Feature in La Creme Magazine about the Specialist Pain Physio approach to the treatment of pain

 

Who’s Who in London Private Healthcare

La Creme Magazine steers the reader through a range of features including health. The soon-to-be-published ‘Who’s Who in London Private Healthcare’ supplement will include interviews with a range of top specialists, covering different branches of medicine and surgery. Our clinic, the Specialist Pain Physio, delivering treatment programmes for pain, in particular complex and chronic cases of pain and injury, was fortunate enough to be part of this group. Richmond spoke with the editor, Sarah Holland, at The Royal Society of Medicine about his approach and work with people in pain.

Read the full interview here

Pain mechanisms (2)

Keith Smart has been looking at a mechanisms-based approach to pain. As you may recall from the first piece on pain mechanisms and previous writings, I am a proponent of the view that we should be thinking about pain mechanisms. There are significant advantages to elucidating the underpinning physiological and pathology including understanding the patient’s description of their experience and to be able to focus treatment upon the mechanism(s) for more successful outcomes. Below are the papers by Keith Smart and others who have looked at pain mechanisms.

RS www.specialistpainphysio.com

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Clin J Pain. 2011 Oct;27(8):655-63. doi: 10.1097/AJP.0b013e318215f16a.

The Discriminative validity of “nociceptive,” “peripheral neuropathic,” and “central sensitization” as mechanisms-based classifications of musculoskeletal pain.

Source

St Vincent’s University Hospital, Elm Park, Dublin, Ireland. k.smart@ucd.ie

Abstract

OBJECTIVES:

Empirical evidence of discriminative validity is required to justify the use of mechanisms-based classifications of musculoskeletal pain in clinical practice. The purpose of this study was to evaluate the discriminative validity of mechanisms-based classifications of pain by identifying discriminatory clusters of clinical criteria predictive of “nociceptive,” “peripheral neuropathic,” and “central sensitization” pain in patients with low back (± leg) pain disorders.

METHODS:

This study was a cross-sectional, between-patients design using the extreme-groups method. Four hundred sixty-four patients with low back (± leg) pain were assessed using a standardized assessment protocol. After each assessment, patients’ pain was assigned a mechanisms-based classification. Clinicians then completed a clinical criteria checklist indicating the presence/absence of various clinical criteria.

RESULTS:

Multivariate analyses using binary logistic regression with Bayesian model averaging identified a discriminative cluster of 7, 3, and 4 symptoms and signs predictive of a dominance of “nociceptive,” “peripheral neuropathic,” and “central sensitization” pain, respectively. Each cluster was found to have high levels of classification accuracy (sensitivity, specificity, positive/negative predictive values, positive/negative likelihood ratios).

DISCUSSION:

By identifying a discriminatory cluster of symptoms and signs predictive of “nociceptive,” “peripheral neuropathic,” and “central” pain, this study provides some preliminary discriminative validity evidence for mechanisms-based classifications of musculoskeletal pain. Classification system validation requires the accumulation of validity evidence before their use in clinical practice can be recommended. Further studies are required to evaluate the construct and criterion validity of mechanisms-based classifications of musculoskeletal pain.

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J Man Manip Ther. 2010 Jun;18(2):102-10.

The reliability of clinical judgments and criteria associated with mechanisms-based classifications of pain in patients with low back pain disorders: a preliminary reliability study.

Source

UCD School of Public Health, Physiotherapy and Population Science, University College Dublin, Ireland.

Abstract

Mechanisms-based classifications of pain have been advocated for their potential to aid understanding of clinical presentations of pain and improve clinical outcomes. However, the reliability of mechanisms-based classifications of pain and the clinical criteria upon which such classifications are based are not known. The purpose of this investigation was to assess the inter- and intra-examiner reliability of clinical judgments associated with: (i) mechanisms-based classifications of pain; and (ii) the identification and interpretation of individual symptoms and signs from a Delphi-derived expert consensus list of clinical criteria associated with mechanisms-based classifications of pain in patients with low back (±leg) pain disorders. The inter- and intra-examiner reliability of an examination protocol performed by two physiotherapists on two separate cohorts of 40 patients was assessed. Data were analysed using kappa and percentage of agreement values. Inter- and intra-examiner agreement associated with clinicians’ mechanisms-based classifications of low back (±leg) pain was ‘substantial’ (kappa  = 0.77; 95% confidence interval (CI): 0.57-0.96; % agreement  = 87.5) and ‘almost perfect’ (kappa  = 0.96; 95% CI: 0.92-1.00; % agreement = 92.5), respectively. Sixty-eight and 95% of items on the clinical criteria checklist demonstrated clinically acceptable (kappa ⩾ 0.61 or % agreement ⩾ 80%) inter- and intra-examiner reliability, respectively. The results of this study provide preliminary evidence supporting the reliability of clinical judgments associated with mechanisms-based classifications of pain in patients with low back (±leg) pain disorders. The reliability of mechanisms-based classifications of pain should be investigated using larger samples of patients and multiple independent examiners.

