Tag Archives: neuroscience

17Dec/13

A quick note on brain~body — body~brain

A quick word, Brain, chronic back pain, Chronic pain, Neuroscience, Pain, Pain and brain, Pain Education, Pain philosophy, Philosophy, Stress, , , , , ,

The brain is where it’s at. Or so it seems if you read the press or look at the bookshelves. The notion that brain is everything has been challenged recently and so it should — see here. We need enquiry at every point, challenging the comfort of thinking that we know.

Despite this, it seems logical to think that the brain is involved with much of our existence. The ‘hows’ and ‘whys’ need continued clarification. In a crude sense, on the end of our brain lies a body. This body is where we feel life whether that be the experience of an external stimulus such as touch or the result of a thought that always triggers a physical and emotional response once we engage with that thought.

The term ‘body-mind’ has been used countless times by both mainstream practitioners of medicine and health and alternative or complimentary therapists. Most people understand the concept although many still try to deny the links. Can a thought really change the physiology in my body? Of course it can. It happens all the time. In fact, I would argue that our body functioning is the emergent physical manifestation of all the processing going on in the mind.

The way in which we move, posture, position ourselves is dependent upon the task at hand but also the task that we may engage with at some point in the near future. The brain is the greatest predictor and will continually analyse the environment, the situation and compare this to what it knows to create the actions necessary. In cases of chronic pain or stress, the brain becomes hypervigilant and responsive to a range of cues that would not normally evoke a protective response but now does via the the autonomic nervous system (‘fright or flight’), the nervous and immune systems.

Much of the activity in our body systems we are unaware of as the brain and reflexive activity takes care so we can attend to the necessary survival tasks. Filtering out the millions of stimuli, the brain draws our attention to what is deemed to be salient for that moment.

In a state of anxiety, this is usually felt in the body — churning stomach, tension, sweaty palms etc. We use the body as a yardstick as to how we are feeling although the thoughts evoking these bodily and physiological responses are not always immediately apparent. The thoughts will eventually pop in there, or emerge, this from an unspecified network of neurons in the brain.

In essence, we can think about the body~brain or brain~body relationship as a needy one; they need each other for full function. To separate makes no sense bit neither does to blame one or the other. Thinking about the emergent features of the synchrony appears to provide a better way of considering problems such as pain, stress and other conditions.

RS — Specialist Pain Physio Clinics, London 

23Oct/13

The dark side — the brain’s creations

Brain, Chronic pain, Lorimer Moseley, Neuroscience, Pain, , , ,

The popular press is awash with neuroscience, now to the point that some authors are becoming ‘anti’. We need debate, so hats off to those contributors who rightly ask questions. We should never sit back and accept a ‘fact’ but instead, test, test, test. Despite this fresh discussion, we do accept that the brain has a great deal to do with our experiences of life.

A single centre for consciousness has not been identified in the brain and is not likely to be discovered. Instead, our unique sensory and emotional experiences are created by vast, interconnected networks of brain cells, maintained and influenced by immune cells that populate the brain and spinal cord. The pain matrix theory of Ron Melzack is a great example of such a functioning network. From these networks emerge feelings, thoughts, movements, senses and pain to name but a few. Where we actually experience these emergent properties can vary enormously, although one could argue that the role of the brain is to create the most biologically appropriate experience for that given moment and context.

Recently, Mick Thacker and Lorimer Moseley wrote a brief paper discussing the idea that pain is emergent. This is a relevant and sensible calling upon philosophy to help us explain pain to patients at a time when there has been a trend to suggest that the brain is at fault. Indeed we need a brain to feel pain — see Lorimer talk here — just as we need a brain to see and hear, but how helpful is this to the patient with back pain? Even if they grasp the concept of the pain neuromatrix, to suggest that the pain is coming from the brain can be a challenging leap. Preferable is the explanation that pain emerges from the body but there is a significant part played by a widespread web of neurons and immune cells in the brain and spinal cord; this requiring a careful description to give meaning to the individual.

