. We studied the neural correlates of body ownership by controlling whether an external object was accepted as part of the body or not. In the rubber hand illusion (RHI), correlated visuotactile stimulation causes a fake hand to be perceived as part of one’s own body. In the present study, we distinguished between the causes (i.e., multisensory stimulation) and the effect (i.e., the feeling of ownership) of the RHI. Participants watched a right or a left rubber hand being touched either synchronously or asynchronously with respect to their own unseen right hand. A quantifiable correlate of the RHI is a shift in the perceived position of the subject’s hand toward the rubber hand. We used positron emission tomography to identify brain areas whose activity correlated with this proprioceptive measure of body ownership. Body ownership was related to activity in the right posterior insula and the right frontal operculum. Conversely, when the rubber hand was not attributed to the self, activity was observed in the contralateral parietal cortex, particularly the somatosensory cortex. These structures form a network that plays a fundamental role in linking current sensory stimuli to one’s own body and thus also in self-consciousness.
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Atkinson Research Laboratory, Barrow Neurological Institute, Phoenix, Arizona, USA. bcraig@chw.edu
An ascending sensory pathway that underlies feelings from the body, such as cooling or toothache, terminates in the posterior insula. Considerable evidence suggests that this activity is rerepresented and integrated first in the mid-insula and then in the anterior insula. Activation in the anterior insula correlates directly with subjective feelings from the body and, strikingly, with all emotional feelings. These findings appear to signify a posterior-to-anterior sequence of increasingly homeostatically efficient representations that integrate all salient neural activity, culminating in network nodes in the right and left anterior insulae that may be organized asymmetrically in an opponent fashion. The anterior insula has appropriate characteristics to support the proposal that it engenders a cinemascopic model of human awareness and subjectivity. This review presents the author’s views regarding the principles of organization of this system and discusses a possible sequence for its evolution, as well as particular issues of historical interest.
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Atkinson Research Laboratory, Barrow Neurological Institute, 350 West Thomas Rd., Phoenix, AZ 85013, USA. bcraig@chw.edu
This article addresses the neuroanatomical evidence for a progression of integrative representations of affective feelings from the body that lead to an ultimate representation of all feelings in the bilateral anterior insulae, or “the sentient self.” Evidence for somatotopy in the primary interoceptive sensory cortex is presented, and the organization of the mid-insula and the anterior insula is discussed. Issues that need to be addressed are highlighted. A possible basis for subjectivity in a cinemascopic model of awareness is presented.
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Atkinson Research Laboratory, Barrow Neurological Institute, Phoenix, Arizona 85013, USA. bcraig@chw.edu
The anterior insular cortex (AIC) is implicated in a wide range of conditions and behaviours, from bowel distension and orgasm, to cigarette craving and maternal love, to decision making and sudden insight. Its function in the re-representation of interoception offers one possible basis for its involvement in all subjective feelings. New findings suggest a fundamental role for the AIC (and the von Economo neurons it contains) in awareness, and thus it needs to be considered as a potential neural correlate of consciousness.
Mastery is defined in the Oxford dictionary as:
The concept of mastery is often applied to a musical instrument, golf, martial arts or a language. The word is rarely used in conjunction with the rehabilitation of an injury or a painful condition. It occurred to me that there are vast similarities between the principles and experience of training for a sport or a skill and the participation in a rehabilitation programme. The difference will be the end goals and the specific reason for the training. In the case of mastering a sport, it is about performance enhancement with greater skill and efficiency to achieve fewer shots or more accuracy for example. In rehabilitation the goal are pain relief, normal mobility, control of movement, restoration of strength, power and a return to daily activities (work, home, exercise).
Undoubtedly the body has incredible mechanisms that heal injured tissue. Unfortunately there are many people who despite the healing process do continue to suffer painful symptoms. We see many cases of enduring and problematic pain at the clinic and set about the problem with a contemporary approach. This involves a range of treatment techniques and strategies including active rehabilitation or training. This training requires instruction, understanding, dedication, awareness, consistency, intention and practice. Just like learning a golf shot or the piano.
Setting up the principles of training (I will refer to the rehabilitation now as training) creates the right context and mindset. This includes pain/condition specific education so that the programme makes sense, the aims of the exercises, when to do them, how often and how to progress or moderate the intensity. In laying out the way forwards, the concept of mastery is introduced. What is it that needs mastery?
When we are in pain we change the way that we move. The longer the condition has been existing, the more the body and brain will have adapted alongside your thoughts and beliefs about the problem. The meaning that you give to the pain can also change with time and this is important. If the ‘meaning’ of the problem is significant, negative in nature and threatening to you as an organism (evolution speaking), the brain is more likely to protect you. This protection includes pain and altered movement, therefore perpetuating the cycle. This subject is for another day, important though it is, but dealing with negative thought patterns and unhelpful beliefs is fundamental, and requires restructuring. Returning to altered movement, this needs to be re-trained to reduce the guarding and protection. Of course this is one aspect of a treatment programme, but it is a great example to use when thinking about how you are going to master normal movement.