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Man Ther. 2011 Nov 8. [Epub ahead of print]

Self-reported pain severity, quality of life, disability, anxiety and depression in patients classified with ‘nociceptive’, ‘peripheral neuropathic’ and ‘central sensitisation’ pain. The discriminant validity of mechanisms-based classifications of low back (±leg) pain.

Source

St Vincent’s University Hospital, Elm Park, Dublin 4, Ireland.

Abstract

Evidence of validity is required to support the use of mechanisms-based classifications of pain clinically. The purpose of this study was to evaluate the discriminant validity of ‘nociceptive’ (NP), ‘peripheral neuropathic’ (PNP) and ‘central sensitisation’ (CSP) as mechanisms-based classifications of pain in patients with low back (±leg) pain by evaluating the extent to which patients classified in this way differ from one another according to health measures associated with various dimensions of pain. This study employed a cross-sectional, between-subjects design. Four hundred and sixty-four patients with low back (±leg) pain were assessed using a standardised assessment protocol. Clinicians classified each patient’s pain using a mechanisms-based classification approach. Patients completed a number of self-report measures associated with pain severity, health-related quality of life, functional disability, anxiety and depression. Discriminant validity was evaluated using a multivariate analysis of variance. There was a statistically significant difference between pain classifications on the combined self-report measures, (p = .001; Pillai’s Trace = .33; partial eta squared = .16). Patients classified with CSP (n = 106) reported significantly more severe pain, poorer general health-related quality of life, and greater levels of back pain-related disability, depression and anxiety compared to those classified with PNP (n = 102) and NP (n = 256). A similar pattern was found in patients with PNP compared to NP. Mechanisms-based pain classifications may reflect meaningful differences in attributes underlying the multidimensionality of pain. Further studies are required to evaluate the construct and criterion validity of mechanisms-based classifications of musculoskeletal pain.

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Pain. 2011 Jul;152(7):1511-6. Epub 2011 Mar 10.

Identifying neuropathic back and leg pain: a cross-sectional study.

Source

School of Rehabilitation Sciences, Faculty of Health and Social Care Sciences, St. George’s University of London/Kingston University, Cranmer Terrace, London SW17 0RE, UK. I.Beith@sgul.kingston.ac.uk

Abstract

Low back pain is a widespread debilitating problem with a lifetime prevalence of 80%, with the underlying pain mechanism unknown in approximately 90% of cases. We used the painDETECT neuropathic pain screening questionnaire to identify likely pain mechanisms in 343 patients with low back pain with or without leg pain in southeastern England referred for physiotherapy. We related the identified possible pain mechanisms nociceptive, unclear, and neuropathic to standardised measures of pain severity (Numeric Rating Scale), disability (Roland Morris Low Back Pain Disability Questionnaire), anxiety and depression (Hospital Anxiety and Depression Scale), and quality of life (Short Form 36 Health Survey Questionnaire Version 2). In addition, we investigated any relationship between these possible pain mechanisms and leg pain, passive straight leg raise, and magnetic resonance imaging evidence confirming or eliminating nerve root compression. A total of 59% of participants (n=204) reported likely nociceptive pain, 25% (n=85) unclear, and 16% (n=54) possible neuropathic pain. The possible neuropathic pain group reported significantly higher pain, disability, anxiety, and depression, reduced quality of life and passive straight leg raise compared to the other pain groups (P<.05). A total of 96% of participants with possible neuropathic pain reported pain radiating to the leg (76% below the knee); however, leg pain was still more common in patients with nociceptive pain, suggesting that leg pain is sensitive to, but not specific to, possible neuropathic pain. No relationship was demonstrated between possible neuropathic pain and evidence for or absence of nerve root compression on magnetic resonance imaging scans. These findings suggest possible neuropathic pain is less common in low back pain patients referred through primary care and clarifies the usefulness of clinical tests for identifying possible neuropathic pain.

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J Pain. 2011 Oct;12(10):1080-7. Epub 2011 Jul 23.

The neuropathic components of chronic low back pain: a prospective multicenter study using the DN4 Questionnaire.