To take this a stage further, one could argue that a depressed state underpinned by ruminating thoughts is emergent from a network of neurons within the brain, yet often felt deep within the body in a multitude of unique ways––visceral. The heaviness of thought is usually reflected within the physical self via posturing, movement and gut instinct. Our minds that exist within the brain networks––who knows where––stream with thoughts that are occasionally useful, frequently the same, and always driving bodily responses. The brain does not discriminate between thinking about being somewhere and actually being there; a similar response ensues. This can be wonderful if the memory or thought cultivates the tape of a happy time. How often does this happen in comparison to a train of worrying or troubling thoughts? Especially if one’s mood is low, the impact of a negative situation or comment is far greater. This is the dark side of the brain’s creation of our multisensory experience; seeing, hearing, feeling, thinking.

The depths to which one can slip or drop are seemingly endless. It does appear modern life is contributing to this endlessness as the figures on depression rise. Perhaps it is the expectation that we should be happy, with all the convenience of immediate service and advancing knowledge, yet there is greater striving for this state. Bookshelves are packed with self-help books, Facebook and Twitter saturated with quotations about how to think positively, and the growing industry that is life coaching all pay homage to the fact that we are not achieving as ‘alchemists of joy’.

Where neuroscience can make a contribution is to give us the understanding of the mechanisms that can be translated into practical tools for everyone. There have been numerous steps in the right direction with some great discoveries that inform; for example: the similarities of physical and social pain (e.g. rejection, isolation), neuroplasticity, the way in which immune cells prune synapses, communication between the gut and the brain, and mirror neurons (a deliberately provocative inclusion — see here) to name but a few.

The idea that experiences are emergent from a neuronal network influenced by many factors including epigenetics (the blend of genetics and experience), is a very credible way of thinking about how we can re-shape our thinking, feeling selves. The basic neuroplastic characteristic of our neuroimmune system, or the ability to learn, means that by creating the right conditions with the right understanding and individualised strategies based upon fact, we can cultivate change. This does not preclude the use of medication or other medical interventions but this alongside sensible and wise action based on sound science to move us into the light.

** Please note that this is not an exhaustive discussion of either depression or neuroscience but rather an observation. I am aware that this may trigger thinking and discussion that are both welcome in the hope of advancement.

Specialist treatment, training and coaching for persisting pain, chronic pain and injury in London – call for appointments 07932 689081

 

21Oct/13

How do you know where you are? | Neil Burgess speaks

Chronic pain, Memory, Motor Imagery, Neuroscience, Rehabilitation, , , ,

It is useful to know where you are. Neil Burgess spends his time studying this important function by looking at the brain, the hippocampus to be specific.

It would appear that the same brain cells that create our sense of where we are and recalling that information for practical use are also at play when we imagine movement, such as a motor imagery task for a painful condition.

15May/13

Neuro……

Flourish, Neuroleadership, Wellness, ,

There is a growing trend to ‘neuroscience-up’ as a way of powering information and concepts. This is no bad thing as it means that current research is being applied to enhance our understanding of who we are, what we do, why we do it and how we can best go about it. Certainly in the world of business the concept of neuroleadership has emerged as a force. The notion can also be used to optimise the self and achieve healthy aims.

Neuroscience for leadership, decision making, performance & health

Employing the notion of neuroscience in health means that we can understand the functioning and interaction between the body systems (nervous, immune, endocrine, autonomic etc), cognitions and emotions. From there, healthy strategies evolve, pointing our natural compass towards wellness. This of course can include how we function as work, developing clarity of thought and resilience in the face of problems that emerge.

Understanding how we can use the body as a yardstick of wellness, for example noting the sensations as a way of detecting a threat, in one of many ways of ‘neuro-self-regulation’ (I just made that term up – it shows how easy it is to ne neuro). We can feel ‘tingling’ in the stomach which is noted as anxiety. Then we need to work out why we are anxious and this may be obvious or may require some thought. This is ironic as anxiety stems from thinking about something that is potentially threatening, albeit on many occasions it emerges from subconscious activity, becoming conscious when we need to attend to the matter. This is ‘self neuroleadership’ – the development of your own toolbox, facilitating a flourishing and flowing lifestyle at home, work and play.

Learn about the science of stress and how to tackle it

Good quality education that is delivered in a way that brains can absorb, process and apply is a further example. Creating the right environment, atmosphere, delivery approach and range of tasks will impact upon the outcomes.

In summary, the neuro-revolution is an important step forward. The science is moving on and we can follow the developments to employ in health and business, and where the two meet. Of course we must look at the science with a critical eye and check the robustness of the data, ensuring we understand the messages before imparting them in an education arena.