Mastering normal movement as mastering a language takes instruction, practice and dedication as mentioned. Often along the road we meet challenges and resistance both physically and mentally. One of those challenges is the plateau when it appears that nothing is happening or changing. The performance still seems to be the same, the outcomes like before. It is during this time that there is change occurring but it has not yet clearly manifest. Understanding that the plateau is an important part of the process and using the time as a chance to learn and an opportunity to create change. The nervous system is very plastic and adaptable according to the stimuli that it receives. In rehabilitation, the repeated stimulus of the right movements, in the right setting and mind set create such an opportunity.
To be good at any skill we must fully engage and spend the time with ourselves practice for the sake of practicing. Applying similar principles to rehabilitation in re-training normal movement, thoughts about movement and exercise and the functional skills of your chosen activity, provides a framework and a well trodden philosophical pathway to success. You will have your chosen goals that you will seek to achieve and on reaching them you will have further targets to attain. This is the journey.
When we sustain an injury or experience a painful condition, our movement changes. In the early stages this can be obvious, for example we would limp having sprained an ankle. Sometimes the limp, medically termed an ’antalgic gait’, persists without the individual being aware. This is the same for other forms of guarding that is part of the body’s way of protecting itself. By tightening the affected area or posturing in a manner that withdraws, the body is changing the way that we work so that healing can proceed. Clearly this is very intelligent and useful. The problem lies with persisting guarding or protection that continues to operate when actually, normal movement is needed.
Practice, practice, practice
We know that when the brain is co-ordinating a response to a threat, a number of systems are active. This includes the nervous system, the motor system and the endocrine system (hormones). This is all part of protection as is pain in the location that is deemed to be under threat. It is important to be able to move away from danger and then to limit movement, firstly to escape from the threat (e.g. withdraw your hand from a hot plate) and then to facilitate the natural process of healing by keeping the area relatively immobilised. Interestingly, at this point our beliefs about the pain and injury will determine how we behave and what action we take. If we are concerned that there is a great deal of damage and that movement will cause further injury, we will tend to keep the area very still, looking out for anything or anyone who may harm us. Over-vigilance can lead to over-protection and potentially lengthen the recovery process. This is one reason why seeking early advice is important, so that you can optimise your potential for recovery.
We have established that we move differently when we are injured and in pain. In more chronic cases, the changes in movement and control of movement can be quite subtle. An experienced physiotherapist will be able to detect these and other protective measures that are being taken. These must be dealt with, because if we are not moving properly, this is a reason for the body to keep on protecting itself through feedback and feed-forward mechanisms. Re-training movement normalises the flow of information to and from the tissues to the brain. Often this process needs enhancement or enrichment as the sensory flow and position sense (proprioception) is not efficient.
To train normal movement is to learn. The body is learning to move effectively and this process is the same as learning a golf shot, a tennis stroke, a language or a musical instrument. Mastery. You are asking yourself to master normal movement. What does this take? Consistency, discipline, practice (and then some more practice), time, dedication, awareness and more. The second part of this blog will look at mastery as a concept that can help you understand the way in which you can achieve success with your rehabilitation.
Evidence based guidelines for CRPS type 1
A CRPS task force looked at the evidence for the treatment of CRPS Type 1 from papers written between 1980-June 2005. A clear limitation is the fact that the search stopped in 2005. Since this time there has been some great work that has considered the cortical and tissue changes that underpin the condition. Treatment advances have really revolved around the brain changes and how we can take advantage of the nervous system’s plasticity to alter pain and function–graded motor imagery.
Clearly we need evidence that treatments are effective. Physiotherapy is the mainstay of restoring function in many conditions including CRPS. However, when working with CRPS it is vital that the knowledge of the evidence base is up-to-date, but also an in-depth understanding of the pathophysiology is vital to be able to both explain the range of symptoms and provide effective strategies in response.
Dear Readers,
Welcome back to the blog. Here is a summary of some of the recent research.
Source
From the Departments of Neurology (M.L., O.H., P.S., S.L., P.S., M.T.) and Pain Management (A.R., J.F., H.R., C.M.), Berufsgenossenschaftliches Universitätsklinikum Bergmannsheil GmbH, Ruhr-Universität Bochum, Bochum, Germany.
In a previous study, we found bilateral disinhibition in the motor cortex of patients with complex regional pain syndrome (CRPS). This finding suggests a complex dysfunction of central motor-sensory circuits. The aim of our present study was to assess possible bilateral excitability changes in the somatosensory system of patients with CRPS.