Source

INSERM U 987, Centre d’Evaluation et de Traitement de la Douleur, Hôpital Ambroise Paré, APHP, Boulogne-Billancourt, France. nadine.attal@apr.aphp.fr

Abstract

The present study investigated the neuropathic components of chronic low back pain (LBP) in patients with and without lower limb pain using the DN4 questionnaire and confirmed its psychometric properties. Patients (n = 132) from 11 French multidisciplinary pain or rheumatology centers were classified by a first investigator into 4 groups derived from the Quebec Task Force Classification of Spinal Disorders (QTFSD): group 1 (pain restricted to the lumbar area); group 2 (pain radiating proximally); group 3 (pain radiating below the knee without neurologic signs); and group 4 (pain radiating towards the foot in a dermatomal distribution, with neurological signs, corresponding to typical radiculopathy). A second investigator applied the DN4 questionnaire to the lower limb (groups 2 to 4) and lower back. A comparison of groups 1 and 4 confirmed the psychometric properties of DN4 (sensitivity 80%; specificity 92%, for a cutoff of 4/10, similar to other neuropathic conditions). In the lower limb, the proportion of patients with neuropathic pain (NP) was related to the distality of pain radiation (15, 39, and 80% in groups 2, 3 and 4, respectively; P < .0001). In the lower back, the proportion of patients with NP was higher for patients with typical radicular pain compared with the other groups (P = .006). Thus, typical radiculopathy has similar characteristics as other neuropathic conditions and is confirmed as the commonest neuropathic syndrome in LBP patients. The observation that neuropathic and nociceptive components of LBP vary in the back and lower limb probably accounts for the discrepancies of reported prevalence rates of NP in LBP. As this study was essentially based on a questionnaire, future studies combining standard clinical sensory testing, specific questionnaires, and more objective assessment of the sensory lesion are now required to further investigate the neuropathic component of chronic LBP. PERSPECTIVE: This study confirms the psychometric properties of the DN4 questionnaire to assess neuropathic pain in patients with low back pain. Neuropathic mechanisms largely contribute to pain in the lower limb as compared to the back, but neuropathic pain is not restricted to typical radiculopathy. This may have significant implications for the choice of treatment strategy in these patients.

CRPS & pain – some things you may not have realised

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

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

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

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

From the book 'Explain Pain' by D Butler & L Moseley

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

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

Below are some interesting abstracts in relation to this blog:

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

Pain sensation evoked by observing injury in others.

Source

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

Abstract

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

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

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

Source

INSERM Unit 280, France.

Abstract

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

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

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

Source

Department of Psychology, Peking University, Beijing 100871, People’s Republic of China. shan@pku.edu.cn

Abstract

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

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

The cerebral signature for pain perception and its modulation.

Source

Centre for Functional Magnetic Resonance Imaging of the Brain, Clinical Neurology and Nuffield Department of Anaesthetics, Oxford University, OX3 9DU Oxford, England, UK. irene@fmrib.ox.ac.uk

Abstract

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

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

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

Source

Nuffield Department of Anaesthetics, University of Oxford, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK. kwiech@fmrib.ox.ac.uk

Abstract

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

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

Mindfulness

Mindfulness has grown in popularity over recent years, and for good reason. Those who regularly practice mindful meditation and mindfulness on a day-to-day basis will tell you about their clarity of thought, their sense of ease and their good physical health. The practice is recommended by NICE for depression as well as the frequent teaching of mindfulness as a way to deal with pain.

At the clinic, I encourage mindful practice to help the individual be released from the pull of negative and unhelpful thinking about pain. We all have thoughts. This is the action of the mind and is a normal process. Automatic thoughts pop into our head and trigger emotional and physical responses–think about a waxy, yellow lemon resting upon a plate; you take a knife and cut into the rind, releasing the citrus odour as you divide the lemon in two, the pieces rolling away from the blade; you further cut the two halves into quarter segments, each time triggering a small burst of juice into the air around; imagine taking one segment and gently placing it into the front of your mouth; what are you experiencing? Thoughts change our physiology because our brains respond to thinking or imagining, just as if we are present. This is why it can hurt when we watch someone else move their body in a way that would be painful for us.


Automatic thoughts are just that. How we respond next we can decide. By being observant of our thoughts we can avoid following an automatic thought with another thought and another that lead to persisting physiological responses and emotions that are unpleasant and unhelpful. In particular those thougths that often recur and create unease and anxiety. They are simply thoughts. They are not us and they are not reality. They are just thoughts. But, they can be powerful unless we can find a way to be observant, non-judgmental, aware and present. That ‘way’ can be mindfulness.

Here are some great people talking about mindfulness and meditation

 

There has been and continues to be a great deal of work looking at mindfulness and how it may work. The Oxford Mindfulness Centre (OMC) undertakes research and provides training.
‘The OMC Team does ground-breaking clinical and neuroscience research on mindfulness. It assesses the efficacy of different forms of mindfulness practice for different types of problem, and is building up a peer-reviewed body of knowledge about what forms of mindfulness intervention best suits which type of person.’
A list of the OMC publications is available here
For further information on our use of mindfulness for pain, please email richmond@specialistpainphysio.com

Imagery & mirrors

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

Body ownership

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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Curr Opin Anaesthesiol. 2011 Oct;24(5):524-31.