Exciting times. Neuro times! (and immune, endocrine, autonomic….)

For further information about the use of neuro in health and business, call us now: 07932 689081 or email: [email protected]

 

11Jul/12

Cervical Dystonia | What can we do?

Cervical Dystonia, Dystonia, Research, Treatments, , , , ,

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

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

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

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

Modern physiotherapy for cervical dystonia at the Specialist Pain Physio Clinics

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

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

Call for appointments: 07518 445493

**********

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

Recent research papers

Behav Neurol. 2012 May 24.

Cervical dystonia: From pathophysiology to pharmacotherapy.

Patel S, Martino D.

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.

********

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.

********

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.

11Feb/12

Manual therapy, pain and the immune system

Back pain, Chronic low back pain, Chronic pain, Complex regional pain syndrome, Joint pain, Low back pain, Neuropathic pain, Pain, Pain Education, Research, Treatments, , , , , , ,

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.

_____

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

Chronic pain, Fibromyalgia, Functional Pain Syndromes, Joint pain, Neuropathic pain, Neuroscience, Osteoarthritis, Pain, Pain Education, Pelvic Pain, Research, Treatments, , , , , , ,

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.

********

 

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.

18Jan/12

Contemporary understanding of factors in joint pain

Chronic pain, Joint pain, Neuroscience, Osteoarthritis, Pain, Pain Education, Research, Understanding pain, , , , ,

Recent research has identified biological reasons for joint pain in arthritis:

  • Interleukin-6, a pro-inflammatory cytokine released both locally at the joint and in the spinal cord, consequently plays a role in the widespread nature of the pain via its role in central sensitisation.
  • Sprouting of sensory and sympathetic fibres at the joint may well have a role in sensitisation
  • Angiogenesis, the growth of new blood vessels, at the joint, perhaps having a role in inflammation

Some of this may sound familiar. IL-6 is known to play a role in the spinal cord following nerve injury, sprouting of the sympathetic fibres at the DRG and in tendinopathy, and angiogenesis also seen in tendinopathy. All are clearly responses by the body and are involved in pain–remembering that pain is a brain experience 100% of the time of course.

Spinal interleukin-6 is an amplifier of arthritic pain (Vazquez et al. 2011)

Objective.

Significant joint pain is usually widespread beyond the afflicted joint which results from the sensitization of nociceptive neurons in the central nervous system (central sensitization). In the present study we explored (a) whether the proinflammatory cytokine interleukin-6 (IL-6) in the joint induces central sensitization, (b) whether joint inflammation causes IL-6 release in the spinal cord, and (c) whether spinal IL-6 contributes to central sensitization.

Methods.

In anesthetized rats electrophysiological recordings were made from spinal cord neurons with sensory input from the knee joint. Neuronal responses to mechanical stimulation of the knee and the leg were monitored. IL-6 and its soluble receptor sIL-6R were applied to the knee joint or the spinal cord. Spinal release of IL-6 was measured by ELISA. Sgp130 which neutralizes IL-6/sIL-6R was spinally applied during development of joint inflammation or during established inflammation.

Results.

A single injection of IL-6/sIL-6R into the knee joint as well as spinal application of IL-6/sIL-6R significantly increased the responses of spinal neurons to mechanical stimulation of the knee and ankle joint, i.e. induced central sensitization. Spinally applied sgp130 attenuated this IL-6 effect. Development of knee inflammation caused spinal release of IL-6. Spinal application of spg130 attenuated the development of inflammation-evoked central sensitization but did not reverse it.

Conclusions.

Not only IL-6 in the joint is involved in the generation of joint pain but also IL-6 which is released in the spinal cord. Spinal IL-6 contributes to central sensitization and thus promotes the widespread hyperalgesia in the course of joint disease.

********

Neuroplasticity of sensory and sympathetic nerve fibers in the painful arthritic joint (Ghilardi et al. 2011)

Objective.

Many forms of arthritis are accompanied by significant chronic joint pain. Here we studied whether there is significant sprouting of sensory and sympathetic nerve fibers in the painful arthritic knee joint and whether nerve growth factor (NGF) drives this pathological reorganization.

Methods.