METHODS:
We measured paired-pulse suppression of somatosensory evoked potentials in 21 patients with unilateral CRPS I involving the hand. Eleven patients with upper limb pain of non-neuropathic origin and 21 healthy subjects served as controls. Innocuous paired-pulse stimulation of the median nerve was either performed at the affected and the unaffected hand, or at the dominant hand of healthy controls, respectively.
RESULTS:
We found a significant reduction of paired-pulse suppression in both sides of patients with CRPS, compared with control patients and healthy control subjects.
CONCLUSION:
These findings resemble our findings in the motor system and strongly support the hypothesis of a bilateral complex impairment of central motor-sensory circuits in CRPS I.
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Source
Royal National Hospital for Rheumatic Diseases, Upper Borough Walls, Bath BA1 1RL, UK; University of Bath, Bath BA2 7AY, UK; Royal National Orthopaedic Hospital, Brockley Hill, Stanmore HA7 4LP,UK.
Abstract
Cortical reorganisation of sensory, motor and autonomic systems can lead to dysfunctional central integrative control. This may contribute to signs and symptoms of Complex Regional Pain Syndrome (CRPS), including pain. It has been hypothesised that central neuroplastic changes may cause afferent sensory feedback conflicts and produce pain. We investigated autonomic responses produced by ambiguous visual stimuli (AVS) in CRPS, and their relationship to pain. Thirty CRPS patients with upper limb involvement and 30 age and sex matched healthy controls had sympathetic autonomic function assessed using laser Doppler flowmetry of the finger pulp at baseline and while viewing a control figure or AVS. Compared to controls, there were diminished vasoconstrictor responses and a significant difference in the ratio of response between affected and unaffected limbs (symmetry ratio) to a deep breath and viewing AVS. While viewing visual stimuli, 33.5% of patients had asymmetric vasomotor responses and all healthy controls had a homologous symmetric pattern of response. Nineteen (61%) CRPS patients had enhanced pain within seconds of viewing the AVS. All the asymmetric vasomotor responses were in this group, and were not predictable from baseline autonomic function. Ten patients had accompanying dystonic reactions in their affected limb: 50% were in the asymmetric sub-group. In conclusion, there is a group of CRPS patients that demonstrate abnormal pain networks interacting with central somatomotor and autonomic integrational pathways.
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Source
Dept. of Neurology, Justus-Liebig-University, Am Steg 14, 35392 Giessen, Germany.
Abstract
Complex regional pain syndrome, which is characterised by pain and trophic disturbances, develops frequently after peripheral limb trauma. There is an increasing evidence of an involvement of the immune system in CRPS, and recently we showed that CRPS patients have autoantibodies against nervous system structures. Therefore we tested the sera of CRPS patients, neuropathy patients and healthy volunteers for surface-binding autoantibodies to primary cultures of autonomic neurons and differentiated neuroblastoma cell lines using flow cytometry. Thirteen of 30 CRPS patients, but none of 30 healthy controls and only one of the 20 neuropathy sera had specific surface binding to autonomic neurons (p<0.001). The majority of the sera reacted with both sympathetic and myenteric plexus neurons. Interestingly, 6/30 CRPS sera showed binding to undifferentiated SH-SY5Y neuroblastoma cells. However, differentiation of SH-SY5Y into a cholinergic phenotype induced a surface antigen, which is recognised by 60% of CRPS sera (18/30), but not by controls (p<0.001). Our data show that about 30-40% of CRPS patients have surface-binding autoantibodies against an inducible autonomic nervous system autoantigen. These data support an autoimmune hypothesis in CRPS patients. Further studies must elucidate origin and function of these autoantibodies in CRPS.
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Source
Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany.
Abstract
A triad of clinical symptoms, ie, autonomic, motor and sensory dysfunctions, characterizes complex regional pain syndromes (CRPS). Sensory dysfunction comprises sensory loss or spontaneous and stimulus-evoked pain. Furthermore, a disturbance in the body schema may occur. In the present study, patients with CRPS of the upper extremity and healthy controls estimated their hand sizes on the basis of expanded or compressed schematic drawings of hands. In patients with CRPS we found an impairment in accurate hand size estimation; patients estimated their own CRPS-affected hand to be larger than it actually was when measured objectively. Moreover, overestimation correlated significantly with disease duration, neglect score, and increase of two-point-discrimination-thresholds (TPDT) compared to the unaffected hand and to control subjects’ estimations. In line with previous functional imaging studies in CRPS patients demonstrating changes in central somatotopic maps, we suggest an involvement of the central nervous system in this disruption of the body schema. Potential cortical areas may be the primary somatosensory and posterior parietal cortices, which have been proposed to play a critical role in integrating visuospatial information. PERSPECTIVE: CRPS patients perceive their affected hand to be bigger than it is. The magnitude of this overestimation correlates with disease duration, decreased tactile thresholds, and neglect-score. Suggesting a disrupted body schema as the source of this impairment, our findings corroborate the current assumption of a CNS involvement in CRPS.