Phantom limb pain and bodily awareness: current concepts and future directions.

Source

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.

Abstract

PURPOSE OF REVIEW:

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.

RECENT FINDINGS:

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.

SUMMARY:

Ultimately, for optimal patient outcomes, treatments should be both symptom and mechanism targeted.

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J Physiol. 2011 Jun 15;589(Pt 12):3009-21. Epub 2011 Apr 26.

Proprioceptive signals contribute to the sense of body ownership.

Source

Neuroscience Research Australia, Barker Street, Randwick, Sydney, NSW 2031, Australia.

Abstract

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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Neuropsychologia. 2010 Feb;48(3):713-25. Epub 2009 Nov 11.

Crossmodal congruency measures of lateral distance effects on the rubber hand illusion.

Source

Macquarie Centre for Cognitive Science, Macquarie University, Sydney, NSW 2109, Australia. regine.zopf@maccs.mq.edu.au

Abstract

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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Neuropsychologia. 2010 Feb;48(3):703-12. Epub 2009 Oct 9.

My body in the brain: a neurocognitive model of body-ownership.

Source

Department of Psychology, Royal Holloway, University of London, Egham, Surrey, UK. manos.tsakiris@rhul.ac.uk

Abstract

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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Cereb Cortex. 2007 Oct;17(10):2235-44. Epub 2006 Nov 30.

Neural signatures of body ownership: a sensory network for bodily self-consciousness.

Source

Wellcome Department of Imaging Neuroscience, Institute of Neurology, University College London, London, UK. e.tsakiris@ucl.ac.uk

Abstract

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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Ann N Y Acad Sci. 2011 Apr;1225:72-82. doi: 10.1111/j.1749-6632.2011.05990.x.

Significance of the insula for the evolution of human awareness of feelings from the body.

Source

Atkinson Research Laboratory, Barrow Neurological Institute, Phoenix, Arizona, USA. bcraig@chw.edu

Abstract

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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Brain Struct Funct. 2010 Jun;214(5-6):563-77. Epub 2010 May 29.

The sentient self.

Source

Atkinson Research Laboratory, Barrow Neurological Institute, 350 West Thomas Rd., Phoenix, AZ 85013, USA. bcraig@chw.edu

Abstract

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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Nat Rev Neurosci. 2009 Jan;10(1):59-70.

How do you feel–now? The anterior insula and human awareness.

Source

Atkinson Research Laboratory, Barrow Neurological Institute, Phoenix, Arizona 85013, USA. bcraig@chw.edu

Abstract

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

Mastery is defined in the Oxford dictionary as:

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

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

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.

Mastering your rehabilitation – Part 1: why exercise & train?

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 (2010)

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.

Training the brain for pain

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.

CRPS medication

When I first meet a new patient who comes with CRPS, I ask about current medication use. The answers to this question vary from over the counter preparations to prescribed drugs for inflammation and neuropathic pain. For example, paracetamol, anti-inflammatories or NSAIDs (neurofen, naproxen, voltarol), opioids (tramadol, oxycodone, codeine), anti-depressants (amitriptyline, nortriptyline) and anti-convulsants (pregabalin, gabapentin). Medication has an important role to play but must be used wisely, appropriately and optimised for the pain type(s), similar to a lock and key. If the key fits the lock the door will open, in other words when the drug attaches itself to the target receptor there will be action but if it does not match there will not be an effect.

Specialist Pain Physio - CRPS London

Gabapentin

There can be different pain mechanisms at the root of the CRPS symptoms. Commonly we see neuropathic pain and inflammatory pain, the latter often due to neurogenic inflammatory mechanisms when the nerves themselves release chemicals–substance P and CGRP–into the tissues that they supply, triggering inflammation. In this case, your doctor could prescribe medication for neuropathic pain such as gabapentin alongside an anti-inflammatory drug.

I believe in a model of care that is inclusive of appropriate physiotherapy, pain medicine and psychology, working together to provide a psychosocial programme of care. Not everyone will require input from all three disciplines, but this model as a start point means that all aspects of the condition and the effects are considered. Further, these disciplines must be providing care that is based upon the latest thinking and science of both pain and CRPS. As a physiotherapist specialising in chronic pain and conditions such as CRPS, I have ensured that those I work with are dedicated to the contemporary provision of treatment. Therefore, returning to the issue of appropriate and effective medication use, when I ask about the drugs and their effect, it is so I can see whether a review is required to optimise the overall programme of treatment. In the case that I feel the medication is not being optimised, I will recommend that you see one of the pain specialists whom I know will be able to advise you on the most appropriate drug for your current state and how best to use it within the programme.

Briefly, I think it is important to point out that I do not prescribe or change patient’s medication. This is the job of your doctor or consultant. If you do not have a nominated doctor or specialist who is looking after your medication use, I will gladly recommend one who can help you.