A painful arthritic knee joint was produced by injection of complete Freund’s adjuvant (CFA) into the knee joint of young adult mice. CFA-injected mice were then treated systemically with vehicle or anti-NGF antibody. Pain behaviors were assessed and at 28 days following the initial CFA injection, the knee joints were processed for immunohistochemistry using antibodies raised against calcitonin gene-related peptide (CGRP; sensory nerve fibers), neurofilament 200 kDa (NF200; sensory nerve fibers), growth associated protein-43 (GAP43; sprouted nerve fibers), tyrosine hydroxylase (TH; sympathetic nerve fibers), CD31 (endothelial cells) or CD68 (monocytes/macrophages).

Results.

In CFA-injected mice, but not vehicle-injected mice, there was a significant increase in the density of CD68+ macrophages, CD31+ blood vessels, CGRP+, NF200+, GAP43+, and TH+ nerve fibers in the synovium as well as joint pain-related behaviors. Administration of anti-NGF reduced these pain-related behaviors and the ectopic sprouting of nerve fibers, but had no significant effect on the increase in density of CD31+ blood vessels or CD68+ macrophages.

Conclusions.

Ectopic sprouting of sensory and sympathetic nerve fibers occurs in the painful arthritic joint and may be involved in the generation and maintenance of arthritic pain.

********

Contributions of angiogenesis to inflammation, joint damage, and pain in a rat model of osteoarthritis (Ashraf et al. 2011)

Objective

To determine the contributions of angiogenesis to inflammation, joint damage, and pain behavior in a rat meniscal transection model of osteoarthritis (OA).

Methods

OA was induced in male Lewis rats (n = 8 per group) by meniscal transection. Animals were orally dosed with dexamethasone (0.1 mg/kg/day), indomethacin (2 mg/kg/day), or the specific angiogenesis inhibitor PPI-2458 (5 mg/kg every other day). Controls consisted of naive and vehicle-treated rats. Synovial inflammation was measured as the macrophage fractional area (expressed as the percentage), thickness of the synovial lining, and joint swelling. Synovial angiogenesis was measured using the endothelial cell proliferation index and vascular density. Channels positive for vessels at the osteochondral junction were assessed (osteochondral angiogenesis). Medial tibial plateaus were assessed for chondropathy, osteophytosis, and channels crossing the osteochondral junction. Pain behavior was measured as weight-bearing asymmetry.

Results

Dexamethasone and indomethacin each reduced pain behavior, synovial inflammation, and synovial angiogenesis 35 days after meniscal transection. Dexamethasone reduced, but indomethacin had no significant effect on, the total joint damage score. PPI-2458 treatment reduced synovial and osteochondral angiogenesis, synovial inflammation, joint damage, and pain behavior.

Conclusion

Our findings indicate that synovial inflammation and joint damage are closely associated with pain behavior in the meniscal transection model of OA. Inhibition of angiogenesis may reduce pain behavior both by reducing synovitis and by preventing structural change. Targeting angiogenesis could therefore prove useful in reducing pain and structural damage in OA.

18Jan/12

Pain – some things you may not have realised

Neuroscience, Pain, Pain Education, Pain Psychology, Rehabilitation, Treatments, Understanding pain, , , ,

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.

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 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.

Osborn J, Derbyshire SW.

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.

********

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

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

Lamm C, Batson CD, Decety J.

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.

********

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

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

Han S, Fan Y, Xu X, Qin J, Wu B, Wang X, Aglioti SM, Mao L.

Source

Department of Psychology, Peking University, Beijing 100871, People’s Republic of China. [email protected]

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.

********

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

The cerebral signature for pain perception and its modulation.

Tracey I, Mantyh PW.

Source

Centre for Functional Magnetic Resonance Imaging of the Brain, Clinical Neurology and Nuffield Department of Anaesthetics, Oxford University, OX3 9DU Oxford, England, UK. [email protected]

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.

********

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

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

Wiech K, Tracey I.

Source

Nuffield Department of Anaesthetics, University of Oxford, John Radcliffe Hospital, Headley Way, Oxford OX3 9DU, UK. [email protected]

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.

********

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.

09Dec/11

Mindfulness

Mindfulness, Neuroscience, Pain, Pain Education, Stress, Treatments, , , , , , , , , , ,

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 [email protected]