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Source
Department of Neurology, Justus-Liebig-University, Giessen, Germany.
Abstract
Complex regional pain syndrome (CRPS) is a painful condition affecting one or more extremities of the body, marked by a wide variety of symptoms and signs that are often difficult to manage because the pathophysiology is incompletely understood. Thus, diverse treatments might be ineffective. A recent report revealed the presence of autoantibodies against differentiated autonomic neurons in CRPS patients. However, it remained unclear how the antibodies act in the development of CRPS. We therefore aimed to characterize these antibodies and identify target antigens. Functional properties of affinity-purified immunoglobulin G of control subjects or CRPS patients were assessed using a cardiomyocyte bioassay. Putative corresponding receptors were identified using antagonistic drugs, and synthesized peptide sequences corresponding to segments of these receptors were used to identify the target epitopes. Chinese hamster ovary cells were transfected with putative receptors to ensure observed binding. Further, changes in the intracellular Ca(2+) concentration induced by agonistic immunoglobulin G were measured using the Ca(2+)-sensitive fluorescent dye fura-2 assay. Herein, we demonstrate the presence of autoantibodies in a subset of CRPS patients with agonistic-like properties on the β(2) adrenergic receptor and/or the muscarinic-2 receptor. We identified these autoantibodies as immunoglobulin G directed against peptide sequences from the second extracellular loop of these receptors. The identification of functionally active autoantibodies in serum samples from CRPS patients supports an autoimmune pathogenesis of CRPS. Thus, our findings contribute to the further understanding of this disease, could help in the diagnosis in future, and encourage new treatment strategies focusing on the immune system.
This was inspirational viewing. We watched these guys make their way to the North Pole across the most challenging terrain but also facing up to their own difficulties. The team bond made you want to be there. The way in which they individually dealt with the obstacles, both mental and physical, was a real lesson in the power of thought and character. No more to be said by me, just watch: http://www.bbc.co.uk/i/b013y230/
What we look at and what we see can be completely different. Our perception is filtered by what we think we know, past experience and expectation. Indeed this is what the brain does before creating a plausible image. When we are looking at an animal in a cage we do not think ‘there is a series of segments of a lion’ when the bars are positioned in front of the animal. No, the brain creates an experience of a lion. Equally, if we have just watched a spooky film and on taking the rubbish out into the alley we see a moving shadow we are more likely to believe that it could be an intruder rather than a cast of a branch.
In the world of neuroscience, all conscious experiences are created by the brain including vision and pain. The world that we see in front of us is no exception, however it is entirely possible that we can miss something right befroe our very ‘eyes’ if the brain does not perceive it to be there or happening. Christopher Chabris and Daniel Simons explain this brilliantly in their book that discusses the illusions of vision, memory and knwledge amongst other functions that we take for granted. Daniel Simons is known for a famous experiment that you can do here:
Have a go and see how you get on. Then ask friends and family! It helps to explain how we can be falsely secure in what we see, know and experience.
The illusion of vision is relevant to daily practice with patients in pain for several reasons. Firstly it demonstrates how we must be targeting the brain and the processing of information to change someone’s experience of their pain and secondly how we can use vision and illusion to ‘train the brain’. In simple terms, the brain is operating in a particular mode or state that is giving the current experience of the body and mind that could include pain.
To alter this experience we need to give the brain something else to do that has meaning and purpose. Of course, the meaning will need to be personal and contextual to that person but could include a position change, an exercise, a change of thought, writing a poem or drawing a picture. Treatment-wise we think about the types of intervention that could either change the flow of informatioin into the brain or to stimulate descending pathways that runs from brain to spinal cord and dampen the activity here in the dorsal horn.
In brain training we are focusing upon particular changes that we know take place in the brain termed cortical plasticity (click here, here and here). This includes the Graded Motor Imagery programme (and click HERE) that we use as part of the treatment programme and training for CRPS and other conditions.
If we are living in an illusion, which many of the leading lights in the field of neuroscience are saying, then this is still our experience and our ‘illusion’. Modern rehabilitation is not only about developing health and function in the tissues, but also changing the brain so that the sense of self is normal in terms of ‘feeling’ the body and in controlling movement. Both of these are developed through redefining the sensory and motor maps that change when we are in pain and not moving properly. Only in achieving this will nomal service be restored in function, confidence and longevity.
